What Disease was Plague? On the Controversy over the Microbiological Identity of Plague Epidemics of the Past (Brill's Series in the History of the Environment)

What Disease was Plague?

Brill’s Series in the History of the Environment General Editor

Aleks Pluskowski, University of Reading

VOLUME 2

What Disease was Plague? On the Controversy over the Microbiological Identity of Plague Epidemics of the Past

By

Ole J. Benedictow

LEIDEN • BOSTON 2010

On the cover: “La peste.” From “Annales de Gilles le Muisit,” Tournai, 1353. Ms. 13076/77 f. 24v Katalog Parler 3, S. 73. Bibliotheque Royale Albert I., Brussels, Belgium. This book is printed on acid-free paper. Library of Congress Cataloging-in-Publication Data Benedictow, Ole Jørgen. What disease was plague? : on the controversy over the microbiological identity of plague epidemics of the past / by Ole J. Benedictow. p. ; cm. -- (Brill’s series in the history of the environment, ISSN 1876-6595 ; v. 2) Includes bibliographical references and index. ISBN 978-90-04-18002-4 (hardback : alk. paper) 1. Plague--Microbiology. 2. Plague-Epidemiology. 3. Plague--History. 4. Communicable diseases--History. I. Title. II. Series: Brill’s series in the history of the environment ; v. 2. 1876-6595 [DNLM: 1. Plague--microbiology. 2. Plague--epidemiology. 3. Plague--history. WC 355] R172.B47 2010 614.5’732--dc22 2010030516

ISSN 1876-6595 ISBN 978 90 04 18002 4 Copyright 2010 by Koninklijke Brill NV, Leiden, The Netherlands. Koninklijke Brill NV incorporates the imprints BRILL, Hotei Publishing, IDC Publishers, Martinus Nijhoff Publishers and VSP. All rights reserved. No part of this publication may be reproduced, translated, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying, recording or otherwise, without prior written permission from the publisher. Authorization to photocopy items for internal or personal use is granted by Brill provided that the appropriate fees are paid directly to The Copyright Clearance Center, 222 Rosewood Drive, Suite 910, Danvers, MA 01923, USA. Fees are subject to change.

For my sons Andreas and Tancred

CONTENTS List of Figures and Tables ........................................................................xiii Preface ......................................................................................................... xv PART ONE

THE ISSUE 1. The Issue and the Problems .................................................................. 3 Introduction............................................................................................ 3 The Human-Flea Theory of Plague Epidemiology ............................ 9 The Revisionists ....................................................................................16 PART TWO

HOW S.K. COHN MAKES PHYSICIANS AND HISTORIANS “SQUARE THE CIRCLE” 2. The Ethics of Scholarly Work .............................................................25 Introduction..........................................................................................25 How Cohn Makes Medical Scientists “Square the Circle” ..............26 Hankin 1: Cohn’s Attack on Hankin’s Observation of Inverse Correlation between Mortality and Population Density ............34 Hankin 2: A Brief Study of Cohn’s Technique of Argument ..........38 “The Ugly Americans” .........................................................................44 Cohn’s Accusations of Racism against J. Ashburton Thompson and L.F. Hirst ................................................................46 How Cohn Makes “Historians Square the Circle” ...........................54 The Attack on Schofield (and Benedictow and L. Bradley) ............62 PART THREE

BASIC CONDITIONS FOR BUBONIC PLAGUE IN MEDIEVAL EUROPE 3. Rats.........................................................................................................73 Introduction: How to Study Rats in History ....................................73 The Nature of Rats and the Frame of Reference of the Medieval Mind .................................................................................78

viii

contents

The Question of the Presence of Rats and the Methodological Fallacy of Inference ex silentio ......................... 85 Ars Moriendi Rattorum: Where Have all the Dead Rats Gone? ........................................................................................91 Zoobiological and Zoogeographical Arguments on the Question of Significant Presence of Black Rats in Medieval Europe ..............................................................................98 The Significance of Evolutionary Theory and Adaptation by Selection.....................................................................................116 Rat Bones: Material Evidence of the Presence of Rats in the Middle Ages .............................................................................122 Sociology of Rat-Based Plague .........................................................142 4. The Spread of Bubonic Plague over Distances ...............................151 Contiguous Spread and Metastatic Spread .....................................151 5. Mortality in India ...............................................................................194 Effects of the Anti-epidemic Efforts by British Colonial Authorities ......................................................................194 6. Was Historical Plague a Viral or Bacterial Disease? The Question of Immunity .......................................................................205 Introduction........................................................................................205 Re-infection or Immunity? ...............................................................212 Did Plague Become a Child Disease after the Black Death? ........218 Plague according to Social Class, Age and Gender .......................235 A Demographic Case Study: The Necrology of the Monastery of San Domenico in Camporegio ............................245 The Real Problem and its Solution: Marriage Rates and Fertility Rates after the Black Death ....................................268 PART FOUR

DEFINING FEATURES Introduction: Concept of Defining Feature ....................................277 7. Defining Feature 1: Latency Periods ................................................279 8. Defining Feature 2: Inverse Correlation between Mortality Rate and Population Density ........................................................289

contents

ix

Introduction ......................................................................................289 More Data on the Inverse Correlation in India and Historical Europe..........................................................................291 Scott and Duncan and the Correlation between Population Density and Mortality ..................................................................301 Epilogue: Sweating Sickness and the Inverse Correlation ..........311 9. Defining Feature 3: Buboes as a Normal Clinical Feature in Epidemics ...................................................................312 General Introduction.......................................................................312 Contemporary Notions and Observations of Buboes (and Associated Secondary Clinical Manifestations) .............322 Scott and Duncan: The Problem of Buboes ..................................334 Cohn: The Problem of Buboes .......................................................340 Cohn and Boccaccio: Buboes, Pustules and Spots ......................359 10. Defining Feature 4: DNA of Yersinia pestis from Plague Graves ...............................................................................381 11. Defining Feature 5: Seasonality of Bubonic Plague .....................396 Introduction: Bubonic Plague’s Association with Moderately Warm Temperatures and Seasons .........................396 Seasonality of Historical Bubonic-Plague Epidemics with Emphasis on the Transseasonal Form ..............................398 The Seasonality of Plague and Mortality in England 1340–1666.................................................................420 Duration of Vacancies in Parish Benefices during the Black Death ...................................................................................436 Temporal Relationship between the Territorial Spread of the Black Death and Increase in Institutions .......................463 Summary and Conclusion ..............................................................482 PART FIVE

THE ALTERNATIVE THEORIES Introduction: The History and Essence of the Alternative Theories ....................................................................487 12. The Beginning: The Alternative Theories of Shrewsbury and Morris ....................................................................................489

x

contents Shrewsbury: the Composite, Low-Intensity Theory ....................489 Morris: The Primary Pneumonic Theory......................................491

13. Gunnar Karlsson’s Alternative Theory: That Historical Plague was Pure Epidemics of Primary Pneumonic Plague ...............493 Introduction ......................................................................................493 Karlsson and Benedictow ................................................................495 Could Plague Have Come to Iceland from Anywhere? ..............502 Pure Epidemics of Primary Pneumonic Plague: Fact or Fiction? .....................................................................................511 Primary Pneumonic Plague in Manchuria: A Model for Iceland? ...................................................................................514 The Spontaneous Decline of Epidemics of Primary Pneumonic Plague .......................................................................518 The Icelandic Climatic Theory of Primary Pneumonic Plague .......................................................................528 Mortality Rate of the Purported Plague Epidemics in Iceland.......................................................................................530 Summary: Why There Never Was a Plague Epidemic in Iceland.......................................................................................533 Was the Black Death in Bergen (Norway) 1349 Primary Pneumonic Plague? .....................................................................536 Summary and Conclusion ..............................................................550 14. Twigg’s Alternative Theory .............................................................553 Introduction ......................................................................................553 The Alternative Theory of Anthrax................................................555 The Historical Basis: The Use of Obsolete and Peripheral Studies .................................................................560 The Telluric-Miasmatic Theory of Anthrax ..................................562 The Pace of Spread of Plague ..........................................................566 Anthrax and the Name Black Death ..............................................571 Anthrax’s Historical Association with Other Epizootics among Domestic Animals and Plague ......................................574 The Black Death’s Origin and Spread and the Anthrax Theory ................................................................................580 Twigg’s Demographic Argument ...................................................595 Concluding Remarks .......................................................................608

contents

xi

15. The Alternative Theory of Scott and Duncan...............................610 Introduction ......................................................................................610 Disparaging Views of Historians and Physicians: Motive and Objective................................................................................611 The Material Scholarly Basis of Scott and Duncan’s Alternative Theory .......................................................................615 The Demography of Historical Plague ..........................................628 The Reed-Frost Theory of Epidemiology ......................................633 The Filoviridal Theory of Historical Plague: A Study in Academic Fiction .........................................................................636 The Significance of Autopsies .........................................................653 The African Confinement ...............................................................661 Summary and Conclusion ..............................................................662 16. Cohn’s Alternative Theory ..............................................................664 Epilogue ....................................................................................................673 Appendix 1 Black Death Mortality in Siena: The Material Provided by the Necrology of the Monastery of San Domenico in Camporegio and Summarized in Table 5 .....................................................675 Appendix 2 The Accounts of the Icelandic Epidemics of 1402–4 and 1494–5 Given in Icelandic Annals ............680 Appendix 3 The Extrinsic Incubation Period and the Structure and Composition of the Latency Period ........................682 Glossary ....................................................................................................688 Bibliography .............................................................................................693 Index of Subjects......................................................................................717 Index of Geographical Names and People ...........................................730 Index of Names ........................................................................................740

LIST OF FIGURES AND TABLES Map 1. Spread of the Black Death in the Old World, 1346–53 ..................... 2 Figures 1. Population density and morbidity (epidemics of plague).............297 2. Plague in Bergen 1565–6. Mortality in the Cathedral’s parish ...............................................................................................408 Tables 1. Life table, model south, level 3: life expectancy and mortality at various ages in a population of females with life expectancy at birth (eo) of 25 years ..............................230 2. Interments by month and week in the Dominican cemetery in Siena in 1348 .............................................................249 3. Interments by month and week in the Dominican cemetery in Siena in 1363 .............................................................250 4. Proportion of child burials in the cemetery of Camporegio in Siena, 1337–78 ...........................................................................254 5. Proportion of child and female burials registered in the necrology of the Dominican cemetery in Siena, 1337–78........258 6. Microbiological identifications of Yersinia pestis: year of publication, time of epidemic(s), and localities .........................390 7. Plague in Bergen 1565–6. Mortality in the Cathedral’s parish ...............................................................................................406 8. Percentage of mortality July–October 1340–500 among English tenants-in-chiefs ..............................................................423

PREFACE Den som vill mitt fotspor fylgje Lær’kje a blidom hjarta. Olav Åsteson

This monograph is not a work of intellectual love and joy, but of scholarly duty. I consider it a duty to examine and repudiate some alternative theories of the microbiological and epidemiological nature of historical plague epidemics. I do so not only because I consider that they are methodologically and factually grossly flawed, but also because they misrepresent the life work of a large number of fine and dedicated medical and historical scholars, many of whom cannot rise from their graves to defend themselves. Against this backdrop, it cannot come as a surprise that I believe that this monograph will provide substantial material for discussion of the ethics of scholarly investigation. I also believe that parts will be useful for the teaching of the basic tenets of the methodology of social science and history. Thus, only very reluctantly have I embarked on writing this monograph, and only because I consider it absolutely necessary and an ethical duty. In the great medieval Norwegian visionary poem the Dream Lay the narrator Olav Åsteson, after having visited hell and a part of paradise in his great dream, warns his audience that “those who follow in my footsteps will not laugh from joy in their hearts.” Long ago, in the autumn term of 1967, I studied late medieval Russian history at the University of Moscow after having received a scholarship from the Norwegian Ministry of Foreign Affairs. The opportunity of meeting Russian scholars and students made a lasting impression on me, not least their icy black humour conveyed in anecdotes that reflected the life of scholars who had endured the not-so-distant years of Stalinist terror. T.D. Lysenko, the fraudulent biologist of Stalinist theory, was not dismissed from his post until 1965. During my work on this monograph, one of these anecdotes repeatedly came to mind: Professor Tarakanov [i.e., “Cockroachson”] carried out a research project on cockroaches. He took a cockroach from his box of healthy and agile specimens, tore off a pair of legs, put it down on the table and screamed at it at the top of his voice: “Run! Run!” And the cockroach crawled across the table as

xvi

preface

best it could. When it reached the end of the table, the researcher grabbed it, tore off another pair of legs, put it down and screamed at it again: “Run! Run!” And the desperate cockroach actually managed to move across the table. However, at the end of the table the researcher grabbed it again, tore off its last pair of legs, put it down on the table and screamed: “Run! Run!” But this time the cockroach did not move. The researcher noted his conclusion in the project’s notebook: “With this experiment, I have proved that cockroaches are animals with their hearing organs on their legs.” However, in upbeat moments I entertain the hope that the medical and historical plague research brought together in this monograph will make it more difficult to launch misguided alternative theories in the future. I also hope that any new alternative theories will take into account the actual tenets of earlier scholars and the latest data of plague research. OJB

PART ONE

THE ISSUE

Map 1. Spread of the Black Death in the Old World, 1346–53

CHAPTER ONE

THE ISSUE AND THE PROBLEMS Introduction Most of our knowledge of bubonic plague was established by medical scholars and entomologists, often organized in research teams who studied the great wave of plague epidemics in China, India, Indonesia, Madagascar, and elsewhere in the period c. 1894–1940, the so-called third pandemic (the early medieval or Justinianic pandemic of 541–766 being the first, and the late medieval and early modern pandemic of 1346–1722 being the second). Much valuable research has also been performed in Russia/Soviet Union and the U.S.A, both with respect to laboratory work and field studies and on endemic cases of plague. Recently, during the Vietnam War, American military physicians found themselves in the midst of the last large epidemics of bubonic plague and produced a number of valuable studies on epidemic plague. Prior to this, at the end of the nineteenth century and in the early decades of the twentieth century, medical scholars from various countries had the opportunity to study epidemics of bubonic plague under various cultural and climatic circumstances. They all reached the conclusion that bubonic plague among human beings was caused by an epizootic among black rats and was spread from these rodents to human beings by their fleas. This is still the prevailing opinion: the World Health Organization (WHO) and Centers for Disease Control (CDC), the leading international organizations in the combat against communicable diseases, are entirely clear on their internet home pages that bubonic plague (for all practical purposes) is rat(-flea)-borne plague.1 Many of the scholars who studied modern plague epidemics in India, China, Madagascar and elsewhere also took a keen interest in the history of plague, especially W.J. Simpson, G. Sticker, M. Greenwood and W.G. Liston of the Indian Plague Research Commission, and W.P. McArthur, L.F. Hirst, R. Pollitzer, J.J. van Loghem, and Wu Lien-Teh.

1

www.who.int/inf, under Global Alert and Response (GAR); www.cdc.gov.

4

chapter one

They produced a number of very fine works which are indispensable for all serious scholars of plague-related research.2 They all concluded that the disease they studied had such close medical, clinical and epidemiological resemblances to the historical plague epidemics that these epidemics must at least mainly have been the same disease.3 The fact that they reached much the same conclusion corroborated their findings. These outstanding scholars who served so valiantly in front-line combat against bubonic plague reached and maintained this conclusion, although they noted that historical sources rarely mention significant mortality among rats.4 As will be shown below, contrary to the impression provided by modern critics, they argued their case with empirical evidence, explaining why this should be the case. In recent decades, this view on the (predominant) identity of modern bubonic plague and historical plague has been challenged by several scholars who have presented alternative theories of the microbiological nature of historical plague and the mechanisms and dynamics of epidemic spread. According to the standard works on bubonic plague, this disease is characterized by a complex clinical and epidemiological panorama. A simplified presentation sufficient for understanding the characteristic manifestations and functions of plague disease and the comparative aspects of the alternative theories of historical plague is given here, beginning with a brief outline of the central epidemiological aspects, which is followed by a similarly brief outline of the main clinical features. Plague is caused by a bacterium called Yersinia pestis. Basically, plague is a disease among rodents, a zootic disease, transmitted by fleas. This means that the terms “enzootic,” meaning sporadic incidence of disease among animals, and “epizootic,” meaning significant incidence of spread of a disease among animals, are usual and useful concepts for many parts of the discussion. These terms correspond to endemic and epidemic incidence of disease among human beings. Bubonic plague. Plague contagion is mainly transmitted to human beings by the normal fleas of the house or black rat Rattus rattus, 2 See especially Hirst 1953, Pollitzer 1954, Wu Lien-Teh 1926, Wu, Chun, Pollitzer et al. 1936. 3 Simpson 1905: 1–39; Hankin 1905: 56–8; Sticker 1908; Greenwood, IPRC 1911b, Appendix: 93–6; Liston 1924: 900–3. McArthur 1925–6: 355–72; Wu Lien-Teh 1926: 1–9; Wu Lien-Teh 1936a: 1–55; Hirst 1953: 1–100, 121–6; Pollitzer 1954: 13, 37, 102–3, 427; Van Loghem 1918. 4 See the standard works on plague of Hirst 1953: 121–35; Pollitzer 1954: 297; Wu Lien-Teh 1936a: 8–9.

the issue and the problems

5

specifically the species Xenopsylla cheopis. Central to the process of transmission and dissemination of plague is the phenomenon of blockage in fleas. When fleas ingest blood with sufficient numbers of bacteria, i.e. a sufficient level of septicaemia, the bacteria will proliferate faster in the stomach system than they are passed through the digestive canal and will eventually form (more or less) a blockage consisting of bacteria and blood mass. This means that when a blocked flea attempts to feed, the ingested blood will hit the blockage and be forced back or regurgitated into the bite wound, taking with it small bits of the blockage containing thousands of plague bacteria. This is the only way that fleas can transmit infectious doses of plague contagion to human beings. Blocked fleas will discharge this contagion at a subcutaneous level suitable for being handled by the body’s first-line defence, the lymphatic system, and the contagion is drained through a lymphatic vein to a lymph node which as a result of the infection swells, producing the characteristic bubo which is the reason the disease is designated bubonic plague. This form is called primary bubonic plague. Because human fleas are bloodsucking insects, they can become contaminated with plague bacteria ingested with septicaemic blood, i.e., blood from patients with plague bacteria in their blood, and could hypothetically become infective and transmit plague bacteria to other persons when they feed again. However, it has been clearly shown that in about half of plague cases human beings develop either insignificant or only slight and transient septicaemia, and that in the other half of cases they do not develop sufficient levels of septicaemia, except perhaps in exceptional cases, to produce (sufficient) blockage of the fleas’ ventricular system which alone makes fleas infective. The incidence of septicaemia is much higher in rats and the level of septicaemia is generally 500–1000 times higher than in humans. This is the reason that rat fleas so often become grossly infected, and since Xenopsylla cheopis also has a particular natural biological propensity for it, develops blockage far more easily and often than any other species of flea. These are two of the main conditions which make these fleas the preeminent vector of plague to human beings and why interhuman cross-infection by human fleas between cases of bubonic plague has not been observed and must be an improbable occurrence.5

5 Wu Lien-Teh 1926: 184–7; Bibikova and Klassovskiy 1974: 110–2. See also Girard 1943: 4–41; Pollitzer 1954: 482–4; Benedictow 1993/1996: 228–64. A brief summary can be found in Benedictow 2004: 11–7.

6

chapter one

All of the above-mentioned leading scholars and researchers of bubonic plague agree on the epidemiological mechanisms and structures governing the spread of bubonic plague. The two main forms are contiguous spread by contact between rat colonies and metastatic spread by the movement mainly of rat fleas, but also of infected rats, by human agency in clothing, luggage or merchandise, which is by far the most important form. The last method of spread is denied by all advocates of alternative theories despite massive empirical documentation in primary studies as well as broad presentation in all standard works, and this denial therefore constitutes a denial of fact. This point will be presented in great detail in chapter 4.6 The fact that bubonic plague has its basis in black rats and their rat fleas gives the disease a characteristic pattern of development. When an infective rat flea of the usual species Xenopsylla cheopis has been introduced into a rat colony, it takes ten to fourteen days before the rat colony has become so decimated that it becomes difficult for the great numbers of fleas which have gathered on the remaining but soon-todie rats to find new hosts. After about three days of fasting, hungry rat fleas will also feed on nearby human beings. When human beings have been infected with bubonic plague, the infection takes on average three to five days to incubate before the disease breaks out: the course of the illness takes on average three to five days. This means that from the introduction of plague contagion among rats in a human habitation it normally takes nineteen to twenty-seven days on average, and usually around twenty-three days, before the first person dies from plague. This time lag or latent period between importation of contagion and the first human case(s) is one of the defining features of bubonic plague. This process is repeated by the spread of infective rat fleas (by contiguous spread or metastatic spread) to other rat colonies where the disease will develop in a similar way. The development of a plague epidemic is characterized by a slow initial phase, an endemic phase, with only a sprinkling of human cases while the underlying epizootic processes acquire increasing momentum, and an epidemic phase in which the disease manifests itself in several concomitant deaths and cases of severe illness. The transition into an epidemic phase takes around forty days after the introduction of plague contagion into a rat colony in a human community. The developmental phases of plague epidemics

6

See below: 151–93.

the issue and the problems

7

from the introduction of an infective rat flea into a colony of black rats to the full-scale epidemic developments are given in more detail below.7 This background reveals a number of basic requirements if an epidemic of bubonic plague is to occur, such as broad distribution of black rats in human habitats and housing and efficient mechanisms of territorial spread in order to occasion high morbidity and mortality rates at various levels of territorial organization: local societies, regions, countries, and so on. This background also produces a number of characteristic clinical and epidemiological features or manifestations of bubonic plague which represent singly or in combination the defining features of the disease and, taken together, constitute a model of the disease. This corresponds to the methodological distinction between necessary conditions and sufficient conditions for the rise and spread of epidemics of bubonic plague. This distinction is the central topics of Parts 3 and 4 of this monograph. Taken together, these conditions for bubonic plague constitute a model which can serve as the basis for comparison with historical plague epidemics and with other diseases, specifically the alternative microbiological theories, in order to examine compatibility or correspondence and by this process determine which of them, if any, could have functioned as the microbiological basis for historical plague epidemics. Septicaemic and pneumonic plague. In around half of the cases of bubonic plague, contagion breaks out of the buboes and enters the bloodstream producing septicaemia, in this case secondary septicaemic plague, because this condition is secondary to the primary bubonic infection.8 This term serves also to distinguish this form from the form of bubonic plague called primary septicaemic plague, which occurs when the flea bites directly into a blood vessel and regurgitates plague contagion directly into the blood stream. Since the contagion is deposited directly into the blood stream, this mechanism of infection avoids the lymphatic first-line defence system and therefore does normally not produce buboes. This condition is so dramatic that the average duration of the illness is about fifteen hours, and normally less than one

7

See below: 279–83. Pollitzer 1954: 205–6: “Of special importance is the fact that the high concentration of toxin within, and in the vicinity of, the primary buboes leads to haemorrhagic infiltration of the walls of the neighbouring veins (first noted by Childe) and consequently to the passage of the bacilli into the blood-stream.” 8

8

chapter one

day.9 This form constitutes normally only a few per cent of cases in a bubonic plague epidemic. Secondary septicaemic plague means that plague bacteria are transported also to the lungs where they may consolidate and cause pneumonia, a condition called secondary pneumonic plague, because the pneumonic condition is derived from and therefore secondary to the primary bubonic infection and subsequent septicaemic developments. This occurs in about 10 to 25 per cent of bubonic cases.10 Such patients tend to develop a cough with bloody expectoration (sputum) containing plague bacteria which occasionally may infect others by droplet infection, a condition called primary pneumonic plague since the disease originates in the diseased person’s lungs. Since a person who has inhaled plague-infected droplets from a case of secondary pneumonic plague may develop a lung infection that reproduces the cough with bloody expectoration, and this person who suffers from primary pneumonic plague may spread the disease to other person(s), primary pneumonic plague can take on an independent epidemic form. Outbreaks of largish epidemics of primary pneumonic plague in Manchuria in 1910–1 and 1921–2 provided ample opportunity to study this form of plague in which Yersinia pestis is spread by interhuman cross-infection by droplets. These are the only known instances of largish epidemics for the reasons explained below. A considerable number of small and even tiny epidemics of primary pneumonic plague have been medically and epidemiologically studied.11 It is also generally agreed among researchers of primary pneumonic plague that epidemics of this type always start from human cases with bubonic plague who develop secondary pneumonia, and thus that this form of plague always originates in a plague epizootic among rodents; as a result, there is no such phenomenon as pure epidemics of primary pneumonic plague.12 Primary pneumonic plague will be discussed in detail below, since it is represented by one of the alternative theories.13 Taken together, cases of primary septicaemic plague which do not exhibit buboes as a clinical feature constitute only a few per cent of the 9

Philip and Hirst 1914–6: 529–30, 534–5; Benedictow 1993/1996a: 23–4. See, Benedictow 1993/1996: 25 and fn. 34. 11 Benedictow 1993/1996: 220–3; and see below: 518–27. 12 See below: 511–4. 13 Below: chapter 13: 493–552. Also see the thorough discussion of primary pneumonic plague in Benedictow 1993/1996: 23–32, 214–27. 10

the issue and the problems

9

victims of a bubonic plague epidemic. Pneumonic plague introduces a tiny element of cross-infection which does not affect the main thrust or character of the epidemiological process of spread. Lethality. The lethality rate, also called case mortality rate or fatality rate, of bubonic plague epidemics is, on average, 80 per cent, meaning that about 80 per cent of those who contract the disease die from it.14 A normal lethality rate of this order of magnitude is highly unusual for epidemic diseases and signals therefore that the disease is bubonic plague. The Human-Flea Theory of Plague Epidemiology The history of alternative theories of the transmission of bubonic plague may be said to have begun with the theory which attributes importance to the role of the human flea (and even lice), usually as a contributory vector. This theory was launched early in the twentieth century and attracted a few loyal supporters. It was revived by the French scholars G. Blanc and M. Baltazard who published studies based on a small outbreak in Morocco in 1941. Their work was carried out mostly in the laboratory, although they also conducted some field work. They argue enthusiastically that the human flea could take on an important role in the spread of plague epidemics in Morocco and perhaps elsewhere in Northern Africa where the density of human fleas is exceptionally high due to particularly favourable climatic conditions and the cultural habits of housing, clothing and (un)cleanliness, and that the density of human fleas could compensate for its poor vector capacity.15 It is important to note that Blanc and Baltazard did not argue for the wide-reaching importance of their findings maintained by some of their self-proclaimed supporters (below). Blanc’s and Baltazard’s studies and conclusions were immediately met with devastating criticism, first, in 1943 by G. Girard, then Director of the Pasteur Institute of Paris.16 Next, L.F. Hirst took a close, comprehensive and very critical view of their studies in his standard work on plague of 1953, closely followed by R. Pollitzer who in his standard

14 Benedictow 1993/1996: 146–9, summarizes all data on lethality in historical plague epidemics. 15 Blanc and Baltazard 1941: 813–6; 1942: 446–8; 1943: 208–16; 1945: 173–354. 16 Girard 1943: 4–43. See also Girard 1955: 253–76.

10

chapter one

work of 1954 thought it was “conceivable” that the human flea “might play” an “important role in the transmission of plague” in Morocco, the exceptional infestation of human fleas “compensating for what it lacks in vector capacity,” but not elsewhere.17 These two scholars had vast experience in the combat of plague in the field and in the laboratory. Finally, in the last standard work, which however is a more general work on Yersinia infections, T. Butler states bluntly: “The human flea Pulex irritans is not an efficient plague vector and rarely, if ever, has transmitted plague from man to man.”18 In my doctoral thesis of 1993, I carefully presented and discussed Blanc’s and Baltazard’s studies and also had to conclude that they were deeply flawed. Thus, the conclusions in my thesis in this respect were in accordance with the highly competent criticism by Girard, Hirst and Pollitzer. However, unlike Hirst and Pollitzer, I believe that “the possibility of occasional or episodic incidence of interhuman transmission” “should be seen as a possible slight undercurrent running concomitantly and as an integral part of bubonic plague epidemics” also in the Nordic countries.19 The internationally acclaimed plague specialist T. Butler was attached to the doctoral committee appointed by the Department of History, University of Oslo, to evaluate my thesis. While his comments were generally very positive, he rejected my acceptance of a small but arguably significant or noticeable role for the human flea. I have since had occasion to reconsider my arguments and acknowledge that Butler was right in his criticism. Decisive significance should have been given to neglected Soviet research I presented which showed that the minimum number of ingested bacteria which induced development of blockage in the superior plague vector X. cheopis was in the order of 50,000–100,000 bacteria, blockage occurring in three of twenty-eight fleas.20 Since only three (20 per cent) of them were blocked, it may appear reasonable to assume that the minimum number of ingested bacteria conducive to the development of blockage under these laboratory conditions would have to be in the upper reaches of this range, in the order of magnitude of 75,000–100,000 bacteria. In order to infect a feeding flea at this level, the host must have a level of septicaemia on the order of 150–200 million bacteria per cc of 17 18 19 20

Hirst 1953: 239–46; Pollitzer 1954: 380–1. Cf. Pollitzer and Meyer 1961: 474–5. Butler 1983: 51. Butler has not changed his mind on this point, see Butler 1993. Benedictow 1993/1996: 263; Pollitzer 1954: 392. Bibikova and Alekseyev 1969: 196–202; Bibikova and Klassovskiy 1974: 111–2.

the issue and the problems

11

blood.21 This level of septicaemia and much higher levels occur quite often in rats, but have never been found in human beings, where the level only in exceptional cases reaches or surpasses one million bacteria per cc, and normally is only a tiny fraction of this level.22 This explains perfectly well why cross-infection of bubonic plague between human beings has never been observed, and will not occur whatever species of flea are present, and why the density of human ectoparasitism does not matter. Butler’s strong negative characterization of the human flea’s vector capacity was repeated by Perry and Fetherston in a long review paper on central points of plague epidemiology published in 1997, where they state that “the so-called human flea (Pulex irritans)” was found to be a “very poor vector.”23 Since then, no new significant research or divergent opinions on this matter have been presented. After the publication of my thesis in 1993, the studies by Blanc and Baltazard have twice been thoroughly re-examined. B.E.B. Persson, the Swedish physician and historian of epidemic diseases, made an independent study of Blanc’s and Baltazard’s works shortly afterwards, motivated perhaps by disbelief of my conclusions, and yet she reached the same conclusions.24 In his monograph of 2003, F. Audoin-Rouzeau takes Blanc’s and Baltazard’s studies to task, especially in a long appendix, revealing unconditionally that they are profoundly flawed,25 apparently independently of my similarly thorough discussion. Neither of the two leading international organizations for the combat of epidemic diseases, the World Health Organization (WHO) and the Centers for Disease Control and Protection (CDC), mentions the human-flea theory on their home pages, instead discussing only rat-borne plague in relation both to modern and historical plague.26 In the WHO’s latest Plague Manual, it is stated that plague “is only occasionally transmitted between humans, either through the bites of human fleas (Pulex irritans) infected after biting patients in the septicaemic stage, or through direct contact between a healthy person with an infected person.” The reference is indirectly to the works of Blanc and Baltazard.27 Thus cases 21 22 23 24 25 26 27

Bibikova and Klassovskiy 1974: 111–2; Benedictow 1993/1996: 257–8. IPRC 1906c: 519–23; IPRC 1906d: 524–9; Benedictow 1993/1996: 242–63. Perry and Fetherston 1997: 53. Persson 1994: 98–102. Audoin-Rouzeau 2003: 68–73, 297–343. www.who.int/inf, under Global Alert and Response (GAR); www.cdc.gov. Tikhomirov 1999: 12, 39.

12

chapter one

of interhuman transmission by the human flea leading to bubonic plague or by droplets leading to primary pneumonic plague occur only “occasionally,” which implies that cases of interhuman transmission by the human flea could have a sporadic incidence. After all this thorough and devastating criticism of the human-flea theory and the formation of a broad consensus, the notion of a significant or important role for the human flea could be expected to have been definitely laid to rest.28 However, it was recently revived by a Professor of Medicine, L. Walløe. He first argued this view in a paper of 1982 which I felt obliged to counter with serious criticism focusing on problematic correspondence between supporting references and their factual contents, and subsequently in my doctoral thesis where diverse points in his paper were discussed and found to be highly problematical.29 In his second paper on plague published in 2008, he provides no new research in support of his stance. In the last footnote, he states that Audoin-Rouzeau is “arguing for the importance of [the flea species] Nosopsyllus fasciatus in northern Europe as a more likely vector than Xenopsylla cheopis.”30 This proves that Walløe also knows AudoinRouzeau’s devastating criticism of Blanc’s and Baltazard’s studies and the foundation of the human-flea theory, yet he is silent on this crucial point. I have already stated that the WHO and CDC do not mention the human-flea theory on their home pages in order to underline the broad consensus on the question of the rat(-flea)-borne foundation of

28 In 2006, prominent French (paleo)microbiologists who had been misled into accepting the notion that plague spreads only between conterminous rat colonies and therefore much more slowly than historical plague epidemics presented a research project with an alternative explanatory model or hypothesis based on G. Blanc’s and M. Baltazard’s theories which include human ectoparasites: see Drancourt, Houhamdi, Raoult 2006: 234–41. However, in a personal communication by e-mail 30 April 2009 Professor M. Drancourt made it clear that this view of bubonic plague’s spread is untenable. Importantly, he also commented that it was a misunderstanding to consider their project as support of the human-flea theory and that they had now abandoned this hypothesis completely but were making studies of a possible role for the human louse. As proof, the central parts of the e-mail of 30 April are cited: “[…] I am not sure that our laboratory in Marseilles supported in particular the human flea theory. We indeed suggested that plague could be transmited by human ectoparasite in special circonstances. We indeed already published experimental work on the potential role of another human ectoparasite, the body louse which is a likely candidate for interhuman transmission of Yersinia pestis […] I can tell you we are going-on this question. Sincerely, Prof. Michel DRANCOURT.” [[email protected]] 29 Walløe 1982: 1–45; in 1995 appeared a translation into English which I have not examined. Benedictow 1985: 84–93; Benedictow 1993/1996a: 126–264. 30 Walløe 2008: 73.

the issue and the problems

13

bubonic plague.31 It is therefore surprising that Walløe is silent on this and asserts in an editorial or leading article in Journal of the Norwegian Medical Association32 in a general fashion that the human-flea theory has been “accepted by plague specialists in WHO, but has not found great influence among Anglophone historians.”33 This is completely untrue. The reference to WHO relates to a misquotation of Pollitzer 1960. In his second plague paper of 2008, which was probably at the publisher when the first statement was made, Walløe maintains that “in an official WHO publication on plague in 1960, Robert Pollitzer concluded ‘Pulex irritans plays the main role in the spread of human plague.’ ”34 What Pollitzer really states, referring explicitly to Blanc and Balthazar, is that: in areas like Morocco where […] thick layers of clothing and lack of cleanliness tend to increase human infestation with ectoparasites, Pulex irritans is apt to take an important part in the transmission of plague, the high incidence of this species compensating for what it lacks in vector capacity. At the same time, however, it is certain that in other plague areas, for example, China, India and also Madagascar, the role of this flea is negligible, the transmission of the infection depending upon the rat fleas, particularly X. cheopis.35

This is a very different assertion. Another issue is that since then, almost fifty years later, this partial and highly restricted admission by one plague specialist has lost influence among historians of plague and physicians alike. This shows that it is impossible for Walløe to defend his position within the perimeters of ordinary scholarly work or methodology. In his pursuit of support for his human-flea theory, Walløe finally states his conclusion couched in terms requiring an ethically impossible experiment for the falsification of his theory: “My point is that we at the present know too little about the vector capability of Pulex irritans, in particular its vector capacity between humans and in the

31

Benedictow 2006: 84, fn. 3. Tidsskrift for Den norske legeforening. 33 Walløe 2007: 3193. My translation from Norwegian. 34 Walløe 2008: 71. 35 Pollitzer 1960: 360–1. Pollitzer should have added here that climate and temperature are exceptionally favorable to the procreation of fleas. Since Pulex irritans does not ride with its host except incidentally, the amount of clothing worn by people is not important nor is lack of personal cleanliness, it is the level of cleanliness within housing or habitation that matters for the level of infestation of human fleas. 32

14

chapter one

environmental conditions found in a bed.”36 Fortunately, however, more is known about the human flea’s vector capacity in relation to human environments and sleeping arrangements than about any other technical aspect of bubonic-plague epidemiology. Despite millions of bubonic plague cases in India, China, Madagascar and elsewhere— over thirteen million in India alone—and despite the extensive field studies of the disease by highly competent teams of specialists, not a single case of interhuman transmission of bubonic plague by crossinfection by the human flea has ever been recorded. This is the biggest conceivable empirical disproof of the potential role of the human flea in the epidemiology of plague. This finding corresponds closely to the study of the required levels of infection of fleas for the production of blockage and the difference in levels of septicaemia between human beings and rats and guinea pigs. On this crucial topic, there is full correlation between the outcome of experiments in laboratories and observations in the field. This demonstrates the problems Walløe must confront as the last protagonist of the human-flea theory and the means he is obliged to employ in order to try to support his argument. It must be emphasized that Blanc’s and Baltazard’s opinions on the significance of human ectoparasitism in historical plague epidemics were very restricted and cannot satisfy the ambitions of Walløe. Blanc and Baltazard maintain that, according to their studies, human fleas, could have played an important part in plague epidemics only in the great cities of the Middle Ages. Human fleas could not have played any significant role in rural plague which exhibited only or mainly an endemic type of spread. Around 1300, some 90 per cent of the population of Medieval Europe lived in the countryside. At most, a couple of per cent lived in urban centres that by any stretch of sociological imagination or even by relative historical standards for the classification of urban centres according to size, could be designated large cities. Thus it is difficult to discern not only the significance but even the relevance of Blanc’s and Baltazard’s views to historical demography and plague studies.37 In view of the fact that Norway, for instance, did not contain any urban centre which can be designated a city (over 10,000 inhabitants), Blanc’s and Baltazard’s studies and views are obviously glaringly incompatible with the Norwegian social realities at the time of the

36 37

Walløe 2008: 73. Benedictow 1993/1996: 230–7, 247–50.

the issue and the problems

15

Black Death. If it were true that the Black Death was mainly spread by human fleas, the effects would hardly have been noticeable, according to the inferences of these scholars from their studies. The mindboggling demographic effects of the Black Death38 presuppose a disease that spreads with enormous efficiency in sparsely populated rural areas. It must also be emphasized that Blanc and Baltazard maintain that plague epidemics are always initiated by a murine epizootic, and that there can be no large-scale epidemic of plague spread by human ectoparasites unless supported by a concomitant epizootic among commensal black rats. Baltazard concludes thus: The duration of the epidemics [in the past: my insertion] must have been dependent on the existence of a large murine background. Indeed, if any proof of the presence of R. rattus in the ancient world is required, it is furnished by the very existence of plague.39

Ignoring briefly for the sake of argument the serious weaknesses of their research, Blanc’s and Baltazard’s studies and opinions are of little consequence for historical plague research and do not provide support for a notion of a significant role of human ectoparasitism in the spread and mortality of historical plague epidemics. They also argue for the pivotal importance of a large presence of black rats and their accompanying of rat fleas. This proves that Blanc and Baltazard have not maintained, in fact that no other scholar than Walløe has ever maintained, that human fleas could play a significant part or main part in the transmission of plague independent of a large presence of black rats. The theory that human fleas could spread plague devastatingly in the countryside in the Late Middle Ages is without basis in any research, and Blanc and Baltazard are certainly not to be blamed for this mistaken theory. Walløe passes in silence by all crucial basic facts that independently invalidate the human-flea theory. It has been shown above that human beings are for all practical purposes excluded as sources of blockageproducing levels of plague infection of fleas and explained that only rats and some other rodents develop required levels of septicaemic blood. He passes also over crucial defining epidemiological features,

38

Benedictow 2004: 273–384. Blanc 1956: 546–8; Baltazard 1960: 261, 251. See also Baltazard, Bahmanyar, Mostachfi et al. 1960: 153–4. 39

16

chapter one

for instance the inverse correlation of morbidity and mortality rates and population density which excludes that bubonic plague is spread by cross-infection, and the latency period of c. 19–27 days which reflects that outbreaks of a plague among human beings are preceded by a plague epizootic in rat colonies, although they are all presented in my doctoral thesis, my Norwegian plague history, and my 2004 history of the Black Death with scholarly references40 (see thorough presentations below in chapters 7–8). The Revisionists The recent history of alternative theories began in 1971, when J.F.D. Shrewsbury published his monograph on bubonic plague in England in which he allotted only a marginal role to bubonic plague as a demographic factor. His work was followed by a number of even more sceptical accounts of the bubonic-plague theory which took on the character of rejection, including C. Morris 1971, G. Twigg 1984, G. Karlsson 1996, S. Scott and C. Duncan 2001 (2004), and S.K. Cohn Jr. 2002, who all insist that historical plague epidemics were not bubonic plague. Instead, they argue that historical plague epidemics were pure epidemics of primary pneumonic plague (Morris) or of a mutated version of that disease (Karlsson) or that they were diseases caused by other microbiological agents disseminated by other means or mechanisms. In the first sentence of his monograph, Cohn states with absolute certainty that the Black Death and subsequent plague epidemics were not bubonic plague caused by Yersinia pestis, but “was any disease other than the rat-based bubonic plague.” However, at the end of the monograph he is completely unable to identify any known disease that could have been the cause of the plague epidemics: “In place of Yersinia pestis I offer no alternatives.”41 The reality of this conclusion is that his particular approach to the subject has led him to a panorama of clinical and epidemiological indications that are incompatible with any known disease—for very good reasons. However, Cohn clearly has in mind a viral disease, since he maintains, for instance, that after the Black Death and increasingly with subsequent plague epidemics plague acquired 40

Benedictow 1993/ 1996: 177–81, 257–8, see also 238–9 for evidence excluding the possibility of mechanical transmission; Benedictow 2002: 35–7, Benedictow 2004: 16–9, 31–3. 41 Cohn 2002: 1, 247.

the issue and the problems

17

the character of a children’s disease, implying that adults were to a large extent survivors who had acquired good and persistent immunity, the hallmark of viral diseases.42 He has also in mind a disease spread by cross-infection with high spread rates as emphasized on the first page and repeatedly later; in a later work he asserts that the speed of spread is similar to influenza.43 These six alternative theories are the subject of this monograph. One should note that Shrewsbury is a bacteriologist, Twigg a zoologist, Duncan a biologist, and the other scholars are historians. In my opinion, as a point of departure it is unlikely that the scholars who worked in the midst of great mass bubonic plague tragedies, each of them having the opportunity to study the spread of plague in the field and the clinical manifestations of thousands of plague cases, should individually and collectively have massively misconceived the comparative clinical manifestations and epidemiological characteristics of historical and modern plague epidemics. It is equally unlikely that modern scholars without medical training or without ever having seen a plague patient should discover the truth in their academic ivory towers: my ivory tower has not bestowed any special insights on me. All theories of the microbiological and epidemiological nature of the Black Death have in common the assumption that it was a new disease in Europe. In order to explain the sudden great mortality, Twigg is obliged to argue that his alternative “Black Death” disease, anthrax, was a new disease to Europe (see below). The alternative theories of Shrewsbury, Morris and Twigg have in common the fact that they are based on known and existing diseases, which ensures their testability and comparability and permit discussion using standard scientific premises. The alternative theories of Karlsson, Cohn and Scott and Duncan have in common that they have “invented” a new contagion/ pathogen (Cohn) or a mutated variant of known pathogens (Scott and Duncan, Karlsson).44 These hypothetical new or mutated pathogens are also all held no longer to exist. This means that the various epidemiological, clinical and demographic features which are attributed to them were until recently materially untestable, and as such unfalsifiable and ipso facto invalid and potentially methodologically fallacious. However, recent developments of genetic science, specifically in 42 43 44

See below: chapter 6. Cohn 2002: 1–3, 138–9, 209; Cohn 2005: 1354–5; Cohn and Alfani 2005: 203. Below: 16–18, 487, 494–6, 636, 662.

18

chapter one

paleomicrobiology, may provide the opportunity of testing genetic material from skeletal remains in historical plague graves for microbiological identification of the pathogen (see below). First (in 2001) Scott and Duncan claimed that they had identified the disease of historical plague to have been a disease caused by a type of filoviridal contagion, a mutated variant of the Ebola or Marburg virus. In their second monograph (2004), mostly a popular version of the first, they wisely chose to be more vague about the type of disease: We can be sure that the virus responsible for the Black Death is not one that is known today, indeed, it is possible that it does not even belong to any of the known families of viruses. However, the symptoms most nearly resemble those of Ebola, Marburg and the viral haemorrhagic fevers and, although it was certainly not identical to any of these, of all the diseases known today they seem to be the most similar to it.45

Scott and Duncan have in reality invented an unknown disease: either a completely unknown type of virus or an unknown variant of Ebola or Marburg haemorrhagic disease. By establishing the term “haemorrhagic plague” at the beginning of their first monograph,46 they erroneously imply that bubonic plague is not characterized by frequent and comprehensive haemorrhaging.47 Later they find it opportune to emphasize the feature of necrosis, pretending (also erroneously) that this is not a usual feature of bubonic plague, and without providing supporting reference(s) to modern research on filoviridal diseases.48 The keen interest that Karlsson, Scott and Duncan and Cohn take in genetics is highly selective, confined to a speculative mutational theory that can be arbitrarily shaped to suit the defence of their alternative theories, or indeed to any alternative microbiological theory they might fancy. Mutations are a fact of (micro)biological life. However, to introduce the theory of evolution without the concept of selection and without any demonstration of how the selection mechanisms produced the specified effects in the case in question, that is, to present in an arbitrary way hypothetical mutations that happen to suits a theory, is obviously unscientific. As it has been aptly put: “mutation absolutely can not explain anything. It is simply an ad hoc call for a miracle.”49

45

Scott and Duncan 2004: 225. Scott and Duncan 2001: 7. 47 See below: 664–72. 48 Scott and Duncan 2001: 71, 381; Scott and Duncan 2004: 224. See below, 423–6. 49 Personal communication from Howard Reisner, Professor of Pathology, University of North Carolina at Chapel Hill. 46

the issue and the problems

19

There is a curious and conspicuous fragmentation of the alternative theories which, except in the case of Morris and Karlsson, have nothing in common with respect to the microbiological identity of the agent and the modes of transmission and pattern of spread. The alternative theories of Shrewsbury (1971), Morris (1971), Twigg (1984), Karlsson (1996), Scott and Duncan (2001, 2004), and Cohn (2002) are all stridently argued, but obviously incompatible, which is a major source of scepticism. The two last alternative theories, for example, are based on paradoxical or contradictory notions of the slowness of spread of plague and the rapidity of spread respectively. Cohn asserts, as mentioned, that plague in the past was a disease spread by cross-infection with high spread rates similar to influenza, Scott and Duncan argue for an extraordinary and uniquely long incubation time and for mysterious infective agents which travel around and spread the disease far and wide, while Twigg argues for anthrax, which has a short incubation time, and claims that its dissemination among human beings is dependent on the spread of the disease among domestic animals and is usually contracted by ingestion of un(der)cooked infected meat. Morris and Karlsson claim that historical plague was caused by some sort of plague bacterium spread by cross-infection and transmitted by droplets. All advocates of alternative theories of the nature of historical plague have in common that they reject all other alternative theories, but only the latest contender entering the fray had the opportunity of rejecting all the other alternatives. It is worth noting that none of them has later retracted their own theory and accepted any of the other theories. Obviously, at least five of them must be wrong, and why not all six? In my opinion, they are all untenable, and for several crucial reasons that ought to be thoroughly analysed and discussed. Thus, for the time being there are seven theories of the nature of historical plague epidemics: the theory that it was the bubonic plague, and six alternative theories. We all reject six of the seven theories; the advocates of alternative theories reject all alternative theories except their own and also the bubonic-plague theory, whilst I reject all six alternative theories for the reasons presented in this monograph. All advocates of alternative plague theories have in common several basic assumptions that they consider sufficient conditions for rejecting the idea that historical plague epidemics were bubonic plague. On this basis, they have developed alternative theories of the microbiological nature and epidemiology of the historical plague epidemics, emphasizing some epidemiological and clinical features which they claim exclude bubonic plague and support their own alternative theories.

20

chapter one

They take, for instance, the slight reflections of rat plague in the sources as strong evidence that the European plague epidemics of the past were not rat-borne bubonic plague transmitted by rat fleas, but some other disease. This situation calls therefore, they assert, for alternative theories of the microbiological and epidemiological nature of historical plague epidemics and forms the background or reason for their endeavours. According to the standards of scholarly discussion, the central views, assertions, and objections of the protagonists or advocates of alternative theories will be addressed here in a serious and focused way. The arguments emphasized by the advocates of alternative theories against the bubonic-plague theory, and which clear the way for their own alternative theories, indicate that the following topics are central to the discussion: (1) They reject the idea that the black rat was a common or widespread animal in Europe in the fourteenth century, and they consequently also deny that rats played a central part in the Black Death and subsequent plague epidemics, concluding that this is a sufficient argument for rejecting the bubonic-plague theory. (2) They assert that bubonic plague spreads only by contiguous dissemination between rat colonies, emphasize the very slow pace of this process of spread and the sharp contrast with the quite considerable spread rates of historical plague epidemics, and maintain that this constitutes a sufficient argument for rejecting the bubonicplague theory. (3) They point out that the human mortality caused by bubonic plague in India was only a few per cent, in sharp contrast to the dramatic mortality rates cause by the Black Death and later plague epidemics, and argue that this in itself constitutes sufficient proof that bubonic plague and historical plague were two different diseases. (4) They point out that epidemics of bubonic plague in India produced higher levels of mortality in villages than in urban centres, and thus exhibited an inverse correlation between population density and mortality, but deny that was the case with historical plague epidemics, which, consequently, would have to have been a different disease. In methodological terminology, each of these four arguments, if valid, represents a sufficient condition for rejecting the notion that historical plague epidemics were bubonic plague. This also means that

the issue and the problems

21

each of them represents a necessary condition for the spread of bubonic plague and that they must be collectively confirmed in order to uphold the tenability of the bubonic plague theory. Discussion of the tenability of the alternative theories must begin by clarifying these basic factual issues, which is carried out in Part 3. If one of these arguments proves to be tenable, historical plague cannot have been bubonic plague, and the quest for a well-reasoned alternative microbiological theory is justified. If none of these arguments is sustainable, all alternative theories will be seriously undermined or falsified, and the bubonic plague theory will be alive and well. The fact that bubonic plague originates in rats and fleas produces a number of characteristic clinical and epidemiological features or manifestations which singly or in combination constitute defining features of the disease. While epidemics of bubonic plague cannot arise if one of the necessary conditions is not met, the identification of one defining feature in modern and historical epidemics of plague suffices to determine the disease with certainty. Defining features are discussed in Part 4. The next task must be to examine the tenability of the various alternatives through systematic comparison between the central clinical and epidemiological features that characterize the alternative theories, bubonic plague and historical plague epidemics, as these features determine compatibility and, thus, identification. This task is performed in Part 5. In principle, and as a point of departure, historical plague epidemics may not have been bubonic plague, but this does not mean that any of the six alternatives is tenable, and it is possible that all currently published theories of the nature of historical plague epidemics are wrong. However, if one of the alternatives can be shown to be tenable, it will represent a very valuable advance in the study of historical plague. It would mean the disclosure of serious misconceptions and the identification of the responsible microbiological agent and its medical and epidemiological characteristics, and would give historical plague research crucial new tools of analysis and important explanatory powers. As the reader will have noted, so far Part 2 has not been mentioned. In the course of denying the conclusions of outstanding scholars and pioneers of plague research, some advocates of new theories about plague have made disparaging remarks which are are utterly

22

chapter one

misleading and in fact destructive of reality-based discussion of the central topics at issue. Cohn’s case is so serious that it is the subject of Part 2: “How S.K. Cohn Makes Physicians and Historians ‘Square the Circle,’ ” which focuses on his accusation of collective intellectual dishonesty and/or scholarly incompetence on the part of dedicated and competent scholars who have argued for the bubonic plague theory. This clarification necessarily precedes discussion of the other issues just mentioned.

PART TWO

HOW S.K. COHN MAKES PHYSICIANS AND HISTORIANS “SQUARE THE CIRCLE”

CHAPTER TWO

THE ETHICS OF SCHOLARLY WORK Introduction Scholars who argue for revolutionary new theories in academic fields where much consensual scholarly work has been performed by dedicated and highly competent researchers must reject a substantial body of previous work. Such rejection has the potential to lead modes of argument that do not fulfill usual academic and methodological standards. Cohn’s monograph is a case in point. He sets the scene in opening chapters titled “Scientists Square the Circle” and “Historians Square the Circle,” in which virtually all medical and historical scholars who have conducted serious research on historical plague epidemics and accepted them as bubonic plague are scathingly criticized. The use of the idiom “square the circle” has unfortunate connotations, implying that those concerned are either intellectually dishonest or incompetent or both. It is hard to imagine that competent scholars would handle their material and apply methodology in such a way as to be open to the severe criticism inherent in this phrase. Cohn also repeatedly strikes out at scholars on subjects that have no, or at best peripheral, relevance to his theory. His attack, for instance, on the Japanese medical researcher S. Kitasato who discovered the plague bacillus at about the same time as A.Yersin does not serve Cohn’s theory, and its unfortunate line of argument is very different from the supportive and positive comments made by leading expert medical plague researchers, for instance L.F. Hirst and T. Butler.1 Cohn makes the most out of the confusion, uncertainties and great range of opinions and suggestions made by researchers in the early years of modern plague research around 1900, by using selective readings of that literature to cast doubt on the research processes and the validity of these early findings and, by implication, to strengthen his

1

Cohn 2002: 7–8; Hirst 1953: 106–9; Butler 1983: 22–4.

26

chapter two

case for an alternative theory. However, as a historian, Cohn might be expected to have been more understanding of the historical context of those studies. In the late nineteenth and early twentieth century, hard facts were few and tentative approaches and hypothetical notions were justified. Gradually more hard facts and consensus emerged and there was a better understanding of the epidemiological processes of transmission and dissemination of plague. This process of accumulation and systematization of knowledge in time formed a consistent and empirically well-founded theory of plague epidemiology and understanding of the physical developments of the course of plague disease and its characteristic clinical manifestations. These developments also gave rise to a universal opinion among plague researchers that the modern epidemics of bubonic plague they studied were the same disease that ravaged late medieval and early modern Europe. This unanimity presents a significant obstacle to Cohn’s theory. For this reason, Cohn has no alternative but to discredit in general terms researchers in the fields of plague medicine, epidemiology and plague history. He vigorously accuses historians and medical scholars of squaring the circle. How then, does Cohn belittle the competence and, as it may seem, the intellectual integrity of so many scholars who have made important contributions to historical or medical plague research?

How Cohn Makes Medical Scientists “Square the Circle” Plague research is blessed with several excellent standard works that bring together and synthesize the vast corpus of medical and historical studies on the disease written by outstanding medical scholars who dedicated their professional lives to combating plague in the late nineteenth and early twentieth century during the so-called “third pandemic.” Since the outcome of their observations and studies are so strongly at odds with the premises of Cohn’s theory, Cohn was obliged to partially or wholly discredit their work. It is a scholarly duty to reveal Cohn’s methods in performing this task. This will be achieved through ample citations which will reveal Cohn’s procedure in detail. Hirst’s standard work The Conquest of Plague is particularly dangerous to Cohn’s theory because it is constructed along medical historical lines. It contains powerful counter-arguments to Cohn’s theory and strongly supports the notion that historical and modern plague epidemics were

the ethics of scholarly work

27

the same disease: “there can be no doubt, however, judging from the detailed descriptions that have come down to us, of the clinical identity of the plagues of ancient and modern times.”2 Thus Hirst’s standard work and his person3 are singled out for misleading and disparaging assertions which can here be demonstrated only through the study of representative quotations. Cohn maintains, for instance, that Hirst’s “insistence that modern and medieval bubonic plague were the same led him into selfcontradictions and other complications” and that his “lifetime thesis […] was brushed aside to explain how the fast-spreading, contagious fourteenth-century and the slow-moving modern plague could be the same.”4 This is not correct. Firstly, Hirst strongly and consistently upholds the opinion that the Black Death and subsequent plague epidemics were bubonic plague, and does not at all believe that these epidemics were contagious in the interpersonal sense of the word cross-infection (excepting cases of primary pneumonic plague).5 Secondly, since Hirst, as shown below in Part 3, strongly emphasizes that bubonic plague spreads (and spread) over considerable distances by (metastatic) leaps through the transportation of goods containing infected rat fleas, especially grain, cotton, woollens, textiles, and over short and medium distances often in luggage and clothing,6 he does not at all have a problem with the spread rates of historical plague epidemics when compared with modern plague epidemics that spread in the same way by ship, train, and so on. Actually, Hirst devotes over 150 pages to this subject of mechanisms, patterns and rates of spread and is not to be misunderstood, certainly not in the way asserted by Cohn. Hirst is entirely clear on the question of spread rates: “All three pandemics spread along the main lines of communication in a similar way at a similar rate; it seems improbable, therefore, that their epidemiology can really be very different.”7 Thus, in strong contrast to Cohn’s assertion on this point, Hirst argues for the identity of the so-called Justinianic pandemic, the late medieval and early modern pandemic and the “third” modern pandemic of 1894-c. 1940, and an important

2 3 4 5 6 7

Hirst 1953: 121; see also below. See below: 46–54. Cohn 2002: 19–20. Hirst 1953: 331–4, 121–7, 189, 246. Hirst 1953: 303–455. Hirst 1953: 122.

28

chapter two

argument to him is exactly the identity of the patterns and rates of spread. Conspicuously, Cohn does not provide footnotes which would make his assertions with respect to Hirst’s opinions testable according to ordinary principles of scholarship. According to Cohn’s theory the Black Death was a viral disease which was spread effectively by interpersonal dissemination of the contagion, while he asserts that modern bubonic plague epidemics spread only exceedingly slowly by contact between contiguous rat colonies (see below). These assertions produce the implication that there would be a great difference in spread rates between the late medieval plague epidemics and bubonic plague. Cohn must misquote Hirst’s text in order to suggest that Hirst brushed aside his long-held theory, and to be able to provide an alleged explanation of what Cohn erroneously claims that Hirst means, namely, that the plague epidemics of the Late Middle Ages spread much more rapidly than “anything seen in Morocco or any other plague epidemic of the twentieth century.” This assertion is again made without a supporting footnote that would enable the critical reader to check its validity. In the following citation from Cohn’s monograph italics indicate an important phrase which Cohn had omitted from his citation from Hirst’s text (Cohn’s footnotes are supplied in brackets): Hirst turned to the improbable Pulex irritans8 to account for the differences, now seeing this flea as an “important auxiliary in transmitting the infection is most plausible for the period of the Black Death” in the late Middle Ages. Such a flea as the late-medieval plague’s vector made it possible to explain away another discordant feature between the two plague pandemics: earlier, characteristic of highly contagious diseases that spread person-to-person, plague deaths clustered in households, while twentieth-century plague shows no such tendency. [fn. 72: Hirst 1953: 246] Thus to maintain the identity between the two waves of disease, Hirst was willing to forego the cornerstone of his life’s work, the central importance of one rat-flea, X. cheopis, for explaining when plague reached epidemic proportions among humans. [fn.73: Hirst 1953: 240, 244]9

Clearly, Hirst does not assert that Pulex irritans was generally an important auxiliary in transmitting plague infection. As can be seen from the phrase which has been restored to the quotation, he makes a highly restricted comment or admission, restricted both with respect to level

8 9

The human flea, my footnote. Cohn 2002: 21.

the ethics of scholarly work

29

of tenability, as indicated by the word “plausible,” and restricted with respect to circumstance, namely to the Black Death. This view is preceded by a statement that explains and again underlines the highly restricted relevance or perspective of his text on this point, which Cohn neglects to cite or mention: “in the medieval and classical plagues” the human flea could have played “a subordinate part in the spread of the disease between members of the same household when present in enormous numbers in the bedrooms of cases of septicaemic plague.” The point is that Hirst in a chapter on “Interhuman plague,” and in the context of an in-depth discussion of the possible role of the human flea, also discusses over a number of pages assertions by the French scholars G. Blanc and M. Baltazard to the effect that the human flea Pulex irritans played a predominant role in outbreaks of plague in Morocco, and that this also had been the case with the medieval plague epidemics in the big cities of the time, though not in the countryside.10 In contrast to Cohn’s dismissive style, Hirst, a gentleman scholar who studied at Oxford, attempts to be as generous as possible with a position with which he fundamentally disagrees. He is willing to consider the possibility that the human flea could have played “a significant part” in the Moroccan plague epidemics, because the human flea was present in truly enormous and amazing numbers in the houses, but only in relation to severe septicaemic cases: “when their density is very high and the blood in human cases contains many plague bacilli.”11 However, Hirst is also very clear in his conclusion: P. irritans occasionally spread plague from man to man in certain parts of North Africa where this human flea is superabundant, though, even in Morocco, it is highly probable that X. cheopis [i.e., the flea of the black rat: my insertion] is the chief vector as elsewhere in the world today.12

It now also becomes clear that it is Blanc’s and Baltazard’s view he is willing to consider as “plausible,” but only within highly restricted circumstances, namely in the Black Death, when the human flea was present in great density in rooms and there were severely septicaemic cases of human plague. Importantly, Blanc and Baltazard restrict their assertions of the importance of the human flea in medieval plague

10 Blanc 1956: 548–9; Baltazard 1959: 519, 521; Benedictow 1993/1996: 234–6, 247–50; Benedictow 2004: 17, fn. 9. 11 Hirst 1953: 241. 12 Hirst 1953: 239–46.

30

chapter two

epidemics to the big cities which at the time cannot have comprised more than two per cent of Europe’s population. Clearly, they have nothing in mind which challenges Hirst’s general opinion or which can confirm or support Cohn’s assertion as to the difference between historic and modern plague epidemics. One should note that Hirst does not say a word about spread rates in this context, neither in Morocco nor in the fourteenth-century epidemics; it is not a problem or concern for him precisely because he is of the strong opinion that the spread rates of historic and modern plague were basically the same. It is Cohn who must insist that that the Black Death spread very rapidly by interhuman transmission, because it is a necessary condition of his theory that the Black Death was a viral infection. Actually, Blanc and Baltazard disagree fundamentally with Cohn and agree with Hirst on a crucial point that upsets Cohn, namely the superordinate importance of rats in the epidemiology of historic plague, namely that: The duration of the epidemics [in olden days] must have been dependent on the existence of a large murine background. Indeed, if any proof of the presence of R. rattus in the ancient world is required, it is furnished by the very existence of plague.13

In addition, regarding my doctoral thesis, Cohn asserts disparagingly that “In the spirit of Shrewsbury, Benedictow simply pushes the evidence aside” and claims that I argue that “evidence of the plague itself […] is itself proof for Rattus rattus’s presence in medieval Iceland and Norway,” referring to pages 159–60.14 However, on these pages no such opinion is expressed, and indeed within the framework of my thesis this would be a circular, and therefore fallacious, argument that would undermine the validity of my efforts to identify the microbiological agent of historical plague epidemics in the Nordic countries, which was my academic mission. In fact in my thesis I discuss Blanc’s and Baltazard’s work and cite the preceding quotation, which Cohn misattributes to me. This exemplifies one of Cohn’s common argumentative techniques: as will be shown also below, he attempts to discredit other scholars by attributing to them opinions or arguments with which they disagree. It was indicated above that Cohn should be quite familiar with Blanc’s and Baltazard’s work not only from Hirst’s quite extensive 13 Baltazard 1960: 261, 251. See also Baltazard, Bahmanyar, Mostachfi et al. 1960: 153–4; Blanc 1956: 546–8. 14 Cohn 2002: 53.

the ethics of scholarly work

31

discussion of it on pages to which he refers, but also from the quite extensive discussion of it in my thesis.15 Thus Cohn should know that Blanc’s and Baltazard’s studies in Morocco are based on just 90 plague cases occurring in a clear pattern of endemic incidence in a small local area.16 The notion that this material could be usable for comparison with the Black Death with respect to pace of spread is erroneous on elementary epidemiological and methodological grounds. The Black Death and the small Moroccan episode are obviously not in pari materia and are unsuitable for the comparative purpose of attaining empirical knowledge of possible differences in spread rates. No such comparison is made either by these two French scholars or by Hirst. It is contrived by Cohn in order to create a fictitious criticism of Hirst’s work. By erroneously attributing to Hirst the claim that he had observed the same difference in spread rates that Cohn asserts to have found, and then asserting that he avoided taking this fact into account, Cohn can undermine Hirst’s standard work to clear the way for his own theory. The considerable effort implied in constructing such an elaborate text to this end is a remarkable feature of Cohn’s work. This also demonstrates how much time and space is consumed in revealing the ways he goes about arguing his case, and that any attempt to document all of his tactics would require a series of monographs. Hence the necessity of making a sufficient and representative sample. Similarly Wu Lien-Teh’s and R. Pollitzer’s outstanding standard works are dismissed by Cohn because the authors are convinced that the Black Death and later plague epidemics of the past were bubonic plague. Cohn asserts that Wu Lien-Teh “expressed doubts about modern and medieval plague as the same” in his important paper on the first large Manchurian epidemic of primary pneumonic plague of 1910–1.17 Cohn does not provide a specific reference to page: several re-readings of this substantial paper have failed to confirm his assertion on this point. The reason is probably that this paper does not provide an historical perspective, but relates directly, concretely and specifically to this epidemic alone,18 which makes Cohn’s assertion on this point untenable and misleading. The same is the case with Wu Lien-Teh’s next paper, this time on the second Manchurian epidemic

15 16 17 18

Benedictow 1993/1996: 232–7, 247–51. Blanc and Baltazard 1945. See also Benedictow 1993/1996: 162, fn. 233. Cohn 2002: 22. Wu Lien-Teh 1913.

32

chapter two

from 1922–3.19 The first time that Wu Lien-Teh considers the Black Death and modern plague from a comparative perspective is in his monograph on primary pneumonic plague from 1926 and he is crystal clear: The fact that the Black Death does not quite correspond to the form of infection as it is known to-day cannot eliminate the ample evidence that it was plague. The descriptions of both the bubonic and the pneumonic types, as given by contemporary observers, leave no room for doubt. We shall not deal with the bubonic form, but it is perhaps necessary to emphasise the large part this type played in the Black Death.20

This opinion is also clearly stated in his later work which was written from a historical perspective.21 Thus Wu Lien-Teh never doubted, even briefly, the identity of medieval and modern plague. Another method employed by Cohn to argue his case emerges: he implies that leading scholars of plague studies and authors of the standard works had briefly seen the light of his own theory, but did not have the courage or competence to delve into it, but instead chose conformity to established opinions and orthodoxy. They were the scientists who squared the circle. This enables him to pretend that the basis or premises of his own theory have been there for a long time for every openminded scholar to see and is therefore not only his personal brainchild. This is true neither for Hirst nor for Wu Lien-Teh. Wu Lien-Teh, like Hirst, is clear on the question of spread rates, arguing squarely against any notion that the Black Death could have spread at a qualitatively different pace than the modern epidemics of bubonic plague that he (like Hirst) observed for several decades.22 This means, of course, that they never observed that bubonic plague spread only contiguously between rat colonies, as Cohn asserts, but observed instead that plague characteristically spread by leaps over distances and developed spread rates comparable to those of the Black Death (see below). One should note that Hirst, Pollitzer and Wu Lien-Teh combined superb qualifications: they combined a strong interest in plague history with very substantial concrete knowledge of plague acquired in active frontline service in combat of the disease and had, in the process, the opportunity to make comprehensive observations of plague’s pattern of 19 20 21 22

Wu Lien-Teh 1922–3. Wu Lien-Teh 1926: 3. Wu Lien-Teh 1936a: 3–4, 9, 14. Wu Lien-Teh 1936a: 3.

the ethics of scholarly work

33

spread and clinical manifestations in thousands of plague patients. In the combat of an exceptional evil, they read voluminously, analyzing and synthesizing all studies of plague they could track down and get hold of, including historical studies. They were dedicated scholars and researchers of the highest calibre. The fact that these excellent scholars with their exceptional knowledge of plague were certain that the disease they used their professional lives to fight uncompromisingly for decades was the same as the historical plague epidemics they encountered in historical contexts would normally, as had been the case prior to Cohn’s study, elicit respect for their judgement. In Cohn’s case, scepticism is also the watchword with regard to such approval as is offered, because it comes at a price. As mentioned above this is the case with the views of the Indian Plague Research Commission (IPRC) on the mechanisms, pattern and pace of spread of bubonic plague, a topic which will be discussed in a separate chapter below. There are many other instances. Cohn asserts, for instance, in his usual disparaging manner that the opinion held by the early plague researchers at the end of the 1890s “that the late-medieval and modern plagues were the same hampered [their] understanding of their own plague” and was an idée fixe. He goes on to state the following: “To their credit, by 1906 the researchers of the Indian Plague Commission were willing to put aside the past and state their findings no matter how opposed to common knowledge of the late-medieval plague.”23 This unfootnoted and unsubstantiated assertion cannot be confirmed. The facts are that the preliminary fact-finding Indian Plague Commission was dissolved in the autumn of 1905 and replaced by the Indian Plague Research Commission. Thus, 1906 is the year when the newly formed IPRC started to publish their findings in The Journal of Hygiene and had no past to put aside. G. Lamb, Senior Member of the Commission, gives a brief history of its formation in the preface and introduction to his summary of its findings up to May 1907.24 Secondly, only two of the Commissions members, namely Greenwood and Liston, published comparative historical plague studies. They conclude, contrary to Cohn’s assertion, on specific and tenable empirical grounds, specifically on the similarity of the peculiar pattern of spread according to 23

Cohn 2000: 41. Lamb 1908: i–iv, 1–3. He includes in his summary studies which were performed at the time but were published in subsequent issues of The Journal of Hygiene. He then became member of the Advisory Committee. 24

34

chapter two

variation in population density (see below), that the Black Death and later plague epidemics were the same disease that they had studied in India.25 No member of the IPRC expressed any doubt as to the overwhelming similarity and identity of the Black Death and subsequent medieval plague epidemics and the plague epidemics they studied in India where there were millions of cases. This shows again that Cohn’s approbation should engender the suspicion that the position he is praising does not reflect the actual opinions or studies, but that Cohn is attributing to others his own opinions in order to forward his own theoretical agenda and make his position seem less isolated. Hankin 1: Cohn’s Attack on Hankin’s Observation of Inverse Correlation between Mortality and Population Density E.H. Hankin was another leading British medical scientist who engaged in the study and combat of plague and who argued for the identity of the Black Death with modern bubonic plague in India. Hankin discovered, among other things, that Indian epidemics of bubonic plague caused higher mortality rates in villages than in urban centres and that the Black Death in England appeared to follow the same pattern and, thus, also was bubonic plague. For this discovery he is severely criticized by Cohn. This strange phenomenon, that mortality rates did not increase with increasing population density, but on the contrary, decreased, is seemingly at variance with the central tenet of epidemiology and must reflect a very special or unique mechanism of dissemination.26 The observation of this unique characteristic is highly important because it may expand epidemiological understanding of the particular process of transmission and dissemination of an infectious disease and, in this case, may serve as a sufficient criterion for identification of the disease because it functions as a defining feature (see below). This represents a serious threat to all alternative theories of the identity of historical plague which are based on an assumption that the contagion was disseminated by interhuman cross-infection, because cross-infection is intimately associated with the opposite principle of increasing infection rates with increasing population density, without exception. 25 26

Greenwood 1911b: 93–7, 150–1; Liston 1924: 900–1. Hankin 1905: 48, 57–8.

the ethics of scholarly work

35

This topic of inverse correlation is so important that it will be discussed in a separate chapter.27 Here the focus is on Cohn’s endeavours to discredit Hankin as a scholar and to deny his important observation. Hankin had an excellent scholarly background: he had been fellow of St John’s College at Cambridge University before he joined the combat of plague in India and became fellow of Allahabad University and Chemical Examiner and Bacteriologist to the United Provinces and to the Central Provinces in India. He was one of the pioneers of plague study in India where he made important contributions to the understanding of the epidemiology and microbiological nature of plague in the years around 1900.28 In his last work on plague published in 1905 he makes clear his view on the identity of medieval plague and contemporary plague in India. It is, so to speak, the final fruit and summary of his work as a scientist who had joined the combat of plague in the laboratory and in the field and in anti-epidemic organizational work. It should be noted that Hankin’s paper was written before the important discoveries made by the IPRC which were published in 1906–14. This provides Cohn with the opportunity of making some cheap points at Hankin’s expense, since he can dispense with the scholarly obligation to consider Hankin’s work within the proper context of the history of medical science and plague research. In Hankin’s substantial paper, the part relating to the epidemiological characteristics of the Black Death and its resemblance to and compatibility with the Indian plague epidemics is a small sub-chapter on pages 57–8 titled “Resemblances of the Black Death to Indian Plague”. It is untrue that Hankin “surveyed the late medieval and early-modern sources” on plague epidemics in Europe and made further comparisons of this type. Cohn asserts disparagingly that Hankin without any reason “presumed identity between these two epochs of bubonic plague” and that this “led him to impose conclusions derived from the present epidemiology of plague on the European past.”29 In the following pages it will be demonstrated that these assertions are groundless. These allegations function as a prelude to a great effort to discredit Hankin’s discovery of inverse correlation between mortality rates and

27 28 29

See below, chapter 8: 289–311. Hirst 1953: 21, 130, 160, 293. Cohn 2002: 16.

36

chapter two

population density. Cohn goes on to state (I place his footnotes in brackets): With the new epidemiological discovery that modern plague mortalities [in India] were inversely correlated with the population size of an infected locality, Hankin stated boldly that the same was found for the Black Death, asserting that mortalities had been high in English villages but that that “no evidence of such depopulation exists for London or other towns” [fn. 51: Hankin p. 58]—this despite Creighton’s analysis of wills from the Court of Hustings published several years earlier that showed a fifteen-fold increase in London’s mortality in 1348–9 [fn. 52: Creighton p. 118].30

This is misleading in several ways. Hankin does not conclude with the demanding concepts of “identity” or “the same” but with the far more cautious concept of “resemblance.” Cohn also neglects to mention that it actually was Hankin who discovered the strange inverse correlation between population density and mortality in bubonic plague, namely that bubonic plague caused much higher mortality in the countryside than in towns of “Bombay Presidency.” Hankin discovered also that this was the case with Indian plague epidemics in 1812 and 1836, and established, thus, the outline of a consistent pattern which implies a systemic causation.31 For this discovery, he deserves praise. As a good scientist, Hankin wished to know whether this was a specific feature of plague in India or a more general and characteristic epidemiological feature. At the time, the scientific study of historical plague epidemics was in its infancy. In order to obtain useful information, he turned to Creighton’s general monograph on the history of epidemic disease in the British Isles of 1891 and found some support in statements indicating extreme mortality and depopulation in the countryside, and lesser mortality in London and other towns. This is a correct understanding of Creighton’s text, which thus represents a threat to Cohn’s alternative theory. In order to undermine the credibility of Hankin’s assertion, Cohn refers to page 118 in Creighton’s monograph asserting that Creighton claims there that his study of wills showed a fifteen-fold increase in London’s mortality in the Black Death. This is not correct: nothing to this effect is found on page 118. The incorrect reference to page 118 provides an opportunity to avoid Creighton’s

30 31

Cohn 2002: 16–7, cf. 44. Hankin 1905: 56–7.

the ethics of scholarly work

37

important specification on the preceding page of the types of information obtainable by the use of wills as source material. According to Creighton, wills are useful in obtaining information about the season and duration of the Black Death, but he says nothing about using them to obtain mortality data: One of the best proofs of the season and duration of the Black Death in London is got from the number of wills enrolled in the Husting Court of the city in the succeeding months.32

Clearly, 118 years ago Creighton had the methodological consciousness and scholarly insight that wills were unsuitable as sources for estimating rates of mortality. There are several obvious and good reasons why this should be so which Cohn ignores; for example, the willproducing social classes constituted only a small fraction of the population at risk and the size of the population at risk was not known. However, there is another sufficient reason. My 2004 monograph on the Black Death includes two substantial chapters on medieval demography and medieval sources for demographic studies with particular emphasis on mortality which function as an introduction to all mortality studies relating to the Black Death. Here it is made clear that wills cannot be used for the study of mortality: Wills reflect more the fear of death than death itself. A large proportion of those who made wills in the face of an immediate epidemic threat to their lives would be alive at the end of the day. Abrupt changes in the number of wills relate to crisis mortality in an impressionistic and flimsy fashion and the correlation between changes in the incidence of wills and death rates is not quantifiable.33

Thus, Cohn misrepresents Creighton’s text on this point in order to lash out at Hankin with a fallacy of methodology based on false and misleading assertions that wills can be used and have been used by Creighton as sources reflecting (f)actual death in order to produce a mortality rate. In fact, according to ordinary methodological considerations, Hankin’s observation of resemblance between the Indian bubonicplague epidemics and the Black Death is valid but at a low level of tenability because of the preliminary character of his Indian observations

32 33

Creighton 1891: 117. Benedictow 2004: 272.

38

chapter two

and the weakness of the comparative historical material he was able to find. Since his observation is valid and at variance with epidemiological orthodoxy on good self-explanatory grounds, it should be of great interest to all open-minded and fair scholars. The question of the inverse correlation between levels of mortality and population density in plague epidemic is, as mentioned, thoroughly discussed below in chapter 8.34 Hankin 2: A Brief Study of Cohn’s Technique of Argument A further sample of the arguments and assertions that Cohn levels against Hankin in order to belittle him as a scholar and person follows here. That almost all arguments or assertions which Cohn attributes to Hankin are false, can be illustrated by citing a paragraph of his text with his few footnotes included in brackets.35 The text is divided into ten constituent parts and rendered in italics, and each of these parts is followed by my commentary. Significant points in Cohn’s text are marked using a self-explanatory number-letter system: (1) Following from the [1A] new discoveries made by the Indian Plague Commission that [1B] the most destitute of India’s population seemed to escape the plague, [1C] Hankin concluded the same for the late Middle Ages, (Comment on 1) All three elements constituting the first assertion Cohn attributes to Hankin are factually erroneous. (1A) The Indian Plague Commission made no such discovery and (1B) Hankin does not make any assertion to the effect that the “most destitute” escaped the plague, in fact it was obvious to him and to the Commission from daily experience that this was not the case. On the contrary, Hankin cites on the first page of his paper a colleague’s statement (which he supports) to the effect that “the houses in the suburban villages near Bombay which suffered severely from plague were not so overcrowded as the houses in the slums of the city which were far less severely attacked.”36 Hankin’s study of the peculiar property of bubonic plague that there is an inverse correlation between mortality rates and levels of population density, which is discussed in detail below, follows from this realisation. It is, therefore, clearly apparent

34

See chapter 8: 279–88. Cohn 2002: 17. 36 Hankin 1905: 48. Much the same perspective is implied by Hankin’s unequivocal statement to the effect that “no definite relation has been observed between intensity of plague (apart from its persistence), and badness of sanitary condition of dwellings.” 35

the ethics of scholarly work

39

that (1C) Hankin had not “concluded the same for the Late Middle Ages.” As can be seen, Cohn provides no footnotes in support of his erroneous assertions. (2) seeing it confirmed by Simon de Couvin’s Black Death poem, which alleged that tanners escaped the plague [fn. 53: “Hankin, ‘On the epidemiology of plague,’ p. 57.”]. (Comment on 2) Cohn refers here to the French ecclesiastic Simon of Couvin who in 1349–50 wrote a Latin poem on the Black Death inspired by the epidemic’s ravages in Paris, where he focuses on astrological explanations but also provides descriptive epidemiological and clinical elements.37 Since Hankin does not hold the opinion which Cohn ascribes to him, that the destitute were not hit by the Black Death, it is unsurprising that Cohn’s next assertion on his behalf is also in error. It is simply untrue that Hankin cited this source for confirmation of an opinion he did not hold. Instead, Hankin refers to Simon of Couvin for support of an opinion he actually holds, namely that mortality rates were higher in the countryside than in the towns: “According to Simon de Covino,38 who observed the Black Death in Paris, Montpellier and probably other places, it was especially severe in the smaller towns (suburbia).”39 As can be seen, Hankin is uncertain about the correct translation of the Latin word suburbia since he renders the original word in a parenthesis; an alternative translation might be to take the meaning to be “villages in the vicinity of/in the surroundings of urban centres,” which corresponds closely to the use of the word “suburban” in the citation from his colleague rendered in comment on (1B). Hankin says not a word about tanners! Cohn’s unjustified criticism of Hankin’s work on this point is apparently designed to challenge his scholarly competence and methodological consciousness, and thus his conclusions. Cohn refers to the correct page in Hankin’s paper where he comments on Simon of Couvin’s statement, so there can be no doubt that Cohn’s allegations are based not on a misunderstanding but on manipulation of facts. Cohn is thus unable to confirm by an accompanying footnote with an appropriate indication of page that Simon of Couvin actually wrote in his poem that tanners escaped the Black Death.

37

Libellus de judicio Solis in conviviis Saturni, seu de horrenda illa peste, published by Lettré 1840–1: 206–43, with introductory comments 231–6. For his biography, see Renardy 1974: 273–92. 38 “Corvino” is the latinized form of “Couvin,” the name of a Belgian town. 39 Hankin 1905: 57: Et nimis immensum sensere suburbia damnum. It is a common misconception that Simon de Couvin observed the Black Death in Montpellier. However, it is unlikely that he observed the Black Death anywhere other than in Paris where he had his benefice: see Renardy 1974: 279. It also seems unlikely that anyone who observed the Black Death in Montpellier and had survived would move to Paris in order to observe it again.

40

chapter two (3) True or false, [3A] tanners, almost invariably a guild occupation, [3B] hardly comprised Europe’s most destitute circa 1348 as Hankin assumed [3C] to make the past fit his present. (Comment on 3) All three assertions in this sentence are untrue and are based on Cohn’s unjustified assertion that Hankin used (3A) a textual element in the poem by Simon of Couvin on mortality among tanners, that (3B) he was so incompetent that he believed that craftsmen like tanners could be among the most destitute inhabitants of Europe at the time of the Black Death, and even more disquieting (3C) that Hankin manipulated this material in order “to make the past fit his present,” or square the circle which is the disparaging phrase that Cohn generally uses to describe the arguments of medical and historical plague scholars that modern and historical plague are the same disease. On the contrary, Simon of Couvin emphasizes that the poorest or destitute masses (vulgus, pauperrima turba) suffered particularly high mortality in the Black Death and that it was not high among the magnates, noblemen and knights (principibus et nobilibus generosis/ Militibus),40 corresponding reasonably well to what Hankin actually wrote. Cohn’s assertions with respect to Hankin’s views in this regard all come from his own imagination; at the same time, Cohn ignores aspects of Simon of Couvin’s description that run counter to his own alternative theory. Simon designates the epidemic pestis inguinaria, expressing his view that the disease had a clinical feature which overshadowed all other clinical manifestations, i.e. buboes in the groin, a defining feature of bubonic plague (see below). In addition, he refers to the characteristic intense pain of buboes: nascitur inde dolor ignites in inguine sepe.41 (4) Using another new and unexpected recent finding—plague in India did not follow trade routes as is normally the case with diseases that spread person-to-person— (Comment on 4) Frankly, Hankin’s statement is confusing. He does indeed remark that plague in India did not show any “tendency to spread along trade routes as such,”42 although the expression “as such” indicates a possible reservation which Cohn omits. However, this is not the main problem, which is that other contemporary medical scholars and researchers in India hold entirely contrary views on the matter. In his great treatise on plague which appeared the same year as Hankin’s paper and which summarizes the Indian experience in the preceding decade within a broad historical perspective, Simpson flatly states that “plague travels by the most frequented trade routes.” He points out that this was the case also with the Black Death, subsequent historical plague epidemics, and also the present

40 41 42

Lettré 1840–1: 236; cf. 204. Lettré 1840–1: 202, 232. Hankin 1905: 56–7.

the ethics of scholarly work

41

pandemic, and Simpson goes on to enlarge on the Indian experience.43 As should be expected from Lamb’s presentation, the IPRC held the same view in a number of papers on the spread of plague.44 Greenwood made a specific study of the spread of plague by railway in the Punjab that confirmed the central importance of this means of long-distance transportation of people and goods in the dissemination of the disease.45 Liston, another of the Commission’s prominent members, summarized aptly its findings in this respect: “Infection was disseminated along the main lines of communication by rail and by ship.”46 Thus, it appears that Hankin is mistaken on this point and he does not corroborate it by any reference in an accompanying footnote. He may have based this point on a non-specialist study of plague in India written in the first half of the nineteenth century but which remained unpublished until 1894, two years before the outbreak in India which is our focus here and before the start of scientific study of the disease.47 However, it is also clear that Cohn is mistaken when he characterises Hankin’s statement as fact, calling it a “new and unexpected recent finding,” which confirms his peculiar reading not only of the relevant plague studies performed before the IPRC began publishing its works the following year but also of Simpson’s treatise which he refers to twice in a form which suggests that he was quite familiar with it.48 However, our focus here is on Cohn’s use of Hankin’s paper. (5) Hankin assumed the same for late-medieval plague (Comment on 5) This is not true. Hankin makes no such assumption for historical plague epidemics, and the statement on trade is made exclusively in an Indian context, comprising the three nineteenthcentury outbreaks of 1812, 1836 and 1896. Within this context, he emphasizes that “though it spreads with facility from a town or village to a neighbouring village, it does not appear often to be carried to great distances in epidemic form” and does not “spread along trade routes as such.”49 In the subchapter on the “Resemblances of the Black Death to Indian Plague,” he does not make any such comparison or present any such assumption with respect to the pattern of spread which Cohn attributes to him.50 Clearly, Cohn’s assertion on this point is incorrect. (6) but for this he did not bother to cite any contemporary evidence. [fn. 54: “Ibid p. 56.”] 43 44 45 46 47 48 49 50

Simpson 1905: 194–5, 200–9. See chapter 4: 151–93. Greenwood 1911a: 47–61. Liston 1924: 950, 997. Hankin, 50, 57. Cohn 2002: 10, 15. Hankin 1905: 56–7. Hankin 1905: 57–8.

42

chapter two (Comment on 6) Cohn’s assertion on this point is not correct, since Hankin does not compare the Indian plague epidemics and the Black Death and subsequent plague epidemics in Europe with respect to the role of trade in the dissemination of the disease, and it is for this reason that he does not “cite any contemporary evidence” to this effect. Probably, Hankin does not comment on this point because he knows that in the Black Death and later European plague epidemics the disease was most efficiently spread along the trade routes. Cohn’s footnote is just plain wrong, since Hankin does not mention late medieval plague epidemics on page 56 of his paper. (7) Finally, Hankin rightly noted from chroniclers characteristics of fourteenth-century plagues that had no parallels with the Indian plague experience, (Comment on 7) This is also untrue. Hankin does not make any use of fourteenth-century European commentary on the Black Death other than the citation from Simon of Couvin’s poetic work which has been cited above in order to reveal Cohn’s false reference to the same author. Hankin uses this citation, as shown above, to demonstrate resemblance between the fourteenth-century epidemics and the Indian plague epidemics, not dissemblance or dissimilarity. Thus, Cohn again mischaracterises Hankin’s paper in order to clear the way for yet another incorrect assertion, namely, that Hankin had collected material from fourteenth-century chroniclers on the characteristic features of plague epidemics that are incompatible with the Indian plague epidemics. This enables Cohn (see below) to concoct the false and disparaging assertion that Hankin had observed crucial or important dissimilarities between fourteenth-century plague epidemics and the Indian epidemics of bubonic plague, but chose to ignore them and pass by the obvious conclusion that they were two different diseases. Cohn by this means contrives to make it obvious to his readers that he (Cohn) has made the discovery that Hankin should have made hundred years ago, but which through scholarly incompetence or intellectual dishonesty Hankin chose to ignore. (8) such as children as the principal victims of the second outbreak of plague in Europe in the 1360s. [fn. 55: “Ibid. 64.”] (Comment on 8) This is also fabricated evidence. Hankin’s only reference to a medieval contemporary writer was clarified in the preceding comments; he does not cite or refer to any commentary other than Simon of Couvin’s (see above) and he cites him on the inverted correlation between population density and mortality rates. He does not write a single word about child mortality in the second plague epidemic (or any other late medieval plague epidemic) and could not have done so also for the compelling reason that Simon of Couvin’s account was written 1349–50 and cannot contain anything about the epidemic in “the 1360s.” Again, Cohn falsely attributes to Hankin (and to other scholars) his own observations, suggesting that the facts had been there for a long time for any competent and honest

the ethics of scholarly work

43

scholar to see, but that it took his own genius to draw the correct conclusions. Cohn’s reference to page 64 in Hankin’s paper is also wrong: on this page, Hankin continues a discussion of the observation by P.L. Simond, the pioneering French epidemiologist, that plague had a latent period of usually around twenty days between the introduction of infection into a locality and the epidemic outbreak, which he correctly points out is incompatible with interhuman spread of a disease. This is a point Cohn must avoid mentioning, since it is incompatible with his assertion that historical plague was a viral disease spread by cross-infection. Hankin goes on to discuss aspects of Indian plague epidemics in 1897–8. Thus, the cited dependent clause in Cohn’s text is simply untrue. Cohn’s argument with respect to child mortality in the second plague epidemic will be discussed in a separate chapter below and will be shown to be untenable.51 (9) Yet, despite discordances between the two plague periods, (Comment on 9) This is a false assertion based on Cohn’s own misleading allegations regarding the contents of Hankin’s text. Hankin did not ignore any “discordances” between the two plague periods, but argues in terms of resemblances between the Indian plague epidemics and the late medieval plague epidemics (see also the following point 10). The only “contrast” he mentions, which Cohn does not find reason to cite, concerns the “extent of area attacked,” but he explains this by arguing that “the present Bombay plague may be regarded as intermediate between the Black Death and the Pali plague.” Thus, Cohn’s use of the term “despite” is groundless as are the alleged “discordances.” (10) he concluded with confidence “all the known plagues of Western India resemble the Black Death and the epidemics to which it gave rise.” [fn. 56: “Ibid. 58.”] (Comment on 10) In this part of the quotation, Cohn manipulates Hankin’s text and misrepresents his line of argument by omitting the explanatory continuation of the text, here rendered in italics: Thus all the known plagues of Western India resemble the Black Death and the epidemics to which it gave rise, in showing a high degree of intensity at one time over a large area, and in the relatively high rate of mortality that they produced in villages as compared with towns. The two groups of outbreaks also resemble one another in their power of spreading with facility from village to village.

Hankin also mentions other resemblances between modern plague in India and the Black Death: “Correlated with the high degree of virulence, there appears to be a certain similarity in the symptoms observed 51

Chapter 6: 212–68.

44

chapter two

in these outbreaks,” which in Hankin’s use of the word indicates a resemblance of level of virulence and a resemblance with respect to clinical symptoms. Hankin argues using valid comparative methodology, the systematic comparison of characteristic features or manifestations of these waves of epidemics which occurred centuries and continents apart. He concludes that there were comprehensive resemblances, and no obvious dissimilarities, which permits him to identify them as the same disease, namely bubonic plague. In my opinion it would be fair to conclude that Hankin’s brief and pioneering comparative discussion of plague in India and late medieval plague contains valuable observations that constitute a reasonable case for a tentative assumption of microbiological and epidemiological identity between the two waves of plague. Summing up, Cohn’s presentation and discussion of Hankin’s paper do not meet reasonable standards of academic work, not because it is amateurish but because such great effort and skill have been invested into producing a grossly misleading presentation of its arguments and of Hankin’s scholarly competence and integrity. This is very far from a comprehensive analysis, but only a sample illustration of Cohn’s handling of the observation of inverted correlation of density and mortality, a point of such great importance that it will, as mentioned above, be discussed in a separate chapter below. “The Ugly Americans” Cohn’s American colleagues may ponder the following general critical statement: “American researchers” in Vietnam “had learnt little from earlier studies in India.”52 The American physicians and other medical personnel who worked in Vietnam during the war had been sent there to serve the military forces, not to make plague research. It so just happened that, to their amazement, they found themselves confronted with a major epidemic of bubonic plague among the Vietnamese population (for example 5,568 registered cases in 1967).53 Thus, they had to

52 Cohn 2002: 37. The criticism is primarily leveled at Marshall, Joy, Ai et al. 1967, but see also the next footnote. I suspect that Cohn’s source of inspiration is Butler’s statement that “American physicians in Vietnam from 1965–1975 were given opportunities to rediscover the dramatic clinical presentations of plague”: see Butler 1983: 77. This is, of course, a very different perspective. 53 Butler, Bell, Linh et al. 1974: S78; Butler 1983: 34.

the ethics of scholarly work

45

join a completely different war, to combat plague in order to protect American servicemen from the disease, and also to help the civilian population and do their very best to prevent or limit its spread and help the diseased. Certainly, they were not sent there as plague researchers, but they took on the responsibilities thrust upon them by fate, so to speak. In my considered opinion they did an outstanding job, often under dangerous and difficult circumstances. In the process, they collected much empirical material and implemented a number of smallscale research projects that confirmed and enlarged on our knowledge of bubonic and pneumonic plague, plague in children, and so on.54 The paper Cohn criticizes scathingly is a preliminary report in the form of a small article of thirteen pages on the plague epidemics of 1965–6, co-authored by six physicians and published the following year, with the best of intentions, namely to make the experience and insights won so far on this terrible disease in Vietnam more generally and usefully known to health personnel. A number of valuable papers with this same background were published subsequently until 1976. T. Butler, who performed valuable studies of plague under these circumstances in Vietnam, takes a very different and positive stance: “American physicians in Vietnam from 1965 to 1975 were given opportunities to rediscover the dramatic clinical presentations of plague.”55 In his much-praised 1983 monograph on Yersinia infections he gives a fine and useful summary of the achievements in plague research by American physicians in Vietnam at the time. What is the reason for Cohn’s highly critical assertion in this case? Is the fact that the American physicians in Vietnam consistently confirmed and supplemented the findings of the IPRC and the presentation of plague in the standard works of Hirst, Pollitzer and Wu Lien-Teh really grounds for criticism? Could it be something like an accusation of having “reinvented the wheel”? However, to the extent that these American physicians performed their research independently of the IPRC’s studies, which Cohn implies they did not know, would that not serve on elementary methodological grounds to strengthen the validity both of their findings and those of the researchers in India? So it seems that there is a different reason for Cohn’s collective attack, or maybe also an additional reason. At least since the 1920s, American 54 See, for instance, references in Benedictow 1993/1996: 252–6; Butler 1983: 34–9, 201–2; Burkle 1973: 291. 55 Butler 1983: 77.

46

chapter two

medical scholars have continuously studied plague in the U.S.A, in the laboratory and in the field. The Centers for Disease Control in Atlanta has since the end of the end of the Second World War monitored plague-related developments and supported research projects and released international reports on plague. On the home page of its “Division of Vector-Borne Infectious Diseases” this leading institution of plague research in the U.S.A., six years after Cohn’s monograph was published, unconditionally supports the notion that modern bubonic plague and the plague epidemics of the Late Middle Ages were the same disease caused by the same bacillary agent, namely Yersinia pestis, and that it is transmitted by rat fleas. Obviously, these leading American medical scholars of plague research were not impressed by Cohn’s arguments. Is it really true that they hold this opinion for unscholarly and unpersuasive reasons? In an ironic twist of research history, the committee which in 1991 was appointed to evaluate my doctoral thesis on plague in the late medieval Nordic countries engaged Thomas Butler as the leading expert on medical plague research in the world at the time. He gave a very positive assessment of my thesis and its epidemiological identification of these historical plague epidemics with bubonic plague. Cohn’s Accusations of Racism against J. Ashburton Thompson and L.F. Hirst There is, however, another aspect of Cohn’s academic “mass execution” of previous scholars which is so outrageous that conscience demands that we address it seriously: his accusation of several early plague researchers of racism,56 specifically J. Ashburton Thompson, the President of the Board of Health and Chief Medical Officer of the Government of New South Wales, and also Hirst for endorsing Ashburton Thompson’s opinions. Cohn’s composite role as accuser, prosecutor, judge and jury is unacceptable and his bombastic convictions of dedicated scholars are grave miscarriages of academic justice which it is a scholarly duty to uncover and repudiate. “Racism” and “racist” are words denoting the notion that one human race is genetically superior to some other human race(s) or all other races. Such notions are completely without basis in scientific knowledge 56

Cohn 2002: 39.

the ethics of scholarly work

47

or research, are conducive to dangerous political ideologies, and should be unequivocally condemned. All other notions of human inequality like ethnocentrism, chauvinism, xenophobia, and negative opinions with regard to people of other religions, social classes, and so on, are not racist, but relate to cultural and social notions of difference and inequality. Such cultural notions are (regrettably) usual all over the world today just as they have been in the past; among the native populations of India where they were systematized according to the notion of cast, and found expressing in tensions between Muslims and Hindus. There are very good reasons for relating to such notions with great scepticism on the basis of a suspicion that they are prejudices and as such detrimental to human relations and social exchange. However, this does not mean that they are always and necessarily erroneous: it should, for instance, be fairly obvious that different cultural notions of the cause and spread of epidemic diseases can have very different functional effects on those diseases’ powers of dissemination and mortality in different societies based on different cultures and civilizations. Thus, from the perspective of preventing epidemic disease and mortality it can be argued on sound scholarly and scientific grounds that there are important and even vital qualitative differences between the various disease-related notions held by various civilizations or ethnic groups at various times in history. Whilst racist notions are completely unscientific and should be condemned in the strongest possible terms, other notions of difference or inequality can be discussed within the parameters of social science according to their functional aspects as more or less tenable, correct or erroneous. This is at the heart of the matter here. Cohn cites a passage in a paper in the journal in which the Indian Plague Research Commission published their own studies and also those of other prominent scholars, namely The Journal of Hygiene, where Ashburton Thompson presents the epidemiological observations and the anti-epidemic countermeasures applied in Australia after plague slipped ashore in 1900:57 Plague has almost always appeared in countries inhabited by races foreign to the observer in their language and modes of thought, who were of little instruction, of an education limited to ancient and immutable conventions, and who lived for the most part under conditions which

57

Cohn 2002: 39, Ashburton Thompson 1906: 537–8.

48

chapter two unavoidably obscured the phenomena. It has thus often been impossible to acquire that exact and complete knowledge of all the circumstances under which the infection had been received by each person attacked, which is the foundation of all investigations into the aetiology of disease by the epidemiological method. [.…] At Sydney the conditions happened to be much more favourable to its employment. The invaded population numbered about half-a-million. It was not merely wholly white, of English extraction and speech, and fully civilized, but intelligent, instructed, and orderly, accustomed to direction and amenable to it.

The passage contains nothing at all indicating that Ashburton Thompson considers that white people are racially, i.e., genetically superior to native people in India or any other race or people. He makes the point that the white (relatively) well educated population of British extraction in Australia accepted the various inconveniences associated with the research efforts and strict anti-epidemic countermeasures which were applied there, partly because there was a long tradition in European culture that, for instance, diseased persons were taken out of their families and isolated in plague hospitals or wards. This meant that the Australian sanitary authorities enjoyed a much more co-operative population than the population to which the British sanitary authorities related in India. The native people(s) in India had a much lower level of education and held very different cultural notions of the cause and spread of disease and of relevant or acceptable countermeasures. For these reasons, they resisted strongly and even violently comparable research efforts and use of the same anti-epidemic measures in the combat of plague in the early years of the plague epidemics. These measures were certainly implemented with the best of intentions, not because the British colonial authorities were “callous” as Cohn maintains. Clearly, this popular resistance impeded the huge efforts to prevent plague from spreading, and had unfortunate effects.58 This is reflected also in the first statement by G. Lamb, Director and Senior Officer of the Indian Plague Research Commission, in the preface of his summary of the results of the Commission’s first years: In the early days of plague in India most strenuous efforts were made to stamp it out by the means adopted in European countries in dealing with epidemic disease, but these efforts failed and they too often led directly to the misfortunes which they were designed to avert. When it was recognized that it was impossible do deal effectively with the epidemic without

58

Simpson 1905: 67–8; Klein 1988.

the ethics of scholarly work

49

the help of the people themselves, a policy of persuasion and assistance was substituted for the more rigorous measures, but this also failed to prevent the extension of the disease, although in many places some degree of success was achieved.59

Lamb makes it clear that the anti-epidemic measures introduced by the British colonial authorities in India based on European experience and culture were implemented with the best of intentions, to save lives by stamping out a murderous disease, but failed because at the outset the authorities did not recognize the importance of relating with sensitivity and insight to the Indian population’s cultures and mentalities. There is no indication of the slightest element of racism in the scholarly meaning of the word, as opposed to its use as an invective, only evidence of deficient knowledge of relevant social anthropology. Thus, the administrators learned a lesson from which the IPRC could benefit. However, the alternative, avoiding efficient countermeasures that might offend Indian sensitivities, also had weaknesses and, according to Lamb, had cost lives. There is no dissonance between Lamb’s statement on behalf of the IPRC and the views presented by Ashburton Thompson; it is Cohn who has contrived a gravely misleading accusation. Thus Ashburton Thompson’s observations and analysis appear correct and relevant. They are therefore supported by modern scholars, for instance by I. Klein, which support exposed him to Cohn’s disparaging assertions about his views.60 One might debate whether some of Ashburton Thompson’s words have ethnocentric connotations, for instance, possibly the concept of “civilization.” However, can we be certain that future generations will not consider with some ambivalence our own choices of words, since the meanings of words develop over time, changing connotations in a changing world with new social and

59

Lamb 1908: i. Klein 1988. As for misleading assertions see, for instance, Cohn’s statement: “Yet Klein, p. 754, still concluded that the reasons for the exceptional mortality from bubonic plague in the early twentieth-century India resulted largely from overcrowding and poor housing”; see Cohn, 2002: 30, fn. 28. In fact, Klein says the opposite, that “plague dwindled and population grew amidst hunger and persistent poverty, misery and environmental decay,” which according to ordinary understanding or interpretation should be taken to mean that plague in India declined despite worsening social conditions. Instead, Klein advocates a very different theory, that the decline of plague was due to biological adaptations by man and rats, with which one can agree or disagree, but has nothing to do with Cohn’s assertion which is, therefore, misleading and designed to devalue Klein as a scholar, since he does not agree with Cohn’s account of plague in India. 60

50

chapter two

political contexts? In order to illustrate the problem, I can mention that in the Scandinavian languages the term “high culture,” “høykultur,” is frequently used synonymously with civilization, a term that could, of course, easily be denounced as containing an ethnocentric notion of cultural superiority over tribal societies, and so on, or even as racist in Cohn’s unscientific abuse of terminology. Actually, it is used more or less consciously in its technical scholarly meaning in social science to refer to cultures that have developed urban structures of settlement, economic production and exchange in contrast to tribal or agricultural societies.61 Is it really necessary for us to appeal to future generations to relate to our choice of words with some lenience and good will and seek a likely or possible positive interpretation? As shown below, Cohn’s negative approach serves a purpose, namely as a pretext to pass by in silence the observations on plague in Australia presented by Ashburton Thompson which would undermine his own theory of plague epidemiology. His contrasting kind words about the IPRC’s attitudes towards the native Indian population serve to portray himself as a reasonable man before ending with highly misleading statements about the IPRC’s findings—which in fact conform entirely with those of Ashburton Thompson (see below). The point is simply that the British colonial authorities and their sanitary agencies learned from the unfortunate early experience of their wholesale application of epidemic countermeasures of European origin to make adjustments that took into account the sensibilities and beliefs of the native Indian populations. Cohn also levels an accusation of racism, as mentioned above, at Hirst, stating that he followed “Thompson’s racist version of events” and goes on to select some words of a passage in Hirst’s monograph so as to incriminate him as much as possible. In order to acquit Hirst of 61 The difference in the sociological meanings of the words “culture” and “civilization” springs from the fact that the basic meaning of the term “culture” is “cultivation” (of land, etc.), while the term “civilization” is based on the Latin word civitas with the meaning “town” or “city”, or derived words like civilis which means “burgher” or “citizen”, implying that the term “civilization” technically refers to cultures that have developed urban structures of settlement, economic production and exchange. “Civilization” is a technical sociological term and does not as such contain qualitative connotations relating to notions of superiority or inferiority of cultures, for instance, in relation to tribal cultures based on agriculture, fishing or hunting and gathering that lack urban formations or structures. The term “civilization” contains, thus, a valuable distinction which makes it useful as an analytical sociological tool for understanding a specific type of societal structures and their function in relation to various other types of societies.

the ethics of scholarly work

51

this scholarly miscarriage of justice and make the true character of Cohn’s accusations entirely clear I will cite both Cohn’s text and Hirst’s original version, Cohn’s text first, with his selection of words from Hirst’s text indicated in italics: […] 50 years later, a researcher in the last stages of the Indian Plague Commission, L.F. Hirst, lost sight of this early twentieth-century history. Instead, he followed Thompson’s racist version of events, concluding that the Australians “enjoyed a considerable advantage over workers in Bombay” because “investigation in Sydney had been conducted in the midst of a civilised and homogenous community speaking the language of the investigator.”62

I also cite the full passage of Hirst’s text, marking again for pedagogical reasons the words Cohn selected with italics, words which he asserts are “concluding,” although, as can be readily seen at a glance, are not concluding. In fact, the passage continues after the end of Cohn’s citation, and Cohn’s mischaracterisation of the passage is not accidental: His reports [i.e., Thompson’s] are models of cogent reasoning from unusually precise epidemiological data. Thompson and his Australian colleagues enjoyed a considerable advantage over workers in Bombay for the purpose of an exact investigation of the factors governing the spatial spread of plague in a particular region. His observation on a series of plague outbreaks in Sydney were conducted in the midst of a civilized and homogeneous community speaking the language of the investigator and already trained, during the course of an epidemic of smallpox, to cooperate with the Department of Public Health: whereas in India the outlook of the polyglot population was restricted by ancient tradition, and the social conditions were such as to make it difficult if not impossible to acquire that exact and complete knowledge of all the circumstances under which the infection had been received by each person attacked, which is the foundation of investigations into the aetiology of disease by the epidemiological method.63

As can now be readily seen, Cohn has selected a few words here and there and has inaccurately represented Hirst’s text with the purpose of incriminating Hirst as racist, although the alert reader will readily discover that even the outcome of this dubious selection technique makes the application of the terms “racist” or “racism” completely groundless. The continuation of the passage after the end of Cohn’s selected words shows clearly what Hirst had in mind, namely that the “polyglot” Indian 62 63

Cohn 2002: 39. Hirst 1953: 144–5.

52

chapter two

population(s) with their ancient and deeply rooted beliefs resisted and prevented good research into the nature of plague epidemiology and hampered efforts to contain the spread of plague.64 His line of argument is entirely based on comparative cultural and ethnological observations and inferences with rational implications for epidemiological research and efficient countermeasures. Taken out of its context, the word “civilization” might also in this case be thought to have been used with ethnocentric connotations. However, seen within the full context it becomes clear that Hirst, with his great experience from work in India and Ceylon (Sri Lanka), agrees with Ashburton Thompson that “investigations into the aetiology of disease by the epidemiological method” were much easier to carry out when the investigators and the population spoke the same language, and the population was trained to understand and accept anti-epidemic measures on the basis of a long cultural tradition of adapting to and understanding the reasons for such sanitary measures and research projects. Thus, the gist of what Hirst says is, as in the case of Ashburton Thompson, that European civilization and populations of European extraction were much better adapted to the implementation of research efforts on epidemiological problems and efficient anti-epidemic measures than the population(s) of the Indian civilization. This is not at all to say that Western civilization as a whole was superior, only that this was the case in this specific field of scientific medical research and anti-epidemic efforts at the time. I would submit that this is true, and that it was at least for the most part the adoption of Western scientific medicine and epidemiology that has raised average life expectancy at birth in India from a maximum of 22–4 years as recorded by the Indian census of 1911 to the present level of 66.46 years.65 There is not the slightest hint in the text that Hirst held the notion that white Australians of British extraction were genetically superior to Indians, and thus there is no justification for describing him as a racist. Clearly, Hirst had the good of the Indian population in mind and wished fervently to find ways to spare as many lives as possible and reduce human misery from plague disease. Those of us who have not served heroically in the fields of combat of plague but live comfortable and safe lives in the ivory towers of academia may note with interest that Hirst, who had spent his professional life in

64 65

Cf. Hirst 1953: 418. Coale and Demeny 1983: 33; www.cia.gov, World Fact Book 2010, s.v. ‘India’.

the ethics of scholarly work

53

active front-line duty in the combat of plague in India and Sri Lanka (Ceylon), almost a generation later strongly supported and enlarged upon this line of argument which was originally presented by Ashburton Thompson. This type of argument consists of scholarly empirical observations and methodologically relevant considerations that can be discussed in an orderly scholarly way. If Cohn had not had such an extraordinary agenda, he could have attempted to show in an ordinary scholarly way why the constituent arguments were not relevant or satisfactory, and in this way produce a case for asserting that the reason for this discrepancy sprang from untenable racist notions. Since this was not possible, Cohn attempts by means of misquotations, incriminations and accusations to degrade and eliminate from serious scholarly consideration an excellent scholar of extraordinary merits. Hirst’s outstanding monograph has obvious mortal implications for Cohn’s theory, exactly because it conforms in its essence to the work of the IPRC. Most importantly, Hirst was convinced that modern and medieval plague epidemics were the same disease, that the plague he had studied intensively in the field and laboratory and combated in India and Sri Lanka and the historical plague epidemics that he studied were the same. Hirst therefore constructed his monograph on plague as a history of the combat and Conquest of Plague from the Early Middle Ages to the present day, presenting a vast amount of historical and modern medical and epidemiological evidence. Thus, Cohn must decide how to dispose of this prestigious plague researcher and author of one of the he most respected works on plague. Cohn attempts to do away with Hirst as a trustworthy and respectable scholar by discrediting him as racist or, what is much the same, asserting that he followed and supported racist views. In addition to Cohn’s false accusation of racism, based, among other things, on misquotations, he also misrepresents other of Hirst’s central views, for instance, those on the spread rates of medieval and modern plague epidemics and on the means of dissemination (below). Cohn ridicules Hirst for having “fabricated the story of an underground war between Rattus rattus and the brown rat to explain the plague’s sudden disappearance from Europe in the eighteenth century.” However, the only fabrication is Cohn’s false reference to p. 141 in Hirst’s monograph where nothing to this effect is stated.66 The reason is that Hirst holds a

66

Cohn 2002: 33.

54

chapter two

very different and very sensible opinion, stating “It is quite possible that advances in building construction and domestic hygiene during the eighteenth century turned the ecological scale against the black rat and encouraged the other species [= Rattus norvegicus] lurking in the outskirts of human habitations to enter them.”67 How Cohn Makes “Historians Square the Circle” In Cohn’s monograph, scholars and colleagues with opinions that differ from his, that is, inevitably almost everyone who has worked in the field of plague research, are scathingly criticised, often repeatedly. His generally disparaging views of historians in this field of study is evident in the name of his chapter “Historians Square the Circle,” a title implying that they are intellectually incompetent or dishonest or both. Here a rapid succession of scholars are ridiculed.68 If their outstanding academic record cannot be denied, they are accused of excelling at concealing what they really are doing: “To square the circle, Ann Carmichael, who combines an expertise in medicine and medieval history [actually in historical plague research, my insertion] was subtler than Shrewsbury…,” and so on.69 And of course, she squares the circle again a few pages later.70 There are quite a number of group executions: A. Zitelli, R. J. Palmer and A. Carmichael are unceremoniously denounced because their views on contemporary notions of the nature of epidemic disease, which are the outcome of serious work and careful studies, undermine a central premise of his theory.71 It is correct of Carmichael to underline that “medical commentary, characteristic of late-medieval plague treatises, was formulated with good Galenic universalism.” This view was based on the notion of miasma which can be understood as a special type of airborne poisonous contagion. This notion was gradually developed into the concept of miasmatic-contagionistic epidemiology, the notion that miasma was infectious and was transmitted between people by contact (per contactum) or by touching objects contaminated with miasma from a diseased person (fomites), or at a 67 68 69 70 71

Hirst 1953: 123–4. Cohn 2002: 41–54. Cohn 2002: 47. Cohn 2002: 49–50. Cohn 2002: 114–5.

the ethics of scholarly work

55

distance (ad distans) when a person exhaled miasmatic air which was inhaled by another person. Over long(er) distances miasma attached to persons, objects or goods that were moved by trade and transportation, and therefore quarantine of ships and people coming from infected places and intermission of trade were introduced early as countermeasures to prevent the importation of contagion or miasma.72 Cohn’s counterarguments for dismissing Carmichael’s view are without value. As proof of plague’s infectiousness he cites Ibn Khatimah: “a well man did not remain long with a sick one without being attacked by the disease.” Firstly, this does not disprove Carmichael’s understanding that such observations or views reflect Galenic miasmatic-contagionistic notions, since miasma was transmitted by contact, also by contact with fomites, objects that a diseased person had touched or used. According to modern notions of plague epidemiology, any person visiting the house of a person diseased by plague would most likely enter a house swarming with dangerous rat fleas and would be at great risk of contracting the disease by flea bite(s) or of bringing infective fleas with him back to his own house where the fleas would seek out rat hosts and unleash an epizootic that after a period of around three weeks would manifest itself in plague disease in the household or in adjacent households. Cohn also cites the Muslim physician to the effect that “in the neighbourhood of Almeria, where the clothing and bed linen of the plague-infected were sold… all died almost without exception.” This observation lends itself well to the same miasmaticcontagionistic understanding, and also reflects reality according to modern plague research in so far as clothing and bedding from persons who had died from plague are liable to contain infective rat fleas. At the end of the same passage, Cohn cites a fourteenth-century Dutch physician on contemporary practice in Italian city-states to the effect that it was “better to burn the commodities of plague victims than to sell them.”73 This point relates to the contemporary concept of fomites, contagious objects infected by miasma, and makes no difference. Carmichael’s view stands undefeated when seen within a proper scholarly context. Undaunted, Carmichael has risen from her academic grave to haunt Cohn, disclosing the unfairness and serious weaknesses of his argument in a fine review paper.74 72 73 74

See, for instance, Hirst 1953: 22–58. Cohn 2002: 234–5. Carmichael 2003: 253–66.

56

chapter two

In his usual disparaging way, Cohn makes the following introduction to the intellectual “liquidation” of a large group of scholars: It is difficult to know why historians and medical scientists have held on so passionately to the notion that the Black Death and its successive waves of pestilence must have been the same disease whose bacillus was discovered in 1894.”75

Here Cohn asserts that historians and medical scientists have been collectively blindfolded by passion and irrational sentiments and excludes the possibility that they have, on the contrary, seen the light through reason and competent scholarly work. He goes on to be more specific both with respect to scholars and his views on their work: For Robert Gottfried and Michael Dols […], Paul Slack […], Brossollet and Mollaret […], and many others, the plague’s bacteriology is simply indisputable; no argument need be made. [….] They then proceed to impose their notions of the aetiology and mechanisms of transmission of the twentieth-century bubonic plague on those of late-medieval and early modern Europe. Worlds of rats and fleas, rat epizootics, and regurgitated bacilli are invented for 1348 and beyond with picturesque vignettes without any grounding in the historical sources […].76

As can readily be seen, in the eyes of Cohn all of these fine scholars “and many others” are irrational persons who hold scholarly opinions based on passion rather than reason and they are collectively incompetent or dishonest or both since they impose notions across centuries and invent their evidence and contrive their conclusions without any basis in sources. The “legal” basis for this awesome ruling in his private court: because they do not agree with his theory that the Black Death was caused by a hypothetical, hitherto unknown and long ago disappeared viral agent. Cohn’s need for group liquidations of researchers can also be well illustrated by his collective execution of E. Le Roy Ladurie, J. Aberth, N. Cantor, P. Slack, O.J. Benedictow, and I. Klein,77 because they all, actually correctly, argue their respective cases on the basis of the IPRC’s well-researched finding that plague was spread over long(er) distances in the guts of rat fleas transported in clothing, luggage, and in shipments of grain, cotton and suchlike (see below).78 This group execution 75 76 77 78

Cohn 2002: 57. Cohn 2002: 57. Cohn 2002: 28–9. This subject is quite exhaustively discussed below: 151–93.

the ethics of scholarly work

57

also reflects the highly problematic character of Cohn’s theory. Their correct knowledge of the IPRC’s epidemiological findings unveils the untenability of his theory of spread which is based on the false assertion that bubonic plague spreads only by dissemination between contiguous rat colonies, and therefore spreads much slower than the Black Death and subsequent plague epidemics. Cohn’s repeated attacks on this author’s doctoral thesis are, in my view, based on gross distortions and misrepresentations motivated by his desire to assert that I am squaring the circle.79 In the following chapters, I will present and discuss a sample of his assertions about my doctoral thesis which I consider objectively untrue and also representative of the way he argues his case. Here I will only make a couple of points: Cohn states that my thesis “shows an impressive but highly selective reading of the epidemiological material on modern plague.”80 He does not indicate in what way my reading is selective, although such a serious accusation of biased collection and use of the scholarly literature should obviously be documented just like any other scholarly argument in order to attain empirical status and some level of tenability or credibility. As it stands, it is a groundless accusation and an academic libel. The assertion is untrue. I started my work on plague with a sceptical attitude to plague as an explanatory cause of late medieval depopulation.81 It was therefore my ambition to read all relevant scholarly literature on plague, the medical and epidemiological, the demographic and historical studies, in order to be able to consider critically and empirically the various views on the plague epidemics of the past and penetrate as deeply into the matter as sources and science would allow, albeit with a particular emphasis on relevance for identifying the microbiological nature and epidemiology of the late medieval plague in the Nordic countries. My thesis was the first monograph to result from this ambition. Its bibliography contains a balanced and for all practical purposes complete reading of modern medical and epidemiological studies and standard works on plague, comprising some 730 studies all used actively in the text and referred to in the footnotes, and the text contains 830 footnotes making it possible to check the premise(s) of even the tiniest detail. Much of what I did not find a

79 80 81

Cohn 2004: 51–2. Cohn 2004: 51. Benedictow 1993/1996: 13–6, 125, 266–7.

58

chapter two

practical evidentiary use for in my thesis has been employed in my two subsequent monographs on plague, while hundreds of other studies have remained unused for lack of relevance or quality. Taken together, my three monographs on plague history contain 2274 footnotes, about 1500 bibliographical entries, more than 1000 individual studies if duplication is deducted, and 1146 pages. This reflects my fulfilled ambition to read all the relevant scholarly literature and to maximize the evidentiary status and empirical testability of my studies on plague. For the same reason, it is easy for me to show, and for anyone interested in this unusual subject to ascertain, that the bibliography of my thesis, which contains only studies referred to in the text or footnotes, is far more comprehensive and balanced than Cohn’s bibliography which exhibits glaring gaps. For instance, the works of Russian and Soviet scholars and of the French researchers in Madagascar and Morocco are completely missing as well as the works of Dutch scholars in Indonesia and plague studies in Egypt, and so on. In short, I would like to ask my readers to consult the bibliography of my thesis under the names of, inter alia, Bibikova (and Klassovskiy), Klimenko, Vasil’yev (and Segal), Fenyuk, Dörbeck, Alexander, Girard, Estrade, Brygoo, Blanc, Baltazard, Van Loghem (and Swellengrebel), de Langen and Lichtenstein, Petrie et al., and Wakil, and compare Cohn’s bibliography. One could also note the remarkable paucity of plague studies by American scholars in his bibliography (see also above). A likely explanation could be that all these scholars consider that historical plague epidemics were bubonic plague, or to be more specific, they consider the similarities between the disease they study and historical plague epidemics of the past so great or comprehensive as to warrant a conclusion of identity. It is also easy to show that Cohn’s reading of the great corpus of works by the Indian Plague Research Commission is quite limited and selective and that he also misrepresents their studies in order to defend his theory: this has already been shown above and will be demonstrated more systematically below. Cohn enters studies in his bibliography that are not mentioned in the text, although there are very strong reasons why he should do so, for instance, a paper by Greenwood, “Statistical investigation of plague in the Punjab. Third Report,” which he dates to 1912, although any scholar who has held this paper in his hand would know that it was published in December 1911, which explains why it is not used in the text, and why he does not mention the important “Second Report: On the connection between proximity to railways and frequency of

the ethics of scholarly work

59

epidemics.” This can be seen as a small beginning of growing evidence of Cohn’s selective reading of the IPRC’s works and his misrepresentation of their results. Cohn has also missed my paper on a feature of bubonic plague which is entirely unique to this disease and therefore can serve as a certain premise for identification, i.e. as a defining feature, namely that morbidity and mortality rates are highest in sparsely populated areas and decrease with increasing population density; in that paper I show that this was the case both in modern epidemics of bubonic plague and in historical plague epidemics.82 Although he demonstrates that he has read my doctoral thesis, he apparently missed the chapter on this subject titled “The Problem of Population Density,” which ends in a comprehensive conclusion written in bold type to indicate the importance I attribute to it.83 This negligence allows him to deny the fact and criticize Hankin for—correctly, as shown above— pointing out this important and characteristic similarity between the Black Death and modern plague, a point enlarged upon below in a separate chapter.84 In short, it is easy to demonstrate that Cohn’s reading of the modern medical and epidemiological studies on plague is very deficient and arguably “highly selective.” These are the reasons Cohn does not substantiate the purported selectivity of my reading of medical plague studies. His reading of my thesis is also highly selective and his understanding of it is surprising and deserving of comment, for instance, his interpretation of the significance of climatic temperature and rats in the epidemiology of plague in the Nordic countries (see below). In this context, it may be useful to describe some problems associated with another instance of how Cohn goes about arguing his case in order to put down other scholars. In order to reveal my incompetence, he discusses the statistical use of the Obituary of the Cathedral of Lund in my doctoral thesis. He begins by presenting the Danish (at the time) cathedral city of Lund (which he misspells “Lunn”), which is in western Scania and faces Copenhagen on the other side of the Sound, as Norwegian. This, despite the fact that in footnote 61 on the same page 51 I dutifully explain the geographical location and historical change of hands of the region, which was not, however, from Norway to Sweden,

82 83 84

Benedictow 1987: 401–31. Benedictow 1993/1996: 177–80. Above: 34–8, below: 289–311.

60

chapter two

but from Denmark to Sweden: Scania has never been Norwegian territory, literally far from it. The point of departure is that my doctoral thesis, in accordance with its title, Plague in the Late Medieval Nordic Countries, relates not only to my Norwegian patria but also to the late medieval plague history of the Nordic countries. In relation to the point at hand I cite two fine studies of the Obituary of the Cathedral of Lund by two Danish historians, namely by J. Kinch (1817–88) and by Emeritus Professor E. Ulsig of Aarhus University,85 the leading specialist on Danish plague history today.86 Thus, it is simply untrue that “Benedictow squeezes from a mere ten deaths records [sic] found in an obituary of monks at Lunn a reading that is far beyond the statistical probabilities of those records,”87 and so on. This is a characteristic and instructive instance of Cohn’s distortions of facts. Obviously, I have done nothing of the kind, I merely cite two studies by competent Danish colleagues which I consider to be of high quality. Ulsig was first opponent when I defended my thesis in 1992 and he had no objections to my citation and use of his own study or of Kinch’s.88 Likewise, I have never seen comments on these studies by Nordic colleagues that have any resemblance with Cohn’s allegations and therefore, by implication, have collectively failed to recognize the crude statistical mistakes that are so self-evident to Cohn. This should make it clear that the disparaging words Cohn heaps on my work since it represents such a serious threat to his theory are misplaced and that he is instead indirectly and on false grounds disparaging Kinch and Ulsig as scholars. I have presented these studies again in my monograph of 2004.89 Cohn ends this chapter on historians (allegedly) squaring the circle by generally disparaging historians working in the field of plague research while singling out for special negative attention one of the greatest scholars of twentieth-century historiography who, fortunately, concentrated increasingly on the field of plague history and made tremendous contributions, namely Carlo M. Cipolla: Historians’ unbending attachment to the Black Death as the same as modern plague illustrates with uncanny precision Cipolla’s observation: “Paradoxical as it may sound, the lesson of history is that all too often

85 86 87 88 89

Kinch 1869; Ulsig 1991. Benedictow 1993/1996: 51. Cohn 2002: 52. Ulsig 1994: 94–105. Benedictow 2004: 165.

the ethics of scholarly work

61

people find it easier to manipulate the facts to fit their theories than to adapt their theories to the facts observed.”90

Cipolla had in mind, of course, people of the sixteenth and seventeenth centuries who had to fight plague on the basis of proto-scientific, deficient and misleading notions of the nature of epidemic disease which affected the way they perceived the epidemic and the conceptual framework within which they endeavoured to understand it. To assert, as Cohn does, that Cipolla with his broad knowledge of the accumulated wisdom of two generations of intensive modern scientific medical and epidemiological studies of plague was a comparable victim of similar misconceptions cannot be taken as a serious scholarly opinion. The heart of the matter is again that Cipolla also considers historical and modern plague the same disease. Does not the notion of “unbending attachment” and its association with manipulation of facts imply intellectual dishonesty on the part of historians in general and of Cipolla in particular? Or can it be understood as an assertion of general gross incompetence on the part of all scholars who have reached conclusions different from Cohn’s own? Later Cohn belittles Cipolla again on as poor grounds as here.91 These examples are only a small selection from the first part of his monograph.92 It should be obvious what sort of need lies behind this profusion of negative and disparaging characterisations and assertions, which collectively degrade plague researchers of both the historical and medical professions: “historians square the circle,” “scientists square the circle,” “historians,’ unbending attachment to the Black Death as the same as modern plague,” “historians and medical scientists have held on so passionately to the notion that the Black Death and its successive waves of pestilence must have been the same disease,” “idée fixe,” and so on. Why is it inconceivable that all of these historians and medical scientists have reached their conclusions and opinions on the basis of dedicated, serious and highly competent research and scholarship? What motive could they conceivably have for squaring the circle in their field of scholarly work? Is that not an accusation of intellectual dishonesty? Or could they all really be grossly incompetent and therefore to be excused of dishonesty?

90 91 92

Cohn 2002: 54. Cohn 2002: 209. Cohn 2002: 11–54, 114–5.

62

chapter two

Why is it only Cohn who has understood the true nature of the Black Death and plague in general? How can it be that all other scholars in the field, physicians as well as historians, are collective victims of an idée fixe, a suggestion with clear psychiatric connotations? Does not Cohn really turn the scholarly usability of the notion of idée fixe on its head? Is not a collective idée fixe a rather strange notion, especially among scholars and trained scientists with their intellectual tools, scientific methodology and long training for disciplined testing of the tenability of scientific hypotheses? Is not an idée fixe much better adapted as an analytical tool at the individual level of (psyco)analysis? If this is correct, is this notion of idée fixe not much better adapted as an analytical tool for understanding the individual scholar with ideas which deviate sharply from those of everybody else, especially if this individual scholar argues his case in a furioso way, disparaging more or less all other scholars in this field of research (if he is not misleadingly attributing to them his own notions)? The Attack on Schofield (and Benedictow and L. Bradley) In his study of the plague epidemic in Colyton 1645–6, a small town of 1500 inhabitants, Schofield focused in exceptional detail on the question of whether or not the pattern of mortality varied according to size of family, and if it did, in what way, and what this could reveal about the mechanisms of spread and the nature of the disease.93 It is useful for several reasons to discuss Cohn’s unwarranted attack on Schofield’s paper because these questions play a significant role in some later discussions. In this attack, he also in his usual disparaging way involves Bradley and me,94 while he forgets to include Slack who entertains the same opinion.95 Schofield’s study is based on a full family-byfamily reconstitution of the population which requires meticulous registration of all inhabitants in order to follow closely their individual and collective fates during the epidemic. This is gruelling timeconsuming work with the objective of performing a detailed empirical analysis of the epidemic, which should make it clear that allegations of

93 94 95

Schofield 1977: 95–132. Cohn 2002: 121. Slack 1985: 177–8.

the ethics of scholarly work

63

arbitrariness are unfounded. Unfortunately, some long citations are necessary to clarify the scholarly problems involved in this case. Cohn makes the following three accusative and disparaging assertions with the footnotes in the running text, and my enumeration in brackets: Curiously, Roger Schofield, “An Anatomy of an Epidemic: Colyton, November 1645 to November 1646,” in The Plague Reconsidered, p. 102, asserts the opposite: [1] that diseases such as bubonic plague cluster in households but airborne infections do not. [2] His claim (and denial of hundreds of years of common sense and epidemiological research) is not, however, based on any new epidemiological findings; no note follows it, but perhaps because of Schofield’s reputation as a demographic historian and his quantitative skills, [3] others have followed blindly: see Bradley, “Some medical aspects of plague” 11–24, ibid.; and Benedictow, Plague in the Late Medieval Nordic Countries, p. 174.96

This passage contains three central accusations: (1) Schofield’s view is obviously and self-evidently untrue and grossly misleading and at complete variance with elementary principles of epidemiology; (2) Schofield’s view is not based on sources or fact but is arbitrary and misleading; (3) Bradley and Benedictow accept uncritically and therefore “blindly” Schofield’s views because Schofield enjoys such high reputation as a demographer. Cohn asserts that his views are based on p. 102 in Schofield’s paper. This page begins with the following statement: Let us take as a first hypothesis the proposition that the more that the chances of catching a disease depend on physical proximity to a localized source of infection, the more deaths will be clustered by household or family, so that some families will be affected whilst others, even near at hand, will escape. In the case of bubonic plague, for example, we would expect the chances of being bitten by an infected rat flea to be higher in a locality where rats had just died of plague than elsewhere. Since the black rat (Rattus rattus) generally stays close to human habitation, a person would be more likely to be infected by a flea in a house where rats had recently died, than by a rat flea hopping across either from a dead rat

96

Cohn 2002: 121, fn. 156.

64

chapter two lying in the gutter, or from someone encountered in the street. Similarly, in the case of typhus, a person would be more likely to acquire an infected louse from someone who had just died in the room in which he was sleeping than from a casual encounter in the street. With airborne infections, on the other hand, transmission occurs much more readily as people breathe out infected droplets as they move around during their normal daily activities. Thus diseases like bubonic plague and typhus are likely to be associated with geographically clustered patterns of death, while airborne infections, such as influenza, will show much less clustering.

Clearly and obviously, Schofield establishes here a very interesting working hypothesis on the basis of a sound and profound knowledge of epidemiological tenets. This puts in perspective Cohn’s assertion that Schofield’s view represents a “denial of hundreds of years of common sense and epidemiological research.” Conspicuously, Cohn is not able to find a single modern epidemiological standard work or paper for support of his disparaging argument of “hundreds of years of common sense and epidemiological research.” For about hundred years, scholars have rejected the common sense of hundreds or even a couple of thousand years of miasmatic epidemiology. The beginnings of bacteriology, and therefore also the beginning of microbiology, was established as late as in the last decades of the nineteenth century and for obvious reasons epidemiological research in the sense of modern scientific research begins at around the same time. There is no factual basis for Cohn’s accusation: Schofield has not denied the tenets of (scientific) epidemiology, but on the contrary, he has used them in a creative and scholarly fashion in order to construct a fine tool for intellectual analysis. Schofield next prepares the ground for empirical testing of his hypothesis and takes time for the pedagogical task of explaining some elementary statistical principles of demographic distribution and the usefulness of the binomial expansion for this purpose to his readers who would tend to be historians without significant statistical training: If we want to discover whether deaths were in fact clustered in families in a particular epidemic, we need to know what the distribution of deaths by family would have been if they had occurred randomly throughout the population […]. In order to calculate this distribution we need to know the chance of dying and the size of the family. This immediately raises the further question of whether the chance of dying in practice varied according to the size of the family […].

the ethics of scholarly work

65

Comparison of the distribution of mortality according to family size with a random distribution will reveal possible deviation, and if there is deviation, the pattern of deviation should enable the identification of social factors that affected the distribution of mortality. After further methodological and epidemiological discussion on pages 102–5, Schofield can finally address his material on the population of Colyton which consists of 406 households containing 1513 persons who suffered 298 deaths or a mortality rate of 20 per cent. Table 2 presents “Death rates by size of family, Colyton. Nov. 1645–Nov. 1646,” and the material is here organized according to size of family from 1 person to 8+, the number of families according to each size, the number of persons each size category contains, the number of persons dying in each size category and the mortality rate for each age category. This provides the basis for studying whether the chance of dying was random or whether it was affected by family size. The conclusion to be drawn from this material is couched in the careful language of an eminent and disciplined scholar: The balance of evidence would therefore seem to suggest that person-toperson transmission of the disease in close physical proximity was not an important element in the Colyton epidemic.97

In Table 3, the material is organized according to “Observed and expected distribution of families, by size and number,” and Table 4 shows “Ratio of observed to expected frequencies ±(0.005),” and “No. dying in family.” Schofield explains: For every family size the number of families with extreme experiences (no-one dying: everyone or almost everyone dying) was greater than expected, and the number of families with some people dying and others surviving was correspondingly far fewer than expected. There was therefore a marked tendency for deaths to cluster in some families and for other families to escape the epidemic altogether […]. Thus in Colyton in 1645–6 an individual’s chance of dying in the epidemic was not independent of what happened to others in the same family […] his chance of dying had little, if anything to do with the size of household in which he lived […] this combination of a strong clustering of deaths with little apparent association between mortality and household size, suggests that the Colyton epidemic is unlikely to have been caused either by an airborne disease or by a contagious disease such as dysentery. It also casts doubt on diseases, such as typhus, which are 97

Schofield 1977: 105–6.

66

chapter two spread by ecological factors, and the most promising candidate would seem to be bubonic plague with the rat fleas as the significant vector.98

It is this result of Schofield’s combination of complete demographic data, careful epidemiological analysis, and mastery of demographic statistical methods that enrages Cohn because it adduces substantial proof to the effect that historical plague was bubonic plague, and represents as such a mortal threat to all alternative theories. This explains why the other advocates of alternative theories pass by Schofield’s paper in silence, even when they cite other papers in the same book, as Scott and Duncan do. This also puts in perspective Cohn’s assertion that Schofield’s views were arbitrary: “His claim […] is not, however, based on any new epidemiological findings; no note follows it.”99 The fact is that Schofield’s views are massively documented and are based on a very careful collection of empirical data through the total registration of the population according to the methodology of family reconstitution. Schofield’s observation fits well with the observations of the IPRC: after the introduction of plague contagion in a rat colony, rats soon begin to die and their fleas to gather on the remaining hosts, until the rat colony is so decimated ten to fourteen days later that released rat fleas have great and increasing difficulties in finding new rat hosts. In this situation hundreds of dangerous rat fleas swarm in the proximity of household members. Since bubonic plague is caused by great numbers of rat fleas released quite closely in time from dead rats, many members of households or inhabitants of adjacent houses would contract the disease at much the same time. This was also observed by plague researchers in India: “[…] when two or more [plague] cases occur in a house, they are attacked practically simultaneously as if from a common source of infection.”100 For this reason, it is an epidemiological misunderstanding when Cohn and Alfani in a recent paper on plague mortality in early modern Milan and Nonantola maintain that the fact that household members typically fell ill in a brief time constitutes evidence that historical plague was a viral disease spread by droplets.101 Instead it is evidence of rat-borne bubonic plague, as shown by Schofield. 98 99 100 101

Schofield 1977: 106–8. See above: 63. Lamb 1908: 67; IPRC 1907i: 881. Cohn and Alfani 2007: 178, 192–6.

the ethics of scholarly work

67

Cohn states disparagingly about Benedictow and Bradley that they “blindly,” presumably meaning uncritically and incompetently, accept and cite the epidemiological principles and findings of Schofield’s paper. So again he levels accusations for incompetence and/or intellectual dishonesty against historians. Are these accusations more tenable than those levelled against Schofield? Benedictow presents the part of Schofield’s paper on clustering of plague cases in Colyton on pages 173–4 of his doctoral thesis. This part will be cited verbatim in its entirety so that the readers can see for themselves and make their own judgement without making an extra effort: Schofield has explored new avenues to obtain insights about modes and patterns of epidemic spread, and has devised methods of determining the nature of epidemic diseases. In the case of Colyton (south-east Devon), in which about 20 per cent of the population were lost in the epidemic of 1645–6, the source material did not allow any study of the territorial distribution or spread of epidemic mortality. Instead, he was able to demonstrate that the pattern of deaths by family or household offered important clues to the nature of the epidemic disease and its mode of transmission and dissemination. He first makes the important analytical distinction that “the clustering of deaths in families, and the variation in the death rate according to family size, are two logically separate aspects of epidemic mortality.” If the chances of catching a disease depend on physical proximity to a localized source of infection, as is the case with rat-borne bubonic plague, deaths will be clustered in some households, whilst others, even in the immediate vicinity, remain unaffected. There should be no association between the chance of being infected and household size. Airborne infections, being transmitted directly between people as they move about during their normal daily activities, show much less clustering, but a strong correlation with household size (cf. Dijkstra’s demonstration of the pattern of spread in Jordan of the influenza epidemic in 1918). Diseases spread by human parasites, like exanthematic typhus (lice) or—according to Biraben—bubonic plague by human fleas and lice, might be expected to show a moderate clustering and a very strong association with household size. The conclusions were unequivocal. There was a “marked tendency for deaths to cluster in some families, and for other families to escape the epidemic altogether”; the “chance of dying had little, if anything to do with the size of household.” This combination points to a disease with a distribution which is largely determined by ecological factors, most probably “bubonic plague with the rat as the significant vector.”102 102

Schofield 1977: 101–6.

68

chapter two As a part of her dissertation on epidemic diseases in early renaissance Florence, A. Carmichael carried out a study of the spread of plague in the quarter of Santo Spirito during the minor epidemic of 1430. In my opinion, the pattern agrees closely with the findings of Dijkstra, Woehlkens, Slack and Schofield.103 The extreme local character of dissemination, the clustering of deaths at first in one part of this traditional working class district and even along certain streets within this small area, the clustering of plague deaths within some families even as the immediate neighbours escaped unharmed, the slow progression of the epidemic, and the impression that many streets seemed to begin to function as local plague foci as the epidemic spread through the summer months, all point to the same explanation. The maps showing the spatio-temporal progression seem close to the maps of Dijkstra and Woehlkens. As Carmichael does not make the important analytical distinction emphasized by Schofield, that clustering of deaths in families, and variation in the death rate in families of different sizes are two logically separate aspects of epidemic mortality, she did not collect the information necessary to decide the type of clustering she had registered. Her own epidemiological analysis therefore becomes ambiguous.104 This illustrates the significant contribution of Schofield’s paper to methodology, he provides the instrument to clarify the issue of clustering and to determine this social aspect of the epidemic as the type of dissemination characteristic of rat-borne plague.

I ask readers to read this text carefully and consider whether it justifies Cohn’s allegation that the author accepts blindly and uncritically Schofield’s text (because of his “reputation as a demographic historian and his quantitative skills.”) In the case of Bradley, no such citation can be made. Cohn refers to Bradley’s paper “Some medical aspects of plague” on pages 11–24 in the same publication with a collection of papers on plague. However, since this paper does not contain a word from or about Schofield’s paper, it is impossible that Bradley in this paper accepts blindly and uncritically anything from Schofield’s paper. It is again an unfounded allegation. Presumably, the crucial point is that Bradley published another paper in the same book, his study of a plague epidemic based on a complete family reconstitution of a parish population, namely the epidemic in Eyam in 1665–6. In this study, which is independent of Schofield’s of Colyton, he reaches the same conclusion as to the nature of the disease, namely that it exhibits the characteristic epidemiological,

103 104

See chapter 9: 142–50. Carmichael 1978: 74–92, 101–8.

the ethics of scholarly work

69

demographic and seasonal features of bubonic plague. Thus, Cohn endeavours, as it seems, to discredit Bradley as a scholar without revealing to his readers that such a paper is published in the same book as Schofield’s paper, and a fine paper it is. In Part 1 of his monograph, Cohn clears the ground for his alternative theory by criticising scathingly the work of various medical scholars and historians in two separate chapters disparagingly titled “Scientists Square the Circle” and “Historians Square the Circle.” As these titles imply, Cohn asserts that the outstanding medical scholars who performed great research effort on plague, many of whom also took a passionate interest in plague history, and the historians who have performed comprehensive studies on plague epidemics in the past, have collectively squared the circle. Thus, they have either been intellectually dishonest or incompetent or both and the outcome of their research has been grossly misleading and untenable since it is incompatible with his alternative theory. Such gross disparaging assertions on behalf of so many fine scholars should meet with profound incredulity. Sadly, I believe that it has been demonstrated here on a broad basis that Cohn’s arguments are severely flawed and are grossly unfair to both medical and historical scholars. The central aspect of the discussion as it unfolds is reflected in the chapter’s title “The Ethics of Scholarly Work,” since it is demonstrated that the means Cohn has employed are very questionable and that it is simply not true that these medical scholars and historians have squared any circles. Instead, as dedicated and conscientious scholars they have followed the tenets of medical and historical methodology and made great and lasting contributions to the epidemiology and medical knowledge of plague as a disease and to the history of plague epidemics.

PART THREE

BASIC CONDITIONS FOR BUBONIC PLAGUE IN MEDIEVAL EUROPE

CHAPTER THREE

RATS Introduction: How to Study Rats in History Advocates of alternative theories on the microbiological nature of historical plague epidemics insist triumphantly that there was no murine basis in the form of black rats in Europe at the time (see below). They concede that there could have been a significant presence in Southern Europe and along the Mediterranean coasts, especially in the urban centres, but elsewhere in Europe, they maintain, there could only have been an incidental and transitional presence caused by ship transportation and they deny that the black rat could have had a permanent presence in Northern Europe. All of these scholars agree that black rats play a crucial role in epidemics of bubonic plague. Thus, the opposite is obviously true: if there were no or only a tiny presence of black rats in medieval Europe restricted to the southern and Mediterranean parts of the Continent, there could not have been epidemics of bubonic plague, or there could not have been more than the occasional small outbreak in the southern parts of it. It is also generally agreed that the brown (or grey) rat did not arrive in Europe until the early eighteenth century.1 Consequently, if there were rats in medieval Europe, they would have to have been black rats. This does not mean, as the zoologist D.E. Davis asserts, that black rats are the cause of bubonic plague.2 These rats have lived peacefully with human beings for thousands of years. Rats are principally victims of bubonic plague. As soon as their dead bodies start to loose temperature, their fleas begin to desert them, fleas which have satiated themselves on septicaemic rat blood and can transmit the real cause of bubonic plague to human beings, namely infective and lethal doses of the bacterium 1 See, Zinsser 1934/1985: 200; Hirst 1953: 123, 142; Twigg 1984: 75; Davis 1986: 456; Audoin-Rouzeau 1999: 423, asterisked footnote. In a personal communication by e-mail of 10 January 2006, Anne Kristin Hufthammer of the Zoological Museum of the University of Bergen, Norway, has confirmed to me that this arrival date for the brown rat is still generally accepted. 2 Davis 1986: 455.

74

chapter three

Yersinia pestis. Methodologically, necessary conditions and causes are very different matters and should also be sharply differentiated from sufficient conditions and causes. Methodology is not Davis’s strong suit, as will unavoidably be shown below. Then there is the question whether or not the brown rat played a part which may affect our understanding of medieval and early-modern plague epidemics. In his “review” of my monograph on the Black Death, Cohn rejects my view that, according to the IPRC’s reports, the black rat was of paramount importance in the aetiology and epidemiology of plague in India: However, he [Benedictow] has read these reports selectively. For instance, he maintains that the black rat (Rattus rattus) was responsible for plague in the years 1346 through 1353 as well as during the 20th century, but the Indian plague researchers found as many dead brown rats as black ones in dwellings where infection was active.3

Cohn’s accusation warrants a closer look at the IPRC’s conclusion as to the relative importance of the brown rat (today called Rattus norvegicus, until 1910 Mus decumanus) and the black rat (today called Rattus rattus, until 1910 Mus rattus): In Bombay city Mus rattus and Mus decumanus both occur in prodigious numbers, in the country villages, however, Mus decumanus is very rarely found. Mus rattus in Bombay is essentially a house rat […] it may almost be said to be a domesticated animal. Mus decumanus, as is well known, is a rat which lives for the most part outside houses in sewers, storm-water drains, stables, etc. Mus rattus is apparently much more common in Bombay than Mus decumanus […]. It is necessary at the outset to insist upon the fact that in Bombay City there is a Mus decumanus epizootic and a Mus rattus epizootic. […] there cannot be the slightest doubt that the place-infection of man is intimately related to that of M. rattus […] that M. rattus is essentially a house-rat and that it lives in close association with man. It necessarily follows from this association that the place-infection of M. rattus must correspond closely to that of man in the sense that both must be referred to inhabited buildings. We think it justifiable to conclude that the epidemic is directly attributable to the rattus epizootic.4

3 4

Cohn 2005: 1354. IPRC 1907g: 743, 746–7, 752, 766–7.

rats

75

This proves that IPRC researchers were of the opinion that the plague epidemics were mainly or wholly a reflection of epizootics among black rats; in the countryside where the brown rat was very rare, the epidemics in the villages would be about entirely based on the black-rat epizootic. This demonstrates also that bubonic plague epidemics can develop and spread on the basis of the black rat alone, a fact that underlies the conclusion that historical plague was bubonic plague. Also in Mumbai where the brown rat had a substantial presence the epidemic was predominantly based on the epizootic among black rats. As can also be seen, the black rat was apparently much more common in Mumbai than the brown rat, and since the brown rat was also largely an out-of-door rat, its significance for the epidemic process would unavoidably be relatively small. Cohn’s assertion that the IPRC found as many dead brown rats as black rats in the dwellings of people in India is spurious. This is confirmed by G. Lamb in his summary of the Commission’s work to May 1907 which is an excellent source for reliable information on the Commission’s findings and views in the early years.5 Clearly, Cohn misrepresents my view.6 Thus the relationship between the rat plague epizootic and human plague epidemic in India must have been very much the same as in historical plague epidemics, if they were indeed epidemics of bubonic plague. Having clarified this point, we can now focus on the presence and distribution of the black rat in medieval and early modern Europe. Leading plague researchers such as Hirst, Pollitzer, Wu Lien-Teh, and J.J. van Loghem who studied the bubonic plague epidemics of the first half of the twentieth century argue for a broad presence of the black rat in medieval Europe. This view is based mainly on contemporary medieval and early modern written sources which also contain some drawings. Their view is also supported by peculiar epidemiological features of the spread and seasonality of the epidemics that were taken as reflections of a basis in rats and their fleas. In support of this conclusion, they emphasized the interval between the first case(s) and the subsequent endemic and epidemic developments, the latency

5

Lamb 1908: 22–3. It is, however, not clear to me what point he is trying to make, since it is quite generally believed, as mentioned above, that the brown rat did not arrive in Europe until around 1700. 6

76

chapter three

period which is a defining feature of bubonic plague,7 and the strong tendency of epidemics to break out in the warmer seasons and disappear or be substantially diminished by cold weather, which they explained, on the basis of the findings of the IPRC and other scholars, through the role of rats and their fleas.8 When Davis refers to Hirst’s monograph and write “that a search for evidence to support these statements [as to the presence and role of rats] produces nothing,”9 this is not correct and also his reference to page 119 is wrong, since this matter is not discussed on this page. Further, his reference to a single page, when in fact Hirst addresses the matter broadly over quite a number of pages elsewhere in the monograph, can also produce an incorrect impression, because Hirst has not taken this question lightly as Davis’s remarks suggest (see below). Since all medieval European references to house rats, both textual and graphical, as a present type of animal clearly refer to black rats, the discussion must address the question of whether or not black rats were present in sufficient numbers and with a sufficiently widespread geographical distribution to constitute the basis for bubonic plague epidemics. Advocates of theories that historical plague epidemics were not bubonic plague but were caused by some alternative microbiological agent assert, as mentioned above, that there either were no rats at all (so Scott and Duncan, with an incorrect reference to Twigg10 and Gunnar Karlsson11) or that the presence of black rats was restricted to a tiny and transient incidence in urban centres, “if it existed at all” (so Davis and also Twigg, who first advocated this view, and who is supported by Scott and Duncan12). Cohn accepts that black rats were present with some unspecified incidence, but maintains that they were not involved in plague epidemics, since dead rats are not mentioned in such circumstances.13 On the first page of his monograph, he declares that “No contemporary evidence links the Black Death or its

7

See below: 279–88. See for instance Hirst 1953: 121–9. 9 Davis 1986: 456. 10 Scott, Duncan and Duncan 1996: 18; Scott&Duncan 2001: 261, 262, 280–1, 357. 11 Karlsson 1996: 263–84. 12 Twigg 1984: 75–89; Davis 1986: 460. Scott and Duncan 2001: 55, 57, 108, 134, 317, 357. 13 Cohn 2002: 82. 8

rats

77

successive strikes in Western Europe to rats.”14 This view is based on three main arguments: (1) the paucity or absence of references to observations of dead rats in contemporary sources relating to historical plague epidemics;15 (2) the climate in the northerly parts of Europe is too cold for black rats, thus the frequent spread of plague epidemics must be seen as proof that they were not bubonic plague;16 (3) Karlsson and Scott and Duncan maintain that they have proved that plague epidemics in Iceland and the village of Eyam in Derbyshire, England, respectively took place without the presence of rats, which constitute proof that historical plague epidemics were not bubonic plague. Since the question of the presence of rats in Europe at the time of the plague epidemics is important, these three main arguments by the advocates of alternative theories should be discussed seriously and satisfactorily, and this is the subject of this chapter. Karlsson maintains that two fifteenth-century plague epidemics in Iceland were pure epidemics of primary pneumonic plague caused by some mutated form of Yersinia pestis, the bacterium that causes bubonic plague, and that this, in his opinion, was the general form of late medieval plague; his theory will be discussed below in a chapter in Part 5. In recent decades an important new source on the history of rats has appeared, namely zoo-archaeology or more accurately archaeological zoo-osteology, the study of animal bones found in archaeological excavations. Bone material of rats constitutes material evidence of the presence of rats with strong evidentiary value. If such evidence is not found or only incidentally found when looked for systematically, this will constitute evidence to the effect that there were no rats in medieval society or alternatively that there was only a tiny presence which cannot constitute a basis for the large-scale spread of bubonic plague epidemics, and consequently, the view of the advocates of alternative theories would be vindicated. However, if rat bones are found quite

14

Cohn 2002: 1. Twigg 1984: 83, 111–2; Scott and Duncan 2001: 54–5, 359. 16 Davis 1986: 455–70; Twigg 1984: 57, 86–8, 99–100, 112, 218; Scott and Duncan 2001: 57, 261, 357. 15

78

chapter three

frequently when looked for as an ordinary part of archaeological excavations of human settlements, and with wide geographical distribution, these advocates’ crucial argument on this point will, on the contrary, be proven invalid. The osteological material and perspective will be presented in the last subchapter of this chapter on rats. The Nature of Rats and the Frame of Reference of the Medieval Mind Clearly, the basic observation with respect to the paucity of references to rat mortality in plague epidemics in historical sources is correct, although as for instance, J.J. van Loghem showed long ago, the silence is not quite as systematic or complete as had been asserted.17 Twigg considers over several pages and with considerable scepticism reports of rat falls associated with bubonic plague.18 However, for several reasons the implications and significance of the relative paucity of observations of dead rats in relation to historical plague epidemics is not at all obvious. As we shall see, relevant studies on rat-plague epizootics associated with plague epidemics have not been considered, and important methodological and source-critical problems have been neglected. In relation to this question, there is a crucial methodological point which the advocates of alternative theories fail to address: the validity of this argument depends on a premise to the effect that contemporary sources should be expected to mention dead rats in connection with bubonic plague epidemics, and that this should be quite a regular feature in accounts of those epidemics. Otherwise, this argument becomes an inference ex silentio, an assumption to the effect that the failure of sources to mention a phenomenon proves that it did not exist or occur, which is a classic fallacy in the methodology of history and social sciences. Firstly, what medieval sources and medieval chroniclers do and do not mention is a continuous source of disbelief and bewilderment to modern scholars.19 Certainly, medieval man had a very different mental frame of reference for the assessment of the relative importance of various types of contemporary events from that of modern man.

17 18 19

See, for instance, Van Loghem 1918 and 1925. Cf. Wu Lien-Teh 1936a: 8–9. Twigg 1984: 25–7. Slack 1985: 34–5.

rats

79

In this context, it might suffice to mention that many chroniclers do not mention the Black Death, although it can be shown that their city, region and country were fiercely ravaged by the epidemic.20 Generally, modern historians find it difficult to accept that outbreaks of mortal epidemic diseases were “determined by divine providence and that their first cause was supernatural: epidemics were God’s punishment for man’s sin,” which was the usual opinion all through the plague era.21 Also historians find it difficult to accept the reality or predictive value of the omens or portents of severe epidemics that contemporaries claim to have observed, for instance, the appearance of a man mounted on a great black horse or a giant striding along, his head far above the roofs of the houses, or the appearance in the night sky of skeletons with swords, hearses, coffins, unknown comets and astrological constellations. It is also difficult to accept the causative implication in the assertion that the first victims of plague fell sick after people had seen “a vision of a corpse or a dead body carried to the parish [church] there to be buried,” and so on.22 Thus, medievalists have to recognize and relate to the fact that medieval man, on the background of medieval culture: (1) believed in types of epidemic manifestations and causation that today will generally be rejected as superstitious or false; (2) did not take the same interest in strict empirical observation, acute analysis and accurate knowledge (in the scholarly meaning of these terms) and, consequently, would not notice the same phenomena as modern man; (3) did not have the same view of what were important and memorable contemporary events as modern man has. Thus, all assertions as to what medieval man should be expected to observe and record must be discussed according to medieval man’s frame of mind and culture and be substantiated according to ordinary

20

See Benedictow 2004: 191–4, and fn. 9 on p. 192, 206–7. Slack 1979: 10. In 1641, John Wright, Jr., published a book called Londons Lamentation. Or a fit admonishment for City and Countrey, wherein is described certaine causes of this affliction and visitation of the Plague, yeare 1641, which the Lord hath been pleased to inflict upon us, and withal what meanes must be used to the Lord, to gaine his mercy and favor, with an excellent sprirituall medicine to be used for the preservative both of Body and Soule. See Cox 1910: 151. 22 See for instance Bell 1951: 1–3; Mullett 1956: 16; Slack 1979: 46; Slack 1985: 34–6, 87–8. 21

80

chapter three

demands for evidence. If the assertion is that medieval chroniclers should be expected to mention rat falls in connection with plague epidemics, such a subject should be shown to belong to the types of events or topics that chroniclers would consider relevant to mention. Empirical orientation increases with modernity, first slowly but clearly from the Renaissance and the Early Modern Period. In order to understand medieval and early modern sources one must understand the frame of mind and understanding of the medieval and early modern people who produced them. To illustrate the significance of this point: Jean de Venette (c. 1307–c. 1370), one of the most prominent and commonly cited chroniclers on the Black Death, states that “the most surprising fact is that children born after the plague, when they became of an age for teeth, had only twenty or twenty-two teeth, though before that time men commonly had thirty-two in their upper and lower jaws together.”23 The fact is that young children have twenty milk teeth, while adults have thirty-two teeth including four wisdom teeth. The idea that plague should have caused such change is not only at variance with modern genetics, but further, Jean de Venette could easily have tested and corrected it by examining the teeth of infants or young children born before the plague and after the plague. This is, then, an illustration of the weak empirical orientation even of educated medieval people. To illustrate the significance of the frame of reference for understanding the reality of observed phenomena, we may note that Anton von Leeuwenhoek, who invented the microscope in the 1670s was the first human being to observe microbes, but neither he nor other researchers for 200 years to come persuasively connected such observations with the idea that such creatures could be causal agents of epidemic diseases. They did not link this type of observation to an explanatory idea of disease for the practical reason that they had no frame of understanding and analysis, no theory, that could lead their thoughts and reasoning to a microbiological theory of epidemiology.24 This puts in perspective medieval man’s great helplessness in understanding the nature and dynamics of epidemic disease. People observe and explain and act according to what their frames of reference and 23

The Chronicle of Jean de Venette 1953: 51. It is true that notions of germs had long been around, but this case history illustrates the lack of real interest in such ideas even after they became to some extent testable by microscopic observation. 24

rats

81

understanding permit or in the direction their thoughts are lead by their preconceptions. Thus, in this context, the beliefs and understanding of people in the past in relation to the cause of epidemic disease and mortality must be taken into account. The great majority, apparently the overwhelming majority of medieval persons, believed that epidemic mortality was an expression of God’s anger and punishment for their sins, and this view was predominant far into the Early Modern Period.25 This belief would not be conducive to observation of natural phenomena and alternative rational interpretations. The limited number of learned persons who had acquired knowledge of Hippocratic-Galenic medicine would have understood epidemic disease as a reflection of the presence of miasma. Miasma was corruption or pollution of the air by noxious vapours containing poisonous elements that were caused by rotting putrid matter, but could also be let out from the ground by volcanic activity or particular constellations of planets. Miasma was spread by wind and could therefore spread speedily, it could enter persons by inhalation or through the pores of the skin. Not until the Renaissance, in the decades around 1500, was this theory of miasma expanded to include the idea that healthy persons could be infected by touching infected persons or objects contaminated by them with miasma (fomites), i.e., a miasmaticcontagionistic theory of cross-infection and epidemic spread, although the idea was for a long time not broadly accepted.26 In the words of C. Creighton, the last champion of miasmatic theory in England, writing around 1890: The virus of plague has its habitat in the soil, although it may be carried long distances clinging to other things. In its most diffusive potency it [miasma] is a soil-poison generated […] out of the products of cadaveric decay; in its less diffusive but hardly less malignant potency, it is a soil poison generated out of the filth of cattle housed with human beings, or out of domestic filth generally […].27

Also, in its medieval form, miasmatic theory allowed in principle empirical observation, but classical medicine’s enormous prestige and medieval man’s weak empirical orientation (in the scholarly meaning of the term) meant that chroniclers and physicians would rather interpret what they saw according to the predictions of classical miasmatic 25 26 27

Slack 1979: 10; Slack 1985: 26, 28–9. See, for instance, Hirst 1953: 222–72, and Creighton 1891: 326. Creighton 1891: 173.

82

chapter three

theory than believe their own eyes: several mention rat mortality in connection with the Black Death, but together with mortality among a combination of other animals that are not susceptible to the same disease, such as birds, horses and snakes.28 Since miasma seeped up through the ground, it would also infect animals that spent much time underground like moles, rats or snakes,29 and since miasma was spread by wind, it was a logical corollary that birds would fall out of the sky, bee hives succumb,30 and so on, and this type of miasmatic inference took precedence over empirical observation. A typical example is provided by the account of the Greek historian Nikephoros Gregoras who witnessed the Black Death in Constantinople: […] The calamity did not destroy men only but many animals living with and domesticated by men. I speak of dogs and horses, and all the species of birds, even the rats that happened to live within the walls of the houses […].31

Since these accounts mention rat mortality in conjunction with mortality of animals known to be refractory to bubonic plague infection and insusceptible to the same pathogen, they are unusable as evidence of reality and rat epizootics in time of plague, and are rather evidence of contemporary culture and mentality and the presence of rats. Lastly in this context, it seems appropriate to mention the almost complete neglect of miasmatic theory by Scott and Duncan in their monographs: in the first monograph the term does not appear in the index, and in the popular version of the monograph of 2004 the word miasma is not mentioned.32 They just assume that contemporary notions of contagiousness can be understood in the light of the modern concept, presumably because this anachronistic approach serves their line of argument. In their original paper of 1996, they mention miasma, but apparently without understanding the concrete contemporary implications.33 An even more demonstrative instance of this

28

Hirst 1953: 127; Wu Lien-Teh 1936a: 8. See for instance Creighton 1891: 173. 30 Twigg 1984: 215. 31 Cited by Bartsocas 1966: 395. 32 See also below: 613–9. 33 Scott and Duncan 1996: 19. Strangely, they do not seem to understand that, according to the theory of miasma, it could be useful to put unslaked lime in plague graves, since it would hasten the decomposition of the bodies and counteract the development of miasma that could seep up through the soil and poison the air. The notion that the use of unslaked lime indicates anthrax is an anachronistic interpretation based 29

rats

83

neglect is their citation from Daniel Defoe’s book on the Great Plague in London where he describes in dramatic literary terms the notion of miasmatic-contagionistic spread of plague by diseased individuals. Whilst Defoe wrote this book in quite a journalistic way, hoping to earn some money in a climate of renewed fear of a plague outbreak, they present his account as proof of his great insight and judgment to the effect that he describes modern ideas of infection. This provides them with yet another opportunity to express their generally disparaging views of historians and medical scholars (the italics are mine): And yet for the whole of the twentieth century, going completely against common sense, it was universally and unequivocally believed that all the plagues were caused by a disease of rodents called bubonic plague, and that the infection was transmitted to people from rats by fleas. Rats and fleas are the established dogma of all history books today. What a pity that little attention has been paid to Defoe’s observation.34

Characteristically, “Debunking History” is the disparaging name of the chapter where this statement is found; the authors scorn historians (and physicians) of plague research for collectively “going completely against common sense” and for collectively being blind supporters of dogmatic beliefs. Defoe was born in 1660; he was five years old at the time of the year of the Great Plague, and his book A Journal of the Plague Year was published fifty-seven years later. The assertion that “Daniel Defoe had perspicaciously noted” the purportedly splendid observations that they attribute to him is obviously untenable and misleading and constitutes no reasonable basis for their disparaging remarks against historians. Defoe was not a scholar or writer of popular science, but mainly a literary author with clear commercial motives whose inaccuracies are legion. In fact, Defoe’s description of the contagiousness of diseased individuals is entirely compatible with and based on contemporary miasmatic theory. Since Scott and Duncan have apparently failed to note this, it seems that they do not have satisfactory knowledge and competence in historical medicine and epidemiology. The use of the term “common sense” as a superior substitute for scientific observation is also noteworthy. Evidently all scholars who have conscientiously and systematically applied scientific methodology and

on modern knowledge and usage. For the same reason, it was also usual to burn livestock which had died from murrain: see below: 580. 34 Scott and Duncan 2004: 165–6.

84

chapter three

empirical observation to their work and made these the basis of their results should have substituted it with “common sense.” Cohn brushes brusquely aside sound studies of contemporary notions of miasma in order to assert much the same (anachronistic) understanding of medieval man’s notion of contagiousness as Scott and Duncan.35 Carmichael has, as mentioned above, since taken Cohn and also Scott and Duncan to task in a good review essay on this point.36 Since bubonic plague, as shown above, is caused by great numbers of rat fleas departing quite close in time from dead rats, many members of households or inhabitants of adjacent houses would contract the disease more or less simultaneously. This was also observed by early plague researchers: “[…] when two or more [plague] cases occur in a house, they are attacked practically simultaneously as if from a common source of infection.”37 Thus, the epidemic scene of bubonic plague would readily lend itself to miasmatic and miasmatic-contagionistic understanding under the assumption of simultaneous contamination by polluted wind or multiple social contacts with a contaminated person. Contemporaries entertained also notions that were closely linked with superstition like the belief in the reality of the evil eye, that healthy people were easily infected by the look of diseased persons. In connection with the Black Death, several chroniclers and commentators venture outside miasmatic epidemiology in this way, insisting that “merely through looking, one person caught it from the other,” which can, of course, support notions of great speed of spread and be taken as confirmation of miasmatic epidemiology.38 Since this chapter is not about contemporary notions of contagion and the spread of epidemic disease, this subject cannot be developed further here. However one should keep in mind that since, in contrast to the claims of Scott and Duncan and Cohn, medieval and early modern man did not know that epidemic disease could be spread and transmitted by insects, they had no alternative to the understanding of contagion and transmission of disease offered by miasmatic theory (or contamination by look).

35 36 37 38

See for instance Cohn 2002: 114. Carmichael 2003: 253–66. Lamb 1908: 67; IPRC 1907i: 881. See for instance Benedictow 2004: 236.

rats

85

The Question of the Presence of Rats and the Methodological Fallacy of Inference ex silentio The advocates of alternative theories contrast the paucity or lack of evidence of dead rats in historical plague epidemics with assertions to the effect that this was a conspicuous feature of modern epidemics of bubonic plague. However, these assertions are typically not accompanied by references to corroborating scholarly studies, but reflect instead what these advocates of alternative theories consider to be self-evidently true, what must have been the case. They all avoid asking the crucial methodological question: on what grounds should people in the past be expected to observe intense rat mortality or at least substantial numbers of rat falls preceding the outbreak of plague epidemics and running concurrently with the epidemics as they unfolded? These researchers are thus committing a methodological fallacy, the fallacy of inference ex silentio, which is to infer from silence in the sources that a phenomenon or event did not exist or occur.39 Twigg, who generally functions as the pioneer of alternative theories, presenting seemingly important arguments that are eagerly picked up by others, is also the first advocate of alternative theories who commits this fallacy of inference ex silentio. He claims that if rats were present when bubonic plague arrived in 1348 there would have been heavy rat mortality, a fact well known and commented upon by people in endemic plague areas, and as this would have been experienced by the English then that fact alone would have been an important feature of the times. So far as I can find there was no occasion when this was recorded in the British Isles in 1348–50.40

This statement contains unsubstantiated and therefore arbitrary assertions as to what people at the time must have seen and what they should have commented on in writing. It contains also an arbitrary argument of fact in so far as Twigg asserts that heavy mortality of rats during plague epidemics was a “fact well known and commented upon by people in endemic plague areas” which is left unsupported by any corroborative evidence or references in the text or in accompanying footnotes. The lack of support is not accidental or fortuitous, for these assertions

39 40

Cf. Benedictow 2004: 192 and fn. 9. Twigg 1984: 111–2.

86

chapter three

as to what people should have seen are misconceived (as we shall see), but they do have a function: they clear the ground for using them as the basis for inference ex silentio that concomitant rat plague did not occur in medieval plague epidemics. When Cohn states on page 1 of his monograph that “No contemporary evidence links the Black Death or its successive strikes in Western Europe to rats,”41 also he commits an obvious fallacy of inference ex silentio, because he claims that such accounts or “links” should have been made by contemporaries without addressing the question of why contemporary people should be expected to note the role of rats and record it in writing. Cohn commits this fallacy of methodology again when he states: “To date, no one has found a description of a rat epizootic preceding or accompanying a plague in late-medieval or early modern Western Europe.”42 He believes that this provides him with another occasion to denigrate historians, stating: “As for the absence of rats associated with the medieval plague, historians have asked us to believe that their ubiquity made them invisible, even though they were noticed in moments other than plague.” He then goes on to cite “the English chronicle of Henry V” where it is related that the besieged inhabitants of Rouen were so desperate from hunger that they ate “all thair cattis, hors, houndis, rattis, myse.”43 Obviously, these two situations are not in pari materia, they cannot be compared in this regard: the English chronicler has a motive to mention rats, he wished to emphasize the English victory, and thus said that the French citizens were forced by the brave English besiegers to degrade themselves by eating animals usually never touched for food. This does not imply that contemporary chroniclers generally had a motive for mentioning dead rats in connection with plague epidemics if they were bubonic plague. However, it does contain evidence that (black) rats were present in this north-western French city in numbers making them usable for supplementary nourishment, and this was evidently acceptable as true by all readers of the chronicle, which is at variance with the insistence of the advocates of alternative theories that only tiny numbers of rats were incidentally and transitorily present in these parts of Europe, a point Cohn does not reflect on.

41 42 43

Cohn 2002: 1. Cohn 2002: 22. Cohn 2002: 82.

rats

87

The fact that Twigg is unable to support his assertion that people usually observe heavy mortality among rats during plague epidemics casts sinister shadows over Scott and Duncan’s repeated assertions to the same effect in their monographs, for instance, that Since bubonic plague is a disease of rodents, the arrival of an outbreak is frequently presaged by rats dying in the streets […].44 It has been regularly reported that the start of an outbreak of bubonic plague spreading to humans is presaged by rats dying in the streets; in a small village perhaps just a few, in a large South African township perhaps many barrowloads. And yet it is generally agreed that there is no mention in any of the accounts of rat mortality during the epidemics in the age of plagues in Europe.45

Thus Scott and Duncan also claim that dying or dead rats in the streets were a regular feature of bubonic-plague epidemics. However, it is a very conspicuous feature of this assertion of a fact purportedly based on frequent or regular observation that it is supported only by one reference to purported observations in a South African township. This is obviously very weak support for a sweeping comparative assertion on a purportedly central feature of contemporary bubonic plague as well as historical plague epidemics, actually they refer to it at least four times.46 Obviously, even if it were correct it is not an adequate basis for the crucial generalizing claim of the high frequency or regularity of this phenomenon. However, as we will see below, it is not correct. Scott and Duncan cross the line into this fallacy again in their second monograph of 2004 when they state disparagingly of historians: it is generally agreed that there is no mention in any of the accounts of rat mortality during the epidemics in the age of plagues in Europe. One comment was that “Historians have noted that contemporary accounts omit any mention of rat mortality,” but they have chosen to ignore this important point.47

Since they do not provide footnotes or literary references in support of their statements and assertions in the second monograph, it is impossible to know the identity of the person represented by “one comment

44 45 46 47

Scott and Duncan 2001: 359, cf. 54–5. Scott and Duncan 2004: 176. Scott and Duncan 2001: 54–5, 65, 359; Scott and Duncan 2004: 176. Scott and Duncan 2004: 176.

88

chapter three

was,” if this assertion has any basis in reality at all. The disparaging remark on historians is, according to the form of the citation from their text, clearly their own, implying that in their view historians in this field of study are generally intellectually dishonest, since they purportedly have collectively chosen to ignore an obvious and important, even crucial fact, and that historians, with their “eyes shut wide open”, have made this choice in order to protect their untenable theories on the microbiological nature of historical plague. It is possible to uncover the basis of these assertions from information supplied in their first monograph of 2001. Here, Scott and Duncan assert that dead rats were swept up by the barrowload in a South African township and that “dead rats littered the streets of an eastern metropolis,” citing “Annotation 1924” and “Liston 1924.”48 This is taken almost verbatim, references and all, from A.B. Christie’s general textbook on infectious diseases. Strangely, they insist that their assertion is based on the first edition of Christie’s textbook, published in 1969 which does not contain a chapter on plague; nor does the second edition of 1974. However, the third edition of 1980 contains a non-specialist chapter on plague, quite flawed, as will be seen.49 This chapter contains the account they cite and also important information which they neglect to mention in conjunction with their repeated assertions that dead rats were collected by the barrowful in the streets. Christie’s account of plague in South Africa is inconsistent, even insouciant. He mentions the purported observation in the South African township twice: on page 758, he uses the wording “dead rodents have been collected ‘by the barrowful,’ ” and two pages later he states that rats “may be swept up by the barrowful in a South African township.” It is this second assertion that Scott and Duncan have chosen to contrast with the lack of similar information in relation to historical plague epidemics in Europe and as proof that these epidemics could not have been bubonic plague. However, one page later, Christie notes that in South Africa “167 outbreaks with 372 cases and 235 deaths have been recorded,” revealing that outbreaks comprised, on average, 2.2 cases with 1.4 deaths, which means that plague did not occur in epidemic form but only in weak endemic form. This is a pattern that on its own raises very serious doubts that it could be associated with open

48 49

Scott and Duncan 2001: 65, cf. 55. Below: M400–5.

rats

89

mass death of rats in a township. Then Christie adds that “apparently plague has not spread in South Africa via the R. Rattus and X. cheopis combination.” This constitutes sufficient grounds for rejecting the idea that these tiny plague episodes can be associated with dead rats, observable or not, and have any significance for the understanding of historical plague epidemics. It can be shown that Scott and Duncan knew these basic facts, but placed them at safe distance from their assertions that rats were collected by the barrowful.50 In support of their various assertions on this point, Christie/Scott and Duncan refer to “Annotation. Reservoir of plague in South Africa,” published in The British Medical Journal, 1924, page 875. However, in this “Annotation” not a word is said about rats, nor is the word barrowful used, and in particular, nothing is said about collection of rats or other rodents according to this gauge or any other measure. Instead, it mentions that wild rodents called gerbilles play the main part in constituting a weak plague focus in South Africa. Rare human cases of plague are mainly associated with plague among these rodents or occasionally with some other wild types of rodents. Gerbilles avoid “human habitation,”51 a fact which explains the miniscule incidence of human cases of plague and also associates the incidence of such cases with rural localities and makes it difficult to relate observations of great numbers of these plague-dead rodents to townships. However, suddenly or inadvertently Scott and Duncan mention that all “367 [sic] human cases” “were confined to the villages,” in short, human cases occurred episodically and were not associated with townships, streets and urban structures but with rural society and African village-structures.52 This shows that they were aware that there were only incidental cases of plague in South Africa. The assertion that rats were collected by the barrowful in a South African township is false. It is this false assertion of the observation of barrowloads of plague-dead rats in South African townships which allows Scott and Duncan to construct a contrast with the lack of similar information in historical plague epidemics in Europe and to consider the difference as proof that the historical epidemics could not have been bubonic plague. The fictitious character of the first half of the comparison invalidates the comparison and the inference. One should keep in mind that the other half of the 50 51 52

Scott and Duncan 2001: 50. Wu Lien-Teh 1936b: 197. Scott and Duncan 2001: 50. No source reference given.

90

chapter three

comparison is also unsupported by evidence, a point that will be discussed below. The brief statement about rats that “litter a street of an eastern metropolis” given by Scott and Duncan is intriguing. They refer to a paper by Liston; however, the statement and supporting reference are taken directly from Christie.53 Unfortunately, Liston’s paper consists of lectures and is unannotated. It contains one passage that could possibly be the source of Christie’s/Scott and Duncan’s account: “It is stated that as many as 20,000 dead rats were collected in a short time in certain quarters of Hong-Kong, and that 1,500 were obtained from a single street.”54 One should note two aspects of this account: firstly, the unspecific nature of the opening words may indicate a reservation or a second-hand origin, and secondly, nothing is said to the effect that rats littered the streets, only that dead rats were collected, also the second part of the passage fits into this framework. All standard works on plague have been searched for corroboration of this information, but nothing was found bearing directly on Liston’s remarks even in the standard work published by the National Quarantine Service, Shanghai Station, by the outstanding scholars Wu Lien-Teh, J.W. Chun, R. Pollitzer et al., Plague. A Manual for Medical and Public Health Workers. Some remarks in the historical introduction could be of interest. It is related that a person called Dr Mary Niles “tells of a Chinese official at Canton” who in 1894 offered to pay out of his own pocket “ten cash” for every dead rat brought to him and collected over 35,000 in the course of a few months. On elementary source-critical grounds, the incidental and uncertain nature of this piece of information is quite obvious and it does not relate to the metropolis specified by Liston.55 It is mentioned in an early standard work on plague that in 1901, thirty men were employed in Hong Kong to collect rats, and “a private firm of 30 coolies employed in sorting, and one of whose duties was to collect dead rats from the godown when required,” and that in another firm rats were dying in the store-room and two men were engaged in removing them.56 Conceivably, this could be the background of Liston’s remarks, but if so, it cannot be considered evidence bearing upon the point, at least not significant evidence: both cases relate to attempts at 53 54 55 56

Christie 1980: 760. Liston 1924: 950. Wu Lien-Teh 1936a: 21. Simpson 1905: 217.

rats

91

reducing the rat population by payment for dead rats or organizations for the collection of dead rats in Canton and Hong Kong. It is not stated that the rats were picked up in the streets, and thus many may not have died by plague, but could have been killed for cash or were picked up or caught in godowns, store rooms or other storage facilities. To my knowledge, evidence of mass deaths of rats is at best sparse or almost non-existent not only in relation to historical epidemics of plague but also in relation to modern epidemics, which explains that only Scott and Duncan attempt to refer to such evidence, erroneously as has been shown. Accounts of purported observations of mass death of rats in plague epidemics in India in the 1830s are mentioned, but these observations were not available in the form of scientific studies.57 Taking a closer look at the few accounts or assertions of observations of widespread rat mortality associated with bubonic plague epidemics, it becomes clear that they are not based on scientific studies but on reports written on obsolete miasmiatic premises, are presented in an untestable or inaccurate form, have the character of hearsay or rumour, or relate to special circumstances that do not clearly imply widespread or mass occurrence of dead rats in streets or other types of open public spaces. It appears impossible to corroborate on the basis of scholarly studies that easily observable mass mortality of rats has occurred either in connection with modern epidemics of bubonic plague or with historical plague epidemics. There is a conspicuous paucity of relevant evidence on this point and its problematic nature must be underscored. This raises the question of why this should be so. Ars Moriendi Rattorum: Where Have all the Dead Rats Gone? Modern plague research started with the outbreaks of plague in Canton and Hong Kong in 1894 which showed that the disease had retained its ability to cause enormous mortality;58 it had also retained its great ability to spread from commercial hubs by ship to countries abroad, as had been demonstrated with enormous vigour by the Black Death.59 In a few years, plague was transported to India, Australia, Indonesia,

57 58 59

Hankin 1905: 55. Cf. Simpson 1905: 43, 46. Hirst 1953: 103; Yersin 1894: 662. Benedictow 2004: Map 1, p. xviii–xix, 60–229.

92

chapter three

Madagascar, Egypt, the U.S.A., countries in South America, and so on. This menacing development was taken very seriously: national health organizations were mobilized, eminent medical scholars with relevant qualifications were organized into plague research commissions equipped with fine medical laboratories and ample assistant personnel, generous grants financed comprehensive studies of the disease’s microbiological, medical and epidemiological properties in order to develop efficient anti-epidemic countermeasures at a time when no medication effective against the disease was available.60 The black rat or Rattus rattus, alias the house rat or ship rat, was quickly singled out as the (main) carrier of the disease. It was pointed out at the very start of modern plague research, in Yersin’s small paper of 1894 summarizing his early findings in Hong Kong, that “it is probable that the rats constitute the main vehicle.”61 Soon it was also suspected that its usual rat flea was the agent of transmission both between rats and from rats to human beings. The Indian Plague Research Commission (IPRC) concluded early on that “the epidemic is directly attributable to the rattus [rattus] epizootic” and that “the rat-flea [of the black rat] and the rat-flea alone is the agent of transmission of the plague bacillus from rat to man.”62 However, the pioneering plague researchers who started their work around 1900 when little scholarly work had been carried out on rats were soon confronted with an intriguing problem, namely the scarcity or even absence of observed rat falls both under ordinary circumstances and during plague epidemics. In their endeavours to acquire indispensable knowledge of the behavioural patterns of rats, especially severely ill or moribund rats, they had to perform much basic work. The IPRC implemented comprehensive studies of natural rat mortality in relatively isolated villages outside Mumbai and in the Punjab. Despite considerable efforts and opening up of rat holes and burrows, so few rats were found that they had to acknowledge that the findings could not “represent the normal rat mortality and it may, therefore, be inferred that the large majority of rats which die from normal causes die in inaccessible places.”63 The IPRC were not unprepared for this conclusion.

60

Hirst 1953: 101–6, 296–300; IPRC. XXII. 1907g: 724–5; Lamb 1908: i–iv; Brygoo 1966. 61 Yersin 1894: 667. My translation from French. 62 IPRC 1907g: 743–62, 767, 777; Lamb 1908: 54. 63 IPRC 1907h: 854; IPRC 1907j: 908; Lamb 1908: 24.

rats

93

In 1906, J. Ashburton Thompson, published, as mentioned above, a paper summarising Australian research after bubonic plague had appeared in Sydney in 1900. In this paper he also addresses this phenomenon and the insights gained by the health authorities under his leadership. He contends that the reason that some scholars thought that there were plague epidemics in India without a basis in rat-plague64 was that a proper search had not been performed.65 “Systematic detection of rat-plague is in reality a difficult business,” he points out. It was not until a “rat intelligence staff ” had been trained and acquired practical experience in the search for plague rats that they were regularly found in the individual houses in which plague cases had occurred, work that started in 1904. Several reasons for this phenomenon were indicated; apparently the basic or crucial reason is that “Rats eat each other in nature.” When rats become seriously ill or dying and cannot defend themselves, they try to hide away as best they can in order not to be eaten more or less alive by their fellow rats when they are no longer able to defend themselves. They tend to die out of sight in obscure and relatively inaccessible places. Therefore, finds or reports of sick rats that had come into the open, “could be counted on the fingers.” Ashburton Thompson goes on to enlarge on his findings: They do die in unusual places, and so regularly that we feel justified in regarding the discovery of three or four carcases at a similar stage of decomposition under floors, or in, or on the tops of cupboards, etc., during known presence of an epizoötic as probable evidence of death from plague. In ordinary, as is very well known, rats generally die out of sight […]. Even when poison has been laid discovery of several dead bodies in such situations should arouse suspicion.66

This makes it clear why it is so important for Cohn to dismiss the findings of Ashburton Thompson by falsely labelling him racist (see above), that is, because they represent a grave threat to one of the pillars of his theory, and why Ashburton Thompson’s observations are generally passed over in silence by the other advocates of alternative theories of plague. The IPRC had ample occasion to observe that rats eat dead rats and rat flesh. In their experimental godowns, the Commission observed that dead or dying rats were eaten: “that of 12 rats proved to have died 64 65 66

See Hankin 1905: 64, 66. The paper was written before the IPRC had commenced publication of its work. Thompson 1906: 548, 550–1. Cf. Hirst 1953: 147–8.

94

chapter three

of plague, the carcases of nine were more or less eaten,” that the “carcases of four inoculated and seven uninoculated were found to have been eaten, several almost completely,” and “in godown No. 9, many of the carcases were eaten.”67 They also carried out experiments by feeding rats highly infected viscera of dead plague rats or “the whole carcases of their plague-infected comrades” which were readily eaten.68 The IPRC made also thorough studies of rat-plague epizootics in selected localities in Mumbai and the Punjab. Again their findings were very similar to those reported by Ashburton Thompson. In 1908, Lamb, the leader of the IPRC, summarized their findings: In proportion to the severity of the epidemic the number of plague-rats found was very small, notwithstanding the very thorough and extensive search made. The experience both in Sion Koliwada [Koliwada is the northerly part of the village Sion outside Mumbai] and in the Punjab village of Dhund in this respect points to the danger of concluding that plague-rats are absent from an infected locality unless a very thorough search is carried out.69

A couple of years later, the IPRC noted the same observation during their study of plague at Belgaum, a small town situated roughly 400 km slightly southeast of Mumbai, where the role of rats was very much in focus and a great program was launched to trap as many rats as possible. Some 39,460 were trapped, while in contrast the number of dead rats obtained being very small indeed […]. Undoubtedly, too, rats may be dying in a house without the inhabitants being aware of the fact. Rats not infrequently die in their burrows, or under cover of boxes or sacks, or amongst rubbish or even in the roofs of the houses.70

A sprinkling of dead plague rats was found in India and China. The reason for this appears mainly to be that the black rat is an excellent climber which finds Indian and Chinese housing well suited for making their nests in the ceilings, and when seriously ill, the occasional rat would fall down on the floor.71 Plague researchers working in an Egyptian village noted that “Dead rats were picked up from the floor of

67 68 69 70 71

IPRC 1910a: 316–7, 318, 321, 324, 326, 331. IPRC 1907a: 373–81; Lamb 1908: 33–6. Lamb 1908: 18, cf. p. 24. IPRC 1910c: 453–4, 456, 469. Pollitzer 1954: 296.

rats

95

most of the rooms, having fallen presumably from the beams of the ceilings.”72 Ashburton Thompson’s strong emphasis on the point that local experience in the habits and haunts of rats was essential in order to conduct successful surveys of rat-plague was a lesson carefully noted by later plague researchers. In 1911, the Department of Public Health of the Egyptian Government appointed a team of British and Egyptian experts on plague research to study plague in Egypt. They made a very thorough study of the rodent populations in selected areas. As soon as plague broke out in a village, the team would move in, see to it that the population was evacuated, and start their investigations. “We first trapped the empty village but did not capture any rats, nor were any dead one seen. This result was puzzling in view of the considerable number of human plague cases.” However, they caught truly extraordinary numbers of rat fleas inside the houses which indicated the recent death of a considerable number of rats. The explanation was uncovered when two of the houses were torn down and “the rat burrows were exposed and traced. A regular system of nests and burrows existed at the bottom of the walls with free communication at their junctions, an arrangement that indicated continuity along the whole length of each block of houses.”73 When plague broke out in Colombo, Sri Lanka, in 1914, W.M. Philip and L.F Hirst were sent to investigate the epidemic. Keeping Ashburton Thompson’s advice in mind, they organized an anti-plague staff and set out to uncover the underlying plague epizootic. The description of the difficulties they met with and how they resolved them on the basis of modern knowledge, technical means and a scientific approach highlights the improbability that medieval populations in times of plague could be expected to observe recurring significant rat mortality that would lead to suspicion of a connection with the human plague epidemic. To begin with Philip and Hirst found few dead rats in the open and conspicuous evidence of a rat epizootic was lacking. In order to reveal the presence of dead plague rats it was usually found necessary to open up rat burrows and thoroughly dissect the tiled roofs of houses or to force surviving infected rats out of their burrows by pumping Clayton gas fumes into their holes. As the

72 73

Petrie, Todd, Skander et al., 1924: 129. Petrie, Todd, Skander et al., 1924–5: 129–30.

96

chapter three anti-plague staff gained experience, the correlation between rat and human plague in space and time became closer and closer.74

This presentation of the rat-related plague studies in Sri Lanka by Hirst and Philip and the final citation are taken from Hirst’s standard work on plague and can serve as yet more evidence of why Cohn felt that he had to do away with this work, and hoped that by labelling him racist (see above) he could make scholars turn away from his work. Twigg gives such a skewed presentation of Hirst’s and Philip’s work in Colombo that the central point is completely obscured.75 This subchapter on the behavioural pattern of dying rats and the great difficulties of finding rats having died either from normal causes or from plague unless a highly competent and very thorough search has been implemented can be closed with the observations of Dutch scholars in Java and their concluding remarks. J.J. van Loghem and N.H. Swellengrebel met with the same curious absence of rat falls and almost had to completely tear down native huts in order to reveal the rat nests and the presence of dead rats. After great efforts, they learned, among other things, that the house rats made their nests in the hollow bamboo frames of the huts and also of the beds; rat nests were found in the roofs, between the walls and in the internal wall covering made of thin bamboo sprouts, and so on, and in these places they also found rats dead from plague.76 The results of research on rats in plague epidemics in the first decades of the twentieth century are aptly summarized by the Dutch medical scholars C.D. de Langen and A. Lichtenstein:77 The most important argument adduced by the opponents of the “RatFlea-Man” theory of the distribution of plague is that in various epidemics no rat plague has been observed, or the epizootic has only developed after the epidemic has started. A really critical examination of the data in these cases shows in every instance that no sufficient search was made for the preceding rat plague. In some cases the mere fact that among 100 rats caught in traps no rat plague could be demonstrated was accepted as sufficient proof that there was no rat plague present! How very difficult it is

74 Here I cite the succinct summary by Hirst 1953: 148, of the original text in Philip and Hirst 1917: 542–5. 75 Twigg 1984: 112. 76 Van Loghem and Swellengrebel 1914: 467. See also the photographs in the appendix. 77 De Langen and Lichtenstein 1936: 185–6.

rats

97

to demonstrate even a very widespread rat epizootic has been shown in Java where, in spite of the most diligent search, no rat plague could be found, until van Loghem easily demonstrated the wide distribution of the disease among the rats by splitting open the bamboos used in building portions of the native houses. The “Rat-Flea-Man” theory as it has now become sharply defined in Java, regards the rat plague as an epizootic disease conveyed by fleas […] it follows that rat plague must always precede human plague; this has almost always been capable of demonstration in Java after a careful enough search has been made.

At the same time, Wu Lien-Teh pointed out: Modern examples could be quoted where not only the population at large but even the medical men believed rat plague to be absent and yet the presence of an epizootic was demonstrated by a proper search.

And he goes on to underline what all the advocates of alternative theories of plague collectively have neglected to take into account: “In old Europe many factors militated against such discoveries.”78 Against this background, the question must be asked: on what grounds should people in the past be expected to have observed intense rat mortality or at least substantial numbers of rat falls preceding the outbreak of plague epidemics and running concurrently with the epidemics as they unfolded? In the preceding subchapter, I showed that the assertions of the advocates of alternative theories that the paucity or lack of historical evidence of dead rats during historical plague epidemics proved that the epidemics could not have been bubonic plague were methodologically flawed, and have the character of inference ex silentio. In this subchapter, material has been presented that demonstates in the clearest possible way the invalidity of their inferences ex silentio: dead rats were not seen during historic plague epidemics simply because it is very difficult to find dead rats, not because they were not present.79 Finally, it must be permitted to ask how so many studies and comments on this rat-related problem can have been overlooked by the advocates of alternative theories if a proper study of the relevant works on plague research published in leading journals and standard textbooks had been performed.

78 79

Wu Lien-Teh 1936a: 8–9. Cf. Benedictow 2004: 192, and footnote 9.

98

chapter three Zoobiological and Zoogeographical Arguments on the Question of Significant Presence of Black Rats in Medieval Europe

A central argument concerning the presence of the black rat in Europe is based on the idea that its geographical distribution is determined by the fact that the species originated in a warm region, Burma and India,80 the North African or Arabian parts of the western Mediterranean as well as the eastern Mediterranean81 or more vaguely that it had an “Oriental origin.”82 Twigg and Davis who are zoologists assert in absolute terms that this origin means that black rats are tender and warmthneeding animals and that the climate in the northerly parts of Europe is too cold to be compatible with a significant and widespread presence of this species; at the most there could have been a more or less sporadic incidence due to importation by ship from Mediterranean ports.83 Consequently, historical plague epidemics in these regions must be some other epidemic disease than bubonic plague. This argument is embraced by Scott and Duncan and Cohn, presumably because it helps clear the way for their alternative cases.84 In this subchapter, I will therefore address this question as a subject suitable for serious discussion. Some priority will be given to Davis’s paper on the matter, since it appears that this is the most influential work in this connection, and also to Twigg’s discussion of this topic, as both are zoologists and operate in this field with some scholarly prestige. Some of the arguments have considerable illustrative powers. Twigg enthusiastically cites a remark by G.M. Thomson who, in a work on the North-West Passage, asserts that the Black Death “struck Greenland even more savagely than Europe.”85 Thomson is neither an historian nor an archaeologist and has no competence on medieval history and no competence on Nordic history, yet Thomson’s assertion permits Twigg to conclude: “It is highly unlikely that Rattus rattus was present there at that time and I can find no records of this species in Greenland in modern times either.” By implication historical plague could not have been bubonic plague. Also this argument is embraced by Scott

80 81 82 83 84 85

Pollitzer 1954: 282; Russell and Russell 1983: 102; Twigg 1984: 86. Zinsser 1934/1985: 198; Davis 1986: 456. Hirst 1953: 126. Twigg 1984: 80, 86–7, 100–1; Davis 1986: 455–70. Cohn 2002: 53; Scott and Duncan 2001: 261; Scott and Duncan 2004: 174–5. Twigg 1984: 86–7.

rats

99

and Duncan who maintain repeatedly that the fact that the Black Death ravaged Greenland and Iceland constitutes proof that it could not have been rat-borne bubonic plague.86 In fact, Nordic scholars, both historians and archaeologists, have taken substantial interest in what happened to Greenland’s Norse population and why it disappeared. This research has been thoroughly and comprehensively summarized in English in a fine paper by J. Berglund.87 It is also succinctly summarized in English by the Finnish scholar J. Vahtola: “In the late Middle Ages the entire Norse population [in Greenland] disappeared. There is no evidence that epidemics of plague or any other disease caused the desertion.” The main explanation of the desertion is ecological: “Recent investigations have demonstrated convincingly that the fertility of the soil was ultimately destroyed by climatically caused erosion and overgrazing of pastures and meadows. In the face of incipient starvation many of the people may have moved to Iceland.”88 This is exactly what is stated on the matter in my monograph on the Black Death.89 Twigg’s and Scott’s and Duncan’s assertions are without foundation in relevant scholarly studies. For the same reason, Scott and Duncan maintain repeatedly that the Black Death raged in Iceland.90 On this point the Icelandic annals are entirely clear: “This disease did not come to Iceland.”91 Scott and Duncan state also that the Black Death crossed “the Baltic to Norway,”92 an impossible feat of geographical dissemination. As a matter of fact, the Black Death did not even spread across the Baltic to Sweden (or from Sweden across the Baltic).93 At the heart of Davis’s line of arguments is a series of interacting methodological fallacies. He presents some selected information from modern studies on the brown rat and the black rat and claims that, although most of this information relates to the brown rat, “enough is known of Rattus rattus [the black rat] to permit conclusions about [the rat] populations at the time of the Black Death.”94 This is an obvious 86 Scott and Duncan 2001: 6, 81, 98, 108–9, 357. Scott and Duncan refer to the uncritical and poor work of Kohn 1995. 87 See the fine summary by Berglund 1986: 113–34. 88 Vahtola 2003: 567–8, 576. 89 Benedictow 2004: 146. 90 Scott and Duncan 2001: 6, 81, 98, 108–9, 357, 374, 376. 91 Islandske Annaler 1888: 276. Lawman’s Annal: “Þessi sott kom ecki aa Island.” 92 Scott and Duncan 2001: 376. 93 Benedictow 2004: 170–8; 196–7, 209–10. 94 Davis 1986: 459.

100

chapter three

instance of fallacious methodology. Historical periodisation is not fortuitous, but reflects historians’ general view that historical processes have changed societal structures so profoundly over time that they are relating to qualitatively different social formations or societal structures. This means that a condition found in one historical period can only provide the basis for a working hypothesis to the effect that it also was the case in another historical period and functioned or interacted in much the same way within different social structures. It is a fallacy of methodology to make inferences across the boundaries of historical periods without due consideration to historical and societal changes and a clear argument as to why a specific factor should nonetheless be able to operate the same way in the specific case under discussion.95 Methodologically, interperiod comparisons or approaches have the character of analogies or parallels which can prove nothing but can serve to construct working hypotheses, while proof requires evidence in the form of empirical data relating to the historical social formation under study. For this reason, observations on aspects of one social formation generally cannot be projected into some other social formation, they can only serve as a base for working hypotheses to the effect that these specific parts of social reality have not changed with the structural societal transformations. If the case were otherwise, if one could legitimately and freely project aspects of one social formation into other social formations, one could legitimately show that medieval society was identical or similar to Early Modern society or even modern society. Therefore, only evidence specific to the period under discussion can be used for evidentiary purposes with respect to any topic; if there is no evidence, the historian has lost. It should be obvious that the biotopes and ecological niches and environments of rats have changed profoundly and fundamentally, and that there is no profound similarity in these crucial respects that will permit argument for historical similarity over these historical periods. Here we may mention the dramatic zoological effects of the introduction of the brown rat in Europe in the eighteenth century on the living conditions of the black rat. Because the brown rat was much stronger and more aggressive, it drove the black rat out of its usual habitats and caused its extinction in many countries and regions (see below). One must also take into account the intensive and fundamental changes of

95

See for instance Benedictow 2004: 387–94; Benedictow 2006: 133–42.

rats

101

human society with respect to types and distribution of settlement and of building structures and of mentality and culture also in relation to animals and insects, which in modern Western society are strongly aligned against the presence of rats and insects in immediate human proximity. These methodological and sociological remarks should suffice to uncover the fallacious and untenable character of Davis’s approach. However, these are the premises that allow Davis to conclude as follows (the enumeration of his assertions is mine): Application of this information to rat populations of the Middle Ages produces the following scenario. [1] Rattus rattus may have persisted in towns, especially grain ports, but the number of buildings with rats was small and the number of rats was stationary. [2] The [rat: my insertion] population in a particular town disappeared in few years but might again become established as a result of new introductions. [3] These characteristics held for northern France, Scandinavia, and the British Isles, but [4] in the more southern Mediterranean region of France Rattus rattus may have lived in small numbers in rural areas.96

All four assertions contained in this citation on the presence and role of rats in medieval society are only speculative or hypothetical. They could legitimately be working hypotheses that could be tested and potentially corroborated through the gathering of evidence. However, Davis has adduced no evidence, and thus, proved nothing. Conversion of working hypotheses into assertions of fact and also inference across the dividing lines of historical periods are fallacious. Another typical instance of a methodologically flawed argument is Davis’s absolute assertion that the black rat lives in trees and roofs of houses […] they rarely if ever inhabit burrows, tunnels in the ground, or aquatic habitats. Thus references to rodents living in burrows or swamps exclude Rattus rattus.97

A number of citations and references has been presented above which demonstrate the burrowing abilities and habits of the black rat in connection with the difficulties of finding rats dead from plague.98 The inherent anachronistic flaw in Davis’s assertion becomes immediately apparent when these assertions are related to Pollitzer’s presentation

96 97 98

Davis 1986: 459–60. Davis 1986: 456, 457. Above: 91–7.

102

chapter three

and discussion of rats, where it is stated that “in the absence of Norway rats, R. rattus may live on the ground floors or even underground.” The point is that in the presence of the bigger and stronger brown rat which aggressively fight the black rat for territory, the black rat which is an “excellent climber, prefers to shelter in the upper parts of buildings.”99 The same perspective is found in the IPRC’s remarks that in contrast with Mus rattus [= Rattus rattus] in Bombay, the Punjab rat burrows extensively […]. It is almost certain that the rat-burrows in the Punjab villages are very extensive, ramifying beneath and opening up communication between several contiguous houses.100 A Punjab village may be looked upon for our present purpose as being honey-combed with rat burrows which ramify in all directions.101 Mus rattus, although typically a climbing rat [in Mumbai], is able to burrow, e.g., in beaten earth floors. We have frequently made this observation and in one instance (in Parel village [outside Mumbai]) have seen exceptionally large and numerous holes and burrows in the earthen floor of a store-roome for grain from which many Mus rattus had been trapped.102

In Mumbai where the brown rat is usual, the black rat prefers to live in the upper parts of buildings, in the Punjab they are typical burrowing rodents, since the brown rat “is not found in the villages of this Province.”103 The IPRC noted that black rats were burrowing extensively in Belgaum (see above) both outside and inside houses where there were no brown rats.104 Again it can be readily seen that Davis just projects into the past the modern situation and the behavioural effects on black rats of the intensely competitive presence of the stronger and more aggressive brown rats, a constellation which did not exist in the Middle Ages or for a long time thereafter. The question of the burrowing of black rats will be discussed below in connection with the history of black rats in the Nordic countries and finds of medieval skeletal remains. From an epidemiological perspective it is also important to note Pollitzer’s point which serves to underline the erroneous character of

99 100 101 102 103 104

Pollitzer 1954: 290. IPRC 1907j: 905. Lamb 1908: 13. IPRC 1907g: 746. IPRC 1907a: 376. IPRC 1910c: 456.

rats

103

Davis’ assertion, namely that “the available evidence shows that X. cheopis has an affinity for rats living underground rather than for those sheltering on higher levels of the houses.”105 Another important question relates to the issue of the density or numbers of rats in relation to the density or numbers of people in an area, because this relationship concerns the necessary conditions for effective spread of bubonic plague epidemics. Twigg and Davis endeavour to play down the relative number of rats as much as possible in order to undermine a necessary condition for efficient spread of bubonic-plague epidemics.106 The central point which they faile to take into account is that the presence of rats in modern cities and settlements tends to be strongly affected by counter-measures by sanitary authorities and extermination campaigns. When Davis studied the rat population of Baltimore in 1947 he estimated their numbers at 200,000, one rat per five inhabitants. However, three years earlier the number had been estimated at 400,000 rats; the rat population in the meantime had been greatly reduced by counter-measures. Thus, again their arguments are based on the fallacy of anachronistically projecting the outcome of modern studies into the Middle Ages. Pollitzer’s following statement is a useful guideline to the question of relative numbers: “There is reason to assume that in less well-sanitated cities, and in smaller settlements in general, the number of rats equals or even exceeds the number of people. This is presumably the rule on farms (Tice).”107 The IPRC’s study of the rat infestation of Parel village demonstrated beyond doubt that the numbers of black rats in the houses far exceeded the number of human inhabitants.108 In Belgaum, the IPRC trapped a number of rats higher than the human population without exterminating the rat population, so the number of rats clearly exceeded the number of inhabitants.109 I have noted with some interest that the responsible municipal authority in Oslo (Norway) cautiously estimates that today the number of rats equals the number of people, despite their efforts at extermination.110 Generally, from the High Middle Ages and through most of part of the Early Modern Period

105 106 107 108 109 110

Pollitzer 1954: 336. Twigg 1984: 88–9. Pollitzer 1954: 292. IPRC 1907h: 844–54. IPRC 1910c: 457. Tollefsen 2005: 7.

104

chapter three

about 85–95 per cent of European populations lived in the countryside on holdings and tenancies of various sizes, each according to local customs with two or more buildings in which colonies of black rats would like to settle: a dwelling house, barn, storehouse, stable, cowhouse, and in addition a cottage to accommodate aging parents and not infrequently “undersettles” (sub-tenancies).111 In the opinion of Davis, it is an important argument that ports can usefully be compared to islands and in order to understand the establishment and persistence of Rattus rattus over time we can follow some principles of island zoogeography. A port can be assumed to have the characteristics of an island because, on the land side, numerous barriers of habitat and frequent hazards prevent rats regularly from spreading far from the wharves. A spread of up to a kilometre or so can nevertheless occur.112

Davis asserts that commercial hubs like Venice, Florence, Genoa, London, Bruges or Lübeck can from a zoogeographical perspective be usefully compared to (more or less isolated) islands. In order to defend this position, Davis resorts to assertions about ports that fly in the face of the amassed knowledge regarding the functions of urban centres in general and specifically also of medieval urban centres, from Max Weber’s classic sociological study of pre-modern cities113 to R.S. Lopez’s classic monograph The Commercial Revolution of the Middle Ages, 950– 1350, Pound’s great summary of medieval economic history, and all serious work that has been published on the subject in the last generation. Urban centres do not function geographically as islands in any significant respect but, on the contrary, as centres of communication lines that radiate out from them and also meet in them. Along these communication lines by land or sea or rivers a great variety of goods are transported and people travel with them or with a great variety of baggage and motives. Microbiological agents, insects and animals will imperceptibly move with goods, people, luggage or clothing. The comprehensive commercial activities of ports and economic hubs were very well suited for the distribution of rats at various distances through the transportation of many types of goods, merchandise, and commodities over land or sea or along rivers by various types of vehicles or vessels or

111 112 113

See, for instance, Astill 1988: 51–2. Davis 1986: 457–8. Weber 1966, Lopez 1976, Pounds 1974.

rats

105

even pack horses.114 One could consider the implications of the IPRC’s observation: “We have seen rats dive, as it were, into bags containing bran and disappear, so that the bags could be moved without any evidence of the presence of the rats within. M. rattus [= Rattus rattus, the black rat] from its habits is particularly liable to be transported in this way […].”115 Davis’s central argument is based on the untenable notion that black rats could spread over land only by individual locomotion, by moving on their feet. According to ordinary scholarly methodological principles, Davis should be obliged to explain to his readers the empirical grounds which permit him to state that in medieval urban centres “A spread of up to a kilometre or so [by black rats] can nevertheless occur.” It is the basic flaws of his theory that force him to found his arguments on such absurd notions as ports as islands suitable for the study of the functions of “the principles of island zoogeography.” In the end, he has to admit that “Factual support for these applications of island geography are regrettably meagre.”116 However, he proceeds unaffected to go on arguing his theory as if this were not the case, which allows him to conclude triumphantly that he has proven that there could only have been an incidental presence of the black rat in the northerly parts of Europe, the concept of proven here being released from its strong evidentiary associations. This line of argument is supplemented by further arbitrary assertions to the effect that because “towns, the ships and the docks were small, we can assume that the rate of extinction was high” and that “persistence of populations of rats would have required frequent arrivals of ships from the Mediterranean, where rats were widely distributed.” In methodological parlance, the concept of “assumption” applies when there is an evidentiary basis that constitutes sufficient ground for making an inference in relation to some part of reality, and this evidentiary basis is more demanding than in the case of other words implying lower levels of tenability such as “plausible” or “possible” or “hypothetical” or “speculative.” When the evidentiary basis is not presented, as in this case, the appropriate terms would be “speculate” or at best “hypothecate.” According to the principles of methodology, each

114 115 116

Pollitzer 1954: 294; Pollitzer and Meyer 1961: 452; Shrewsbury 1971: 29. IPRC 1908b: 255. Davis 1986: 458.

106

chapter three

of these assertions is a speculative working hypothesis that requires corroborative evidence in order to cross the dividing line between speculation or hypothesis and valid statement on reality at some level of tenability, however slight. Eventually, this point also occurs to Davis since he states that from “these principles we can construct a hypothetical history of rats in Europe.” However, he immediately leaves the methodological implication of this characteristic, concluding in terms requiring a significant empirical basis: “The available evidence indicates that Rattus rattus was rare and erratically dispersed both geographically and temporally at the time of the Black Death.”117 However, no evidence to this effect has been presented. This unsubstantiated history is based on the speculative view that black rats could not uphold an autonomous widespread presence. Finds of rat bones force a small admission to the effect that black rats may in Roman times have been spread from the Mediterranean region by ship transport to ports in Western Europe in a continuous process that secured a small and continuous presence of the black rat in ports. According to Davis, the decline in shipping with the break down of the (Western) Roman Empire and the beginning of the Middle Ages meant that ports became so small that “it resulted in the extinction of rats in most cities of the north” and “the size of remaining ports were not adequate to maintain large rat populations.” This is plainly serial speculation that can provide premises for any hypothesis. It is also an expression of ignorance: there was no direct shipping between Mediterranean ports and Western Europe in Roman times and up to the end of the thirteenth century, rats would have a local origin and a continuous presence. It ignores also the widespread finds of rat bones from Roman times far from ports in many parts of Europe (see below). Davis goes on to argue that the “increase in shipping and the size of ports in Columbian times released an avalanche of rats which has been reduced only in recent decades.”118 Around 1500, the size of Europe’s population was close to the late medieval minimum after the ravages of the Black Death and subsequent plague epidemics. The intensity and volume of international trade, the size and ramifications of banks, and so on, were vastly greater around 1300 than around 1500, as were the size of populations and volume of general economic activity. This is the

117 118

Davis 1986: 468. Davis 1986: 458–9.

rats

107

reason Lopez writes about the commercial revolution of the High Middle Ages, and I write about the plague history of the Late Middle Ages. If there was to have been an avalanche of imported rats into northwestern Europe, the High Middle Ages up to 1350 would have been the period of pre-eminence. Davis’s arguments are without basis in the economic and demographic history of the Middle Ages. This leads Davis to a peculiar conclusion: “Evidence for this chronology is meagre, but it offers a plausible explanation of changes in rat populations.”119 Since he has not presented any empirical evidence in support of this chronology of rat history, and even characterizes it himself as a “hypothetical history of rats in Europe,” it is not “meagre,” it is non-existent. Methodologically, this relates to the fact that the concept of “plausible” relates to a level of tenability which requires sufficient evidence to position it between the level of possible and the level of likely. Davis appears unwilling to accept that what he really is doing is constructing an explanatory model on entirely speculative and hypothetical grounds. He also appears unable to accept the fact that a model is an intellectual tool that proves nothing, but which in the hands of a conscientious scholar can be useful for the collection, organization and analysis of empirical material. In addition, Davis’s knowledge of plague disease is unsatisfactory. It is not true that “most cases during the Black Death were of pneumonic plague” and that this “is now documented.”120 He refers for support to Biraben 1975: 86, where the opposite is maintained, namely that there could have been some episodes of primary pneumonic plague, but that “everywhere else it appears in the bubonic form with secondary pneumonic or haemorraghic manifestations.” In the immediate continuation of this statement, Biraben also makes it clear that these epidemics of bubonic plague which dominate the scene “are arrested or diminished by the cold season,”121 Davis is aware that primary pneumonic plague “occurs all year round,” he knows also that bubonic plague is “a disease [typically present: my insertion] in late summer,”122 and he has seen Biraben’s strong evidence to the effect that the Black Death was

119

Davis 1986: 459. Davis 1986: 460–1. See Benedictow 2004: 27–31, 233–41. Davis does not differentiate between primary and secondary pneumonic plague, but has apparently primary pneumonic plague in mind. 121 My translation from French. 122 Davis 1986: 460. 120

108

chapter three

bubonic plague, which does not accord with his assertion on the predominance of primary pneumonic plague. This puts in perspective Davis’s assertion that “fall and winter epidemics were surely not the result of the transmission by fleas from rats.”123 In the accompanying footnote he refers to (1) Gras 1939: 305, (2) Simpson 1905: 159, (3) Gasquet 1893: 43, and (4) The Indian Plague Research Commission 1907: 324–476. I will comment on these references below in paragraphs marked by corresponding number. First, it must be pointed out that he calls the IPRC the “Indian Advisory Commission,” which reflects his confusion of the scientists who made the research and wrote the papers or reports with “The Advisory Committee” which was responsible for controlling the quality of the papers and arranging for their publication. Lamb makes painstakingly clear the difference between the Advisory Committee and the Research Commission in his summary of their work up to May 1907: “It was arranged that reports of the work done by the Commission should be published by the Advisory Committee in the Journal of Hygiene.”124 Since it can be shown that Davis has not read the papers contained in these pages (see below, paragraph 4), this confusion may be taken to be a consequence of Davis’s hasty look at the title on the opening page of this sequence of papers in the Journal and its last page in order to produce a seemingly normal reference. This is not, as will be shown, the only case. (1) Gras’s paper is a study on the Black Death in the small Burgundian town of Givry on the basis of the only surviving complete parish register in Europe from the time of the epidemic. However, according to this study, the first victim of the Black Death died 17 July, the epidemic slowed down sharply in October and petered out in the first half of November, and in the second half of November three final cases are registered on the 19th.125 This is not a case of a “fall and winter” epidemic, but instead in conforms to Biraben’s general account of the seasonality of the Black Death in France. Clearly, this reference is also fictitious. One should note that rat fleas are typical fur fleas (and not nest fleas),126 which means that they spend much of their adult lives in the 123

Davis 1986: 467. Lamb 1908: ii–iv. 125 Gras 1939: 305–6. 126 IPRC 1908b: 245–6, 258; Liston 1924: 997; Pollitzer 1953: 321; Pollitzer and Meyer 1961: 461; Busvine 1976: 37. 124

rats

109

fur of their hosts, enjoying there a relatively warm microclimate even in chilly or cold weather and ample feeding opportunities. This explains why plague epidemics can produce cases in chilly or cold autumnal weather, although at a rapidly diminishing rate, until the depletion of the number of rat fleas and the reduction of septicaemia in plagueinfected rats caused by cold weather stop the epidemic or it manifests itself by only occasional cases. The idea that plague epidemics must stop abruptly with the advent of chilly or cold weather is untenable.127 (2) Simpson 1905: 159, does not relate to the Black Death or the subsequent late medieval or early modern plague epidemics. This page is the first in a chapter on “Variation in Virulence of Plague Epidemics” which has nothing to do with Davis’s subject. Consequently, this is also a fictitious reference. Evidently, Davis has again arbitrarily picked some pages in order to produce a false impression of a normal reference in a footnote. (3) Gasquet 1893: 43, relates to the Black Death in Avignon. The course of this epidemic cannot be followed closely, but the epidemic continued during the winter months. It is generally agreed, especially on the basis of the clinical descriptions of Guy de Chauliac, the pope’s personal physician, that this phase of the epidemic was predominantly primary pneumonic plague or rather a mixed epidemic.128 Since this is a unique case, as no other case of an epidemic of primary pneumonic plague or more likely a mixed epidemic is known, it does not at all support Davis’s assertion that the Black Death was at least predominantly primary pneumonic plague. Much has been written on the Black Death in Avignon after 1893. (4) Davis’s reference to IPRC 1907: 324–476, comprises not one but ten studies which all have in common that they do not relate to the subject in question and do not, consequently, contain support for his assertion which therefore is arbitrary. On the same page, Davis asserts that “Human plague can occur without involvement of Rattus. For example in India only eight of forty local epidemics had obvious mortality of Rattus.” In the accompanying footnote, Davis provides three references to scholarly works in support of his assertion, all of which need close and sceptical scrutiny: (1) Hirst 1953: 121; (2) Martin 1913: 63; and (3) Hirsch 1883, Vol.1: 494–544. I now comment on each of these references: 127 128

See below: 396–8. Benedictow 2004: 97–8, 236–8.

110

chapter three

(1) Hirst 1953, 121: Hirst’s monograph is devoted to the study of the history of human combat of bubonic plague. He does this in a broad and in-depth historical perspective of the development of medicine and epidemiology and concludes with a strong case for the rat-flea theory of bubonic plague. Every scholar who has read this outstanding standard work on bubonic plague will immediately recognize that Davis’s reference is fictitious. Far from providing support for Davis’s assertion, Hirst argues strongly against it. On page 121, which is sited by Davis, starts Chapter VI on the role of “Rats and Plague”; the subchapter starting on this page relates to “Rats and the First Two Pandemics.” Thus, this chapter does not relate to the third pandemic and developments in India in this period. On page 121, Hirst begins by emphasizing very strongly the early resistance among scholars to the rat-based rat-flea theory of bubonic plague. (2) It is on the following page, Hirst 1953: 122, that Davis had the luck to find his next reference, namely Martin 1913: 63. Here Hirst states that “the paucity of records directly and clearly associating human plague with mortality among rats in medieval literature has led some authorities, including Sir Charles Martin and Professor Jorge, to postulate the human flea as the chief transmitter of the bubonic element of the Black Death.” This view asserts the importance of interhuman spread of plague which begins from rat plague but then continues independently of rats by cross-infection, a view with which Hirst entirely disagrees and against which he argues intensively over many pages. Davis has, thus, made a misleading reference to Hirst’s monograph in support of his own view. He makes no reference to Hirst’s comprehensive discussion leading to his conclusion on the fundamental role of rats and rat fleas in the epidemiology of bubonic plague among human beings, including in India. A huge number of studies have appeared after Martin published his study in 1913, among them quite a number relating to the possible role of the human flea, and they affect the tenability of Martin’s opinion. Many of these studies are used and referred to by Hirst. Certainly Hirst disagrees, this is at the heart of his monograph: the role of fleas is discussed in the following chapter, the question of interhuman spread in Chapter IX, and the spatio-temporal patterns of plague epidemics in Part III, Chapters X-XII. In fact, even the most ardent supporters of the human-flea theory, namely G. Blanc and M. Baltazard, do not maintain that the Black Death or subsequent plague epidemics were in the main spread by the human flea, only that it could be of importance in the great cities of the Middle Ages, which

rats

111

means that at most 2 per cent of Europe’s population would be at risk, and the hypothesis of little consequence even if it were tenable.129 The main reason that the human-flea theory is untenable is that plague sepsis in human beings is generally far too weak to infect fleas sufficiently for development of blockage other than in sporadic cases.130 (3) Davis’s third and last reference in support of his view on this point raises immediate scepticism, namely that to August Hirsch’s twovolume Handbook of Geographical and Historical Pathology of 1883, which is an English translation of the two-volume German edition of 1860–4. This work is surely much too old to contain scientifically tenable information on the matter. I have taken a look at the original German edition and also the second edition of 1881–6 (three volumes) which are the versions owned by the University Library of Oslo. In the first edition, bubonic plague is presented in Volume 1, in a chapter of twenty-three pages, which fits very poorly with the fifty pages to which Davis refers. This chapter does not contain anything to the effect that involvement of rats was observed in only eight of forty plague epidemics in India. Since the presentation of plague in the original first edition starts on page 192, it may seem quite impossible that this chapter in the English translation should start on page 494, at which point the original German edition is in the middle of a 312-page discussion of chronic diseases. One could also take into account that the properties of the English language make translations from German shorter, not longer.131 Hirsch’s work is, of course, unscientific, based on the theory of miasma in both editions, and it contains no reference to bubonic plague later than 1850.132 This makes it clear that the author could not consider any theory of bubonic plague involving bacteria, rats and rat fleas as agents, carriers and transmitters of bubonic plague among human beings. Hirsch has of course not had the opportunity to learn from and take into account the modern scientific studies performed by Ashburton Thompson, the IPRC or van Loghem and Swellengrebel who discuss the behavioural patterns of rats and revealed that epizootics among rats were, in fact, at the basis of epidemics of bubonic plague.

129

Benedictow 1993/1996: 228–37. Cf. Benedictow 2004: 17, fn. 9. Benedictow 1993/1996: 243–63. 131 In the much expanded second edition, the chapter on bubonic plague runs from page 349 to page 384. 132 Hirsch 1860: 211. The chapter on bubonic plague in the second edition of 1881 contains a few later references to plague epidemics, but not in India. 130

112

chapter three

Davis’s reference to Hirsch is fictitious; Hirsch’s book cannot be the source of his assertion that only eight of forty plague epidemics in India exhibited evidence of involvement by rats. The real basis for Davis’s assertion is taken from Hankin’s paper of 1905. Here Hankin summarises a report by Planck relating to the Garhwali area where plague tends to be “endemic” in the Annual Report of the Sanitary Commissioner for the North-West Provinces and Oudh for the year 1876.133 While Davis presents his assertion as if it were based on scientifically tenable research, for instance Hirst’s monograph, it can now be seen that the basis is another proto-scientific report written many years before the establishment of bacteriology and therefore also based on the miasmatic theory of epidemic disease and without notions of any role for rats or insects. On the basis of relevant scholarly studies, the question of why rat falls are such rare sights during plague epidemics has been quite extensively discussed above. This makes it clear that Davis’s assertion could not be based on valid evidence. Importantly, Hankin uses the term “endemic,” which means sporadic cases, so that in this context the term “outbreak” does not refer to epidemic plague and a large number cases. This means that the role of rats would not be obvious because of the sporadic and endemic incidence of the plague cases, in addition to the other factors cited above. The report Davis refers to is not relevant for the understanding of epidemic plague. Davis asserts in seriousness that the human flea might have been involved in the dissemination of plague, because they “can transmit the bacillus that appears in saliva and human feces.”134 Human fleas like other types of fleas are ectoparasites, bloodsucking insects, and do not ingest human saliva both because they do not have access to it, and because it would not be useful as nourishment or as a necessary basis for the production of eggs which unconditionally requires blood. Certainly, human fleas are not dung insects and will not touch human faeces with their proboscises. Davis asserts also that “Buboes can occur in cases of pneumonic transmission and cannot be construed as proof of transmission by fleas that infest either rats or humans.”135 In support of this statement, he

133 134 135

Hankin 1905: 49–50, 66. Davis 1986: 461. Davis 1986: 461.

rats

113

refers to the following standard works on plague, namely Wu Lien-Teh 1936b: 409, Hirst 1953: 29, Pollitzer and Li 1943: 161/212–6136 none of which works contains anything that supports his assertion, neither on the indicated pages nor elsewhere. They are fictitious references.137 Wu Lien-Teh’s standard work on primary pneumonic plague makes it clear that the pneumonic mode of infection does not give rise to buboes.138 Davis goes on to present other misleading statements on plague. He asserts, for instance, that the Black Death “travelled across or around the Alps in the winter.”139 This is not correct, the Black Death’s advance into the Alpine area stopped with the advent of cold autumn weather which extinguished its epidemic manifestations, and it did not re-emerge until the advent of spring temperatures when it started penetrating into Southern Germany. Its spread in this region was also temperature-dependent, requiring temperatures of the warmer seasons, which can be easily explained by a rat-based and flea-transmitted disease.140 Davis asserts also that in “Europe the spread of plague was rapid,” its “speed and intensity was remarkable” and incompatible with spread rates characteristic of contiguous spread between rat colonies. His empirical examples of rapid spread of the disease are that it travelled to: (1) (2) (3) (4)

Paris in six months, and to southwestern England by December; it spread to northern Norway (Bergen and Trondheim) in a year; it permeated all of England within months.141

The enumeration is mine, and my comments below are marked by corresponding numbers. Davis does not mention the point in time of the start of epidemic spread from the chosen point of origin and the time of its arrival at the chosen destinations. Neither does he clarify his concepts of speed or rapidity by providing his readers with his criteria and explaining why he considers these characterizations suitable. As will be

136 The discrepancy in the page numbers is due to my use of the version published in Chinese Medical Journal 1943: 212–6, while Davis refers to a somewhat shorter version published at the same time in Journal of Infectious Diseases 1943: 160–2. 137 Neither does Wu Lien-Teh mention such cases in his monograph on pneumonic plague. Wu Lien-Teh 1926: 241–73. 138 Wu Lien-Teh 1926: 184–7. 139 Davis 1986: 460. 140 Benedictow 2004: 186–90. 141 Davis 1986: 460–1.

114

chapter three

seen, they are not only arbitrary in form but also erroneous and confused in fact. (1) The first outbreak in France was noted in Marseilles 1 November 1347, and the outbreak in Paris was noted at the end of August, which means that ten months passed between the arrival of the Black Death in France and its arrival in Paris. However, the part of the Black Death that spread northwards from the original epicentre at Marseilles killed its first victim in Givry in Burgundy on 17 July (according to the parish register), which means that in mid-July the epidemic was more than 300 km from Paris as the crow flies, and much further by ground transport. It also means that by the end of August it would have moved only about 60–70 km further on its way northwards and still be several hundred km away along the main roads to Paris.142 The crucial point that Davis has missed is that the Black Death was shipped out of Bordeaux to Rouen in Normandy in time to cause a recognized outbreak there in June and could cover the much shorter distance thence to Paris in time for an outbreak at the end of August, a spread rate that would quite likely have been hastened by ship transportation up the R. Seine.143 The basic problem here is that Davis does not recognize the importance of metastatic leaps which will be comprehensively discussed below in the next main chapter. (2) Davis’s assertion that it is an example of remarkable speed of spread that the Black Death could spread from Melcombe Regis (Weymouth in southern England), where it broke out shortly before 24 June 1348, to southwestern England by December is intriguing, since the Black Death started in southwestern England. It has long been known that by the beginning of August most of the tenants of Frome Braunch in Somerset had died and that peasants had died on other manors in the area. It has also been long known that the Black Death broke out in Bristol on 15 August, shortly afterwards in Gloucester (and that it had broken out in coastal towns of the Pale in Ireland by early August).144 The reason Davis again is so out of line with historical plague research and reality here is that he does not recognize the crucial importance of metastatic leaps in plague epidemiology and he has poor knowledge of the relevant historical studies.

142 143 144

For spread rates in this part of France, see Benedictow 2004: 106, 230. Benedictow 2004: 72–3, 96–108. Benedictow 2004: 126–8, 130–1, 143–4.

rats

115

(3) As a Norwegian scholar who has specialized on plague history and who has written his doctoral thesis on the late medieval plague epidemics in the Nordic countries and a complete history of plague epidemics in Norway (1348–1654),145 I do not understand what Davis means when he states that the Black Death spread to “northern Norway (Bergen and Trondheim) in a year” and one should take into account that Norway is a very long country, over 2000 km long. Bergen is situated on the western coast of southern Norway and is only slightly more northerly than Oslo, while Trondheim (Nidaros at the time) is situated in central Norway. In short, these two cities are not situated in northern Norway, literally far from it. There are no sources on the history of the Black Death in northern Norway or even north of Trondheim/ Nidaros; all medieval Norwegian sources have been published and I believe that I have identified every source that could have a bearing on the history of the Black Death in Norway. The history of the Black Death in central Norway north of Trondheim and in northern Norway is unknown and may remain so, although the new scholarly discipline of paleomicrobiology holds out promise of microbiological identification of Yersinia pestis in archaeologically datable plague graves.146 Obviously, this part of Davis’s statement reflects great historical and geographical confusion or disorientation, and what Davis has in mind may therefore just be confused and disoriented. The only possible realistic interpretation I can make is that the Black Death spread to Bergen and Trondheim in a year, taking into account these cities’ correct geographical position. In this case, the facts on the ground are that the Black Death was introduced to Bergen directly from England, probably by a ship transporting grain from King’s Lynn; the disease broke out in Bergen some time in the second half of August 1349, and was transported by ship thence to Trondheim where the outbreak appears to have been in full development at the end of September. At the time, the usual duration of a voyage from Bergen to Trondheim (or vice versa) was a fortnight.147 Obviously, these developments cannot support an argument that the Black Death spread so rapidly that it could not have been bubonic plague. There is nothing in the pattern of spread which is at variance with the normal assumptions of the spread rates of 145 For the history of the Black Death in Norway see Benedictow 1993/1996: 73–102; Benedictow 2002: 46–96; Benedictow 2004: 146–58; Benedictow 2006: 83–163. 146 See below: chapter 11: 249–58. 147 Benedictow 2002: 67–80; Benedictow 2004: 102, fn. 20.

116

chapter three

bubonic plague if the erroneous assertion that bubonic plague spreads only between contiguous rat colonies is discarded and we take into account metastatic spread over long(ish) distances by ship and by land and over short and intermediate distances by the agency of human beings transporting rat fleas in clothing, luggage, or goods (see below). The average daily spread rate along the main roads was about 1.25–1.5 km.148 (4) It would have been a proof of remarkable speed of spread if it were true that the Black Death “permeated all of England within months,” actually it would have been a remarkable feat for any contagious disease whatever its mechanisms of dissemination and transmission, especially under medieval conditions of communication and transportation. However, this assertion is without basis in research. The Black Death broke out in Melcombe Regis shortly before 24 June 1348 and petered out in northern England in the late autumn of 1349.149 The Significance of Evolutionary Theory and Adaptation by Selection Despite the agreement among advocates of alternative theories of plague that black rats are too warmth-needing to establish more than a sparse and transient presence in the northerly parts of Europe, it has been easy to demonstrate that this view has been argued in ways that makes it untenable on source-critical and methodological grounds. The lack or paucity of references to dead rats in contemporary accounts of plague epidemics does not support the assertion that there were no dead rats; instead this inference is a fallacy of methodology. This makes it clear that the argument that black rats are too warmth-needing to have a significant presence in the northerly parts of Europe has a principally explanatory character. This explanatory function can only be relevant and activated when it has been empirically proved that rats were, in fact, absent or few and far between in these parts of Europe and such an observation needs explanation. Consequently, it is also a fallacy of methodology to use this explanatory potential as factual evidence to prove the absence or approximate absence of rats, as all these advocates of alternative theories do. Instead, the methodological status 148 Benedictow 2002: 35–40, 319–20; Benedictow 2004: 151–3, 157–8; Benedictow 2006: 91–5, 107–8, 113. 149 Benedictow 2004: 126–31, 138–42.

rats

117

of this notion is that of a working hypothesis that must be corroborated by evidence in order to assume the character of valid assertion with some level of tenability. It has also become clear that this argument is methodologically problematic in yet another respect: the plague epidemics of the past could in principle provide the basis for a hypothesis that they represent a reflection of a broad presence of black rats and, consequently, that the epidemics were bubonic plague. These two legitimate hypotheses are diametrical opposites, a fact which demonstrates that up to this point in the discussion nothing has been precluded: it is universally agreed that there must have been at least a tiny sprinkling of rats, not necessarily enough to generate epidemics of bubonic plague. The crucial question is how these two hypotheses can be empirically tested. Twigg and Davis and other advocates of alternative theories assert that in the Middle Ages there could only have been autonomous or self-maintaining small rat colonies in Mediterranean ports, and possibly also in some rural districts. In the ports of northwestern Europe there were no rats or only a tiny and transient population of rats which could not reproductively maintain itself and establish itself there permanently, and their presence was dependent on a trickle of new rats by ship from Mediterranean ports. As pointed out above, regular direct voyages between Mediterranean ports and northwestern Europe did not begin until quite late in the thirteenth century. On logical grounds alone there could not have been any rats in these parts of Europe before that time if the assumptions of the advocates of alternative theories were tenable. Instead, the implication is that there was a continuous presence of rats. It has been shown above that negative assertions in this respect are not empirically based but are speculative notions or working hypotheses awaiting corroboration. In this connection, another methodological point should now be mentioned, namely that the methodological requirements for proving that some phenomenon did not exist or taken place tend to be rather more demanding than for adducing positive proof of a phenomenon or event. The argument asserted by advocates of alternative theories that since the black rat originated in a warm region means this species is too warmth-needing to have a significant and continuous self-maintaining presence in the northerly parts of Europe is based on a very narrow view of the question: it neglects to consider the possible significance of evolutionary theory and the process of adaptation and development of

118

chapter three

species by natural selection. In the words of Pollitzer, rats are “extremely fertile.” They reach sexual maturity long before they have completed their growth, when they are about three months old. The females have a sexual season extending for about nine months of the year, during which they are “in heat” at intervals of about ten days, the period of gestation is about twenty days, parturition tends to be immediately followed by “heat” so that a female can be impregnated a few hours after the birth of a litter. This means that there are many litters during a year and the number of young per litter is, on average, 5.4–6.150 The mortality rate of sucklings is quite high, but this also means that the forces of evolutionary selection are intensely at work, making for relatively rapid adaptation to changing circumstances.151 The view that a species with such enormous fertility and brief generational cycle as the black rat should not be able to adapt to various biotypes, ecological niches, and climates, is obviously untenable. Clearly the advocates of alternative theories accepted this hypothesis without careful consideration simply because it agreed with their theories. The heart of the matter can easily be put in perspective. The Vikings brought horses to the Shetlands and to Iceland when they began to settle there at the end of the eighth century and in the 860s ad respectively.152 Within a few hundred years, these horses developed into the Shetland pony and the Iceland pony characterized by considerably reduced size, a rough coat, and a long mane and tail as evolutionary adaptations to the new environments. Thus, new, smaller and hardier breeds of horses had come into being in these islands as early as the High Middle Ages. When horses with only a tiny fraction of the fertility of rats and much longer generational cycles can adapt so readily to new and difficult climatic and ecological circumstances, the complete rejection by all advocates of alternative theories of plague of the possibility that rats could have any such adaptability becomes the more remarkable. Can it really be true that rats arriving in the northerly parts of Europe would not develop by the process of evolutionary selection into a hardier breed with size and coat adapted to the climate? Does not such a surprising assertion demand a specific and empirically based

150 IPRC found an average of six foetuses in 975 pregnant rats in the Punjab, IPRC 1907j: 907, and 5.4 in 4841 pregnant rats in Belgaum in Bombay Presidency. IPRC 1910c: 457. See also Liston 1924: 998. 151 Pollitzer 1954: 290–1. Cf. IPRC 1907 g: 750. 152 Lamb 1995: 173–4; Sawyer 2003: 106, 112.

rats

119

defense? Do not the bare assertions that this is excluded or improbable in the case of rats and the complete absence of empirical arguments to this effect represent a fallacy of methodology? Would it not be logical to consider adaptation by degrees, as black rats were transported northwards in Europe over the centuries, which would introduce a long-term evolutionary perspective? M. McCormick emphasizes that to assume that “only human support can sustain rat populations outside a Mediterranean ecology is to underestimate rats’ adaptability.” He underlines this point by referring to the fact that burrowing black rats are found thriving in subantarctic conditions on Macquarie Island, latitude 54.30° S, longtitude 159° E, not far from Antarctica. Black rats are also living in the chilly and windy north Atlantic climate of the Shiant Islands in the Hebrides (Scotland). Interestingly, the zoologists who studied these black rats in the Shiant Islands, in stark contrast to Davis and Twigg, state firmly and unconditionally that “Rattus rattus was once widespread throughout the UK.”153 The black rat was also present until recently on Lundy Island off the northwestern coast of Devon,154 having survived from the Middle Ages in the absence of the brown rat. Size is important for the survival or improvement of the competitive situation of rats (as for other animals). According to the same evolutionary reasoning, McCormick emphasizes that “the size of modern black rats might be a misleading criterion, since substantially larger ones are documented in medieval Corsica.”155 This is also the case with finds of medieval rat bones both in England, Norway and Sweden (see below). Correspondingly fleas which have much higher fertility and shorter generational cycles than rats, would readily adapt by selection—fleas might, in the words of Bacot, “adjust itself to the varying conditions of climate experienced in its geographical distribution.”156 This is also underlined by Pollitzer: As shown by its wide geographical distribution, X. cheopis is able to adapt itself to a considerable range of climatic conditions. It is, as have been 153 McCormick 1998: 22–3; Key, Fielding, Goulding et al. 1998: 228–33. Under ordinary circumstances, I would have tended to think that these studies would have been of interest to Icelandic scholars. 154 James 2001: 12, and pers. comm. These rats have subsequently been exterminated. 155 McCormick 2003: 3. 156 Bacot 1914: 449–50.

120

chapter three previously noted, the common rat-flea in Manchuria and is also the prevalent species in the tropical section of Brazil.157

Another error at the heart of the arguments of Davis and Twigg is that they project anachronistically into the Middle Ages the modern situation of black rats. In modern Western society, black rats arriving in the northerly parts of Europe or North America by modern means of transportation directly from warm countries are not only poorly adapted to the new environments; further, their situation with respect to having the opportunity of going through a process of evolutionary adaptation is very different from what it was in historical European societies, for three important reasons: (1) they are mercilessly fought by the larger and more aggressive brown rat which did not arrive in Europe before the eighteenth century; (2) modern buildings and settlement structures are poorly suited for the establishment of colonies of house rats; (3) modern man has a very hostile attitude towards rats in their habitations. These three factors cause too high mortality rates among these rats to allow adaptation by selection before they are exterminated. In these circumstances, their presence will be dependent on fresh arrivals by ship, according to the model constructed by Davis and Twigg, but applied anachronistically by them to the Middle Ages. Rats have a rich and complex history which is structured according to a number of evolutionary developments and a plethora of social, economic and cultural factors in the human societies on which they depend. To project the situation of black rats in modern Western society back into the Middle Ages is obviously fallacious. The inherent dangers in neglecting to address the theory of evolution by natural selection for a species can also be demonstrated in relation to rats in several ways with profound theoretical and empirical implications. It has been shown, for instance, that black rats in the northerly parts of Europe could have had several different origins. Since both Twigg and Davis refer to Hirst’s monograph of 1953, it may be instructive to cite his statement that “the fossil remains of a very similar species [to black rats: my insertion] have been found near

157

Pollitzer 1954: 327.

rats

121

Geneva, in Lombardy, Bohemia, and Crete in Pleistocene strata, and numerous bones among the pile dwellings of Mecklenburg.”158 Thus, several finds of fossils of animals very similar to the black rat have been made from a pre-historical period starting more than a million years ago and stretching to about 10,000 years ago, covering several very cold periods or ice ages. This suggests that the black rat or rather a closely related species may have been present continuously in Europe, retreating with expanding glaciers and following in the wake of their withdrawal much like reindeer, bears, wolves and many smaller mammals. This notion is supported also by the fact that numerous bones of this rat or a similar rat have been found in excavations of human settlements in northeastern Germany from about 4000 to 2500 years ago. This can be taken to indicate the continuity of a species of rat very or at least quite similar to the black rat which was well adapted to life in northerly climatic zones. It also suggests that this rat rapidly found a new and attractive environment or ecosystem with the advent of human beings and their housing, settlements and economic activities, especially farming and animal husbandry with their corresponding products and outbuildings. As pointed out by Hirst, this indicates that “rats were associated with man since his first cultural beginnings, since the time when he first began to store large quantities of cereals in granaries.” Since this provides evidence of a species of rat which is quite closely related to but not identical with the black rat, it may usefully be taken as evidence of the black rat’s adaptability by evolutionary selection to northerly climates and environments, and evidence that black rats have adapted to northerly climate at least once, and quite likely twice in the past. The material is too small to constitute proof of the continuous presence of this species of rat from the Pleistocene or the Bronze Age to the Middle Ages, or of its early and continuous association with man. However, this evidence may serve as the basis for a wellfounded working hypothesis calling for further investigation. Davis and Twigg would have been right in their view that the black rat and its accompanying fleas would quite likely not have survived in the northerly parts of Europe if specimens were picked up in India and dropped there by parachute. However, if a long time perspective and conditions for adaptation are introduced in an evolutionary model which lets rats and their accompanying fleas start from southern

158

Hirst 1953: 126. Davis 1986, refers erroneously to page 121.

122

chapter three

Europe and gradually spread northwards over centuries, both black rats and their fleas would easily produce variants or biovars adapted to the new conditions. It is therefore a fallacy of methodology and evolutionary theory to assume, without empirical evidence, that black rats of modern India and black rats in the northerly parts of Europe in the Middle Ages or Early Modern Period were biologically identical in the sense of having the same biological adaptation to environments, biotopes and climates. This is a valid argument also for a comparison of black rats in southern Europe and northern Europe at the time. This perspective will now be tested against the sources and material evidence. The presence of rats in Europe at the time of the Black Death is the focus here. In consideration of the large time spans in question, we must take into account the possibility that there may have been another later independent introduction of the black rat, representing a second or third introduction, and another subsequent evolutionary process of adaptation. If it were correct that it was too cold in the northerly parts of Europe to allow a broad presence of black rats and that nonetheless the same disease ravaged this part of Europe as southern Europe, this would constitute independent and sufficient proof that the Black Death must have been some disease other than bubonic plague. Consequently, evidence on the presence of rats in Europe, especially the northerly parts of Europe in the preceding centuries, would be of pivotal importance. Rat Bones: Material Evidence of the Presence of Rats in the Middle Ages In Europe, rat bones older than ca. 300 years must be remains of the black rat. Twigg argues that it is reasonable to dismiss the significance even of archaeological finds of rat bones in medieval layers on the grounds that the “Black rat in temperate latitudes today lives only in the warmer parts of towns and it is likely that it has always done so” and adds that “Rattus rattus is essentially a sedentary animal, therefore in temperate climates its occurrence in towns where it does not leave the warmth of buildings is a fact of great significance in the aetiology of bubonic plague and one we should remember when viewing past epidemics of that disease.”159 As shown above, this type of argument is

159

Twigg 1984: 80, 88.

rats

123

fallacious. It represents an attempt to make an argument which is at variance with the elementary methodological principle that all scientific and scholarly arguments must in principle be open to falsification. Twigg also attempts to undermine the significance of finds of rat bones in layers of medieval remains on the basis of two other premises, namely that (1) the brown rat is known for its prowess in burrowing, and (2) the bones of the black rat and the brown rat are quite similar and their remains are therefore often difficult to separate. For this reason, he holds that finds of rat bones in archaeological excavations of medieval sites do not constitute evidence of the medieval presence of the black rat, but could reflect the burrowing capacity of the brown rat.160 However, Twigg does not take into account any limit to the depth to which brown rats were apt to burrow. It is therefore important to emphasize that brown rats’ “burrows for shelter and nesting rarely exceed 18 inches (approximately 45 cm in depth),” and that they will only dig deeper in order to “gain access to food-supplies.”161 Since there is not much food to be found in medieval strata even for rats, burrows of the brown rat will normally be significantly shallower than 45 cm, and will, consequently, often or normally not reach medieval layers that will tend to be deeper, especially in urban and village environments where deposits from daily life tend to increase the ground level. Another point is that rat burrows tend to be archaeologically traceable and their origin identifiable.162 For this reason, finds of rat bones in medieval layers will normally be remains of black rats and only exceptionally come from a brown rat, and then under circumstances where this will tend to be recognizable. The brown rat is normally larger than the black rat, also the size of the bones provides some useful if not decisive indication of the type of rat. While it is true that the burrows of brown rats may occasionally have penetrated into medieval layers, and that this should be taken into account, finds of the remains of rats in medieval layers are now so numerous that the great majority of them must be of the black rats. Different types of evidence and arguments can be accumulated to produce a solid case for identifying rat bones found in excavations of Roman or medieval sites as medieval remains of the black rat. 160

Twigg 1984: 78, 80. Pollitzer 1954: 286; he cites US Public Health Service, Communicable Disease Center (1949). 162 Rackham 1979: 112–20. 161

124

chapter three

The main conditions of source-criticism and the significance of finds of rat bones must also be assessed in a historical perspective. Zooosteological studies of finds in archaeological excavations are recent features of archaeological work, having been taken up beginning in the 1970s; this is especially the case with small bones. Earlier studies of small bones are so few that they can be considered exceptional, for instance, finds of two-thousand-year-old rat bones in Pompeii.163 This also means that while excavations up to about 1970, and to a large extent also later, have undoubtedly made significant contributions to our knowledge of the past, they have also destroyed much valuable evidence for the study of bones, insects, and plants, and so on, which could help to form a more complete picture of human environments and ecology in the past. Much of medieval Oslo was destroyed when the first railway was built in the early 1850s and also in the subsequent decades as the railway network was expanded; as late as around 1970, excavations of some remaining medieval sites were performed without sieving for small bones (such as rat bones).164 Wars have also been destructive, especially the mass aerial bombardments and massive use of artillery along the front lines and in urban battles which are characteristic of the Second World War. Archaeological excavations tend also to be performed in urban centres or at the manors and castles of the rich and mighty, whilst peasant houses and settlements have attracted much less interest and are often much less amenable to such studies. Black rats are nimble climbers and like to nest in the roofs or ceilings of human housing where they are safer from predators like cats, and also because warm air rises from the hearth and produces better living conditions there. This means that their bones and their nests will often be long gone or be dispersed in a way that will make finds very unlikely. Black rats are also, as mentioned, burrowing animals, and they have been burrowing away from human habitation also in the Nordic countries (see below). They could have burrowed within medieval and early modern houses with beaten earthen floors until it became usual to build houses with timbered floors as in the Nordic countries or with tiled floors as in the more southerly parts of Europe, and subsequently and gradually also on low stone foundation walls, a process that appears 163

MacArthur 1952: 209. Lie 1988: 159. I thank Professsor Egil Mikkelsen, Director of the Historical Museum, University of Oslo, for useful comments on this point in a personal communication by e-mail 25 January 2010. 164

rats

125

to have started in many places some time in the sixteenth century and to have been largely completed by 1800. This meant that the black rats increasingly had to focus on nesting in roofs or ceilings, outbuildings and burrows which increased their vulnerability, especially after the arrival and growth of the brown rat populations.165 One should note that it was usual in the past that live-in farm workers slept in the outbuildings, especially in stables and cowhouses where the dense housing of large animals produced a significantly higher temperature which also would be attractive to rats, as would the opportunities for finding food. Unfortunately, in the large regions of the Nordic countries characterized by detached or semi-detached peasant holdings, houses have over many centuries and even millennia been reconstructed or replaced on the same or partially overlapping sites (tofts). In the villages of manors, especially in medieval Denmark, the lords in the process of socalled equalization organized the holdings into units of equal size more or less unhindered by customary rights typical of, for instance, contemporary English manorial economy. This makes it unlikely that medieval rat burrows will be found in such sites, or that such finds will be exceedingly rare. The fields from the Viking Period and the Middle Ages are also largely long gone, having been reworked many times and in recent generations by heavy machinery which crushes burrows in the ground or works so deep into the soil that burrows will be destroyed. And of course archaeologists rarely study undisturbed fields of the Viking Period or the Middle Ages, so rat burrows in the fields near human habitation will remain undiscovered. Another factor is that undisturbed fields or tofts over such a long time will tend to be unrepresentative for some of the same reasons that have made them unattractive for re-settlement. For all of these reasons, the chances of finding medieval rat bones or rat burrows may appear small, but such finds would be more likely in urban centres than in the countryside for reasons that may not have anything to do with the territorial distribution of black rats in the past. Consequently, the incidence and number of archaeological finds of rat bones should be expected to be small, but will increase as archaeologists more often look for small bones of animals and take a more complete interest in human environments of the past.

165

Benedictow 2002: 250, 276–8.

126

chapter three

The substantial number of finds of rat bones from the Middle Ages that is now available for analysis and their wide distribution across Europe is therefore a surprising result of archaeological investigations in this regard. The source-critical problem of the representativeness of archaeological finds of rat bones can also be illustrated in another way on the basis of the report that B. Hårding, the former Swedish osteologist, produced on the study of bone material found in excavations of the original area of the small town of Sigtuna (north-west of present-day Stockholm) which developed beginning in about 975 a.d. An area of about 1,100 m2 was excavated, bone material was collected from about 400 m2, but small bones from small mammals were only searched for with adequate methods in a sample of eight squares of 2×2 m, a miniscule fraction of the excavation area. Since the osteologist nonetheless found twentytwo rat bones of which fifteen could be identified with certainty as black rat,166 it would be inadequate to conclude that these bones represented just a few rats; instead it would be more realistic to infer that black rats were ordinary animals in the small town at the time, in the late Viking Period and the early High Middle Ages. As new archaeological finds of rat bones were steadily reported over the last decades, patterns of development and spread became observable. I produced the first preliminary overview of finds up to 1991 in the medieval Nordic countries and northern Europe in my doctoral thesis.167 The first full inventory of finds was published by F. AudoinRouzeau and F.-J. Vigne in 1994.168 After this date, more than thirty new finds from about twenty ancient and medieval sites169 have been recorded and presented in a broad historical perspective by M. McCormick in 2003,170 a paper that appeared when my typescript on the history of the Black Death was with the publishers. However, in my monograph I give a broad account of such finds in the chapter “Rat History.” McCormick and I independently reached the same crucial conclusions about this material, although I have chosen to ignore the

166

Hårding 1992: 0–1 (sic), 4, 27. Benedictow 1993/1996: 157–60. The writing of the dissertation was finished in 1991, it was defended in 1992 and was published in a slightly revised form in 1993 and reprinted in 1996. 168 Audoin-Rouzeau and Vigne 1994: 125–45. Cf. Aduoin-Rouzeau 1999: 220–6. 169 McCormick 2003: 6, fn. 7. 170 McCormick 2003: 1–25. 167

rats

127

question of geographical origin of the black rat as being peripheral to my subject. A useful point of departure is the numerous finds of rat bones in Roman imperial territories in the West and also in its northern territories. McCormick summarizes finds of rat bones in sixty-five sites from the Roman period up to the eighth century. Several finds of the skeletal remains of black rats dating back to Roman times have been found in Italy, they are widespread in Roman Gallia/Gaul (France), have been found near Amsterdam and in Valkenburg in the Netherlands, in southern Belgium, in Roman Austria and are widespread in Roman Germania all the way to about the city of Cologne (a Roman military camp called Colonia = settlement) in the northwest.171 In Switzerland, skeletal remains of two black rats have been found in excavations of a Roman villa near the city of Bern, the remains of one rat in the Roman town Augusta Raurica, present-day Augst, and the remains of a rat dating to the 4th–8th century have been found near Geneva.172 Many of these finds come from rural inland regions, and only a few from ports. In England, several finds have been made of the skeletal remains of the black rat dating back to the time of the Roman occupation, namely in York and London, at a Roman settlement (Gorhambury) near St Albans roughly 35 km north of London, in Wroxeter (Shropshire), and of two rats from the first century a.d. in a Roman villa in Beddingham situated inland in East Sussex. Remains of three rats found in Walton, Aylesbury, in Buckinghamshire, the very heartland of rural England, have been dated to the 5th–7th centuries, and may therefore be from the late Roman period or transitional early AngloSaxon England; subsequent finds at this location up to the 9th–12th centuries reflect a presumably continuous presence. These finds are widely distributed in the northeast, southeast, central and western parts of England, respectively. They are certainly not restricted to ports or to cities, which are the case only with the finds in London and York. The devastating implications of these findings for advocates of alternative plague theories are demonstrated by the complete silence on these finds by Scott and Duncan in their monographs of 2001 and 2004. This permits them to maintain that “the black rat had not spread to northern Europe by the time of the plague of Justinian [540–1]” and 171 Armitage, West and Steedman 1984: 379; Audoin-Rouzeau and Vigne 1994: 129; McCormick 2003: 6, fn. 7. 172 Stampfli 1965–6: 454–5; Audoin-Rouzeau and Vigne 1994: 129, 134–5.

128

chapter three

that the black rat may have arrived in England in the Middle Ages, but “a variety of dates have been suggested.”173 In support of these assertions they refer to Matheson’s book of 1939 and Shrewsbury’s monograph of 1971, again seeking refuge in obsolete works in relation to an important point. In the later popular version of their monograph, they express the same opinion and again pass in silence by all the finds of rat bones from Roman England and Northern Europe.174 Despite the fact that animal bones, especially of small animals, have attracted the interest of archaeologists and osteologists only in recent decades,175 it has been shown that the black rat was widely dispersed in Roman Europe, from Italy to England, to “Belgium” and the Netherlands and all over Roman Gaul in the west to the Roman military settlements on the borders with the Germanic tribes along the R. Rhine and the R. Danube. The pattern of finds in time and space indicates that the black rat was spread over Roman Europe by the movement of the legions, by their long logistical train of wagons with sufficient food stuffs to support 4000–6000 men in each legion over time, and through the market-oriented network that was established by the Roman Empire. This is one of the important observations that McCormick and I made independently.176 This is really not surprising in view of the fact that there was no commercial (or military) sailing from the Mediterranean to western and northwestern Europe, and legions and goods moved by land from Italy to Britain, to Gaul and Roman Germania. Up to 1984 when Twigg’s monograph was published there had been six finds in England of skeletal remains of the black rat dating back to the Early Middle Ages, and also one find in Ireland. As mentioned above, at Walton, Aylesbury, finds were made dating back to the 5th– 7th centuries, the late Roman period or transitional early Anglo-Saxon England, while other finds at this location date to the 9th–12th centuries, indicating a continuous presence. Twenty-seven finds dating back to the 11th–15th centuries with a wide territorial distribution in England have also been made.177 After 1984, many new finds of remains of rats have been made in England from Anglo-Saxon times

173

Scott and Duncan 2001: 56. Scott and Duncan 2004: 174–5; Davis 1986: 463–4. 175 McCormick 2003: 6. 176 McCormick 2003: 9; Benedictow 2004: 22. 177 Armitage, West and Steedman 1984: 381; Rackham 1979: 112–20; AudoinRouzeau and Vigne 1994: 129–35; McCormick 2003: 6, fn. 7. 174

rats

129

and subsequent periods of the Middle Ages. They show a wide distribution in the country, as far north as the Brough of Birsay on the western tip of the main island of the Orkneys where they dated back to the 9th–12th centuries.178 Nonetheless, Scott and Duncan state that Dr Twigg has continued with his careful study of the black rat in England during the age of the plagues and has collated overwhelming unpublished evidence that it did not spread to rural areas.179

This raises a number of questions: How can Twigg maintain that the black rat only had had a sporadic incidence in English ports in the Middle Ages and later, when the material skeletal finds on the ground prove a much longer history of wide distribution back to Roman times, also in inland regions, when he shows knowledge of several of the studies that present this evidence?180 How can Scott and Duncan refer to “overwhelming” unpublished evidence collated by Twigg which confirms that rats did not spread to rural areas in the face of substantial published empirical zoo-osteological evidence to the contrary? How could Twigg collect and collate “overwhelming” evidence bearing on the matter which is unknown to archaeologists and osteologists who would have had to produce it? And why is this “overwhelming” material still not published? Fortunately, Scott and Duncan mention two arguments based on Twigg’s unpublished material which afford the opportunity to test its quality or tenability, especially since these arguments must be assumed to have been selected for their importance and evidentiary powers. Conspicuously, these arguments have no relation to zoo-osteology or finds of rat bones, which presumably would be the only powerful material evidence in this case. Instead, these two supposedly important pieces of evidence relate to (1) changes in the design of dovecots in the 1720s and (2) changes in the design of storage facilities for grain in 1730s, which purportedly constitute proof of the normal absence of the

178 James 1999: 20–1; James 2001: 12; Audoin-Rouzeau and Vigne 1994: 129–31; McCormick 2003: 7–9. McCormick’s information is not as well arranged and easily surveyable as that of Audoin-Rouzeau and Vigne and therefore not easily structured and summarized at the level of finds, but is updated and contains more valuable perspectives and analyses. 179 Scott and Duncan 2004: 175. 180 Twigg 1984: 80–1.

130

chapter three

black rat back in English history. It is also asserted that these two developments reflect the contemporary spread of the brown rat which arrived in England in 1728 or 1729. These two arguments contain several elementary methodological fallacies. The notion that observations regarding technological developments in the third and fourth decades of the eighteenth century can prove anything about reality in Roman, Anglo-Saxon, medieval or Early Modern Periods in England is obviously untenable. The argument that the advent of the brown rat in 1728 or 1729181could be the cause of widespread change in the construction of dovecots in England in the 1720s is obviously also an anachronistic assumption of causation and as such fallacious. The idea that a tiny and growing number of brown rats which probably numbered in the hundreds and was distributed over a tiny area in the course of the 1730s could affect how grain was stored in England in the 1730s reflects the same temporal problem of causation but also again the fallacious anachronistic implication that it would have evidentiary relevance for a discussion of the presence of black rats in preceding historical periods. The explanatory potential of the modernization of mentality and culture in the early phase of the Industrial and Scientific Revolutions should also be considered. This could make it clear that these authors will have to device a methodologically tenable research strategy that will uncover material with unambiguous evidentiary and explanatory powers relating concretely to the historical process in question. To my knowledge, a generation later Twigg has still not published his purported material, the outcome of his “careful study of the black rat in England,” although Scott and Duncan characterize these two arguments as “splendid pieces of scholarship.” In conclusion, it can be emphasized that despite the fact that animal remains have only quite recently attracted the interest of archaeologists and osteologists,182 it has been shown by numerous finds of skeletal remains that the black rat was widely dispersed in England in Roman times and was distributed all over the country in the Middle Ages. The difference in the incidence and distribution of finds between these two historical periods is probably due to two facts, firstly that there are fewer physical remains from Roman England than from medieval England that can be examined and, secondly, that Roman remains have

181 182

Shrewsbury 1971: 9. McCormick 2003: 6.

rats

131

attracted relatively greater interest from English archaeologists and to a greater degree had been excavated before they started to take interest in small bones, and relevant skeletal material has inevitably been destroyed en masse. From the Roman border provinces, the black rat could easily have been spread further into Germanic and Slavic territories through trade. Actually, remains of black rats dating back to late Roman centuries have been found in the excavation of a Germanic settlement at Waltersdorf in eastern Germany near present-day Berlin, and in Slavic settlements in present-day northwestern Poland (Smuszewo) and on the eastern side of the Gulf of Gdansk (Tolkmicko). There has also been a find in Szczecin (Stettin) dating from the 4th–8th centuries. Thus, it is not surprising that numerous finds of skeletal remains of the black rat dating back to the early medieval period have been made in northern and northeastern Germany, and in Poland, including sites on the Baltic Sea.183 In the most important commercial centre in Northern Europe in the Early Middle Ages, namely the town of Haithabu situated north of present-day Hamburg, several finds of skeletal remains of the black rat have been made.184 From this important commercial centre black rats must have been distributed into the Nordic countries by ships—the black rat is not only the house rat but also the classic ship rat. Again, a long temporal process of spread and adaptation is indicated. The lines of trade and communication extended much farther around Northern Europe: Franks and Frieslanders traded with the Nordic countries in the Early Middle Ages and the Vikings sailed all around Western Europe trading and plundering as they saw fit. In the 880s, the Norwegian merchant Ottar who lived in northern Norway, visited King Alfred the Great of Wessex in England. He told the king about Norway and the other Nordic countries, an account that was included in the geographical section of the translation of the Roman author Orosius’s History of the World, a project in which the king eagerly participated. Ottar’s account produces a vivid picture of trade by ship that in the ninth century interconnected the whole of Northern and northwestern Europe in a commercial network along which black rats, the classic ship rats, would almost inevitably have been widely distributed.

183 184

Teichert 1985. Reichstein 1974 and 1987.

132

chapter three

Against this backdrop, it is unsurprising that finds of black rats in the Nordic countries date back to the Early Viking Age. Recently the archaeologist B. Wigh published a monograph on excavations at Birka, an urban centre which developed in the second half of the eighth century on an island in the big L. Mälaren west of present-day Stockholm. Within a chronology of stratigraphic phases he reports that the remains of a rat were found in phase 3 covering the period c. 810–30 a.d., thirteen remains of four rats were found in phase 4, a stratum pertaining to c. 830–45 a.d., the remains of another rat date back to the subsequent phase 6, the period c. 860–900, and from phases 7–8 covering the period 900–50 twenty-four bone fragments of black rats were identified,185 before the town disappeared around 975.186 Finds of skeletal remains of the black rat dating back to the end of the Viking Age around 1050 have been made in other urban centres, in Lund187 near the western side of the Sound, and in Sigtuna situated on L. Mälaren north of the former town of Birka and northwest of presentday Stockholm. As mentioned above, twenty-two bone fragments of rats of which fifteen were identified with certainty as black rat have been found in a special study of a tiny part of the excavation area in Sigtuna. Within this area, the bone fragments were quite dispersed and presumably represent several specimens. These finds suggest that black rats were ordinary animals in the urban environment of the time.188 In all three cases, the presence of the black rat in these urban centres occurred quite early in their developments, and they may have been present about as early as urban growth first started, which appears to have been the case in Birka. The appearance of rats in the first phase of the formation of new urban centres in the Viking Period indicates that rats at the time were widespread and usual on board ships and were easily spread to new ports that would act as epicentres of spread inland with the further distribution of goods by boats or pack horses. Also the remains of two rats datable to 1220–60 have been found in Lund.189 Large numbers of skeletal remains of the black rat dating back

185

Wigh 2001: 29, 54, 125–6. A small first excavation at the location was performed in the early 1870s and among the finds were the remains of a rat, but since the find was not handled according to modern standards nothing more can be said than that it dates from the ninth or tenth century. See Wigh 2001: 29, 125; and Audoin-Rouzeau and Vigne 1994: 129. 187 Bergquist 1957: 98–103. 188 Hårding 1992: 27; Hårding 1993: 25. Cf. Wigh 2001: 125. 189 Bergquist and Lepiksaar 1957: 11–84. 186

rats

133

to the thirteenth century and the late medieval period have been found in excavations in Stockholm.190 Excavations of a settlement on the Baltic island of Öland unearthed the remains of three rats dating back to the 11th–13th century.191 In excavations in Visby in Gotland Island, G. Malmborg, the osteologist at the University of Gotland, has in recent years found many remains of the black rat from the 13th and 14th centuries. In a personal communication, he states that he finds it improbable that the black rat was not spread to all parts of the island in the medieval period, and suggests that the brown rat did not arrive until around 1800.192 Remains of two black rats from the decades around 1400 have been found in Hälsingland,193 a completely rural region along the Baltic coast in northern Sweden, namely in the royal bailiff ’s fort at Faxeholm,194 after only four per cent of the site has been excavated.195 J. Lepiskaar, the osteologist, has identified the remains of twenty rats found in the site of a monastery in Gudhem in western Sweden (specifically the southwestern region of Västergötland) dating back to the fourteenth and fifteenth centuries. The same scholar found bones from a rat in Uppsala north of Stockholm datable to the fifteenth century and another from about 1470–1530 at a nunnery in Ny-Varberg, a small town situated on the Sound (close to Varberg).196 A find of rat bones in the site of a hostel for travellers in Ramundeboda in the district of Tiveden, in a central region of Sweden (county of Örebro) is dated to the fifteenth century197 (Ny-Varberg and Lund are situated in regions that today are Swedish but in the Middle Ages belonged to the Kingdom of Denmark). Finds of rat bones in Sweden now date back to the early Viking Period and throughout the whole medieval period; they have a wide territorial distribution from Scania in the southwest to Hälsingland in the northeast. These finds were made in both urban and rural ecological environments. This corresponds to interesting linguistic evidence 190

Vretemark 1983: 294, 467. Boessneck and von den Driesch 1979: 214–5. 192 Personal communications from G. Malmborg in e-mails dated 19 June, 20 June and 21 June 2006. 193 Hälsingland is situated roughly 250 km north of Stockholm. 194 Faxeholm is situated not far from the present-day small town of Söderhamn that, please note, was established at the beginning of the seventeenth century. Faxeholm was quite a small and simple fortified place, not really a castle. Mogren 2000: 251–2. 195 Mogren 2000: 119–20, 249. 196 Lepiksaar 1965: 96–7; 1969: 38; 1975: 230–9. 197 Audoin-Rouzeau and Vigne 1994: 131. 191

134

chapter three

which needs some general introductory comments. The major language families do not contain a specific word for rat in their basic vocabularies. In the past, people were not zoologists and had no scholarly or scientific education, and they used the same word to designate a number of animals that looked quite alike to them such as mice, rats, stoats and polecats. In languages of Indo-European origin, the basic word is “mus,” e.g., in Latin, Norse and modern Scandinavian languages “mus,” German “Maus,” English “mouse,” Russian “mysh.” Up to 1910, the scientific name of the black rat was Mus rattus and of the brown rat Mus decumanus. For this reason, it is often impossible to know which animal a writer has in mind when the word “mus” or “mouse” is used.198 When a writer for some reason wished to be more accurate, additional information was needed to identify the specific animal referred to. Medieval authors writing in Latin might resort to the current vernacular word: a chronicler provides an account of an Irish bishop of the fifth century whose library was destroyed by majores mures que vulgariter rati vocantur, i.e., “big ‘mice’ that in the vernacular [by common people] are called rats.” Thus, in fifth-century Ireland, ordinary people had acquired a specific word in order to distinguish vermin in the form of mice from vermin in the form of rats, probably from the Anglo-Saxon invaders who appear to have had such a word.199 Also in the Norse language of the Vikings a specific term came into use when people wished to identify the animal in question as a rat (long before the word rat entered the Scandinavian languages), namely “vǫlsk mus” which can be literally translated as “Frankish mouse.”200 In view of what we know of the history of the brown rat, there can be no doubt that this term refers to the black rat. The adoption of the term may reflect either the fact that the black rat was a new animal in the early Viking Period or that the Vikings learned a specific term abroad that they found useful. The term “Frankish mouse” may contain some indication of the geographical origin and the time of frequent and widespread introduction of black rats to the Nordic countries. It suggests that the time was the Viking Age, quite likely in the first half of the ninth century, when Viking fleets frequently sailed up the large French rivers, landed hosts of armed men which ravished the countryside and formed armies which besieged Paris. Since the black rat is not only the 198 199 200

Cf. for instance McCormick 2003: 4. McArthur 1949: 170, fn. 2. An Icelandic-English Dictionary 1975: 440, ‘mýss valkar’; Fritzner 1954: 755.

rats

135

house rat but also the ship rat, this means that there must have been many introductions of black rats into the Nordic countries as early as the ninth century and also frequently later, also from other sources, for instance, from Haithabu or England. This explains the frequent archaeological finds of rat bones from the early ninth century and later periods. These were rats which would have had centuries of adaptation to the climates of northwestern France, England, and northern Germany. Consequently, there would also be ample time for the evolutionary development of an even more hardy and rough-coated breed of black rats that would have been adapted to life under the prevailing climatic, economic and social conditions of the Nordic countries. This process would allow the development of a widespread and numerous population of rats and the murine potential which could play a tragic part in the spread of the Black Death and subsequent plague epidemics. The early introduction of the specific term “vǫlsk mus” is probably the reason that the word “rat” is not registered Scandinavian sources until the Late Middle Ages.201 The numerous finds of medieval rat bones in the Nordic countries present the proponents of alternative theories with great problems which they handle in interesting ways. Davis discusses Scandinavia in this regard under the pretence that there has been made only one find of rat bones, namely in Lund, despite the fact that quite a number of the finds of rat bones presented above had been published before he wrote his paper. It is not true that Lund is a port, as Davis maintains:202 Lund is situated on a fertile plain about eight km from the Sound without pronounced commercial functions. In the Middle Ages, Lund’s growth was mostly stimulated by its establishment as a national religious centre, a cathedral city, and as the site of the archdiocese of Denmark. It is not readily comprehensible what Davis means in this context by stating that “none were found in Holland” which is a province in the Netherlands. Perhaps, it is a garbled form of Halland which is a longish region (at the time Danish) situated along the Sound (north of Lund), in which case he is wrong, since Ny-Varberg was a small town in Halland near present-day Varberg. Relating to my discussion of the presence of rats in the medieval Nordic countries in my doctoral thesis,203 Cohn asserts in his 201 202 203

Bernström 1969: 578. Davis 1986: 463. Benedictow 1993/1996: 157–60.

136

chapter three

monograph that in “these Nordic countries no skeletal remains of rats has been found.”204 Clearly, this assertion is wrong. Most of the finds of skeletal remains of rats mentioned above were published before I wrote my thesis and they are all included in my presentation of this material with a discussion of their epidemiological implications. At the time Cohn was writing his monograph, he had the opportunity to avail himself of the overview of archaeological findings of black rats published by Audoin-Rouzeau and Vigne in 1994 in which my information on Nordic finds is included and greatly enlarged upon within a Europewide perspective, and subsequent publications of finds up to 2002. Instead, he denies the facts and makes disparaging comments on the earnest efforts of colleagues to interpret the significance of these finds. In my doctoral thesis I argue that the absence of finds of rat bones in Norway so far was probably due to the incipient stage of development of zoo-archaeology, and for this view I am ridiculed by Cohn.205 However, at the time Norwegian archaeologists had not begun searching for and studying small bones in their excavations; such bone material might be collected and stored but was not actively studied. In recent years, the study of such bone material has begun, in the words of Ann Kristin Hufthammer, the osteo-archaeologist who has taken the first initiative in this field of study in Norway: “only recently have we begun to sieve and systematically collect bones also of small species.”206 Up to the time of writing, this has led to the following identifications of skeletal remains of the black rat: in Trondheim (medieval name Nidaros) skeletal remains of the black rat have been found in several sites from the early High Middle ages, among them in the sites of Folkebibliotekstomten and Televerkstomten; finds have also been made in sites from the seventeenth century in the archiepiscopal mansion and in Televerkstomten. In Stavanger, rat bones archaeologically dated to the early twelfth century have been found in strata at Skagen. The oldest radiological dating of bone material of a black rat in Bergen is 750 years before present time, calibrated to ad 1225–95. In Tønsberg, archaeologists have succeeded in finding a rat nest containing several individuals. Skeletal remains of a rat found in it have

204 205 206

2006.

Cohn 2002: 53. Ibid. Personal communication from Ann Kristin Hufthammer by e-mail of 10 January

rats

137

been radiologically dated to 700 years before present, calibrated to ad 1265–1375.207 It is tempting to consider this find a possible reflection of the Black Death. The finds of medieval rat bones in Norway are consonant with literary evidence. In Snorri Sturluson’s Saga of St Olav, the need for a specific designation of rats is resolved by using the description “mice as big as cats” with obvious resemblance to the Latin wording of the Irish chronicler mentioned above mures majores, “big mice” (in the vernacular called rats). This description is used for animals which are said to have appeared when St Olav crushed a big wooden statue of the god Thor to which food was sacrificed daily.208 This brief legend of St Olav linked to his missionary work takes place in the principal inland valley of Gudbrandsdalen, a completely rural region of central southern Norway. This implies that at the time this saga was written, i.e. shortly before 1230, the listeners or readers were comfortable with the notion that rats were usual animals in central rural districts of southern Norway and that this had been the case two centuries earlier. When rats surface in this saga, it is in a context that demonstrates the ordinary presence of rats in the middle of the high medieval Norwegian countryside. Again, the crucial source-critical question is: why are rats mentioned? Sagas are heroic tales of kings and warriors and serve the ideological and political purposes of state-building and of confirming the prestigious (and profitable) roles of kings and aristocratic elites. Comments on rats have no useful practical or ideological place in this literature and should not be expected to occur, particularly as they were pests in human habitats. In this case rats are mentioned because they serve a religious propagandistic function, demonstrating the stupidity of serving food to heathen wooden gods. The great saga writer who constantly seeks literary effects does not use the term “vǫlsk mus” because he wishes to dramatize his story and enhance the impact of its moral teaching by emphasizing the ludicrous point that the heathen peasants had fed rats so lavishly that they had grown big as cats. The question of evolutionary adaptation to northerly climates by rats and the quantitative and distributive aspects of their presence in the Nordic countries can be enlarged upon on the basis of written sources. There are so many references to rats in literary works that a leading

207 208

Personal communications by e-mail 10 January 2006. Snorri Sturluson 1899/2003: 295.

138

chapter three

Swedish scholar in this field of study concludes: “During the late medieval period, rats and mice are mentioned as generally known pests in and around human buildings”; and “it appears likely that this animal [the black rat] at the middle of the fourteenth century had a numerous presence in Scandinavia’s and Denmark’s rural districts.”209 “Rats and even mice must have been very troublesome pests for medieval man,” as evidenced by both the great number of maledictions and curses and also the extensive use of rat traps.210 For zoo-historical reasons, all of these references must be to the black rat. This literary evidence and the conclusions drawn by Nordic scholars with respect to the quantitative aspects of the presence of black rats and their territorial distribution in the Nordic countries accord with the material finds of rat bones, and we may be certain that rats had a broad rural presence. This presentation of skeletal remains of the black rat so far found in Norway and Sweden puts in perspective Twigg’s assertion that Norway and Sweden are countries “which provide especially poor conditions for Rattus rattus,” and makes it clear that his view is based on preconceived and arbitrary assumptions which are at variance with historical reality as reflected both in the form of rat bones and in literary sources.211 This confirms O. Nybelin’s view which he formed long before archaeological finds of rat bones were made to the effect that the black rat was spread all over medieval Sweden and the southern parts of Norrland. To him it was important that this was still the case in large parts of Sweden in the nineteenth century, but at the time the black rat was in rapid decline because of the expansion of the brown rat and the modernization of housing. Nonetheless, the black rat was still observed in inland rural regions with very cold winters such as Värmland and Småland, and at the time it was still common in southern Norrland, especially in Hälsingland. Actually, in Hälsingland the black rat was still living in four rural parishes in the early 1920s as well as in seven rural parishes in Halland, in northeastern and southwestern Sweden respectively. In Finland, black rats were observed in about 20 localities, mostly in rural regions, in the first decades of the twentieth century.212 For obvious reasons, the brown rat spread first to ports and urban 209 210 211 212

Bernström 1969: 577–83. My translation from Swedish. Törnblom 1993: 367. Berg 1969: 576–7. My translation from Swedish. Twigg 1984: 57. Nybelin 1928: 852–5.

rats

139

centres and from there to rural districts, thus, logically the last surviving “tribes” of the old black rat were found in peripheral rural districts. However, this also constitutes evidence that the black rats in the Nordic countries were spread all over these countries, and that they were usual rural animals not at all confined to ports or urban centres. Sweden and Finland have colder winters than large parts of Norway because they are situated further way from the warming effects of the Gulf Stream.213 In this respect, there is complete compatibility and accordance between the written sources and the material finds of skeletal remains of these animals. This point should be considered from wider chronological and geographical perspectives. Until the 1790s, the black rat was the only rat in Sweden and Finland, the Nordic countries with the coldest winters. The arrival of the brown rat meant that the black rat was gradually driven from its habitats by the brown rats, and was prevented from seeking alternative refuge or habitats by contemporaneous changes in the construction of buildings and increasingly hostile countermeasures implemented by the human inhabitants against rats in their houses and immediate vicinities However, in the first decades of the twentieth century black rats were still found in a number of urban and rural areas in these countries; in Sweden the last colonies could still be observed in the 1950s.214 In Norway, the black rat may possibly still live in a few rural localities.215 In the Middle Ages, Finland had a tiny and territorially widely dispersed population numbering about 65,000 persons at the time of the Black Death. There was only one small urban centre, namely Åbo (Turku),216 consequently, rats would have to be animals living in conjunction with rural human settlements. In fact, black rats were still observed in the remote rural districts of the region of Tavastland in Central Finland in the 1920s.217 Presumably, rats were introduced into Finland by Swedish peasants who moved across the Baltic Sea and

213 Eldevik 2006: 48. Eldevik is researh leader at the G.C. Rieber Climate Institute at the Nansen Environmental and Remote Sensing Center and Bjerknes Centre for Climate Research. The average temperature in these parts of Norway is 10 °C higher than other regions situated at the same northerly latitudes. 214 www.skansen-akvariet.se/vara_djur/html/svartratta.html 215 Personal communication from Rolf Lie, Zoological Museum, University of Bergen, in 1991. 216 Benedictow 2004: 216–7. 217 Vilkuna 1969: 584.

140

chapter three

settled there in the Viking Period, but, of course, these rats might have a much longer history. And these black rats were also burrowing and living in the vicinity of human habitation,218 despite Twigg and Davis’s assertions to the contrary.219 Davis actually consistently calls the black rat a “roof rat.” As shown above, the black rat can, in fact, freely burrow, in nature as peridomestic rodents and in beaten earth floors and walls of human housing220 on the condition that they are not exposed to brown rats which will hunt them down, kill them or drive them out of their burrows, and that would not happen before the late eighteenth century in Europe. As mentioned also above, in Macquarie Island which is situated quite close to Antarctica (54° 30ʹ S, 158° 57ʹ E), in a very inhospitable cold climate and subantarctic ecology, thriving colonies of black rats have settled as burrowing rodents, temperatures in the burrows ranging from 4.8 °C. to 9.2 °C.221 Largish specimens of the black rat have been found in England at Faccombe Netherton on the Hampshire-Berkshire border,222 among the Norwegian finds in Bergen and the Swedish finds in Visby,223 and also in Corsica (see above). This can be taken as further evidence of the adaptability of rats by selection, which also adapt by size to environmental challenges by selection of larger animals with improved chance of survival in competition with other small rodents and which would make them less vulnerable to small predators like stoats or polecats. Perhaps rounding off of body-shape could also increase resistance to cold (which could not have been a selective factor in Corsica).224 Under the circumstances, the wide geographical spread and the substantial number of finds of medieval rat bones in the northerly parts of Europe are quite remarkable. In the words of McCormick: “Judging from 143 rat contexts of the ninth to the fifteenth centuries, medieval Europe’s rat colonies were extensive and abundant […].” And these

218

Nybelin 1928: 850–7; Bernström 1969: 578–9, 584; Vilkuna 1969: 583–4. Twigg 1984: 80; Davis 1986: 456–7. 220 See. for instance, IPRC 1907 g: 746; Lamb 1908: 9, 13. 221 McCormick 2003: 22–3. 222 James 2001: 12. 223 Malmborg, personal communication by e-mail 19 June 2006: “Even here we have a morphological variant which appears a little larger than the black would be expected to be.” My translation from Swedish. 224 I have noted with interest that the IPRC found that black rats in Belgaum 400 km southeast of Mumbai were much larger than in Pune (Poona) about 120 km southeast of Mumbai. IPRC 1910c: 456. 219

rats

141

rats were not far and few between at the time: in sixty-six cases the archaeologists estimated the minimum number of individual rats, which proved to be 601 rats or an average of 9.1 per site, and twelve of the most-infested sites were from the thirteenth century or later. “Overall, the raw rat counts hint at hugely expanding rat populations around the fourteenth-century plague.”225 Clearly, the arguments of the advocates of alternative theories against a numerous and broad presence of the black rat in medieval Europe, including in the northerly parts and in the Nordic countries, are not tenable and represent serious underestimation of “rats’ adaptability” by evolutionary selection and the development of regionally adapted variants or biovars.226 As pointed out above, this is also the case with rat fleas, X. cheopis: “As shown by its wide geographical distribution, X. cheopis is able to adapt itself to a considerable range of climatic conditions. It is, as has been previously noted, the common rat-flea in Manchuria and is also the prevalent species in the tropical section of Brazil.”227 This shows that a full potential for epidemics of bubonic plague must have been present in the Scandinavian countries at the latest from the High Middle Ages. This does not prove that epizootics among rats fuelled historical plague epidemics, but does constitute crucial evidence which permits solid assumptions to the effect that there was a sufficient murine basis all over Europe, that the potential for epidemics of bubonic plague was present. Whether or not this potential was realized must be demonstrated through manifestations of the epidemiological processes that are explicable only by a concomitant epizootic of plague among rats. Central aspects of this question will be discussed in the next subchapter on the sociology of rat-based plague, and in Part 4 on defining features in chapters on epidemic latency periods and other temporal aspects of the development of plague epidemics, the inverted correlation between population density and morbidity and mortality rates in modern as well as historical epidemics of plague, and on the seasonality of plague epidemics, and elsewhere. Assertions that historical plague epidemics could not have been bubonic plague because there was not a murine basis must be rejected.

225 226 227

McCormick 2003: 14. McCormick 2003: 22; Wigh 2000: 125; Nybelin 1928: 855. Pollitzer 1954: 327.

142

chapter three Sociology of Rat-based Plague

Social conditions can systematically affect the intensity of infective processes in relation to particular social categories of persons according to the distributive functions of relative risk of exposure. At the heart of the matter is the fact that epidemiology is fundamentally a subdiscipline of sociology which aims to explain how various social conditions and interrelated patterns of behaviour of human beings, animals and insects affect the probability of contagion being transmitted to human beings or between human beings. It is, therefore, important to note Wu Lien-Teh’s general statement: Most investigators are agreed that, on the whole, differences in the age, sex, racial and also occupational incidence of bubonic plague are due to differences in exposure to infection as brought about by varying modes of life and not to intrinsic causes.228

Pollitzer supports this position unequivocally when he cites it quite closely: “Most workers are agreed that differences in the race and sex incidence of bubonic plague cases, as well as […] among certain occupational groups […] are due merely to differences in the degree of exposure of the various groups to the infection and not to intrinsic causes.”229 Population density affects the intensity of social interaction and therefore also the probability of being infected and also of being infected repeatedly and, thus, by multiple infective doses, which produce different morbidity and lethality rates according to social class and other social categories. This explains the typical supermortality in epidemic disease of indigent and destitute people who tend to live in overcrowded rooms and in overcrowded quarters. On the other hand, diseases spread by cross-infection may also negatively affect the affluent classes who tend to have large households with several or many servants and an active social life, producing a high level of social interaction and a corresponding increase in exposure to contagion by droplets. R. Schofield remarks in his study of the plague epidemic in Colyton on the sociological dimension of epidemiology that “men and women living in isolated farmsteads may be less

228 229

Wu Lien-Teh 1936c: 399. Pollitzer 1954: 503.

rats

143

likely to meet infected people than would those living in a village street. Also the chance of catching a disease may […] vary systematically with the social and economic status of the household.”230 R. Engelsen found that affluent or well-to-do farmers in Norway at the end of the eighteenth century had a slightly higher risk of contracting infectious diseases than the poor rural classes who tended to live more isolated on their sub-tenancies (“undersettles”) or small holdings.231 This pattern of social variation in the incidence of epidemic disease is basically associated with risk of exposure. This demonstrates the important point that risk of exposure in relation to diseases spread by crossinfection, by droplets or inter-personal physical contact should be expected to produce clearly different social manifestations from the pattern of epidemic bubonic plague disseminated and transmitted from rats by rat fleas to human beings. Sticker, summarizing in his big two-volume work of almost thousand pages an almost incomprehensibly wide reading of sources and studies written in classical and modern European languages, pointed out the great variation in the incidence of plague among people of different occupations. Persons working with food stuffs and in environments where food is stored, bakers, millers and butchers, were particularly at risk of contracting the disease and dying from it.232 In E. Woehlkens’s outstanding study of plague in Uelzen (northern Germany), six of seven bakers, ten of twelve linen weavers, and five of six butchers died in the plague epidemic of 1597 but only two of nine smiths, and only four of the town’s fifteen carpenters, wheelwrights and coopers.233 This is clear evidence of the workings of the rat epizootic associated with an epidemic of bubonic plague, because the activities of some occupations attract rats while the activities of other occupations drive them away. Bakers, linen weavers and butchers are very vulnerable to plague disease because their work material is highly attractive food for rats (flax seeds in the case of linen weavers), while the shops of smiths, coopers and wheelwrights do not contain significant amounts of edible material attractive to rats, and rats avoid high sharp sounds produced by their work, so these occupations are little exposed to rats. Thus, the human sociology of a plague epidemic reflects the sociology 230 231 232 233

Schofield 1977: 103–4. Engelsen 1983: 161–202. Sticker 1910: 266–8. Cf. Mate 1984: 351–2. Woehlkens 1954: 72–5.

144

chapter three

of rats which is influenced by human activities which are attractive or repellent to rats. Woehlkens who could follow the spread of the epidemic house by house concluded that the direction of spread of the epidemic, the formation of new centres in the specific phases and the progress from block to block were determined by the localization of these houses: the topographic course of plague was governed by the places with the highest accumulation of food stuffs for rats (bakers, linen weavers, butchers). A comparison of average numbers of deaths shows that the probability of being killed by plague in such a place was more than five times higher than in the case of occupations working with wood or iron.234

The crucial sociological point is that this differential pattern of mortality among various occupations and types of artisans or craftsmen can be easily explained as reflections of rat-borne plague transmitted by rat fleas, and is inexplicable as reflections of a disease spread by crossinfection. This pattern constitutes therefore sociological evidence of bubonic plague. Woehlkens makes also quite a number of other observations that reflect the workings of rat-based plague, for instance that the affluent citizens who lived in housing of stone or bricks with tilecovered roofs were largely spared by the epidemic while poor people living in housing suitable for nesting of rats were violently attacked, a pattern that also took the form of strongly differential mortality according to social-class divisions by side of street.235 Notable is also the formation of new centres of spread, demonstrating metastatic spread of plague by transportation of rat fleas. Cohn has not noted this important aspect of supermortality among occupations working with food stuffs attractive to rats and submortality among occupations repellent to rats. In his discussion of differential mortality among occupational categories, he is only able to mention supermortality among professions like notaries, attorneys, and parish priests on the one hand, and of gravediggers according to two chroniclers and of wax chandlers of London according to an “apocryphal” personal communication, on the other. Wax chandlers are supposed to suffer supermortality because they did not only supply candles for funerals but also quite remarkably are asserted to have embalmed

234 235

Woehlkens 1954: 74. My translation from German, and my italics. Woehlkens 1954: 70–1.

rats

145

bodies,236 which may be the reason that such assertions have not been accepted for publication. The point is that supermortality among these professions does not obviously imply the role of rats and their fleas but can be associated with diseases spread by cross-infection and professional exposure; in the case of gravediggers and wax chandlers they are surprisingly supposed to contract the disease from dead bodies. However, Cohn must ignore the fact that these professionals would tend to enter houses with persons dying or dead from plague and that this behaviour would produce high exposure to infective rat fleas. If we take seriously the assertions with respect to gravediggers and to wax chandlers in the purported role of embalmers, one must also take into account the possibility that they could be infected by rat fleas hidden in the clothing of dead plague victims. On page 122, Cohn maintains that gravediggers according to two chroniclers suffered great supermortality in plague because this seemingly serves his case for cross-infection. However, on page 138 he cites another chronicler to the effect that he “marvelled at the gravediggers, who he said were rarely struck by plague or died from it by his day (the mid-fifteenth century),” because this diametrically opposite view now seemingly serves his argument for immunity among survivors. This is just one of many instances of weak consistency and high tolerance of cognitive dissonance in Cohn’s work, since his selection of material is governed by his ambition to establish a pre-conceived revolutionary theory of historical plague. He only cites occupations or professions with supermortality or a pattern of death which seem at least superficially to suggest cross-infection; why butchers, bakers, millers, linen weavers, and so on, should suffer supermortality from cross-infection and smiths, carpenters, wheelwrights and coopers should on the contrary suffer submortality is not readily understandable. In fact, only bubonic plague can provide a cogent explanation for these patterns of occupational supermortality and submortality. In his study of the plague epidemic in Colyton 1645–6, Schofield puts forward a working hypothesis which predicts that, among other things, “diseases like bubonic plague and typhus [transmitted by insect vectors] are likely to be associated with geographically clustered patterns of death, while airborne infections, such as influenza, will show much less clustering.” As shown in quite some detail above, Schofield

236

Cohn 2002: 121–3.

146

chapter three

succeeded in uncovering the typical pattern of clustering in families characteristic of rat-born plague transmitted by rat fleas.237 Dijkstra carried out a study of the pattern of spread of plague in the Jordan quarter of Amsterdam during the epidemics of 1617 and 1624. The clustering of plague cases, the contiguity of spread, and the type of progression showed that “plague in the seventeenth century has been dependent on rat plague.” As the Jordan quarter had changed little physically between the seventeenth century and the first decades of the twentieth century, he is able to elaborate further on the topic of epidemic spread. With a number of maps he illustrates the strongly contrasting patterns of epidemic spread in Jordan during the plague epidemics of the seventeenth century on one hand, and the influenza epidemic in 1918 on the other. The latter represents the pattern predicted by the interhuman model of transmission and dissemination.238 As a part of her dissertation on epidemic diseases in early Renaissance Florence, Carmichael conducted a study of the spread of plague in the quarter of Santo Spirito during the minor epidemic of 1430. In my opinion, the pattern agrees closely with the findings of Dijkstra, Woehlkens, Slack (see immediately below) and Schofield. The extreme local character of dissemination, the initial clustering of deaths in one part of this traditional working class district and even along certain streets within this small area, the clustering of plague deaths within some families even as the immediate neighbours escaped unharmed, the slow progression of the epidemic, and the impression that many streets seemed to begin to function as local plague foci as the epidemic spread through the summer months, all point to the same explanation. The maps showing the spatio-temporal progression resemble quite closely the maps of Dijkstra and Woehlkens. Slack’s analysis of plague in Bristol in 1540–60 also provides acute observations of rat-borne plague and the relative risk of exposure of various social classes. He could identify the typical slow spread of plague which reflected its movement through contiguous rat colonies: “The disease was carried relatively slowly through the town by rats,” and it “moved haphazardly, sometimes missing out two or three households in its progress along a street.” He registered sudden leaps to a house surrounded by uninfected houses,239 which then might or might 237 238 239

Schofield 1977: 102–8. Above: 62–9. Dijkstra 1921: 64–74. My translation from Dutch. Cf. above: 67. Slack 1977: 53–7.

rats

147

not start to function as new infective centres of spread. The conspicuous outcome of his study is “the variations which emerge between parishes and their apparent coincidence in many cases with social class differences. For plague mortality was not spread evenly over the town.” Christ Church parish comprised broad, fine streets inhabited by affluent citizens and also the poor and the overcrowded back street of the Pithay: The Pithay lost a higher proportion of its inhabitants in both epidemics than any other part of the parish […]. Bubonic plague was concentrated in the back street of this otherwise prosperous parish.

Slack concludes in this way: “Plague thus had a socially selective impact on Bristol in these years, and this is important for any understanding of its demographic and economic effects.” His sociological explanation of the social variation in plague mortality is clear: The vital determinants behind this association were of course variations in standards of housing and hygiene which might attract or repel the rats and fleas which carried plague.240

This view accords with the fact that there exists much evidence showing that ecclesiastics, aristocrats, well-off urban residents and other persons living in houses built of stone or brick in relative terms contracted plague far less frequently than social categories living in other types of housing, e.g., the poor in Milan’s “stalli” or in London’s outparishes.241 Mortality among the English baronage was much lower than among the peasantry.242 A.E. Nash is quite probably correct in assuming that many of them escaped infection because they lived in “stone-built accommodation.”243 Cazelles concludes his study of the differential social impact of the Black Death by stating that “the nobility apparently lived through the mortality without significant losses.”244 In the Black Death, monasteries, churches and hospitals in Avignon were left unscathed whilst the city in general was cruelly ravaged. This cannot be explained by acquired 240

Slack 1977: 54–7. Cipolla 1974: 283; Cipolla and Zanetti 1972: 201; Bell 1951: Chapters 4, 6, and pp. 158a, 329; Hirst 1953: 128; Dyer 1978: 309. 242 Benedictow 2004: 343, 360–77. See also below: 383–92. 243 In the epidemics of 1369 and 1374, the “lords of the manor” appear to have been left almost unscathed. Nash 1980: 39. 244 Cazelles 1962 (165): 300: “la grande noblesse traverse apparement la mortalité sans pertes sensibles.” My translation from French. 241

148

chapter three

immunity, as it was the first plague epidemic in southern France for about 700 hundred years. In the terrible epidemic of 1720–2, mental hospitals and closed monasteries remained untouched. The previous epidemic, which killed about 8,000 persons, occurred in 1649.245 Only a very few members of the resident regular clergy (living in a population with an average life expectancy of c. twenty-five years246), could possibly have acquired immunity to plague. Closing such institutions to the outside world would not have provided protection against the plague, if the stone buildings had not prevented rats from entering the premises. In Moscow, the Imperial Orphanage which contained a thousand children and a staff of 400 was similarly spared in the violent plague epidemic which ravaged the city in 1770–1.247 At that time, there had not been plague in Moscow since 1665,248 so neither children nor adults could have been protected by immunity to plague. The reason for this pattern is that houses built of stone or brick were far less amenable to rats than houses built of wood or wattle and daub and roofs covered by thatch. In fact, the increasing use of stone and brick for house construction beginning in the seventeenth century was for quite some time the favourite explanation with historians for the disappearance of plague from Europe.249 In more recent times, the IPRC concluded that the extensive use of stone and brick for house construction constituted an important explanation of why East Bengal and Assam were only lightly hit by plague.250 This fact is flatly rejected by Cohn. Encouraged, perhaps, by his being in the favour with the editors of The New England Journal of Medicine Cohn apparently does not fear that his scholarly reputation will be affected by the following assertion in his review of my monograph on the Black Death:251 Benedictow maintains that people in well-built stone housing were protected against plague because rats could not enter these dwellings. The plague commissioners [IPRC: my insertion] again discovered the opposite: that rats penetrated stone and brick houses, even those with cement

245

Colonna d’Istria 1968: 18–9. Fourastié 1972: 30. 247 Sticker 1910: 264; Alexander 1980: 263–4. 248 Biraben 1975: 429. 249 See e.g., Clark and Slack 1976: 142–9; Liston 1924: 902–3; Appleby 1980: 166–7; Slack 1981: 472. 250 IPRC 1911c: 187–92. 251 Cohn 2005: 1354. 246

rats

149

floors, inflicting some of the highest rates of death in these residences, whereas often some of the poorest people, living in bamboo huts, fared much better.

The IPRC comments on these matters in Report No. XLVI of 1911, “Observations On Plague in Eastern Bengal and Assam,” in Chapter H. “The Causes for the Comparative Scarcity of Rats in the Houses.” In the second sub-chapter titled “The Structure of Their Houses,” the following statements can be found: the Bengali seems to have adopted a method of house construction which succeeds in practically eliminating rats from his house, be the house a pucca or kutcha one. “Pucca” houses, being built of stone or brick or mortar, often with concrete roof, from the very nature of the materials used in their construction afford little harbourage for rats. These animals may however effect an entrance from outside either through the floor or by the door. Many Bengali houses however have been so constructed as to prevent rats gaining an entrance in these ways, being built on raised plinths of special construction. These plinths are erected with a brick or masonry facing, along the upper border of which runs a bead of varying depth which projects for from four to six inches or more over the base. The floor is made of a layer of concrete faced with hard polished cement, below which is a layer a foot or more deep of dry sand. These devices are said to have been adopted for a number of reasons: […] (3) to prevent the access of rats which cannot make their burrows in the sand or climb the overhanging plinth […]. The “kutcha” houses, too, afford little shelter for rats. For, being constructed of thin bamboo matting or wattle covered with a thin layer of mud, the walls afford no shelter for these rodents. The roofs too, being made of corrugated iron, split bamboo, or thin grass thatch, fail to shelter these animals. Perhaps one of the most noteworthy features of the buildings in this province is the almost complete absence of tiled roofs which are so commonly seen in many other parts of India.252

The Commission summarized their findings in its “General Conclusions”: (3) The freedom of the province from plague can chiefly be attributed to the scarcity of rats in the houses as compared with other parts of India […]. (5) The structure and design of the Bengali homes, whether it be of the solid masonry type on the one hand or of the flimsy matting or grass type on the other, afford little shelter for rats.253 252 253

IPRC 1911c: 190–1. IPRC 1911c: 192.

150

chapter three

Thus, Cohn’s assertion on this point is contrary to fact. It is a clear misrepresentation of the findings of the IPRC and their unequivocal conclusion which indisputably supports the notion that stone, concrete and masonry protects against rat invasion and the establishment of rat colonies in human habitation. Nothing is said to the effect that the small incidence of plague cases in this region was higher in the “pucca” houses than in the “kutcha” houses, as Cohn’s maintains. Thus the sociology of historical plague epidemics exhibits the characteristic reflections of rat-based bubonic plague and constitutes evidence of the presence of black rats.

CHAPTER FOUR

THE SPREAD OF BUBONIC PLAGUE OVER DISTANCES Contiguous Spread and Metastatic Spread The advocates of alternative theories, particularly Twigg,1 Scott and Duncan,2 and Cohn,3 deny that bubonic plague spreads by leaps (per saltum) by the movement of people or goods, technically often also called metastatic spread. Although they must have seen Shrewsbury’s presentation of the principle and mechanisms of metastatic spread of plague by transportation of rats and rat fleas,4 they insist that bubonic plague spreads only by contact between adjacent rat colonies, technically called contiguous spread. In the words of Twigg: An important aspect of plague spread is the continuity across a rat population. The more isolated the rat units the slower will be the movement of plague amongst rats, and ultimately, to people.5

Among the specific examples he cites in accordance with his view that this factor alone has the power of invalidating or undermining the ratand-flea-based bubonic-plague theory is the following: The disease would be expected to have spread northwards from the counties of East Anglia, which it had reached in May 1349, spreading through the rat population and causing local epizootics. Yet throughout this large area the high mortality occurred only one month later over the whole diocese. Plague is said to have reached York on 21 May but according to Thompson (1914)6 the deaths of clergy over the whole of this vast 1

Twigg 1984: 57, 100, 185. However, Twigg acknowledges that plague can be spread by fleas over various distances on pages 128–9, see below. 2 Scott and Duncan 2001: 79–80; Scott and Duncan 2004: 177. 3 In his monograph, Cohn accepts that bubonic plague can be spread by shipments of grain, but denies all other types of spread by goods, textiles or clothing: see Cohn 2002: 29, 31–2. However, later, in a review of my monograph on the Black Death, he denies flatly the relevance of the concept of metastatic spread and the fact of spread by leaps, see Cohn 2005: 1354–5. Cohn repeats this view in a recent paper, Cohn and Alfani 2007: 178. 4 Shrewsbury 1971: 29–34. 5 Twigg 1984: 100. 6 A.H. Thompson has written two valuable papers on the mortality of the beneficed clergy in the Black Death which will be discussed at some length below in the chapter on seasonality. See also the bibliography.

152

chapter four northern diocese were on the increase soon afterwards. As we have seen, bubonic plague can be excluded from the reckoning if these facts are correct, and there is no reason to doubt them.7

Objections against this account of the spatio-temporal pattern of spread are not important at this point; I cite the passage to illustrate the implied unconditional view that plague spreads according to a territorially contiguous epizootic process, by direct contact between adjacent rat colonies, and, consequently, that the Black Death could not have been bubonic plague. Presumably the advocates of alternative theories all adhere to this view of the very slow territorial spread by contact between rat colonies because it is obviously incompatible with the real spread rates of historical plague epidemics. Since this can be seen as a sufficient condition for rejecting the conclusion that historical plague epidemics were bubonic plague, they can therefore triumphantly conclude that historical plague epidemics must have been a different disease, which justifies their endeavours to identify an alternative disease. This erroneous view is misleading other serious scholars in the field, derailing potentially good research.8 The time is ripe for taking the advocates of these assertions to task. The metastatic mode of spread has long been empirically established as a characteristic feature of the epidemiology of bubonic plague (as of most other epidemic diseases). Since the advocates of alternative theories deny or ignore the facts on this crucial point in order to save their theories, I will now not just paraphrase or summarise the scholarly literature on the mechanisms of spread of bubonic plague, but will supply a broad collection of citations from the primary studies and standard works on plague which should settle the matter definitively. However, Cohn’s assertions on the matter in particular are so extraordinary that they warrant some concluding remarks on the background of the evidence presented. In this chapter, the citations constituting the heart of the subject will be presented chronologically to demonstrate the history and development of this insight, how conspicuous this feature of plague epidemiologically was, how early plague researchers identified these mechanisms

7

Twigg 1984: 185. Wood, Ferrel, DeWitte-Aviña 2003: 444; Drancourt, Houhamdi, and Raoult 2006: 234–41; below: 193–4, 461. 8

the spread of bubonic plague over distances

153

of spread and the consistency and firm tenability of these findings over time. Observations of these features were first made several years before the IPRC began its work. The first standard work on bubonic plague based on modern medical studies in India, China and elsewhere was published by Simpson in 1905. Twigg cites and refers to it twice9 and must be presumed to know it. Nonetheless, Twigg passes over in silence Simpson’s information on the great importance of metastatic spread, for example, that in Canton, many persons, especially the well-to-do, removed to the country, thus forming fresh foci for its dissemination; and in the same way the outbreak in Hongkong no doubt arose from persons having migrated from Canton to Hongkong.10

He notes that in China, “the infection on land has followed chiefly the routes of busiest intercourse.”11 Simpson also provides much information on spread by leaps in India in connection with the mass exodus out of Mumbai, for instance, when the plague epidemic suddenly blazed up: “Fugitives from Bombay and the Bombay Presidency were not long in carrying infection to the other provinces of India.”12 W.G. Liston, who joined the IPRC in 1905 as the Commission’s entomological specialist, stated in a paper published earlier the same year that infection could be conveyed from one place to another, either by infected rats and fleas transported by ships and trains conveying merchandise or by infected fleas carried on the clothing of man.13

In 1906, W.B. Bannerman, the director of the modern medical laboratory that had been built outside Mumbai at Parel and was placed at the disposal of the IPRC,14 published a paper in The Journal of Hygiene where he summarized plague-related research in India: Spread of Infection by Means of Clothes […] Major Collie, I.M.S. (1898), relates the following striking instance from his experience. “A man lost his wife from plague in Bombay, and ten days later he brought her clothing and ornaments to his house in a village near Harnai in the Ratnagiri Collectorate. In about a week dead rats were found in this man’s house and neighbourhood, then one relative after 9 10 11 12 13 14

Twigg 1984: 135, 212. Simpson 1905: 62. Simpson 1905: 65. Simpson 1905: 71. IPRC 1907f: 713. IPRC 1907g: 725; Lamb 1908: ii–iii.

154

chapter four another sickened and died from plague, and ultimately the man himself became the sixth victim. None of his relatives had been out of their village. Eventually, this village and others suffered severely, and many lives were lost. No plague cases had occurred up to the direct infection.” Captain W. Ronaldson Clark, I.M.S. (James, 1899, p. 152) brings forward several instances in which conveyance of infection by clothes seems the most likely means of introduction in some villages in the Punjab […]. In the report of the fifth season of plague in the Punjab (Wilkinson 1904, a, p. 29) it is recorded: “That infection could be carried by clothes was however recognised by the people of Ambala district fairly soon, and in all towns the practice of burning the clothes of persons who died of plague was introduced and acquiesced in by sweepers who had previously suffered severely from taking the abandoned clothes of the dead.” In Patiala State it was noticed that infection was also conveyed by clothing and bedding of persons who had died from plague, and this was so borne in upon the sweepers of Patiala that they refused to touch these articles, which often had to be burnt where they lay in consequence […]. In the report in the Punjab for 1902 the following information is given on what is regarded as “fairly definite” evidence. The mode of communication from one place to another was considered to be: “Human communication in 88 instances. Probably human communication in 7 instances. Clothes in 25 instances. Probably clothes in 7 instances.” The Government review in commenting on these results says (Wilkinson, 1902, p. 15), “It is therefore clearly established now that plague is spread from infected to uninfected places almost entirely by personal communication on the part of persons who have resided in, or visited the infected places during the existence of plague there.” It serves to explain the infectivity of clothes so often noticed. It is probably the fleas in the clothes that are the danger, not the clothes themselves. We may sum up the above evidence as follows: —As regards introduction into a new area remote from a focus of disease, it seems certain that human beings are the carriers of infection.15

Persuasive cases of spread of plague over considerable distances in clothing were among the early observations made by British medical personnel in India. Cohn and Twigg refer to Bannerman’s paper, which they therefore presumably have read, but completely ignore these findings, which are here presented in the form of a number of extracts that easily could have been multiplied.

15

Bannerman 1906: 189–95, 208.

the spread of bubonic plague over distances

155

Similar observations were made during the plague epidemics in Australia which occurred more or less simultaneously with these early Indian epidemics. These observations were presented in a paper published by the distinguished leader of the combat of plague in Australia, Ashburton Thompson, in The Journal of Hygiene immediately after the publication of the first reports released by the IPRC. His observations pre-date shortly the establishment of the rat-flea theory of spread over distances by the IPRC: Extension of local infection by contiguity The infection always first made its appearance at some one spot; never at more than one. From that spot it extended continuously. […] this way of spreading I distinguish as “extension by contiguity.” Extension of local infection per saltum While infection was apparently present only at the point of invasion or central focus, it often made appearance quite suddenly at some distant point, and there created a new focus […]. It appeared that the infection could be transported safely, be planted afar, and could there take effect. In that there is nothing novel, for the same happens with several communicable diseases. It becomes remarkable and important when it is remembered that, in accordance with our fundamental observation, the infection of plague is not maintained or diffused by communication with the sick. This way of spreading I distinguish as “extension per saltum.” For convenience of description outbreaks which result from extension per saltum may be called “sub-epidemics.” In reality they have their own independent status. […]. The numerous secondary outbreaks which we have witnessed were not the less independent that they were isolated by but a mile-wide ring of plague-free houses, nor the more independent had they occurred (as we have seen) 70 or 2300 miles away from the point of primary invasion.16

Ashburton Thompson introduced the concepts and terms of spread or extension by contiguity and spread or extension per saltum, in English “spread by leaps.” These concepts and terms were, as we shall see, accepted and used by members of the IPRC, although they often relied on accurate descriptions rather than on specific terms and concepts, writing that infection was transported, imported, carried, transferred or conveyed, or with other similar words and corresponding nouns, from one place to another. As their studies progressed, they tended to

16

Ashburton Thompson 1906: 542–3, 546, 561.

156

chapter four

develop supplementary terminology and write for example of the, “implantation” of infection and of infections which are “implanted.”17 Thus observations of these modes of spread of bubonic plague belong to the initial phase of scientific plague research, before the IPRC had set to work, as a consequence of their being very obvious features of the characteristic modes of spread of this disease. Ashburton Thompson’s paper can either be ignored and passed over in silence, which is the strategy adopted by Twigg and Scott and Duncan, or it can be viciously attacked without mentioning these observations, which is the course chosen by Cohn (see above), in both cases presumably because they recognized its disastrous consequences for their own alternative theories which are based on the denial of spread by leaps of bubonic plague. The IPRC’s first observations on the spread of plague by the agency of rat fleas were presented in a study of rat fleas’ willingness and ability to use man as a host. Some central findings were: We have made many observations which show that P. cheopis [= Xenopsylla cheopis] will make use of man as a host, and may be captured in large numbers on men in houses infested with rat fleas […]. We have on many occasions caught rat fleas on our own persons, as well as on those of the attendants […]. From the above experiments it is seen that we were able to keep rat fleas alive for nearly four weeks by feeding them on human blood […] (a) that they fed readily on man, and (b) that some of them were still alive after 25 days.18

The willingness of rat fleas to attack men and the great number of fleas involved were underlined by the outcome of another experiment. A (vaccinated) person went inside a house in Mumbai which had been evacuated after finds of dead rats and human cases of plague, and stayed in one room only briefly. After he came out, a flea count was made, with the following result: April 18, 51 rat fleas, April 19, 34 rat fleas, April 20, 60 rat fleas.19 As Liston, a former member of the IPRC, later commented: It is quite possible that, had we not examined this man’s legs and removed the fleas from them, he might have carried some of these fleas to his home […].20

17 18 19 20

IPRC 1910d: 528, 534. IPRC 1907e: 472–3. IPRC 1907e: 474–5. Liston 1924: 997. Cf. below: 164–5.

the spread of bubonic plague over distances

157

Scott and Duncan refer to this paper, but apparently did not see these central statements.21 Summing up their findings, IPRC also stated that this study “shows how readily and in what large numbers rat fleas may under certain circumstances come on to man.” They also concluded that the experiments “indicate that rat fleas may often be transported in this way from place to place, especially from plague-infected houses.”22 The next step was to study the arrival of plague in isolated villages on the outskirts of Mumbai, specifically the villages of Sion, Wadhala, Parel and Worli. A useful illustration of the IPRC’s work and methodology and the observations they made in these villages is provided by the following example from Worli village: Jankibai was a woman close on 70 years of age who lived in Worli. She left the village in perfect health on the 14th February to attend the funeral of her nephew, Laxuman Narayan, who lived at 94–6 Sonapur Street in Bombay City. Motiram Ramji, another relative of the old woman, was ill with plague in the same house in which Laxuman had died. After the funeral Jankibai remained on at Sonapur Street nursing this latter patient. Dead rats had been found in the house at Sonapur Street, and many dead rats, found in the neighbourhood at this time, were proved by us to be plague infected. Motiram died on the 18th February. Jankibai in the meanwhile had developed fever. She came back to Worli on the 19th suffering from plague, as evidenced by high fever and a well-marked bubo in the groin. She went to a house in Block I, building No. 54, where we saw her on the 21st February. Two days after Jankibai came to the village, we placed two guinea-pigs in her house […]. One of the two guinea-pigs which had been placed in Jankibai’s house after isolation in the laboratory died of plague on the 9th March […]. Taking all the facts into consideration it seems to us that the guineapig which contracted plague in Jankibai’s house probably derived its infection from infected fleas imported by Jankibai from Sonapur Street in Bombay City. This case closely resembles one recorded in Parel village. In this instance, it will be remembered, another such woman, coming from the city, appeared to have brought infected fleas to that village (Case 1; Parel village).23

21 22 23

Above: 88, 90. IPRC 1907i: 888. IPRC 1907h: 869–70.

158

chapter four

The IPRC concluded their study of Worli village thus: Three cases of plague which occurred in the village were investigated. It is probable that these three cases all contracted the infection outside the village. In two instances there is evidence which points to infection having been introduced in the clothing or persons of people [sic! my insertion], and of this spreading in one instance to a guinea-pig, and in the other instance to rats.24

Thus, at the very beginning of their studies of the mechanisms and patterns of spread of bubonic plague the IPRC ascertained that plague spread over distances, in this case from “Bombay City” into villages on the outskirts of the city. They were also able to establish empirically at a substantial level of tenability that in two of these cases the infection had been imported in the clothing of a person and in a form that caused spread of plague to a guinea-pig or rats, which strongly incriminates rat fleas as the agent of transportation of the infection, riding in clothing from the city into houses of the village, attacking their preferred hosts, namely the black rat or alternatively other available rodents. This explains also that “the carrier of the infection may not contract the disease, as the Sion and Wadhala cases show.”25 Clearly this material exposes some central flaws of Scott and Duncan’s work, since they repeatedly refer to this report for their views on the role of rats in plague epidemiology,26 while maintaining throughout their monographs that plague spreads only by contiguous contacts between rat colonies, not by leaps. If they had really read the report, they should have known better and ought to have eagerly acquired more knowledge of the Commission’s work or at least have read Lamb’s ninety-three page summary. However, as will be shown below, they apparently had not read the IPRC’s reports, although it is a overriding motive of their work to show that the results of the Commission’s work is not compatible with the manifestations of historical plague epidemics. Instead, they think it is adequate to build on Hankin’s pre-IPRC paper of 1905 for their assertions regarding the epidemiology of plague in India.27

24 IPRC 1907h: 873. The word “persons” could conceivably by a slip of the pen for luggage. 25 IPRC 1907i: 891. 26 Scott and Duncan 2001: 72–3, 112, 357. 27 Scott and Duncan 2001: 77–8.

the spread of bubonic plague over distances

159

Inspired by their early observations, the IPRC moved briskly to expand and deepen their knowledge on the spread of bubonic plague. First, they did so by extending their studies of the spread of plague in “Bombay City and Island.” In their next Report (no. XXIV), Section III is called “The Transportation of Infection to a Distance,” which all advocates of alternative theories have avoided or evaded, whilst it should have been of great interest and of obvious crucial importance to their projects. The IPRC begin by stating their principal explanatory theory: If we can exclude modes of spread of the infection of plague other than the rat flea, we must conclude that the transportation of infection to a distance is attributable solely to the conveyance of the infection in the rat flea. A little reflection suffices to show that transportation of infection in this medium is not only conceivable, but that under certain circumstances it may be a very likely contingency.

They go on to discuss “Transportation in Merchandise, Grain etc.” and “Transportation of Rat Fleas in Clothing.” The last subtitle is too brief, since it does not reflect an important experiment described in this section which took into account an expanded concept of implicated textiles: Bundles of clothing, bedding, etc, were sent to the laboratory from houses in the City in which plague cases had occurred. The bundles after being opened out were kept in a flea proof godown28 for several days […]. Along with the clothing guinea-pigs were placed in the godown. In some instances the animals were allowed to run free, in other cases they were placed in pairs in cages, the control animal being protected from fleas either by means of a layer of tanglefoot or by a curtain of wire gauze […].

The result of the experiment was that two rat fleas were caught on the animals, that one of the free-roaming guinea-pigs died from plague, and that one of the three rat fleas caught on the tanglefoot of one of the cages was shown to contain plague bacteria in its stomach contents. This permitted the IRPC to conclude: (1) that rat fleas may be transported to a distance in bedding and clothing removed from plague houses; and 28 “So convinced were Colonel Bannerman and Captain Liston of the tenability of the flea-transmission theory that they had designed and built at the Plague Research Laboratory, Parel, special godowns or cabins, in which it was proposed to carry out large series of experiments to test and prove this theory.” Lamb 1908: 2, 38.

160

chapter four (2) that such rat fleas may prove infective if transferred to a susceptible animal in the place to which they are carried. We would point out that in whatever way rat fleas are transported, whether in clothing or merchandise, they will select, when carried to their new surroundings, either their true host, i.e., the rat, or the next best available animal. If then infected fleas are imported into a house they will by preference attack the rat rather than the human occupants of the house. It is apparent from the account we have given of the rat infestation of houses in Bombay, that under such circumstances opportunities for transference of infected rat fleas to rats in houses are abundant. It would appear, then, that the introduction of infected rat fleas into a hitherto uninfected locality may lead to serious consequences by giving rise to an epizootic amongst the rats. It has been shown that infection may be transported to a distance by means of rat fleas in clothing or merchandise and that such infection, when imported into a hitherto uninfected locality, may give rise to an epizootic in the rats.29

We may in effect complete this statement by mentioning that an epizootic among commensal rats is the point of departure of plague among human beings in their proximity. The following year, 1908, the IPRC published another study on fleas containing specific subchapters on rat fleas and “The Mode of Dispersal of Fleas.” Among their findings were: That rat fleas may be attracted to man, jump on him but take some time to feed on him. Plague infected fleas might in this way be carried from one place to another without infecting the man, but would, when brought near a rat, attack it in preference to man. We would, however, like to draw attention to the ease with which rats with their fleas can be transported in certain kinds of merchandise. We have seen rats dive, as it were, into bags containing bran and disappear, so that the bags could be moved without any evidence of the presence of the rats within. M. rattus [= Rattus rattus, the black rat] from its habits is particularly liable to be transported in this way […]. From what has been said above it will be apparent that merchandise and grain, which have been visited by rats, may have fleas deposited on them and these fleas may be transferred with these articles to distant places […]. Fleas will be more readily carried on the clothes of a person, in that the man who wears the clothes forms an attraction for the insects […] experiments carried out in the godowns […] show how readily and in what large numbers rat fleas may, under certain circumstances, come on to

29

IPRC 1907i: 886–90, 894.

the spread of bubonic plague over distances

161

man, and leave us certain that rat fleas must frequently be transported in this way from place to place, especially from plague infected houses, where they are more likely to take to man because of the absence of their true host. In whatever way fleas are transported, whether in clothing or merchandise, etc., they will select when carried to their new surroundings, their true host or the next best available animal.30

Also in 1908, G. Lamb, the Director of the IPRC, published a summary of the Commission’s studies in the period 1906–May 1907 as published in The Journal of Hygiene, some of them in the second half of 1907. This summary is a good alternative source of knowledge of the opinions of the IPRC on various issues, particularly on the subject of mechanisms and types of spread discussed here. There is no excuse for the advocates of alternative theories not having used at least this easy way to obtain basic knowledge of their results, but none of them availed themselves of this opportunity. Part VII is called “The Importation of Infection from an Infected to an Uninfected Locality.” In this part, the main points are presented in three easily readable pages. In conclusion, then, we may state that all evidence points to the usual method of the importation of plague from an infected to an uninfected locality being by means of infected rat fleas and to the fleas being brought in by human agency, namely, by healthy men, by plague cases or in their belongings.31

In the following years, the IPRC continued to deepen and enlarge on these findings. In their study of plague in Belgaum, a small town situated roughly 400 km south-east of Mumbai, in 1908–9, the Commission noted that plague probably was introduced into the urban centre from an outside village and that there arose three effective centres of spread in the town and that, in addition, plague was transferred in a bag of bran over a distance of about two km from the centre to the fort on the outskirts of the town. The Commission also emphasizes that Given an epizootic such as we have seen raging in the Market it would be difficult to imagine more favourable conditions for the dissemination and spread of infection than this weekly gathering afford, a spread not only to other parts of Belgaum but to surrounding villages. The commission agents, such as those whose stores, as we have seen above, were harbouring plague infected rats, import and export grain etc. by road and rail and sell it to retail and other wholesale dealers. The grain is contained

30 31

IPRC 1908b: 253–5. Lamb 1908: 81–3, cf. 91, 93. See also IPRC 1911b: 76.

162

chapter four in gunny bags which are capable of harbouring not only rat fleas but rats as well. It requires little imagination to picture what a serious danger a market such that of Belgaum is, in times of plague, not only to itself but to all places with which it has trade intercourse […]. There is always a danger of importation of plague infected rats or fleas or both in the sacks of grain and other stores that are continually being imported into these godowns and when once introduced with the large rat population that these buildings shelter there is nothing in he plague season to prevent the disease spreading and an epizootic and epidemic resulting.32

As can be clearly seen, the fact of metastatic spread or spread by leaps over small and intermediate distances is very obvious to the IPRC as is the importance of grain and grain trade in the spread of infected rats and rat fleas. At about the same time, a similar study was carried out in Pune (Poona), a city situated about 120 km south of Mumbai, with similar results which however deepened the Commission’s understanding of some aspects of the mechanisms of spread. As in the study of how infection was introduced into villages outside Mumbai, special emphasis was put on the introduction of infection into the city. The pressure of infection on the city was obvious; since the earliest cases of plague were imported from Mumbai by the railway, people were either sick on arrival and were taken to hospital directly from the train or fell sick soon after their arrival. The IPRC suspected that the first indigenous plague cases would be associated with the railway station. This hypothesis was borne out: rats dead from plague were first found in the goods sheds of the railway close to the station. Thus, the early history of the epidemic and epizootic “started in the neighbourhood of the station, the rats acquiring the disease from infection probably imported by the railway.” The first indigenous plague case occurred in the sweeper’s chawl, the railway servants’ quarters at the station and soon nearby hotels and restaurants where people contracted plague and could act as carriers of infected rat fleas to other parts of the city.33 The IPRC also observed that a number of infective centres arose in the city that could not be linked directly to persons coming from Mumbai or elsewhere, a development with which they were familiar and which reflected the fact that infected rat fleas carried in luggage or clothing would often first seek out rats at their place of arrival and trigger an epizootic which

32 33

IPRC 1910c: 466–7, 470–1. IPRC 1910d: 506–07.

the spread of bubonic plague over distances

163

would run its imperceptible course and in due time manifest itself in human cases. This pattern was particularly likely in this case because it took only four hours by train from Mumbai to Pune. At the same time, the IPRC were closely monitoring the situation in the part of the city called the “Poona Cantonment.” As the epidemic situation in the region unfolded, large numbers of people meanwhile were flocking into the city from the surrounding infected areas to live there with friends […] one would expect to find therefore, first a number of imported cases of the disease, occurring in widely scattered localities: then later a large number of indigenous cases, also widely scattered, arising from numerous infected centres […] especially when we bear in mind the fact that rat fleas are readily carried by man, almost unknown to himself, from one place to another, and that the fleas by choice select rats for their hosts rather than man. Centres of epizootic infection arise in this way in areas where a history of the importation of the infection could only be obtained with the greatest difficulty. The history of the epidemic in the city will be seen to bear out this latter hypothesis.

Next there follows a detailed description of the early appearance of plague cases which corresponds closely to this outline of the epidemic process and to the IPRC’s notions of plague epidemiology as developed in their research projects in the field and in the laboratory.34 Other aspects of spread over distances were studied in especially designed research projects. Greenwood’s major epidemiological study “On the Spread of Epidemic Plague Through Districts with Scattered Villages,” namely villages in three districts situated in the northern provinces of the Punjab and the United Provinces (corresponding roughly to the present-day province of Uttar Pradesh) is of particular interest. He was able to conclude that the origin of the great majority of village outbreaks was the importation of the disease from elsewhere, and the corollary that recurrence of plague could in the main be attributed to re-importation of the disease, and that the chance that a village would be attacked increases with increasing population.35 The implication was that plague was spread by leaps between scattered villages by human agency by old-fashioned means of transportation. It was also shown in another study that certain regions were conspicuously exposed and that the proximity to habitual lines of travel and

34 35

IPRC 1910d: 510–18, 527–9, 534–5. IPRC 1910b: 361, 363, 368, 371, 374, 377–9, 443.

164

chapter four

transportation, especially railways, was a factor in this result; this study also emphasized the importance of metastatic spread, this time by modern means of communication.36 Shortly afterwards, Greenwood published yet another report on the epidemiological structures of plague in the Punjab and pointed out, among other things, that “effective centres of spread” arose in three ways: (1) By the introduction of an infected human being. (2) By the human importation, on the person or in the clothing, of infective fleas. (3) By the importation of infective fleas or infected rats in merchandise. All the methods by which a centre is established ab extra, will still apply for the establishment of secondary centres within the community, and in addition we have to reckon with chances of spreading through the rat population by the transference of infective fleas from individual to individual. […] What is material, however, seems to be the apparent fact that the extent of an epidemic must largely depend upon the number of “effective” centres established early in the epidemic. The diffusive power of plague is evidently not so great that one “effective” centre is sufficient to develop a wide-spread outbreak […] many conflagrations will be required.37

Indisputably, the IPRC showed that bubonic plague was spread by human agency both between communities and within communities and that the central means were importation and spread by infective rat fleas in clothing or merchandise, and that spread between contiguous rat colonies was only of minor importance, the epidemic process being mainly dependent on an increasing incidence of new “effective centres” where each new “conflagration” tended to increase the dynamics of spread by multiplicative powers. This shows how completely erroneous Twigg’s, Scott and Duncan’s and Cohn’s assertions are with respect to the IPRC’s views on the mechanisms and dynamics of the spread of bubonic plague. In 1924, Liston, formerly a member of the IPRC, published a short outline of bubonic plague. In the part on epidemiology of plague he takes as his point of departure the study in which a vaccinated person on three successive days went inside a house in Bombay which had been evacuated after finds of dead rats and human cases of plague,

36 37

IPRC 1911a: 47–61. IPRC 1911b: 76, 78.

the spread of bubonic plague over distances

165

stayed in one room only briefly, and attracted 144 rat fleas that were picked off his legs (see above). He writes: “It is quite possible that, had we not examined this man’s legs and removed the fleas from them, he might have carried some of these fleas to his home, and there they might have transferred their attraction to their natural hosts,” unleashing a rat epizootic among the rats that would translate into plague cases among the persons in the house. He continues: These observations show that infected rat fleas do not generally travel far from the spot where they left their host; they generally lie in wait for the passing of another host. If this new host is a rat, the fleas are readily attracted to it and may then be carried to a distance limited by the extent of the rat’s wanderings. If the new host is a man, then the distance over which the fleas can be carried may be considerably greater, and will be limited by the distance and by the speed at which the man travels. Plague thus progresses in two very distinct ways: first, to contiguous areas—here infection is carried chiefly by rats; secondly, to more distant centres per saltum—in this case infection is transported by men. Men may carry rat fleas either on their person or in their clothing, or they may transport rats and their fleas with merchandise, in which case railways and ships materially assist the dissemination of the disease.38

This may be considered a final summary of the IPRC’s findings. As can be seen, Liston underscores the fact that plague spreads in two main ways, by contiguous spread between rats and per saltum, that is by leaps. However, in the last case, Liston clearly distinguishes between spread by rat fleas over short or intermediate distances by human beings in clothing or luggage, and spread over long distances in merchandise by ship, railway or lorry; in a pre-modern perspective one could also add by horse and cart or pack horse. In this way he distinguishes between more or less local spread in short-range leaps establishing new centres of spread in a locality in a more or less multiplicative way and, thus, constituting an important and even crucial element in the dynamics of the development of plague epidemics in urban centres, localities or districts; and longer distance disseminations. This view is clearly completely compatible with the presentation of IPRC’s work above. The IPRC’s findings are not unique, they do not differ from the results of epidemiological studies of the modes and mechanisms of

38

Liston 1924: 997, 999, 1001.

166

chapter four

spread of plague elsewhere. Plague researchers working on plague epidemics in Egypt stated that they were of the opinion that the creation of apparently independent foci of rat and human plague in a town like Qûs is attributable to the transportation of infective ratfleas by persons who inhabit or visit infected areas in the town; these persons may or may not suffer from plague in consequence. The possibility of the carriage from one hamlet to another of infected fleas by human beings is strengthened by the results of examining the clothes of four plague patients from Atmour Mistigid. Only two P. irritans [human fleas] were found in the four lots of clothes, and the numbers of X. cheopis were 4, 4, 4, and 1 […]. And, further, 185 X. cheopis were taken from the clothes of three of our rat-catchers after they had dug out [rat] nests in houses in Atmour Mistigid.39

The highly localized character of the work of these plague researchers and its consequent short-range perspective is reflected in these conclusions, which emphasize that in local towns or villages the spread of plague is engendered by the movement of rat fleas in the clothing of human beings. In a manual for medical and health workers working in China written by several leading plague specialists, C.Y. Wu agrees completely with the IPRC and subsequent researchers’ findings that plague is spread by infected rat fleas in clothing and goods, the central statements here being enumerated from 1 to 5: (1) “All the evidence available goes to prove rather […] that infected fleas imported into a locality through human agency first cause plague among the rats, than that human beings are directly attacked.” (2) It is accepted that “X. cheopis may be carried great distances on human beings or in their baggage,” (3) It is also accepted that in this part of Asia the “medium of transportation of infected rat-fleas over long distances [was] by ship transporting rice and grain,” and it is specifically mentioned that Rangoon had acquired a “sinister reputation” as a source of importation of plague in these commodities. (4) Wu notes that “Cotton is another effective vehicle for the transportation of X. cheopis,” and that Hirst had come to the conclusion that

39

Petrie, Todd, Skander et al. 1924: 128, 131.

the spread of bubonic plague over distances

167

“raw cotton, weight for weight, is an even more dangerous vehicle of X. cheopis than grain or any other kind of merchandise.” (5) He also underlines the “ever-present menace of dissemination by infected rats hidden in cargo or by infected fleas secreted in grain and cotton shipments.”40 Obviously C.Y. Wu here describes spread of plague over various distances by transportation of rat fleas in clothing, luggage or commodities. The term spread per saltum is used by Wu Lien-Teh in this composite standard work on plague written by several specialists and, in his monograph on primary pneumonic plague, he distinguishes between contiguous spread and spread per saltum for this type of plague.41 He also cites J.D. Long’s observation in a report on plague on the West Coast of South America, that under favourable climatic conditions, such as low temperatures and relatively high humidities, “fleas can act as reservoirs of plague infection, carry it over long distances and later under favourable conditions transmit the disease.”42

In 1914, J.J. van Loghem and N.H. Swellengrebel, two Dutch researchers, published a study on the epidemiology of plague in Java (Indonesia) titled “Contiguous and Metastatic Spread of Plague.” For reasons that will become clear below, the gist of this paper will be presented in more detail than would be necessary under normal circumstances. At the heart of the matter is a discussion of the pace and pattern of spread as defining features that can distinguish between modern bubonic plague and historical plague epidemics. Van Loghem and Swellengrebel note that at the start of an epidemic of human plague it seems often as if the plague has moved by leaps: the neighbouring localities of a plague infected village remain often untouched while villages situated farther away become involved in the sufferings […]. There can hardly be any doubt that ratborne plague can be introduced from far away by human agency. The epidemic in Java is no exception in this respect. The question is how this rapid transfer over longer distances (metastatic spread, as we will call it) comes about.43

40

C.Y. Wu 1936a: 285–90, and 1936b: 485. Wu Lien-Teh 1936b: 204; Wu Lien-Teh 1926: 182–3. 42 C.Y. Wu 1936a: 286–7. 43 “Kontinuerliche und metastatische Pestverbreitung” = “Contiguous and Metastatic Spread of Plague.” My translation from German. See also below: 176–7, 179, 182–3. 41

168

chapter four

They point out that the IPRC explained “metastatic spread over land by the assumption that human beings transport rat fleas in their clothing or luggage,” but also that the conditions in Java were fundamentally different for two main reasons: (1) because there were far fewer cases of human plague in Java than in India, “which indicates a lower intensity of plague among rats” and (2) because the number of fleas on the rats was far smaller. For these reasons “the likelihood that rat fleas would ride with human beings and that human beings would assume a significant role in the transfer of plague, seemed therefore at the outset smaller than in British India,” although the occurrence of metastatic spread of plague between distant villages had been noted and discussed with interest. In this context, they point out that a leading Dutch medical scholar (Dr de Vogel) had shown that in the city of Malang the centres of infection were in places where large quantities of rice were stored and then distributed to the surrounding districts. He had also shown that the beginning of plague epizootics in Java occurred shortly after the importation of large quantities of rice from plague infected areas abroad (Rangoon and Singapore). Plague was first introduced into the harbour of the city of Surabaya, and subsequently several smaller urban centres connected with Surabaya by railway were attacked almost simultaneously and large numbers of dead rats were found in goods wagons of the railway: This indicates the predominant significance of transportation of commodities for the metastatic spread of plague.

This view was corroborated by a study of the clothing and luggage of inhabitants of Malang that wished to leave the city because of the epidemic there. Only very few rat fleas were found, and the case was much the same in the plague hospitals, evidence that supported the view that it was transportation of commodities and not transportation by human agency that played a predominant role in the metastatic spread of the epizootic. [….] Furthermore, it has been shown that the epizootic was spread along the lines of communication and that, in this connection, we have also been able to ascertain the transportation of house rats and their fleas in public means of transportation (railways, ships). We would also like to mention that the different conditions in British India are at least

the spread of bubonic plague over distances

169

partly due to the fact that there the flea numbers are much higher than in Java.44

As the reader will have noted, the concept of metastatic spread appears not only in the paper’s title, but also six times in the passages just cited from van Loghem and Swellengrebel’s paper (other instances could have been quoted). This suffices to show and to prove that this concept is real and represents the same notion of the mode of spread by plague over considerable distances that the IPRC and other plague researchers call spread per saltum45 or spread by leaps. This clarification is necessary to a discussion of Cohn’s misleading assertions in his “review” of my monograph on the Black Death in The New England Journal of Medicine: Benedictow casts aside any rate of disease spread that was faster than he likes: at these junctures, the Black Death made “metastatic leaps.” But even with his various stratagems, his results still show the medieval plague travelling 30 times as fast as the modern one—a discrepancy he does not explain or even admit to.46

The meaning of the word ‘stratagem’ should be explained, in this case according to Oxford Advanced Learner’s Dictionary of Current English: “trick, plan or scheme to deceive sby [= somebody] (esp an enemy).” This means that Cohn accuses me of doing my best to deceive colleagues, students and other readers who are interested in the Black Death, and that at the heart of this alleged stratagem is the concept of metastatic leaps. According to Cohn, then, this concept is not based on scholarly studies and facts but is fabricated,47 in order to preserve by dishonest means my conventional theory of the microbiological nature of the Black Death as bubonic plague. Clearly, Cohn’s assertion is completely unfounded and untrue in every respect. Cohn maintains that medieval plague spread thirty times faster than modern bubonic plague. This assertion is obviously based on his false assertion that bubonic plague does not spread by metastatic leaps. He also asserts that

44 Van Loghem and Swellengrebel 1914: 460–1, 468, 470–80. My translation from German. 45 See also Wu Lien-Teh 1926: 182, and 1936b: 204. 46 Cohn 2005: 1354–5. 47 See also above: 151 and fn. 3.

170

chapter four Historians have realized since the work of Graham Twigg, in 1984, that the Black Death and the subtropical Y. pestis traveled at vastly different speeds. Even with the railway and the steamship, the 20th-century plague, because of its dependence on the homebound rat, spread overland at about 8 miles per year, whereas the contagious Black Death almost equaled that speed per day.48

The only correct assertion in this citation is that Twigg also claims that bubonic plague spreads only contiguously between adjacent rat colonies. However, Twigg does not assert that the modern spread rate according to this mechanism of dissemination was “about 8 miles per year,” since he correctly refers to IPRC’s observation on the spread rate of contiguous rat plague (see below),49 so the spread rate of 8 miles per year is falsely attributed to Twigg by Cohn. The assertion that the yearly spread rate of 20th-century plague was about eight miles or 12.9 km per year is at variance with the studies of the IPRC and subsequent researchers on plague epidemiology broadly presented above and also with all standard works on plague: it is simply a fictitious figure. One could also wonder how it might be possible that so many excellent plague researchers, many of them with strong interests in the history of plague, should collectively have overlooked the fact that the Black Death and modern plague “travelled at vastly different speeds.” Accurate information on the pace of contiguous spread of plague among colonies of black rats was obtained in one instance by the IPRC, namely 300 feet or 91.4 m in six weeks, corresponding to 792 m in a year. The IPRC organized some large-scale projects in order to study the mechanisms and process of the spread of plague over considerable distances, what they called spread per saltum50 (which Dutch scholars called metastatic spread). The observation of the territorial spread rate between conterminous rat colonies was made in one of several quite remote and isolated villages on the outskirts of “Bombay Presidency” selected by the IPRC in order to study how plague arrived.51 It was observed in Sion Koliwada, Sion village’s northerly part (see above) after it had been evacuated by inhabitants following the discovery of a dead rat and the occurrence of a case of human plague.52 Thus in

48 49 50 51 52

Cohn 2005: 1354–5. Twigg 1984: 131–2. IPRC 1907h, 1907i, 1907j. IPRC 1907h: 799–873. IPRC 1907h: 805–28.

the spread of bubonic plague over distances

171

Sion Koliwada the plague could not be spread further by the dynamics of human agency,53 by persons picking up rat fleas in their clothing at home or elsewhere or in locally purchased grain and redistributing them among neighbours in a process that would establish new effective centres of spread at a multiplicative rate, as would be the case in historical plague epidemics. The observation of spread between rat colonies was an unplanned result of the experiment and occurred under highly artificial circumstances. The study corroborated (again) the by then well-established observation that plague is spread over short and intermediate distances by persons carrying rat fleas in their clothing or luggage or to a distance especially by transportation of certain types of merchandise by ship or railway. The crucial part of the study of this specific case in Sion Koliwada is that the IPRC investigated the origin of the infection there, identified the person who had arrived with it and whence she had arrived: “the infection of Koliwada was not of indigenous origin but was imported, as it were by mere chance, from “Bombay City,” having been brought by a woman who resided in an infected quarter of the city.” In other words, plague arrived in Koliwada by a metastatic leap trough the agency of a person coming from an infected locality. One could also take interest in the relationship between the first find of a dead rat in Koliwada and the subsequent first human death there in plague, which shows that the woman had brought with her an infected rat flea which had first sought out its natural host, a black rat, unleashing an epizootic and soon the release of a swarm of increasingly hungry rat fleas.54 Conspicuously, Cohn does not mention that the central objective of the IPRC’s studies on the mechanisms of spread of plague around Mumbai (and in the Punjab) was specifically to study metastatic spread of plague, the type of plague spread which Cohn denies that the Commission observed or found to be crucial in the epidemiology of bubonic plague. Cohn can only make such a highly misleading and unfair assertion as a basis for his attack on my monograph exactly because he denies established fact, that bubonic plague spreads metastatically and that the usual vehicle of this mode of spread is infected rat fleas.

53 54

IPRC 1907h: 827; Lamb 1908: 19. IPRC 1907h: 805–7, 835.

172

chapter four

To my knowledge, none of the scholars who has studied plague epidemiology in the last hundred years has suggested that bubonic plague spreads over land by movement of black rats between rat colonies, as maintained by Twigg, Scott and Duncan and Cohn. The fact is that the black “homebound” rat is exactly that, and the technical names for the animal are the Latin-derived terms “commensal rats,” meaning rats which are associated with the table, or “domestic rats,” meaning rats which are attached to or associated with human housing. Rats do not, or are loath, to move “over land” but are sedentary animals seeking shelter in burrows and nests near their source of food. If possible, they avoid the dangers from birds and beasts of prey inherent in crossing open land, and for the same reason they are nocturnal animals, leaving their nests or burrows for foraging at night.55 Scholars generally deny that bubonic plague is spread by black rats by movement over land. The IPRC never found infected black rats at any great distance from human habitation. Only in Java has it been reported that black rats “may be trapped almost a kilometre along the side of roads between villages.”56 Rats are inadvertently spread in goods by human agency, by ship, railway, cart, or packhorse, or other means of transportation. Cohn maintains that He [Benedictow: my insertion] speeds up the 20th-century plague by reporting infection times only for California, where the disease is carried by the prairie dog, not the homebound rat, and has been known to move as fast as 15 miles per year.57

The fact is that the geographical term California is never mentioned in my monograph which can be easily ascertained in the “Index of Geographical Names and Peoples,” and I have never stated anything to this effect. In order to produce this spurious assertion, Cohn must confuse the pace of expansion of plague foci by wild rodents in nature58 with the spread rates of rat-plague epizootics and plague epidemics among human beings in their human social contexts, which makes his disparaging comment obviously fallacious and unfounded. To my

55 Pollitzer 1954: 285–6; Wu Lien-The 1936b: 213–5. In the countryside, black rats may move from their nests and burrows associated with farm houses and into the fields when crops are harvested, later to return to their home base. This is, then, a highly localized cyclical occurrence. 56 Hirst 1953: 305–6. 57 Cohn 2005: 1355. 58 See Benedictow 2004: 46–8.

the spread of bubonic plague over distances

173

knowledge, conterminous colonies of black rats which cover contiguous large areas outside urban structures are not found anywhere in the world, presumably for the reasons mentioned above. In contrast to Cohn, and in contrast to what Cohn maintains, in all my monographs I have endeavoured to gather all information on spread rates of plague epidemics. In my monograph on the Black Death, all available information on the spread of the Black Death across Europe is presented in 180 detailed pages with an accompanying map; the factual circumstances on the ground can be scrutinized, tested and pondered59 (six years after its publication, no one has pointed out relevant material that I missed). This material is easily accessible for all readers interested in the material facts. Adequate information on the findings of the IPRC on the mechanisms and patterns of spread of bubonic plague is also presented.60 In this comprehensive work, which takes into account contemporary means of transportation, I have found nothing in data about the Black Death that is at variance with the spread rates and pattern of spread of modern bubonic plague, and my findings are broadly similar to the small material gathered by Biraben on this topic. In general terms, the Black Death can be seen to spread over land by an average pace of 0.5–2.5 km per day, and along main roads usually on average by 1–2 km per day.61 It must therefore again be emphasized, now with the ample background of the facts just presented, that the observations of the IPRC on the pace of spread of plague between rat colonies in Sion Koliwada in the absence of human beings constituted only a tiny part of their observations on the spread of plague. The IPRC emphasize that, taking into account spread by leaps in a normal epidemiological plague process, many other centres of spread would arise and the spread rate of the epidemic as a whole would be very much higher and would tend to increase multiplicatively in the first half of the epidemic. As shown above, the IPRC also established comprehensive evidence to the effect that bubonic plague is spread by rat fleas in clothing, luggage and merchandise by human agency, and that the spread rates of bubonic plague under similar climatic circumstances are decided by two main factors, 59

Benedictow 2004: 44–224, Map 1 opposite page xvi. Benedictow 2004: 11–21. 61 Biraben 1975: 85–92; Benedictow 1993/1996: 78–80; Benedictow 2002: 33–8, 50; and Benedictow 2004: 227–33, where the material is summarized and generalized. See also the index under Plague, Pace of spread, and p. 418 for local data according to country and region. 60

174

chapter four

by the underlying rates at which human beings or commodities travel or are transported, on foot, on horseback, by horse and cart, by railway or by ship,62 and by the time needed for plague disease to develop at each place of arrival. Modern bubonic plague tends to spread faster than medieval plague because modern means of travel are much faster and more efficient, but the type of spread is metastatic. Cohn’s assertion flies in the face of the obvious outcome of elementary analyses and comparison of the means of transportation in the Middle Ages with modern means of communication and transportation. The discrepancy that he presents as scientific “truth” is therefore merely something invented by him. Cohn unconditionally denies all of these facts, asserting that against earlier speculation [fn. 14], the commissioners [of the IPRC: my insertion] found that plague was not transmitted through clothing or baggage of travellers, or other effects of infected persons.

In footnote 14, Cohn cites The Journal of Hygiene, Vol. 7, 1907, page 541, as corroborating evidence where, according to Cohn, the IPRC state: We have no ground for suspecting that the infection of plague can be spread by clothing, bedding or other articles of household use.63

In fact the citation comes from The Journal of Hygiene 1906, p. 541, in the paper by J. Ashburton Thompson which Cohn used to level the accusation of racism discussed above and found to be groundless (above: 46–50). This means that Cohn’s line of argument is doubly false and misleading: the citation is not taken from a publication by the IPRC and it does not represent the Commission’s opinion, in fact, it does not relate to any Indian experience at all. Ashburton Thompson’s paper presents and discusses the findings of Australian scholars under his leadership who studied a number of small plague outbreaks in Australia in the period 1900–5. These plague epidemics occurred in a population overwhelmingly of British extraction and culture and living in a modern social system with modern medical education and facilities and level of hygiene. In these circumstances, it is not surprising that transportation of rat fleas in “clothing, bedding or articles of household use” was of no significance. However, as shown above, “Ashburton

62 63

Cf. Wu Lien-Teh 1926: 182–3. Cohn 2002: 28.

the spread of bubonic plague over distances

175

Thompson introduced in relation to plague epidemiology the concepts and terms of spread by contiguity and spread per saltum,” thus, he made it clear that plague did not only spread contiguously but also, and very importantly, spread by leaps (metastatically) and in this way established new and independent epicentres of epidemic spread which greatly contributed to the pace and dynamics of spread. In the quite comprehensive citations from Ashburton Thompson’s paper above, which easily could be multiplied, this is made abundantly clear. Ashburton Thompson explains that in Australian society plague was spread per saltum by transportation of “produce-trade in hay, straw, chaff in bags, maize and potatoes.” He emphasizes the difference between the mechanisms and dynamics of spread of plague and suitable measures for the combat of plague in modern Australian society and in traditional un(der)developed Indian society, which is the basis for Cohn’s malicious attack on him for racism. This means that Ashburton Thompson’s findings and conclusions cannot be taken in support of Cohn’s position and that Cohn unavoidably must know this fact. Thus, in flagrant contradiction of both Ashburton Thompson’s and the IPRC’s clearly stated views, Cohn takes Ashburton Thompson’s paper falsely in support of his own position after having transformed it from the work of the “racist” Asburton Thompson on plague in Australia into a study by the IPRC’s on the pattern of spread of plague in India. Since the IPRC’s results on the mechanisms of spread by leaps by human transportation of infected rat fleas represent a dire threat to Cohn’s alternative theory, their work cannot be presented correctly. He endeavours to convey the impression, by reiteration as it may seem, that their findings support his view. He makes, for instance, a similarly misleading reference to the IPRC in his paper in The American Historical Review 2002 in order to be able to defend his repeated assertions that the IPRC found that plague can only spread contiguously between conterminous rat colonies and therefore exceedingly slowly, only 300 feet in six weeks.64 In footnote 51, he purportedly refers for support to the “Indian Plague Commissions,” but none of the references is to any member of the the preliminary fact-finding Indian Plague Commission or of the Indian Plague Research Commission which replaced it in 1905. The reference to IPRC 1907h: 839, pertains

64

See Cohn 2002b: 712, and fns. 51–2 where he misrepresents IPRC 1907 e,g,h,i.

176

chapter four

to the end of a small preliminary survey of the findings in Sion Koliwada but he avoids the substance of the study of this village and also the early part of the survey where it is stated, for instance, on page 735, that “the available evidence inclines strongly that the infection in Koliwada was not of indigenous origin but was imported, as it were by a mere chance, from Bombay City, having been brought by a woman who resided in an infected quarter of the city.” He also avoids the final summary of this report on page 873 where it is stated that positive evidence had been adduced that contagion was introduced into these villages by transportation of rat fleas in the clothing of persons. Cohn’s assertion that studies of other villages had shown the same slow spread as evidenced by the special study in Sion Koliwada is not correct and the implication that this should also be corroborated by the same reference to IPRC 1907h: 839, is therefore also not correct. As emphasized above, the study of these peripheral villages outside Mumbai was designed to find out exactly how plague was transported from the city to the villages, it was designed to study spread of plague by leaps, exactly the opposite of what Cohn claims. In reality, nothing supports Cohn’s statement that “Without the assistance of the railway or the steamship, the fourteenth-century disease spread almost as fast per day over land as modern plague does per annum.” In his “review” of my monograph in The New England Journal of Medicine, Cohn attributes to the IPRC that the assertion that from studies of the clothing and luggage of tens of thousands of people migrating from plague-stricken regions, the plague commissioners concluded overwhelmingly that Y. pestis was not transmitted by these means.65

As so often, Cohn presents this assertion without a supporting footnote. However, the IPRC have made no such study and drawn no conclusion to this effect. Possibly, Cohn has attributed to the IPRC the study in Java by van Loghem and Swellengrebel presented above where such a research project is described and the results are cited and explained,66 at least this is the only study I know that fits the description. If this is the case, it would be remarkable that Cohn pretends not to know the term ‘metastatic spread’ which is the central subject of the paper and which is included in the title, and that he does not discuss 65 66

Cohn 2005: 1354. Above: 167–9; below: 182–3.

the spread of bubonic plague over distances

177

the Dutch researchers’ explanation which incorporates this finding within the conceptual framework of the theory of plague epidemiology constructed and established by the IPRC. The true epidemiological findings of IPRC are presented above and document the completely misleading character of Cohn’s assertions. In fact, Twigg also mentions the terms contiguous and metastatic spread of plague in a brief comment on these observations in Java.67 Thus Cohn, who repeatedly refers to Twigg’s monograph, certainly had the opportunity to acquaint himself with this term there. I note that Cohn repeats this false assertion in his “review” of my monograph on the Black Death as evidence that my epidemiological analysis is unfounded and deliberately misleading.68 In support of his assertions on these crucial points of plague epidemiology Cohn refers also to a paper by Pollitzer and Meyer from 1961, page 435. On this page, nothing in support of Cohn’s assertion is mentioned, but on the contrary, it is stated that plague “is primarily an insect-borne, especially a flea-borne, disease.” Thus, this is also a false reference. Twenty pages later Pollitzer and Meyer comment directly on the means, modes and mechanisms of spread and their true views on the matter can be ascertained beyond doubt or dispute from this quotation: A distinction has to be made between what Gill adequately called the “intramural” spread of the disease from one house, block or part of a settlement to adjacent houses, blocks, or precincts or, as observers in Java have called it, “metastatic” spread. It is easy to understand how plague, conveyed either by the rats themselves or by their fleas, may creep from one house or group of houses to others […]. Such a spread of the infection may be extremely slow. One instance has been reported in which a rat epizootic in India took six weeks to travel 300 feet (approximately 91 m.) [….] The question of whether active movements of the rats are responsible for the long-distance spread of plague, and if so to what extent, has been the subject of considerable debate. In the opinion of the Plague Research Commission, this factor was of no importance because the spread of infection per saltum was effected by the passive transportation of rats or their fleas by goods or human traffic. This opinion has been shared by most subsequent observers.69

67

Twigg 1984: 131; see below: 181–3, Twigg explains away the Dutch researchers’ findings with respect to metastatic spread and provides no reason for why they needed this concept. 68 Cohn 2005: 1354. 69 Pollitzer and Meyer 1961: 454.

178

chapter four

Here it is unequivocally stated by two of the Grand Old Men of plague research that the IPRC rejected the theory that long-distance spread of plague takes place through dissemination between rat colonies. Instead, the IPRC concluded on the basis of great research efforts that contiguous spread was not important for the spread of bubonic plague but that saltatory or metastatic spread was of pre-eminent importance, and this view has later come to be shared by most scholars observing plague epidemics in the field. This is why this view is emphasized in all standard works on plague. This is what Twigg, Scott and Duncan, Cohn and other advocates of alternative theories purportedly have collectively failed to notice. They maintain that they have only noticed the tiny remark on contiguous spread in Sion Koliwada on page 827 in a paper of seventy-five pages, also that this is the main topic of the Report containing the study of plague in Sion. The great mass of research on saltatory spread has been overlooked by the advocates of alternative theories. Also this citation of Pollitzer and Meyer confirms that Cohn’s denials of the reality and concepts of metastatic spread or spread per saltum are made against his better knowledge. Furthermore, Pollitzer and Meyer return to the question of spread per saltum. In a sub-chapter titled “Role of Flea Transport in the Spread of Plague,” they first state: Fleas can be passively transported by (1) their specific hosts or temporary hosts […]; (2) transport vehicles; (3) the persons or the baggage of travelers; and (4) the movement of goods. While it is generally admitted that plague-infected fleas may be carried on the persons or in the baggage of travelers, in the opinion of most observers this means of spreading plague is of comparatively limited importance, and, in particular, is never responsible for a carriage of the disease to far distance localities. Most observers agree that the transport of infected fleas in goods, particularly in grain, raw cotton, gunny bags, rags, and hides is of great importance in the spread of plague.70

This shows that Pollitzer and Meyer support the view that bubonic plague spreads by metastatic leaps or per saltum, but that they, like Hirst, place less emphasis on the importance of transportation of rat fleas over great distances in clothing or luggage, and more on the importance of transportation in commodities by railway or ship. This

70

Pollitzer and Meyer 1961: 469–70. Cf. Pollitzer 1954: 335.

the spread of bubonic plague over distances

179

should be compared with the continuation of Cohn’s assertion cited above: Instead, adult fleas outside their normal host, the rat, rarely live more than five days and do not travel in passengers’ baggage, in wool packs, or cotton bales as recent historians such as Le Roy Ladurie, John Aberth, and Norman Cantor for medieval Europe, [fn. 15] Paul Slack for Tudor and Stuart England, [fn. 16] Ole Jørgen Benedictow for late-medieval Scandinavia, [fn. 17] and Klein for twentieth-century India, [fn. 18] continue to report as solid epidemiological facts of modern plague.71

As can be readily seen, Cohn’s assertion that all these serious historians have fabricated similar erroneous and misleading assertions to the effect that rat fleas were transported over long(er) distances in various types of goods, but also in the luggage of travellers, is without foundation. On the contrary, as shown above, the IPRC, van Loghem and Schwellengrebel, Pollitzer72 and Meyer,73 Hirst,74 and C.Y. Wu,75 all strongly support this view. Much eminent scholarly work has produced a truly impressive corpus of evidence to the effect that bubonic plague is mainly spread over short-range and medium-range distances by rat fleas in clothing or luggage and over longer distances in grain, rice, raw cotton, textiles and other commodities, and all leading plague researchers agree on the importance of these means of spread. This view is also comprehensively presented in all standard works on bubonic plague. Cohn’s assertions to the contrary are unfounded, and his disparaging characterisations of plague historians groundless. Cohn argues that spread of plague over distances cannot occur because “fleas outside76 their normal host, the rat, rarely live more than five days.” This assertion is based on obsolete research from the very infancy of rat-flea studies, research that was soon corrected. In the words of Hirst: The contention that rat fleas, when separated from their host, have too short a life to survive long journeys in the midst of merchandise and then transmit the plague bacillus, has substance when the climatic conditions en route are exceptionally unfavourable and not otherwise […]. In the light of recent research it is evident that rat fleas are much hardier than 71 72 73 74 75 76

Cohn 2002: 28–9. Pollitzer 1954: 385–7, 389–90. See Pollitzer and Meyer 1961, and the preceding pages here. Hirst 1953: 306–13, 316–23. C.Y. Wu 1936a: 285–90; 1936b: 485. Presumably he means away from their hosts.

180

chapter four was formerly imagined. Earlier ideas on this question were based mainly on the results of experiments on the viability of starved fleas isolated in test tubes. We now know that experiments on the bionomics of fleas in a highly unnatural environment are very apt to be misleading. In this respect the observations of Estrade [fn. 8577] on the prolonged survival of X. cheopis in cereal dust in Madagascar are especially relevant […] long after the rats have died of plague […] Not infrequently such infected fleas are transported considerable distance by human agency and give rise to sporadic outbreaks of plague at destination […]. At temperatures below 15° C. the chief vector of bubonic plague [X. cheopis] can certainly survive in a very heavily infected state for at least fifty days […]. Macchiavello has found X. cheopis still alive after six months unfed in a protected rat burrow (personal communication).78 [.…] It is highly improbable, however, that the maximum longevity of unfed, infected rodent fleas is known.79

Since ships appear to have sailed, on average, around 40 km per day in the Middle Ages,80 a voyage of fifty days would correspond to a distance of 2000 km; in natural conditions of 27° C X. cheopis transmitted plague after 29 days of starvation,81 corresponding to transportation over a distance of 1160 km. Clearly, Cohn’s assertion flies in the face of basic facts and misrepresents Pollitzer’s and Meyer’s view on the matter, and also the view of all other serious scholars who have studied the epidemiology of plague. His disparaging remarks on historians are unwarranted. Twigg was the first advocate of an alternative theory of plague who denied the reality and importance of metastatic spread of plague by rat fleas, a denial of which all later advocates of alternative theories have availed themselves. Twigg’s point of departure is a double assertion: (1) there were hardly black rats in medieval Europe, thus, there could not have been bubonic plague. (2) “An important aspect of plague spread is the continuity across a rat population.” Since bubonic plague spreads contiguously only between conterminous rat colonies, contiguous distribution of this animal must be a necessary condition for spread over distances, it is impossible that the Black Death or medieval plague epidemics 77

Hirst refers to Estrade 1935. This piece of information can be found in a paper by Machiavello published in 1917, see Pollitzer and Meyer 468, fn. 74, p. 586. 79 IPRC 1914a: 437; Hirst 1953: 322–4. 80 Benedictow 2004: 102–3, fn. 20. 81 Hirst 1953: 330–1; Pollitzer and Meyer 1961: 468. 78

the spread of bubonic plague over distances

181

could have been bubonic plague: “If it is assumed that rat populations were contiguous throughout the region—and they would need to have been—then the rate of spread across France is as follows […].”82 These assertions are presented as objective facts. The comprehensive empirical material documenting the reality of the broad presence of the black rat all over medieval Europe, also in the northerly parts of the Continent, has been presented above, and Twigg’s denial is untenable. No plague researcher has ever asserted that colonies of black rats are distributed contiguously over the landscape and as such could provide the basis for contiguous territorial spread over districts, areas, regions or countries. About seventy pages later,83 Twigg’s line of argument takes a different turn. He states, seemingly on the basis of an independent reading of the works of IPRC, that: From their experiments the Plague Research Commission concluded that the spread of infection at a distance was effected by infected fleas carried either on a person or in the bedding of travellers who had either lived in plague houses or had visited them.

Although this is not incorrect, it is, as shown above, highly unrepresentative since the IPRC rapidly reached the conclusion that infected rat fleas in various types of goods also played a major role in the spread of plague over distance and with increasing importance with the distance (see also below). Twigg does not refer to the works of the IPRC in a footnote; the reason is that he has in fact based his discussion on a chapter in Pollitzer’s monograph of 1954 titled “Role of Flea Transport in Spread of Plague,” but only discusses it very selectively in a small sub-chapter called “Transport by Travellers and their Baggage.”84 Twigg goes on to state that such persons would not be bitten and infected themselves, which is not correct: it is quite a usual occurrence.85 82

Twigg 1984: 57–9, 100. Twigg 1984: 128. 84 Pollitzer 1954: 386–7. 85 This may or may not occur depending on the duration of starvation of the rat flea from the time it leaves a dead rat and the time of the person’s arrival at the destination, since rat fleas of this type normally endure about three days of starvation before they attack human beings. Apparently, Twigg insouciantly cites Pollitzer’s statement that “such fleas [that were carried on persons or in bedding] were not directly responsible for the causation of human plague (even the travellers carrying flea-infested baggage were able to escape infection) […]”: Pollitzer 1954: 386. 83

182

chapter four

However, the main point is made, namely that the IPRC were of the opinion, based on their empirical studies, that rat fleas in the clothing or luggage of persons moving from a plague infected place to an uninfected place would on arrival at the destination preferably seek out rats in the immediate proximity, and thus could trigger a rat epizootic and spread plague over a distance. Next, Twigg continues to follow Pollitzer’s text (without acknowledgement) and mentions that Petrie and Todd [and Skander et al.] reached the same conclusion in Egypt. Then, Twigg sets out to refute the tenability and significance of these opinions. He does this by paraphrasing in a highly selective fashion Pollitzer’s presentation which is a tertiary source based on van Loghem’s and Swellengrebel’s brief presentation of the results of Dr de Vogel’s largescale study of the clothing of plague refugees from Malang and of patients in plague hospitals there which produced insignificant evidence of rat fleas.86 This study has been quite thoroughly discussed above and the reason for this finding and de Vogel’s conclusions presented. Twigg omits the title of van Loghem’s and Swellengrebel’s paper which contains the terms contiguous and metastatic spread which are at the centre of the paper’s contents and restricts his discussion to contiguous spread87 in accordance with his need to make bubonic plague theory incompatible with the epidemiology of historical plague. However, on methodological grounds it is impossible to reject the validity of the empirical findings of the IPRC in India or of the researchers in Egypt of rat fleas in clothing or bedding on the basis of different results in Java. These findings in India and Egypt remain tenable and valid, as do similar findings in Madagascar and South America mentioned on the same page by Pollitzer, and results from China could have been added. In order to refute these findings, Twigg would have to show that they were untenable and based on invalid studies, or else he would have to search for an empirical explanation of why the case should be different in Java. However, the strong limitations of this approach, which leaves unaddressed the great mass of evidence to the contrary elsewhere, would not provide the general refutation which his theory requires. Like Cohn, Twigg fails to cite or consider the Dutch researchers’ explanation of the outcome of Dr de Vogel’s study, which explanation underscores the special conditions underlying this finding in Java, 86

This study is cited and discussed at some length above: 168–9. “Kontinuerliche und metastatische Pestverbreitung” = “Contiguous and Metastatic Spread of Plague.” 87

the spread of bubonic plague over distances

183

namely that both the intensity of plague was much lower and the number of fleas on rats was much lower than in India. Consequently, the incidence of rats dying from plague was much smaller and also the number of fleas leaving each rat dead from plague was much smaller, facts that epidemiologically relate multiplicatively to each other and as such produce a corresponding order of reduction of the number of infected rat fleas which could attack human beings in Java compared to the situation in India. In short, the chance that plague-infected rat fleas would attach to clothing or bedding was much smaller in Java than in India or Egypt. As shown above, the two Dutch scholars incorporate their findings on plague in Java within the conceptual framework of the theory of plague epidemiology established by the IPRC. Dr de Vogel’s findings in Java do not falsify the findings in India or Egypt or elsewhere, but serve only to describe a special case that can be adequately explained and understood within the framework of the established ratflea theory of the spread of bubonic plague. Twigg’s attempt to refute the rat-flea theory of the spread of plague in clothing, bedding or luggage is methodologically and empirically invalid and dependent on a flawed and selective presentation of van Loghem’s and Swellengrebel’s paper. However, the rat-flea theory of the spread of bubonic plague also has another dimension, namely spread over considerable or long distances in merchandise. Again the discussion will be based on a citation from Twigg’s monograph which will shed light on his way of arguing his case on this crucial point: Pollitzer (1954) says that one ought to agree with the opinion of Hirst that, in general, a spread of flea-borne plague through travellers is of comparatively limited importance. The transport of infected fleas in goods, especially in raw cotton, gunny bags, rags and hides is generally agreed to be of great importance in the spread of plague. There has, however, been plenty of debate on just how far the infection can be carried by such fleas. Hirst (1931) said that the available evidence pointed to the fact that when an overseas source of infection was only a few days away, an infected flea might be readily transferred directly in grain from the port of origin to the port of entry but otherwise it would be inferred that a plague epizootic had occurred among the rats aboard ship […]. After examining various evidence of plague transport, Pollitzer (1954) concluded that it was unlikely that long-distance transportation of infected fleas played a generally important role in plague dissemination.88

88

Twigg 1984: 129.

184

chapter four

Twigg unfortunately omits a crucial word in his citation of Pollitzer’s 1954 text on the types of goods that are especially important for the transport of infected rat fleas, namely “grain,” which can be seen from the verbatim citation of this point in Pollitzer and Meyer 1961 cited above on page 178. The meaning or conclusion Twigg here endeavours to achieve and convey to his readers is obviously at variance with the citations above from Pollitzer and Meyer, which gives grounds for scepticism. In the first passage, the central point is associated with the words “travellers” and “comparatively little importance.” The word “travellers” should be seen in light of the problem of transportation of plague over considerable or great distances. It is in this connection that Pollitzer and Hirst opine that transportation in the clothing or luggage of travellers is of comparatively little importance, that is in relation to other means of transportation of plague. This passage should be seen in immediate connection with the following passage. Here the crucial words are “generally agreed,” i.e. Twigg suggests that it is the general opinion of plague researchers who have studied the mechanisms of spread of bubonic plague that transportation of infected fleas in goods, in raw cotton, gunny bags, rags and hides, is of “great importance” in the spread of plague over considerable or great distances (a fact flatly denied by Cohn, as we have seen). As can be seen from the citations above, the IPRC and the research team in Egypt maintained that they had succeeded in showing that plague was distributed locally or at relatively short distances by rat fleas in clothing, bedding or luggage, and that this process by engendering new centres of spread fuelled the powers of spread of local epidemics. The heart of the matter according to Pollitzer’s text is very different from the meaning Twigg attributes to him in his presentation, because he has omitted the crucial passage. This passage addresses the question of whether metastatic leaps of plague are mainly effected by the transportation of rat fleas in goods or by transportation of infected rat fleas on rats in goods. On this issue, Pollitzer takes a clear stance that Twigg does not mention, namely: There can be no doubt, therefore, that infected rats, rather than infected fleas, carried in consignments of goods are responsible for this dissemination of the infection.89

89

Pollitzer 1954: 389–90.

the spread of bubonic plague over distances

185

Based on the passages cited above it is clear that among serious scholars of plague research there is no disagreement that bubonic plague spreads by metastatic leaps or per saltum. And clearly Pollitzer is of the same opinion as other plague researchers on this point, that metastatic spread is of great importance. There is, however, a debate on the relative importance of the various mechanisms which effect spread over considerable or great distances. To be more precise, at the centre of this discussion is the question of whether this transportation to a distance is dependent on the presence of rats with which rat fleas can travel for a substantial part of the voyage, or whether rat fleas can make a long(ish) voyage on their own. Twigg misrepresents Pollitzer’s view on the matter by using an incomplete citation which omits Pollitzer’s central opinion. Pollitzer’s opinion is also of great interest in relation to Twigg’s view that the Black Death could not have been transported all the way from Constantinople to Italy on board the big Italian galleys that sailed this route, which ships certainly could accommodate more than one rat colony. One must take into consideration the fact that from the infection of a rat colony on board it would be about twenty-one days before the first death among the people on the ship, providing that the rat fleas did not find new rat hosts in another colony which expanded into the area of the decimated rat colony in order to take advantage of their food resources, and the whole process would have to be repeated.90 A few other clarifying comments are warranted in relation to Hirst’s opinions, since Twigg attributes to Hirst the view that plague could not be transported over long distances by ships, for instance the 1985 km from Rangoon in Burma/Myanmar to Colombo in Ceylon/Sri Lanka even by steam ship,91 which makes it surprising that plague could have been transported the much longer distance from Hong Kong to Kolkata (Calcutta) in 1896. Since it is well known that around 1900 plague was transported repeatedly by steam ships all the way from India to England, obviously with infected rat fleas which triggered outbreaks of plague on arrival, Twigg’s opinion would appear to go against observed fact. Surprisingly, eighteen pages later in a chapter called “TwentiethCentury Plague in Britain […]” Twigg mentions a number of these outbreaks, for instance in Glasgow, Liverpool, Cardiff, Hull, Bristol,

90 91

Below: 582–3. Twigg 1984: 129.

186

chapter four

London, and Freston (Suffolk), and he could also have mentioned other instances of long-distance transportation of plague to Australia, the Americas, and so on. Unexpectedly, Twigg refers to Hirst’s monograph of 1953 for support,92 and he could therefore also have cited Hirst to the effect that “the disease broke out in Hong Kong in 1894 and commenced to spread overseas to the ports of several continents,”93 which seems to indicate that Hirst considered spread over much longer distances than from Rangoon to Colombo as fully possible. Twigg’s statement of Hirst’s purported view to the contrary eighteen pages earlier is supported by a reference to a rather peripheral work by Hirst published in Sri Lanka (Ceylon) in 193194 that is very difficult to get hold of, at least my efforts have not succeeded, although the librarians at the University Library of Oslo are excellent. One could suspect that Twigg has taken the reference from Pollitzer’s monograph.95 However, Hirst’s excellent 1953 monograph on plague provides easy access to his views on all matters of importance, and moreover gives his final views after he had had the opportunity to bring together and structure his vast knowledge of the scholarly literature on plague and his unique personal experience in the laboratory and in the field and in the combat of this epidemic evil. This is, of course, the work that Twigg should have used, and Hirst’s opinion is clear. His opinion on the matter is cited at length above in my discussion of Cohn’s assertions; Hirst emphasizes that rat fleas are much hardier than formerly assumed and that such fleas in moderately warm and humid circumstances can survive unfed and in heavily infected conditions under transportation for at least fifty days.96 Seen against the background of the usual situation on board ships which commonly contain several rat colonies, this fifty-day interval could be activated after a considerable time at sea, producing a much longer total duration of journey for infected fleas as they successively found new hosts on rats invading the territories of rat colonies decimated by plague which could not any longer defend their food

92

Twigg 1984: 147–8. Hirst 1953: 332. 94 L.F. Hirst, The protection of the interior of Ceylon from plague with special reference to the fumigation of plague-suspect imports. Municipal Printing Office: Colombo, Ceylon 1931. 95 See, for instance, Pollitzer 1954: 387or 404; Pollitzer and Meyer 1961: 467–71, 585. 96 Above: 179–80. 93

the spread of bubonic plague over distances

187

resources. In this context, a brief supplementary citation from Hirst’s monograph removes any doubt about his opinion on the subject: In view of the observations on flea longevity shown on pages 330–1, there seems no reason to doubt the theoretical possibility that infection might be carried in the bodies of live, unfed fleas half-way around the globe.97

If we consider these diverse materials together, it might seem that Pollitzer and Hirst tend to underrate the great importance that the IPRC attribute to transportation of merchandise for the spread of plague over considerable or long distances. In the case of spread over short or intermediate distances, the commissioners seem to put somewhat more weight on the significance of rat fleas in clothing, bedding or luggage. In general there is great continuity in the views on the mechanisms and modes of spread of bubonic plague, but it is also clear that there are regional variations due to differences in climatic and social conditions and customs, traditions of clothing, communication technology and social structures. Spread per saltum or metastatic spread explains the ability of bubonic plague to spread quickly over long distances, particularly by ship, but also to some extent by land with transportation of goods, or over shorter distances in the luggage of travellers or in people’s clothing. This must also have been the case under medieval conditions when ships sailed at an average pace of forty km a day, so that infected rat fleas surviving for fifty days could have travelled 2000 km, and as we have seen, there are good reasons to assume that the duration of their survival at sea and the distance they travelled could easily have been considerably longer. Much evidence to this effect is presented in my monograph on the Black Death.98 The findings of the IPRC and other modern researchers in frontline combat of plague during the first half of the previous century in this respect are contrary to what is loudly asserted on their behalf by the advocates of alternative theories. Scott and Duncan insist repeatedly that bubonic plague spreads only contiguously between rat colonies,99 and despite the abundant documention that the disease has spread spread per saltum, they repeatedly 97

Hirst 1953: 327. Benedictow 2004: map by p. 1, 20, 227–3, for general discussion, and Index under Metastatic spread p. 418 for accounts of concrete events. See also the comprehensive discussion below. 99 See for instance Scott and Duncan 2001: 45–6, 57, 79–80, 98–9, 280–1, 350, 358, 361, 383, 394. 98

188

chapter four

deny that bubonic plague can spread by “saltatory”100 movement or “transmission,” for instance: these stories of a blocked flea carrying bubonic plague over very long distances through the countryside and starting an epidemic are quite impossible.101

They make this same denial in a passage which is so comprehensively flawed that the constituent assertions must be enumerated for comments following the quotation: [1] Bubonic plague could not have spread in the saltatory fashion seen in many of the epidemics in England and, particularly, in France when it jumped more than 30 miles in a few days with no intermediate outbreaks. In the outbreak at Malpas [Cheshire] (section 9.3) it travelled nearly 200 miles in this way. The speed of this transmission is completely inconsistent with bubonic plague: [2] the Plague Research Commission (1907a,b) gave an example where the epidemic [sic!] in rats took 6 weeks to travel 300 feet; [3] this slow diffusion is one of the most common characteristics of bubonic plague and [4] we see this pattern in the hinterland of Marseilles in 1722 (Chapter 12). [5] Bubonic plague in South Africa in 1899–1925, moved about 8–12 miles per year and this spread may have been aided by steamtrains (Twigg, 1984). [6] The Black Death, in stark contrast, spread from the toe of Italy to northern Europe in 3 years […].102

(2) Scott and Duncan contend that “The speed of this transmission is completely inconsistent with bubonic plague: the Plague Research Commission (1907a,b)103 gave an example where the epidemic [sic] in rats took 6 weeks to travel 300 feet.” The first of these reports does not relate to questions of spread rates but to other aspects of the role of rats and rat epizootics in Mumbai and is not relevant for the subject in question. The second report is relevant and is a careful and detailed study how plague spread from Mumbai to villages on the outskirts of

100

Scott and Duncan 2001: 317, 347, 358, 361, 372. Scott and Duncan 2001: 262–3. This assertion should be seen in relation to their great efforts to prove that the famous epidemic at Eyam (Derbyshire) could not have been bubonic plague. 102 Scott and Duncan 2001: 358. 103 The two reports are: (1) Indian Plague Research Commission. 1907g. Reports on Plague Investigations in India, XXII. “The Epidemiological Observations made by the Commission in Bombay City.” The Journal of Hygiene. 7: 724–98; and (2) Indian Plague Research Commission. 1907h. Reports on Plague Investigations in India, XXIII. “Observations made in four villages in the Neigbourhood of Bombay.” The Journal of Hygiene. 7: 799–873. 101

the spread of bubonic plague over distances

189

the city. In other words the report is a study of metastatic spread or spread per saltum, also called saltatory spread by Scott and Duncan, exactly the opposite of what Scott and Duncan maintain is the typical or normal pattern of spread of bubonic plague. Within this large-scale study, the IPRC also made some incidental observations which have been referred also above, and will now be repeated since all advocates of alternative theory cite this account of slow spread rate but all are in denial regarding the contextual facts. Sion was one of the villages studied, and the observation area in question was in a part of this village called Koliwada after it had been evacuated by the inhabitants after the find of a dead rat and the occurrence of a case of human plague. Thus, the plague could not be spread further by the dynamics of human agency, and for this reason this case is not directly comparable to epizootic spread in populated environments; rather it is a study of spread under artificial conditions.104 The IPRC succeeded in identifying the person who had brought with her an infective rat flea from a contaminated part of Mumbai. This case history provides a corroboration of the rat-flea-based theory of saltatory spread. The fact remains that Report XXIII by the IPRC provides a comprehensive collection of material on and analysis of saltatory spread by bubonic plague—this is the purpose of the Report, and strong empirical confirmation of the process was observed and reported. If Scott and Duncan had read the report, it is a serious matter that they pretend not to know this; if they have not read it, it is also a serious matter, because it would demonstrate unsatisfactory attitudes to scholarly research and the responsibility of honesty to readers. They have these serious issues in common with all other advocates of alternative theories. (2 + 3) It has been shown above in this chapter that the IPRC did not think that slow diffusion is the characteristic pattern of spread of bubonic plague. The Commission maintain that plague is spread according to at least two main patterns, by contiguous spread and by metastatic spread. (1 + 4) These assertions deny central epidemiological facts relating to the pattern of spread of historical and modern bubonic plague. It has been documented above that bubonic plague spreads at rates and in a pattern corresponding to the ways and means of movement, travel and

104 IPRC 1907h: 807–28, the oft-mentioned finding on the spread rate under these conditions is found on page 827.

190

chapter four

transportation of persons and goods. The fact that many times there are not intermediate outbreaks between an established plague centre and an outbreak some distance away is characteristic of the metastatic spread of bubonic plague; neither of the two examples or illustrations mentioned provides any proof that it was not bubonic plague, but are compatible with the pattern of metastatic spread of bubonic plague. (4) Here Scott and Duncan misrepresent the realities of the epidemic in southern France in 1720–2 and indeed their own knowledge of it. A few pages earlier, in their discussion of this epidemic which Scott and Duncan in the face of overwhelming evidence, must admit was bubonic plague, they also have to concede that there “were examples of saltatory behaviour.”105 This is a minimized admission of the facts. Instead of addressing the evidence for saltatory behaviour, they endeavour to convey a picture of an epidemic spreading slowly and contiguously,106 and claim that: The epidemic continued to spread slowly from these foci to the east of the Rhône, affecting neighbouring villages […] the movement was gradual, travelling to nearby localities, but there were examples of apparently saltatory behaviour.107

However, metastatic spread was the ordinary, dominant way this great epidemic of bubonic plague spread in Provence, the Comtat and the Languedoc, at short distances or over hundreds of km. This can be easily ascertained from Biraben’s lengthy discussion of it in the first volume of his plague history to which Scott and Duncan also refer. It can be easily ascertained also by studying Biraben’s chronological table of the attacked localities which shows the beginning and end of the epidemics. The point can be illustrated by a small excerpt from the first page relating to the year 1720: 1 August – Aix; 1 August – Apt; 2 August – Vitrolle; 7 August – Sainte-Tulle; 8 August – Riez; 15 August –Aubagne; 15 August – Mayrargue; 15 August – Mirabeau and Les Pennes-les-Septèmes; 15 August – Gignac; and so on. As can be readily seen, the plague appeared simultaneously or almost simultaneously over considerable distances with no intermediate outbreaks, and this occurred all over these large regions.108 Biraben himself is very clear on this point and directly contradicts Scott and Duncan’s 105 106 107 108

Scott and Duncan 2001: 347. Scott & Duncan 2001: 346–51. Scott and Duncan 2001: 347. Biraben1975: 240–87.

the spread of bubonic plague over distances

191

endeavours to minimize the prevailing saltatory pattern of spread to a distance when he states: If one marks on a map all the localities touched by the epidemic, it is remarkable to ascertain that, far from spreading between neighbourhoods, it is compartmentalized in small centres [“foyers”], almost all isolated from each other by parishes that remained healthy […]. This extension did not, by the way, come into being by chance, but mainly along the roads […] the chronological order is not the same as the geographical succession [of localities] out of […] a result of transportation by human beings.109

Thus, Scott and Duncan’s assertion that bubonic plague in Southern France in 1720–2 predominantly and typically spread contiguously and in accordance with the observation by the IPRC that plague in an instance used six weeks to move 300 feet [91.4 m) is not correct. (5) “Bubonic plague in South Africa in 1899–1925, moved about 8–12 miles per year and this spread may have been aided by steam trains (Twigg, 1984).” As will be clear from the discussion of Scott and Duncan’s presentation of purported South African evidence on the epidemiology of bubonic plague above,110 their assertion on this point is misleading. This observation does not relate to contiguous spread between rat colonies, but relates to the spread and development of a plague focus among wild rodents, predominantly gerbilles. This development was reflected in a highly sporadic incidence of cases of bubonic plague among human beings with an average of 2.2 cases per incidence and 1.4 deaths. This is not an epidemic of bubonic plague, but an episodic endemic manifestation of enzootic plague among rural rodents, and consequently there is no case of spread of a bubonic plague epidemic based on black rats in South Africa and no evidence of spread rate. (6) Scott and Duncan’s assertion that the Black Death spread from the toe of Italy to northern Europe in three years is erroneous: the Black Death did not spread contiguously from Italy’s toe, it arrived by longdistance ships in Genoa and Venice whence it spread into parts of France and Central Europe; it spread from the original epicentre of Marseilles to the northerly parts of Europe in a process that comprised a number of metastatic leaps, as I show in my monograph on the

109 110

Biraben 1975: 285–6. My translation from French. Above: 87–90.

192

chapter four

Black Death and as can easily be ascertained by a glance at the map in that book.111 After having rejected the microbiological evidence produced by M. Drancourt and D. Raoult in two papers of 1998 and 2000 to the effect that the identity both of modern and historical plague contagion was Yersinia pestis on the basis of speculative arguments about laboratory contamination, which arguments are shown to be groundless below in Chapter 10 (and having apparently overlooked two other studies (namely nos. 3–4 in Table 6), J.W. Wood, R.J. Ferrel, and S.N. DeWitteAviña had cleared the ground for arguing against the bubonic-plague theory. Firstly, they have maintained that a difference in the temporal progression of the Black Death as reflected in institutions of (new) parish priests (after the incumbents’ death) in the diocese of Coventry and Lichfield in 1349 and general mortality of bubonic plague in Kolkata (Calcutta) (1903) constitutes evidence that the Black Death could not have been bubonic plague. According to the principles of comparative methodology, I cannot accept that a comparison can be valid and tenable when performed without active interest in the significance of spatial-territorial, urban-rural, housing-related, religious, cultural, political-organizational, public sanitary, medical, and climatic differences.112 These are all societal dimensions that make for vast differences in the interrelationship of behavioural patterns and physical structures with epidemic disease, even the same epidemic disease. The territorial and demographic comparability of modern Hong Kong, Kolkata or Mumbai around 1900 with archdeaconries in the diocese of Coventry and Lichfield at the time of the Black Death seem unconvincing, a point that the authors appear eventually to realize but not really to understand.113 The central methodological question must be asked: is it not similarity of historical circumstances that make phenomena in pari materia and comparable, and must not historical, cultural and societal structures therefore be made part of the study? Should not differences of circumstances be carefully taken into account in order to explain differences of manifestation in different countries and different historical periods? Is it not only when intensive study of the differences of circumstances and their significance has failed to provide explanatory grounds and culture-specific and period-specific factors of causation 111 112 113

Benedictow 2004: 50–224, map xviii–xix. Wood, Ferrel, and DeWitte-Aviña 2003: 429. Ibid.: 436–7, 441. Wood, Ferrel, and DeWitte-Aviña 2003: 436–7, 441.

the spread of bubonic plague over distances

193

have been eliminated that the comparison can be taken further and resemblances determined, because this analytical and methodological process has established elements that are in pari materia? Finally, they admit that the inference from the comparison of such diverse materials from so different cultural and organizational settings so many centuries apart “can be challenged on both statistical and substantive grounds,” however, the main objections are methodological. When such methodological weaknesses are linked with erroneous assertions which limit the spread of plague to contiguous spread between rat colonies,114 the outcome will be invalid. Metastatic spread of bubonic plague was observed in the last largescale epidemics of this disease, although none of the advocates of alternative theories has taken notice. The observations of American physicians during the Vietnam War are summarized by Butler who present “three factors responsible for the spread of plague,” of which the second factor is of interest to us: 2. Transportation network. Vehicles carried goods from remote villages to cities, junks and boats transported goods between coastal cities, planes shared in the transportation of passengers, and highways were built. Thus, plague spread from provinces, which were considered as foci, to neighboring provinces along the ways of communication and highways.115

The importance of grain transports was also noted, since plague often arrived in an uninfected locality or town with shipments of rice,116 as was observed also by plague researchers working in Asia half a century earlier.117 Summing up, all advocates of alternative theories misrepresent the work, research and opinions on the mechanisms and modes of spread of plague published by leading plague researchers, from the IPRC to Hirst and Pollitzer. Spread of bubonic plague by leaps over short or long distances is at the heart of their work and their understanding of the disease’s powers of spread.

114 115 116 117

Wood, Ferrel, and DeWitte-Aviña 2003: 444. Butler 1983: 37. Marshall, Joy, Ai et al. 1967: 604–5, 610. Above: 166, 168, 179. Cf. Benedictow 2004: 20–1.

CHAPTER FIVE

MORTALITY IN INDIA Effects of the Anti-epidemic Efforts by British Colonial Authorities In the previous chapter, the subject was introduced of the great efforts made by the British colonial authorities in India to combat plague immediately after its outbreak in Mumbai in 1896. This provides a background for discussions of the assertions first made by Twigg and after him by Karlsson, Cohn, and Scott and Duncan to the effect that the consistently relatively small human mortality rates in India, in sharp contrast to the mortality rates caused by the Black Death, show that the late medieval and early modern plague epidemics must have been different diseases.1 Some of these scholars correctly point out a clear difference in the distribution of mortality, specifically that multiple plague cases in the same household were rather “uncommon” in India,2 but usual in historical plague epidemics, a fact they argue constitutes an independent argument to the same effect.3 Recently, related assertions have been presented by other scholars with respect to the dissimilarity of the temporal progression of mortality in Kolkata (Calcutta) in 1903 and in the Black Death. It may seem that this misunderstanding or misconception is taking hold.4 At the heart of the matter is the fact that all of these advocates of alternative theories have overlooked or ignored important differences between India around 1900 and historical Europe of the plague era which make their use of comparative methodology fallacious. Firstly, they appear to have overlooked the fact that when, in the decades around 1500, it was more widely recognized in Europe that plague was a communicable disease, this brought about great and decisive change. In their monograph, Scott and Duncan mention related subjects on

1

Twigg 1984: 187–9, 195–9; Karlsson 1996: 283; Cohn 2002: 2; Cohn 2005: 1355; Scott and Duncan 2001: 112. 2 IPRC 1907i: 878–81; IPRC 1907j: 922, 956. 3 Cohn 2002: 102, 119–21; Cohn 2005: 1354; Cohn and Alfani 2007: 179, 194–6, 202–3; Scott and Duncan 2001: 361. 4 Wood, Ferrel, and DeWitte-Aviña 2003: 429.

mortality in india

195

pages 118, 204, 278, 283, 358, 366, 379, but without taking them into consideration or understanding the implications, as it seems. Although this early epidemiological theory was distorted by many misconceptions and an incomplete understanding of the epidemiological processes, it nonetheless gave rise to important notions to the effect that it was important to avoid contaminated houses or areas and clothing or goods coming from contaminated persons or areas, and that plague, consequently, could be effectively combated by administrative countermeasures like quarantines of ships, isolation of infected communities and diseased persons, trade embargoes, and so on. On this basis, European governments and municipal authorities soon drove plague back to such an extent as to allow vigorous population growth and recuperation of pre-plague population levels.5 This means that mortality from plague at a generalized demographic level of analysis was reduced to about the average annual level of mortality found in India around 1900 and in the following couple of decades, that is, to a level compatible with population growth. Around the middle of the seventeenth century, European authorities succeeded in stamping out the plague from most of Europe, namely the modernized parts (and, thus, with the exception of Russia, parts of Eastern Europe and Turkish Balkan), rearing its ugly head only on a few occasions when it succeeded in slipping through the anti-epidemic barriers. Against this background, I find it entirely reasonable that the British colonial authorities in India, by using the same countermeasures from the very beginning of the outbreak of plague, including at the outset some of the misguided ones, made substantial and comparable success in the combat of the disease. Lamb, the Director the Indian Plague Research Commission, begins the preface to his summary of the Commission’s research up to May 1907 with the following statement: In the early days of plague in India most strenuous efforts were made to stamp it out by the means adopted in European countries in dealing with epidemic disease.6

5

England’s population started to grow some time in the second quarter of the 1500s (about the same time as in Norway). It is well known that England’s population did not reach pre-plague levels until hundred years after plague disappeared. However, the reason that England’s population recuperated later than most other populations must therefore be unrelated to plague and appears primarily to be associated with the early and strong transition to the so-called western European marriage pattern characterized by relatively late age at marriage and relatively high percentage of permanently celibate persons and consequent relatively low fertility. 6 Lamb 1908: i.

196

chapter five

Thus, from the very beginning of plague in India the British colonial authorities made enormous efforts to combat the disease, and although mistakes were made, especially with respect to the cultural differences between Europeans and Indians in the face of epidemic diseases, these mistakes were soon corrected and the measures adapted to Indian society (see above). This puts into perspective Cohn’s assertion that “the British medical corps in India faced the plague’s mounting annual death tolls from plague with fatalistic resignation.”7 It is true that the British colonial authorities were confronted with the very unmedieval problems of mass transportation of people and goods by railway and steam ships. On the other hand, they enjoyed important advantages over their European predecessors: the new sciences of bacteriology and epidemiology provided a far better framework for integration of empirical observations into a rapidly developing factual understanding of the processes of transmission and dissemination of plague. Of particular importance was the fact that they had at their disposal a vastly superior and larger organization which permitted comprehensive control of travellers and of the transportation of goods. They could also almost immediately implement mass vaccination, and millions of doses of Haffkine’s anti-plague vaccine were administered.8 The truly gigantic scale of the measures implemented from the very beginning can be indicated by mentioning that in February 1897, six months after the appearance of plague, the Municipal Council of Mumbai employed a staff of 30,699 persons in anti-plague work. All travellers leaving infected localities by road or rail were medically inspected, and systematic medical inspection of fugitives from Mumbai by rail was initiated as early as October 1896. When Kolkata (Calcutta) was believed to be threatened, 1,800,000 travellers were medically inspected, 40,000 detained as suspects, and so on. Mass flight out of these cities when plague broke out was partly a solution, and partly a problem to be confronted.9 Importantly, the climate allowed the widespread use of mass evacuation of populations of infected villages into nearby camps. In this

7 Cohn 2002: 240, repeated verbatim in Cohn 2002b: 738. He refers for support to Hirst 1953: 451, where the perspective is very different but not to the relevant pages that would demonstrate that his assertion is contrary to fact and Hirst’s real opinion, Hirst 1953: 115–8, 416–7. 8 Sticker 1910: 438–61. Cf. Simpson 1905: 402–9. 9 Hirst 1953: 115–8, 416–7.

mortality in india

197

early phase, the best measures to restrict mortality from plague proved to be evacuation of infected areas and so-called “health camping,” the effects of which were reported to be “almost magical”. When the population of an infected area could be deported in bulk into the country, leaving the rats behind them, plague returns fell with striking rapidity to zero. Such measures were practicable and were carried out in the case of small towns and villages, but were impracticable in large towns such as Bombay.10

The early conviction among British medical personnel and British authorities that house rats played an essential part in plague epidemics and the early observation that immediate evacuation of the populations of infected local towns and villages into camps in nearby fields until the plague season was over functioned perfectly in the sense that not a single certain instance of a person infected with plague in any of these camps was ever recorded: it is well known that the evacuation of an infected village by its inhabitants and their removal into a temporary camp, if only a short distance away, is one of the best measures for checking an outbreak of plague.11

This gave the anti-plague campaign organized by the British authorities a great and effective strategy which was implemented on a grand scale. In 1907, the British colonial Government appointed a committee of influential Indian gentlemen and placed in their hands funds to be used for measures against plague. This enlightened committee carried out an extensive scheme of operations which resolved itself in instructing the people by holding public meetings and circulating popular pamphlets on the most recent views of the manner in which plague is spread, and urging and encouraging the people by pecuniary assistance and otherwise (a) to resort to evacuation of their houses as soon as rats were observed to be dying, and before cases of the disease occurred among the household, (b) to be inoculated with anti-plague vaccine if evacuation was not possible, (c) to destroy rats.12

Soon, the Indian population recognized the dangers when a person suddenly died from plague or they came across a rat fall in the plague 10 Brownlee 1917–8: 130; the quotation is taken from a comment by a physician who took part in the anti-epidemic work in India at the time. 11 IPRC 1907i: 882. 12 IPRC 1910d: 497.

198

chapter five

season, and it became usual that they immediately and on their own initiative emptied their villages and moved into temporary camps in the fields. For instance in the case of Sion Koliwada:13 On 28th January the occupants of [building] A14 according to their own admission found a dead rat in their house and threw it away. On the same day these people and their neighbours in the other house of the building vacated it and went to live in a building a short distance away, namely building C […]. By the 11th February the Koliwada inhabitants with a few exceptions had removed to a temporary camp in the neighbouring fields a few hundred yards from the village. This action on the part of the villagers was undoubtedly the outcome of severe lessons learnt during the earlier years of plague in Bombay. For the past four or five years [1901–2] they have been accustomed, acting on their own initiative, to leave the village and to go into camp whenever human deaths associated with dead rats begin to occur.15

Similarly, the inhabitants of Belgaum evacuated their dwellings and went to live outside the city, also in huts especially constructed for the purpose, either when there was a plague case in their vicinity or in their family, and also when dead rats were found in their houses—this “caused householders to suddenly vacate their houses.”16 Much of this can be summarized and illustrated by the case of Pune (Poona), a city situated roughly 120 km south-east of Mumbai.17 According to the Government’s guidelines, the chief measures that were adopted until 1907 had been disinfection of infected houses with perchloride of mercury, evacuation of infected houses (when they were not disinfected), isolation of the sick in hospital and inoculation with anti-plague vaccine: there were both a General Plague Hospital and hospitals in the administrative divisions of the city called cantonments to which plague patients were admitted. Also, a campaign against rats had been in force in the city for some years, a rat catching staff had been established consisting of a “Rat Inspector” and ten “coolies” working under the supervision of the Health Officer of the Municipality.

13 Koliwada is Sion village’s northerly part. Map I on Sion village, IPRC 1907h: by page 800. 14 Building A refers to Map II–III on Koliwada, Map II–III, IPRC 1907h: by page 802. 15 IPRC 1907h: 806, 808. 16 IPRC 1910c: 452–3. 17 See also above: 162–3.

mortality in india

199

The Health Officer was responsible for registering all plague cases and to implement suitable anti-plague measures. According to the municipal authorities, during the epidemic of 1908–9 4,900 persons occupied municipal huts in the plague camps, and 5,000 persons lived in private huts in the fields; they also estimate that 15,000–20,000 persons left the city for the surrounding towns and villages. This indicates that around one-fourth of the city’s population evacuated their houses during the epidemic. Furthermore, 16,998 persons had been inoculated with antiplague vaccine.18 Thus, there was in operation a comprehensive anti-epidemic organization which worked efficiently in accordance with modern epidemiological and bacteriological principles and with considerable means at its disposal in order to reduce the impact of plague on the population. The IPRC characterized these anti-plague measures as “elaborate arrangements for the suppression of plague,” emphasizing particularly the importance of the large-scale implementation of preventive vaccination and “the enormous extent” of evacuation, and concluded that “these measures had a marked effect in checking the epidemic.”19 Compared with the epidemiological understanding and the administrative counter-epidemic methods at the disposal of early modern European municipal and government organizations there can be no doubt that the Indian anti-plague organization which operated in Pune was greatly superior. Nonetheless, the historical European authorities succeeded in driving back and eventually in defeating plague and keeping the scourge out of their countries with only a few unfortunate episodes. Why should British colonial authorities in India have not had even greater success? Evacuation of infected local societies as an integral part of the strategy for combating plague is the reason why multiple cases of plague in Indian households were quite rare, in contrast to the situation in medieval and early modern Europe. As the IPRC stated in connection with local studies of plague: “evacuation of houses soon after the finding of plague rats in them appreciably reduces the incidence of plague among the occupants.”20 I have also pointed this out in a paper published in Population Studies in 198721 which was known to Scott and Duncan, 18 19 20 21

IPRC 1910d: 497–9. IPRC 1910d: 534. IPRC 1907j: 959. Benedictow 1987: 427–8.

200

chapter five

who refer to it twice but failed to take into account its central points, which go directly against their theory (see below).22 Since the extent and effects of evacuation in India appear to be poorly understood or known, I here provide a footnote with several references for further reading.23 When Cohn and Alfani in 2007 repeat that the usual incidence and pattern of clustering of multiple cases in the early modern Italian urban centres of Milan and Nonantola is very different from the pattern in India, this does not, as Cohn and Alfani assert, prove that the epidemics were different diseases, since they have not taken into account the effects of the gargantuan anti-epidemic measures implemented in India on the basis of rational modern medicine and epidemiology and the significance of differences with respect to climate and other factors.24 Further, the observation that household members tended to fall ill and die in close succession does not, as Cohn and Alfani assert, prove that historical plague was a viral disease spread by cross-infection: the IPRC commission observed in village studies of bubonic plague in the Punjab that “when multiple cases did occur in a house they were attacked practically simultaneously, as if from a common source of infection.”25 The explanation is associated with the process of the rat epizootic. As rats of a plague-infected rat colony die off, their fleas leave their dead hosts’ bodies and gather on the remaining living rats. When a colony of house rats is severely decimated, over a hundred rat fleas are usually released from each dead rat and they have great difficulties of finding a new rat host. At this point of the rat epizootic suddenly over a hundred and very soon hundreds of rat fleas, many of them infective, swarm in the immediate proximity of the household members, which means that they will be infected closely in time and exhibit the epidemic pattern of falling ill almost “simultaneously, as if from a common source of infection.” Thus, there is nothing pertaining to the Indian plague epidemics with respect to pattern of spread, household clustering of cases or mortality that can be used as evidence against the notion that historical plague epidemics were bubonic plague.

22

Scott&Duncan 2001: 315, 377. Bannerman 1906: 186; IPRC 1906a: 468, 480–1; IPRC 1907f: 711; IPRC 1907h: 806, 808, 812, 828, 830, 833, 840, 842, 870–1; IPRC 1907i: 882; IPRC 1907j: 958–9; IPRC 1908c: 294; IPRC 1912: 210–2; Lamb 1908: 18, 25; Liston 1924: 998. Hirst 1953: 416–7. 24 Cohn and Alfani 2007: 177–205. See also Cohn 2002: 119–21; Cohn 2005: 1354. 25 Lamb 1908: 65. 23

mortality in india

201

For climatic reasons, European populations could not so readily evacuate their houses, but I have noted some examples from fifteenth and sixteenth-century Europe of mass exodus from plague-infected towns into the immediate surroundings, in Alessandria in the Piedmont and in Poitiers in western France, respectively.26 The affluent classes which could afford to leave and stay away for the duration of the epidemic may, to some extent, have practised evacuation from the very beginning, as is suggested, for instance, by Boccaccio in his introductory description of the Black Death in Florence in the Decameron.27 In sixteenth-century Scotland, evacuation of infected houses was implemented on a more systematic basis.28 This behaviour can only be explained on the basis of concrete observation of the plague’s attachment to houses and locality and that moving out was a good way to avoid the disease. Of course, in the case of diseases spread by interpersonal cross-infection, by droplets or otherwise, such action would be useless and quickly revealed as such by the epidemic’s immediate continuation among the evacuees. Analytically, this type of action must be distinguished from another behavioural strategy for evading plague: “When the plague hit an urban center, most of those who could afford it left the town for the countryside.”29 With this background in mind, it would in fact be difficult to understand how high mortality rates, rapid succession of multiple cases, or household clustering of cases could become usual in India, in other words, how the manifestations of plague in India could be similar to the manifestations of plague in late medieval and early modern Europe. The advocates of alternative theories have ignored important research bearing on the matter, excepting Cohn who, as shown above, makes misleading assertions instead.30 Since they have not taken into account important differences between the two parts of the historical comparison, their use of comparative methodology is fallacious. Clearly, the underlying observations are explicable in terms of the effects of antiepidemic organization and epidemiological knowledge of plague. It is not correct that modern bubonic plague did not retain its inherent ability to cause great mortality. Where traditional administrative

26 27 28 29 30

Roccatagliata 1976: 210; Favreau 1967: 354–5. Boccaccio 1982: 11–6. Simpson 1905: 348. Cipolla 1981: 102. Above: 26–69.

202

chapter five

structures more or less broke down and countermeasures of European origin were weakly or reluctantly applied for cultural reasons, as in the case of the Mandarin authorities, bubonic plague showed its old epidemic might. In 1894, probably 70,000 and perhaps as many as 100,000 persons died from plague in Canton. In sharp contrast, when plague reached Hong Kong later the same year, the British authorities managed to keep the mortality down to about 3,000 persons, demonstrating the great efficiency of European epidemic countermeasures.31 To this day, no one has doubted that this was the same disease and contagion that reached India in 1896 in a long-distance metastatic leap by ship. There, the British authorities immediately implemented the same epidemic countermeasures as in Hong Kong, only on a much larger scale, demonstrating their excellent administrative skills and putting to good use the rapidly improving knowledge of the nature and epidemiology of plague disease and recently developed vaccines,32 all to very good effect. One of the previous century’s leading historical demographers, R. Schofield, asked some acute questions in the analysis of the data resulting from a family-reconstitution of the population of Colyton which was ravaged by the plague epidemic of 1645–6. The town contained a population of 1513 inhabitants of whom 298 or about 20 per cent died. He pointed out the crucial distinction that strong clustering by household would indicate a disease spread by the rat flea, while a strong association with household size would indicate a disease spread by cross-infection, because if the disease was spread by cross-infection, infection rates should increase with increasing family size and the consequent increasing household density and intensity of interaction. If this was not the case, the disease would have to be transmitted according to a different mechanism, as for instance in the case of bubonic plague from rats to human beings by the agency of rat fleas. He therefore organized his material on deaths also according to the size of families. The conclusion of the analysis was that “person-to-person transmission of the disease in close physical proximity was not an important element in the Colyton epidemic.” This analysis was followed by another in which the number of persons dying in families was correlated with size of family. It appeared that the number of families with extreme experiences (no-one dying; everyone or almost everyone dying) was greater than would be statistically

31 32

Hirst 1953: 103; Wu Lien-Teh 1936a: 20–1. Simpson 1905: 402.

mortality in india

203

expected by chance, and the number of families with some people dying and others surviving was correspondingly far fewer than would be statistically expected by chance. There was therefore a marked tendency for deaths to cluster in some families, and for other families to escape the epidemic altogether.

The outcome indicated that a person’s chance of dying “had little, if anything, to do with the size of household in which he lived”. Schofield concluded therefore that “it points to a disease whose distribution is largely determined by ecological factors, and the most promising candidate would seem to be bubonic plague with the rat flea as the significant vector.”33 Thus, clustering of deaths in families is not a one-dimensional, mechanical manifestation of an epidemic process. It contains important epidemiological and sociological information which can be revealed by the acute and creative mind of a dedicated scholar and can provide important evidence that historical plague was bubonic plague. For two main reasons, it should not come as a surprise that the British authorities did not succeed completely in their endeavours to stamp out plague: (1) As mentioned above, the Indian population in accordance with ancient traditions and beliefs in relation to epidemic disease resisted some of the effective countermeasures based on modern scientific medicine or European experience. As pointed out by Lamb,34 this resistance caused “the extension of the disease”; (2) Plague in India found an extra-urban murine basis for continuous enzootic existence, which functioned as a murine plague reservoir (plague focus) from which new outbreaks could easily spring.35 In practice, it was impossible to root out murine plague in the large cities like Mumbai where the rat populations were so immense that

33

Schofield 1977: 104–8. Lamb 1908: i. 35 For the period before the Indian Plague Research Commission, see for instance Simpson 1905: 333–456; Indian Plague Commission. Minutes of Evidence: 1998–9; Hankin 1905: 75–6, 78–9; Bannerman 1906: 186, 197–9; Lamb 1908: 25. I would like to underscore the importance of Simpson’s work, the first standard work on plague written on the basis of the early development of modern scientific medicine and on the basis of observations of plague epidemics and plague cases on a large scale. It surprises me that it is possible to read this work and the works of the IPRC and not note the comprehensive anti-epidemic measures that were implemented by the British authorities in India, and see their efforts as a great success story of early modern European governments. See also Hirst 1953: 115, 117, 131–2, 416–7. 34

204

chapter five they could bear the continuous circulation of plague for many years, causing a number of cases between large-scale outbreaks, much as in London in the period 1550–1670.

Some of the anti-epidemic measures applied by the British colonial authorities in India from 1896 were undoubtedly misguided and possibly to some extent counterproductive, especially in the early years, much like the measures applied by early modern authorities. However, they made tremendous achievements, as did early modern European authorities in their combat of plague, by relying on the notion of contagiousness, although they were otherwise dependent on misconceived theories of epidemic disease. For these reasons, it is an error to think that the quite small mortality rates in the Indian plague epidemics constitute evidence that late medieval and early modern plague epidemics were two different diseases. It is also an error to assume that differences in clustering constitute evidence that these waves of epidemics were two different diseases. It is completely untrue that the British colonial authorities made these huge efforts to save lives from plague for any other reasons or motives than European authorities would try to protect their own populations, as Cohn falsely asserts, making groundless accusations of Imperialistic callousness (see above).

CHAPTER SIX

WAS HISTORICAL PLAGUE A VIRAL OR BACTERIAL DISEASE? THE QUESTION OF IMMUNITY Introduction Cohn and Scott and Duncan advocate alternative theories to the effect that historical plague was a viral disease and maintain, in accordance with this view, that survival of plague infection provided persistent and strong immunity. As a rule, bacterial diseases confer only modest and transient immunity in survivors who therefore may repeatedly fall ill from the same bacterial diseases; it is viral diseases such as small pox, chicken pox, measles and mumps that produce persistent and strong immunity in survivors. Most medical authorities on plague who had the opportunity of observing large plague epidemics in the first decades of the twentieth century agree that survival of plague infection conferred only weak and transient immunity (see below).1 If the observation or assertion were correct that survivors of historical plague disease acquired strong and persistent immunity, it would constitute substantial evidence that historical plague epidemics could not have been bubonic plague or indeed any other bacterial disease, and probably was a viral disease instead. Since this type of assertion, like the assertions on the manifestations of plague discussed above, tend to falsify the bubonic plague theory and to justify the search for a tenable alternative, this subject of immunity must also be examined sufficiently thoroughly to decide the matter. Twigg, who advocates a bacterial alternative, has not recognized that there is such a problem and does not discuss it, which in itself can be taken as an indication of the weakness of this case. Theoretically, a dangerous epidemic disease producing high morbidity and lethality rates can produce a violent reduction of a population, but some essential distinctions must be made. Diseases producing strong and persistent immunity in survivors are characterized by strong

1

Benedictow 1993/1996: 126–30.

206

chapter six

limitations with respect to possible long-term demographic effects. In naïve populations (i.e. populations without prior experience with the disease) exceeding 500,000 to one million persons, after a first onslaught which may be dramatic, such diseases will recur in the constituent local societies normally in a five to ten year cycle, in the meantime circulating elsewhere. This is the period needed to bring into existence sufficient numbers of interacting persons without previous infectious experience with these pathogens to allow rise of epidemic spread among them (as distinct from endemic spread). In other words, in ordinary populations there must have come into being a sufficient number of susceptible children to assure that each case of an epidemic disease will be transmitted to at least one other child or susceptible person,2 otherwise no epidemic will arise and the disease’s presence will take on an endemic (sporadic) pattern or disappear. The older populace will contain too large proportions of resistant survivors to be much involved in the epidemic. In the typical mortality pattern of, e.g., smallpox, the rate of mortality in no age group older than 5–10 years amounts to even one-fifth the rate in the age group 0–5 years.3 Even smallpox, which is characterized by high virulence and extraordinary powers of spread, will therefore normally produce modest general mortality rates in populations where adult generations have previous infectious experience with the disease. Scott and Duncan correctly point out that recovered “persons were immune to the smallpox virus for a long time so that each new epidemic swept with high infectivity through only the children who had been born in the interim, of whom about 20% died […].”4 This corresponds to a rate of population mortality of a few per cent, which does not prevent local or regional societies from rapidly recuperating their demographic strength and producing population growth between epidemic outbreaks, so that this epidemic pattern is compatible with long-term population growth. This is a specific reflection of a general pattern which ensures that, in substantial populations, recurrence of acute infectious diseases which produce strong and persistent immunity in survivors will normally have quite limited demographic effects over quite short periods. In order to cause a large-scale and protracted diminution of the

2 3 4

Cf. Scott and Duncan 2001: 37–8. Greenwood 1935: 240. Scott and Duncan 2001: 376.

was historical plague a viral or bacterial disease? 207 population like those witnessed in Europe in the late medieval period, a disease must display a pattern of dramatic recurrence, sparing no substantial sections of the populations. Obviously, epidemic diseases which do not produce good persistent immunity in survivors will have much larger powers of spread, recurrence and mortality than diseases conferring persistent immunity. Consequently, other factors being equal, they will also tend to produce much higher mortality rates over time, since the whole population will be at risk every time they recur. This is therefore a question of considerable epidemiological and demographic importance which will have to be sufficiently discussed to reach a certain conclusion. The analysis above reveals that failure to produce strong and persistent immunity in survivors is an essential property for a disease if it is to function as a causal explanation for the type of demographic developments which took place in the Late Middle Ages. Thus, epidemiological theory militates against the notion that the Black Death and subsequent plague epidemics could have been a viral disease but is compatible with a bacterial disease. Nonetheless, Cohn argues that historical plague epidemics after the Black Death assumed the character of a child disease, and that this shows that historical plague was a viral disease conferring persistent immunity on survivors, a position that will be discussed below. Scott and Duncan, who also maintain that historical plague was a viral disease that should, accordingly, produce immunity in survivors, conspicuously refrain from addressing this question in a focused or systematic way, since children are strongly underrepresented in registered cases of filoviridal diseases, represented by Ebola disease and Marburg disease.5 At various places in their monograph they present a number of purported instances of possibly increased resistance or immunity in persons or populations which have in common that they do not constitute valid material for tenable inference—what they present is speculation without a firm evidential basis.6 Although Scott and Duncan combine the professions of demographer and biologist, they do not discern between incidence as related to degree of risk of exposure to infection and susceptibility. They assert that Pollitzer should have maintained that “adolescents and adults aged

5

Khan 2003: 1167. Scott and Duncan 2001: (104), 121, 139, 145, 155, 205, 232, 281–2, 329, 355–6, 377–8, cf. Index under immunity. 6

208

chapter six

up to 45 years displayed the greater susceptibility.”7 However, Pollitzer states that “according to most observers” “the incidence of bubonic plague was highest in adolescents and in adults up to the age of about 45 years” which is certainly a very different opinion.8 It is, therefore, important to note Wu Lien-Teh’s general statement on the matter: “Most investigators are agreed that, on the whole, differences in the age, sex, racial and also occupational incidence of bubonic plague are due to differences in exposure to infection as brought about by varying modes of life and not to intrinsic causes.”9 Pollitzer supports this position unequivocally when he paraphrases it quite closely: “Most workers are agreed that differences in the race and sex incidence of bubonic plague cases, as well as […] among certain occupational groups […] are due merely to differences in the degree of exposure of the various groups to the infection and not to intrinsic causes.”10 “Differences in the degree of exposure of the various groups to the infection” is a key phrase. Too often it is forgotten that epidemic appearances can be deceptive, because social conditions can systematically affect the intensity of the infective process in relation to particular social groups according to the distributive functions of relative risk of exposure. In this context it must be emphasized that this occurs in ways that mimic the workings of acquired differences in immunity. As explained above,11 at the heart of the matter is the fact that epidemiology is fundamentally a subdiscipline of sociology, and attempts to explain how various social conditions and patterns of behaviour affect the probability of contagion being transmitted to human beings or between human beings in a population of susceptible people. In short, age-specific role-patterns may produce particular risks of exposure and age-specific patterns of morbidity and lethality. This is the essence of Wu Lien-Teh’s and Pollitzer’s statements on the matter. Likewise, changes in mortality rates cannot be taken as evidence of increasing immunity or resistance in a population as Cohn and Scott and Duncan argue. It is important to take into account the fact that human understanding of the contagious nature of epidemic disease may lead to changes in individual behaviour and the implementation

7 8 9 10 11

Scott and Duncan 2001: 139. Pollitzer 1954: 504. Wu Lien-Teh 1936c: 399. Pollitzer 1954: 503. Above: 142–9.

was historical plague a viral or bacterial disease? 209 of more or less efficient countermeasures which will tend to reduce mortality at national, regional and local levels and may affect the social distribution of the intensity of exposure and the relative social incidence of cases. Thus, epidemic case histories can only have evidential value for a particular (type of) disease if there is no alternative independent sufficient explanation. On the basis of the fact that “plagues in Florence after 1424 killed many fewer people than they did in the 14th century,” it is fallacious to infer, as Scott and Duncan do, that this “suggests a greater resistance in the population or a decrease in the virulence of the causative agent,”12 when alternative explanations are not considered. The two main points are that (1) a dramatic fall in the numbers of dead persons can reflect a drastic fall in the population as was the case in Florence,13 and that (2) decreasing rates of mortality are independently fully explicable by cultural and social factors, by increasing recognition and understanding of the contagious nature of epidemic disease which translate into increasingly rational social behaviour and efficient administrative countermeasures in the face of epidemics. In fact, northern Italy is the part of Europe where the Renaissance originated and where effective anti-epidemic organizations were for the first time established, as described by Cipolla in several fine studies.14 This point is also underlined by L. Del Panta in his fine overview of Italian epidemic history,15 and by Ciano in his general study of the development of sanitary precautions for shipping by Italian commercial city states in the period c. 1300–1700.16 Scott and Duncan note the anti-contagious and anti-epidemic actions of populations and authorities in England several times in their monograph, but only incidentally. They do not consider the fundamental significance and explanatory potential of these developments, and the likelihood that along the time axis of this historical process mortality rates would tend to decline independently of their discussion of immunity and resistance.17 This implies also that they have not understood the central aspects or core of Slack’s monograph which they refer to several times, in which he shows how increasing understanding of the nature of epidemics

12 13 14 15 16 17

Scott and Duncan 2001: 376. Herlihy and Klapisch-Zuber 1978: 165–88. Cipolla 1973, 1976a, 1976b, 1977, 1978, 1979, 1981, 1986. Del Panta 1980: 187–91. Ciano 1976. Scott and Duncan 2001: 118, 204, 356, 358, 366, 379.

210

chapter six

induced people to change behaviour and authorities to implement measures for protection of the population, leading to the disappearance of plague from England after the last Great Plague of 1665–6.18 When plague disappeared from the British Isles after 1666, is the reason that immunity or resistance had become total or that plague bacteria had completely lost their virulence? It appears that Scott and Duncan do not recognize that at the heart of their line of reasoning is the concept of lethality, also called case fatality or case mortality: increasing resistance and/or decreasing virulence will be reflected in reduced case mortality rates and can only be tenably studied in this perspective. I have done my best to collect and present all historical and modern information on lethality in plague epidemics, covering the period from the mid-fifteenth century in Italy to modern studies in developing countries, and in the past eighteen years I have not come across additional material. The conclusion of this study of lethality is that lethality in plague epidemics appears to have been quite constant throughout the whole period and at the same level in historical epidemics and in developing countries (before the advent of efficient medication), namely about 80 per cent.19 This represents a strong indication of stable level of virulence and that historical and modern plague epidemics were the same disease. This strong indication of stability of plague virulence is strengthened further by the establishment of an empirically well-founded explanation. The reason for this stability of virulence over such a long period is the close relationship between the virulence of plague bacteria and their ability to cause blockage in fleas on which they are dependent for securing transmission to new hosts and their survival as a strain of a species with particular genetic properties for this process. Milder strains are often observed in laboratories, but these cannot satisfy the relentless demands of natural selection for the survival of the fittest, thus, only the highly virulent strains remain in operation. These findings, which were originally made by Soviet scholars,20 have been supplemented and supported by later Western research.21 Some of this

18

See my review of Slack’s monograph in Benedictow 1989: 655–9. Benedictow 1993/1996: 146–9. 155. The only piece of information on this subject I have found later is IPRC 1910c: 468. 20 Tiflov 1964: 181–98; Bibikova and Klassovskiy 1974: 115–23; Bibikova 1977: 28. Cf. Benedictow 1993/1996: 241–2. 21 Hinnebusch, Perry and Schwan 1996: 367–70. 19

was historical plague a viral or bacterial disease? 211 Western research is known by Scott and Duncan who have recognized a couple of points of importance, for instance, the general point that “the evolution of the pathogen is highly dependent on this coupling between transmissibility and virulence” and that “only those fleas that were infected with normal [plague] bacteria developed blocking.” However, they do not recognize the link to the high and constant level of virulence of plague bacteria and the consequent high and stable lethality rates characteristic of bubonic plague.22 They cannot, therefore, recognize the strong argument which these findings represent against their opinion of increasing resistance and immunity and therefore against their alternative theory. The constancy of a very high lethality rate reflecting an underlying constancy of virulence, which is characteristic of plague, is at variance with the typical historical tendency of reduction in the virulence of diseases which are spread by cross-infection. This tendency of weakening virulence occurs because highly virulent strains tend to kill their victims rapidly and will tend to have lower success rates of transmission and therefore fewer opportunities to reproduce their genetic properties. Weaker strains which cause milder and more protracted courses of disease will more often succeed at being transmitted and will therefore increasingly establish genetic (pre)dominance.23 Scott and Duncan touch rather casually upon this subject without showing recognition of its significance.24 These aspects of plague disease and plague history are compatible with Cipolla’s findings that the reduction in the importation and spread of plague and the related diminution of population mortality from the mid-fifteenth century to the mid-seventeenth century are due to increasing human understanding of contagiousness and ability to translate this understanding into anti-epidemic behaviour and rational administrative anti-epidemic actions, which may serve to explain Cohn’s disparaging attacks on him.25 This brief analytical and structural discussion paves the way for identifying some decisive criteria which this viral-immunity theory must satisfy in order to be viable or tenable:

22 23 24 25

Scott and Duncan 2001: 64–5. See, for instance, Greenwood 1936: 240–3. Scott and Duncan 2001: 376. Above: 60–2; below: 226, 293–4, 352–3.

212

chapter six

(1) absence of re-infection of survivors; (2) after the first outbreak of an epidemic disease in a naïve or previously unaffected population, which may cause havoc in people of any age, gender, or social class, recurrent epidemics will tend to cause relatively small mortality rates because large proportions of the adolescent and adult population are immune; (3) corollary: recurrent historical plague epidemics take on the character of a child disease. These questions will be discussed (further) in the subsequent subchapters. Re-infection or Immunity? Neither Cohn nor Scott and Duncan take interest in the question of re-infection which is so crucial to their theories, which are based on alternative assumptions of viral contagion. If their theories were correct, re-infections should not occur or be exceedingly rare, and even the single incidental mention in historical sources would be surprising. As mentioned above, most medical authorities on plague who had the opportunity to observe large epidemics of plague in the first decades of the twentieth century and therefore to observe the potential for reinfection agree that survival of bubonic-plague infection confers only weak and transient immunity, as would be expected in the case of a bacterial disease. Meyer states, for instance: The immunity which follows a natural plague infection is probably temporary and relative in nature. De Langen and Lichtenstein state, in their Textbook of Tropical Medicine, that “reinfection with plague may occur within a few months; surviving an attack gives but a very limited immunity.”26

A decade later he reiterated his position in a standard work on microbiology.27 The other standard monographs on plague similarly state tersely that survival from an attack of plague confers only a transient and weak immunity.28 Pollitzer states in his central standard work that

26 Meyer 1946–7: 434. Meyer’s citation contains a number of small insubstantial deviations from the original text. De Langen and Lichtenstein 1936: 195. 27 Meyer 1957: 414. 28 Sticker 1910: 265; Dieudonné and Otto 1928: 256.

was historical plague a viral or bacterial disease? 213 immunity to this disease, acquired under natural conditions, was evidently relative in degree and limited in duration.29

This means that re-infections of survivors of bubonic plague should be expected to occur and be recorded both in connection with modern plague epidemics and historical plague epidemics. If this prediction can be corroborated, the alternative theories of Scott and Duncan and Cohn are ipso facto invalidated. The views of the authors of the standard works on plague to the effect that acquired immunity in survivors was weak and transient imply that re-infections were observed. In fact, re-infections have been documented in modern epidemics, for instance in India by the Indian Plague Commission and other medical observers: one case was a woman who had first contracted plague in Hong Kong in 1894 and subsequently contracted the disease in Mumbai in 1896; another person, a native Indian, fell ill from plague 30 October 1896 and again 2 December. It was also noted that subsequent attacks could be survived or end in death.30 Wu Lien-Teh recorded the case of a patient who contracted bubonic plague only four months after having recovered from primary pneumonic plague.31 There are numerous other observations of re-infections in historical plague epidemics which, because of the crucial importance of this topic and its great evidentiary powers, will be discussed in detail in the pages that follow. Beginning around 1700 medical science had developed to a level where empirical observation and systematic study led to quite detailed accounts of individual cases in epidemics, including cases in plague epidemics, and this produced quite frequent and welldocumented observations of re-infections. For this reason, I will documentation will begin by describing these observations to provide a background for earlier historical observations. Historical observations of re-infections were first collected by Sticker.32 G. Kirchoff, the physician, in 1714 published his observations of the Austrian plague epidemic the preceding year,33 and he relates that persons who had survived bubonic-plague disease in a previous epidemic or had survived plague disease in the present epidemic 29 30 31 32 33

Pollitzer 1954: 138. Simpson 1905: 294–6; Sticker 1910: 437–8. Wu Lien-Teh 1927–8: 84, fn. 4. Sticker 1910: 434–8. See Sticker 1908: 449, bibliography.

214

chapter six

contracted plague again. During the epidemic of 1720–2 in southern France, J.B. Bertrand observed some persons who were attacked three times.34 Bertrand’s work was published in English translation in 1973 and is used and cited by Scott and Duncan, who nonetheless do not take note of these observations.35 In a contemporary study of the plague epidemic in Aleppo in 1760–2, P. Russell recorded twenty-eight cases of re-infection among 4400 plague cases, and several of the patients contracted plague more than twice.36 G. von Orraeus, the Finnish physician, observed re-infections in the Moscow epidemic of 177137 as did D. Samoilowitz, the Ukrainian epidemiologist, who himself contracted plague three times.38 A. Chenot mentions several cases of re-infection which he observed in the plague lazaretto at Kronstadt in 1755, among them his own servant who contracted plague three times, at the end of June, in mid-September, and in November when he died.39 In an Egyptian plague epidemic in 1834–5, A.B. Clot-Bey observed so many re-infections that he argued directly against the notion that survival of plague conferred significant immunity according to the pattern of small pox.40 Of course, at the time bacteriology was not established as a medical or microbiological discipline and the vital differentiation between bacteria and viruses and their immunity effects had not been made, thus, the difference could not be understood or explained, only observed. By implication, re-infections in earlier historical plague epidemics should be expected, and if documented, this would constitute strong evidence that these plague epidemics could not be a viral disease but could be bubonic plague. In fact the history of observation of reinfections of plague is as old as the history of plague in Europe. Sticker collected a considerable number of statements on this subject by physicians of the past. He points out that Evagrius observed numerous cases of re-infection in the Justinianic epidemic of the early 540s,41

34

Simpson 1905: 296. Scott and Duncan 2001: 338–9. 36 P. Russell 1791: 190. See also Simpson 1905: 296. 37 Gustavus Orraeus, Descriptio pestis quae anno 1770 in Jassia et 1771 in Moscua grassata est. Petrepoli [St Petersburg] 1784. Cit. Simpson 1905: 296. Sticker 1910: 436, 467. 38 Kowal 1972: 434–46. 39 Sticker 1910: 334. Cf. Sticker 1908: 433. 40 Clot-Bey 1851b: 89: “nous avons vu de fréquentes récidives.” Sticker 1910: 437. 41 Sticker 1910: 434–8. Cf. Meyer 1946–7: 434. 35

was historical plague a viral or bacterial disease? 215 a point that was first made by Clot-Bey in 1851.42 Surprisingly, there are quite numerous observations of re-infections in the period 1480–1714, most of them are registered by Sticker,43 and I have come across some other instances. This material on historical cases of re-infections will be presented in chronological order. Marsilio Ficino [Marcilius Ficinus], the Florentine physician and philosopher (1433–99),44 observed several cases of re-infections in the epidemic of 1478:45 And say not that he who has survived from the disease once cannot any more succumb, because one of our Florentines fell ill three times in this year: the first two times he survived intact; the third time he could not survive. Again, in this year, in September, I cured a woman completely of plague, becoming as sound as any other person, then she conversed with diseased and fell ill again eighteen days later and perished.46

This is a work that Cohn knows well, as he refers to it at least eight times, but he has apparently overlooked this piece of information that is incompatible with his theory.47 Again one should note that a person could be attacked three times in the same epidemic and also the brief time that elapsed between the time a person had completely recovered and fell ill again, which explains how the disease could be contracted three times in the course of the same epidemic. W.P. MacArthur found information about a baker’s wife who contracted plague three times in the London Epidemic of 1563, first around mid-summer, then in August, and then again at the end of September, when she died.48 A. Massaria, the Venetian physician, relates in his two-volume work on plague of 1579 that he observed numerous cases of re-infection in

42

Simpson 1905: 296. Sticker 1910: 434–8. 44 See Bibliography in Sticker 1910: 502. 45 Del Panta 1980: 118, 128. See also fn. 49. 46 Ficino 1983(/c. 1481): 105. My translation from the original text which is written in the vernacular. For dating see Cosmacini 1979: 22. 47 Cohn 2002: 62, 95, 133, 209, 214, 230, 231, 240, where he refers concretely to pages 56, 57, 92, 109, 110, in Ficino’s work but has apparently not seen page 105. Cohn states repeatedly inaccurately that Ficino related to the epidemic of 1480, but there was not plague in Florence this year. Ficino makes it clear on page 109, to which Cohn refers, that this epidemic occurred in 1478, the year identified also by Del Panta in his history of Italian epidemics (see fn. 45). 48 MacArthur 1925–6: 358. 43

216

chapter six

the Venetian epidemic of 1575–749 which swept away 46,752 of the city’s c. 180,000 inhabitants.50 In the epidemic in Rotterdam in 1624–5 a woman contracted plague twice and survived both times.51 John Woodall, physician at St Bartholomew Hospital in London, who published a plague tractate in 1639, informs his readers that he contracted plague twice and developed buboes both times. This case is mentioned also by Creighton52 and on a page which Cohn asserts that he has read and refers to in the accompanying footnote.53 I. Diemerbroeck, the famous Dutch physician (1609–74), published a plague treatise in 1644 based on observations of the plague epidemic in Flanders in 1636–7. In this work he set new standards of empirical approach and scientific rigor and he introduced, among other things, the standard of providing numerous case histories in which the disease was clinically described in some detail. His treatise was rightly admired by contemporaries and posterity and it was published posthumously in English in 1722. He states that he had seen many persons who contracted plague twice, among them a knight who after having recovered completely fell ill from plague with a bubo a second time five weeks later. G.O. Giseler, the physician, published his medical observations on the plague epidemic at Brunswick (northern Germany) in 1657:54 he noted, among other things, that several children in a family contracted plague a second time, when most of them died, while other persons died in the third attack. W.G. Bell cites Dr Hodges who wrote after the plague in London 1665: “I have known many infected who although all things succeeded well the first and second time, and each cure was perfected, yet the third seizure, upon the account of a new infection and not a relapse, hath proved fatal to them.”55 A prominent Capuchin priest contracted bubonic plague twice in the plague epidemic in Mainz in 1666. Ludwig von Hörnick, Dean of the Medical Faculty in Mainz, contracted plague twice and survived both times.56 The Nordic experience agrees with this material. M.G. Block, the Swedish physician who wrote an extraordinarily valuable account of

49 50 51 52 53 54 55 56

See Bibliography in Sticker 1908: 456. Del Panta 1980: 146. Moquette 1925: 19. See also Creighton 1891: 122. Cohn 2002: 212 and fn. 73. See Bibliography in Sticker 1908: 442. Bell 1951: 213, (244). Sticker 1910: 436.

was historical plague a viral or bacterial disease? 217 his observations during the plague epidemic in Norrköping in 1710–1, states: “I never imagined that a person who so recently had been to bed with plague, should so soon be attacked again, as it happened.”57 Inspired by Diemerbroeck, Block provided detailed and acute observations of the epidemic process and numerous detailed clinical case histories and descriptions which leave no doubt about the nature of the disease: it was bubonic plague. This links Nordic plague history chronologically with European plague history, where it continues with the observations of Kirchoff and Bertrand, and so on. As can now be seen, and without forgetting Evagrius’s observations, there are numerous records of re-infections in historical plague epidemics, starting in 1478 and becoming quite frequent in the period 1563–1835. Records on observations of re-infections in plague epidemics begin as far back in time as one could reasonably expect that the development of culture, mentality and sources would convey such information to posterity, demonstrating that re-infections were a normal part of historical plague epidemics all over Europe. Also the continuity in time and European geography is interesting, particularly because Scott and Duncan are willing to accept that the epidemic in southern France 1720–2 was bubonic plague. These observations can, as shown above, be readily linked with similar observations in India from 1896. I will submit that the material on case histories of re-infections presented above constitutes substantial evidence that historical plague epidemics cannot have been a viral disease, but could according to the criterion of re-infection have been a bacterial disease, for instance, bubonic plague. Since many of the physicians who provided these case histories also specifically mention that these cases had plague buboes or pestilential buboes, I submit that this combination of information constitutes crucial evidence to the effect that historical plague epidemics were bubonic plague. As is shown below, buboes as a normal clinical manifestation of epidemic disease are an exclusive feature of bubonic plague and constitute therefore a defining feature of this disease (see below). This combination of information of buboes and re-infections constitute a coherent pattern of clinical manifestations which constitutes evidence of bubonic plague.

57

Block 1711: 104. My translation from Swedish.

218

chapter six Did Plague Become a Child Disease after the Black Death?

At the core of Cohn’s monograph is the alternative theory that historical plague was a viral disease, albeit with very different apparent properties from the viral agent of Scott’s and Duncan’s alternative theory, almost as different as possible. At least one of them must for this reason alone be incorrect, at least one of these theories must have been constructed from virtually nothing, at least one of them must be the outcome of a great input of unscientific and unscholarly work. Since Cohn’s alternative is a completely unknown disease which is presumed to have disappeared long ago, the testability of this theory is problematic but not impossible, since the compatibility of observed epidemic manifestations with a viral disease can be studied. This can be a useful approach, although the fact that no new disease has appeared in the significant number of studies of microbiological DNA taken from the skeletal remains of historical plague victims,58 whilst Yersinia pestis is systematically found, could justify the dismissal of Cohn’s theory as being based on a phantom disease. As the only advocate of an alternative theory, Cohn argues that plague epidemics subsequent to the Black Death assumed the character of a child disease which must reflect the fact that a large proportion of adults had survived previous plagues and acquired good and persistent immunity, the susceptible part of the population being to a large extent children born later, a characteristic manifestation of viral diseases. His view is based on an analysis of the Necrology of the Monastery of San Domenico in Camporegio in Siena (see below) and statements by some contemporary chroniclers who call the epidemic of 1360–3 a child disease, pestilentia puerorum, pestis puerorum, “la mortalite des enfauntz,” and the like, and the fact that a few plague epidemics up to 1400 were characterized in this way by some chroniclers.59 In his words: “after several strikes, it became domesticated as a disease largely of children,” and “by the end of the [fourteenth] century it had become largely a disease of children.”60 This is obviously at variance with the material on re-infections presented on the previous pages and also with the constant and high levels of lethality documented above. It is also very problematic for a number of other reasons, as will be seen below. 58 59 60

Below: chapter 10: 381–95. Cohn 2002: 213. Cohn 2002: 212, 238.

was historical plague a viral or bacterial disease? 219 In Cohn’s monograph, which purports to study the greatest demographic catastrophe ever caused by an epidemic disease, Cohn has no chapter or section focusing on mortality rates in the Black Death or subsequent plague epidemics. This is a reflection of his weak interest in demography and consequent unfamiliarity with demographic science and its emphasis on stringent concepts, intensive analysis and hard facts. His monograph contains only a couple of attempts at producing demographic data, and as we shall see below, his handling of demographic material is gravely flawed. My endeavours to collect Cohn’s statements or views on mortality rates in order to form a general impression of his opinion on the matter by use of the entry “mortality” in his index led nowhere, and the subentry “statistics of ” does not contain a single piece of statistics in any scholarly meaning of the term, only untestable, subjective and arbitrary assertions of the chroniclers’ opinions. In a section on epidemiology within a chapter on “Chroniclers and Doctors” Cohn insouciantly discusses mortality in the Black Death over a few pages by citing various chroniclers’ more or less fanciful or absurd assertions.61 Nearly 200 scientific demographic studies of mortality in various localities caused by the Black Death are all ignored.62 Readers interested in this subject are referred to my monograph on the Black Death. Cohn’s chronicle-based material on mortality in the Black Death serves as a basis for his subtheory that plague developed into a child disease in the subsequent epidemics. Cohn consistently ignores the available demographic studies of mortality in the second plague; this means that his subtheory that plague developed into a child disease is not based on hard demographic facts. Instead, he builds his case on chroniclers and a minimalistic application of source-criticism. This approach has the strangest consequences in the eyes of an historical demographer (see below). I have above made clear my reservations and cautiousness in relation to medieval chroniclers and the need for unrelenting source-criticism and independent testing of their assertions. Late medieval chroniclers have a wide range of opinions, many of which all modern scholars would reject as superstitious, prejudiced, ignorant or plainly wrong. Most chroniclers believed in an other-worldly explanation of epidemic disease, specifically that it was an expression of God’s wrath over man’s

61 62

Cohn 2002: 106–9. Benedictow 2004: 272–376.

220

chapter six

sinfulness. No modern scholar would accept their alternative miasmatic causal views on epidemic disease and the mechanisms of epidemic spread or those of contemporary physicians who were the chief proponents of miasmatic theory.63 Chroniclers’ opinions on subjects related to demography or social science and their notions of numbers tend to be demonstrations of ignorance, subjectivity and rhetorical extravagance. Their assertions with respect to mortality in plague epidemics vary enormously and are quite often rhetorical exaggerations or phrases not intended to be accepted at face value as factual. When they can be tested on independent material they quite regularly prove to be not just unrealistic but outright fanciful, bizarre or absurd. According to one chronicler, 57,000 people died from the Black Death in one month alone in Marseilles, which Twigg, for instance, accepts as credible information.64 However, Baratier, the outstanding demographer of medieval and early modern Provence, estimates the number of inhabitants before the catastrophe at only 15,000,65 which makes it understandable but not credible that another chronicler cited uncritically by Cohn asserts that the city became “uninhabited.”66 Similarly, Cohn uncritically cites the fanciful figures of another chronicler who maintains that in Avignon 62,000 persons died in the three months following 25 January 1348 and that the epidemic peaked on 14 March when 11,000 bodies were buried.67 There is no way that Avignon could have had over 35,000 inhabitants on the eve of the Black Death,68 and the only reason Cohn believes that the epidemic peaked 14 March is that he accepts the chronicler’s ludicrous fantasy figure. The epidemic in Avignon lasted seven months, so if we accept the chronicler’s figure, 62,000 persons died before half the epidemic period was over. Assuming that the disease was bubonic plague with a normal lethality rate of 80 per cent,69 this would mean that 77,500 persons had 63

Above: 78–84. Below: M377–8. 65 Baratier 1960: 66–7. 66 Cohn 2002: 102. 67 Cohn 2002: 141. 68 Pounds 1974: 261 and 266. At the beginning of the fourteenth century, Avignon was in the category of a large medieval city containing 10,000–25,000 inhabitants. The arrival of the papal court in 1309 meant an influx of over 4000 court functionaries and the city’s population may have increased by around 10,000 inhabitants. 69 All data on lethality rates in historical and modern plague epidemics are presented in Benedictow 1993/1996: 46–149. 64

was historical plague a viral or bacterial disease? 221 contracted plague, and a population far above 100,000 persons is indicated. Cohn arbitrarily (but not consistently, as will be seen) implies a much lower lethality figure for his unknown viral disease since he also assumes that the survival rates were sufficient to turn the subsequent plagues into a child disease, thus he implies in this case a correspondingly very much higher population. This view is well adapted to the chronicler’s assertion that 150,000 persons died in the Black Death in Avignon.70 If half the population perished in the epidemic, this implies that Avignon’s population was 300,000 persons, almost as many as the whole population of Provence (350,000–400,000) at the time,71 twenty times higher than Marseilles’ population, three times bigger than Florence’s, and very much larger than Paris’s population, which was probably twice as big (200,000) as any other city in Europe at the time. Interestingly, Sticker cites a Dutch canon to the effect that 11,000 persons were buried in Avignon in the six weeks after 13 March.72 This is only a small illustration of the nonsense that results from placing any faith in chroniclers’ population figures or mortality figures and the unrelenting need for merciless source-criticism and material testability on the firm grounds of scientific historical demography. Obviously, no person with elementary knowledge of demography and source-criticism would land in such outlandish trouble. While reading Cohn’s monograph the warning of John Hatcher, the leading scholar of medieval demography in the world today, regularly comes to my mind: “substantial advances in knowledge and technique have enabled us to proceed far beyond the overwrought imaginings and hopelessly inaccurate quantification of the chroniclers.”73 In short, chronicles are unusable sources for serious demographic research; all serious demographic research is based on registrations of populations, manorial records, tax lists, burial lists, censuses, and the like. It is the uncritical use of chronicles by Twigg, Scott and Duncan, and to an incredible extent, Cohn, which makes it necessary to emphasize this elementary point. Cohn employs the “overwrought imaginings and hopelessly inaccurate quantification of the chroniclers” in order to construct a basis for, among other things, his immunity argument with its obviously important implications for the possibility of developing an alternative theory 70 71 72 73

Sticker 1908: 57. Baratier 1960: 67. Sticker 1908: 57. Hatcher 1977/1987: 21.

222

chapter six

of plague. Cohn takes medieval chroniclers at their word, or more accurately, some medieval chroniclers at their word, when they state that plague epidemics took on the character of child disease. This implies that he considers contemporary chroniclers’ use of the concept of child disease reasonably equivalent to a modern medical scientific concept of child disease, and to be useable in a modern monograph of epidemic history without a significant input of source-criticism, demography, epidemiology and social science. Representativeness is a crucial tenet of the methodology of social science and source-criticism. According to this tenet, presentation of some chroniclers’ opinions to the effect that children suffered supermortality in plague can only be accepted as methodologically valid material for inference, and therefore as material of scholarly value or interest, if the following necessary condition is fulfilled: it must be demonstrated that it is not possible to present a more or less similar number of chroniclers’ opinions to the effect that plague had (an)other marked specific social predilection(s) according to age, gender, social class or occupation, for example that plague had a predilection for women, or for men or for the poor or for noblemen or, conversely and importantly, that many chroniclers did not observe any special social predilections, and so on. There is a methodological and source-critical condition or demand that Cohn demonstrates that his collection of data is not a biased and unrepresentative sample resulting from a single-minded quest for statements on child mortality, selected and gathered to serve his alternative viral theory, but is, in fact, generally representative of chroniclers’ statements on plague’s social predilections. A discussion of this issue can only begin with the second Europewide plague epidemic of 1360–5 on which Cohn focuses. It is easy to illustrate the inherent methodological fallacy of Cohn’s approach. Cohn states that “numerous chroniclers in Britain […] noted that it [the second plague of 1361] struck down greater proportions of children than the first, so much that they called it ‘the child plague,’ ” and cites one chronicler and refers to some other chroniclers to this effect, which he believes supports his view of the viral immunity effects among survivors of the Black Death.74 Whether the word “numerous” is an apt

74

Cohn 2002: 213.

was historical plague a viral or bacterial disease? 223 term is open do debate; the term “several” is probably more appropriate. Among the chroniclers he refers to but does not cite is Henry Knighton’s chronicle, which, however, takes a more complicated view: it mentions “the Second Pestilence ‘in which great and less died, but especially young men and children.’ ”75 Knighton appears to have made quite a composite observation of the social pattern of supermortality and by implication of submortality among various social classes and other demographic categories. He certainly emphasizes supermortality among children, but also among young men who, being differentiated from children, must be assumed to be older than twelve or fourteen years and thus to have lived through the Black Death, and also among the upper classes and the lower classes, and it is a relative emphasis, not a description of more or less overwhelming dominance of children. It is intriguing to consider why young men should have had much less immunity than young women? And what happened to the middle classes? What is it that Knighton observed, if that is what his text reflects? Even a quick glance at Shrewsbury’s presentation of this second British plague epidemic provides a much more complicated picture of contemporary observations of the pattern(s) of mortality in this plague epidemic of 1361. “Adam of Murimuth calls it a great mortality and records that ‘of it there died in England some outstanding people and noblemen, and a very large number of churchmen, both secular and regular.’ ” The chronicle called “The Brut notes that it especially slaughtered men, whose wives ‘as women out of control,’ proceeded to consort with any men that were available.’ ” John of Reading describes the mortality pattern as sexum masculinum valde consumens, meaning that the plague had a very strong predilection for, or to a very high degree consumed or destroyed the male sex, which again raises the question of why men should be much less immune than women. In the Calendar of the Close Rolls, which is not a chronicle but which in this case provides a contemporary observation of much the same character, it is stated on 10 May 1361: “great multitudes of people are suddenly smitten with the deadly plague now newly prevailing as well in the city of London as in neighbouring parts, and the plague is daily increasing.”76 Jean de Venette, the prominent contemporary French chronicler, 75 76

Shrewsbury 1971: 128. Shrewsbury 1971: 127–8.

224

chapter six

asserts that there was substantial mortality in Paris, “notamment parmi les pauvres”=“especially among the poor.”77 As can now be readily seen, it is possible to select a number of chroniclers’ statement on the differential social impact of this plague epidemic to the effect that it especially swept away men or adults or the poor. Taken together, the chroniclers’ statements could also be interpreted to indicate that this plague epidemic hit seriously various main social categories with respect to age, gender and social class, but perhaps not so much women. However, women apparently tended to be present in the chroniclers’ minds primarily as morally weak or outright immoral sexual beings and to be out of focus as a demographic category, which may raise doubts and inspire source-criticism or outright source-scepticism. There will be occasion to return to Cohn’s statement cited above. It is important to remark that the scholarly meaning of the concept of “infectious child disease” is not, as Cohn would like us to believe, a disease with disproportionately high distribution of epidemic cases among children. Most modern medical textbooks on child infectious diseases do not consider the term “infectious child disease” or “infectious paediatric disease” to mean a disease with an imbalanced distribution of cases between different age groups. Instead, they define infectious child diseases as diseases spreading among and between children independent of proportions in different age groups.78 Thus, there are two highly different concepts of infectious child disease with very different operational properties, and Cohn’s intuitive understanding of the concept is not self-evidently valid, but it does serve his purpose. In the present discussion, this intuitive meaning will be the focus of endeavours to clarify its scientific, medical and demographic connotations and validity. According to Hatcher, Christ Church Priory in Canterbury was visited by plague during fourteen years between 1413 and 1507, that is on the average once every 6.7 years; if we take into account the fact that on two occasions the same plague epidemic appeared also a second consecutive year, the number of epidemics was twelve and plague epidemics recurred on the average every 7.8 years.79 If the plague epidemics were as frequent among the population from which the monks were recruited, which must be a rather cautious assumption, many monks 77 78 79

Glénisson 1968–9: 32. See for instance Donowitz 2003: 17. Hatcher 1977: 17; Hatcher 1986: 29–30.

was historical plague a viral or bacterial disease? 225 must be presumed to have survived at least one, often two plague epidemics as a child, before they entered cloistered life (age at profession for all novices was eighteen years80). However, the monks suffered great mortality from plague. So what happened to immunity? In his huge corpus of wills produced in southeastern England in the period 1430–80, Gottfried registered evidence of eight plague epidemics in these fifty-one years which correlate well with other contemporary registrations of plague epidemics; on average, a new epidemic occurred every 6.4 years.81 And there are many large collections of wills from this period which exhibit tremendous increases in numbers during periods of plague.82 But why would adults abruptly start making wills in the face of a threatening plague epidemic if they mainly were immune? And surely the pervasive immunity of those who had survived plague in childhood or adolescence must have been conspicuous, people must have observed that those who had survived the plague rarely contracted the disease again? Mortality of children would not be relevant to adult fear of dying intestate. So what happened to immunity? In Norway, there were three grave plague epidemics in the years 1521–9(−30); in 1525 and in 1529 the epidemics were in the southeastern region, and both must have started in Oslo and spread out of the town over the region. So what happened to immunity?83 In my history of plague in Norway, I have registered as fully as possible all plague epidemics in Norway, England, the Netherlands and northern Germany in the period 1348–1666, which made it possible to create comparative tables for the periods 1348–1500 and 1500–1666.84 I registered fourteen plague epidemics in England in the 1500s, on the average a new wave of epidemics every 7.2 years, and seven epidemics in the period 1600–66 indicate on the average a new epidemic every 9.5 years. Much the same pattern occurred in the other countries. Norway mostly imported plague from England and thus showed much the same temporal rhythm.

80

Hatcher 1986: 27. In the period 1430–80, there appear to have been seven epidemics of plague in England of a national or extra-regional scale, in 1433–4, 1438–9, 1452–3, 1457–9, 1463–4, 1467, 1471–3, and 1478–80; locally there were many more. 82 Some of them are mentioned or presented in Benedictow 2004: 81, 106, 119, 121, 135–7, 178, 197–8, 272, 336. 83 Benedictow 2002: 131, 146–56. 84 Benedictow 2002: 102–09, 129–37. 81

226

chapter six

In the period 1500–1666, the quality and quantity of textual sources increased greatly, which is reflected in modern archives. So why has no earlier scholar asserted that the historical plague epidemics of the period exhibited the general pattern of child disease and acquired immunity? The answer is very clear, because there is overwhelming demographic evidence that this was not the case, that the mortality rates among the adult population were usually tremendous in all of these epidemics, which also explains the very strong correlation between the mass production of wills and plague epidemics. This is the reason that scholars who have made comprehensive in-depth studies of historical plague epidemics have not so much as hinted that post-Black Death plague epidemics took on the character of child disease. Since Cohn mainly bases his assertion on this point on English and Italian material, it must be emphasized that E. Fiumi, M. Livi-Bacchi, L. Del Panta and C.M. Cipolla, the highly admired Italian historical demographers, have not observed plague as a child disease at any time during the plague period in Italy. This seriously undermines Cohn’s assertion on this point and may also serve to explain his ill-natured attacks on Cipolla’s work85 and why the important works by Fiumi, Livi-Bacchi and Del Panta are passed by in silence. No Italian historian has formed such an opinion; it is Cohn’s arbitrary idea. The same is true of all of the prominent scholars of English medieval and early modern demography and epidemic history, Postan, Russell, Shrewsbury, Hatcher, Slack, Schofield, and Wrigley. Prominent French and Dutch scholars in this field of research like Biraben, Dubois, Nordergraaf and Valk have also failed to note any such development, and this is also the case with the authors of the first volume of Histoire de la population française,86 the authoritative summary of French demographic history. Nordergraaf and Valk have registered a plague epidemic somewhere in the Netherlands about every year from the time their registration starts in 1450 until the last plague epidemic in 1668. In some urban centres plague epidemics broke out in quick succession, in Amsterdam for instance in 1550, 1554, 1557, 1558, and 1559, and in 1616, 1617, 1618, 1623, 1624, 1625, 1626, and 1629.87 So what happened to immunity? This evidence and perspective makes it urgently necessary to examine Cohn’s evidence. However, in order to understand the significance

85 86 87

Above: 60–1, 209, 226, 293–4, 352–3, and in subsequent contexts. Dubois 1988: 324–66. Nordergraaf and Valk 1996: 225–8.

was historical plague a viral or bacterial disease? 227 of his evidence, suitable analytical tools are needed. Unavoidably and centrally, the concept of child disease must be clarified. Such a clarification is crucial since the concept of child disease in the loose sense suggested by Cohn’s intuitive (and self-serving) use of it only implies that children constituted something like a highly disproportionate part of the total mortality in plague epidemics. It also entails the corollary that this highly unproportional mortality among children reflects widespread or comprehensive acquired immunity among the adult population who had survived earlier epidemics of the disease, this manifestation being the hallmark or defining feature of viral disease. In order to acquire a more accurate and operational concept of child disease, it is necessary to make explicit some central demographic aspects of medieval population structure, especially the proportion of children among the living and the dying in normal populations both in normal circumstances and in plague epidemics. Only on the basis of such information can a realistic and operational definitional notion of the disproportionality of child mortality as evidence of child disease be considered. The concept of child disease according to Cohn’s notion must relate to epidemic morbidity and mortality rates among children of ages c. 0–14 as proportions of concomitant morbidity and mortality rates among the older segments of the population. Or more accurately: the demographic and epidemiological concept of child disease must relate to or reflect a notion of the proportion of sick and dying children usually caused by an epidemic disease which differentiates it from concepts of population mortality or adult mortality in a way that makes it useful as an analytical tool. Since Cohn has not provided any idea of these proportions and their relative dimensions, his conceptual notion is obviously as impressionistic and intuitive and unanalytical and therefore unscientific as the impressions of the chroniclers on which he bases it, and can as such be summarily rejected as useless as an analytical tool. Greenwood provides some of the data needed for the definition of the proportional concept of (infectious) child disease in an historical perspective, when he states: as recently as 1851–60 the rate of mortality [in smallpox] in no age group later than 5–10 amounted to one-fifth the rate in the age group 0–5, and the mortality at 5–10 was one-quarter the mortality at 0–5. In the epidemic of 1881–2 the relative predominance of the first age group was considerably lessened; the mortality at 5–10 was half that of 0–5 […],

228

chapter six

and so on.88 This shows that when Cohn does not specify the constituent definitional elements and their interrelationships, that is, the correlates of his definition of the concept of infectious child disease, it clearly becomes well-nigh impossible to test the material tenability or relevance of his assertion. Without real testability, not only the tenability but also the validity of his assertion can be rejected. Notions of disproportionality of morbidity and mortality according to age in the face of epidemic disease relate by implication to notions of normal proportions. Any serious approach to this definitional problem must therefore also take into consideration the fact that these relationships or notions of interrelated proportions are not constant but vary with social structures. Any realistic and useful definition of child disease derived from studies of epidemic child mortality as a proportion of adult mortality in modern Western society will be highly different from an historical definition derived from studies of relative proportions of child mortality in medieval or early modern populations, and would therefore be unusable for the study of this topic in these societies. This is the case for several crucial reasons: (1) because there are vast differences in demographic structures, and in particular, children constitute far smaller proportions of the populations in modern Western society; (2) because the incidence, prevalence and effects of epidemic diseases in modern and old-time society are tremendously different; (3) because normal levels of population mortality in these periods are extremely different; (4) because the pattern and distribution of normal mortality according to age are extremely different. This means that the definition of an operational concept of child disease or child mortality according to the distribution of cases by age in a population will vary greatly with changing demographic and other societal structures and historical periods, a fact all too often overlooked. Therefore, concrete data of the proportion of children in populations at the time is needed in order to gain knowledge of the relative size of the pools of children and older age categories which are exposed to epidemic disease and epidemic death. Only on this basis can mortality rates in particular age groups which are out of proportion with their

88

Greenwood 1935: 240.

was historical plague a viral or bacterial disease? 229 numerical representation in the population be identified and analyzed for an understanding of causal factors. Intuitive, impressionistic and other arbitrary or subjective notions of such conditions must be rejected as methodologically invalid and materially untenable. Since Cohn focuses on Italian material, it will be reasonable and fair to put a certain emphasis on Italian demography here in an otherwise general discussion. Life expectancy at birth in the Late Middle Ages and the first half of the sixteenth century appears to have been twenty and twenty-five years, respectively.89 Belletini indicates the same life expectancy as normal in old-time Italy, “oscillating usually between twenty and twenty-five years, rarely reaching the limit of thirty years.”90 A useful point of departure for a realistic understanding of demographic structures under such circumstances can be seen in Table 1 which is a life table, Model South level 3,91 showing life expectancy and mortality at various ages in a population of females with life expectancy at birth (eo)92 of twenty-five years, the number of deaths at each age level and the number alive at the start of each age level out of an original population of 100,000 persons. Among other things, this life table shows that 54.6 per cent of all children born died at ages 0–14, and over one-fourth of all children born died as infants, in the first year of life. This pattern of child mortality corresponds to Belletini’s view on child mortality in old-time Italy: “normally a fourth of all new-born babies (neonatus) died in the first year of life, but that the death toll not rarely reached or exceeded one-third of births, while half of the

89 See the summary and discussion of normal levels of mortality in the Middle Ages in Benedictow 2004: 250–6. Since the work on this monograph was finished in 2003, two very important works on the subject have been published. The first is Hatcher’s outstanding and, one must hope, final breakthrough in the understanding of late medieval demography, Hatcher 2003: 83–130. In 2006 Hatcher Piper and Stone published a study of monastic mortality in Durham Priory in the period 1395–1529. The latter work accords with Hatcher’s study of late medieval monastic mortality at Christ Church Priory in Canterbury and Harvey’s study of monastic mortality at Westminster Abbey in about the same period. These studies accord with and corroborate my presentation of medieval mortality in my monograph. Cf. Benedictow 1996b: 36–42. 90 Belletini 1973: 494. My translation from Italian. 91 Coale and Demeny 1983: 11–2, 31–4. For a similar table of Model West, see Coale and Demeny 1983: 43, or Benedictow 2004: 249. 92 The differences between this table and a similar table for males are negligible in this context. eo is a standard abbreviation in demography meaning life expectancy at birth, e being an abbreviation of the Latin word eta(ti)s (aetas/aetatis) in nominative and genitive cases meaning (of) age, o referring to age at birth. Life expectancy at other ages, at age 15, for instance, would correspondingly be written e15.

230

chapter six

Table 1. Life table, model south, level 3: life expectancy and mortality at various ages in a population of females with life expectancy at birth (eo) of 25 years, and the number of deaths at each age level and the number alive at the start of each age level out of an original population of 100,000 persons Age

Number of deaths

Number alive

Life expectancy

0 1 5 10 15 20 25 30 35 40 45 50 55 60 65 70 75 80 85 90

26433 22263 3799 1892 2490 2931 2935 2836 2759 2588 2519 2980 3572 4810 5335 5029 3319 1193 286 30

100000 73567 51304 47505 45613 43123 40192 37257 34421 31662 29074 26555 23575 20003 15193 9858 4829 1510 317 31

25.00 32.85 42.57 40.80 37.38 34.39 31.71 29.00 26.18 23.23 20.07 16.73 13.52 10.47 7.96 5.86 4.26 3.13 2.24 1.59

new-born babies of a generation did not live beyond the fifth year of age.”93 This means that at the time, according to this life table, of 100,000 persons born, 54,387 would die before their fifteenth birthday while 45,613 would not. That is, among death’s normal yearly harvest in a normal population, almost 55 per cent were children of ages 0–14. At the time, the normal level of mortality in a normal population under normal circumstances should, thus, be expected to have a large

93

Belletini 1973: 494. My translation from Italian.

was historical plague a viral or bacterial disease? 231 component of child mortality according to modern notions of the relative distribution of mortality. In other words, in the period under consideration the proportion of normal child mortality in a population would easily qualify as the outcome of a very serious child disease according to modern notions. Contemporaries considered this, on the contrary, to be the normal distribution of mortality among the various constituent age groups of the population under normal circumstances. Carmichael is right when she points out that 50–60 per cent of those dying from plague in the epidemic of 1400 were children, and that “this was close to the proportion of children in the population.”94 The usefulness of a realistic understanding of the normal rates of child mortality at the time can be demonstrated in relation to Cohn’s discussion of the first part of the Necrology of the Dominican monastery in Siena containing burial lists for the cemetery in Camporegio 1336–1430. Cohn asserts, for instance, that it contains representative information on child mortality when the entries of interments, according to his inaccurate figures, produce a child mortality rate of 9 per cent in the year of the Black Death, 1348, and (erroneously, as can be seen from Appendix 1 and Tables 4–5 below) one-third in 1363,95 the year of the next plague epidemic. Comparison of these data with Table 1, Life table, Model South, level 3, life expectancy at birth (for females) of 25 years, makes it clear that Cohn’s assertions are completely untenable as assertions of demographic reality in the meaning of registrations of the deaths in a normally constituted contemporary population at the time, whatever its social-class composition, pattern of territorial location, types and structure of habitation or occupational structure. This can be put in a realistic perspective by considering more fully the Necrology as a source on contemporary child mortality in Siena. As can be seen from Tables 4 and 5 below,96 in all non-plague years in the period 1337–78, thirty-nine years out of forty-two years, the average proportion of child burials is 7.6 per cent and never exceeded 11.3 per cent but could be as low as 2.5 per cent. In the three plague epidemics, the proportions of child burials were 11.0, 46.6 and 59.6 per cent, respectively, according to the Necrology. The figure for the Black Death is obviously without contact with reality, in the two following 94

Carmichael 1983: 514. Cohn 2002: 212. 96 Below: Table 4, 254, Table 5, 258. The material on which these tables are based is cited in Appendix 1. 95

232

chapter six

epidemics the figures are within the realm of normalcy, and in the last epidemic within the higher reaches of the range of normal levels of mortality. The strong increase from the Black Death to the two subsequent epidemics is interesting and will be addressed below. However, Cohn’s claim that this Sienese cemetery population reflected the normal process of dying in a normal parish population can be unceremoniously rejected. The very high normal mortality rates among children imply that children constituted a much higher proportion of the population in medieval society than in modern society, and the very high normal mortality had to be balanced by high fertility or the population would diminish and become extinct. This is what Table 1, Life Table, Model South level 3, predicts. Few direct demographic studies of the composition of medieval populations according to age are available for empirical testing of the prediction. Herlihy and Klapisch-Zuber have presented material on the age structure of the population in Florence in 1427. Since this population is affected by plague epidemics and the effects of plague on populations is at the heart of this discussion, this material is methodologically problematic as it would tend to invite a circular argument. However, as it is, it implies a proportion of children ages 0–14 of 45–50 per cent. In my analysis of the studies of medieval skeletal populations in Scandinavian cemeteries in my monograph on Nordic medieval demography, I reached the same conclusion, that the proportion of registered children in these ages was 45–50 per cent.97 In addition, there is always a significant and even serious problem of underregistration of infants and young children both in population registers and in cemeteries, as the bones of infants and the youngest children would tend to disintegrate beyond any possibility for registration or recovery. For this reason, the real proportion of children under age fifteen constituted probably a significantly higher proportion of the population than fifty per cent, which figure accords with the predictions of Life Table, Model South, level 3. Taking into account normal variation, a normal medieval mortality rate among ages 0–14 can be estimated at 50–60 per cent. Taken as they are, these registrations show that the very high normal rates of child mortality at the time, constituting 50–60

97 Herlihy and Klapisch-Zuber 1978: 427, cf. also p. 456 where the probability of underregistration and underestimation is pointed out. Benedictow 1996b: 29–36, cf. p. 156–9, 162.

was historical plague a viral or bacterial disease? 233 per cent all mortality, occurred in a population where children below the age of fifteen constituted around half of the population. This confirms the impressionistic notions of mortality in the minds of the contemporaries and that they were extremely different from modern notions or impressions. To the irreparable and irremediable damage of Cohn’s views on immunity, he has avoided to address the crucial question: How much increased relative mortality among children would be needed for the chroniclers to consider a disease a child disease, according to their impressionistic notions of such matters? Only an operational answer to this question can serve as a base for possible inference to immunity. This conclusion must be seen in the perspective of available historical and other relevant knowledge of the relative impact of plague on children, which will be the next point to consider. Generally, children are particularly vulnerable to infection due to immaturity of the immune system.98 A clinical study of plague among Vietnamese children of ages 0.25–16 years compared with adult cases published in 1973 concluded that adults resist the disease better than children: “the usual illness was more fulminant in children, and the mortality seemed to be higher.”99 A study of plague patients over six years of age in Vietnam from 1970 concluded thus: “The adolescent age group were most affected and were also the most toxic […]. These age correlations suggest that younger patients may be more susceptible to infection and to the toxic manifestations of the disease.”100 Clearly this indicates that children and adolescents tend to have weaker innate resistance to plague infection, are therefore relatively more likely to succumb to plague infection than older persons and will, thus, suffer higher lethality rates and supermortality in plague epidemics for this biological reason. In fact, this was observed in the Black Death: Chalin de Vinario, one of the pope’s personal physicians, points out that children and youngsters frequently died quite suddenly,101 which accords with the fulminant course of plague disease in children and youth due to weaker innate resistance to plague infection relative to adults observed by modern physicians. However, children also suffer supermortality for social reasons, because they were especially vulnerable to the detrimental effects of the 98 99 100 101

Donowitz 2003: 17. Burkle 1973: 296. Butler 1972: 274. Sticker 1908: 58.

234

chapter six

breakdown of families visited by plague. Many children, especially in the age brackets up to about 10–2 years, would succumb for lack of nourishment and normal care, even if they were not infected. In his study of the plague epidemic in the provincial English town of Colyton in 1645–6, which is based on family-reconstitution of the population according to parish registers (see above), Schofield addresses this question. His study shows that if the father survived and the mother died, nine out of ten children died; if the mother survived and the father died, nine out of thirteen children died; if both parents survived, eleven out of forty-seven children died, corresponding to mortality rates of 90, 70 and 23 per cent respectively.102 Thus mortality among children in plague epidemics was a variable dependent on the fate of parents. This point is also made by Del Panta in his history of epidemic disease in Italy.103 However, this point is not taken into account by Cohn, although he has read Schofield’s study, albeit with ill-will (see above); scholars in the field may be surprised that he evidently has not read Del Panta’s standard work on Italian epidemic history, since so much of Cohn’s material is Italian. In modern plague epidemics, the incidence of plague mortality among older children and youngsters is much higher than their relative proportion of the population. This was observed in India, China and Manchuria in the first decades of the twentieth century. Later, the same observation was made also in the U.S.A. where 55 per cent of all plague cases in the period 1950–79 were children aged 0–16 years. Clearly, in plague epidemics children and youth are strongly overrepresented in relation to their proportion of the population and the relative number of age classes that they represent. The plague epidemics in Vietnam during the war in the 1960s and early 1970s were the most recent to produce many thousands of cases which permitted a thorough demographic analysis. In 1967 there were 5,547 recorded plague cases,104 and children and youth under twenty years constituted between half and two-thirds of all plague cases.105 The researchers explain this skewed distribution of plague cases according to age by the play-oriented behaviour and generally active behavioural patterns of children and youngsters which increase the level or intensity of their exposure to 102 103 104 105

Schofield 1977: 118–9. See also, for instance, Hirst 1938: 690. Del Panta 1980: 48. Reed, Palmer, Williams et al. 1970: 467. Marshall, Joy, Ai et al. 1967: 605, 612.

was historical plague a viral or bacterial disease? 235 infection relative to most other parts of the population.106 Supermortality among children in plague epidemics is also a function of children’s and adolescents’ behavioural patterns which entail increased exposure to infection relative to adults. This point is also made by Del Panta.107 Thus, children should be expected to suffer substantial supermortality in plague epidemics for biological and social reasons. Carmichael found that the Florentine Books of Dead “give strong evidence of heavy mortality among dependent children during the early fifteenth century,” and that “during epidemic years [in the decades around the mid-1450s] more than 70 per cent of those dying from all causes were children.” She is surprised that in the plague epidemic of (1429–)1430, “the relative losses of children exceeded the percentages that would be expected if plague alone were the principal determinant of mortality patterns, since there is no reason that bubonic plague would selectively affect the young.”108 As shown above, there is no ground for her surprise, because for various reasons plague produces supermortality in children and adolescents; instead her findings confirm what should be expected. This proportion of child mortality in plague epidemics would definitionally be distributed over only fourteen age groups, whilst the remaining well under half of all deaths would be distributed among the remaining about fifty significant age groups. No doubt, this pattern of mortality according to age would easily produce an impression among contemporary observers that plague caused extraordinary high mortality among children which could, according to their culture and meaning of words, permit or inspire the use of the expression “child disease.” The assumption that such impressions constitute certain evidence of immunity among the adult population is clearly unwarranted. Plague according to Social Class, Age and Gender These preliminary conclusions can be considered as a hypothesis to be tested on the Black Death which, being the first plague epidemic, hit a so-called naïve population (without prior contact with the contagion) in which no population element could enjoy the alleged advantage of

106 Wu Lien-Teh 1936c: 399–400, 417, Pollitzer 1954: 503; Payne, Sandwell and Hennessy 1946: 993; Reed, Palmer, Williams et al. 1970: 470, 472–7. 107 Del Panta 1980: 48. 108 Carmichael 86: 91–2.

236

chapter six

acquired immunity. If chroniclers or other contemporaries observed supermortality among children, this constitutes corroborative empirical evidence to the effect that supermortality among children is a normal aspect of the mortality effects of plague epidemics which is unrelated to acquired immunity among other sections of the population. In this context, M.R. Cazelles’ study of the differential social impact of the Black Death in France (excluding Languedoc109) according to chroniclers and other contemporary observers takes on particular importance. Its title speaks loudly about his findings, that the Black Death was an “Épidémie prolétarienne et enfantine,” that is, an “Epidemic of proletarians and children.”110 Cazelles cites, among others, Simon of Couvin, whose account of the Black Death in verse Cohn knows and cites falsely in his attack on Hankin.111 In this case, Cohn does not attribute to Simon de Couvin a statement he does not make, but passes in silence by his statement on the particularly great mortality afflicted on the “splendid youth” by the Black Death. He also passes in silence by Simon de Couvin’s poetic description of the particularly fulminating course of the disease among the young which led to death in a day: “who perishes before a day is over like a flower which born in the field, in the morning greening flowers, in the evening completely withers.”112 Instead, Cohn refers to Simon of Couvin’s work on another aspect of the differential social impact of the Black Death: “all doctors of Montpellier perished in the plague of 1348.”113 Cazelles cites to the same effect other prominent chroniclers of the time, prominent in the sense of being among the most often cited because their chronicles are considered among the most valuable of their kind, namely those of Jean de Venette and Gille le Muisit.114 In Histoire de la population française Dubois cites most of Jean de Venette’s account of the Black Death, including the statement that “All this year 109 Cazelles employs the old geographical term “Langue d’oïl” which denotes the main part of France where the word for “yes” is “oui,” in contrast to “Langue d’oc” where the word for “yes” is “oc,” derived from Latin hoc. Languedoc is not included because contemporary chroniclers there held other views, but because they do not provide views or observations pertinent to the matter in question. 110 Cazelles 1962/1965: 293–305. 111 Above: M26–7. 112 Littré 1840–1: 233: Illic strata jacet hominum speciosa juventus,/ Quæ perit ante diem quasi flos qui natus in agro/ Mane virens floret, et vespere totus arescit;. My translation from Latin. 113 Cohn 2002: 121. 114 Cazelles 1962/1965: 304–5.

was historical plague a viral or bacterial disease? 237 and the next, the mortality of men and women, of the young even more than of the old, in Paris and in the Kingdom of France, and also, it is said, in other parts of the world, was so great that it was almost impossible to bury the dead.”115 In fact, Cohn cites this chronicler quite often in his monograph, twelve times, and even cites the following sentence,116 but on a minor point and without taking interest in the chronicler’s view on the Black Death’s predilection for young persons or children. Also Gille le Muisit, Abbot of St Martin’s in Tournai (modern Belgium), states in his chronicle that in Tournai more young persons than old perished in the Black Death. Cohn has used also this chronicle and cites it twice on points regarding differential social mortality, namely on the supermortality of the beneficed parish clergy and to the effect that “neither the rich, the middling sort, nor the pauper was secure.”117 Thus, all three chroniclers are well known by Cohn118 who pretends, nonetheless, that he has overlooked their statements on the supermortality of young persons or children in the Black Death. Conspicuously, Cohn knows and cites Cazelles’s paper but pretends to know only half of the paper’s title and half of its conclusion, writing that “Raymond Cazelles, has claimed that from the beginning the Black Death was ‘a proletarian epidemic.’ ” Thus, Cazelles’s view that also children, according to the chroniclers, suffered conspicuous supermortality from the Black Death is deleted and the author’s opinion is misrepresented. In the same vein, Cohn goes on to state falsely (footnote included in brackets): but more convincingly others, such as Geneviève Prat and Edouard Perroy, relying on local studies with land registers and fiscal records, have corroborated the message heard from the mass of the chroniclers: initially the Black Death was egalitarian in its onslaught [fn. 207: “Carpentier, ‘Famines et épidémies,’ pp. 1069–70, summarises this historiography.”]119

This short statement contains three assertions: (1) that empirical evidence like “land registers and fiscal records” represents the most valuable and crucial material for the study of the Black Death;

115 116 117 118 119

Dubois 1988: 317; The Chronicle of Jean de Venette 1953: 48. Cohn 2002: 110, cf. p. 310. Cohn 2002: 121, 126. Cohn 2002: 310, 312, 316. Cohn 2002: 127.

238

chapter six

(2) that the Black Death was “egalitarian in its onslaught”; (3) that the studies based on manorial registers and fiscal registers corroborated the assertions or statements of the “mass of chroniclers” to this effect, that there is full agreement or identity between the information provided by these two categories of sources on this point. As emphasized several times above, Cohn is a scholar who consistently avoids documentary empirical evidence like population registers, tax registers, and manorial rolls. As shown in my monograph on the Black Death, there are available almost 200 demographic studies of mortality in the Black Death based on such material, but Cohn has not taken interest in any of them. Instead, Cohn relates to the problem of the nature of historical plague as a cultural historian attempting to make his case primarily on the purported amassment of chroniclers’ views, enumerating in his bibliography 407 “chronicles, annals and calendars.” This is the material that constitutes the basis for his main argument for an alternative theory of the microbiological nature of the Black Death.120 Thus, the thrust of Cohn’s remarks just cited is quite astonishing: if documentary empirical evidence like censuses, tax registers, and manorial rolls are considered superior medieval demographic sources, then any serious scholarly study of the Black Death, its mortality, differential social impact according to social class, age and gender, and the question of the microbiological nature of historical plague epidemics would be very different from Cohn’s, as my monograph is for exactly this reason. The assertion that a mortal epidemic disease like “the Black Death was egalitarian in its onslaught” is at variance with epidemiological and social sciences’ general observation of epidemic diseases’ characteristic predilection for particular sections of populations, for the poor and destitute, for the old and the elderly, for infants and children, and so on. It must be treated with caution and even suspicion. In my monograph on the Black Death which takes into consideration all relevant studies, it is shown that the disease was socially selective and non-egalitarian (see below).121 Hence Cohn’s assertion must be materially untenable, and it is important to take a closer look at his arguments and supporting references. 120 121

Cohn 2002: 99 and bibliography: 255–73. Benedictow 2004: 259–68.

was historical plague a viral or bacterial disease? 239 Prat’s work of 1952 is a study of the Black Death in the city of Albi on the basis of two registers in which the population is recorded according to household and their assets are surveyed in order to assess their taxes, including those who were too poor to pay taxes who are registered only by name without tax assessment (compoix d’Albi). Thus, her sources record households according to householders, always adult persons, overwhelmingly men.122 Unsurprisingly, her paper does not mention the words “child” or “children,” does not contain a single reference to a chronicler, and does not show mortality according to various social divisions and, thus, certainly does not argue that the “Black Death was egalitarian in its onslaught.” However, Prat’s paper contains a comparison with the compoix of 1357 which shows that the proportion of those who were too poor to bear any tax assessment had fallen from 42 per cent in 1343 to 28 per cent in 1357, which could legitimately be taken to indicate considerable supermortality among the poorest classes of the city. Cohn’s assertion with respect to Prat’s conclusions, cited just above, is misleading. Perroy’s paper of 1949 “On the Origin of a Contracted Economy: The Crises of the Fourteenth Century”123 likewise does not mention the words “child” or “children” or use or refer to chronicles or argue that the Black Death was socially egalitarian in its onslaught. Cohn’s assertion is misleading. Prat’s and Perroy’s papers are not entered in Cohn’s bibliography. For support of his assertion and two scholarly references, Cohn refers in the accompanying footnote to a paper by E. Carpentier published in 1962 which he asserts “summarizes this historiography.” Carpentier wrote a synthetic paper on the significance of famines and epidemics in the fourteenth century; she does not mention the mortality of children in the Black Death, she does not maintain that mortality in the Black Death was “egalitarian in its onslaught” or that mortality did not vary according to social class, gender, or age, neither on pages 1069–70 to which Cohn refers nor anywhere else in the paper. She does not summarize the views of chroniclers, as they are peripheral to her material. She refers to chroniclers three times, twice in relation the famine and epidemics of the years 1315–6, and once to make the point that chroniclers enumerated the plague epidemics, the first plague, the second

122 123

Benedictow 2004: 265, 332–3. My translation from French, see bibliography for the original French title.

240

chapter six

plague, and so on, to show that the Black Death and subsequent plague epidemics by contemporaries were perceived as representing a new disease.124 Everything Cohn states about Carpentier’s paper is simply misleading. The assertion that Prat, Perroy and Carpentier in these papers “corroborated the message heard from the mass of the chroniclers” is therefore wrong in all tree cases. Cohn’s use of false references to these early papers on these subjects, which are good in their own right, must serve a need and a purpose. A possible explanation could be that if the Black Death did not ravage the populations in an egalitarian way, various social categories would, according to his line of reasoning, suffer different rates of morbidity and mortality and, consequently, contain higher or smaller proportions of persons with immunity, which in subsequent plague epidemics should be observed with marked consistency by chroniclers. This would seriously complicate and potentially undermine his argument on differential immunity and the development of plague as a child disease. In view of the topic of immunity and purported development of plague into a child disease that allegedly was very clear in the second plague epidemic, it is a conspicuous feature of Cohn’s argument that he avoids or evades presenting the two most important papers on the subject of what happened to children in the Black Death and the subsequent epidemic, namely Cazelles’s paper of 1962 on the fate of children in the Black Death which I have discussed above, and J. Glénisson’s paper of 1968–9, the most important paper on the second plague epidemic of 1360–3. In his paper, Glénisson accepts Cazelles’s finding of supermortality among children in the Black Death according to the chroniclers.125 Although these two papers are central in relation to the question of the pattern of mortality of children in the Black Death and in the second plague epidemic, they do not appear in Cohn’s bibliography. Cohn has also avoided presenting the findings of any of quite a number of papers and monographs based on manorial records and fiscal records which were published after Prat’s, Perroy’s, and Carpentier’s and which show that children and the poor suffered considerable and even dramatic supermortality in the Black Death. In order to

124 125

Carpentier 1962: 1072, 1081–2. Glénisson 1968–9: 35.

was historical plague a viral or bacterial disease? 241 emphasize this point, a small sample of these studies will be presented in detail instead of just enumerating them; I also invite the reader to consult my monograph on the Black Death. In his study of the manor of Halesowen (Worcestershire), Z. Razi found evidence showing that “child mortality in the Black Death was very heavy,” in fact, “child mortality in the plague must have been catastrophic.”126 His perspective is also very different from Cohn’s in relation to the subsequent epidemics: “it would seem that infants and children were as susceptible to these plagues as they were to the pestilence of 1349.”127 M. Ecclestone’s study of mortality among the “garciones,” the (allbut-)landless men aged twelve and older at seventeen of Glastonbury Abbey’s manors, uncovers considerably higher mortality among this rural proletarian class than among the customary tenants, the landholding classes of peasant society.128 On some manors of the bishopric of Winchester, the (all-but-)landless classes were liable to pay death duties in the form of small money payments called heriots in order to obtain the right to transfer cottages and tiny plots of land to inheritors. Heriots are thus a special type of death duty that would reflect the number of deaths or level of mortality among this proletarian social class. The heriot registers appear to be complete from 1270 through the time of the Black Death. The studies of these registers reveal very high supermortality among this proletarian class relative to that suffered by the customary tenants.129 In three parishes near Chambéry in the County of Savoy in southeastern France, mortality in the Black Death has been studied on the basis of records registering small money payments made by the households for permission from the lord to collect firewood. These lists record most of the landless classes who also needed firewood for cooking and heating. New lists of these rural householders were produced each year, also in the year of the Black Death, and they reflect directly the impact of the Black Death. The study of these lists reveals clear supermortality among the poor and proletarian classes.130

126

Razi 1980: 104. Razi 1980: 129. 128 Ecclestone 1999: 6–29. See also Benedictow 2004: 265, 364 fn. b, 368, 374–6. 129 Ecclestone 1999; Postand and Titow 1958–9: 408; Ohlin 1966: 84–9; Benedictow 2004: 259, 364–5 fn. g, 376–7. Cf. Arthur 2005: 113–20, 123–7. 130 Brondy 1988: 88. See Benedictow 2004: 259, 264–5, 320–1. 127

242

chapter six

Thus, Cohn’s assertion that studies based on fiscal and manorial sources confirm the socially egalitarian character of the Black Death’s onslaught is three times false, (1) false because such studies generally prove the contrary, (2) false because the studies he cites do not provide evidence to this effect, and (3) false because Prat’s paper provides good evidence for the opposite view, namely that the poor and proletarian social classes suffered a marked supermortality in the Black Death. The Black Death’s onslaught was socially non-egalitarian both according to social class and according to age. In the page preceding the quotation under discussion, Cohn himself cites several chronicles which clearly demonstrate that the social impact of the Black Death exhibit a highly varied and differential social pattern, i.e. that it was non-egalitarian. He asserts that The Paris Medical Faculty, Geoffrey le Baker, the Abbot at Tournai [Gille le Muisit: my insertion], and Henry of Hervordia even saw the first plague striking down the strong and rich in greater numbers than the weak and ill.131

This is seemingly the opposite of Cazelles’s findings of chroniclers’ observations on the differential social impact of the Black Death presented above. However, the Paris Medical Faculty is not a chronicler and has not addressed differential mortality but rather the cause of the Black Death.132 Cohn refers to two chroniclers. As usual he has only picked what suits his case and thus has produced a skewed impression of the opinion expressed in the source. What Le Baker really states is, according to Creighton, that:* Few of the first rank died, but of the common people an incalculable number, and of the clergy and the cleric class a multitude known to God only. It was mostly the young and strong who were cut off, the aged and weakly being commonly spared.133

Clearly, Le Baker gives quite a complicated picture of differential mortality, and he obviously agrees with Cazelles or rather Cazelles’s

131

Cohn 2002: 126–7. This statement is cited with valuable introductory comments in Hoeniger 1882: 149–56. Cf. Sticker 1908: 60–2. 133 Creighton 1891: 122. 132

was historical plague a viral or bacterial disease? 243 informants among French chroniclers that the Black Death also visited the poor and proletarian classes with particular ferocity. It can be proven that Cohn knows better since almost a hundred pages later he refers directly to Creighton’s text on this page, but again in a way that misrepresents not only Le Baker’s statement but also Creighton’s rendering of it, namely: Similarly, Creighton, History of Epidemics in Britain, p. 122, found that the plague of 1348–9 in England carried off able-bodied young adults and not the young, weak or elderly.134

Here, Cohn paraphrases, or more accurately apparently paraphrases Creighton’s view on the differential social impact of the Black Death, but deletes Creighton’s emphasis on the great supermortality among the poor thus producing a great distortion of Creighton’s view. Cohn states that “Various chroniclers claimed that the first wave of plague hit populations indiscriminately, regardless of age, sex, or social class,”135 in other words in a socially egalitarian way. Conspicuously, in the accompanying footnote he succeeds in mustering only two chroniclers for support,136 while as seen above he inadvertently provides four references for an entirely different view among chroniclers or contemporary observers and, as demonstrated by a correct paraphrasing of Le Baker’s statement on the matter, this material could easily be augmented. According to my experience, it would be possible to find two or more chroniclers who express a particular opinion on any conceivable point, which means that Cohn’s references in this case can only have illustrative function and serve as a basis for formulating working hypotheses. Thus, a quick look at Cohn’s documentation shows that he is not able to provide significant evidentiary support for his central assertion: “the message heard from the mass of the chronicles: initially the Black Death was egalitarian in its onslaught.” It is one of his numerous arbitrary assertions formed to serve his great objective, his great 134

Cohn 2002: 212, fn. 73. Cohn 2002: 126. 136 Cohn 2002: 126. He also supports this view by citing Matteo Villani who maintained, or in Cohn’s unfortunate choice of word “suggested,” that the poor were especially severely hit but also called the Black Death “a pestilence among men of every condition, age and sex.” However, there is no logical or factual contradiction between maintaining that the poor were especially severely hit and that all social classes, ages and both genders suffered severe losses; it means that the Black Death did not take an equal toll among all main social categories of people and therefore was not egalitarian in its impact. 135

244

chapter six

revolutionary ambition, an alternative theory of the nature of the Black Death. His misrepresentation of Prat’s, Perroy’s, Carpentier’s, and Cazelles’s paper and Le Baker’s views reflects the grave problems he has with his sources and the means he must employ in order to form a semblance of supporting evidence. The reference to “message heard from the mass of the chroniclers” is fundamentally a statistical assertion implying a very large number of persons. Central to Cohn’s assertion is the implied claim that he has gathered the views or opinions on the matter of such a large number of chroniclers that it constitutes a mass of material. Whether 407 chroniclers constitute a mass of persons according to the terminology and conceptual notions of historical science and social science more generally is a definitional question open to debate and dispute. However, the sociological term “mass [of persons]” should satisfy also other criteria than numbers, for instance, “a very diverse population that has no social organization,” which makes it unlikely that chroniclers would constitute a mass of persons according to formal sociological criteria, since they tend to be interconnected with respect to social class, education, ideology, values and norms, frame of mind and outlook on life. If ordinary sociological demands for definitional clarity and specificity are left aside, it must be pointed out that the meaning and statistical implication of the expression “message heard from the mass of chroniclers” is unclear. Primarily, it must be taken to mean that contemporary chroniclers as a mass, massively, held a certain opinion. This is obviously untenable, since chroniclers held a great variety of opinions, as documented above. However the expression could possibly with maximum goodwill be understood to mean that the vast majority of chroniclers held a certain opinion. In this context, expressions like “the (great) mass of ” or “the vast majority of ” must mean that the proportion holding this opinion must be very high, at least 75–80 per cent, in order to discern the expression notionally from formulations like “over half,” “the majority,” “the substantial majority” or even “the great majority,” so that the implied meaning would at least approach something like “the overwhelming majority.” Thus, Cohn’s assertion must be taken to imply that at least 300–25 chroniclers should have expressed this specific opinion. Of course, anyone knowledgeable of medieval chronicle(r)s will know that this is taken out of thin air in order to serve Cohn’s argumentative objective. If Cohn’s assertion were to have any scholarly relevance or significance in the form of any level of tenability, it would need to be underpinned by explicit and systematic

was historical plague a viral or bacterial disease? 245 empirical data: the relevant statements of the (mass of) chroniclers must be quoted and marshalled in some type of table or register which renders the vital statements with footnotes which alone can satisfy the crucial criterion of testability. Only in this way can the assertion be made methodologically valid and materially tenable. These citations, which would have been useful both for his supporters and his critics, could have been presented in a fourth appendix and be used for crossreferences in his monograph. Cohn has refrained from performing this work although he asserts that he has the material at his disposal. Scientifically and methodologically, his approach is arbitrary, his argument invalid and untenable. However, any scholar knowledgeable of the cultural attitudes of contemporary chroniclers to the Black Death would know that many of them, quite possibly the majority of them, do not mention the Black Death,137 and that the great majority of those who mention the epidemic do not provide any information on differential social mortality, but make only some terse statement about great mortality. Only a tiny fraction will mention the Black Death and also provide opinions on the social distribution of mortality. Cohn’s reference to 407 chroniclers and the opinions of the mass of chroniclers constitutes fictitious evidence which is unavoidably misleading and forms the basis of quasistatistics. In fact, chronicles can rarely be used for the study of generalized or sociological aspects of social, demographic or epidemic reality. To the extent that their writings attract interest, it is usually in connection with the study of cultural history, medieval mentality and outlook on life, and in some cases of political history. Their statements on demographic or soci(ologic)al issues must be exposed to relentless and merciless source-criticism and be testable on independent material, tests they regularly (but not always) fail to pass. A Demographic Case Study: The Necrology of the Monastery of San Domenico in Camporegio Cohn also argues his case for immunity on the basis of a purported demographic study of a necrology associated with the Dominican monastery of San Domenico in Siena which was mentioned above. 137

Benedictow 2004: 192–4, 207.

246

chapter six

Since he ascribes great importance to the evidentiary value of his study of this Necrology, especially with respect to immunity and its great significance for the understanding of the microbiological nature of the disease, it should be taken seriously. As a medievalist historical demographer, I have taken upon myself the task of producing a responsible study of the central part of the Necrology which can be usefully compared with Cohn’s study and serve as a base for a serious discussion of the purported facts. First, the medievalist demographer must make some highly specialized initial comments. A necrology is not a burial register comparable to parish burial registers as Cohn gives the impression. The typical necrology is a monastic (or ecclesiastical) death-roll or register containing entries of the deaths or more usually, as in this case, burials of persons which was usually kept in the chapter’s assembly hall where it was used for brief commemorations of the dead in the morning. Such commemoration services were normally associated with honourable places of burial in the cemetery or monastic buildings and normally required significant payment. Consequently, persons entered in a necrology did not constitute a normal population of dead persons but were overwhelmingly persons who could afford such investment in a better afterlife in relation to God and to prestige among the local population. Interments in the cemetery of the monastery of San Domenico in Siena are known by name in lists running from 1336 when it was started and are published as I Necrologi di Siena di San Domenico in Camporegio. As pointed out repeatedly, a conspicuous aspect of Cohn’s monograph and his approach to scholarly work is his lack of interest in taking into account many of the central works of Italian historical demography on the late medieval period. This Necrology has been briefly studied in relation to the Black Death by two of Italy’s leading historical demographers of the twentieth century, Professor M. Livi-Bacchi and Professor L. del Panta in central works of Italian historical demography, namely Livi-Bacci’s La société italienne devant les crises de mortalité [Italian Society in the Face of Mortality Crises], and Del Panta’s standard work Le epidemie nella storia demographica italiana (secoli XIV–XX) [Epidemics in the Demographic History of Italy (Fourteenth to Twentieth Centuries)]. These works remain unmentioned in both Cohn’s book and his bibliography, and he discusses the Necrology as if he has discovered it and pioneered research on it. I have made a complete demographic registration of all entries from the first full year, namely 1337, to 1378, that is, for forty-two years and

was historical plague a viral or bacterial disease? 247 through three plague epidemics, in all 1644/46 persons, with accurate registration of all demographic vital information on age, gender, day of burial, and so on. The material is summarized in Table 5 according to year, gender and age; in order to ensure easy testability all of the material is presented in Appendix 1. The Necrology contains ample information showing that burials normally took place on the day of death or the following couple of days, a delay which is of no significance for this type of study. The editor of the Necrology has enumerated the acts of interments but not the number of interred. Since there is an incidence of two or more simultaneous burials in the same grave and also other “irregularities,” use of the enumeration for production of numerical data will lead to inaccurate figures, which is the case for all three scholars. According to Agnolo di Tura, the Black Death broke out in Siena in May,138 which may quite likely be when it became observable to contemporaries. To the historian’s prying eyes there is, however, a suspicious sprinkling of burials in the Necrology starting 12 April and which by 7 May comprised eight interments139 corresponding to about ten in a month or 120 burials a year, about four times the yearly average in the ten preceding normal years. This can be considered the endemic phase of the incipient plague epidemic, the ten interments on 10 May representing the start of burials from the initial epidemic phase. It is useful to see how prominent Italian historical demographers relate to this source and the problems associated with it in order to put Cohn’s handling of it in perspective. In the words of Del Panta who has enlarged on some of Livi-Bacchi’s original findings, over a hundred deaths were recorded in the period including 10 May and 6 June [1348];140 then, abruptly, the registrations break off and are not taken up again with regularity until the end of August. If the curve is extrapolated for the period in which there are no registrations, we reach an estimate (obviously only suggestive) of about 400–20 deaths in the whole year.141

Del Panta clearly includes the whole part of the Necrology which covers continuously the course of the plague epidemic until it breaks

138 Cited in The Black Death. A Turning Point in History? 1971: 13. Cf. Del Panta 1980: 112; Benedictow 2004: 92, 94. 139 Nos. 739–46. 140 The correct figure is 111 persons buried: there are a number of burials of two or more persons in the same grave. 141 Del Panta 1980: 115. My translation from Italian.

248

chapter six

off 6 June; only a few episodic interments are registered later, two on 12 June, three 17 June, three 6 August, four single interments in the days 28 August–2 September, and only three more burials for the rest of the year. These ten episodic entries in the second half of 1348 cannot be taken as evidence that systematic registration of burials was resumed. The four entries performed around 1 September are not different from the previous three instances of entries of burials and are followed by only three burials for the rest of the year, only a fraction of the usual number of burials for normal years before the Black Death (see Table 5). This must be taken to indicate that regular registration of burials was discontinued after 6 June for the rest of the year. Instead, the ten episodic interments in the cemetery in the second half of the year can be usefully seen in the light of the personal tragedies so graphically described by the city’s well-known chronicler Agnolo di Tura who buried his five children with his own hands, and also relates that “none could be found to bury the dead for money or for friendship. Members of a household brought their dead to a ditch as best they could, without priest, without divine offices.”142 Table 2 shows that, in 1348, there were seven burials in April, fifty-five in May and sixty-four or sixty-six in June, in all 126/128, which all may be presumed to reflect the effects of the Black Death. Quite likely this was also the case with six burials in August and two burials in September, so in all there were 134/136 plague-related burials. In the whole year there were 144/146 burials. As can also be seen, the registration of burials breaks off at a time when the number of daily and weekly burials was rising steeply, that is, it breaks off before the first epidemic phase was completed by reaching the apex of epidemic intensity. Thus, the burials recorded in the Necrology reflect only a small part of the plague period and lack the remaining part of the phase of increasing epidemic intensity, the whole period of maximal intensity and the decline of the epidemic to its final phase and end. In fact, the lacuna is so huge and devastating for the Necrology as a source on the Black Death that the number of burials recorded in the year of the Black Death is considerably smaller than in the severe year of dearth and hunger-related epidemics of 1340 when 176 persons were buried in the cemetery, and much smaller than in the subsequent plague epidemics when 328 persons were entered in the

142 Rendered in The Black Death. A Turning Point in History? 1971: 13. Cf. Bowsky 1964: 15; Del Panta 1980: 112; Benedictow 2004: 91.

was historical plague a viral or bacterial disease? 249 Table 2. Interments by month and week in the Dominican cemetery in Siena in 1348 Month

January February March April May June July August September October November December

Week

No

1

2

3

4

5

0 0 0 0 2 57/59 0 3 1 0 0 0

0 0 0 3 5 4 0 0 0 1 0 1

2 1 1 1 14 3 0 0 1 0 0 0

1 0 2 2 21 0 0 1 0 0 0 0

0 0 1 1 13 0 0 2 0 0 0 0

Total number of interments

3 1 4 7 55 64/66 0 6 2 1 0 1

144/146

Necrology in 1363 despite three lacunae, and 231 persons in the epidemic of 1374, as will be seen from Table 5 and Appendix 1. Cohn mentions that the Necrology is not complete for the time of the Black Death,143 but over forty pages from where he presents most of the results of his purported demographic study of it,144 at quite a safe distance, presumably, for the memory of most readers, and in a way that seriously understates the size of the lacuna and its numerical significance.145 He does not anywhere in his monograph specify the grave significance of this lacuna or include it in his discussion. He does not mention at any time that there are three large lacunae in the Necrology for the time of the next plague epidemic of 1363, as will be seen from Table 3, or that there is also a probable but not clearly significant lacuna in connection with the third plague epidemic of 1374. Instead, he uses 143 144 145

Cohn 2002: 171. Cohn 2002: 211, 212. Below: 256–7.

250

chapter six

Table 3. Interments by month and week in the Dominican cemetery in Siena in 1363 Month

January February March April May June July August September October November December

Week

No

1

2

3

4

5

0 0 1 5 10 39 22 2 0 0 1 0

1 0 1 5 14 28 17 2 0 0 0 0

1

1 2 0 9 16 0 5 34 0 0 0 1

3 0 1 3 9 0 2 10 0 0 0 0

Total number of interments

8 12 20 4 13 24 2 0 0 0

6 2 11 34 69 71 59 72 2 0 2 1

328

crude and inaccurate figures summarizing the entries on these three plague epidemics for comparative purposes, making strong inferences as to immunity and differential mortality, which are obviously methodologically invalid and materially untenable (see below). A plague period for the Black Death of only four months for such a large city, according to Del Panta’s assumption, would be highly unusual. In fact, there is, as mentioned, really no reason to assume that normal burial practice and regular registration of burials in the Necrology was resumed at the end of August, and the four single interments around 1 September have, as mentioned, the same character of episodic or incidental interments as those made 12 June, 17 June and 6 August. This means that there is no real empirical basis for assuming that normal keeping of the Necrology was resumed before the start of the next year. This source-critically based view can be empirically supported with an important piece of information given by Agnolo di Tura, namely that the epidemic continued in full force “until September.”146 Thus, more 146

Cited after Bowsky 1971: 14.

was historical plague a viral or bacterial disease? 251 likely the epidemic began to decline some time in September and petered out during October, quite likely ending with a few endemic cases sometime in November, the epidemic lasting, as one would expect, eight months (at least). This time perspective corresponds much better to the size of the city of Siena and the time needed for a plague epidemic to spread effectively across it, a time perspective well known from other plague epidemics in big(ish) cities at the time. This means that the lacuna is much larger than assumed by Del Panta and that his extrapolation is much too small. An extrapolation along more realistic lines suggests a much higher number of persons who potentially would have been recorded as being interred in the cemetery if the process of registration had not broken down: over 600 potential burials seems more realistic on these premises. The estimated number and distribution of burials according to these extrapolations are based on general knowledge of the pattern of development and duration of plague epidemics and on a Necrology recording only the main part of the first phase of the epidemic as reflected in interments in this cemetery. Obviously, the empirical basis is weak and the extrapolation is hypothetical. These mortality figures can usefully be seen in the perspective that the population loss in Siena in the Black Death appears to have been of the same order as in Florence, namely about 60 per cent.147 Del Panta erroneously claims that the number of yearly interments entered in the Necrology in the previous years was, on average, twenty, which means that he assumes that the mortality in the Black Death increased by a factor of twenty or twenty-one. Since the average yearly number of interred persons in the ten normal years preceding the Black Death was 31.2,148 the increase, according to Del Panta’s extrapolation, would be around thirteen times the average of normal years. A more realistic period of extrapolation would suggest an increase in the potential number of burials of at least around twenty times or somewhat in excess of 600 burials, if the system had not broken down and interments in the cemetery and entries in the Necrology had proceeded as usual. Instead, only 144/146 interments are recorded in the Necrology

147

Benedictow 2004: 299–300; Carmichael 1983: 514. See Table 5 and Appendix 1. In the decade 1338–47, 438 persons were interred in the cemetery, a yearly average of 43.8 persons. If the severe crisis year of 1340 is deleted (176 burials) and substituted by the interments in the normal year 1337, the number of interred persons in the ten normal years would be 312, and the average number of interred persons in normal years would be 31.2. 148

252

chapter six

for the whole year or an increase of only 4.6 times relative to the previous ten-year average. This shows again that the lacuna has devastating effects for any demographic use, a point which Cohn disregards at the cost of making all his assertions and statistics and comparisons based on the Necrology untenable. The outcome of this analysis of the registrations relating to the Black Death appears more realistic also when compared with the next plague epidemic of 1363 which was generally much smaller than the Black Death and generally caused much lower mortality rates. This is the crucial epidemic for Cohn’s argument that survivors of the Black Death acquired persistent and good immunity according to the pattern of viral diseases and that plague’s consequent development into a child disease was reflected now for the first time. According to the Necrology, this second plague epidemic lasted at least six months in Siena, namely March to August. In this period, as shown in Table 3 and Table 5, 328 persons were interred in the cemetery, 182 more persons or 25 per cent more interments than were registered in the Black Death, which certainly does not support a notion of widespread immunity among the survivors. However, in January 1363 there are six registrations of interments in the cemetery, the largest number recorded in the Necrology for this month from the first full year in 1337 to the end of my demographic registration forty-two years later in 1378. This indicates that plague contagion arrived in the late autumn and that the epidemic was in incipient development but was slowed down almost to a halt by chilly or cold winter weather. In this phase, its presence took on the character of a smouldering epizootic spreading among the rat colonies, a process manifesting itself in a few episodic human cases and preparing the ground for a rapid epidemic rise with the advent of warmer early spring weather. This explains the early start of the plague epidemic in the middle of March. However, as can be seen in Table 3 and Appendix 1, the Necrology’s registration of burials also broke down in the 1363 epidemic, three times, the first breakdown started 16 June and lasted fifteen days until 1 July when registration was resumed; a new breakdown started 26 July149 and lasted for twenty-one days, during which time there were only seven episodic burials, until 16 August when systematic registration of burials were resumed, but only for fifteen days until the

149

Or perhaps 27 July, since there is one burial 26 July.

was historical plague a viral or bacterial disease? 253 registration again broke off 30 August, this time for good. In the two weeks preceding the first breakdown of registration there had been twenty-eight burials, in the fifteen days following the resumption of burials there were sixty-eight entries. This shows that the registrations first broke off when the epidemic was in a process of intensification, that it was resumed at the height of the epidemic, and that it broke down completely and finally when the epidemic was still at its apex. It may also suggest that during the twenty-two days of intermission of registration there may have been a loss of 50–60 potential burials. The third and final breakdown came at a point when the epidemic apparently still raged with full force. Indisputably, these three lacunae are so large and disastrous for the Necrology as a demographic source also for this plague epidemic that to present any crude figure for burials in the cemetery as reflecting the reality of mortality and to use it for comparison and inferences to immunity and differential mortality by gender or age is clearly fallacious and misleading. This source-critical demonstration of the comprehensive lacunae in the Necrology and their devastating effects on its usability as a demographic source for the study of plague mortality is not the only devastating blow. Even a quick glance at Tables 4 and 5 and Appendix 1 will show, as documented above, that the proportion of child burials in the cemetery does not reflect the normal process of dying in a local society/parish society. In the eleven years preceding the Black Death, from the first full year of the Necrology in 1337 to 1347, thirty-two interred persons could have been children below age fifteen;150 in the same period a total of 519 burials were registered in the Necrology, so children constituted consequently a very low 6.1 per cent of the interred. This period includes the severe dearth year of 1340 with a greatly enhanced number of burials, namely 176, about five times the average number of burials in the ten normal years of the period 1337–47, however, the number of children interred was only nine and the proportion of children 7.4 per cent. Correspondingly, children constituted 8.2 per cent of the interments in the inter-plague period of 1349–62. In the next inter-plague period, 1364–73, the percentage of child burials was 8.2 per cent, in the following four post-plague years the percentage was 11.3. As shown in Table 5, in all of the non-plague years 1337–78 taken together, the total number of burials was 938, the total number of child

150

See Appendix 1.

254

chapter six

Table 4. Proportion of child burials in the cemetery of Camporegio in Siena, 1337–78, according to the Necrology. Non-plague years (N.P.), crisis year 1340, plague years (P.Y.), in italics 1348, 1363, 1374.151 Period

Burials

Adults

Children

%

1337–39 1340 1341–47 1348 1349–62 1363 1364–73 1374 1375–78

119 176 224 144/46 208 328 158 233 53

116 163 208 128/30 191 175 143 94 47

3 13 16 16 17 153 15 139 6

2.5 7.4 7.2 11.0 8.2 46.6 9.5 59.6 11.3

Total Total N.P. Total P.Y.

1643/45 938 705/07

1265/67 868 397/99

378 70 308

23.0 7.6 43.6

burials was seventy, so the proportion of child burials was 7.6 per cent. Even in the Black Death, the proportion of child burials was only 11 per cent. Since normal child mortality in ages 0–14 in normal years at the time would be in the range of 50–60 per cent of total mortality, this makes it entirely clear that the cemetery population was grossly unrepresentative of populations in normal local societies or parishes and that its recruitment did not reflect the normal process of dying in a normal population. Clearly, this age structure reflects special cultural and religious attitudes and practices associated with social class within a broader context of civilization. The great majority of the children of the adults interred in the cemetery must have been buried elsewhere, presumably in the cemeteries of the parishes in which their parents’ habitations were located, whilst their parents purchased expensive and religiously attractive burial places in the cemetery of the Dominicans. Obviously the increase in the proportion of child burials from the Black Death to the two subsequent plague epidemics is interesting and will be addressed below. However, the fact that the proportion of child burials

151

The material on which this Table is based, is presented in Appendix 1.

was historical plague a viral or bacterial disease? 255 reverted nearly to the pre-Black Death level in the normal years between the plague epidemics is also interesting, and must also be explained. The central point of Cohn’s argument is that he claims to have succeeded in proving that the plague epidemics repeatedly ravaging Siena in this period caused immunity in the surviving adult population and that this is what is reflected in the greatly increased percentages of child burials in the plague epidemics following the Black Death. What should now be clear is that the material he cites is grossly deficient, that the entries in the Necrology generally cannot support realistic demographic statistics or Cohn’s mortality statistics more specifically. The facts are that all child mortality statistics based on this source are methodologically invalid and factually untenable: the percentages of child burials before the Black Death and in the inter-plague periods represent only a tiny proportion of normal child mortality, and the percentages of child mortality for the plague years, disregarding for a moment the fact that they are not based on valid source material, are all within the range of normalcy of child mortality in normal years at the time and provide therefore no specific empirical reflection of child mortality in plague epidemics. Cohn’s statistics are quasi-statistics, they resemble statistics but are not. They are quasi-statistics because the registration breakdowns at an early stage of the Black Death and covers only a minor part of the epidemic. They are quasi-statistics because Cohn avoids pointing out and taking into account that there are three large breakdowns of the registrations in the Necrology in relation to the next plague epidemic of 1363. Cohn pretends that he can compare a grossly deficient part of the Necrology relating to the Black Death with another grossly deficient part relating to the second plague epidemic without having any possibility for identification of the missing parts in order to produce corrections that could make it feasible to establish tenable comparability. This is obviously methodologically fallacious independent of the phoney character of his mortality statistics. In English historiography, the term ‘bastard feudalism’ is applied to situations that resemble feudalism but are not, for instance, enlistment in royal armies of gentlemen warriors for longer periods of service than the forty days associated with feudal obligations or services given by a retainer to his lord in exchange for a fee and livery.152 In this sense, we have here bastard statistics, what

152

See for instance Hicks 1995; Bellamy 1989.

256

chapter six

resemble statistics but are not. And this is only the beginning of bastard statistics, there is much more to come. When this presentation of the Necrology’s burial register is compared with Cohn’s handling of it, interesting and revealing aspects can be observed. It may be useful to start with Cohn’s presentation of the register and its contents and then we will examine the demographic information he maintains to have extracted from it: For burials of the laity in Dominican grounds at Siena, the figures for 1348 show the same seasonal trajectory: they mounted in May, jumping from seven to 54, and continued to climb in June (66 burials), but for July the scribes ceased their reporting, perhaps turning to unrecorded mass graves or dying themselves. When the register was resumed in August, its count had returned almost to normal (6).153

Cohn maintains that he has found 127 burials in the register in the months from April to June before it breaks off, which is quite correct (126/28), but also maintains that the number of interments in the whole year is 136,154 which is not correct, as can be seen from Tables 2 and 5, and reflects a pervasive tendency of looseness with his figures. In this citation, the crucial point is that Cohn endeavours to make the period of registration seem much longer and by implication the lacuna much shorter than in fact is the case and, thus, to upgrade its quality and potential usability far beyond the limits that source-criticism will allow. He neglects to inform his readers that it broke off 6 June, misleadingly and erroneously implying that instead it continued throughout June and did not break off until some time in early July, about a month later. He also pretends that normal registration of burials was resumed in August, while the reality is that there was an episode of three burials 6 August which was followed by a lacuna lasting to 28 August, when there was a new episode of four registrations, followed by a breakdown lasting for the rest of the year when only four episodic burials are recorded. Cohn’s account would clearly tend to suggest to the unsuspicious mind that registration was resumed quite early in August and that the epidemic had declined radically at this point. For this reason, Cohn cannot inform his readers that the “66” (64/66) burials in June (Table 2) occurred in the first six days of the month and that, in fact, half of the total number of deaths for the whole epidemic as recorded in the Necrology are from these six days and, consequently, can 153 154

Cohn 2002: 171. Cohn 2002: 211.

was historical plague a viral or bacterial disease? 257 represent only a small fraction of total mortality in this month. This is a point of crucial importance since it shows that the epidemic was under explosive development when the register broke off. This indicates also that the keeping of the Necrology was discontinued because the great mortality at the time affected the monastic administration and made the organization of prestigious individual interments in the cemetery (well-nigh) impossible. Thus, Cohn’s presentation of the registrations of this Necrology for the time of the Black Death appears to be profoundly characterized by misinformation. While the lacuna in the form of absence of regular registration of burials lasts for the rest of the year, Cohn makes it seem as if it lasts about thirty-five days. Presumably his motive is to increase the register’s seeming value as a demographic source in order to make his “data” appear more plausible when he presents, forty pages later, the essence of his purported “demographic” findings or data in the form of quasi-statistics (in this quotation the footnotes are in brackets; for the correct figures, see Table 5): lay burials at Siena’s Camporeggio bear out even more forcefully the same patterns. In 1348, men and women were buried in almost equal numbers, the same as in non-plague years. [fn. 65: I Necrologi di Siena di San Domenico, 66 of 136 were female, or 49 per cent] But, with the plagues of 1363, 1374, 1383, 1400, and 1411, women consistently fared better than men, accounting respectively for 43, 45, 42, and 43 per cent of the burials, [fn. 66: In 1363, 143 of 331 were women; in 1374, 104 of 233; in 1383, 110 of 260; in 1400, 78 of 182; and 52 of 120 in 1411.]155

Unusually, and in an obvious and amateurish breach of demographic terminology, Cohn claims to have registered women when he also has included female children, which would require use of the term “females.” The records of Camporeggio (Siena) are the only ones I know to record the burials of the laity across the plague experience from the Black Death of 1348 to the fifteenth century. Here we witness a remarkable transformation. Of 136 Sienese buried in the Dominican cemetery in 1348, only 12 or under 9 per cent, were identified as children (simply filii or filie without their own names) [fn. 73].156

155

Cohn 2002: 211. Cohn 2002: 212: “Similarly, Creighton, History of Epidemics in Britain p. 122, found that the plague of 1348–9 in England carried off able-bodied young adult and not the young, weak, or elderly.” This citation is commented on above: 243, and shown to be false. 156

258

chapter six With the second strike in 1363, their proportion increased to 116 of 331, over a third of the plague burials. The change corresponds with what chroniclers across Europe were saying. As we saw earlier with sex and social class, they emphasised the plague’s indiscriminate killing in 1348. Matteo Villani called it “a plague among men of every condition, age, and sex.” [fn. 74: Matteo Villani, Cronica, I, p. 9.]157 Instead of 1361 [sic! (should be 1363), my insertion] being exceptional, the burials plot this second plague on a trend-line of increasing proportions of childhood deaths through the fourteenth century. In the third plague of 1374, the death of children in Siena increased from a third to over a half (136 of 233).158

Table 5. Proportion of child and female burials registered in the necrology of the Dominican cemetery in Siena, 1337–78. Non-plague years (N.P.), crisis year 1340, plague years (P.Y.) 1348, 1363, 1374. A = Adults, F = Females, C = Children Period

Burials

1337–39 1340 1341–47 1348 1349–62 1363 1364–73 1374 1375–8

119 116 59 176 163 91 224 208 103 144/46 128/30 15964 208 191 69 328 175 66 158 143 71 233 94 40 53 47 20

Total Total N.P. Total P.Y.

157

A

FA F A %

1643/45 1265/67 583 938

868 413

705/07 397/99 170

C

%

50.9 3 2.5 55.8 13 7.4 49.5 16 7.2 52.9 16 11.0 33.1 17 8.2 37.7 153 46.6 49.7 15 9.5 42.6 139 59.6 42.6 6 11.3

FC FC % All F% 1 8 7 8 6 75 4 62 5

33.3 61.5 43.8 50.0 35.3 49.0 26.7 44.6 83.3

50.4 60.7 49.1 52.6 36.1 43.0 47.5 43.8 47.2

46.0 378 23.0 176 46.6 46.1 47.6

70 7.6

31 44.9 47.3

42.6 308 43.6 145 47.1 44.6

Cohn 2002: 212–3. Cohn 2002: 214–5. 159 The number of adult men and women is smaller than the number of adults because in two cases of simultaneous burials of three and 4–6 persons respectively the gender of the interred is not given, no. 796–3, and no. 839–4/6, which give 64 women and 57 men. Thus, the population of gendered burials in 1348 is 137 persons when children are included, of whom women are 64 plus eight female children, in all 72. 158

was historical plague a viral or bacterial disease? 259 One should note that the Latin terms filius and filia do not mean “child” as maintained by Cohn but “son” and “daughter.” This is a point of some of importance in the present circumstances since all human beings are sons or daughters, including adults, but not all sons and daughters are children. Latin has words specifically denoting children or youngsters, for instance, natus, infans, puer/ puella, parvulus/ parvula, juvenis. The five last words are employed by the Dominican scribes, but only in twenty-eight cases160 or 1.7 per cent of the burials in the period. This confirms that neonatals, infants, toddlers and young children were not normally buried in the cemetery, although they constituted a large part of total normal mortality, probably about 45 per cent (see Table 1). Even as a point of departure for a realistic discussion of child mortality, this should be taken to suggest that also older dead children were often not buried in the cemetery with their parents or relatives. These terminological considerations agree completely with the empirical picture of the proportions of child mortality provided by the Necrology for normal years and the crisis year 1340. On the other hand, since sons and daughters also are children, many of them, quite possibly a large majority of those who are registered without indication of marital status or other indications of adult age, will be children. Importantly, there can be no doubt that the identification of all entries of unnamed sons or daughters as children will produce an unrealistically high figure, but since there is no means of “sieving” this material, it is probably best to do as Cohn does and identify them all as children, as I have also done. However, Cohn neglects to inform his readers about his choice and its consequences (see Appendix 1). One should also note that the term juvenis meaning “youth” could also denote persons of age 15 and a few years older, but this problem is of no real significance since it used only in five cases.161 As can be seen from Table 5 and substantiated by the presentation of the underlying material in Appendix 1, Cohn’s figures are inaccurate to the point of being erroneous and misleading: the number of recorded burials in 1348 is 144/46, not 136, and the number of children is sixteen, not twelve. In 1363 the number of burials is 328 and the number of children is 153 and not 116, seventy-eight boys and seventy-five 160 I Necrologi di San Domenico 1337: Nos. 466, 843, 881, 896, 913, 976, 996, 1176, 1189, 1212(1229), 1224, 1227, 1231, 1233, 1234, 1425, 1427, 1450, 1509, 1839; 1116–2, 1550; 1054, 1070–2, 1071, 1667. 161 I Necrologi di San Domenico 1337: Nos. 1054, 1070–2, 1071, 1667.

260

chapter six

girls; the proportion of child burials is thus 46.6 per cent and not 33 per cent. This discrepancy is so large that it is inexplicable as the outcome of serious research but could possibly be explained on the assumption that Cohn wishes to produce a larger rise in the proportion of immune persons in the population as the logical consequence of repeated plague experience. Further comments must start with elementary source-criticism which predictably levels more devastating blows at Cohn’s use of the Necrology. It is not true, to put it in the mildest possible terms, that the Necrology of San Domenico at Camporegio contains continuous records of the “plague experience from the Black Death of 1348 to the fifteenth century.” Cohn knows, and the readers now know, and also know that he knows, that for most of the period of the Black Death there are no registrations in the Necrology, simply because the registration of burials broke down early in the development of the epidemic162 and that there are three large lacunae in the Necrology for the period of the plague of 1363. Cohn does not subject his purported demographic data from the Sienese Necrology to the usual source-critical and analytical tests by presenting and addressing crucial questions: Did the burials in this prestigious cemetery recorded in the Necrology really reflect the normal process of living and dying in a normal population of a local parish? Could they have been affected by religious and social prestige, social class and cultural notions which attracted deceased for burial from elsewhere or from special segments of local population or the Sienese population? Could the interred for these reasons be socially skewed also according to age or gender? True, ten pages before his presentation of his purported demographic data from this source he states: the demand to be buried in Siena’s Dominican cemetery also appears to have risen in tandem with the rising prestige of the Dominicans in postplague Siena, as illustrated in the pious choices of the laity in their last wills and testaments.163

In a much used technique, Cohn separates this important sourcecritical information from his discussion of the source and presentation

162 Here it is not of significance whether or not this reflected the actual breakdown of the process of interments. 163 Cohn 2002: 200–1.

was historical plague a viral or bacterial disease? 261 of his purported demographic results. This reveals that Cohn recognizes that the cemetery population was not recruited from the local parish population, at least to a considerable extent, but attracted people living elsewhere, in other localities and parishes, for religious and devotional reasons in the hope that a burial place there would enhance their afterlives and also out of social ambition associated with prestigious religious burial places in those days. The Necrology contains much material showing that burial places were often expensive, and the scribe functioning in the years c. 1368–74 provides a particular abundance of such information.164 In this context, Cohn supports his argument by stating: “the number of burials recorded at Santa Maria Novella in Florence during the second plague of 1363 also outstripped those of 1348 (90).”165 Cohn neglects to mention that this burial register also breaks off during the peak of the Black Death and therefore is grossly incomplete, a fact that the responsible historical demographer Livi-Bacchi conscientiously underlines. He also scrupulously underlines the very special character of this burial list, namely that it recorded those interred with the Dominican habit, a ceremony performed with some pomp, an honour that only devoted upper-class people could afford.166 These central source-critical facts are also carefully emphasized in my discussion of this source and its potential usefulness in my monograph on the Black Death.167 Thus, this register is socially unrepresentative as well as highly incomplete, and Cohn’s use of it is misleading and fallacious. The burials of persons in the habit of the Dominicans in the cemetery of Santa Maria Novella in Florence was not unique; according to the Sienese Necrology this was also the case with quite a number of those interred in the Dominican cemetery there. Unfortunately, this information cannot attain further source-critical function since Cohn does not discuss this Dominican cemetery’s religious and social prestige before the advent of the Black Death but links it directly to his presentation of his purported demographic data from the Necrology. Although it is not stated explicitly, it seems that this was a prestigious burial ground also before the Black Death; according to Cohn its religious prestige increased in post-plague Siena, but perhaps it would be more accurate 164 165 166 167

I Necrologi di San Domenico in Camporegio 1937: 104–22. Cohn 2002: 154. Livi-Bacchi 1978: 14. Benedictow 2004: 292.

262

chapter six

to say that it continued to increase.168 There is strong evidence for assuming that the cemetery population was skewed not only by age, but also by social class. Also Cohn’s claim that “women consistently fared better than men” in subsequent plague epidemics according to the Necrology of San Domenico in Siena, in the meaning that they suffered lower mortality rates, is obviously fallacious and untenable. The distribution of burials of female and male adults and female and male children in the period 1337–78 are shown in Table 5 below and in Appendix 1. The Necrology’s burial figures from the time of the Black Death cannot be compared with later burial figures for two independent sufficient reasons. Firstly, the comparison is fallacious for the fundamental source-critical and methodological reason that it represents only a small fraction of the Black Death and cannot, therefore, be compared with purportedly complete but, in fact, also grossly incomplete registrations of burials in the 1363 epidemic or with the registrations of burials during the subsequent plague epidemic of 1374. Secondly, the comparison is fallacious as the social origin and composition of the population of living which was recruited into the cemetery population has not been usably clarified. It is clearly not a normal local population or parish population as is overwhelmingly demonstrated by the gross deficit of children in normal years. These two conditions represent two independent sufficient conditions for concluding that it is fallacious to maintain that the somewhat lower proportions of women’s burials in subsequent plague epidemics reflect lower female mortality. Instead, the small tendential underrepresentation of females could reflect the fact that men in this society were considered more important than females and that, for this cultural reason, males were more often given prestigious and costly burials. Thus, what the Necrology’s burial lists quite probably show is not that “women consistently fared better than men” in plague

168 Cohn ignores the usual source-critical question of the extent to which the seeming increase in this burial ground’s prestige is real, and not affected by other factors, for example, by the fact that wills and testaments which he refers to for substantiating his point became more usual in the period following the Black Death (and subsequent plague epidemics), which resulted in larger numbers of inheritances and increased the affluent proportion of the population, and/or also as a consequence of intensive changes in culture and mentality associated with the development of Renaissance society. Perhaps even more important were the lessons learned from the difficulties of making wills during such a tremendous mortality crisis as the Black Death, emphasizing the importance of preparing for calamities of a new dimension.

was historical plague a viral or bacterial disease? 263 epidemics but that they consistently fared worse than men with respect to getting burials in prestigious burial grounds. Only this explanation contains a causal factor and must therefore be deemed superior. As underlined above, it is fallacious not to take into account the fact that social, cultural and religious factors could affect the cemetery population and the relative distribution of burials according to the main socio-demographic divisions of social class, gender and age which may produce alternative explanations. The social unrepresentativeness of the cemetery population stands out in glaring clarity when child mortality, which is at the heart of the matter under discussion here, is considered more closely.169 As shown above in Table 5, in all non-plague years 1337–78 taken together the proportion of child burials was 7.6 per cent. In the Black Death, the proportion of child burials was only eleven per cent. Since normal child mortality in ages 0–14 in normal years at the time would be in the range of 50–60 per cent of total mortality, the recorded level of child mortality is clearly grossly unrepresentative of normal local societies or parishes at the time and the recruitment of the cemetery population was not the result of the normal process of dying in a normal parish population, but reflects special cultural and religious attitudes and practices associated with social class and a wide(r) catchment area. As pointed out above, the great majority of the children of the adults interred in the cemetery must have been buried elsewhere, presumably in the cemeteries of the parishes in which their parents’ habitations were located, while their parents purchased expensive and religiously attractive burial places in the cemetery of the Dominicans. Obviously, the strong increase in the proportion of child burials from the Black Death to the two subsequent plague epidemics from 11 per cent in the Black Death to 46.6 per cent in the second plague epidemic and 59.6 per cent in the third epidemic is interesting and must be explained. However, also interesting is the fact that the proportion of child burials in the second and third plague epidemics does not exceed the level of normal child mortality at the time of 50–60 per cent, which shows that these strongly increased mortality rates do not reflect or indicate specific levels of plague mortality. The fact that the level of child mortality reverted nearly to the pre-Black Death level in the normal years between the plague epidemics must also be explained.

169

See also above: 228–35.

264

chapter six

Cohn asserts that in the plague of 1400 in Florence, the “gravediggers identified two-thirds” of burials as children, however, he does not provide a footnote.170 Despite considerable efforts, I have not been able to identify the possible source with certainty, but it could be a table in Carmichael’s monograph.171 As mentioned above, Carmichael found that the Florentine Books of Dead “give strong evidence of heavy mortality among dependent children during the early fifteenth century,” and that “during epidemic years [in the decades around the mid-1450s] more than 70 per cent of those dying from all causes were children.”172 Thus, it may appear that Cohn understates the significance of Carmichael’s findings and that the threat they represent to his alternative theory may be the reason for his unreasonable attacks on her work which is, in fact, of high scholarly standards (see above). Also the purported further increase in the proportion of child burials in the next plague epidemic of 1374 to over half reflects underregistration of child mortality as a proportion of normal mortality in plague epidemics, since children are particularly at risk in plague epidemics and child mortality increases as a proportion of total mortality, but also this mortality rate is within the range of normal child mortality in normal years. Obviously, the proportions of child burials according to the Necrology are gravely deficient and grossly unrepresentative, they cannot serve as evidence of the real level of child mortality in normal years or in plague years or be taken to demonstrate any change in children’s proportions of mortality between the two first plague epidemics or in relation to later plague epidemics. Consequently, the increases in registered proportions of child burials in the two post-Black Death plague epidemics in this cemetery do not constitute evidence that this development represents increasing levels of immunity among survivors so that groups of children born after the previous epidemic constituted increasing proportions of the susceptible part of the population. Instead, one must consider other reasons for the increase, especially changes in religious attitudes and practices under the traumatic psychic impact of the Black Death. When the Sienese chronicler Agnolo di 170

Cohn 2002: 215. Carmichael 1986: 94. Cf. however, Carmichael 1983: 514. In Herlihy and Klapisch-Zuber 1978, which would be a likely source for such information, the entries on gravediggers = becchini/(fossoyeurs) match with “peste 1400” only on pages 453 and 456 where nothing to this effect is stated. I have also checked all pages which the index indicates contain references to gravediggers or to “peste 1400.” 172 Carmichael 1986: 91–2. See above: 235. 171

was historical plague a viral or bacterial disease? 265 Tura informs his readers that he buried his five children with his own hands, we can only attempt to understand the psychic trauma, and since this terrible experience, according to his account and other contemporary accounts, appears to have been quite usual, its generalized psychological effects on Sienese mentality and culture must also be taken into account. It is also important to take into account the fact that these informal burials were unlikely to have been registered anywhere, and the possibility cannot be excluded that Agnolo di Tura buried them in the cemetery of San Domenico in Camporegio. Of particular importance in this context is the following quotation from Agnolo di Tura, which shows that not only the mind-boggling mortality of the Black Death but also the breakdown of burial services impressed itself on contemporary observers: And so they died. And none could be found to bury the dead for money or friendship. Members of a household brought their dead to a ditch as best they could, without priest, without divine offices. Nor did the death bell sound. And in many places in Siena great pits were dug and piled deep with the multitude of dead. And they died by the hundreds both day and night, and all were thrown in those ditches and covered over with earth. And as soon as those ditches were filled more were dug. And I, Agnolo di Tura, called the Fat, buried my five children with my own hands. And there were also those who were so sparsely covered with earth that the dogs dragged them forth and devoured many bodies throughout the city.173

The last rites were a necessary condition for salvation according to the teachings of the Church, as was burial in a consecrated burial ground, and a proper funeral was considered indispensable for the profoundly religious and devotional minds of contemporary medieval persons. Nothing worse could happen to them than the events so graphically described by Agnolo di Tura, that the dead were unceremoniously thrown into ditches. Agnolo di Tura’s account does not stand alone: other contemporary chroniclers, for instance Marchionne di Coppo Stefani in Florence described the social scene in a similar way: All the citizens did little else except to carry dead bodies to be buried; many died who did not confess or receive the last rites; and many died by themselves and many died of hunger […]. At every church they dug deep pits down to the water-table; and thus those who were poor who died

173 Cited in The Black Death. A Turning Point in History? 1971: 13. Cf. Del Panta 1980: 112; Benedictow 2004: 92, 94.

266

chapter six during the night were bundled up quickly and thrown into the pit. In the morning when a large number of bodies were found in the pit, they took some earth and shovelled it down on top of them; and later others were placed on top of them and then another layer of earth, just as one makes lasagne with layers of pasta and cheese.174

Evidently, the most frightening features of this enormous demographic disaster in the authors’ mind are, in accordance with the religious beliefs and mentality of the time, that people died without priestly administration of the last rites, and, thus faced perdition and eternal punishment, and that their loved ones were unceremoniously and humiliatingly thrown into mass graves or, even worse, unconsecrated ditches, which was an independent sufficient condition for perdition or at least prevented salvation. There is every reason to believe that such very frightening and humiliating events on a mass scale would have jolted many persons into action to save themselves and their spouses and children and other loved ones from such a fate in the future and there is every reason to believe that the representatives of the Catholic faith, both the secular and regular clergy, took the same view and also considered how this could be avoided in the future. In other words, when the second plague epidemic and subsequent plague epidemics arrived, there was a mental and practical preparation of all parties concerned for a tremendous onslaught, among the laity as well as the clergy. This explains the tremendous efforts by the Dominicans of San Domenico in Camporegio to re-establish the functioning of the Necrology and burials during the second onslaught of plague, twice succeeding in reorganizing a functioning administration after breakdowns. This explains on source-critical grounds some peculiar features of the Necrology over time: it seems that parents who had purchased costly and prestigious burial places in the Dominican cemetery acquired the right to have their children buried properly there and preferably in their own graves or sepulchres in order to be certain that their children would not be unceremoniously thrown into mass graves or unconsecrated ditches if they died when they were sick themselves or after they had died and were unable to take care of the children’s burials. In this perspective, it is also important to take into account the fact related so graphically by contemporary chroniclers that the

174

Cited after Henderson 1992: 145.

was historical plague a viral or bacterial disease? 267 mind-boggling mortality in the Black Death had the effect that many survivors received inheritances and acquired a new wealth or good fortunes, and many also entered good economic positions due to opportunities created by the epidemic. Survivors of the Black Death and later plague epidemics were quite likely to be lucky twice. Agnolo di Tura, for example, states that “all money had fallen into the hands of nouveaux riches,”175 which is certainly logical: when a great proportion of the population, probably over half, dies in a few months, many of the survivors must receive an inheritance and often multiple inheritances. This meant that many people could now afford not only to raise their standards of living substantially but also acquired the means to raise the standard of their afterlife by the purchase of attractive burial places for themselves and their spouses and ascertaining that also their dead children would be properly taken care of when the burial process in their local parish cemeteries broke down, as it so often did in the Black Death. This is only a well-founded explanatory hypothesis which, however, integrates much important material and many important perspectives of the contemporary scene, is not a variance with known facts, and is a methodologically and materially tenable hypothesis, which Cohn’s immunity theory is not. Crucially, this hypothesis is materially testable, and I can only hope that historians of contemporary culture and mentality will address it from a scholarly basis that I do not possess. This discussion of the material bearing on Cohn’s alternative theory to the effect that plague was a viral disease, that survivors acquired strong and persistent immunity and that plague epidemics subsequent to the Black Death developed into a child disease can now be summarized. Much of the purported material from chroniclers and burial lists which Cohn produces to support his theory is not valid and must be rejected as evidence for his theory. At a closer look much of his material does not agree with his theory or is incompatible with it. It has also been necessary to cite a number of studies and much material left out by Cohn which is at variance with his theory. It has also been made clear that Cohn does not base his discussion on adequate demographic competence, as reflected in the absence of realistic notions of normal levels of child mortality in medieval society and the normal proportion of child mortality of total mortality, and in his flawed terminology.

175

The Black Death. A Turning Point 1971: 15.

268

chapter six

It has also been shown that he has not taken into account the frequent fulminant course of plague disease in children and youth with a consequent increased level of lethality or their supermortality from secondary catastrophic effects in plague epidemics, which increase children’s relative proportion of mortality above the normal proportion of 50–60 per cent in normal times. Unsurprisingly, it is possible to find chroniclers who make this point, that children and youth also suffered a disproportional level of mortality or supermortality in the Black Death. In addition, Cohn has ignored or neglected Cazelles’s study on this point as well as Glénisson’s study of the second epidemic. Cohn has not presented tenable evidence to the effect that the relative or absolute level of child mortality increased from the Black Death to subsequent plague epidemics. Cohn has also neglected to take into account several important pieces of research with direct bearing on his theory of immunity effects associated with historical plague: the material on re-infections, the stability of lethality rates, the pattern of clustering of plague cases according to size of family, and so on, which represent further evidence that historical plague could not have been a viral disease spreading by cross-infection. Cohn’s assertions to the effect that plague epidemics subsequent on the Black Death took on the character of a child disease are untenable. The Real Problem and its Solution: Marriage Rates and Fertility Rates after the Black Death In the chronicles it is possible to discern a stronger emphasis on the perceived level of child mortality in the second plague epidemic than in the Black Death. This impression is, then, the real problem to be addressed which has been overlooked or ignored by Cohn since it does not imply any potential for support of his great revolutionary alternative virus-based theory. A real interest in this impression and a scholarly will to examine and explain it in its own right rather than turning it into a case for a revolutionary new theory could usefully start with another point made by chroniclers. As pointed out by Glénisson, “The contemporaries have noted that, after the plague epidemic [the Black Death], there was an epidemic of marriages and the number of births rose.”176 Jean de 176

Glénisson 1968–9: 30. My translation from French.

was historical plague a viral or bacterial disease? 269 Venette’s description of how survivors of the Black Death reacted to the post-plague social scene and the new sociology of opportunity can be a useful point of departure: After the cessation of the epidemic, pestilence, or plague, the men and women who survived married each other. There was no sterility among the women, but on the contrary fertility beyond the ordinary. Pregnant women were seen on every side. Many twins were born and even three children at once.177

Jean de Venette claims to have observed that, in the wake of the Black Death there was a great upsurge in marriages and a great consequent increase in fertility. As usual, chroniclers’ statistics cannot be taken literally, and there is no biological reason to accept that sterility among women disappeared in the wake of the Black Death, or that there was an increase in individual natural fertility, or that there would be any increase in the incidence of births of twins or triplets, but one may take serious interest in the generalized impression of great increase in marriage rates and a consequent strong increase in fertility rates. Chroniclers’ statements in this regard can be taken seriously because this type of development should be expected for three main reasons. In the decades before the advent of the Black Death life was difficult for the great majority of common people both in the towns and in the countryside. Great population pressure on the resources for production and income made it difficult for young adults to find work and income that could serve as a base for sustaining a family, thus there was a pool of young persons ready to marry and on the lookout for opportunities. This is a Malthusian explanation based on comprehensive economic and social research and appears to be tenable for most of Europe, from Norway in northern Europe to Spain in southern Europe, from England and France in Western Europe all the way to Poland178 in Eastern Europe.179 Secondly, great mortality entails that many people will receive inheritances, often from more than one relative, so the 177

The Chronicle of Jean de Venette 1953: 51. See for instance Pelc 1937. His price history of Krakow agrees completely with the price history of Western European countries and both reflect great Malthusian pressures before the Black Death and a late medieval fall in grain prices and increase in wages which must reflect a great contraction of the population which allowed peasants and their lords to concentrate grain growing on the best and most productive lands while the demand for workers produced an upwards pressure on wages. Cf. Benedictow 2004: 219–21, 387–94. 179 Benedictow 2004: 177–9, 388–91. 178

270

chapter six

economic situation of survivors would tend to be strongly improved. Thirdly, the social situation would now be very favourable for marriage because great mortality creates attractive vacant positions in the labour market and the housing market.180 Young adults entered them, acquiring the economic ability to realize marriage ahead of plans, often even making dreams come true. Thus, not only would young widows and widowers soon remarry and keep up normal reproduction, but also many young unmarried persons would now be in a good position for entering into matrimony producing in due time a large increase in realized fertility, a baby boom, that would produce a corresponding increase in the proportion of infants and children in the population. The period from the Black Death to the second plague epidemic covers the whole span of child years, ages 0–14, as in Siena where the Black Death raged in 1348 and the second plague raged in 1363, or almost the whole span of child years in Norway, where the main year of the Black Death was 1349 and the second epidemic raged in 1360.181 In fact, quite a number of studies of various plague epidemics reveal that a strong increase in marriage rates was a characteristic feature of post-plague social developments. With the usual time-lag, birth rates increased briskly.182 There is also significant and important empirical evidence associated with the aftermath of the Black Death. This pattern is clearly reflected in the only extant parish marriage register from the time of the Black Death, that of Givry in Burgundy. In the years 1336– 41, for which the register appears to be complete, the mean number of marriages was 17.5, varying between eleven and twenty-nine. In 1348, the year of the Black Death, no marriages were recorded in this small Burgundian town, either because the keeping of the register broke down or because the ravages of the Black Death had made it impossible to arrange new marriages either for the hopeful or for the parish priest and his auxiliary personnel. However, in 1349, the number of registered marriages was eighty-six, a quintupling of the pre-plague mean. And for a number of subsequent years the number of marriages was considerably higher than in the pre-plague period: in the year 1350 there were thirty-three marriages, and the number did not fall under 180

Cf. Herlihy and Klapisch-Zuber 1978: 194–8. Benedictow 2002: 44–81, 91–2, 115. Cf. Benedictow 1993/1996: 73–102, 141–5. 182 Bickel 1956: 515; Russell 1958: 41–2; Le Méné 1964: 196, 209; Croix 1967: 77; Croix 1981: 264–345; Dupacquier 1972: 199–204; Clark and Slack 1976: 88–9; Hatcher 1977: 56–7; Herlihy and Klapisch-Zuber 1978: 208; Perrenoud 1978: 265–88; Vaquer Bennassar 1987: 133; Weiner 1970: 50–1. 181

was historical plague a viral or bacterial disease? 271 the pre-plague level until 1355, when there were twelve marriages followed by ten marriages in 1356.183 Since the post-plague population must have been much smaller than before the plague, the marriage rate was quite likely still significantly higher in 1355–6 than before the Black Death. The same was the case in Florence after the Black Death: “The memories of the Florentine families show well the cascades of marriage contracts which followed a great epidemic.”184 The same development has been noticed in England by several scholars. T. Lomas found that at the manor of Norton in County Durham “there were a great many grants of licence to marry [merchets] in 1350.”185 J. Ravendsdale found in his study of the manor of Cottenham in Cambridgeshire a rush to the altar (or should it be the church door) in 1349 [which] represented marriages that would have been postponed even longer but for the plague, the average age at marriage would have been depressed, thus bringing increased fertility within marriage. The crop of marriages in 1349 must have been followed by a baby boom among the villeinage.186

In his study of the manor of Halesowen (Worcestershire), Razi found that in the three-year period which immediately followed the Black Death, “proportionally more marriages were contracted in Halesowen than in any other three-year period in the fourteenth century.”187 The number of marriages in Halesowen “rose sharply again in the years 1361–3 as a reaction to the second visitation of the plague,” which is evidence that mortality among adult members of the manorial community was high. If mortality had been concentrated among children because many or most of the adults were immune, the second plague would not have been followed by an upsurge in new marriages. It is also evidence to the effect that supermortality among children is a general feature of plague epidemics. Razi concludes that “during the first two decades following the Black Death the marriage rate in the parish was high […] the birth rate must have been at a high level.”188

183 184 185 186 187 188

Gras 1939: 303. Herlihy and Klapisch-Zuber 1978: 196. My translation from French. T. Lomas 1984: 260. Ravensdale 1984: 212, cf. 209. Razi 1980: 132–3. Razi 1980: 134.

272

chapter six

This means that in the years following the Black Death, the proportion of children (ages 0–14) in society would have increased considerably and even substantially above the normal level of around 50–60 per cent. Since children constituted a considerably or substantially higher proportion of the population at the time of the second plague than before the Black Death, children would also constitute a correspondingly higher proportion of total mortality than in the Black Death. If child mortality normally constituted 65–70 per cent of population mortality in the Black Death, this explains why some chroniclers noticed a relative increase in child mortality in the second plague compared with what they had seen in the Black Death. A substantially increased proportion of child mortality above this level would readily affect the impressions of contemporary observers, and this is what probably occurred in relation to the second plague epidemic. On this solid background of facts and studies, the fact that some chroniclers designated the second wave of plague epidemics as a child disease can reasonably be taken to reflect a perception of a real phenomenon: children below the age of fifteen constituted an unusually high proportion of the population, and children in general died in correspondingly higher proportions which also were affected by the additional specific increase related to plague disease, and produced an impressionistically observable higher proportion of the victims than people were accustomed to.189 These impressions reflected social and demographic reality but had nothing to do with immunity among survivors in the Black Death or subsequent epidemics. This is a sufficient and satisfactory explanation of the tendency among chroniclers to emphasize the high proportion of child mortality in the Black Death and the stronger tendency to emphasize the high proportion of child mortality in the second plague epidemic. This resolution of the problem addressed in this chapter corresponds also to the observations by chroniclers of the socio-demographic distribution of mortality in the second plague epidemic, for instance, by Knighton: Eodem anno mortalitas generalis oppressit populum quae dicebatur pestis secunda. Et moriebantur tam majores quam minores, et maxime juvenes et infants. Et de congregatione nostro xi canonici mortui sunt.

189

Benedictow 1993/1996: 144–5. Cf. Bridbury 1973: 591.

was historical plague a viral or bacterial disease? 273 This year a widespread mortal disease visited the population which is called the second plague. Both the upper and lower classes died, and especially youth and children. And in our congregation eleven canons died.190

As can readily be seen, the contemporary observer Knighton was of the opinion that all main social classes suffered serious mortality; adults were not spared, as is also shown by the Dominican Necrology of Siena, but children and youth suffered even higher proportions of mortality than in the Black Death. This is what should be expected according to ordinary demographic and sociological considerations and has nothing to do with acquired immunity in any part of the population. This account explains the phenomenon in the basic scientific meaning that all relevant evidence can be satisfactorily incorporated within a normal demographic explanatory framework based on ordinary demographic developments in the wake of plague epidemics. After I first pointed out this resolution of this problem in my doctoral thesis,191 I have noted that both L. Genicôt and A. Bridbury have suggested a similar explanatory model and it seems also to be implied in Herlihy’s and Klapisch-Zuber’s study of late medieval Florence.192 Cohn discusses quite a number of points mentioned in my doctoral thesis and exhibits quite comprehensive knowledge of it. One may again note with interest that his reading is selective, and he takes no notice of the sections on immunity and on the inverse correlation between population density and mortality in modern as well as and historical in plague epidemics, epidemic manifestations with evidentiary powers of falsification of his alternative theory.

190

See Shrewsbury 1971: 128; Russell 1948: 229 and fn. 24. Benedictow 1993/1996: 141–5. 192 Genicôt 1966: 675–5; Bridbury 1973: 591; Herlihy and Klapisch-Zuber 1978: 195–7. 191

PART FOUR

DEFINING FEATURES

INTRODUCTION: CONCEPT OF DEFINING FEATURE In principle, all diseases are identified by comparison with known defining properties or a set of characteristic features according to a level and range of compatibility. A standard case definition serves as the base for description of the epidemiology of a disease or health event. This comparative methodological approach must also be used in all endeavours to identify historical diseases, including the question whether or not historical plague epidemics were bubonic plague or had a different microbiological identity according to any of the alternative theories. In the Part 3 above, it has been decisively shown that all fundamental requirements for the rise and spread of bubonic plague epidemics were operative in medieval and early modern Europe. It has also been shown that the central aspects of spread and mortality were not at variance with the observations on bubonic plague made by the IPRC when proper account is taken with respect to the extent and modernity of the epidemic countermeasures implemented in India at the time. It has also been clearly demonstrated that the pattern or dynamics of spread and the level or social distribution of mortality did not militate against the disease being bubonic plague. All assertions of the advocates of alternative theories of historical plague to the contrary were shown to be untenable. The fact that the fundamental requirements for bubonic plague were operative in European society at the time obviously suggests the possibility of epidemics of bubonic plague. A defining feature of an epidemic disease is characteristic only of that disease and permits therefore certain identification. In medical or epidemiological terminology, the term is “pathognomonic feature” or also “cardinal feature,” while in the terminology of social science it is a “defining feature,” a self-explaining term that will be used here. Defining features can be ordinary clinical and epidemiological manifestations of a disease caused by a specific infectious pathogen and its process of transmission or demographic manifestations in the form of a unique level or pattern of morbidity or mortality according to age, gender, social class or population density. Positive identification of the microbiological agent of historical plague epidemics can be achieved by direct positive identification of

278

introduction

the genetic or biological material, the DNA or proteins of Yersinia pestis, taken from skeletal remains in plague graves of the past. Such findings will constitute evidence to the effect that the pathogen of bubonic plague was present at the time and was spread in epidemic form and, consequently, independently make a strong or decisive case for the identity of historical plague epidemics with bubonic plague. This topic will be discussed below in the chapter “Defining Feature 5: Reclamation of Yersinia pestis from Plague Cemeteries or Graves.” It can also be identified by unique clinical or epidemiological properties like, for instance, the normal occurrance of buboes or latency periods. Defining features can also have a composite character, that is, they can consist of two or several characteristic features each of which may not be unique to a specific disease but which taken together constitute a unique combination of concomitant manifestations which satisfy the definition of a defining feature. Shrewsbury is very clear and firm on this point on page 1, specifically in connection with the identification of historical diseases: The confirmatory evidence that is required to identify a pestilence in olden times as an epidemic of bubonic plague may be either a contemporary description of the clinical picture of the pestilence that is pathognomonic of plague or a conjunction of certain observations that are exclusive to the epidemiology of plague. Unless, one—and preferably both—these conditions are fulfilled the assumption that an ancient pestilence was an epidemic of bubonic plague is not justifiable.

These general comments on the concept of defining features pave the ground for presentation and discussion of some specific reflections or manifestations of bubonic plague that constitute a definitional feature suitable for comparison with historical plague for the purpose of identification of the nature of the disease. These features can, as mentioned, usefully be divided into clinical, epidemiological, and demographic. This provides a basis for presenting a sample of cases suitable for identification of historical plague.

CHAPTER SEVEN

DEFINING FEATURE 1: LATENCY PERIODS Bubonic plague epidemics have a distinctive temporal pattern of development from the introduction of plague contagion into a rat colony in a locality to the first human case or cases which can usefully be divided into several phases (see also Appendix 3): (1) The temporal pattern of plague-infected rats and fleas (1a) Normally, when an infective rat flea of the usual species Xenopsylla cheopis has been introduced into a rat colony, it takes ten to fourteen days before the rat colony has become so decimated that it is difficult for the great numbers of fleas which have gathered on the remaining but soon-to-die rats to find new hosts.1 (1b) After about three days of fasting, hungry rat fleas will turn on human beings in their immediate surroundings.2 This initial epizootic phase of a bubonic-plague-epidemicto-be lasts thirteen to seventeen days. (2) Temporal pattern of the first human case or cases (2a) Time of incubation: When human beings have been infected with bubonic plague, the infection takes on average three to five days to incubate before the disease breaks out. (2b) Duration of illness: The course of illness takes on average another three to five days before the diseased in most cases die.3 Thus, the development of a human plague case from

1

IPRC 1907g: 764; Lamb 1908: 21, 51; Wu Lien-Teh 1936b: 222. IPRC 1907g: 765; Lamb 1908: 52; Wu Lien-Teh 1936c: 387; Pollitzer 1954: 485. 3 IPRC 1907g: 765; Lamb 1908: 52; Chun 1936: 309–10, 313; Wu Lien-Teh 1036c: 387; Pollitzer 1954: 409–11, 418, (485). The IPRC estimates the average duration of illness in fatal cases at 5.5 days. This figure is the outcome of the fusion of two sets of figures, namely the average duration of illness of 100 fatal cases reported on their case cards, which was 3.6 days, and the average of 64 hospital cases which was 7.5 days. I cannot agree with the IPRC that the average duration of illness according to these two sets of figures is 5.5 days: instead the average is 5.12, which should be rounded to five days. In my opinion, this estimate is probably flawed also for methodological reasons. 2

280

chapter seven infection to death takes usually six to ten days, on average, eight days.

(3) Latency period, first part From the introduction of plague contagion among rats in a human community it normally takes nineteen to twenty-seven days, on average around twenty-three days, before the first person dies from plague. This time lag or latent period between the importation of contagion and the first human case(s) is one of the defining features of bubonic plague: no other epidemic disease exhibits a similar pattern of early development. New research has fully clarified the biological premises.4 (4) Endemic phase Since this process will have to be repeated by the spread of infective rat fleas (by contiguous spread or metastatic spread) to other rat colonies where the disease will develop in a similar way, the development of a plague epidemic is characterized by a slow, incipient initial phase, an endemic phase, with only a sprinkling of cases while the underlying epizootic processes acquire increasing momentum and eventually become manifest by several concomitant deaths and cases of severe illness. (5) Transition from the endemic into the epidemic phase and the full latency period The transition into an epidemic phase takes around forty days after the introduction of plague contagion into a rat colony in a human community. In this phase the epidemic developments become more immediately observable and recognized in village Quite likely, cases arriving at hospitals would tend to live longer and have a better social background than the average of Indian plague cases. One misses therefore considerations relating to questions of social and illness-related representativeness. The numbers of patients constituting the two sets of figures appear to be used unweighted according to notions of representativeness and the reasons for the great discrepancy between the two figures are not commented on. Taken together, these factors represent significant methodological problems. I prefer therefore later estimates which also take into account subsequent experience, namely that the duration of illness is normally three to five days, which also corresponds better to the information taken down on the IPRC’s case cards. Since the IPRC gives a shorter average period of incubation (three days) than later estimates (three to five days), the duration of these two elements taken together does not differ significantly from the average represented by later estimates. If the small correction noted above is taken into account, the figures will be identical and average eight days. In a later study of the duration of the course of illness, the Commission estimated the average for thirty-eight fatal cases at “a little over four days.” IPRC 1907j: 943. This accords with Pollitzer’s information. 4 Appendix 3: 682–7.

latency periods

281

communities. In larger towns, cities and metropolises, the process of recognition will be delayed from a few days up to two weeks according to the size of the city, because the immediate observability of the early epidemic developments will be affected by increased social and territorial distance between the first cases and the great majority of the population and representatives of the social classes who would note the occurrence in writing in some form that eventually might be available to historians.5 This delay from the first death to an early epidemic situation characterized by several or more concomitant deaths and severely diseased persons is therefore also social in construction, and more complex social contexts require a higher degree of epidemic development before the epidemic becomes more generally observable and obviously significant to the observers. The episodic occurrence of deaths in epidemic disease was a fact of daily life in medieval and early modern society, in urban society as well as in rural society. This period while plague disease rages among house rats up to the time the epidemic flares up and becomes readily observable and recognizable is called the (full) latency period and “is characteristic of plague of rat origin.”6 For these reasons, epidemics of rat-based bubonic plague are generally also characterized by protracted duration in the same locality. The recognition of the existence of a latency period belongs to the very early days of modern plague research. It was first noted by P.L. Simond, the pioneer French epidemiologist who, in a paper published in1898, noted that plague had a latency period of usually around twenty days between the introduction of infection into a locality and the epidemic outbreak. Simond points out that this feature is incompatible with inter-human spread of a disease. Hankin knew Simond’s paper a few years later and put his observation to good use in his endeavours to understand the Indian plague epidemics in the years around 1900. In these early days, terminology as well as the understanding of the mechanisms of spread of bubonic plague were rudimentary, but the reality is clear when Hankin states in a chapter called “Simond’s Latent Period in the Locality”: This undeniable fact of the frequent occurrence of a long period of incubation in the locality independently of the incubation period in 5 6

Benedictow 2004: 57–9, cf. 124–5. See also Sticker 1910: 369. Hirst 1953: 125.

282

chapter seven the human body, indicates that, as a rule, plague spreads not by simple contagion from patient to patient, but by some deep-seated and perhaps complicated method.7

Here for the first time the term “latent period” emerges, but is not established in the community of scholars and presumed to be unfamiliar to the readers and is therefore pedagogically explained by Hankin as an incubation period of the locality which precedes the incubation period in the infected person. Clearly, these two incubation periods correspond quite closely to the term of the first latent period. Hankin illustrates the point by an account of the introduction and first development of bubonic plague in the village of Mahlgahla in the Punjab in 1898: The infection was introduced by a woman who was attacked by the disease, and who on the day following her attack, with her whole family, was removed from the village to an isolated camp. Twenty-one days later seven of the inhabitants of the village were attacked […] disinfection of the evacuated quarters of the village in which no human cases had occurred, was commenced. Numbers of dead rats were found in each of these quarters […].8

The latent period is also described by the IPRC, now with an accurate temporal and factual description of the epizootic process among the rats, the consequent release of infective fleas, their subsequent attack on human beings in their proximity, and the duration of the incubation period and the course of illness.9 These findings by the IPRC confirmed and explained Simond’s and Hankin’s observations of a latency period and their view that this latency period ruled out the possibility that bubonic plague was spread by cross-infection. In the second volume of his standard work on historical and modern plague published in 1910, Sticker emphasized the significance of the latent period, “Latenzzeit” or “Latenzperiode,” as a defining feature of rat-based plague.10 He illustrates his point by several case histories. Its status as a defining feature was also pointed out by Hirst who also employs the term “latent period.” Both the first phase of the latent period and the full latent period reflect a plague of “rat origin,” both these temporal manifestations of the pace of development of rat-based plague are unique and function independently as defining features. 7 8 9

Hankin 1905: 63–4. Hankin 1905: 71. IPRC 1907g: 764–5 and fn. 6 above; Lamb 1908: 51–2. Cf. Wu Lien-Teh 1936c:

387. 10

Sticker 1910: 220, 227–32.

latency periods

283

Thus, latency periods as defining features of bubonic plague were such an obvious characteristic manifestation of bubonic plague that the phenomenon was observed by the first modern scientific medical scholars who studied the outbreaks of plague at the end of the nineteenth century and was soon conceptually and materially clarified and entered in the standard works on plague. The broad negligence of the significance of latency periods as defining features of bubonic plague by the advocates of alternative theories is thus all the more remarkable. The exception is Twigg who has noted Shrewsbury’s presentation of the latency period, how it reflects rat-based plague,11 and he understands its grave implications for his alternative theory.12 In contrast to Cohn and Karlsson, he does not pass this problem by in silence, but the way he goes about handling it is disappointing. Shrewsbury gives a historical case illustration of a latency period based on an account by Bishop Gregory of Tours of the development of plague in Marseilles in 588 as it was hit by the fourth wave of epidemics in the Justinianic pandemic of 541–766. The bishop relates that the contagion had been introduced into the harbour of Marseilles by a merchant ship. Many citizens purchased goods from it, and soon the contagion broke out among a family of eight who died rapidly and the house stood empty. However, the disease did not go on to spread through the residential quarter, there was “a certain interval,” and “then, like a wheat field set on fire, the entire town was suddenly ablaze with the pestilence.”13 What Bishop Gregory without any knowledge of rat-based plague had observed and what puzzled him was the latent period while plague worked its way through adjacent rat colonies and, as it seems, also through rat colonies in houses at a distance where rat fleas might have been introduced in visitors’ clothing, until the rat fleas released from dead rats began to attack human beings in their proximity and plague’s presence re-emerged among the inhabitants in the form of dramatic human mortality.14 Shrewsbury correctly points out that “plague did not spread immediately after its introduction to a town, as a disease that is spread by human contacts would do.” This point must be emphasized: no disease spread by cross-infection would for any reason exhibit

11 12 13 14

Shrewsbury 1971: 19. Twigg 1984: 172–5. Little 2007: 11; Twigg 1984: 35. Shrewsbury 1971: 19.

284

chapter seven

an interval with no epidemic activity, and certainly not anthrax which is mainly spread by the eating of un(der)cooked contaminated meat: such diseases would develop according to a bell-shaped continuous curve. Twigg focuses on Bishop Gregory’s dramatic description of the development of the epidemic, maintaining that the plague in India did not produce “epidemics that flared in that way” and avoids in this way to relate seriously to the significance of the description of the latency period. He does not discuss the idea that Bishop Gregory’s choice of words could have anything to do with rhetorical dramatization,15 although dramatic rhetorical figures of speech were a central part of classical education and they lived on in the medieval world as an ordinary part of chroniclers’ writings. The central methodological point is that in order to preserve his theory Twigg is required to reject the fact that a silent interval, a latent period, is an ordinary part of bubonic plague, and to document that a latent period was characteristic of anthrax disease and explain how this feature sprang from this disease’s properties. He appears not to have noted that the Indian epidemics, according to the IPRC, were characterized by this silent interval or latency period(s), as shown above.16 Sticker who had studied plague in India points out that this epidemiological feature was observed in Mumbai in 1896 at the very start of this plague period in India, and in Hubli in 1897, and so on.17 This means that Twigg’s argument on this point is not based on the work of the IPRC or earlier plague researchers in India and must be considered unfounded. Next, the way Scott and Duncan address this topic must be considered. It begins with their study of post-medieval plague in Penrith (Cumbria) during 1597–8 based on parish records which provide good data on the early epidemic developments of mortality as reflected in the burial records, which in the case of medieval epidemics tend to remain more or less veiled to the historian’s prying eyes. The first victim of plague was a stranger named Andrew Hogson who was buried 22 September 1597. Conspicuously, the next burial did not occur until 14 October, twenty-two days later, and the epidemic progressed slowly in the following couple of weeks.18 Obviously, the stranger had 15 16 17 18

Twigg 1984: 35–6. Twigg 35–6. Sticker 1910: 228. Scott and Duncan and Duncan 1996: 3; Scott and Duncan 2001: 116, 128.

latency periods

285

introduced plague contagion into the small town; he must have been a fugitive from some locality in the region where outbreaks of plague were quite widespread at the time.19 The delay between the two first burials is a defining feature of bubonic plague corresponding exactly to the first latency period, and the ensuing slow developments are compatible with the whole latency period and as such also a defining feature of bubonic plague. Scott and Duncan decline to take these basic facts into account,20 they remain unacknowledged and ignored in all of their works. This may indicate that they do not have basic knowledge of bubonic plague’s temporal structure of development and are unable to add up the duration of the various subphases. However, several aspects of their monograph make it difficult to accept the idea that they have no knowledge of bubonic plague’s typical latency period(s). In their monograph of 2001, they refer, for instance, to Shrewsbury and his monograph 116 times, or on almost 20 per cent of the pages, and often more than once on a page,21 and Shrewsbury presents this feature of bubonic plague at the very beginning of his monograph, on page 3, giving the first latency period the self-explanatory name of “lag interval.” In their account of the plague epidemic at Eyam, they do not test their theory according to usual methodological principles. Instead of providing the time of the first deaths and examining whether or not it could be compatible with bubonic plague, they introduce as fact an invalid estimate of an incubation period of thirty-two days for filoviridal disease (Ebola and Marburg diseases), a figure unknown in the modern literature on these diseases, which will be discussed below. On this arbitrary basis, they proclaim that the first victim had been infected “about 1 August” and that the “first secondary infection took place on 16 August.”22 The crucial methodological point is that they do not test their material according to the known properties and characteristics

19

Scott and Duncan and Duncan 1996: 12. Scott and Duncan 2001: 128, 137. 21 Scott and Duncan 2001: 6, 14, 16–2, 18, 80–3, 81–3, 89–2, 90–2,91–4, 94–2, 95, 96, 98, 99–4, 100–3, 101, 102–3, 104, 106–2, 110, 111, 112, 113–2, 114, 115, 122, 149, 151–2, 152–6, 153–5, 154, 163, 165, 166–4, 167, 168, 176, 177, 179, 181, 182,193, 202– 2, 204, 205, 207–2, 209, 212, 215, 220, 232, 233, 238–2, 245, 247–2, 250–2, 253, 256–2, 257, 258, 261, 262–2, 265–2, 284, 357, 359–3, 360–2, 374, 375, 377, 380, 395. First figure is page number, and the number after the hyphen indicates the number of times Shrewsbury is referred to by name on the page. 22 Scott and Duncan 2001: 265. 20

286

chapter seven

of bubonic plague and prove that they are incompatible with the events of the epidemic. The first victim died 6 September after three days of illness when he developed swellings in the groin and neck and the fatal token, the plague spot. The clinical manifestations and the duration of the course of illness are typical of bubonic plague, buboes are a defining feature of bubonic plague and have not been observed in relation to cases of filoviridal disease (see below).23 None of these features conforms to the theory of filoviridal disease according to currently available medical information. The duration of the course of illness takes the case history back to 3 September. Assuming that the disease was bubonic plague, a normal assumption of incubation period indicates a time of infection c. 31 August. According to local oral tradition taken down in writing about 1840, the first victim was a tailor who received a box with cloth from London where the last great plague was raging. This account is credible in so far as transportation of plague in cloth(ing) over considerable distances is, as shown above, a usual mechanism of metastatic spread, and an infective rat flea (or more) could have emerged when the box was opened, and, desperately hungry and thirsty, have bitten the tailor and next searched for its natural host, a black rat. If this traditional information is reasonably correct, this would constitute an ordinary scenario of the beginning of a plague epidemic which would manifest itself in a sequence of epidemic events characteristic or defining of bubonic plague. It is therefore of crucial importance that the second victim, who lived in the same house, was interred 22 September, twenty-three days after the beginning of the process of infective transmission.24 As can be seen, this is a very fine match for the general time structure of the two first cases of an epidemic of bubonic plague, and the twenty-three day period is the first latency period which is a defining feature of bubonic plague, and as such represents sufficient evidence that the epidemic disease under development at Eyam was bubonic plague. Thus, even the introductory evidence displays two defining features of bubonic plague, namely the buboes and the duration of the first latency period. The other serious scholars who have made in-depth studies of the epidemic at Eyam have readily recognized this.25

23 24 25

See below: 652–3. Bradley 1977a: 64–5. Shrewsbury 1971: 523; Bradley 1977a: 64–5, 69–71, 73; Coleman 382–3.

latency periods

287

What about Slack’s observation in relation to the plague epidemic in Devonshire in 1546–7, which he makes on the basis of extensive empirical evidence: “the apparent slow movement of disease from place to place, burials rising in one village a fortnight or a month after they had done so in another a few miles away”? Does this not constitute interesting evidence of short-range metastatic leaps and the latent period, conforming to and reflecting the rhythm of development and pattern of spread of bubonic plague?26 These grave flaws in their argument perhaps explain why Scott and Duncan fill their book with declamatory assertions of the truth of their findings and of the great weaknesses of the work of other scholars, as if to veil the realities behind a verbal smoke-screen: “the details of the epidemic demonstrate clearly again, as at Penrith in 1597–8, it is a biological impossibility that Yersinia pestis was the causative agent”; the conditions at Eyam “would be completely unsuitable for the establishment of a colony of black rats”; and the usual disparaging remarks on the incompetence of historians “who all assume without question that this was an outbreak of bubonic plague,” and once “blind acceptance of bubonic plague has been abandoned, the sequence of events […] fit readily into the pattern of a ‘standard’ infectious disease which was transmitted person-to-person.”27 Their principal monograph contains several similar instances— examples of epidemics with latency periods that clearly suggest bubonic plague as the disease in question—that remain ignored and unrecognized. For instance, they discuss an epidemic in 1665–6 in Neston, a small port on the R. Dee, about 16 km north of Chester, and give some examples of “spread of the infection within households”:28 “George Leene (son of William Leene) brought the infection into his family and died on 13 September 1665. He infected other members immediately at the end of his latent period and they died on 24 (father), 25 (sister),

26

Slack 1985: 84. Scott and Duncan 2001: 261, 269. 28 Scott and Duncan 2001: 252–5. This epidemic is not mentioned by Shrewsbury and it is not clear on what material Scott’s and Duncan’s account is based. It could possibly be a pre-modern amateur work by W.E.A. Axon, “Chronological Notes on the Visitations of Plague in Lancashire and Cheshire”, Transactions of the Lancashire and Cheshire Antiquarian Society, 12 (1894): 52–99. This paper is used by Shrewsbury who, as it seems, does not let any epidemic go unmentioned, but does not mention the alleged outbreak at Neston. Since I have not have succeeded in identifying the paper and acquiring it, I have not been able to examine the account. 27

288

chapter seven

26 (brother), 26 (‘base child which William Leene’s wife nursed’), 28 (sister) September. On this basis, Scott and Duncan announce “35 days as the minimum duration of the latent and infectious periods.”29 If it is assumed that this was bubonic plague and deduct an average of eight days for incubation and duration of illness, George Leene would have been bitten by an infective flea 5 September, the flea would then have searched for its natural host the black rat and triggered a rat epizootic that, according to the first latent period, would manifest itself in human cases nineteen to twenty-seven days later, which fits absolutely with the sequence of epidemic events and deaths in the family. This sequence of events corresponds perfectly to a defining feature of bubonic plague, namely the first latency period. Scott’s and Duncan’s assertion that George Leene infected the other family members immediately at the end of his latent period is unconvincing for several reasons. The sequence of events does not fit with an incubation period of thirty-two (here thirty-five) days according to their invalid assertion on this point for filoviridal diseases: no such latent period or extraordinary long incubation period has been observed in research on filoviridal diseases (see below). Scott and Duncan have not only invented this imaginary incubation period of thirty-two days (see below), but have also taken out of thin air the idea that infected persons in this period were extremely contagious. This is yet another assertion which they are unable to document or prove30 for the obvious reason that all medical research on the two filoviridal diseases agrees that there is not a “carrier state” and that infection requires direct transmission of living cells.31 This is an awkward and inefficient mode of transmission which explains why this type of disease “typically appears in sporadic outbreaks” which are also typically small. This makes it surprising that Scott and Duncan should not have met with latency periods as a characteristic feature of bubonic plague.

29

Scott and Duncan 2001: 363. Scott and Duncan 2001: 384–9 (or anywhere else in the monograph). 31 www.cdc.gov/ncidod/dvrd/spb/mnpages/dispages/ebola.htm 2003: 2; www.who .int/inf-fs/en/fact103.html 2003: 1; Dowell, Mukunu, Ksiazek et al. 1999. 30

CHAPTER EIGHT

DEFINING FEATURE 2: INVERSE CORRELATION BETWEEN MORTALITY RATE AND POPULATION DENSITY Introduction At the heart of modern epidemiological theory is the notion that E.M. Burnet, the Nobel Laureate, in his standard work Natural History of Infectious Disease formulates thus: no matter by what method a parasite passes from host to host, an increased density of the susceptible population will facilitate its spread from infected to uninfected individuals.1

A representative sample of Cohn’s unfair discussion of Hankin’s paper of 1905 has been commented on above. The central reason for Cohn’s misrepresentation and disparagement of Hankin as a scholar is his (Hankin’s) discovery that Indian epidemics of bubonic plague caused higher mortality rates in villages than in urban centres and that the Black Death in England appeared to follow the same pattern and, thus, also was bubonic plague.2 This strange phenomenon, that mortality rates did not increase with increasing population density but, on the contrary, decreased, is at variance with the central tenet of epidemiology and must reflect a very special or unique mechanism of transmission and dissemination. Observation of a unique feature of bubonic plague is of particular importance, because a unique feature is obviously synonymous with a defining feature and can, as such, serve as a sufficient criterion for identification of the disease and invalidation of all theories based on other diseases. Clearly an inverse correlation between morbidity or mortality rates and population density is incompatible with and falsifies all alternative theories of the identity of historical plague epidemics based on diseases spread by interhuman

1 Burnet and White 1972: 11. This standard work was written by Burnet, the 4th edition is revised by White. 2 Hankin 1905: 48, 57–8. Above: 21–3.

290

chapter eight

cross-infection, primarily Cohn’s, Scott and Duncan’s, and Karlsson’s alternative theories. In a paper published in Population Studies in 1987, I developed Hankin’s point by introducing much more evidence to the same effect and also succeeded in presenting an explanation for it that so far, over twenty years later, appears to have been generally accepted. The gist of this paper was presented in my doctoral thesis of 1993, which Cohn knows, but nonetheless he ignores this point in his monograph of 2002. However, since the gist of this paper is also presented in my monograph on the Black Death and the cat is out of the bag, so to speak, Cohn attacks my findings in his “review” of my monograph in The New England Journal of Medicine (see below). It is interesting to note how the advocates of alternative theories relate to this epidemic evidence. Cohn’s efforts to misrepresent and belittle Hankin as a scholar are commented on above. Twigg admits that Hankin’s finding can be correct for India, but maintains on quite speculative grounds, as it may seem, that “constraints of climate and other factors might have resulted in a different situation in northern Europe.” The comparative evidence Hankin gathered on the Black Death showing the inverse pattern of correlation in England and additional European historical evidence to the same effect presented later by other scholars are ignored.3 Scott and Duncan do not discuss this point. This allows Scott and Duncan to construct a line of argument to the effect that historical plague epidemics were density dependent in their restricted meaning of the term, i.e. that mortality rates increased with population density (as if the inverse correlation is not also a structure of density dependence), which seemingly satisfies the epidemiological principle for diseases spread by cross-infection formulated by Burnet. This makes it important to perform two tasks: (1) to present an outline of the evidence passed over in silence by all advocates of alternative theories which provides proof that the inverse correlation was a characteristic feature of historical plague epidemics; and (2) to consider Scott and Duncan’s attempt to make a case for the positive correlation of levels of population density and mortality in historical plague epidemics, which will be carried out in a subsequent subchapter.

3

Twigg 1984: 55–6.

mortality rate and population density

291

More Data on the Inverse Correlation in India and Historical Europe In India the inverse correlation to the effect that “plague is much more severe in country villages than in towns” was so obvious that it was mentioned briefly in passing by Bannerman a year after Hankin published his findings.4 In the following year (1907) the IPRC published a study of the relationship between population density and mortality in various sections in Mumbai, i.e., an intra-city study, and to their surprise noted that there is no relation between the severity of plague in these sections and any of the facts which contribute to overcrowding of the population […]. Viewing the evidence as a whole we are of [sic] opinion that there is no relation between overcrowding and plague incidence.5

This observation is an important contribution to the study of the inverse correlation because it strengthens and expands the systematic or pervasive character of the phenomenon from an urban-rural dimension by showing that it also holds good in an intra-urban perspective. This instils it with a generalized character which must reflect important basic factors in the mechanisms of spread of bubonic plague which permits us to establish the concept of the principle of inverse correlation for the pattern of distribution of mortality rates according to population density in bubonic plague epidemics, decreasing with increasing population density. Interestingly, the IPRC’s observation suggests that the principle of inverse correlation should also be a structural densitydependent feature in the countryside, that is, that mortality rates should be higher in hamlets and small villages than in large villages. Empirical data to this effect would make the principle of inverse correlation completely generalized, a hypothesis that must be tested on relevant data as they become available. If it is not substantiated, a separate explanation would be called for. However, for some years, the study of the inverse correlation slipped out of the IPRC’s focus. In 1911, Major Greenwood, the epidemiologist and also the statistical specialist of the IPRC, published a study “on some of the factors which influence the prevalence of plague” in the

4 Bannerman 1906: 195. Later, it was observed also in China, see Wu Lien-Teh 1936c: 396–7. 5 IPRC 1907g: 780–1.

292

chapter eight

Punjab, where he found that “given an equal period of exposure to infection, small villages suffer more severely from plague than large ones.” “These curious and interesting facts” caught his attention exactly because they were at variance with the central principle of epidemiology, and being an eminent scholar he asked the pertinent methodological question whether “the same or similar circumstances have been noticed before.”6 This led him to Hankin’s observation of a similar or closely related pattern, that villages outside “Bombay Presidency” had much higher mortality rates than towns, which corroborated the central aspect of his own finding. In view of Cohn’s negative assertions and characteristics, it is of particular interest that Greenwood then points out that “Hankin also called attention to the probable occurrence of a similar phenomenon in the Black Death,” showing that it is not difficult for a fact-oriented scholar to cite Hankin’s pioneering finding correctly on this comparative point. He then proceeds to test also Hankin’s historical finding: In Appendix I,7 I deal with such statistics as I could obtain bearing on the historical plagues: it will be found that these, so far as they go—unfortunately not very far—bear out Hankin’s suggestion. They lend some support to a belief that we here have to deal with a general epidemiological phenomenon […].8 it would appear probable that the rule deduced from the Punjab village statistics, viz. that the rate of plague mortality tends to increase as the absolute population of the infected community diminishes, may apply to European epidemics.9

Concluding, Greenwood points out that his own study enlarged on the knowledge of the observed phenomenon in so far as “the difference is found to be carried further and still to prevail amongst communities of the same general type,” i.e., among villages (of various sizes).10 Suprisingly, Twigg displays knowledge of Greenwood’s first report on plague in the Punjab, IPRC 1910b: 349–443 + 48 maps, “On the Spread of Epidemic Plague through Districts with Scattered Villages,” but in his bibliography he discloses that he refers only to Part II (pages 416–42) constituting 28 per cent of the running text,11 which means 6 7 8 9 10 11

Greenwood 1911b: 74–5. Greenwood, IPRC 1911b: 93–6, 150–1. Greenwood, IPRC 1911b: 75. Greenwwod 1911b: 95. Greenwood, IPRC 1911b: 74–5. Twigg 1984: 187, 243.

mortality rate and population density

293

that he avoids having to admit knowledge of metastatic spread of bubonic plague from this paper. He displays no knowledge of the important second and especially third reports on plague in the Punjab published the next year where metastatic spread is the central topic (see above).12 As can be readily seen, Cohn’s, Twigg’s and Scott and Duncan’s assertions that the inverse correlation between population density and mortality has been observed only in relation to modern bubonic plague are not correct: both Hankin and Greenwood adduced evidence of the same pattern in historical epidemics. Clearly, Hankin’s discovery is important and valid and strengthened by Greenwood’s similar finding on independent material. The problem confronting Hankin and Greenwood was the early and low level of development of historical plague research which restricted the level of tenability that it was possible to achieve by the comparative approach, but tenable their results were, and taken together, at a significant level both with respect to plague in India and with respect to historical plague epidemics in Europe. Cohn enters Greenwood’s study of 1911b in his monograph’s bibliography and can therefore be assumed to know it, although he refrains from mentioning it in his text. Despite this silence it can be assumed that Cohn also knows that Greenwood addressed Hankin’s finding that the inverse relationship between levels of plague mortality and population density appeared to be characteristic also of historical plague epidemics, and that Greenwood adduced significantly more historical evidence to the same effect and strengthened the empirical status and level of tenability of this observation. More evidence showing the main outline of the same pattern of inverse correlation between levels of mortality and population density in European historical plague epidemics was published around 1980. In their monographs of 1978 and 1981 respectively, both R.S. Gottfried and C.M. Cipolla noted the basic point: the effects of plague epidemics were at least as severe in rural areas as in urban centres in fifteenth century England and seventeenth century Italy, despite much lower population densities.13 Cohn knows Cipolla’s monograph (Fighting the Plague in Seventeenth-Century Italy), since he refers to

12 13

IPRC 1911a: 47–61; IPRC 1911b: 62–156. Gottfried 1978: 138–54, 226–7; Cipolla 1981: 102.

294

chapter eight

page 14 in it,14 although at a safe distance from page 102 where Cipolla addresses this subject. Thus, Cohn has again overlooked significant evidence bearing on this important point which undermines his alternative theory and corroborates the bubonic plague theory. He does not enter Gottfried’s monograph in his bibliography, which is surprising from an author who accuses his adversaries for “highly selective” reading of the scholarly literature (see above and below). Cohn’s comments on Cipolla’s work have been discussed also above and shown to be misleading: Cipolla is not an historian “squaring the circle.” Unfortunately, Cipolla is not in a position to defend himself against these unjustified accusations. While working on my monograph on the Black Death and making my way through the Spanish studies of historical plague epidemics, I noted that three scholars, P. Vilar, M.V. Shirk, and M. Berthe had observed that the Black Death ravaged the countryside even more severely than the towns in the Spanish regions for which there was mortality data, namely Catalonia and the Kingdom of Navarre.15 Cohn has overlooked all three studies. In 1985, Paul Slack published his large and important monograph on plague in Tudor and Stuart England where he unreservedly identifies the demographic and epidemiological patterns and clinical descriptions of the epidemics as bubonic plague, and is for this reason severely criticized by Cohn, who also criticizes a number of other notable scholars, including me, albeit on untenable grounds, as shown above.16 Since Slack had not discovered Hankin’s and Greenwood’s pioneering studies on the inverted relationship between population density and mortality rates in plague epidemics, he was unprepared for making the same curious finding. However, he has used Greenwood’s standard work of 1935 on epidemic diseases and has also read the chapter on plague, actually citing it on a point five lines before the following statement: “the smaller the community the greater the rate of mortality if it becomes infected.”17 Being a historian, not an epidemiologist, and expecting a conventional pattern, Slack treated this curious finding 14

Cohn 2002: 14, fn. 75. Vilar 1962: 464; Shirk 1981: 365; Berthe 1984: 314. 16 Cohn 2002: 28–9. See above: 56. 17 Slack 1985: 94; Greenwood 1935: 300–1. Greenwood’s italics. Cohn also enters this work in his bibliography and refers to it once in the text, but does not cite the chapter on plague and the statement on the inverse relationship between plague mortality and population density. 15

mortality rate and population density

295

with circumspection, and, as it seems, uneasy disbelief. However, his in-depth studies of plague in Devonshire in the years 1546–7 based on a broad sample of parish registers showed that the variations in mortality […] appear to bear no relation to the size of the community involved. The epidemic was as bad in the small parish of Bridford, south-west of Exeter, consisting mainly of scattered farms, as it was in the large village of Ugborough […] and it was less serious in the market town of Colyton in east Devon than in either of these […].

Incidentally Slack might also have said that it was less serious than in Exeter. Clearly, mortality was higher in villages than in urban centres and there was also clearly a general inverse correlation between the size of communities involved and the level of mortality. Slack also made in-depth studies of the effect of plague in quite a number of parishes in Devonshire in the period 1568–1626. The gist of his findings is revealed in his Table 4 and show a similar pattern: small rural parishes like Widworthy and Dean Prior suffered extreme mortality, much higher than urban centres like Exeter, Tiverton or Plymouth.18 Thus, the same pattern emerges in mid-sixteenth-century England that was first observed by Hankin in India, that village mortality was much higher than in towns. Deeper insights into the matter could have been achieved if Slack had organized the material in a table according to the size of the communities and the mortality rates they suffered. As it is, Slack has contributed valuable historical evidence to the effect that mortality rates in epidemics of bubonic plague did not increase with size of community in sixteenth-century England but, on the contrary, tended to be (much) higher in villages than in towns. The significance of this observation is clear: these historical plague epidemics did not spread by crossinfection but by some other mechanism which produced this inverse correlation of mortality rates and population density or, at least, prevented correlation of mortality rates with increasing population density. Finally, I think it is fair to point out the central role of British scholars in the discovery and development of this topic. Shortly before Slack’s monograph appeared, I was setting up tables of plague mortality in Italian localities in 1630–2 and in French localities in southern France in 1720–2, when it struck me that village mortality was much higher than that in towns. Next, I remembered that Hankin 18

Slack 1985: 88–9, 94.

296

chapter eight

and Greenwood had noted the same peculiar pattern which they, however, were unable to explain, and I delved eagerly into this exciting problem. In order to avoid methodological problems from possible differences between morbidity rates, which directly reflect the dynamics of the epidemic process of spread, and mortality rates, which might vary according to lethality rates, I endeavoured to collect all available information on morbidity rates. I also collected some series of mortality rates and at the end of the day it was clear that these two types of data was similar, reflecting the historical stability of plague lethality. Inevitably, this emphasis on the quality of data in the form of morbidity rates had the effect that my data was associated with quite late historical epidemics of bubonic plague in Europe, namely the Italian epidemic of 1630–2 and the French epidemic in 1720–2. However, these data expanded substantially in time and geography the English data of Hankin and Greenwood on the Black Death, Gottfried’s data on epidemics in fifteenth-century south-eastern England, and Slack’s on sixteenth-century England. It emerged that the mortality data of these two epidemics showed the same pattern and contributed to the formation of a systematic pattern covering the whole of the plague period from the Black Death to the last, the French epidemic of 1720–2. The inverse correlation was a systematic characteristic feature of historical plague. Since this feature was a characteristic feature of bubonic plague epidemics both in India and in historical Europe it constituted indisputable evidence to the effect that historical plague epidemics were epidemics of bubonic plague. The outcome of my endeavours was published in a paper in the demographic journal Population Studies in 1987 and it contains a broad range of historical evidence. It shows a systematic inverted correlation between levels of population density and mortality, that mortality rates are highest in small villages, tend to fall with increasing village size, and fall abruptly in towns (urban centres with 1000–9999 inhabitants). It thus confirms the hypothesis constructed on the basis of the IPRC’s paper of 1907f that the inverse correlation held at the level of villages or rural settlement more generally. Since the vast majority of European populations lived in the countryside in relative small agricultural settlements, this finding also conforms with the extreme mortality of the Black Death. However, in the evidence I studied the mortality rates start to increase in the big cities and the metropolises of the time, so that a bimodal pattern emerges. This means that the expression “inverse correlation” is inaccurate. My data is summarized in Figure 1, where

mortality rate and population density Morbidity rates (per cent) France 1720-2

297

Morbidity rates (per cent) Italy 1630-2

80

80

70

70

60

60

50

50

40

40

30

30

20

20

10

10

0

0 Small Village Large Small Samll Town village village town 1 town 2

City

Metro

Small Village Large Small Samll Town village village town 1 town 2

City

Metro

Figure 1. Population density and morbidity (epidemics of plague)

they produce a sort of bimodal correlative histogram. Specification of data and source-critical points is presented in my paper; see the footnote here for demographic explanation of the terms describing the sizes of the settlements.19 A detailed summary of this study is given in my doctoral thesis.20 Cohn has apparently read it not only in a biased way, but also in a selective way, since he failed to notice my discussion of this phenomenon in a separate subchapter aptly called “The Problem of Population Density” complete with Figure 1 and a conclusion written in bold type to underline its importance (see below). This topic is also discussed and enlarged upon in my monograph on the Black Death, first in a subchapter called “Can It Be True that Plague Spreads More Effectively in the Countryside than in Urban Areas?”21 All mortality data was tested for further evidence on the matter. In the 19 Settlements and population centres are categorized in an approximate fashion according to demographic and sociological criteria taking into account contemporary societal realities and cultural notions: a village has up to 1000 inhabitants; a town from 1000 to 10,000 inhabitants; a city 10,000 to 100,000 inhabitants; a metropolis 100,000 inhabitants and upwards. Metro = metropolis. The French data refer to the following numbers of inhabitants: small village = 74–109; village = 213–450; large village = 540– 850; small town 1 = 1,000–1,750; small town 2 = 2,000–3,000; town 2 = 4,200–6,000; city = 22,500–24,000; metropolis = 100,000. The Italian data: village = 190–640; town = 2,025–3,900; city = 12,000–76,000; metropolis = 130,000–140,000. 20 Benedictow 1993/1996: 177–80. 21 Benedictow 2004: 31–4.

298

chapter eight

case of Spain, it is pointed out that several scholars have noted that the Black Death ravaged the countryside even more severely than the towns in the regions for which there is mortality data, namely parts of the Kingdom of Navarre and Catalonia, an observation my work confirmed.22 The Italian mortality data on the Black Death is too few to constitute a good material for this discussion. In San Gimignano, mortality in the town was higher than in the countryside, in Prato the data suggests that mortality was about the same in the city and in the countryside, and the mortality rate in a number of villages in Valle Susa in the Piedmont was about 52.5 per cent. Taken together, it appears that the available Italian data indicates about the same level of mortality in the urban centres as in the countryside, which still is incompatible with the epidemiological principle that mortality rates should increase with increasing population density and, thus, support the inference that it was bubonic plague.23 In the case of France, a similar pattern of mortality in the Black Death appears in Provence where the data comprises nine urban centres, which according to the registration of household(er)s containted roughly 1350–6700 inhabitants, and seven villages with roughly 130–650 inhabitants. For urban centres and rural communities the mortality rate of householders was about 52–3 per cent, and measured as part of the population about 60 per cent. However, a closer look at the rural data makes it possible to discern a pronounced tendency towards higher mortality rates among the smaller villages and lower mortality among the larger villages. Despite the fact that the lowest rate is found in the smallest village, the two second smallest villages, both with forty householders, lost more than 70 per cent of them, while the two largest villages comprising 144 and 122 household(er)s lost 48 and 46 per cent of their householders respectively.24 The material for villages in the County of Savoy also shows a tendency, albeit quite weak, to the same effect, the largest villages or small towns lost a somewhat smaller proportion of their population than medium-sized and small villages, and there is no tendency to the positive correlation on which Cohn’s and Scott and Duncan’s alternative theories depend.25 This evidence tends to support the prediction (above) that mortality rates in 22 23 24 25

Benedictow 2004: 284. Benedictow 2004: 307. Benedictow 2004: 311. Benedictow 2004: 318–31.

mortality rate and population density

299

bubonic-plague epidemics should tend to be higher in small rural settlements than in large villages. The available English mortality data on the ravages of the Black Death does not include information on urban populations and cannot be used for ascertaining relative levels of mortality between urban and rural environments. It is, however, hard to envisage that urban mortality can have exceeded the average mortality rate among seventy-nine manorial communities of about 55 per cent among the householders of the customary tenantry, and over 60 per cent (c. 62.5%) among the rural population as a whole, quite likely the highest rate in Europe. The mortality rates among landless or all-but-landless men are known for seventeen of the manors of Glastonbury Abbey. They show a tendency to higher mortality rates on manors of under-average size than on those of over-average size.26 Thus, even in these early days in the development of medieval demography the surprisingly numerous and territorially quite widely dispersed mortality data that is available for populations visited by the Black Death shows a consistent pattern to the effect that the epidemic either ravaged the countryside even more harshly than urban centres or that the mortality rates may have been at about the same level. They also indicate that population losses were more severe in small villages than in large villages. Since this monograph appeared after Cohn’s monograph, he may be excused for not knowing it, but not for ignoring all of the relevant data or for his misleading comments in his “review” of the monograph, when he realized that the cat was out of the bag and the issue had to be addressed.27 In this chapter it has been empirically shown at a high level of tenability that a mainly inverse correlation between levels of mortality and population density in epidemics of bubonic plague is an inherent, historically stable and unique property of this disease, at least this is the case for communities up to the size of big cities or metropolises of the Middle Ages. For this reason, it is also incompatible with and invalidates all alternative theories of the microbiological nature and mechanisms of spread of the Black Death and subsequent plague epidemics based on assumptions of interhuman spread, specifically the alternative theories of Karlsson, Scott and Duncan, and Cohn.

26 27

Benedictow 2004: 374–6. Cohn 2005: 1354–5.

300

chapter eight

However, the question remains of whether this defining feature can be explained on the basis of unique aspects of the epidemiology of bubonic plague which set it epidemiologically apart from all other epidemic diseases. The point of departure must be that the central tenet of epidemiology predicts in a sweeping and general fashion that no matter by what means or method a disease is transmitted from person to person, morbidity and mortality rates will increase with increasing density of the susceptible population. If this general prediction can be shown on solid empirical grounds not to be fulfilled by an epidemic disease, but that the disease, on the contrary, exhibits a pattern of mortality that is inversely correlated with or unaffected by population density, as is the case with bubonic plague, the reason or cause must be sought in the only reservation, namely that this is generally true only of diseases spread by cross-infection. Consequently, diseases that are not disseminated or transmitted directly from person to person can, in principle, exhibit other types of correlation. In this context, it is also important to emphasize that the study of the correlation between levels of mortality and population density did not exhibit a linear decreasing development along the population-density axis, but unexpectedly and conspicuously began to increase when population density reached the level of the big cities and metropolises of the Middle Ages. This peculiar feature must also be explained by a satisfactory explanatory model or theory. In my paper on the inverse correlation between levels of morbidity/ mortality and population density in bubonic plague epidemics, an explanatory model or theory was presented that so far has not been criticised or countered. In the interest of encouraging regular scholarly discussion and development of the topic, the compressed version given in my doctoral thesis will be cited at quite some length: We have also been able to demonstrate that this seemingly unique, according to basic epidemiological theory inverted relation between morbidity rates and population densities, may be explained only by assuming that epidemics of plague reflect epizootics among commensal rodents. In other words, it reveals that the rat flea is of paramount importance for dissemination and transmission of plague among human beings. In the case of diseases spread by cross-infection, the density pattern is, so to speak, one-dimensional, comprising only humans; the density of susceptible humans will, accordingly, in the main decide the powers of spread. In the case of rat-based plague, the density pattern is three-dimensional, comprising the density not only of humans but also of rats and rat fleas. The latter two density-factors will tend to co-vary strongly and, therefore, to override the significance of the density of humans.

mortality rate and population density

301

Rats are social animals defending territories. This means that in the countryside at least one rat colony will normally co-reside with a household, whereas in urban environments several households will usually crowd together within the territory of a rat colony. The ratio of humans to rats and fleas will, accordingly, tend to be lower in urban environments than in rural, there would be more persons to share between them the dangerous rat fleas let loose from an afflicted rat colony. This epidemiological model provides a basic explanation why plague may wreak havoc after having arrived at some small-scale residential unit, and why, in the case of plague, severity of impact on human populations does not increase with mounting density of human settlement. This finding is of crucial importance. Only an epidemic disease with these disseminative properties could possibly have brought about the demographic developments observed in the Nordic countries in the Late Middle Ages (and also in most other European countries). Thus, another necessary condition has been identified as being fulfilled.28

In this summary, one point is not included, namely the tendency of mortality rates to rise again in large cities and metropolises as shown in Figure 1. Again a reasonable explanation can be found within the theory of rat-and-flea-based bubonic plague. In large late medieval and early modern urban centres, often surrounded by walls, the price of building sites would induce building of multi-storey houses, quite often with two or more living units at the same level. This would create new ecological niches or habitats for black rats where colonies would settle in the space provided by floors, in the walls between living units and in the ceiling or roof, according to a pattern observed in India and commented on by the IPRC,29 “the fact that R. rattus lived at all levels of the houses and therefore in close contact with man.”30 This would produce the effect of increasing the number of rats and fleas relative to the human population within the territories of rat colonies, causing morbidity and mortality rates to rise again and surpass the level characteristic of small or middle-sized towns. Scott and Duncan and the Correlation between Population Density and Mortality In their monograph of 2001, Scott and Duncan refer to my paper on the inverse correlation twice: 28 29 30

Benedictow 1993/1996: 179–80. See, for instance, Lamb 1908: 22–3. Pollitzer and Meyer 1961: 452.

302

chapter eight

(1) “Naples, with about 300,000 inhabitants, suffered 150,000 deaths in 1656. The morbidity in the countryside has been estimated at 66% (Benedictow, 1987).”31 First, one should note the juxtaposition of mortality and morbidity data without mediation of lethality data that would allow real comparison of mortality—and lethality data is provided in the paper. Unfortunately, the morbidity rate of 66 per cent in the countryside given by Scott and Duncan with reference to my paper is erroneous and therefore misleading for two reasons: because it is taken from a table which does not contain morbidity data on the epidemic of 1656, but on the epidemic of 1630–2, and because these data does not relate to the countryside around Naples as asserted by Scott and Duncan, but to Tuscany almost a generation earlier.32 Disquietingly, the combination of these two sets of erroneous data can hardly be accidental; they are carefully selected from page 405 and page 424 in the paper, twenty pages apart. As shown above, mortality rates start to increase again in the big cities and increase further in the metropolises of the time, and Naples is obviously one of the largest metropolises of the time with correspondingly high(er) relative mortality. This constellation of selected data serves to conceal the fact that morbidity data is also generally higher in the countryside than in urban centres in Italy. Scott and Duncan could have avoided the misleading combination of data from two different epidemics by choosing from the page that contains the piece of information on Naples the brief passage on Venice, for instance. The mortality in Venice in the epidemic of 1575–7 was considerably higher than in the next epidemic of 1630–1 when the population had fallen by about a quarter; it is also pointed out that urban mortality rates in Venice and Terrafirma were considerably lower than rural plague mortality. (2) “During the 17th century, there is evidence that the mortality and relative severity of the plagues in London were declining slightly (Sunderland, 1972; Benedictow, 1987).”33 The citation is accurate, and the reference to Sunderland is taken from my brief discussion of this minor or rather peripheral point in my paper. However, the

31 32 33

Scott and Duncan 2001: 315. Benedictow 1987: 405–8, 413–5, 418–24. Scott and Duncan 2001: 377. Cf. Benedictow 1987: 424.

mortality rate and population density

303

heart of the paper, the presentation of comprehensive historical evidence from Spain, Italy and France and other countries showing a strong tendency of inverse correlation between levels of mortality/ morbidity and population density up to the level of large cities or metropolises, when the tendency reverses, a pattern constituting a defining feature of bubonic plague, remains ignored. Thus, Scott and Duncan ignore all historical evidence for the inverse correlation between levels of mortality and population density in plague epidemics, although they cannot have avoided acquiring knowledge of it. Their silence on this topic seems to produce a clean sheet that, apparently enables them to make a case that the powers of spread and mortality of historical plague epidemics in England were positively correlated with increasing population density. A positive correlation would, as they emphasize repeatedly and correctly, constitute proof that historical plague epidemics were spread by cross-infection, and thus proof that these epidemics could not have been bubonic plague. In view of the broad empirical documentation of the inverse correlation supplied in the preceding subchapter, these endeavours deserve a closer examination. Scott and Duncan’s highly divergent and self-contradictory opinions on this phenomenon in India indirectly provide an impression of being shattered, as it were, for instance: Bubonic plague in India was primarily a disease of the smaller towns: the intensity of an outbreak in 1897–8 was inversely proportional to the size of the community, with the maximum mortality in the villages rather than towns (Hankin, 1905).34

Thus, within this sentence Scott and Duncan state that bubonic plague in India was primarily a disease of small towns and also that the levels of mortality in the epidemic of 1897–8 were highest in villages. Scott and Duncan isolate this purportedly observed self-contradictory feature to one epidemic wave and, thus, reduce its significance by avoiding mentioning that Hankin found the same characteristic feature in two earlier Indian waves of plague epidemics, in 1812 and 1836 (above). This was, therefore, a general feature of Indian plague epidemics in the nineteenth century. In view of the fact that India’s population was overwhelmingly rural at the time, the plague epidemics would obviously

34

Scott and Duncan 2001: 77–8, 103.

304

chapter eight

also have to be mostly rural, the pattern mainly being that plague first arrived in urban centres and from there fanned out into the surrounding countryside. In fact, this point is not unknown to Scott and Duncan about a hundred pages later: […] authentic outbreaks of bubonic plague in India, where it is essentially a rural disease of village communities.35

They also maintain that Endemic bubonic plague is essentially a rural disease because it is an infection of rodents. The Black Death, in contrast, struck indiscriminately in the countryside and in the towns.36

Here, Scott and Duncan compare endemic bubonic plague with epidemic plague, actually the largest plague epidemic ever to visit humankind called the Black Death. Clearly, in this context these two phenomena are not comparable, are not in pari materia, and the juxtaposition and comparison on this basis is fallacious. They maintain that endemic plague was essentially a rural disease because it is an infection of rodents without presenting arguments for why rodents in the form of rats (mice?) were not generally amply present in urban centres, and, as so often, they fail to provide a supporting footnote. It has been an accepted opinion among English plague researchers for some time that plague developed a more or less continuous endemic presence in the larger English cities, which can especially be clearly discerned with the advent of bills of mortality around 1550 when systematic registration of deaths discloses the quite continuous incidence of plague cases.37 Slack points out that plague “was certainly endemic for long periods in major towns, in Norwich as well as in London,” and after the last great plague in London 1665–6, cases of plague continued to occur until 1679. The only periods of any length when the country appears to have been free from epidemics of plague were the period 1612–24 and the period 1654–64.38 Scott’s and Duncan’s assertion that endemic plague was a phenomenon of rural districts seems unfounded and the lack of supporting footnote or reference is explicable. Before proceeding, it is useful to compare the previous citation with another citation from Scott and Duncan’s monograph, this time on the 35 36 37 38

Scott and Duncan 2001: 173, cf. 75. Scott and Duncan 2001: 359. Slack 1985: 239–45. Slack 1985: 68–9, 133.

mortality rate and population density

305

epidemic that broke out in Marseilles in 1720 and spread over large parts of southern France in the following couple of years, and which they recognize as bubonic plague: The plague struck indiscriminately at towns as well as the tiniest hamlets (some with only four houses) so we conclude that it was not density dependent.39

When this citation and the previous citation from their monograph are juxtaposed for comparison, it can be readily seen that the Black Death, which Scott and Duncan fervently assert is not bubonic plague, and the southern French epidemic of 1720–2 exhibit an identical basic pattern or structure of spread; in the co-authors’ terminology, the Black Death “struck indiscriminately in the countryside and in the towns”40 and the French epidemic about 370 years later struck “indiscriminately at towns as well as the tiniest hamlets.” According to ordinary methodological considerations, these citations should provide good evidence to the effect that both waves of epidemics were the same disease since they exhibit the same basic pattern of spread. Since the last epidemic’s microbiological nature is known and it is generally agreed upon to be bubonic plague, also by Scott and Duncan, the Black Death should consequently be bubonic plague. Admittedly, it is difficult to understand what Scott and Duncan mean by maintaining that the Black Death struck “indiscriminately” in the countryside and in the towns, and efforts to understand are much frustrated by the fact that Scott and Duncan make this assertion with respect to the Black Death’s pattern of spread without a supporting footnote and also without clarification of the types of spread, in this case specifically the scholarly meaning of the concept of “indiscriminate.” If the meaning is that as many people died in urban centres as in the countryside it is clearly erroneous and without support in demographic studies; if they mean that as many urban centres were visited as villages it is also obviously erroneous and without support in demographic studies. The point is that the overwhelming part of the English population lived in the countryside, quite likely about 85 per cent,41 much like in India around 1900. For this reason, the Black Death in 39

Scott and Duncan 2001: 349–50. Cf. Scott and Duncan 2001: 366: “We have little quantitative evidence concerning exactly how the Black Death struck at the different naïve communities in the vast metapopulation of Europe but it appears that it attacked largely indiscriminately.” 41 Hatcher and Bailey 2001: 140. 40

306

chapter eight

England, like the epidemics of bubonic plague in India, struck far more villages than urban centres and killed far more rural inhabitants than townspeople. The basic pattern of spread of Indian plague epidemics and the Black Death are also similar or closely related: plague arrives first in coastal urban centres and spreads out along main lines of communication with goods and people along the coast and to inland urban centres and thence into the countryside along local tracks and footpaths.42 In the words of P. Slack: “They [plague epidemics] began in ports and major towns; they spread along main routes of communication to other urban centres and from there to smaller communities and to some of the less isolated villages.”43 Indisputably, in relative terms a much higher proportion of urban centres than villages or rural communities were ravaged by the Black Death.44 This appears to have occasionally dawned upon Scott and Duncan: Each epidemic was introduced from the Continent or Ireland. Some outbreaks were also spread by boats trading up the east coast at ports between London and Scotland. The inhabitants were well aware of the dangers of transmission by this means […].45

It is erroneous that the Black Death struck “indiscriminately” in a scholarly meaning of the term. It is true that it spread efficiently in the countryside in times when there was no real knowledge of the nature of epidemic disease, no knowledge of the mechanisms of spread of bubonic plague, and no effective anti-epidemic organization, in contrast to the situation in India around 1900. What Scott and Duncan avoid admitting or recognizing is that the Black Death, the last wave of epidemics in France in the early 1720s, and the plague epidemics in India around 1900, exhibited the same unique and defining feature of bubonic plague, namely that mortality rates did not increase with increasing population density, but on the contrary decreased. This is what is concealed by their assertion that the Black Death or the last plague epidemic in France “struck indiscriminately.” The same purpose is served by their strange terminology, that bubonic plague in France in 1720–2 was “not density dependent”

42

Above: chapter 4: 151–93, Benedictow 2004: Map xviii–ixx, 17–22, 31–4, 57–241. 43 Slack 1985: 66. 44 Benedictow 2004: 227–33, and under the spread of plague in various countries. 45 Scott and Duncan 2001: 358.

mortality rate and population density

307

because it did not spread according to the epidemiological pattern of diseases that spread by cross-infection, namely that levels of mortality increase with increasing levels of population density. The fact that the pattern of spread of bubonic plague does not agree with this principle but, on the contrary, exhibits increasing mortality rates with decreasing population density, does not mean that bubonic plague is not density dependent, but that the spread of this disease functions according to a different structure of density dependence, namely the inverse correlation. The scientific and methodological point is that there is systematic co-variation between mortality rates and population density. This is the reason Scott’s and Duncan’s use of the word “indiscriminate” can be considered unscientific, since the term implies that bubonic plague spreads in an erratic, haphazard, random or fortuitous manner and does not spread according to systemic structures, patterns and mechanisms providing regularity that can be scientifically disclosed and applied in the form of predictions. According to the methodological tenets of science, there is an unbridgeable abyss between asserting that a phenomenon is systematically random, haphazard or fortuitous and therefore cannot be understood according to rules of causation, and the view that its character or dynamics are poorly understood or not understood. In fact, the mechanisms of the dissemination of bubonic plague that produce the inverse correlation are understood; I presented the solution twenty years ago and it has not been challenged, not even by Scott and Duncan, who have read the paper containing it, but ignore its central topic. As shown above, British colonial authorities in India made tremendous efforts to fight the plague epidemics and under the circumstances succeeded in reducing strongly the impact of plague. However, Scott and Duncan go on to assert that Major epidemics of later plagues were mostly, but not entirely, confined to the towns. In summary, haemorrhagic plague epidemics were density dependent whereas bubonic plague (as in the Mende area at Marseilles) was not.46

It is not a slip of the pen when Scott and Duncan state that the Mende area is situated “at Marseilles,” when in fact this area is situated more than 200 km away from Marseilles as the crow flies, and much further away on the ground. It is as misleading as asserting that Sheffield is 46

Scott and Duncan 2001: 359.

308

chapter eight

situated at London. By stating that these two places were in proximity, they avoid confronting the way a bubonic plague epidemic spreads by leaps or per saltem over considerable distances as demonstrated amply also by this wave of epidemics, and thus are able to stick to their false assertion that bubonic plague spreads only between adjacent rat colonies (see above). It is not true that bubonic plague in the last French epidemic was not density dependent: mortality shows a very clear pattern of diminishing rates with increasing population size and density and, conversely, increasing levels of mortality with diminishing population size and density as shown in Figure 1 above and with empirical detail in Benedictow 1987. It has been documented above that Scott and Duncan have read this work.47 Scott and Duncan point out that about 200 years after the Black Death or “in the 16th and 17th centuries” plague epidemics increasingly became an urban phenomenon and that this development reflected the fact that “haemorrhagic plague” was density dependent in their amputated meaning of the term, because it spread by crossinfection, while this was not the case with bubonic plague which is not spread by cross-infection: Two hundred years later, after a succession of epidemics, the dynamics of the epidemics were more formally established. In general, the outbreaks were density dependent, with the major epidemics confined to towns with some 1000 inhabitants or more. In villages or hamlets or in parishes where the population was scattered, the epidemics rarely exploded and the mortality was usually confined to a few dozen households and we have given examples in Chapter 9. This is the normal pattern of infectious diseases spread person-to-person (smallpox and measles are examples) where a sufficient population density is necessary to establish an epidemic […].48

One questions why the pattern or dynamics of spread should change from the Black Death to later plague epidemics if it was the same disease throughout the period caused by the same contagion and was transmitted and spread by the same mechanisms, as Scott and Duncan imply here. Why plague should need 200 years in order formally to establish its “dynamics” is incomprehensible and indicates fallacious reasoning. Such change in the pattern of spread of a disease must

47 48

Scott and Duncan 2001: 315, 377. Above: 301–02. Cf. Benedictow 1987. Scott and Duncan 2001: 366, 392.

mortality rate and population density

309

presumably be due to and reflect changes in people’s perception of the disease and consequent change in their pattern of behaviour or fundamental changes of society and social structures or both. In their rhapsodic casuistic presentation of outbreaks of plague in their chapter 9, Scott and Duncan cannot prove that outbreaks in the countryside were usually confined to a few dozen households. Instead, one should note, for instance, Slack’s fine study of plague epidemics c. 1500 to mid-1660s where he concludes: when plague did strike a village, it often raised mortality by well over 100 per cent. ‘Plague comes seldom, but then very sore’ was the saying in rural England.49

Contrary to Scott and Duncan’s assertion, the usual pattern of mortality in villages was not confined to a few households, but took the form of very serious outbreaks, a pattern that constitutes evidence to the contrary of Scott and Duncan’s inference. Also the reason that plague in England became increasingly an urban phenomenon was very different from Scott’s and Duncan’s assertion on this point, and in fact Scott and Duncan provide, albeit inadvertently, elements of the explanation on the preceding page and a few other places, namely that ordinary people discovered that plague accompanied refugees from plague-stricken urban centres and therefore drove them away by all means: The people fleeing from the plague in London met with a poor reception in the country towns and villages, as in 1603. Creighton described how “They are driven back by men with bills and halberds, passing through village after village in disgrace until they end their journey; they sleep in stables, barns and outhouses, or even by the roadsides in ditches and in the open fields. And that was the lot of comparatively wealthy men.” A stranger from London arrived in Southampton on 27 August and died in the fields […].50

Scott and Duncan’s unsatisfactory practice with regard to references again makes for extra work: the information on popular reactions cited in their text is not taken from Creighton’s account of the epidemic of 1603, instead it is found in his account of the epidemic of 1625.51 Creighton also provides related types of information on the epidemic

49 50 51

Slack 1985: 84, and chapter 4. Scott and Duncan 2001: 204, cf. 118, 359. Creighton 1891: 517–8.

310

chapter eight

of 1603.52 At another place in their monograph, pursuing a different line of argument, Scott and Duncan again reveal knowledge of this topic of popular resistance in the countryside: Some outbreaks were also spread by boats trading up the east coast at ports between London and Scotland. The inhabitants were well aware of the dangers of transmission by this means and, by the late 16th century, they were prohibiting from docking boats that came from ports where the plague was raging.53

Certainly, these comments are not exaggerated: Bell states dramatically that London was at open warfare with the countryside. Always there were people seeking the safety of the country. Where the highways entered towns and villages armed watchmen turned the travelers back […]. Suspect to all, travel-stained, tired and dispirited, the flying Londoners were kept outside towns and forced to find refuge in the fields. A few, the most fortunate, carried tents. Others crept for cover beneath trees and hedges, into cow-byres and dirty hovels of the farms.54

This pattern of anti-epidemic behaviour represents a sufficient explanation for the new pattern of plague epidemics that emerged in England and elsewhere in which outbreaks were mainly limited to urban centres, from which the epidemics occasionally spread into the countryside.55 This development is based on contemporaries’ observation and increasing understanding that plague was spread by people and goods and that it was desperately important to prevent persons coming from plague-stricken urban centres or areas from entering their community. In Slack’s words: Villagers’ suspicions of strangers in plague-time were founded on hard experience […]. People with houses or friends in the country fled from infected towns, only to meet with suspicion and hostility wherever they went.56

Thus, the reason for the development of the pattern of plague epidemics as being increasingly associated with urban centres has nothing to do with higher population density in urban centres than in the

52 53 54 55 56

Creighton 1891: 483, 492. Scott and Duncan 2001: 358. Bell 1951: 137, 138–44. Slack 1985: chapter 4. Slack 1985: 19, 87.

mortality rate and population density

311

countryside, and everything to do with increasing human understanding of the basic mechanisms of spread in dynamic interaction with human observation and consequent efficient anti-epidemic action taken on this basis. Scott’s and Duncan’s attempts to establish a case for positive correlation between levels of mortality and population density in English plague epidemics can be shown to be untenable. On the contrary, substantial evidence can be marshalled to the effect that there was an inverse correlation from the Black Death to the last plague epidemics in England. Epilogue: Sweating Sickness and the Inverse Correlation Sweating sickness suddenly appeared in England in 1485, recurred in a few epidemics in the years 1507–8, 1517, 1528, and 1551 and then disappeared. Reading Slack’s valuable account of the epidemics of sweating sickness in England, the mortality patterns seemed familiar. The demographic effects of the epidemics of the disease appear generally to have been quite small, “only in the smallest villages did this short-term increase in mortality amount to a serious loss of population,” and it had only minor effect on mortality in larger communities.”57 In reality, this appears to be a description of a disease producing higher mortality rates in human habitats of small population density and lower mortality rates in human habitats of high population density, in other word the inverse correlation of mortality rates and population densities, mortality rates increasing with decreasing population densities, and vice versa. This suggests that sweating sickness was transmitted by insects with a zootic background. This understanding is supported by the fact that sweating sickness was more prevalent in the warmer seasons, especially summer and autumn, much like bubonic plague. One interesting candidate for the cause of sweating sickness could perhaps be a virulent biovar of murine typhus.

57

Slack 1985: 70–1.

CHAPTER NINE

DEFINING FEATURE 3: BUBOES AS A NORMAL CLINICAL FEATURE IN EPIDEMICS General Introduction The great pioneers of the modern study of plague epidemiology and medicine saw thousands of cases of bubonic plague in the field and in hospitals. They were certain that the disease they observed had to be the same disease as they saw described in historical sources about the Black Death. There is a curious contradiction between their understanding and the opinions of the advocates of alternative theories who have never seen a plague case in their lives and are, nonetheless, entirely sure that historical plague could not have been bubonic plague. One of the central arguments of the pioneers of modern plague medicine and epidemiology for the identity of historical and modern plague was the descriptions of buboes and their accompanying clinical features which they met in historical sources. Advocates of alternative theories (must) make great efforts to disprove that the usual or normal appearance of buboes in diseased persons is a unique and therefore a defining feature of bubonic plague for the simple reason that this would rule out or invalidate their alternative theories. In these endeavours, they argue either that (1) buboes are not a characteristic clinical feature of historical plague epidemics and consequently do not constitute a defining feature, or (2) buboes are not a defining feature of bubonic plague because buboes are more or less a characteristic clinical feature of at least one other disease which corresponds closely to their own alternative theory, or (3) that the incidence or locations of buboes in historical plague or the clinical panorama within which buboes occur in historical plague epidemics are so different from those characterizing modern epidemics of bubonic plague that they must be two different diseases. Karlsson and Morris follow the first type of approach which cannot be taken as a serious position. Nonetheless, a fresh look at Karlsson’s

buboes as a normal clinical feature in epidemics

313

theory will be taken below in Part 4 since it has found favour with the Journal of Medieval History as a serious publishable theory. The term “bubonic plague” reflects the characteristic development of buboes on persons suffering from the disease. When a person is bitten by an infective flea, plague contagion is discharged in the bite site at a subcutaneous level suitable for normally draining it along a lymph vessel to a lymph node that consequent upon the infection swells to form a bubo.1 Occasionally, the infection may be drained to glands, especially the parotid glands.2 The element of reservation expressed in the choice of the word “normally” stems from the fact that one form of bubonic plague does not exhibit buboes. In a small percentage of cases, infective fleas bite directly into a blood vessel so that the plague bacteria will be discharged directly into the blood stream and avoid the lymphatic system which constitutes the body’s first line of defence, and in these cases the infection will not give rise to buboes. Since the infection is discharged directly into the blood stream, this form is designated primary septicaemic plague in order to differentiate it from secondary septicaemic plague when contagion enters the blood stream secondarily after having broken down the bubonic tissue by the effects of toxins. Primary septicaemic plague is so fulminant that the diseased usually dies the same day; the course of illness lasts an average of c. 15 hours,3 which means that the course of illness is exceptionally short. This form accounts for the many terrified observations of dramatic brief courses of the disease and physicians who remark that plague without buboes is the most dangerous form.4 However, as an epidemic disease, bubonic plague is characterized by the normal occurrence of buboes on those who contract the disease.5 1 Historians commonly and physicians occasionally use the anatomical term (lymphatic) gland instead of node, however, by definition glands produce something, e.g. hormones, enzymes or saliva, but lymph nodes do not, they constitute part of the body’s immunity apparatus. 2 Choksy 1909: 352. It is the major salivary glands that are called parotid, the submandibular and sublingual glands. The parotid glands are thus, found in association with mouth and throat. Cf. also the preceding footnote. 3 Philip and Hirst 1917: 529–30, 534–5. 4 See, for instance, G. Block, the Swedish physician, who wrote a remarkable protoscientific study of a plague epidemic in his home town of Norrköping in 1710–1, Block 1711: 21, 24–5: “That plague is the most dangerous which leaves no external signs, attacking directly the spirits of life in the heart itself.” My translation from the original Swedish edition of 1711. 5 Epidemics of bubonic plague include also a tiny incidence of primary pneumonic plague rising from cases of secondary pneumonic plague by cross-infection with

314

chapter nine

Plague can affect the lymph nodes in any part of the body,6 but will for obvious reasons tend to affect concentrations of lymph nodes, especially in the groin or nearby femoral area, in the axillas or on the neck, in the latter case often under the jaw or ear. Since bubonic plague is (normally) transmitted by rat fleas, this mode of transmission will decisively affect the distribution of sites of buboes, although one must take into account that the distribution of sites is variable as it can be affected by various local customs of clothing and footwear.7 A typical distribution of the sites of buboes, according to Pollitzer and two studies based on ample evidence which are cited by him, would be: in the groin or nearby femoral area around 55 per cent (with a somewhat higher proportion in the femoral area, about 31 per cent), in the axillas around 24 per cent, and on the neck around 9 per cent.8 Cohn maintains that the proportion of buboes in the groin can be as high as 75 per cent; the assertion is not supported by a footnote on page 64 where it is made, but he states thirteen pages later9 that this figure is given by A. Yersin in a paper of six pages on the plague in Hong-Kong from 1894. In this brief paper, Yersin reports on his discovery of the plague bacterium which was since named after him and provides impressionistically quantified figures on the location of buboes, figures that are not the outcome of systematic clinical observation.10 This is the very beginning of modern medical plague research,11 and this paper is cited at the expense of leaving unmentioned later studies of the locations of buboes which show substantially different figures. In fact it is a factually misleading reference which could permit raising the question of motives (see below). Cohn also refers to the 19th edition of 1987 of Manson’s Tropical Diseases, the general standard work on tropical epidemic diseases, where the proportion of inguinal-femoral buboes is estimated at 70 per cent,12 which has been a consistent piece of information at least since the seventh edition of 1921,13 the oldest edition I have found any plague-infected droplets which will likewise not develop buboes. Davis’s assertion to the contrary is commented on below: 321. 6 Butler 1983: 90. See also illustration in Sticker 1910: 382–3. 7 Pollitzer 1954: 421; Chun 1936: 315. 8 Pollitzer 1954: 420. 9 Cohn 2002: 77. 10 Yersin 1894: 663. 11 Cohn 2002: 64. 12 Manson’s Tropical Disease 1987: 593. 1921: 267, 1982: 340. 13 Manson’s Tropical Disease 1921: 267; 1982: 340.

buboes as a normal clinical feature in epidemics

315

reason to consult. One should keep in mind that the chapters on plague in such general standard works on infectious disease are tiny summaries of the material presented in general standard works on plague, in this case, it constitutes, for instance, just 2.2 per cent of Pollitzer 1954. However, since Manson’s Tropical Disease up to this edition of 1987 is not a specialist standard work in the sense that most of the chapters on various infectious diseases are not written by specialists on plague, and since no supporting footnote is given in the first nineteen editions which would allow confirmation of sources, I do not understand the significance which Cohn attributes to it and why he avoids the standard works on plague. However, in the 20th edition of 1996, which Cohn has also used and refers to elsewhere in his monograph, chapters are written by specialists and equipped with footnotes. In the small chapter of 6.5 pages on plague representing less than 1 per cent of Pollizer 1954, the two authors state in a general way that 70–80 per cent of buboes are located in the groin.14 For support of this assertion, they refer to Butler 1972: “A Clinical Study of Bubonic Plague. Observations of the 1970 Vietnam Epidemic with Emphasis on Coagulation Studies, Skin Histology and Electrocardiograms.” The title reveals immediately that this must be a very restricted paper with respect to area and number of cases. In fact, it is based on forty Vietnamese cases who, the author explicitly states, “were not a representative sample of the epidemic” for a number of reasons. Also importantly, the number of cases is much too small to warrant statistical stability and representativeness.15 Perhaps even the authors became uneasy confronted by their figures which showed that in 88 per cent of the thirty-five cases the buboes were located in the inguinal-femoral area,16 since they arbitrarily reduce the percentage to 70–80 per cent. A couple of years later in 1974 Butler et al. published a paper based on the study of twenty-two Vietnamese plague cases in which 66 per cent (14) of the patients presented with inguinal-femoral buboes.17 A paper relating to the study of twenty-one Vietnamese patients presented a very different distribution of the locations of buboes.18 Obviously, the materials are too small to provide statistical

14 15 16 17 18

Smith and Thanh 1996: 918–24. Butler 1972: 274. Butler 1972: 272. Butler, Bell, Linh et al. 1974: S78–9. Legters, Cottingham and Hunter 1970: 639–40

316

chapter nine

stability and relate to a specific Vietnamese cultural background that could also affect the distribution of buboes for various reasons which the researchers under the circumstances have not studied. Unsurprisingly, Cohn must admit that “Manson, his successors, and Yersin have not tabulated or quantified the positions of the plague scars,” nor have they provided the material basis for their quantifications, but the numbers involved are, as we have seen, very small. Given this background, it is necessary to increase the level of empirical documentation and mention that Chun cites four studies on the location of buboes according to mass materials from China and India around 1900, but none of them show 70–5 or 70–80 in the groin plus femoral area. Instead, they show the proportion of femoral-inguinal buboes varies between 48 and 68 per cent; in Mumbai in 1900, two independent studies provide figures of 55 per cent and of 68 per cent. Chun comments on the considerable difference between these figures: “It may be that this discrepancy is due to the difference in the style of dress adopted by Indians and northern Chinese,” and he goes on to address this issue in considerable detail.19 Yersin’s impressionistic guesstimate and Butler’s small study of Vietnamese cases which is explicitly characterized as an unrepresentative sample cannot be used for generalization, as Cohn appears to assume; these studies do not provide alternative evidence which allows one to neglect or ignore or override the statistical materials for Mumbai and Hong Kong provided in the special standard works on plague which also have in common that they are meticulously annotated. The only statistically valid material Cohn refers to on p. 74 is also from the infancy of modern medical plague research, namely, reports from Mumbai’s plague hospitals for the plague year 1896–7, the first plague year in India and Mumbai. In this study 58 per cent of the patients who developed buboes had them in the groin or nearby femoral area, a figure which agrees with the data given by Pollitzer and Chun. Cohn’s predilection for obsolete data and disassociation between argument and data are typical features of his monograph. The reason that buboes arise more frequently in the groin or nearby femoral area than anywhere else on the body is not that a flea “can bite no higher than just above the ankles” as Cohn asserts.20 However, 19 20

Chun 1936: 314–5. Cohn 2002: 64.

buboes as a normal clinical feature in epidemics

317

people can be bitten by fleas not only when they walk about or sit down but also when they lie down to rest or sleep. This is the obvious reason that plague buboes also develop on the upper part of the body and that persons can develop two or more buboes at various locations of the body. Plague buboes develop most commonly in the groin or femoral area because the legs constitute a large part of the body’s surface and because people can be bitten in the legs both during the day when walking about or sitting down and also when lying down to rest or sleep: legs have a twenty-four-hour exposure to flea bites, but the rest of the body only around one-third of this time. Not only ethnic and historical differences of clothing and footwear can affect the distribution of the location of buboes but also sleeping arrangements. For this reason, contrary to what Cohn may seem to assume, variation in the statistical distribution of the location of buboes is of little or modest significance for identification of the disease or at least present some stringent demands for empirical explanation. The crucial fact remains that buboes as a regular manifestation of an epidemic disease, according to present medical knowledge, are associated only with bubonic plague. The causes of this fact will now be considered more thoroughly. Together with its numerous other functions, the skin protects the human body from invasion, including by infectious agents. If the skin is broken, infection may enter, but it will encounter the body’s first line of defence against invasion, namely the lymphatic system. Most infections can under varying circumstances and by varying mechanisms enter through abrasions or cuts in the skin and be drained through a lymphatic tract to a lymph node and occasionally cause a swelling and the development of a bubo. However, this means that infection by the cutaneous route is dependent on the presence of a cut or abrasion in the skin before exposure to contagion and that contagion accidentally meets the skin exactly at the point where it is punctured, cut or broken. These circumstances produce the typical pattern of rare, occasional or episodic occurrence of buboes. Thus Twigg is certainly correct when he states that “buboes may occur in other bacterial and viral diseases.” Surprisingly, he goes on to maintain that this is “notably” the case with “anthrax and small pox.”21 For this important assertion, he does

21

Twigg 1984: 36.

318

chapter nine

not provide a supporting reference to any scholarly study, and it therefore unavoidably takes on the character of an arbitrary assertion. The reason is probably that he advocates anthrax as an alternative microbiological theory of historical plague and is concerned about the conspicuous role of buboes as an ordinary clinical feature of epidemic bubonic plague, a clinical criterion of identification that anthrax cannot satisfy. This is not accidental, it is due to a crucial difference in the modes of infection: (1) in the case of bubonic plague, infection is transmitted by the bite of infective flea(s) which combines puncturing of the skin with the depositing of contagion at a subcutaneous level suitable for being drained from the bite site through a lymphatic tract to a lymph node, thus, the puncturing of the skin is a part of the process of transmission; (2) in the case of anthrax, smallpox and other infectious diseases, in order to produce buboes the contagion must by chance meet with an accidental portal through the skin and then be moved by some mechanism through the broken skin to a subcutaneous level suitable for being drained to a lymph node. These two points explain that buboes can be a regular feature of plague and not of other infectious diseases, specifically the anthrax and smallpox mentioned by Twigg, although buboes can be a rare contingency in these diseases. In epidemic form, anthrax is ordinarily contracted by the eating of contaminated un(der)cooked flesh, while smallpox is transmitted by inhalation of contaminated droplets. Since there are no lymph nodes in the gastro-intestinal system or in the lungs, epidemics of these diseases are not associated with buboes; instead other defensive functions of the human immune apparatus are activated. Twigg significantly and misleadingly understates the difference in the relative incidence of buboes when he reduces it to buboes being “more regularly present in bubonic plague than in any other disease.”22 If Twigg wishes to maintain that anthrax or smallpox quite often present with buboes, he cannot neglect to explain how these infections could be often— or usually—transported from the normal site of introduction, the gastro-intestinal tract or the lungs, to lymph nodes. In the case he cannot find support in the medical literature for the frequent incidence of buboes in cases of anthrax or small pox or other diseases

22

Twigg 1984: 36. See also Sallares 2007: 237.

buboes as a normal clinical feature in epidemics

319

transmitted by similar mechanisms, together with a medical explanation of how this could occur in any standard work on epidemic diseases, he must obviously have a very poor case. The crucial fact remains that bubonic plague is the only epidemic disease known by medical science which presents with buboes as a normal feature of the clinical panorama. This fact is based on hard evidence. For this reason, it must be addressed by all advocates of alternative theories of the microbiological nature of historical plague. In order to be viable theories, they must contain specific empirical explanations for why infected persons should regularly present with buboes; if not they are ipso facto falsified. A generally overlooked point of considerable importance is that another disease is characterized by the development of buboes, namely tularaemia. Tularaemia is a bacterial disease of wild rodents, especially of beavers, hares, muskrats, rabbits and squirrels and is mainly contracted by hunters. In Europe, this disease is associated with rabbits and hares on the Continent, in the Nordic countries with hares and lemmings, and is also called “lemming fever” or “hare pest.” In infected persons, this disease presents in a number of ways dependent on the route of infection: it may occasionally infect by ingestion of contaminated water and also of un(der)cooked meat or by inhalation. The main form characterized by “fever and a bubo” is transmitted by ticks or deer-flies, but hunters can occasionally also contract infection and develop a bubo in the process of skinning sick animals if they have cuts or abrasions in the skin of their hands.23 Helpfully, Butler presents the clinical and epidemiological elements of bubonic plague and tularaemia in a table for immediate comparison and differentiation: tularaemia is easily distinguishable from bubonic plague according to a number of criteria, for instance: (1) it is restricted to wilderness and hunters (today occasionally also campers) and, thus, ordinarily exhibits an endemic or episodic type of occurrence; (2) the course of illness is “usually indolent and self-limited”; (3) the buboes are normally located on the upper part of the body in the axillas or on the neck (reflecting the position of ticks or deer-flies in the vegetation); (4) the level of mortality is much lower, and so on. These two diseases cannot be confused at the epidemiological level or at the level of clinical

23

Butler 1983: 90–1; Manson’s Tropical Disease 1982: 355–9.

320

chapter nine

analysis. Since epidemics of bubonic plague definitionally spread in human societies in sharp contrast to tularaemia, bubonic plague is the only epidemic disease in human habitats, rural or urban, which is characterized by the typical formation of buboes. Therefore, this feature constitutes a defining feature of bubonic plague. Recent genetic research has also revealed that Yersinia pestis target “lymph tissues during infection and carry a virulence plasmid, pCD1, which is required for infection in these tissues, as well as to overcome the hosts’ defence mechanism.”24 This contributes to explaining why buboes constitute a predominating and definitional clinical feature of bubonic plague. An important fact should now be clear, which is that the only other case of a disease characterized by the usual development of buboes is directly associated with insect bites and bacterial infection. The crucial point is that the development of buboes results from insect bites which deposit contagion at a subcutaneous level which is then normally or usually drained through a lymphatic tract to a lymph node. In such diseases, and according to present medical knowledge only in such diseases, the appearance of buboes is an ordinary or usual clinical feature because it is systematically related to the mode of transmission of infection by insect bites. Bubonic plague and tularaemia have in common the fact that they do not spread by interhuman cross-infection but are transmitted by ectoparasites conveying contagion from rodents to human beings. It is of crucial significance in this context that for technical reasons associated with the mode of transmission no disease spread by interhuman cross-infection can be characterized by ordinary epidemic occurrence of buboes. This corresponds completely and without exception with observed fact. Conspicuously, the advocates of alternative theories make no attempt to explain how normal manifestation of buboes should be physically realized in persons contracting the alternative type of epidemic disease they advocate. The fact that they pass by in silence this crucial problem must be taken as an indication that they are unable to provide reasonable medical explanation. Their silence on this point constitutes therefore crucial evidence of the untenability of their assertions and the incompatibility of their alternative theories with this basic fact. All alternative theories of historical plague

24

Dongsheng, Yanping, Yajun, et al. 2004: 1229.

buboes as a normal clinical feature in epidemics

321

based on microbiological contagion spread by cross-infection are ipso facto invalid; this is the case with the alternative theories of Karlsson, Morris, Scott and Duncan and Cohn. Karlsson and Morris who advocate theories of primary pneumonic plague must ignore the obvious fact that buboes are the most usual clinical feature mentioned by contemporaries from the Black Death to the last plague epidemics more than 300 years later. Davis, who recognizes the inherent danger, makes a disquieting attempt at doing away with this problem by asserting that Buboes can occur in cases of pneumonic transmission and cannot be construed as proof of transmission by fleas that infest either rats or humans.25

In support of this statement, he refers in the accompanying footnote to an impressive number of works on plague, among them the following standard works: Wu Lien-Teh 1936b: 409, Hirst 1953: 29, Pollitzer and Li 1943: 161/212–6.26 All of these fine works on plague have in common that they do not contain anything that supports Davis’s assertion, neither on the indicated pages nor elsewhere—they are spurious references (who was the journal’s consultant?). Davis leaves out the only standard work on primary pneumonic plague, Wu Lien-Teh 1926. The reason is clear: no such case is mentioned.27 In this footnote, Davis goes on to refer also to historical plague works, Biraben 1975: 73, 129, and Nohl 1961: 18. These works likewise contain no support for this assertion on the indicated pages, and to anyone knowing these works it will be obvious that support is not to be found anywhere else in them, and that these references are also spurious. Davis does not attempt to explain medically how plague contagion could spread from the lungs to the lymph nodes nor does he explain how a non-episodic, regular pattern of incidence could occur. All assertions to the effect that the epidemic occurrence of buboes is associated with any other epidemic disease than bubonic plague are untenable.

25

Davis 1986: 461. The discrepancy in number of pages is due to my use of the version published in Chinese Medical Journal 1943: 212–6, while Davis refers to a somewhat shorter version published at the same time in Journal of Infectious Diseases 1943: 160–2. 27 Wu Lien-Teh 1926: 241–73. 26

322

chapter nine Contemporary Notions and Observations of Buboes (and Associated Secondary Clinical Manifestations)

Sticker’s ambitiously broad account of all historical plague epidemics in his old but impressive two-volume work on plague28 has inevitably become partly obsolete at least in the sense of having become increasingly incomplete as new research has been published. However, somewhat disappointingly it still provides more concrete information on clinical features than any other history of plague, and as a physician Sticker exhibits strong interest in medical or epidemiological concepts and terminology. Having studied plague in India at the beginning of the twentieth century and having contracted and survived plague, he is in a unique position to put his seemingly boundless energy into good scholarly use. His standard work will be supplemented from later works in the following discussion. “There was little appreciation that individual diseases were separable entities before 1600,” Slack states,29 I would rather say before 1550. In his diary for the years 1550–72, Absalon PederssØn, the Norwegian humanist, identifies a number of diseases with specific terms: plague (“pestilence”), syphilis (“pocks”), small pox (“small pocks”), tuberculosis (“consumption”), exanthematic typhus (“spotted fever” or “soldiers’ disease”), dysentery (“flux”) and leprosy (“[ho]spital disease”).30 This development appears to be closely related to a growing recognition from about 1510–20, associated with the Renaissance, of the contagiousness of epidemic diseases. In Norway and Denmark this development is noticeable from the 1520s at the latest and was apparently influenced by the University of Rostock and presumably other institutions of learning in northern Germany where students of these countries often studied at the time.31 The famous pioneering physician J. Fracastoro systematically discerned plague from exanthematic typhus in Italy around 1530.32

28

Sticker 1908: 42–107. Slack 1985: 25. 30 Benedictow 2002: 204. The term “[ho]spital disease” for leprosy in the Nordic languages refers to the early establishment of particular hospitals for lepers in the High Middle Ages. In English it may have a certain parallel in the contemporary term “lazarhouse disease.” 31 Benedictow 2002: 179–86. 32 Sticker 1908: 106; Ackerknecht 1963: 30. 29

buboes as a normal clinical feature in epidemics

323

Against this background, it is a very noticeable fact that when the subject is broached of how late medieval and early modern historical plague disease presented to contemporaries, there is broad agreement among scholars that one clinical manifestation in particular impressed itself on their minds. From the beginning of the Black Death in the Crimea and Constantinople, and as it spread all through Europe, contemporary commentators who generally had at best very confused ideas about the nature of epidemic disease mention with conspicuous regularity, if they present even minimal clinical detail, buboes as the distinguishing clinical feature. This was also the case in connection with plague epidemics in the following centuries. This clinical feature impressed itself so strongly on contemporaries and distinguished this disease so sharply from all other epidemic diseases ravaging contemporary populations that contemporaries from the very beginning constructed specifying designations or identifications of plague epidemics which reflect the appearance of buboes as a conspicuous characteristic and distinguishing clinical manifestation.33 The clinical manifestations which impressed themselves on contemporaries and led to the development of generalizing terminology can be seen in Matteo Villani’s chronicle, for example, where he relates in connection with the Black Death in Florence in 1348: “in most [of the infected] there were growths in the groin, and with many in the pits under the arms, under the right and the left, with others in other parts of the body, so that almost generally some single swelling manifested itself on the body of the infected.”34 Clearly, Villani was of the opinion that buboes were a general and characteristic feature of the disease which distinguished it from all other diseases known to him and his contemporaries, and this is the basis of the generalizing terms which he goes on to form. When he reverts to the subject in connection with the second plague in Florence in 1362, he can avail himself of generalized

33 Cohn 2002: 63–4, 68–9, has also to some extent noted this development, but since his aim of necessity is to reject the possibility that this proves that the disease was bubonic plague, although he knows of no other disease characterized by this clinical feature, his presentation becomes episodic and his discussion superficial and tendentious. Of course, this development was not especially associated with Florence, it is his narrow perspective that associates it with Florence and Italy. 34 Matteo Villani, Cronica 1995–1: 9: “e a’ piu ingrossava l’anguinaia, e a molti sotto le ditella delle braccia a destra e a sinistra, e altari in alter parti del corpo, che quasi generalmente alcuna enfiatura singulare nel corpo infetto si dimostrava.” My translation of the chronicle’s text. Cf. ibid.: 11.

324

chapter nine

terms referring to buboes for identification of the disease and as the same disease as the Black Death (see below). It is also noteworthy that he gives main locations of buboes which are similar to those observed in cases of modern bubonic plague. These generalizing designations focus on buboes of the groin area (in Latin inguen, in modern Italian “inguinàia” or “inguine”/ “inguinale,” in contemporary northern Italian often slightly changed into “anguinaia”/ “anguen”), or provide more generalized expressions of a disease characterized by buboes, especially in the groin area, and great mortality: “pestis inguinaria”35 (= inguinal pestilence, Modena 1348),36 glandular plague, “mortalité des boces”37 (= mortality of buboes, Rheims 1349), “l’épidémie des boces” (Narbonne 1349),38 “sterffde van den droesen” (= mortality of the buboes, Cologne 1350),39 or characterized by “dolor ignitus in inguine” (= a fiery pain in the groin, France, Paris).40 Cohn 2002: 64, cites three generalizing expressions “inguinarie,” “pietolenzia dell’anguinaia” (= pestilence of the groin), and “mortalità dell’anguinaia” which I have not mentioned above as associated with “Florence after 1348.” In the accompanying footnote 51, Cohn refers to Matteo Villani, Cronica con la continuazione di Filippo Villani 1995, Volume 1: 273, 300, 514, 585–6, 660–1, 663. However, on these pages nothing is said about plague or buboes—all of these page references are erroneous. As we shall see, the second and third of the medical terms for plague that Cohn cites are instead associated with the second volume of Matteo Villani’s chronicle and with the next plague epidemic in Florence of 1362; the first term may be associated with the second plague epidemic in Siena in 1363 and a different source (see below). Cohn also asserts in this connection that the development of terms to describe plague in connection with the Black Death which were “derived from the boil’s position in the groin” took place “particularly in Florence.” As we have seen this was not the case; this assertion depends on false references to Matteo Villani’s chronicle and a narrow

35

Sticker 1908: 51, without specification of source. Cohn 2002: 64. 37 Desportes 1977: 794. 38 Sticker 1908: 59. For his account of the Black Death in Narbonne, Sticker refers to works which I have not had occasion to get hold of, namely Cayla 1906 and Martin 1859. 39 Sticker 1908: 75. 40 Littré 1840–1: 202, 232. Cf. Gasquet 1908: 40–1. 36

buboes as a normal clinical feature in epidemics

325

Florentine or Tuscan perspective. Such terms arose in connection with the Black Death elsewhere in northern Italy and also in France and Germany and also in connection with subsequent plague epidemics elsewhere, in Ireland, Belgium, and Russia. In the subsequent plague epidemics, the use of generalized designations continued to be developed, strengthened and familiarized. Matteo Villani comments on plague in Germany and Brabant in 1358 calling it “pistolenzia dell’anguinaia” and mentions in another chapter “moria dell’anguinaia” in Brabant which also spread to some areas in Italy, and he refers to the second plague in England also with the characteristic expression “pistolenzia dell’anguinaia.”41 Matteo Villani makes it clear that the plague of 1362 was the same disease as the Black Death, calling the first chapter on it “How the Mortality of the Groin Recommenced in Various Parts of the World,”42 and after having used the expression “mortality of the groin” in the chapter’s title, he goes on to state in the first line of the text: “the mind-boggling disease of the groin recommenced this year, similar to that which had begun in 1348.”43 He reverts to this plague epidemic later in his chronicle using in the chapter’s title the expression “mortalità dell’angunaia” and in the opening text of the chapter the expression “pistolenza dell’ anguinaia (= pestilence of the groin area, Florence 1362).44 In the Necrology of the Dominican cemetery in Siena it is casually written in the margin in 1363 when there is a huge increase in interments: mortalitas generalis inguinarie45 (= general inguinal mortality). Also elsewhere in Europe such expressions or terms were developed 41

Matteo Villani Cronica 1995–2: 273, 300, 514. “Come mortalitá dell’anguinaia ricominció in diverse parti del mondo,” my translation. 43 “la moria mirabile dell’anguinaia in questo anno ricominciata, simile a quella che prencipio ebbe nel MCCCXLVIII […],” my translation. Matteo Villani Cronica 1995–2: 448. 44 Matteo Villani Cronica 1995–2: 585–6, see also pages 660, 663. Cohn 2002: 138, makes a free translation of the introductory passage, again showing, as pointed out by Carmichael, a strange reluctance to use the word buboes, perhaps because of its strong association with bubonic plague, instead translating the expression “pestilence of the groin area,” with “pestilence of the glandular swellings” which ignores the original text’s unambiguous association of the disease with the groin and indication that it was characterized by clinical features associated with the groin. 45 I Necrologi di San Domenico in Camporegio 1937: 95. Written rather casually in the margin of the necrology, which in this case is a burial register, this expression indicates quite a widespread term and notion. Cohn erroneously includes this source in his reference to the development of such terminology in post-Black Death Florence (see above). 42

326

chapter nine

to designate plague: disease of buboes or mortality of buboes (Russia 1360, 1387),46 pestis inguinaria (Cologne 1365),47 pestis glandium/ glancium (Ireland 1369), disease of buboes (Liège, “Belgium” 1370),48 infirmitas carbunculi et glandulae (= disease of carbuncles and glands, Parma 1371),49 peste anguinaia (Florence 1449),50 and so on. The process of familiarization with the specificity of bubonic plague can be illustrated by Marchionne Stefani’s statement on the plague of 1374 which was to him the “usual pestilence of inguinal or axillary swellings,” and in 1383 commented that the plague killed “in the same way as the other mortalities, with that sign of great swelling under the arm and over the leg at the groin.”51 Another related development is that bubonic plague was considered such a conspicuously specific disease that a distinguishing term for this disease was needed according to the medical notions of the time. First, the term “epidemic” was employed for specific designation of bubonic plague in order to distinguish it notionally and terminologically from other contagious diseases which generally were called “pestilence” or “pestilential.” The generalized expression “l’épidémie des boces” was used in Narbonne to designate the Black Death in 1349,52 under the influence, as it may seem, of the medical faculty of Montpellier. In Paris physicians called the Black Death “épidémie,” as also was the case with a chronicler discussing plague in the area around Trier in western Germany (epidemia).53 This terminological development appears in strengthened form when the plague in Hesse and Westphalia in 1371 was characterized by the term pestilentia epidemiarum54 = the epidemics’ pestilence, implying that that plague was considered the essence of epidemic disease, the highest and most dangerous refinement of miasmatic poison, the King Death of epidemic diseases. A related term, pestis epidemialis was used in Thuringia, especially in Frankfurt and Eisenach.55 The link becomes obvious with the expression inguinaria 46

Sticker 1908: 76, 80. Sticker 1908: 77. 48 Sticker 1908: 77. 49 Cohn 2002: 61. 50 Herlihy and Klapisch-Zuber 1978: 375. 51 Carmichael 1986: 11. 52 Sticker 1908: 59. The Black Death was recognized as present in Narbonne around 1 March 1349, Benedictow 2004: 101. 53 Sticker 1908: 60, 67. 54 Sticker 1908: 77. 55 Sticker 1908: 81. 47

buboes as a normal clinical feature in epidemics

327

pestis seu epidemiae morbus = “inguinal pestilence or disease of epidemic” used to designate the plague which reigned in Wittenberg in 1535.56 Thus, logically the term “epidemie van die pestilentie”57 = “epidemic of pestilence” was developed, showing that “pestilence” could be used as a specific term for bubonic plague, producing, therefore, a need for another general term for contagious diseases, a role which was increasingly filled by epidemia or “epidemic,” which has retained this position to this day, while the form “pest” has retained its position as a specific word for bubonic plague. In English, the word “plague” reflects the fact that the English found another solution to the need for specificity in the designation of this disease, taking this term slowly into specific use as an Anglicized form of Latin plaga with the meaning of “a blow,” which originally was a general term for a dangerous disease, a development that was becoming pronounced by the late sixteenth century.58 In a document of September 1349, Magnus Eriksson, King of Norway and Sweden, used the word plaga to designate the Black Death.59 This perception of plague as dominated by buboes did not start with the Black Death; it has been a consistent feature of how people of the past perceived plague and what really characterized the disease, besides the exceptional mortality. Twigg rejects the fact that Gregory of Tours uses the term lues inguinaria = “disease of the groin” to designate the first plague epidemic of the Justinianic pandemic of 541–76660 which spread over southern France and conquered Old Gaul in the years 543–4.61 However, he does not point out any alternative specific disease which could fit this clinical descriptive term, presumably because every specification easily could be rejected by anyone knowledgeable of epidemic disease or with access to a standard textbook on epidemic diseases. Since small pox (variola maior) was probably not present in Europe at the time or for a long time to come,62 the alternative Twigg has in mind would have to be anthrax. Any reader interested in the matter is encouraged to look up anthrax (or smallpox) in any standard work on epidemic disease and see whether buboes are mentioned at all or as more than episodic individual occurrences that would never give 56 57 58 59 60 61 62

Sticker 1908: 92. Sticker 1908: 99. Slack 1985: 64–5. Benedictow 2002: 22, 96–7; Benedictow 2004: 152, 160, 171–2. Twigg 1984: 35–6. Simpson 1905: 15; Sticker 1908: 30: Little 2007: 11. Cartwright 1977: 76–7; Greenwood 1935: 227; Copeman 1960: 127–8.

328

chapter nine

rise to a generalized designation of the disease as involving this symptom. Twigg ignores the accounts of the violent plague epidemics in Constantinople given by the Byzantine physician Procopius which contain quite detailed clinical information on buboes,63 for instance: “On a sudden they became feverish […] in some cases, on the same day, in others on the next, in others in a few days after there arose a bubo, not merely on what is called the groin, but under the armpit; in some cases the bubo appeared behind the ears and in other parts.”64 Also in this pandemic of plague, similar generalized terms referring directly to the ordinary occurrence of buboes as a characteristic clinical feature of the epidemics are in frequent use: inguinarium (550), inguinarium morbum, fever with buboes, glandulae (561), morbus inguinarius (582), clades65 inguinaria, pestis inguinaria (589), lues inguinaria (591), pestis inguinaria (599), clades glandolaria (600), and so on,66 which about exhausts the potential of Latin for forming clear designations of a disease characterized by the formation of buboes, especially in the groin and nearby femoral area. Buboes in the axillas or on the neck are also specifically noted quite often.67 Recently, M.G. Morony has supplemented and corroborated this with information from Syriac sources on the Justianic pandemic focusing on epidemics specified by the use of the clinical term “sharcūṭā” “which refers both to the swellings or tumors and to the disease itself,” and the term “mawtānā de sharcūṭā” meaning epidemic of tumors.68 Also the corresponding Arabic term “ṭācūn” is used in this meaning. The terms (“mawtānā de) sharcūṭā” or “ṭācūn” were used to designate the first plague epidemic of 541–4, next in connection with epidemics of 562, 573–4, 600, 639, 686–7, 698–9, 713, 744–5.69 One should note that a plague focus running in quite a broad territorial band from the Persian Gulf up to eastern Syria and south-western Turkey was established at the latest during the Justinianic pandemic and would give rise to local outbreaks of plague.70

63

See, for instance, Simpson 1905: 6–14. Cited after Simpson 1905: 7–8. Cf. Little 2007: 8–9. 65 The word clades here has the meaning of “mortality”; it usually has the related meaning of military losses. 66 Sticker 1908: 31–4; Simpson 1905: 15–16. 67 Ibid. 68 Morony 2007: 61. 69 Morony 2007: 61, 65–6, 70, 73, 76. 70 See for instance Benedictow 2004: 37–40, 44–8. 64

buboes as a normal clinical feature in epidemics

329

By now, quite a number of scholarly studies on this pandemic provide ample material for the identification of the disease as bubonic plague.71 Importantly, new developments in paleomolecular analysis of DNA have in recent years given rise to several papers reporting reclamation of DNA of Yersinia pestis from skeletal remains of the time of the Justinianic pandemic a.d. 541–766, from the second half of the sixth century or later, from Sens in northern France, Aschheim near Munich in Upper Bavaria and from Vienna,72 providing independent and substantial, even decisive evidence to the effect that Gregory of Tours’s use of the term lues inguinaria, disease of the groin, refers to bubonic plague. The tendency towards generalized designation of the epidemics with reference to buboes is reflected in numerous accounts or descriptions of buboes from the very beginning of the Black Death to the final paroxysm of plague in southern France in 1720–2. When the inhabitants of the north-eastern French city of Rheims in 1349 use the term “mortalité des boces” (= mortality of buboes) to designate the Black Death, the reason must be that plague cases in this city conspicuously and ordinarily presented with this clinical feature. This is corroborated by a list established in order to register by name, approximate age, and social status persons who had been miraculously healed from plague disease by prayer to St Remi, in which list some of the entries include some basic clinical description as proof that the disease really was plague. A mother declared to have seen her small boy be healed from three buboes, two buboes in the groin (area), and one in an axilla; at the time of Ascension Day (21 May), a young girl first had a bubo under her arm, and then a second bubo appeared on her neck; a married man had an enormous bubo on his neck 17 July; Jehan de Blanzy, a man of some learning, related that his wife’s disease began with strong fever, next buboes appeared in the groin (area) and her condition began to improve 29 July after intercessory prayer to St Remi had been said. The local canon and poet Guillaume de Machet emphasizes buboes as the distinguishing feature of the disease. All information about the locations of buboes on the body is consistent with modern bubonic plague. Thus, not only the general terminology but also all the individual pieces of clinical information provided by contemporaries are consistent with 71 See for instance Russell 1968; Biraben and Le Goff 1969; Allen 1997; Keys 1999; Sarris 2000. 72 See below: 389–90.

330

chapter nine

bubonic plague—only with bubonic plague and with no other disease. This is also the case with the seasonality of the epidemic in Rheims, arriving in the autumn of 1348, being suppressed by cold winter weather, developing rapidly with the advent of warmer spring weather, and fading away in the autumn.73 Correspondingly, the inhabitants of Narbonne not only used the generalized term of an epidemic of buboes (“l’épidémie des boces”) but also used more individualized clinical information to the effect that plague cases started abruptly with fever and headache and then developed buboes in the groin (area) and in the axillas,74 again a description which is entirely compatible with modern bubonic plague both with respect to the start of illness, the typical early symptoms of high fever and severe headache, and the development of buboes and their location.75 In Strassbourg a local chronicler relates that all victims died from buboes or (enlarged) glands which swelled under the arms or high up on the legs, and when the bubo appeared, they died on the second, third or fourth day.76 When Dubois concludes with respect to the Black Death that “everywhere in France, the plague has taken on the bubonic form with secondary manifestations,” he has a solid empirical foundation for this summary of the evidence.77 In “Germany” it is stated in the Upper Palatinate (Ober Pfalz) that persons developed a bubo and died on the third day, and in Cologne there was a “great mortality from the buboes.”78 In addition to the presentation of more generalized terms and expressions used by contemporary Florentines, it can be mentioned that in the north-eastern Italian provinces of Friuli and Istria the diseased generally presented with three main clinical manifestations “in glantia (= in the glands), carbuncle et sputo sanguinis (= carbuncle and bloody expectoration).”79 Carbuncles are a normal part of the clinical panorama of modern bubonic plague: they may either develop at the bite site as a local infection caused by remaining plague bacteria, often called primary plague 73

Desportes 1977: 794–9. Cf. Dubois 1988: 320. Sticker 1908: 59. 75 Simpson 1905: 263; Chun 1936a: 310; Pollitzer 1954: 411; Butler 1983: 73. 76 Sticker 1908: 67. 77 Dubois 1988: 316. My translation from French. With the term secondary manifestations he has probably in mind bloody expectoration in cases of secondary pneumonia. 78 Sticker 1908: 75. My translation from contemporary German: “groß sterffde van den droesen.” 79 Sticker 1908: 50. 74

buboes as a normal clinical feature in epidemics

331

carbuncles, or may, like pustules, be due to an invasion of the skin through the blood-stream, and may, thus, be considered secondary and consequent upon the development of septicaemia.80 Carbuncles as a usual clinical feature of an epidemic disease cannot be associated or explained by any of the alternative theories, although they occur episodically in relation to anthrax in cases where contagion is contracted through abrasions in the skin. As a usual clinical feature carbuncles could probably represent a defining feature or a very strong indication of the nature of the disease as bubonic plague. This explains why carbuncles are not entered as a clinical feature of any epidemic disease in the indices of general textbooks on epidemic diseases,81 in contrast to the standard works on (bubonic) plague where this is an ordinary entry.82 In his historical presentation of plague, Sticker cites a great number of historical sources in which buboes are mentioned, often with specification of locations on the body, that buboes were associated with sharp intense pain, and other clinical manifestations that are consistent with modern bubonic plague: severe headache, spitting of blood, rapid course and brief duration of illness, and so on. For sceptics it can be mentioned that, in the case of the pandemic that started with the Black Death and petered out in the seventeenth century and ended (except in Eastern Europe) at the beginning of the eighteenth century with a couple of explosive outbreaks, Sticker provides such information in the first volume for the Black Death on pages 45, 47, 49–54, 57–60, 64, 65, 67–8, covering most of Europe, from Kaffa on the Crimea and Constantinople to Northern Germany and Poland, but misses out England (see below). For the next wave of plague epidemics of 1361–5, see pages 76–7, also with great geographical distribution, for the third wave of 1368–71, see page 77, and so on through the centuries. The total amount of evidence is massive.

80

Pollitzer 1954: 206, 425. See, for instance, Manson’s Tropical Diseases 1982, Jawetz, Melnick and Adelberg 1982, with their indices. 82 Usually carbuncles are associated with boils or abscesses caused by yellow staphylococci and have an individual type of occurrence. The cutaneous type of anthrax may develop into carbuncle-like forms, but will be closely associated with a few occupations using wool or hides where workers with abrasions on their hand will be exposed to infection by the cutaneous route. Carbuncles with this background are for obvious reasons unlikely to appear in epidemic form or to assume the character of a usual clinical feature. See also below: 556–8. 81

332

chapter nine

British chroniclers and other contemporary observers and commentators provide little clinical detail on the Black Death, however, when they do, it is consistently compatible with bubonic plague. The most informative chronicler is the Irish friar John Clyn of the monastery of Kilkenny: […] many died of boils and abscesses, and pustules on their shins [= legs] and under their armpits; others frantic with pain in their head, and others spitting blood […].83

As can be seen, John Clyn refers to buboes (boils), and specifies the characteristic and usual locations on the legs and under the armpits. However, the friar is perhaps shy when it comes to identifying the sexually sensitive area of the groin and the nearby femoral area, but feels free to specify the location in the armpits. The excruciating headache which tends to drive people out of their minds is also a characteristic accompanying clinical feature of bubonic plague.84 John Clyn’s observation that some died spitting blood cannot be taken as evidence to the effect that the Black Death was an epidemic of primary pneumonic plague as asserted by Morris (see below). The strongly restricted reference to the occurrence of cases with bloody expectoration, i.e., the fact that only some developed this feature, indicates clearly the normal proportion of plague cases which develops secondary pneumonic plague in epidemics of bubonic plague. The friar also mentions abscesses and carbuncles,85 and he mentions pustules which are quite a usual cutaneous manifestation.86 This account contains, then, a good description (for the time) of an epidemic of bubonic plague, and is thus a good source on the medical and epidemiological character of the Black Death in England. Other accounts and descriptions are compatible with John Clyn’s but contain fewer details. Galfrid le Baker states, for instance: Swellings suddenly breaking out in various parts of the body, racked the sick. So hard and dry were they that, when cut, scarcely any fluid matter 83

Hirst 1953: 13. Simpson 1905: 263; Chun 1936a: 310; Pollitzer 1954: 411; Butler 1983: 73; Benedictow 2002: 208, where two cases in the epidemic in Bergen of 1565–6 are described in Absalon Pederssøn’s diary: “A man was ill with pestilence, he raged, he stood up in his rage and ran to L. Lundegaard where he drowned himself.” A clergyman of one of the Hanseatic congregations in Bergen died in the plague “and raged somewhat in his head in his illness.” My translations from contemporary Norwegian. 85 Pollitzer 1954: 424. 86 Pollitzer 1954: 427. See below: 557. 84

buboes as a normal clinical feature in epidemics

333

came from them. From this form of the plague many, through the cutting [incision?], after much suffering, recovered. Others had small black pustules distributed over the whole skin of the body, from which very few, and indeed hardly anyone, regained life and strength.87

Le Baker mentions buboes without localization and says that they were incised, and that many of those who underwent this treatment survived, an indication that he has his information from a barber-surgeon or perhaps physician who apparently added some self-serving comments on the efficacy of this treatment. On the other hand, the assertion that buboes hardly contained any fluid appears to be incorrect and is inconsistent with other contemporary and later accounts.88 He mentions also that some of those diseased from plague developed widespread dark pustules, a clinical feature which is associated with septicaemic developments and are observed also in modern observations of plague cases and discussed at length below.89 Standard works on English plague history like Creighton 1891 and Shrewsbury 1971 must for various reasons be used with caution but can provide additional interesting concrete clinical detail. Valuable information is also provided in Slack 1985 and in Bell 1951 who gives detailed and informative material for the London epidemic of 1665.90 Johan van Beverwijk, the Dutch physician, described plague as “manifestation of buboes” (“manifestatie van bubonen”), and Jacobus Viverius noted that buboes appeared on the neck, in the armpits and in the groin, mentions carbuncles and that buboes suppurate (if not incised).91 W. Swinnas, another physician, considers “pest-buylen, Pestkoolen en peperkoorens,” i.e., buboes, carbuncles and dark-coloured spots in the skin called peppercorns (caused by haemorrhages) as “convincing” indications of plague, but mentions also headache and other secondary accompanying clinical features as indicative.92 Although there is considerable variation in the clinical panorama of bubonic plague, contemporary observers of historical plague epidemics nonetheless focus on certain features, first of all on buboes and the

87

Cited after Gasquet 1908: 136. Chun 1936: 316. Cohn 2002: 60, cites the account of Michael of Piazza (Michele da Piazza) to the effect that buboes “filled with a putrid liquid,” but this must be a mistranslation. Nohl 1961: 9; Sticker 1908: 49. 89 Below: 370, 372–8. 90 Bell 1951: 126–7. 91 Noordegraaf and Valk 1996: 25–6. 92 Dijkstra 1931: 13–7. 88

334

chapter nine

great sharp pain associated with them,93 but also on carbuncles, sudden onset of high fever, early appearance of splitting headache, purple or black spots, pustules, and spitting of blood. All of these clinical features noted by contemporary observers are also mentioned by modern specialists on plague on the basis of vast numbers of medical observations in India, China, Madagascar, and elsewhere, and are described in all standard medical works on bubonic plague.94 I cannot see that further amassing of evidence would be of any additional use in disproving the alternative theories about the plague: this evidence is to be found everywhere in serious scholarly work on historical plague epidemics. Scott and Duncan: The Problem of Buboes Scott and Duncan follow the second of the approaches mentioned above in their attempt to reject the conclusion that buboes are a defining feature of bubonic plague, that is, they claim that buboes are a characteristic clinical feature of at least one other disease. However, they do this in a special way that deserves closer attention. They do not at the beginning of their monograph present filoviridal contagion and the Ebola and Marburg forms of disease caused by this pathogen and its variants in order to test the historical material against this epidemiological and clinical presentation. Instead, and at variance with normal scholarly practice, Scott and Duncan (like Cohn) start their monograph by asserting their thesis and conclusion to be true, that historical plague epidemics were not bubonic plague but rather haemorrhagic disease, or “haemorrhagic plague” as they arbitrarily go on to call it, and that this was some type of Ebola or Marburg filoviridal disease.95 In consequence, they pretend that they can legitimately conclude that any characteristic feature of historical plague epidemics must be reflections or manifestations of their phantom haemorrhagic disease. When historical sources state that persons diseased with plague presented with buboes, this simply proves that the normal occurrence of buboes is a characteristic feature of “haemorrhagic plague” (see below). When contemporary physicians or barber-surgeons incised mature buboes, this proves that such simple surgery was a suitable treatment for

93 94 95

Below: M346–54. See, for instance, Pollitzer 1954: 411–40; Chun 1936: 309–17. Scott and Duncan 2001: 1, 7–10.

buboes as a normal clinical feature in epidemics

335

haemorrhagic buboes.96 When historical plague epidemics show strong seasonality with a very pronounced prevalence for the warmer periods of the year, this proves that this feature is characteristic of haemorrhagic filoviridal disease.97 When the duration of the disease is three to five days, this proves that this is the duration of the course of illness of haemorrhaghic plague,98 and so on. Clearly this is an instance of the fallacy of methodology called circular inference, and these examples show that it is an integral part of the construction of Scott and Duncan’s alternative theory. Thus, in the view of Scott and Duncan the ordinary clinical occurrence of buboes does not prove that a disease is bubonic plague but proves that buboes are a characteristic and defining feature of haemorrhagic plague.99 The two crucial parts or arguments in the following citation are enumerated by me and will be commented on following the citation with references to these numbers: Indeed, apart from [1] the fact that the victims of both diseases presented with enlarged glands and subcutaneous swellings, it is difficult to suggest a more unlikely candidate than Yersinia as the infectious agent of haemorrhagic plague. [2] In the 1720s, 60 years after the disappearance of the plague, London was swept by a series of epidemic fevers which were characterised by buboes and carbuncles [Creighton, 1894100], confirming that these clinical signs were not exclusively diagnostic of bubonic plague.101

(1) The crucial assertion that buboes are an ordinary and characteristic clinical feature of any or some form of Ebola or Marburg haemorrhagic disease is not given support in the form of reference(s) in the text or in a footnote to studies providing such clinical evidence, not here or anywhere else in the monograph, and this assertion is ipso facto unfounded and arbitrary. When Scott and Duncan at the very end of their monograph at long last finally provide some systematic, but highly deficient clinical and epidemiological information on filoviridal types of disease, their presentation does not contain a word about

96

Scott and Duncan 2001: 388. Scott and Duncan 2001: 148, 152–4, 193, 252–3, 364–6. 98 Scott and Duncan 2001: 85, 107–8, 144, 207–9, 380–1. 99 Scott and Duncan 2001: 6–7. 100 In 1894, the complete work of Creighton appeared, where the first volume is a reprint of the edition of 1891 and the second volume completes Britain’s epidemic history “to the present time.” See bibliography. 101 Scott and Duncan 2001: 362. 97

336

chapter nine

buboes.102 They are completely unable to provide any support from primary medical studies on filoviridal diseases or standard works on infectious diseases for the suggestion that any strain or variant of Ebola or Marburg filoviridal contagion produces haemorrhagic disease which presents with buboes. In fact, they are unable to document that any bubo has ever been observed in any patient diseased by any known (and therefore testable) form of filoviridal disease. The assertion in the citation to this effect, which is at the heart of their alternative theory, is arbitrary. This explains their choice of a methodologically fallacious approach. (2) The fact that Scott and Duncan are unable to adduce evidence to the effect that buboes are associated with the clinical panorama of filoviridal diseases should, according to ordinary methodological considerations, have settled the matter. Even if it were true that other diseases presented with buboes, it would obviously not support the validity or tenability of their specific alternative theory. Nonetheless, they assert that other diseases do present with buboes and maintain that support for this view is provided in the second volume of Creighton’s great work on Britain’s epidemic history published in 1894 covering the period from 1666 to “the Present Time,” which, they maintain, contains descriptions of epidemic diseases in London in the 1720s “characterised by buboes and carbuncles.” No footnote with identification of page is given. After having done my best to identify the textual source, I have had to throw in the towel. In this volume, epidemic diseases in London in the 1720s are discussed in a chapter called “The Epidemic Fevers of 1726–9: Evidence of Relapsing Fever.” In this chapter, the words buboes or carbuncles are not mentioned.103 Relapsing fever is, of course, an entirely different disease and the victims of this disease do not present with buboes. Consequently, Creighton states nothing “confirming that these clinical signs were not exclusively diagnostic of bubonic plague.” This claim is taken out of thin air in order to create a false argument in support of their theory which reveals again the untenability and arbitrariness of their alternative theory. The curious reader may here become an inquisitive reader and ask pointedly why Scott and Duncan must make this important point for the viability of their theory on the basis of purported historical

102 103

Scott and Duncan 2001: 384–9. Creighton 1894–2: 66–74.

buboes as a normal clinical feature in epidemics

337

evidence in a proto-scientific history of epidemic diseases based on miasmatic theory, and why they do not base their view on modern medical or historical studies of epidemic diseases. The answer can be given on their behalf: no such studies can be found because there are no such studies to be made because there are no such diseases; the epidemic occurrence of buboes is a unique and defining feature of bubonic plague. In the popularized version of their book published three years later, they revert to the problem of buboes in a related way; again the crucial points in the citation are enumerated by me and will be commented on following the citation with references to these numbers: The characteristic [1] (but not specific symptom) of bubonic plague is the appearance of the bubo. [2] Once Yersin had announced his seminal results, [3] it was realized that victims of haemorrhagic plague also sometimes presented with swollen lymph glands.104

These assertions are presented without any evidentiary support and, as shown above, the reason is that there is no support for any of them. (1) It has been documented above that bubonic plague is the only epidemic disease that presents with buboes as an ordinary clinical feature, the reasons for this have also been given. Scott and Duncan’s assertion that the bubo is not a “specific symptom” remains unsubstantiated by evidence and is as such arbitrary. (2) Yersin’s discovery of the plague bacillus in 1894 was published the same year and contains nothing in support of Scott and Duncan’s position (what do they mean by “announced”?). Filoviridal haemorrhagic disease was discovered in 1976,105 eighty-two years later, and it is obviously not true that “once” Yersin had published his discovery anything “was realized” about the clinical manifestations of cases of filoviridal disease. (3) Consequently, it cannot be true that it was recognized in 1894 or for eighty-two years to come that “haemorrhagic plague” “also sometimes presented with swollen lymph glands.” In the research literature published in the three decades following the discovery of Filoviridae not a single patient has been recorded who has

104 105

653.

Scott and Duncan 2004: 167. www.who.int/inf-fs/en/fact103.html 2003: 2; Manson’s Tropical Diseases 1996:

338

chapter nine presented with a bubo or “swollen lymph glands.” This is the reason Scott and Duncan are unable to present a single case in support of their assertion, despite the fact that most infectious diseases may occasionally infect by the cutaneous route, be drained to a lymph node and cause the development of a bubo. The three assertions constituting the passage are all spurious. Throughout their monographs, Scott and Duncan presume identity between the incidence of buboes in cases of bubonic plague and in “haemorrhagic plague.” The present formulation “sometimes presented with swollen lymph glands” approaches a notion of episodic or individual occurrence, although as emphasized above, they are unable to supply a reference to a single victim of filoviridal disease who has, in fact, presented with a bubo, so this formulation is also unfounded. But in any case, episodic or individual occurrence would not have epidemiological significance for the present discussion, since the point is that bubonic plague is the only epidemic disease that presents with buboes as an ordinary feature of the clinical panorama and this feature is therefore a defining feature of bubonic plague. For these reasons, the unnamed scholars implied in the formulation “it was realized” are fictitious, they do not exist, and this is the reason Scott and Duncan are unable to substantiate their assertions to this effect in their monograph of 2001 or in the popularized version of 2004.

Since Scott and Duncan proclaim at the opening of their monograph that their alternative of haemorrhagic filoviridal disease is the “truth” about the microbiological nature of historical plague, which entails as a logical consequent the flat rejection of bubonic plague as an alternative possibility, they can pretend that they do not need much information on bubonic plague. They can therefore pretend that it is adequate to rely on a chapter in a general textbook of infectious diseases by A.B. Christie for their information on bubonic plague, a chapter consisting of twenty-four pages of which only three pages relate directly to clinical and medical features of human plague.106 Intriguingly, all through their monograph Scott and Duncan consistently refer to the first edition (1969) of this textbook which in fact does not contain a chapter on plague. A chapter on bubonic plague does not appear until the third edition of 1980, which attests to the author’s peripheral interest in 106

Christie 1980: 760–2. See also below: 621–8.

buboes as a normal clinical feature in epidemics

339

bubonic plague, which according to ordinary principles of scholarly work should be very much in focus in Scott and Duncan’s monograph. Unsurprisingly, Christie’s account of plague has many unsatisfactory aspects (see below) and provides a clinical description of bubonic plague of uneven quality, though it does also contain valuable information. Scott and Duncan cite Christie’s concluding clinical statement in this extraordinary way: Most importantly for our purposes, he [Christie: my insertion] continued, “The picture is non-specific: it might be any severe septicaemic illness, or typhus, typhoid, malaria and the like [our italics]. The only distinguishing feature is the bubo.”107

Astonishingly Scott and Duncan cite this statement under the assumption that they can “legitimately” focus solely on the initial words in Christie’s statement, that the “picture is non-specific,” emphasizing this point with italics, and can infer that Christie asserts that bubonic plague has no defining feature. This is what they consider “Most importantly for our purposes.” This is clearly not compatible with the last sentence of Christie’s statement where it is unequivocally stated that bubonic plague has, in fact, one distinguishing feature, namely “the bubo,” a crucial statement that should have been emphasized by bold type but is left also without italics and is completely ignored. A distinguishing feature sets a phenomenon apart from all other phenomena and constitutes a defining feature; for this reason the terms “distinguishing feature” and “defining feature” are synonymous. Consequently, even Scott and Duncan’s brief and peripheral source of modern medical information on bubonic plague in Christie’s general textbook makes it clear that description of buboes as an ordinary clinical feature of diseased persons in an historical plague epidemic constitutes a sufficient condition for the identification of the disease as bubonic plague. It provides also a sufficient explanation of why Scott and Duncan do not present a model of filoviridal diseases at the beginning of their monograph which would enable readers to perform continuously a critical comparative analysis. Comparison of the clinical panorama of known diseases with the clinical panorama of historical plague is the crucial methodological approach for resolving the problem of the identity of

107 Scott and Duncan 2001: 68. Scott and Duncan do not provide footnotes, however, information on buboes is given in Christie 1980: 761–2. Scott and Duncan’s italics.

340

chapter nine

historical plague. Their failure to present (sufficient) material premises for performing a valid comparison means that readers cannot perform ordinary critical functions and will tend to become helpless victims of their arguments. This is the reason why when a presentation of filoviridal diseases can no longer be postponed and at long last appears at the end of their monograph in an unsatisfactory brief and cursory form, it does not contain a word about buboes. In the end, reality can no longer be evaded: they have invented a phantom disease. Cohn: The Problem of Buboes In the very first sentence of his monograph, Cohn states unreservedly that “The Black Death in Europe, 1347–52, and its successive strikes to the eighteenth century was any disease other than the rat-based bubonic plague.” At the end of his monograph he lamely admits that he has no idea what disease it could have been, except that it must have been a viral disease that since has disappeared, which means that he ends arbitrarily with an untestable hypothesis (see below). Cohn’s approach to the problem that epidemic occurrence of buboes represents to his alternative theory is very different from Scott’s and Duncan’s: he primarily seeks support in the writings of contemporary chroniclers and physicians. He does not deny that contemporary accounts and descriptions of plague disease often mention buboes as an ordinary clinical manifestation. The pivotal point of his line of argument is that contemporaries provide descriptions of the localizations of buboes and the wider clinical panorama of the disease which differ so greatly from those of modern medical studies and textbooks that they would have to be two different diseases. This paves the way for his own alternative theory, a viral disease spread by cross-infection which since has disappeared and cannot therefore be tested. At the heart of this line of argument, as so often in Cohn’s work, is the notion or assertion that chroniclers and especially contemporary physicians provide epidemiological, medical or clinical evidence that was obtained by basically rational, systematic and quite scientific observation. According to his view, this evidence is therefore suitable as hard evidence for statistical inference, comparison with modern medical data, and other forms of generalizing at a high or substantial level of tenability, and as such forms the basis of strong arguments in important or crucial matters. In a characteristic fashion, Cohn argues seemingly effectively on the basis of the amassed evidence of chroniclers

buboes as a normal clinical feature in epidemics

341

and physicians, but without actually presenting the material. Therefore, his assertions must either be believed at his word, which is not something scholars usually demand from their readers, or must be rejected as methodologically incomplete science: the point is that at the heart of scholarly work are the concepts of testability and falsifiability, so that scholars are obliged to present evidence in a way that makes its validity and (level of) tenability readily testable and falsifiable. Cohn maintains that he consulted “407 chroniclers, calendars and ‘necrologies’ covering the plague years from 1347 to 1450” and that “I have been able to read in various libraries in Britain, France, and Italy.”108 He is not so specific about the number of physicians’ plague tracts that he maintains to have consulted but states that at least fiftyfive of these tracts provide information on the localization of buboes;109 in his Appendix III, he enters the titles of nearly a hundred “Plague tracts cited from Sudhoff Archiv für Geschichte der Medizin,”110 which presumably represent the majority of them.111 Thus, Cohn pretends that it is an acceptable procedure of scholarly or scientific work to confront those of his readers who wish to perform the ordinary critical obligation to test the material basis of his assertions with an ultimatum: (1) that they either repeat his “work,” that they should travel to academic libraries in England, France, and Italy, in order to get access to these works and spend great amounts of money and years of their precious scholarly lives just to test the material basis of his assertions or (2) eat out of his hand. I will submit that this is not compatible with the methodological requirements of scholarly or scientific work and that his generalizing assertions on the supposed basis of chronicles or plague tracts should also for this reason be rejected as invalid because they have (so far) no practically testable evidentiary basis and therefore (so far) have a fundamentally arbitrary character. Cohn is not averse to appendices, actually he has three of them in his monograph, but he does not use this opportunity for presenting his primary material, i.e. citations from chroniclers or plague tracts.112 According to the

108

Cohn 2002: 99. Cohn 2002: 69. 110 Cohn 2002: 274–9, cf. 66–7. Cohn’s italics. 111 Cohn 2002: 66–7. 112 Actually, Cohn uses his Appendix I, “Miraculous Plague Cures,” to present material according to sources, while the two other appendices are supplementary sections of the bibliography. Appendix I demonstrates that Cohn is fully aware of the usefulness of appendices for presenting material evidence in tabular form. 109

342

chapter nine

basic methodological principles of scholarly or scientific work, no scholar has the right to demand to be believed on his/her word, (s)he has instead the right to try to persuade on the basis of the material evidence which (s)he presents and the quality of source-criticism and the general methodological framework of interpretation. Cohn’s point of departure is his assertion that of the 407 chronicles, calendars and necrologies, covering the period 1347–1450 which he has consulted, barely 16 per cent of them (68) identified the plague by pointing to cutaneous signs—the bubo, gavòcciolo, biscica piena di veneno, apostemata, macchie, rossorie, or even with just the adjectival phrase “pestis inguinaria.”113

Since cutaneous manifestations other than buboes are included (macchie and rossorie), the passage implies that even fewer works and a smaller percentage actually mention buboes, which could be taken to signify that this feature was not as important as usually assumed. This impression is strengthened by his subsequent remark that the sixtyeight chronicles which mention buboes include “double counting of chroniclers.” Cohn asserts also that thirty-five of these chronicles are Italian, that only three of forty-five English chroniclers refer to buboes “or other skin disorders,” and that only nine of 117 German chronicles, annals and calendars mention buboes, and so on. This may resemble some sort of fact-finding on the basis of sourcecriticism, but it is not. Central in this context is the question of what chroniclers should be expected to mention according to their medieval scholarly training, social status and cultural mindset. The inherent methodological point has been demonstrated above. It was shown that Cohn and other advocates of alternative theories commit the methodological fallacy called inference ex silentio when they infer from the fact that chroniclers do not mention dead rats in connection with plague epidemics that there were no rats around.114 In this case, Cohn unquestioningly presumes that chroniclers should be expected to mention buboes, and when only a small percentage does, he infers that buboes cannot have been an ordinary or usual part of the clinical panorama of the Black Death and subsequent plague epidemics. However, if epidemics, including severe epidemics, were not among the subjects 113 114

Cohn 2002: 99. See above: 85–91.

buboes as a normal clinical feature in epidemics

343

that chroniclers, according to their prestigious classical models, considered important to record, it is, on the contrary, to be expected that many chronicles would not mention the Black Death or subsequent epidemics. And if they do not mention the Black Death, why should they mention buboes? As now should be clear, Cohn’s unquestioning assumption that chroniclers should be expected to mention (severe) epidemics with concrete clinical detail involves again the fallacy of methodology of inference ex silentio and makes him dependent on luck not to be led into false conclusions. However, his luck fails him also in this case. It is known that the Roman Empire was swept by great waves of severe epidemics, especially at the time of Emperor Marcus Aurelius (161–80), Emperor Commodus (180–92), Emperors Valerianus (253– 60) and his son Gallienus (253–68) (with whom he co-ruled for some years), and again under Emperor Diocletianus (284–305). Arguably, all of these severe waves of epidemics could have been bubonic plague. However, very little is known about them. Roman chroniclers generally took little notice of epidemic disease, not only because epidemics were common but importantly in this context because epidemics were not considered an appropriate subject according to the humanistic ideals of writing in which they were trained. Extraordinarily severe epidemics could be briefly mentioned, but usually without any diagnostic or epidemiological information that would allow identification of the disease(s).115 These ideals associated with the writing of chronicles were those taught in medieval schools with great authority and admiration and moulded the intellectual framework within which educated medieval people functioned. However, from the end of the thirteenth century, these ideals were in the process of being weakened in Northern Italy within the framework of societal developments termed the Early Renaissance, a modernization of culture and mind or mentality that apparently was arrested by the onslaught of the Black Death and subsequent plague epidemics, but was resumed around the mid-fifteenth century. At the cultural level, this modernization was reflected in the increasing use of the vernacular instead of Latin by the educated classes, even in the case of such a high-brow, high-social-status work as Dante’s La Divina Commedia (1307–21). At the time of the Black Death Italian chroniclers usually

115

See for instance Gilliam 1961: 225–51; Russell 1958: 37; McNeill 1979: 112–3.

344

chapter nine

wrote, like the Villani brothers, in the vernacular and this was also the case with the novels written by the learned humanist Boccaccio, including his novel Il Decamerone, a frame story set in Florentine environments at the time of the Black Death. There were also corresponding pioneering developments of substance with respect to both literature and chronicles (Giovanni Villani’s chronicle is truly remarkable for its empirical orientation). These developments had hardly started in many other parts of Europe, and this is reflected both in the fact that most chronicles in those regions were still written in Latin and also in the fact that many chroniclers do not mention the Black Death at all. This is especially the case with German and Dutch chroniclers, which makes it difficult to produce even a general outline of the spread of the Black Death in these countries. In fact, in the case of the Low Countries the total lack of notices on the Black Death in chronicles and other narrative sources is conspicuous. Despite the fact that these areas were characterized by high standards of education and literacy for their time […] no source is produced with the objective of handing down information on this exceptionally grisly event to posterity.

This central source-critical and historical point regarding the subjects that chroniclers would like to include and which they would tend to leave out whatever their significance has been made by several historians.116 This topic demonstrates again the fallacy of methodology inherent in argumentum e silentio or inference from silence in the sources to assumptions that a phenomenon did not occur or exist. So far the discussion has focused on the conditions that would affect the chances of whether or not chroniclers would mention the Black Death at all. It is an obvious corollary that if chroniclers do not mention the Black Death nothing will be said about buboes, but it is also an obvious corollary that if the Black Death’s ravages of the cities or localities in which chroniclers lived tended to be a peripheral subject for them, it is rather unlikely that a terse statement to the effect that the Black Death ravaged the local population would be accompanied by descriptions of clinical details like buboes. This historical context explains why, according to Cohn, thirty-five, or slightly over half of the chronicles in which buboes are mentioned are Italian. Even if Cohn’s figures are reasonably correct, it must be emphasized that this 116

See my discussion in Benedictow 2004: 192–3 and fn. 9, 206–7, cf. 114–6.

buboes as a normal clinical feature in epidemics

345

does not at all signify that buboes were not a usual feature of the disease. At the heart of the matter is also an implicit comparative perspective with important methodological implications which Cohn ignores: if it was the case that chroniclers should be expected to comment on epidemics with clinical detail, this view must have an empirical basis documented by studies of contemporary chroniclers. Thus, Cohn is obliged to demonstrate that he has found such a material in a specified and testable manner. His readers are entitled to know the answers to the following two questions: (1) what other type(s) of epidemic disease(s) did chroniclers tend to mention and (2) for what other epidemic disease(s) did they provide clinical details? If these central questions cannot be answered positively with good empirical evidence, the view will stand corroborated that, under the historical circumstances, the Black Death is mentioned by surprisingly many chroniclers and with surprisingly frequent additions of clinical detail. Unfortunately, Cohn’s attitude to source-criticism is so deficient that problems abound, especially since he uses his data for direct or implied comparative statistical inferences. He neglects to ask a number of important critical questions and clarify their implications. (1) If the vast majority of chroniclers did not mention the Black Death and buboes, around 90 per cent of them as it seems according to Cohn’s figures, why does this not represent a serious problem of representativeness? The inherent source-critical implication indicates that the relatively small proportion of chroniclers who (against the odds) actually mentioned the Black Death and buboes did so because they were different persons socially, educationally, economically, culturally, and so on, and different personalities from the great majority of chroniclers who did not mention the Black Death and buboes. In order to make use of this material on chroniclers Cohn should have satisfied a number of methodological demands for clarification of the problem of representativeness, a problem that can be potentially resolved only by source-critical means, i.e. individualized study of these chroniclers. Since Cohn specifies the number of Italian chronicles that mention “cutaneous signs” but not the number of Italian chronicles he consulted, the same problem also looms large in this case. In short, he must relate the number of chroniclers who mentions a certain phenomenon to the total number of chroniclers, indirectly indicating also the number and proportion that does not mention it. Since Cohn purportedly sums up chronicles from all over Europe in order to produce

346

chapter nine

his quasi-statistics on the matter, he must also methodologically clarify on what grounds he can lump together Italian chroniclers with German or English or Polish or Dalmatian chroniclers, demonstrating that he satisfies the methodological condition that he lumps together only similar chronicles, and not similar and dissimilar or like and unlike. (2) How can Cohn attribute importance to the information given by chroniclers and other literary sources on clinical manifestations of plague when he does not ask the crucial question: What is the basis of this information, how was this information obtained? Is it based on observation? Is it based on statistically valid samples or numbers of cases? Is it based on physical examination of a statistically valid sample of the diseased? Or is it based on hearsay, rumours and flimsy impressions? Did the chroniclers who mention specific clinical detail really attempt to provide a realistic and medically satisfactory clinical description of plague disease as Cohn implies, or did they provide some graphic detail in order to impress their readers according to the rhetorical classical tradition in which they had been educated? Cohn relates that the chronicler Giovanni da Parma called the plague of 1371 an “illness of spots and glandular swellings” which seems trustworthy. However, when he goes on to state that that he had observed with his “own eyes” a peculiar difference between the effects of buboes that formed on the right as opposed to the left side of the body, “claiming that none survived with them on the right, whereas some, even if only a few, recovered with them on the left,” it becomes clear that his statements are not based on systematic observations of plague cases as he maintains, but on rumours or hearsay, and that the assertion that he has seen this with his own eyes is only classical rhetorical technique applied for the purpose of literary dramatization.117 Conspicuously, Giovanni da Parma freely makes clinical and medical assertions on the basis of purported personal observation which to modern scholars are obviously fictitious. This is not because he is a liar, but because, as demonstrated above, medieval man had a much weaker empirical orientation and much weaker requirements for repeating assertions of fact and because they liked to form their assertions and accounts according to prestigious classical Greek and Roman models.118 When even a chronicler who insists that he had seen clinical and medical facts with

117 118

Cohn 2002: 61. See above: 78–84.

buboes as a normal clinical feature in epidemics

347

his own eyes freely and unembarrassed presents fantasy data, why should any other chronicler be trusted and taken at his word? This illustrates the important point which also has been made above in other connections that chroniclers are not trustworthy even when they claim to have observed something with their own eyes. Chroniclers’ statements must be generally and unrelentingly tested by source-critical and empirical means in order to be usable and useful. Thus, when Cohn points out that a few chroniclers mention only buboes in the groin, “and no chronicler, not even the statistically minded Florentines, ever suggested that the vast majority of plague boils appeared there,” and that some chroniclers mention two locations of buboes, namely in the groin and axillas, and others mention three locations, including also the neck, and others do not mention any locations of buboes,119 why is this significant for any scholarly discussion of the microbiological nature of the Black Death? The assumption that the “vast majority” of buboes should have appeared in the groin, is as shown above not based on the mass of evidence gathered in connection with modern plague epidemics and provided in the standard medical works on plague, where it is indicated that around or more usually somewhat above half of the cases normally have inguinal-femoral location of bubo(es). Cohn’s comparatively based assertion on this point is therefore a misleading piece of quasi-statistics. It is also a misleading piece of quasi-statistics because Cohn does not address the question of the circumstances to which these statements refer. Were they based on personal clinical inspection of plague cases? If they were, were they based on a statistically tenable sample? Were they affected by the sexual connotations of the groin and mostly based on what could be observed in sexually less sensitive parts of the body? Were they based on hearsay? And so on. Also the spectre of a fallacy of distribution looms large over Cohn’s argument. The assertion that the Florentines were generally “statistically minded” is not supported by any evidence and is as such arbitrary. Certainly this was the case with Giovanni Villani, but he died in the Black Death and did not provide posterity with a word on the disaster in Florence. Real statistical orientation can only be said to be weakly discernable in a couple of other Florentine chroniclers, for instance Giovanni di Pagnolo Morelli. Crucially, Cohn maintains without any

119

Cohn 2002: 65–6.

348

chapter nine

justification that Florentine chroniclers should have been expected to provide empirically based scientifically tenable statistics on the location of buboes when he is completely unable to document that contemporary Florentines implemented a systematic medical examination of a valid sample of plague cases in order to determine (inter alia?) the distribution and localization of buboes. Instead, the only significant information that can be obtained from chroniclers is that contemporaries noted according to various pieces of hearsay or incidental observation that the single most conspicuous clinical feature of the disease was buboes and that these buboes strongly tended to be localized in the same parts of the body as buboes of bubonic plague. Does Cohn possess the scholarly qualifications necessary to evaluate evidence statistally and to make demographic analyses? Cohn maintains that “at least four chroniclers saw the first plague killing more women than men”120 and assumes throughout his monograph that this is tenable information. Next, he goes on to claim that for “the next plague, however, several chroniclers saw the sex bias swing in the opposite direction.” But what about all the other chroniclers, in both cases the vast majority of them, who did not make such comments, do they not count? Why? The assertions that the Black Death killed more women than men or the other way around are demographic and statistical in nature. How did these chroniclers observe or obtain tenable demographic information of a statistical nature? How were their materials gathered or constituted? Were the chroniclers’ statements based on anything of real substance, does they constitute real demographic data? Were these materials representative and valid samples suitable for forming statistical valid statements about reality? Or was it all just flimsy impressions or hearsay affected by prejudice, preconceived assumptions and superstition and without evidentiary or scholarly value? If the scientific validity and tenability and representativeness of their materials and the premises on which their assertions or statements are made cannot be ascertained, how can it be possible to use these opinions for a demographic purpose? Is it not in fact possible to find four chroniclers who hold much the same opinion about any contemporary matter, even the most outrageous and fantastic nonsense? According to the tenets of historical demography, Cohn’s approach is invalid and his estimates on these matters are quasi-statistics. Maybe

120

Cohn 2002: 129.

buboes as a normal clinical feature in epidemics

349

painstaking hard work on the individual chronicles with intensive application of source-criticism might provide tenable material, but this work has not been performed by Cohn. He has no real material basis for his assertions and his demographic qualifications may be called into question. It seems that Cohn’s ambition to present a revolutionary theory of the nature of historical plague forced him into variance with the tenets of the methodology of historical and social science. All of Cohn’s premises and arguments are arbitrarily chosen and are presented in a way so as to produce the resemblances of statistical evidence. As mentioned above, in English historiography the term “bastard feudalism” is used to mean what resembles feudalism but is not, for instance, enlistment in royal armies of gentlemen warriors for longer periods of service than the forty days associated with feudal obligations. In this sense, Cohn’s various estimates are bastard statistics: they resemble statistics but are not. And this is only the beginning of bastard statistics in this context. Attempting to pave the ground for more seemingly supporting quasi-statistics, Cohn goes on to argue that the plague tracts of contemporary physicians are more useful than the chronicles, because (footnote in brackets) (1) these fourteenth- and early fifteenth-century plague tracts turned on practical experience of treating plague patients. [fn. 77] [.…] (2) Doctors, by contrast [to chroniclers: my insertion], because of their attempts to cure the plague by addressing its surface manifestations, focused consistently on these cutaneous signs.121

Cohn indicates the relevant period for his material by the formulation “fourteenth- and early fifteenth-century,” which I will take to mean the early plague period 1347–c. 1410 or about the first sixty-five years of it. Cohn provides a supporting footnote only for the first of these crucial but also surprising two assertions, so the second assertion may immediately be judged arbitrary. In support of the first assertion, he refers in the accompanying footnote 77 to a single brief paper and states: “For this impression, see Andreina Zitelli and Richard J. Palmer, ‘Le teorie mediche sulla peste e il contesto veneziano’ [= The Medical Theory of Plague and the Venetian Context], Venezia e la peste 1348–1797 (Venice, 1979), pp. 21–8, esp. 24.” Recognizing uneasily that this reference could appear suspiciously tiny and unimpressive for the evidentiary demands 121

Cohn 2002: 68.

350

chapter nine

put on it and that some of his readers might be puzzled and ask why he does not refer to the central standard works on Italian medical history, he adds: “For these doctors’ emphasis on practical experience, see chapter 9.”122 This means that these two references must be commented on. Anyone familiar with Italian and contemporary medical history will immediately recognize that this tiny paper by the outstanding scholars Zitelli and Palmer, a 6.5-page summary of medical history 1348–1631, i.e. almost three centuries, contains nothing that would faintly corroborate Cohn’s assertion. On pages 21–4 the two scholars summarily but excellently present the miasmatic theory of epidemic disease in which physicians of the time generally believed and which they generally used to explain epidemic disease, and specifically plague, from the advent of the Black Death to the end of the fifteenth century. The key words, opening a new theme on page 24, are “A partire dal tardo secolo xv” = “From the end of the fifteenth century,” there were some new developments inspired by the “humanistic intention of returning to the pure sources of classical knowledge,”123 reflecting the development of the culture and mentality of the Renaissance. In this context, two important late medieval physicians are mentioned, first Marsilio Ficino whose plague tract Consilio contra la pestilenzia from c. 1480124 reflected the “spirit of the Renaissance” and contains a discernable increased element of empirical observation,125 and Alessandro Benedetti who published a plague tract in 1493 titled De observatione in pestilentia. However, these pioneering physicians represented only the start of a long-term slowly developing trend towards more empirical observation of epidemic disease throughout the Renaissance and the Early Modern Period. According to Zitelli and Palmer, Benedetti asserted that plague was introduced through the skin, since persons diseased with scab were immune, a view which is certainly not based on empirical observation. The remaining 2.5 pages of their paper relate to this long line of development through the sixteenth century with a clear emphasis on the second half of the century and the decades up to the city’s last plague epidemic of 1630–1. It has long been recognized that

122

Cohn 2002: 68, fn. 77. My translation from Italian. 124 According to Zitelli and Palmer it was written 1478; according to the editor of this plague tract, it was written c. 1480, see Ficino 1983: 6. 125 Cf. above: 209, 343. 123

buboes as a normal clinical feature in epidemics

351

the Renaissance from the end of the fifteenth century brought an increasing tendency towards empirical orientation based on real observation, as has been repeatedly stated also in this monograph, but this is not the issue here. Instead, it is Cohn’s assertion that Zitelli’s and Palmer’s paper supports his view that physicians contemporary with the Black Death and subsequent plague epidemics examined their patients physically in order to cure them: this assertion has now been shown not to be correct, which means that the assertion is unfounded and spurious. In Chapter 9, Cohn is not able to present empirical support for his two assertions. He maintains that Perhaps the most incisive and detailed of such attempts to understand the rise of plague in human terms was that of the Gatari chroniclers of Padua for the plague of 1405. Their reasoning is closer to the nineteenthcentury understanding of crowd diseases than it is to the Black Death mindset of floods of frogs.126

It is interesting to note the way Cohn now disparages the medieval mindset—the very mindset of the chroniclers and physicians whom he held in such high esteem when the subject was buboes 175 pages earlier (see above). However, Cohn’s subsequent lengthy citation of the text does not confirm his view as to the increased empirical orientation and scientific epidemiological understanding of epidemic disease. The Gatari chroniclers underline the importance of the overcrowding in Padua caused by the on-going war which made the peasantry of the surrounding rural districts flee into the city with their domestic animals. This caused extreme overcrowding and unhygienic conditions, and meant that many of the domestic animals died and began decomposing: Manure and mud beyond measure filled the city outside as well as within houses, and the stench was so great that it putrefied the air, corrupting the entire city. And there was a dearth of basic necessities beyond measure, […]. And these conditions combined with other forces of darkness sparked a ferocious plague in the city of Padua with little nuts forming on some around the throat, on others, on the arms, and on some, on the thighs, along with an intolerable and burning fever with discharges of blood. With this illness the victims lived two or three days at the most and died.127

126 127

Cohn 2002: 230. Cohn 2002: 230.

352

chapter nine

Clearly, the Gatari chroniclers interpret events according to the ordinary miasmatic theory of plague and are in this respect representative of chroniclers and physicians of the late medieval period up to the end of the fifteenth century. Their description of buboes and plague disease is quite inaccurate and does not reveal any personally acquired clinical knowledge, as was the case with some other chroniclers who commented on the Black Death and the following plague epidemics for almost 150 years. Parts of this clinical description of bubonic plague cases are compatible with inaccurate, flimsy or casual observation of diseased reaching the writers’ ears in the form of rumours or hearsay. Next, Cohn mentions Marsilio Ficino’s plague tract,128 written around 1480, which for temporal reasons has no relevance for his two assertions that are under discussion here. Chapter 9 is the last chapter of Cohn’s monograph and is oriented towards concluding and synthetic inferences; it is therefore permitted to wonder why new material that relates to earlier chapters and discussions is introduced there. It is a conspicuous feature of Cohn’s discussion of this topic that he gives the impression that the history of Italian medicine has not been written. Actually, there are several fine monographs on this subject. We must particularly emphasize G. Cosmacini’s fine history of medicine and hygiene in Italy from the Black Death to 1918 which appeared in 1987.129 I. Naso has published a fine monograph on physicians and sanitary structures in late medieval society in the Piedmont. Cohn refers to two papers by A. Castiglioni (1874–1953), the leading Italian medical historian of the first half of the twentieth century, but he has avoided Castiglioni’s highly admired history of Italian medicine of 1927, so excellent that it was published in French in 1931 and in English in 1941 and reprinted as late as 1975. Thus, Cohn consistently avoids the fine standard works on Italian medical history which summarize the endeavours of generations of Italian scholars in the field. The reason, perhaps, is that they are incompatible with his assertions on this subject and provide collectively a broad and solid basis for rejecting them. This puts in perspective another of the misleading accusations that Cohn levels against Cipolla: 128 129

Cohn 2002: 231. I was lucky and acquired a copy of the sixth edition in Milan in 1994.

buboes as a normal clinical feature in epidemics

353

Others such as Carlo Cipolla in glancing at them [the plague tracts] have judged that it was not until the seventeenth century that doctors would tear themselves free from the “scientia” of ancient authorities.130

In fact, Cipolla, the Grand Old Man of Italian historical plague research, did not take this subject lightly with a quick glance at these sources; it was consistently a central topic in his numerous books. Let me mention Cristofano and the Plague. A Study in the History of Public Health in the Age of Galileo (1973), Public Health and the Medical Profession in the Renaissance (1976a), Faith, Reason, and the Plague in Seventeenth-Century Tuscany (1979), Fighting the Plague in SeventeenthCentury Italy (1981), Contro un nemico invisibile. Epidemie e strutture sanitarie nell’Italia del Rinascimento (= Against an Invisible Enemy. Epidemics and Sanitary Structures in Renaissance Italy) (1986), and finally Miasmas and Disease. Public Health and the Environment in the Pre-industrial Age (1992) containing chapters titled “The Health Boards in Italy and Epidemiological Concepts” (pp. 1–9), “Medical Reports and the Florentine Health Magistrates” (pp. 27–65), and “Doctors, Diseases and the People” (pp. 66–73). Cipolla has formed his opinions on the matter on a truly extraordinary broad basis of his own research and also on other available research and the standard works of Italian medical history. It will easily be seen that Cipolla’s studies of these subjects are in accordance with those of the standard Italian works on medical history which Cohn has avoided. It is Cohn’s view that deviates sharply from the established scholarly knowledge on the subject. His disparaging comments on the works of Cipolla and other fine historians all the way through his monograph131 should be seen with this background. Elsewhere in his monograph, when Cohn focuses on other subjects, material contrary to his theory with clear power of falsification slips through. We are informed, for example, that The famous doctor Giovanni da Santa Sofia, professor of medicine at the University of Padua, advised that a plaster of pig fat be applied to the larger plague boils but a plaster made from pigeon dung (de stercore columbino) be put on the smaller anthrax and carbuncles because of their more “vehement heat.”132

130 131 132

Cohn 2002: 234. See above: 54–69, in the case of Cipolla, see 60–1, 211, 226, 293–4, 352–3. Cohn 2002: 62.

354

chapter nine

Obviously, Giovanni da Santa Sofia (†1389), who was a professor of medicine at the University of Padua, freely makes medical assertions which are flatly untrue and simply fictitious, not because he is a fraud, but because, as demonstrated above, medieval man had a much weaker empirical orientation and much weaker requirements for repeating assertions on reality or fact.133 Although Professor Giovanni da Santa Sofia was a prestigious medical figure of his time, here is not a trace of the empirical orientation which Cohn attributes to physicians of that period. Since Cohn’s assertion with respect to the increased empirical orientation of contemporary physicians of the second half of the fourteenth century and early fifteenth century has now been analyzed and shown to be untenable, the original discussion of the contemporary material on buboes can again be addressed. It now appears reasonable to assume that Cohn’s two assertions to the effect that physicians’ plague tracts show significant or substantial empirical orientation in the aftermath of the Black Death were formulated to serve as the basis of more bastard statistics on buboes. The following citation illustrates this point (I place Cohn’s footnote in brackets): The positions of the buboes pinpointed in these texts [physicians’ plague tracts] are at variance with those give by the chroniclers. Only one plague tract, and that one not by a doctor but by a German schoolteacher, located the plague boils in a single bodily spot. Furthermore, it was in the armpit, as opposed to the most usual place with modern plague, the groin.[fn. 80134] Even more curious, the pairing of boils in the groin and under the armpits, which the chronicles to some extent and modern historians more often have seen as the late-medieval plague’s unmistakable signs, is almost wholly missing from the tracts.135

This citation should be seen in the source-critical light of Cohn’s admission three pages later that “the plague texts rarely described individual patients with the exact locations of their boil or boils” and that they are “generally prescriptive rather than descriptive.”136 In the cited text, Cohn sees his case served by not addressing the question of whether the purported high incidence of more than one bubo reflects the fact that physicians “rarely” described individual cases but “generally” made

133

See above: M50–4. “Konrad von Megenberg, ‘Tractatus de mortalitate in Alamannina [sic],’ in Sabina Krüger, ‘Krise der Zeit als Ursache der Pest?,’ p. 865.” 135 Cohn 2002: 68. 136 Cohn 2002: 71. 134

buboes as a normal clinical feature in epidemics

355

prescriptive or generalizing comments on the locations of buboes, which would strongly tend to imply plurality. In the final sentence, Cohn asserts that some chroniclers and modern historians, in contrast to contemporary physicians, quite often have seen the pairing of buboes in the groin area or under the armpits as “the late medieval plague’s unmistakeable signs.” But this assertion is unaccompanied by a supporting footnote, which means that it is arbitrary and fictitious. One would have liked to know which chroniclers and which modern historians held or hold this view. Until tenable facts are presented in support, these are all bastard statistics. As can be seen from Cohn’s footnote, the only contemporary scholar identified by name in support of this citation in Cohn’s footnote 80 is Konrad von Megenberg who was not a physician but a natural scientist, best known for his Book of Nature. Surprisingly, Cohn calls him a schoolteacher, although he earned a Master degree at the University of Paris, lectured at the university for a number of years and died as a canon of the Cathedral of Regensburg. According to the principles of the methodology of social science, the works of just one natural scientist cannot provide empirically tenable insights or knowledge about the scholarly attitudes of contemporary physicians. The works of a natural scientist, including just one book, could function as a basis for establishing a working hypothesis about the attitudes or works of contemporary physicians, which, according to the methodological principles of scholarly work, should lead to an active search among physicians’ medical writings for confirmation. Konrad von Megenberg did produce two small plague-related works: in 1349 he wrote Causa terre motus on the association between earthquakes, which let out miasmatic poisonous gases from the ground, and plague epidemics, which, according to his profound religious views, had God’s anger over men’s sinfulness as their final cause, the causa remota. It does not contain traces of empirical attitudes or approaches but represents a combination of intense personal religiousness with speculative scholastic reasoning which was so typical of scholars at the time. Later he wrote Tractatus de mortalitate in Alemannia (= Tract on mortality in Germany). Cohn cites a paper by S. Krüger for support of his claims about Megenberg’s medical and epidemiological views. However, Krüger clearly argues that Megenberg’s views were exactly the opposite of those Cohn ascribes to him: she shows how Megenberg attempts to align the notions of God’s wrath as the cause of severe epidemic disease and the Black Death with miasmatic theory, arguing that God used earthquakes to let out miasmatic poisonous gases from the

356

chapter nine

ground into the human sphere. Krüger describes Megenberg’s views as based on “simple, tradition-based, tradition-burdened/traditionloaded piety” which understood “the plague as God’s punishment.”137 Thus, Megenberg does not discuss plague in an empirically oriented way, but as a pious scholastic. The idea that persons diseased from plague should be physically examined is entirely alien to him, and there is no indication that he ever did so, or that he ever thought that a statistically valid sample should be studied in a scientifically valid way. This is, consequently, also a fictitious reference. In short, the cited text consists of bastard statistics. Cohn goes on to mention that physicians in their plague tracts linked the locations of buboes to “Galen’s three emunctoria” and that this was the reason that buboes formed on the thighs or in the groin, in the axillas or on the neck (I indicate Cohn’s footnote in brackets): Except for the two tracts mentioned above, every other one that pointed to plague boils (at least 55 tracts) said they formed in these three zones. [fn. 84] According to the position of the boils, the doctors would then advise where to place their plasters and of what materials they should be composed, and more often, which veins were to be tapped for bloodletting.138

The supporting footnote 84 contains references to forty-three plague tracts in Appendix III enumerated according to Sudhoff ’s enumeration in his edition in Archiv für Geschichte der Medizin;139 in addition there are references to three other works by named physicians. Thus, Cohn provides forty-six references, not (at least) fifty-five, as should be expected. Of the forty-three enumerated plague tracts, two refer to the same work, namely nos. 27 and 28, which reduces the number of tracts to forty-two. Of these forty-two plague tracts, two refer to numbers not entered in Appendix III, which are therefore irrelevant;140 eight are, according to the temporal information given by Cohn in the Appendix, later than the early fifteenth century141 and are therefore also irrelevant

137 Krüger 1972: 839–83. My translation from German: “Seine einfache, traditionsgebundene, traditionsbeladene Frömmigkeit deutet diese Entwicklung als schuldhaftes Verhalten der Menschen, die Pest als Strafe Gottes.” In an appendix to this paper Krüger publishes the full text of Tractatus de mortalitate in Alemannia, Krüger 1972: 862–3. 138 Cohn 2002: 69. 139 Vols. 4–9, 11, 14, 16, 1910–25. 140 Nos. 99, 111. 141 Nos. 26, 58, 75, 182, 192, 193, 265, 285.

buboes as a normal clinical feature in epidemics

357

as support for the assertion under discussion; eleven are not dated142 and their relevance is therefore uncertain and as such they are not usable. Thus, over half of these references are invalid. Cohn also refers, as mentioned, to three other works by physicians: Marsilio Ficino’s plague tract of 1480, Antonio Guaineri’s rare Practica (Antonii Guainerii) from 1517,143 which is not a plague tract but a more general medical work; and a work written in 1382 by Chalin de Vinario who worked as a physician at the papal court in Avignon.144 Thus, two of these three works are anachronistic in relation to the topic under discussion and must be grouped with the other eight works outside the temporal parameter of the issue. Taken together, ten of Cohn’s references contain nothing on physicians’ empirical practices and cures in the second half of the fourteenth century or early fifteenth century, and thirteen other references are invalid, so in all twenty-three out of forty-five, or over half, are irrelevant or invalid. This means that only twenty-two methodologically valid references remain which shall cover for at least fifty-five plague tracts; this is obviously fallacious and must be rejected. Materially, Cohn’s readers are left to eat out of his hand, since the evidentiary material is not gathered and presented for ready testability (for instance in an appendix) as is the scholarly norm. This material is for several obvious reasons flawed and unusable as the basis for valid and tenable statistics. However, it is not difficult to give Cohn a helping hand by providing the necessary additional information from Sudhoff ’s edition of late medieval plague tracts: the two tracts with numbers not entered in his Appendix, nos. 99 and 111, are temporally acceptable since they appear to have originated at the beginning of the fifteenth century, and among the eleven tracts without dating nos. 19, 27, 50, 61, 97,113 are temporally acceptable, while nos. 9, 49, 116, 117, 184 must be rejected as anachronistic. This means that of the forty-five references145 thirty are formally relevant and fifteen are irrelevant and misleading. Methodologically, it is a very serious matter that thirty references

142

Nos. 9, 19, 27, 28, 49, 61, 97, 113, 116, 117, 184. Practica Antonii Guainerii Papiensis doctoris clarissimi et omnia opera. (Impressum Venetijs: mandato and expensis nobilis viri Luceantonij de Giunta, 1517. die 13 mensis Julij). As can be seen, it was published in Venice, not in Florence as Cohn claims. 144 Hoeniger 1882: 171. 145 42 plague tracts + 3 other works by the physicians Ficino, Guaineri, and de Vinario = 45. 143

358

chapter nine

should cover for at least fifty-five plague tracts that Cohn claims constitute his evidential basis, and that fifteen plague tracts which are introduced and mixed up among them are irrelevant and distort his remaining relevant material. Inevitably, this undermines the validity of his discussion or rather leaves it invalid for formal methodological and material reasons. I have read through the thirty relevant plague tracts; many of them are quite brief. They do not provide any support for Cohn’s assertions as to the clear empirical orientation of post-Black-Death physicians, on the contrary, the established view in the history of medicine on this matter stands vindicated. Cohn appears unwilling to recognize that the condition for making valid and tenable assertions on this matter is to present sufficient evidence from the plague tracts which can, taken together, demonstrate that physicians at the time (c. 1347–1410) actually examined their patients bodies reasonably thoroughly and noted down their findings in a sufficiently systematic way in order to be usable for producing (valid and) tenable statistics on clinical manifestations. On the contrary, physicians’ tracts provide hardly any evidence of such empirical attitudes. This explains or accords with Cohn’s later admission that “the plague texts rarely described individual patients with the exact locations of their boil or boils” and that they are “generally prescriptive rather than descriptive.”146 On the contrary, the little evidence there is on such matters from this period (c. 1347–1410) points rather in the opposite direction, as do much later plague tracts. A plague tract written shortly before 1450 advises physicians who visit plague patients to stay at a good distance from patients and turn their faces towards the [open] door or the window, an attitude that would of course exclude real physical examination of patients for identification of clinical features, but makes good sense according to miasmatic reasoning. The author also states that indications of a patient’s chance of survival can be obtained by dripping breast milk in one’s own hair.147 This accords with Cohn’s citation of a chronicler elsewhere in his monograph to the effect that “no one dared use or even touch the clothes of the plague-stricken” and his statement that “Chroniclers of later plagues continued to see touching the infected and their belongings as a sure means of catching the

146 147

Cohn 2002: 71. Archiv für Geschichte der Medizin, 11, no. 117: 132, 135.

buboes as a normal clinical feature in epidemics

359

plague.”148 This material makes it hard to understand how anyone would dare to physically examine plague patients. For the same reason Carmichael, a leading scholar on the medical plague history of the period (although not according to Cohn’s disparaging remarks149), concludes: “This kind of medical commentary, characteristic of latemedieval plague treatises, was formulated with good Galenic universalism. It is difficult to deduce physicians’ first-hand experience from the information included.”150 This confirms that Cohn’s various statistics are misleading bastard statistics without evidentiary power, but not without power for misleading readers. In my opinion, the preceding citation from Cohn’s text on the great influence of the Galenic concept of “emunctoria” as a contemporary medical explanation of the location of buboes can be read very differently from Cohn’s intentions. Cohn admits that, with only a couple of exceptions, late medieval physicians state that in plague epidemics buboes formed in these three areas of the human body, in the inguinalfemoral area, in the axillas and on the neck.151 These are the same main areas for the formation of plague buboes registered by modern physicians.152 Thus, if the quasi-statistics and unrealistic claims for empirical orientation at the time are dispensed with, contemporary evidence provides in a general fashion support for the identity of historical and modern plague. Cohn and Boccaccio: Buboes, Pustules and Spots Although chroniclers’ and physicians’ various writings seemingly constitute the central evidence for Cohn’s argument on buboes and some other clinical manifestations, he places great emphasis on the evidentiary value of Boccaccio’s account of the Black Death in Florence in the introduction to his amorous novel and frame story Il Decamerone, written c. 1350.153 In order to claim that Boccaccio’s literary account 148

Cohn 2002: 113. Above: 54–5, 84. 150 Carmichael 1998: 158. See below. 151 Cohn 2002: 69. The use of the term “late medieval” reflects the fact that most of these plague tracts are from the fifteenth century. 152 See also above: 314–9. 153 According to the editor C.S. Singleton, nothing more precise can be said about the date this work was written than that “a few years have elapsed” since the Black Death. Boccaccio 1982–3: 804–5. 149

360

chapter nine

has this value he must dispense with source-criticism (as he also does with other types of sources): “Boccaccio’s description cannot be simply dismissed as poetic license to heighten the plague’s horror,”154 he states. This urging can be accepted, but The Decameron is, indisputably, a literary work, and thus the central source-critical point remains and gives Cohn a task, namely to identify the author’s literary intentions and to separate the literary functions of dramatization from the realityoriented parts. Instead, Cohn invites his readers to swallow Boccaccio’s text hook, line and sinker (see below). This point relating to the functions of literary technique and poet’s license which Cohn should have addressed can be put more concretely. Clearly, some of the frequently cited contemporary accounts and descriptions of the Black Death were quite likely not written by persons who lived through the epidemic.155 Much like the young persons in Boccaccio’s frame story these authors seem to have fled from its ravages and returned after it had subsided; according to Matteo Villani, this was quite a usual strategy employed by Florentines, at least by those who had the means or opportunity to do so.156 There are, in fact, clear indications in Boccaccio’s text that this was also the case with him. Boccaccio’s use of the narrator’s I-form, which provides the impression of personal experience and observation and hence increases the credibility of what is being told, is a usual literary technique for dramatization. Boccaccio employs it not only in the introduction but also in connection with the constituent stories, particularly in their openings. He insists, for instance, that the disease spread as easily from plague cases to animals as to other human beings, and with the same deadly effects. This claim is highly suspect to put it mildly; what disease could that be? A marvellous thing to hear is that which I have to tell and one which, had it not been seen by many men’s eyes and by my own, I should scarcely have dared credit, much less set down in writing, even though I had heard it from one worthy of belief, I say, then, that of such virulence was the pestilence […] a thing which had pertained to a man sick or dead of the aforesaid sickness, being touched by an animal foreign to the human species, not only infected this latter with the malady, but in a very brief space of time killed it. Of this my own eyes […].157

154 155 156 157

Cohn 2002: 59. This seems to be the case, for instance, with Michael of Piazza (see below). Villani 1979: 297–8. Boccaccio 1982–1: 9–10.

buboes as a normal clinical feature in epidemics

361

Boccaccio’s ample use of the narrative I-form his references to personal observations are conspicuous in the introduction to this incredible story, but he also records some information from hearsay. Is not deep scepticism of Boccaccio’s assertion that he has seen this with his own eyes the correct scholarly attitude? Fortunately, Boccaccio dramatizes this point by going on to give a concrete example, the account of the two hogs which rooted with their snouts in rags of clothes that had belonged to a pauper dead from plague, and almost immediately “fell down dead upon the rags.”158 There is no disease presenting with buboes in human beings, as described by Boccaccio, which is hyper-dangerous to pigs; pigs are refractory both to plague and tularaemia. Such a disease is unknown both to medical and veterinary sciences, Boccaccio’s anecdote must be rejected as empirical evidence. The overwhelming probability is that he relates in I-form an anecdote which in fact is based on hearsay; as such it becomes evidence not of reality but of his literary technique and medieval humanist mindset. On the other hand, this anecdote is compatible with the miasmatic theory of contagious disease which for quite some time now has been out of fashion for extremely good reasons, but was fashionable in Boccaccio’s time. There are overwhelming reasons for considering this an anecdotal story made up or repeated by Boccaccio and related in the I-form in order to dramatize the introduction to his novel. It serves a literary purpose and would be perfectly acceptable to his audience according to their miasmatic epidemiological notions, but it should not be acceptable to modern scholars. Boccaccio’s account of the Black Death in Florence is compatible with conveyance of second-hand information or hearsay on the disease and is moulded to serve his (legitimate) literary purpose of dramatization. Boccaccio must be understood on his own terms. He was a humanist writer of his time and a pioneer of this form of the art of literary entertainment, not a modern scientist, and he had no intention of including a study of the Black Death with medical information of scholarly value for posterity. For these reasons, it is clearly fallacious when Cohn fails to fulfi l the scholarly imperative for adequate source-criticism and neglects to consider elementary critical questions with regard to Boccaccio’s account: Did Boccaccio recognize the importance of empirical observation?

158

Boccaccio 1982–1: 10.

362

chapter nine

Did he have the methodological knowledge or understanding to carry out observations of plague cases according to scholarly principles? Did Boccaccio base his clinical description of plague cases on observation? How can we know that he has seen plague cases at all and did not practise the strategy of his novel’s characters, i.e. that he did not flee the city and avoid the plague by strict isolation from the surrounding world? If he has seen plague patients, did he perform a physical examination? Did he perform physical examinations of a valid sample of patients? If this can be shown to be the case, what was his frame of medical reference for understanding what he observed? If he did not base his description on personal observation, did he base it on observations made by others? If that was the case, who were those others and how did they perform and pass on their observations? As Cohn does not ask these basic source-critical questions, he does not know that Boccaccio’s description is not based on rumours, hearsay and a poet’s license for producing literary effects. In short, it is Cohn’s scholarly task to prove that Boccaccio’s clinical description represents valid source material for modern historians. If he should succeed in making this point, it would be his task to clarify at what level of tenability it would be usable and to identify and specify which parts are usable as evidence. Only such identified valid and tenable parts of the text will be usable for empirical comparison with modern medical materials on the clinical manifestations of bubonic plague obtained by scientific means. However, Cohn does not ask a single one of these elementary and indispensable source-critical questions, which means that his use of this account as hard evidence on the clinical panorama of plague disease is fallacious for two independent reasons. Firstly, it is fallacious to accept as hard evidence historical sources which have not been source-critically scrutinized and had their potential evidentiary value ascertained. Secondly, it is fallacious to use it for comparison with modern medical clinical descriptions because he cannot demonstrate or ascertain that the two sides of the comparison have similar scientific and scholarly status, and are thus in pari materia, in other words are comparable and as such valid and usable for the comparative methodology of analysis. Since chroniclers and physicians cannot be seen to have significant or pronounced empirical orientation on the matter, and certainly were too scared of being miasmatically contaminated by contact with the diseased or their belongings, or even by look, to examine patients, why on earth should Boccaccio, a literary artist, examine patients? In fact,

buboes as a normal clinical feature in epidemics

363

Boccaccio asserts demonstratively for every scholarly supporter of source-criticism to see that this pestilence was the more virulent in that, by communication with those who were sick thereof, it got hold upon the sound […] for not only did converse and consortion with the sick give to the sound infection or cause of common death, but the mere touching of the clothes or of whatsoever other thing had been touched or used by the sick appeared of itself to communicate the malady to the toucher […].

Obviously, Cohn should have underlined this evidence and asked the crucial question of how Boccaccio, holding these beliefs about the dangers of talking with or touching persons diseased or dead from plague, would have dared to approach such persons, to converse and consort with them, and to touch their clothing and examine them physically. Clearly, to take Boccaccio on his word is methodologically flawed and fallacious but to dismiss his text, in the meaning of ignoring essential pathways to the understanding of it, can cause neglect of valuable knowledge and also be reprehensible. It is the challenge of source-critical scholars to sail their ships safely through the strait between (the whirlpool of) Charybdis and the (sea-monster) Scylla and like Odysseus put wax in the ears to avoid the Sirens’ lovely but dangerous song of the revolutionary new theory. This does not mean that Boccaccio’s informants could not have picked up factual clinical elements and that his account cannot contain valuable or tenable information, only that source-criticism will have to be applied in quantum satis. Boccaccio states that In men and women alike there appeared, at the beginning of the malady, certain swellings, either on the groin or under the armpits, whereof some waxed to the bigness of a common apple, others to the size of an egg, some more and some less, and these the vulgar [ordinary people] named plague-boils [gavocciolo].159

These pieces of clinical information are mostly credible and acceptable: the early appearance of buboes corresponds to many other descriptions of the initial phase of bubonic plague, and the locations are those usual in bubonic plague, although the neck is left out. These basic elements are compatible with the disease being bubonic plague. Buboes as large as apples or even bigger, if they existed, must be quite or even 159 Boccaccio 1982–1: 8–9. As for the vernacular term “gavòcciolo,” see also Sticker 1908: 84.

364

chapter nine

very rare in bubonic plague, but this is legitimately explicable as literary exaggeration and also as a reflection of the sensational augmenting tendencies of information transmitted by hearsay. This prepares the ground for taking a closer look at Cohn’s concluding assertions on the matter of buboes and other clinical manifestations: Boccaccio recorded buboes and then their spread along with black pustules over the entire body. Nor was his description unique, or the Black Death’s first appearance a radical departure from the “normal” signs of the disease once it became established. Other contemporary texts— chronicles, plague tracts, saints’ lives, and poetry—attest to the persistence of these pustules’ spread […]. Further, the medieval plague boil was neither singular, as in 94 per cent of the cases with modern plague, nor located predominantly in the groin as happens with the flea-conveyed modern plague. Instead, they often formed under the breasts, on the shin, the face and even up the nose—places not mentioned in the 3000plus cases reported from hospitals around Bombay City during the plague years 1896–7. Mostly, these late-medieval sores formed higher up the body than those that characterise modern bubonic plague, in the cervical region, higher than a flea can possibly jump. To keep the paradigm, should we hypothesise that medieval men and women were more supine than modern Indians or Glaswegians?160 The cutaneous signs of the two [late-medieval and modern plague] hardly match in their positions on the body, number, or character. The Bombay plague report at the end of the nineteenth century showed that in 94 per cent of cases, the victims had only a single boil, that 57 per cent of them were in the groin and in not a single case of over 3000 clinical studies did the boils spread from the lymph nodes, bursting into tiny black, green, and red pustules across the body. By contrast, for the medieval plague two-thirds of the cases showed multiple boils; the neck, not the groin was the boils’ pride of place, and one chronicler after another from Wales to Novgorod, Sicily to Uzbekistan described the invasion of small pustules preceding, accompanying, or following the formation of boils. In place of Yersinia pestis I offer no alternatives […].161

Cohn has not furnished these numerous assertions with supporting footnotes that would allow evidential testing, which means they are arbitrary according to the basic tenets of methodology. The only

160 161

Cohn 2002: 81. Cohn 2002: 247.

buboes as a normal clinical feature in epidemics

365

references are those given in the text to Boccacccio and to “The Bombay plague report at the end of the nineteenth century,” a surprising reference to the report on plague in Mumbai of 1896–7, only one of several reports on plague written at the end of the nineteenth century, a fact that will be considered more closely below.162 The juxtaposition of these two sets of information in a formal comparison of important clinical manifestations of late medieval and modern plague is clearly fallacious. The late medieval side of the comparison consists of pre-scientific types of information which in not a single case can be shown to be based on physical examination of a valid sample of plague cases and must therefore be assumed to have an impressionistic and unsystematic character, constituting on the whole quasi-empirical material. This quasi-empirical material cannot be compared with a scientifically valid sample of scientifically studied modern plague cases for the purpose of demonstrating valid differences between the two clinical panoramas. These two materials can only be legitimately juxtaposed for comparative purposes in order to reveal the unscientific aspects of medieval accounts or presentations of the matter. For the same reason, the other juxtapositions of materials on the distribution of buboes on the body are further instances of quasistatistics. Importantly, one should note that Cohn has not presented the evidence for his statistical assertions as to the location of buboes according to late medieval sources; his statistics have no empirical basis, they are taken out thin air, which means that they are invalid and untenable. His citation of Boccaccio does not corroborate or support his assertion with respect to the distribution of buboes on the body. If it was really the case that late medieval buboes formed more often on the upper part of the body than in modern bubonic plague, why does Boccaccio not mention buboes on the neck? At variance with normal methodological considerations Cohn does not think that this has any source-critical significance and does not affect the reliability of this source. On the contrary, Cohn goes on to cite Boccaccio’s account as the very truth, his assertion that the original buboes “would begin to spread, and within a short time would appear at random on every part of the body” is taken as cast-iron scientifically acquired evidence, although he is not able to cite any chronicler or physician who

162

Below: 371–4.

366

chapter nine

has made a similar observation. Thus, in essence Cohn asserts that Boccaccio’s account on this point overrides the significance of all other medieval comments on the matter—but without affecting the value or tenability of this evidence when that evidence is useful for his argument. It now becomes clear why Cohn must reject or ignore the fact that Boccaccio’s account was affected by literary intentions and functions, since this could undermine his use of the dramatic account of how buboes spread all over the body as hard evidence with crucial significance. For the same reason, Cohn must refrain from asking the obvious anatomical question: Can buboes really spread all over the body, can buboes arise where there are not lymph nodes or glands? He has also dropped his own argument that late medieval physicians with only a couple of exceptions located buboes in relation to the Galenic concept of emunctories163 which means that they would predominantly form in relation to the inguinal-femoral area, the axillas and the neck. However, it is not correct that in India buboes only arose in those parts of the body, as Cohn asserts; there was also a significant incidence of other locations. Choksy sums up the medical experience on this point in India around 1900, using the term “gland” both for glands and lymph nodes:164 Such glands may be situated in different parts of the body, the order of frequency being the femoral, inguinal, and iliac165 glands, separately but more often in continuation, the axillary, and the brachial166 chain with epitrochlear,167 the cervical, parotid168 and submaxillary169 glands, and but rarely also in other positions, such as the femoral chain, the popliteal,170 in the calf, at the ankle, at the bend of the elbow, pre-auricular or even occipital.171

Many of these locations of buboes are illustrated with photographs from the Indian plague epidemics in Simpson 1905: 275–83, 285–6,

163

Above: 356, 359. Choksy 1909: 352. 165 Iliac artery = each of the two arteries, right and left, into which the abdominal aorta divides. The common iliac lymph nodes, four to six in number, are grouped behind and on the sides of the common iliac artery, one or two being placed below the bifurcation of the aorta. 166 Brachial = belonging to the arm. 167 Epitrochlear gland, situated just above the elbow. 168 Gland situated besides or near the ear, producing saliva. 169 Situated under the jaw. 170 Pertaining to the ham or the hollow at the back of the knee. 171 Belonging to or situated in or on the occiput or back of the head. 164

buboes as a normal clinical feature in epidemics

367

which is a standard work Cohn refers to three times and must be assumed to be acquainted with. True, nothing is said about an instance of a bubo up the nose that Cohn refers to, but is this statement true? Was the existence of this bubo ascertained by adequate anatomical means? Which lymph node or gland is implied? Could this not reflect an observation of a patient with septicaemia where bursting blood vessels in the nose due to vascular damage by plague toxin had occasioned epistaxis, “bleeding from the nose,” as observed also in modern plague epidemics and described in the standard works of plague?172 Bleeding from the nose is repeatedly mentioned in the historical sources, and why could it not lead to the notion with people who did not perform anatomical dissection and analysis that this was caused by a bubo in the nose? No doubt because it would put another critical question mark on Cohn’s assertions about the empirical orientation of late medieval physicians. It now becomes clear why Cohn cannot exercise source-criticism and ask the crucial question: How were the clinical elements of Boccaccio’s account obtained, did he or anyone else examine plague cases physically? If they did not, how would this affect the clinical opinions that would come into circulation? Are there not very good reasons for assuming that the very bashful or shy attitudes towards sexual matters of these times would affect how often buboes in the groin would be mentioned? If plague cases were not physically examined, would not more easily observable buboes on the upper part of the body, in the axillas, on the neck, and so on, be relatively more often noted than buboes in the groin area, and would that not skew the relative incidence of the locations of buboes as mentioned in the writings of the time? Thus, again the conclusion must be drawn that Cohn argues his case on the basis of bastard statistics. The application of elementary source-criticism also reveals that Cohn’s sarcastic question whether one should assume that medieval persons “were more supine than modern Indians or Glaswegians” simply reflects his neglect of source-criticism and the pervasive methodological weaknesses of his discussion. Cohn has not furnished these concluding and crucial extractions of his text cited above with supporting footnotes. However, there are clearly two clinical features at the centre of Cohn’s line of argument,

172

Simpson 1905: 265; Chun 1936: 313. Cf. Manson’s Tropical Diseases 1921: 268.

368

chapter nine

namely the location and number of buboes, and the appearance of pustules, Boccaccio recorded buboes and then their spread along with black pustules over the entire body […]. not a single case of over 3000 clinical studies [in the Bombay report of 1896–7] did the boils spread from the lymph nodes, bursting into tiny black, green, and red pustules across the body […].173

Pustules appear to be the single most important criterion, since according to Cohn, this type of clinical manifestation was unknown or unregistered in studies of plague in India or elsewhere: with no modern plague have black pustules spreading randomly all over the body been reported […].174

For historical documentation he refers in identifiable and testable form only to Boccaccio’s description of plague cases in Il Decamerone and he adds in order to strengthen its significance: “Boccaccio’s description cannot be simply dismissed as poetic license to heighten the plague’s horror […].”175 However, this reference to pustules can be revealed to be fictitious, even when compared with Cohn’s own citation of Boccaccio’s text on this point176 twenty-two and 206 pages later: From the two areas already mentioned [the groin and the armpit], the aforementioned deadly gavòcciolo would begin to spread, and within a short time would appear at random on every part of the body. Afterwards, the illness would change with the appearance of black or blue spots (macchie nere o livide) forming on their arms, thighs, and other parts of the body, sometimes large and few in number, at other times tiny and closely spaced.177

Clearly, nothing is said about pustules, only about (buboes and) darkly coloured spots and, as shall be expanded on below, pustules and spots are different categories of clinical manifestations. This shows that Cohn’s assertion to the effect that Boccaccio emphasized the importance of black pustules as a clinical feature is spurious (and that he

173

Extracted from the citations above on page 364. Cohn 2002: 59. 175 Cohn 2002: 59. 176 Cohn refers to an edition which I have not succeeded in getting hold of, namely V. Branca, Boccaccio 1976: 10–1. 177 Cohn 2002: 58–9. Gavòcciolo = bubo. 174

buboes as a normal clinical feature in epidemics

369

probably knows better). Nonetheless, it is in connection with the text just cited that he for the first time links Boccaccio to the topic of “black pustules.”178 This assertion is based on a false translation of the infamous “petechiae” as “pustules.” In the case of bubonic plague, the appearance of petechiae reflects the fact that bacteria have reached the small subcutaneous blood vessels and by toxic effects on the walls of the vessels (and a tendency of clotting) caused them to burst, letting out drops of blood that through the skin take on the form of black, bluish or livid spots. These are the indications of imminent death that made early modern Englishmen call them “the tokens,” “God’s Token” or “God’s Mark.”179 This demonstrates again the means Cohn must resort to in order to form a seeming evidential basis for his grand theory. Thus, Cohn has constructed an important or even crucial argument for rejecting the identity of late medieval and modern plague by making a false translation of words meaning “darkly coloured spots” as “pustules” which is at variance with all scholarly translations and editions of Boccaccio’s text,180 including the one that he himself used.

178

Cohn 2002: 59. See, for instance, Bell 1951: 127; Slack 1985: 65. 180 Boccaccio 1982: 8–9: “but in men and women alike there appeared at the beginning of the malady, certain swellings, either in the groin or under the armpits […] and these the vulgar named plague-boils [gavòccioli]. From these two parts of the aforesaid death-bearing plague-boils proceeded, in brief space, to appear and come in every part of the body; wherefrom, after awhile, the fashion of the contagion began to change into black or livid blotches, which showed themselves in many on the arms and about the thighs and (after spread to) every other part of the person, in some large and sparse and in others small and thick-sown; […] a very certain token of coming death […].” Nohl 1961: 10–11: “it began with young children, male and female, either under the armpits, or in the groin, by certain swellings […] which (in their vulgar Language) they termed to be a Botch or Boil. In very short time after, those two infected parts were grown mortiferous, and would disperse abroad indifferently to all parts of the body; whereupon, such was the quality of the disease, to shew itself by black or blue spots, which would appear on the arms of many, others on their thighs, and every part else of the body, in some great and few, in others small and thick. Now as the boil (at the beginning) was an assured sign of near approaching death, so proved the spots likewise to such as had them.” Sticker 1908: 54, strictly, this is not an exact translation but an almost verbatim rendering of Boccaccio’s text: “es entstanden, als sie begann, bei Männern wie bei Frauen entweder in der Weiche oder unter der Achsel Geschwülste […] Das Volk nannte sie gavoccioli, Drüsenbeulen. Von jenen Körperstellen aus verbreitete sich das tödliche Pestgift rasch in alle Teile. Später nahm di Krankheit eine andere Gestalt an; es kamen schwarze oder bläuliche Flecke an den Armen und an den Beinen und weiterhin über den Leib hervor; bei dem Einen groß und spärlich; bei dem Anderen klein und dichtgedrängt. Und wie anfangs die Pestbeule das sichere Zeichen des herannahenden Todes war, so wurden es jetzt die Flecken für Jeden, an dem sie sich zeigten.” 179

370

chapter nine

However, Cohn has actually collected material purportedly showing an incidence of pustules which is described in Appendix I, “Miraculous Plague Cures.”181 I have not checked this material, but it purportedly shows that out of fifty-six instances of miraculous plague cures, seven, or 12.5 per cent, mention pustules as a clinical feature. However, can this material be taken seriously and be allotted any significance or tenability when Cohn does not present his material in the form of texts that allow readers to check out whether pustules are really mentioned or whether these statistics are based on false translations of words meaning “spots” or “blotches” as “pustules,” as he demonstrably has done with Boccaccio’s text? Even if it is assumed that the translations are correct or acceptable, the source-critical problems attached to any attempt at using this material for any other purpose than to show that pustules occurred within the broader pattern of late-medieval plague disease is formidable for several elementary source-critical and methodological reasons. Firstly and devastatingly, they do not represent a physically systematically examined sample of cases. Next, the elementary source-critical questions which Cohn has neglected to ask queue up, for instance: Are the reports of miraculous cures real? Were miraculously cured plague cases systematically physically examined and their clinical panorama ascertained in a scientifically tenable manner? Were reports of pustules relatively over-reported as a grisly feature that made the cures even more miraculous? And so on. Nonetheless, it can be accepted that this material shows that pustules were observed by contemporaries, but the significance of this material for Cohn’s arguments depends heavily on the following question: Is it true that pustules are not normal part also of modern plague cases, that this clinical feature was not observed in studies of plague in India or elsewhere? As can be seen especially clearly from the second and concluding citation above on page 364, Cohn denies that pustules were a feature of plague in India and of modern plague more generally, referring indirectly to the report Brigadier-General Gatacre compiled from evidence collected at plague hospitals in and around Mumbai in the plague year 1896–7 to this effect. I understand that Carmichael is puzzled by Cohn’s insistence of sticking uncritically to this report alone which he cannot praise enough182 while ignoring all other reports and studies, also contemporary and also based on the Indian experience around the turn of 181 182

Cohn 2002: 253–4. Cohn 2002: 16, 26.

buboes as a normal clinical feature in epidemics

371

the previous century. One should note that Gatacre was a military man, not an army medical officer, and most renowned for his leadership of the 3rd Brigade of the Chitral relief force, and was honoured with the publication of his biography.183 In this context one may legitimately wonder whether it is accidental that Gatacre’s report is extremely difficult to get hold of for critical examination. After having ordered this work at the University Library of Oslo I got the following exceptional e-mail from the librarian handling the order: “We have not found that this work (it appears to consist of three volumes) is in the possession of any library in the Nordic countries, Germany, Austria, Switzerland or several other countries. It is found in several libraries in Great Britain, but none of them permits loan. Neither is the copy in Bibliothèque Nationale (Paris, France) available for loan. The National Library of Medicine (NLM), Bethesda, Maryland has a microfilm edition of it? Do you wish that we attempt to have it loaned in for you?”184 I responded affirmatively to this question, but a couple of weeks later I received the following notice from the librarian: “This library does not lend this copy outside the U.S.A.”185 All the other more extensive, thorough and more mature studies published in the following decades are far easier to get hold of and provide enormous amounts of new and valuable information. Much of it is also found in compressed form in the standard works on plague. Why do these standard works on plague not mention Gatacre’s report? Is not the probable answer to this question that the material contained in Gatcre’s report lost its significance in the light of the great volume of outstanding research produced in the subsequent years? Is it unreasonable to consider the possibility that Cohn has chosen this work because it makes it so difficult to check out his assertions with references to this work to which he attributes such great importance? However, whatever his motives, the great volume of subsequent research based on a wealth of new experience and insights will have great precedence over such material from the earliest phase of modern research on plague. As pointed out by Carmichael, the outbreaks of bubonic plague epidemics in India in 1896 put extreme strains on medical facilities which were entirely unprepared for such an enormous epidemic onslaught on the population. In February 1897, when there were 900–1000 weekly 183 184 185

Develin 1896; B. Gatacre 1910. Librarian Eli Fjeld in e-mail of 1 August 2007. My translation into English. My translation into English.

372

chapter nine

deaths from plague in Mumbai, at the most 300 hospital beds were available. Many diseased persons resisted hospitalization because caste and ethnic groups were insufficiently separated. In short, there was a plethora of grave problems. The desperate endeavours of the English colonial authorities to build a great anti-plague organization which could cope with the tremendous tragedy unfolding before their eyes absorbed much of the available resources. The production and gathering of material for Gatacre’s report concomitantly with the unfolding epidemic catastrophe was unavoidably also adversely affected by lack of competent personnel, deficient understanding of bubonic plague as a disease, the relevant questions to be asked and which types of information should be gathered, and it was prepared for publication in great haste in the autumn of 1897.186 It must also be relevant to ask the question why Cohn only uses this report which obviously represents the earliest phase of the combat of plague in India, the scientific study of the disease and the collection of evidence? In critical minds, this should raise the question of why Cohn avoids later information based on much larger and more composite material, far better medical understanding of plague disease and far better resources for making research into the disease. Is it because black pustules are mentioned as a normal clinical feature of bubonic plague? It comes therefore as no surprise that Carmichael can cite another contemporary report to the same effect based on the medical study of 939 plague cases at the “Municipal Hospital for Infectious Disease at Arthur Road Bombay” in the period 24 September 1896 to February 28 1897. The study of these cases was thus produced concomitantly with Gatacre’s: The so-called black boils were observed in a large number of cases, and they seem to bear a distinct causative relation to the buboes in their neighbourhood. They differed from ordinary boils in that no inflammatory areola surrounded them. They consisted essentially of a blister in which the cuticle had become raised sharply and evenly from the skin, without any redness or signs of inflammation. In fact it appeared as if a glass circle had been fixed over the skin and its top tied with transparent tissue paper.187

Indisputably, here the clinical phenomenon of black pustules is identified in great detail and it is explicitly stated that it was observed in a 186 187

Carmichael 2003: 257–8. Carmichael 2003: 258.

buboes as a normal clinical feature in epidemics

373

large number of cases. This confirms the assumption of why Cohn sticks to a report compiled by a military officer and impossible to get hold of for most scholars, and why he passes in silence by or ignores all other important evidence on the matter produced by physicians in much the same circumstances. In 1905 there appeared the first standard work synthesizing the medical and clinical knowledge won by the British medical service in India authored by W.J. Simpson, Professor of Hygiene at King’s College in London, and Lecturer on Tropical Hygiene at the London School of Tropical Medicine and “formerly Health Officer, Calcutta.” These qualifications may usefully be compared with Gatacre’s credentials in relation to the matter at hand. Simpson’s standard work appeared shortly before the IPRC started late the same year, and it provides the following presentation of some clinical features central to the present discussion: petechiae and ecchymotic patches188 are generally over buboes or on the abdomen, but they may be found in other parts of the body, such as the face, neck, breast, and extremities […] the petechiae and ecchymotic patches probably correspond to the tokens in the Great Plague of London which appear to have been a common feature in fatal cases. In addition to patches of dark-coloured petechiae or ecchymoses there has been occasionally an eruption of pustules. The pustules on the skin may be of a variable nature, and in some cases they have been so numerous as to raise a doubt as to whether it was not a case of small-pox that was being dealt with. […] the pustules usually commence as ecchymotic or petechial spots […] these ecchymotic patches rapidly increase in size and then rise in the form of blisters […].189 Carbuncles, boils, vesicles, or pustules may be present on any part of the body.190

In connection with a post-mortem examination of a Chinese plague victim in Hong Kong: On superficial examination the case looked like one of small-pox, vesicles and pustules being scattered over the face, shoulders, arms, body, and leg.

188 Ecchymosis designates the passage of blood from ruptured blood vessels into subcutaneous tissue, marked by a purple discoloration of the skin. An ecchymotic patch in the skin is typically larger than a petechia, forming a non-elevated, rounded or irregular blue or purplish patch. 189 Simpson 2005: 284. 190 Simpson 2005: 227.

374

chapter nine The caretaker of the mortuary, who has had a large experience, pointed out the case as one of small-pox. An eruption covered the skin. Papules, vesicles, and pustules were present side by side. They were numerous over the neck, back, shoulders, back of arms, ventral surface of the abdomen, the extensor surfaces of the thigh and the buttocks […]. The pustules were the most numerous […]. There was no question of small-pox.191

The first citation makes it clear that petechiae and ecchymoses corresponding to Boccaccio’s account on this point are usual clinical features of bubonic plague in India and of modern bubonic plague more generally. Simpson’s view that they probably correspond to the tokens in the Great Plague of London of 1665 is confirmed by Bell’s monograph of 1951, who cites contemporary sources on this clinical feature which show great similarity to the descriptions just cited in reports from India. “The tokens” were spots upon the skin. Breaking out in large numbers, varying in colour, figure, and size […]. The colour might be red, with a surrounding circle inclining towards blue; in others a faint blue, the circle being blackish; others again took a dusky brown tone […] no part was immune from these round spots, though the neck, breast, back, and thighs were the most common places for them, “the tokens” sometimes were so numerous as to cover all the body. It was “the tokens,” so universally dreaded, that gave to the Plague the name of “the spotted death.”192

The citations from Simpson’s standard work on plague make it clear that that Indian plague patients presented with pustules and that this was observed from the beginning of plague in India and was well recognized before the IPRC began its work. A severe case of pustules in a plague patient had also been observed and described clinically in Hong Kong a few years earlier. Simpson makes it clear that the darkly coloured spots of petechiae and ecchymoses are distinctly different clinical feature from pustules, the confusion on this matter being entirely of Cohn’s own construction and, unfortunately, may appear to serve an argumentative objective. It also becomes clear that historical plague cases presented with buboes, pustules and darkly coloured spots which correspond to similar clinical features in modern bubonic plague and that this fact constitutes a strong argument to the effect that they were the same disease. Cohn’s use of Gatacre’s report can now be seen to be 191 192

Simpson 1905: 246. Bell 1951: 127–8.

buboes as a normal clinical feature in epidemics

375

misleading and is so throughout his monograph. One should note that Simpson’s work is entered in Cohn’s bibliography and referred to three times in his text, so arguably he is not unacquainted with this information. Pustules and petechial or ecchymotic spots as quite usual clinical features of bubonic plague are not confined, of course, to India, but are general clinical features of this disease. Summarizing the observations of bubonic plague in China, Chun states: Vesicles appearing on the hands, feet and pectoral193 region may be converted into pustules which were described by old writers during the Plague of London in 1665 as “blains.” The pustules may coalesce and form areas of necrosis, the so-called carbuncles. […] In some plague cases, the vesicles and pustules may resemble those of chicken pox or smallpox. […] There are often haemorrhages in the skin and elsewhere. […] Haemorrhages may occur in different parts of the body, so that we find petechiae, or ecchymoses […].194

Cohn has used this outstanding standard work on plague,195 which is a composite work written by a number of distinguished plague researchers, but he has evidently failed not only to consult the section on clinical features but even to look up the terms “pustule” and “petechiae” in the index, as he has generally failed to consult the sections on “Immunology,” “Hosts and Carriers,” “Insect Vectors,” “Clinical Features,” and “Epidemiological Factors.” Chun’s identification of the “blains” described by “old writers during the Plague of London in 1665” with pustules is confirmed by Bell: “The ‘blains’, so-called, were like blisters on the skin, obscurely ringed about.”196 Descriptions of pustules and petechiae in modern bubonic plague are ordinary information of the standard works on plague. Hirst mentions, albeit briefly, that the “vesicular variety of plague may simulate smallpox, but the pustules contain plague bacilli” and that “before death dusky stains or blotches appeared on the skin of the body.”197 In his standard work, Pollitzer cites Simpon’s description of the “formation of ecchymotic or petechial spots” which develop into the form of blisters and underlines that the “appearance of numerous petechiae 193 194 195 196 197

Of the chest or breast. Chun 1936: 311, 313, 316, 329. Cohn 2002: 301. Bell 1951: 126. Hirst 1953: 30, 32.

376

chapter nine

or ecchymoses, particularly early in the disease, is an ominous sign.”198 This shows that Simpson’s presentation of these clinical features of bubonic plague displayed knowledge and competence that were fully adequate fifty years later to an outstanding scholar who had lived his professional life in the first line of combat of plague in the field and the laboratory. Next, Pollitzer provides the following relevant clinical comment on the present topic: The appearance of generalized pustular eruptions (“plague pox” or “plague variola”) has been recorded by several observers. According to Macchiavello, instances of this kind were frequent in South America.199

This comment reflects the fact that pustules may be so widespread and numerous on the body that the disease may resemble small pox, a point also made by Simpson and Chun. Cohn has entered Pollizer’s impressive standard work on plague in his bibliography and refers to it nine times in the text according to the index (in one case the reference is erroneous).200 Purportedly, Cohn has not used the opportunity to find out whether Pollitzer had something to contribute on such a vital point for his theory as the clinical feature of pustules and petechiae; he could have done so by consulting the index under the entries “Plague pustules” and “Skin plague.” Machiavello’s statement that plague pox or plague variola was quite usual in South America can be independently confirmed. C.R. Eskey states in his report on this in his study of bubonic plague in Ecuador: Viruela pestosa begins as the ordinary bubonic disease, but the skin eruption that follows is likely to obscure the buboes. Vesicles develop which pass through stages very similar to those of varicella. The vesicles may be few in number or present to the extent that they are found in a severe case of chicken pox. The mortality of viruela pestosa is relatively high. Doctor Martinez states that when the vesicles exceed 50 the result is nearly always fatal.201

198

Pollitzer 1954: 425, 426. Pollitzer 1954: 425–7, see also p. 206. 200 Cohn 2002: 314 (the reference to page 189 should be 188 n). The erroneous reference is given on page 215: “the ones called iuvenis or young adults between around 20 and 30 years old—the ones most susceptible to new diseases in general and to modern bubonic plague in particular[fn. 100].” In the accompanying footnote 100, Cohn refers to Pollitzer 1954: 516, where statistics on the distribution of victims of primary pneumonic plague according to age is given, not in relation to bubonic plague. 201 Eskey 1930: 2082. 199

buboes as a normal clinical feature in epidemics

377

The frequent occurrence of plague pox in South America is also interesting because it may give a clue or key to the medical understanding of the cause of this phenomenon, whether it could, for instance, be due to peculiarities of food or drink or variants of malnutrition or undernutrition. According to my knowledge, the cause of widespread eruption of pustules in plague cases has so far not been studied; all knowledge appears to be descriptive or statistical. In the most recent standard work Butler, as a matter of course, makes the following description of usual cutaneous manifestations or skin lesions in cases of bubonic plague, mostly based on his experience and observations in Vietnam: The most common were pustules, vesicles, eschars,202 or papules near the bubo […].203

Cohn has entered also this work in his bibliography and refers to it four times in his text. Of particular interest is a passage where he insists that with no modern plague have black pustules spreading randomly over the body been reported. At most, a few points might form around the fleabite, but such marks are rare and usually occur with pneumonic or septicaemic plague, when buboes do not have time to form at all.[fn. 9]204

In the accompanying footnote 9, Cohn refers to page 17 in Butler’s monograph where nothing to this effect is stated. This is a spurious reference. Cohn has avoided page 79 where the chapter on “Cutaneous manifestations” starts and the information on pustules is given. All of Cohn’s assertions with respect to pustules and plague are erroneous and misleading. Puzzlingly, in view of all of these standard works on plague which Cohn has purportedly held in his hands, he refers for support of his assertion that pustules did not occur or only rarely occurred in modern plague to the short chapters on plague in three editions of Manson’s Tropical Diseases, the 10th edition of 1935: 254, the 19th edition of 1987: 591, and the 20th edition of 1996: 920, hoping, as it would seem, that none would make the effort to check them all.205 One should again

202

In the case of plague, a slough produced by gangrene. Butler 1983: 79. 204 Cohn 2002: 59. 205 It is not easy to get hold of so many editions, it actually requires some effort and I only managed to get hold of the American edition of the 10th edition published in 1936, but the contents should be identical with the British edition. 203

378

chapter nine

keep in mind that the chapters on plague in such general standard works on infectious diseases are very brief summaries of the material presented in general standard works on plague; in the case of the two last editions, of 1987 and 1996, they constitute 2.2 per cent and 0.97 per cent of Pollitzer 1954. This also means that the information they include on clinical matters vary considerably according to their assessment of what is sufficiently important to warrant inclusion in consideration of the medical circumstances of the contemporary world. However, since the editions of Manson’s Tropical Diseases up to the 19th of 1987 are not furnished with footnotes which allow basic checking out of the information, the significance which Cohn attributes to them and the scholarly argument(s) for not using the standard works on plague are quite intriguing. Nonetheless, in the 19th edition of 1987 of Manson’s Tropical Diseases’s section on “Skin affections” it is stated: A generalized popular rash on the hands, feet and pectoral region has been described. Should life be continued sufficiently long, the vesicles become converted into pustules resembling smallpox. These observations confirm in a remarkable manner the old writers who described manifestations, in the Plague of London of 1665, as “blains.”206

In the general introduction to the section “Human plague” it is also stated that the clinical panorama is very frequently characterized by ecchymotic spots or patches […]. Occasionally there are also furuncles, pustules and abscesses […] ecchymoses are common in all serous surfaces.207

Is it really possible that Cohn who claims to have held in his hand the 19th edition of 1987 and refers specifically to page 591 in the chapter on plague has not seen the relevant information in the general introduction to human plague on page 591, or the even more relevant section on clinical manifestations on the skin on page 593? Is it really credible that Cohn can have used all the modern standard works on bubonic plague from Simpson 1905 to Butler 1983 without having taken interest what they state about cutaneous manifestations? Is it really credible that he even by accident could have missed all references in them to pustules? But then Cohn’s reference to pustules in

206 207

Manson’s Tropical Diseases: 1987: 593. Cf. 1982: 340; 1996: 920. Manson’s Tropical Diseases: 1987: 591. Cf. 1982: 339.

buboes as a normal clinical feature in epidemics

379

Boccaccio’s Il Decamerone is also, as shown above, spurious in the sense that it is based on a mistranslation. In place of Yersinia pestis I offer no alternative […],208 Cohn admits. Crucially, Cohn does not take interest in the problem of why he is unable to present a single viral disease spread by interhuman crossinfection which is known to modern medical science in which patients present with buboes as an ordinary clinical manifestation. Viral diseases that spread by cross-infection are not rare. On the contrary, crossinfection is the usual way viral diseases are disseminated, and there must be hundreds of them. In epidemic or endemic form of spread, they have in common that diseased persons do not present with buboes as an ordinary clinical feature. According to ordinary methodological considerations, this elementary test of Cohn’s alternative theory which now has been performed for him provides abundant empirical evidence—without exception or loophole—for asserting that whatever disease historical plague could have been or whatever microbiological contagion could have caused it, it could not have been a viral disease spread by cross-infection. According to ordinary methodological considerations, this is a sufficient condition for rejecting Cohn’s theory that he should have recognized early in the process of planning his alternative theory. According to the elementary principles of methodology and social and medical science, the complete absence of a viral disease which presents with buboes provides maximum evidentiary powers to the fact. This invalidates Cohn’s alternative theory. This fact implies that there must be a very strong systematic cause or combination of causes which excludes any exception, i.e. which excludes the possibility that the disease could have been a viral disease spread by cross-infection. This systematic cause is probably identified since the only two diseases which regularly present with buboes, namely bubonic plague and tularaemia, are transmitted by ectoparasites which systematically deposit bacillary contagion at a subcutaneous level suitable for being drained through lymphatic vessels to lymph nodes (see above). This distinguishes these diseases from all diseases spread by crossinfection in which the contagion is normally inhaled into the lungs in droplets, landing the infection in an anatomical location without contact with lymph nodes, which is the reason no scholar has intimated the occurrence of pneumonic buboes. This clarifies the question

208

Cohn 2002: 247.

380

chapter nine

of crucial importance which Cohn has ignored, which is: How, by which physical routes or mechanisms or properties, should his purported viral disease spread by cross-infection have been regularly transported to lymph nodes? What Cohn is trying to make his readers believe is that he in confused and unscientific medieval texts has found tenable evidence of the only viral disease which regularly produce(d) buboes in diseased persons and that this (miraculously) is his purported alternative microbiological theory of historical plague. Cohn is unable even to make an attempt at explaining the medical or epidemiological process of causation. What was so unique about this viral disease that buboes should be expected to be an ordinary manifestation of the infection in contrast to all other viral diseases known by medical science? Cohn simply maintains that it was spread like hundreds of other viral diseases, namely by cross-infection, but in an obvious breach of elementary methodology pretends that he is not obliged to explain why this mode of (viral) transmission of infection should uniquely produce buboes only in the case of his purported disease without a unique and specific mechanism of transmission which leads to the regular infection of lymph nodes. As now should be clear, what Cohn has constructed is not an alternative theory, it is an alternative speculative flight of the imagination, a phantom disease which has not the slightest resemblance with any viral disease known to medical science. It is overwhelmingly probable that such a disease has never existed and never disappeared because it never appeared in the real world but lived its entire short life as a brainchild in an academic ivory tower.

CHAPTER TEN

DEFINING FEATURE 4: DNA OF YERSINIA PESTIS FROM PLAGUE GRAVES The advocates of alternative theories of the microbiological identity of historical plague find themselves dramatically confronted by modern microbiological and genetic sciences which have now reached a level of sophistication which provides entirely new opportunities for historical studies of biological material of the past and the development of the new science of paleomicrobiology. Identification of the microbiological agent of historical plague epidemics can be achieved by reclamation of genetic material or specific proteins of plague contagion taken from human remains in historical plague graves. Reclamation and study of such biological material will provide certain evidence of the microbiological identity of historical plague if the results from a significant number of excavated plague graves with significant geographical spread are consistent. Since the development of the scientific discipline of paleomicrobiology is quite recent, starting in 1993,1 the following presentation will give a brief outline of the research history and the results up to the present be summarized in Table 6. In 1998 a team of French scholars, M. Drancourt, G. Aboudharam, M. Signoli, O. Dutour and D. Raoult, published a study of DNA recovered in dental pulp2 taken from unerupted teeth extracted from individualized skeletal remains excavated from two mass graves of plague victims in Provence. This material was taken from a mass grave containing the skeletal remains of 133 plague victims buried after a plague epidemic in Lambesc3 in 1590 and from a mass grave in Marseilles containing skeletal remains of 200 plague victims buried in May 1722. The scholars extracted dental pulp from the teeth of two individualized skeletal remains in Lambesc and from the remains of three individuals

1

Drancourt and Raoult 2008a 55. See La, Aboudharam, Drancourt 2008: 175–96. 3 Lambesc is a town situated c. 45 km north of Marseilles. Cf. Les saison d’une peste (avril–septembre 1590): Le cimetière des Fédons à Lambesc. B. Bizot (ed.). 2005. Rouen: CNRS Editions. 2

382

chapter ten

in Marseilles. In seven of the eight cases,4 the scholars found DNA of ordinary strains of the plague bacterium Yersinia pestis which causes bubonic plague (and the variants and modalities of plague disease that can develop from such cases).5 In 2000, another group of French researchers (including three of the scholars who participated in the 1998 study) published a similar study performed with improved techniques aimed at molecular identification by so-called “suicide PCR” which should exclude any possibility of contamination of the material. The study was nonetheless carried out under the observance of draconian precautions to exclude contamination; it was, among other things, performed in a building where plague contagion never had been introduced before, and the dental pulp was extracted with techniques which were specifically designed to exclude any form of contamination with extraneous DNA. The material was dental pulp, in this case extracted from twenty-three teeth of three skeletons, two adults and a child, buried hastily and without shroud in the same grave in a cemetery in the city of Montpellier some time in the period 1348–1400, probably in the Black Death (1348). As a negative control, four unerupted teeth were collected from ancient skeletal remains excavated from a medieval grave in Toulon, France. In this period, Montpellier was ravaged by plague in 1348, 1374–5, 1385 and 1397, and the number of registered households fell from c. 9500 in 1348 to c. 1000 in 1397. This means that a large majority of the buried persons must have died in these plague epidemics, indicating that the recovered genetic material is probably connected with the Black Death. In one of the four teeth taken from the child and in all nineteen teeth taken from the adults, the researchers found Yersinia pestis-specific DNA fragments representing the genetic code of ordinary strains of this contagion. None of the four negative control teeth tested positive for plague contagion.6 It must be highly improbable that a few episodic cases of deaths from bubonic plague in the historical past should be found by chance. The consistent identification of Yersinia pestis constitutes therefore substantial evidence to the effect that bubonic plague spread in epidemic form in southern France in the period 1347–1722 covering the whole second 4

Drancourt, Aboudharam, Signoli et al. 1998: 12638. Drancourt, Aboudharam, Signoli et al. 1998: 12637–40. 6 Raoult, Aboudharam, Crubézy et al. 2000: 12800–3. Cf. Drancourt and Raoult 2002: 5–6. 5

dna of yersinia pestis from plague graves

383

plague pandemic from the Black Death to the last great epidemic. Since these epidemics have the same characteristics as historical plague epidemics elsewhere in Europe, this genetic evidence constitutes significant evidence that the plague epidemics in the second pandemic were generally epidemics of bubonic plague. The scholars conclude triumphantly (but arguably prematurely): “We believe that we can end the controversy: Medieval Black Death was plague.” In later papers, presenting the further development of this type of research, they have had occasion to repeat this conclusion on an even more certain basis, last time in 2008: “Our results enabled us to resolve the long dispute over the aetiology of the Black Death by showing that the disease was in fact plague caused by Y. pestis.”7 In 2002, a comprehensive study appeared of genetic material taken from individualized skeletal remains in mass graves in seven localities, namely Aubagne, Cassis, Puy-Sainte-Réparade, Marseilles, Martigues, Salon, and Vitrolles relating to the plague epidemic in Provence in 1720–2. This genetic material was studied by use of improved molecular biology techniques on dental pulp which determined the infectious agent with even greater certainty. Yersinia pestis was identified in all cases.8 Now microbiologists from other countries have begun to make similar studies and make similar findings. The same year, two Australian scholars published a study in which they had succeeded in identifying the DNA of Yersinia pestis in skeletal material taken from a putative plague grave from the Black Death in London (1348–9) using the PCRtechnique (see below, Table 6 and fn. 28, no. 3). Frequent, usual or consistent identification of Yersinia pestis in plague victims of the past without concomitant identification of any other alternative mortal pathogen should put and end to all microbiological alternatives argued by the revisionists. For this good reason, a team of scholars set out to test the almost sensational results obtained by the French scholars by carrying out an independent study with microbiological techniques of other samples of dental pulp taken from skeletal remains in presumed plague graves in various countries. A preliminary negative communication was published in Science by 7 Drancourt and Raoult 2002: 105–9; Drancourt and Raoult 2008b: 153. Drancourt and Raoult 2008c: 182. 8 Signoli, Séguy, Biraben et al. 2002a: 838–9, 841; Signoli, Séguy, Biraben et al. 2000b: 846, 849.

384

chapter ten

A. Cooper and H. Poinar in 2000 to the effect that it had not been possible to reproduce the results of the first French study,9 the final study, also negative, was published by Gilbert and al. in 2004. They had studied dental material taken from putative plague victims in five burial sites from the late thirteenth century to the seventeenth century with wide territorial distribution in Europe using a sample of 108 teeth taken from sixty-one individuals, however, without succeeding in finding the DNA of Yersinia pestis.10 Unimpressed by the French scholars’ descriptions of the impressive pre-cautions taken to avoid contamination and their insistence in the first paper that “Contamination of the samples during handling is highly improbable”11 and in the second paper that the researchers had used a special technique that would “avoid any possibility of molecular contamination of the ancient DNA,” Gilbert et al. suggested that “the DNA-sequences […] derive from the contamination of DNA extracts with formerly amplified or extracted Y. pestis DNA.”12 However, Gilbert et al. do not attempt to explain concretely how contamination could have occurred in view of the French researchers’ descriptions of their techniques and anti-contamination measures and they did not test the French researchers’ more specific techniques and the use of “suicide PCR.” Gilbert et al. overlook the fact that the French scholars also tested control samples taken from non-plague sites, and that they tested negatively,13 which constitutes strong evidence against contamination in the laboratories. Gilbert et al. did not comment on the positive findings presented in the paper of 2002 which was produced by another team of French scholars attached to other institutions using other laboratory facilities and who insisted on the “absence of contamination of the research workers.”14 Also, they did not comment on the positive identification of DNA of Yersinia pestis relating to the Black Death in London performed by entirely independent scholars, despite the troubling fact that they had not succeeded in identifying such DNA from two sites with plague burials in London.

9

Cooper and Polnar 2000: 1139. Gilbert, Cuccui, White et al. 2004a: 342–9. Cf. Prentice, Gilbert and Cooper 2004: 72. 11 Drancourt, Aboudharam, Signoli et al. 1998: 12637, 12640. 12 Gilbert, Cuccui, White et al. 2004a: 352. 13 Drancourt, Aboudharam, Signoli et al. 1998: 12637–8. 14 Signoli, Séguy, Biraben et al. 2002a: 838–9; Signoli, Séguy, Biraben et al. 2000b: 846. 10

dna of yersinia pestis from plague graves

385

Gilbert et al. argue also that it is suspect that the French scholars found Yersinia pestis-specific DNA in all cases, since “during an epidemic, not all deaths can be expected to arise due to the specific pathogen […]. Therefore, it seems unlikely that, among the eight individuals sampled in these two studies, only one negative for Y. pestis was observed.”15 However, this argument does not bear the significance allotted to it, since the mortality caused in historical plague epidemics was so enormous that normal mortality from other causes would be strongly affected by the fact that many of those who in normal circumstances would have died from other caused died from plague instead. This greatly affects the numerical relationship and the statistical probabilities. Although it is true that persons died from other causes during plague epidemics, it is also true that the probability of selecting by chance the remains of such persons in mass graves with plague victims would be small, even tiny. I have had the opportunity of approaching the problem in my Norwegian plague history on the basis of continuous information on the number of corpses brought to the Cathedral in Bergen during the plague epidemic of 1565–6 in its capacity as parish church. This is material which provides the opportunity for deleting all persons dying outside the plague season and a number of persons about whom it was specifically stated did not die from plague. This process would be much the same in a plague year, when people dying outside the plague season would receive normal burials and the mass graves of plague victims would tend to contain very few non-plague deaths. About 40 per cent of Bergen’s population perished in the epidemic, and I could conclude: “the material on the deaths in the plague epidemic was probably affected by slightly below 0.5 percentage point of normal mortality for each of the two years in which the epidemic took place.”16 In their monograph of 2004, Scott and Duncan refer to a talk given by one of the members of the team, A. Cooper of the University of Oxford, at a meeting of the British Society of Microbiology in Manchester in September 2003 in which he apparently suggested that the DNA analysis technique used by Drancourt and Raoult was flawed. He also purportedly maintained that “splitting the teeth and scraping out the inside, as the French team did, contaminated them with

15 16

Gilbert, Cuccui, White et al. 2004a: 351. Benedictow 2002: 201. My translation into English.

386

chapter ten

bacteria.” In the opinion of Scott and Duncan, this justified calling the findings of the French scientists “A Red Herring.”17 However, later in 2004, Drancourt and Raoult responded briefly to Gilbert et al.’s paper and pointed out a serious flaw in the critics’ work: Gilbert et al. did not test systematically “our dental technique” and that they had only tested dental pulp in seven suspected specimens. This included five teeth from a cemetery in Verdun: in their work they had tested three teeth from this cemetery which also had tested negative for Yersinia pestis. “Therefore this result did not surprise us.” Moreover, we found that the recovery of dental pulp via the tooth apex, as described by M.T.P. Gilbert, is almost ineffective. In our work, we always recovered dental pulp after complete opening of the dental pulp cavity. This approach is more difficult to perform and a dentist is probably necessary here. This allowed the recovery of all the pulp remnants. When this technique was applied, only two dental pulps, recovered by a different technique, from patients sampled in Copenhagen gave results different from ours. The use of the less satisfactory technique makes a very weak basis to contest our data.18

Drancourt and Raoult also point out that another strategy of genetic research, PRC techniques (“suicide PCR”), as practiced by Gilbert et al. was open to substantial criticism and was “very different from what we reported […]. We therefore believe that our test conditions were not reproduced.” “We therefore disagree with the authors’ conclusion that they failed to reproduce our results since they did not use our techniques to obtain material of our PCR testing techniques.”19 The defensive response from Gilbert et al. shows that the serious flaw Drancourt and Raoult had pointed out was justified and tenable.20 The tenability of 17

Scott and Duncan 2004: 185–90. Drancourt and Raoult 2004: 263–4. 19 Drancourt and Raoult 2004 : 263–4. Cf. Drancourt and Raoult 2008: 153. 20 Gilbert, Cuccui, White et al. 2004b: 264–5. Gilbert, Cuccui, White et al. 2004a, has also other weaknesses. For their information on the Black Death they refer only to Cohn 2002 and Scott and Duncan 2001 without taking interest in the fact that these monographs are not devoted to the general study of the Black Death, and without taking any interest in the fact that their alternative theories on the microbiological nature of historical plague are entirely incompatible, so that at least one of them must be massively erroneous, which may be taken to indicate a certain element of preconception. Surprisingly, they argue that since the mortality rates were 40–50 per cent, this can be taken as a serious argument in favour of Scott and Duncan’s filoviridal virus theory, a type of disease that for transmission and dissemination requires direct physical contact involving transmission of cellular material. This is compatible with the fact that these diseases produce only small or tiny outbreaks, and are, furthermore, dependent on a highly local African animal reservoir (see below). One would also like to have seen a 18

dna of yersinia pestis from plague graves

387

the important points made by Drancourt and Raoult have since been confirmed by the continuous stream of new positive studies (Table 6) and the fact that apparently no other microbiologists have failed to identify Yersinia pestis in biological material taken from plague graves since 1998. Revisionists are also rejecters and have consistently continued to refer to the preliminary negative communication by Cooper and Poinar from 2000 and Gilbert et al.’s paper from 2004 in order to reject the significance of the French scholars’ research.21 This is what Cohn does briefly and superficially in his monograph of 2002 and in his paper in The American Historical Review the same year.22 This attitude requires that subsequent studies exhibiting positive identification of bubonic plague DNA, also by other scholars associated with other research institutions in other countries, must also be overlooked. This is what Cohn still does in 2008 (see below).23 In 2007, Drancourt, Roux, Dang et al. published a study designed to resolve another controversy and enlarged in the process the pool of examinations of dental pulp taken from plague graves of the past. They took up again a central team of the paper of Drancourt, Roux, Dang et al. of 2004 (above) concerning the historical role of various types of Yersinsia pestis. In 1951 R. Devignat published a very interesting paper where he identified three biovars of plague characterized by special properties, namely ability to convert nitrate to nitrite, or to ferment glycerol, or both, and he assumed that each were responsible for an independent pandemic, namely Antiqua, Medievalis and Orientalis.24

reference to at least a single modern case of filoviridal haemorrhagic disease that has presented with a bubo. It is also surprising that they evidently have a positive view of Cohn’s theory involving an unknown virus that long ago has become extinct. Is this a testable theory? Why do they not take interest in the crucial fact that Cohn does not underpin his alternative theory with a single example of a viral epidemic disease that ordinarily presents with buboes in the diseased? Would it not be reasonable that they at least attempt to identify a viral epidemic disease which ordinarily presents with buboes in the diseased, and if this proves impossible, to establish a rule of regularity that would include untestable assertions with respect to viral theories of the nature of bubonic plague? These and other relevant issues or topics have partly been discussed above in relation, for instance, to buboes; other points will be discussed and clarified below. Here, it is the lack of questioning and critical attitudes in these scholars’ paper that have attracted attention. 21 See, for instance, Christensen 2003: 417, fn. 16; Knudsen 2005: 25. 22 Cohn 2002a: 248–9; Cohn 2002b: 735–6. 23 Cohn 2008: 88–9, 100. 24 Devignat 1951: 247–63; Devignat 1953: 509–14. Cf. Pollitzer 1954: 103.

388

chapter ten

Drancourt, Roux, Dang et al. confirmed by molecular analyses that these three biovars existed, but found also that the biovar Orientalis was involved in all three pandemics and probably was the main biovar also in the two first pandemics. They also found that isolates of biovar Antiqua are more distantly related to other isolates than biovars Orientalis and Medievalis, and that one Y. pestis Antiqua isolate formed a fourth branch, which “suggests that Y. pestis may comprise four different lineages instead of the three that have been recognized so far.” In the new paper, the French team of researchers expanded their territorial search for biological material to include teeth taken from twelve skeletal remains including five children buried within the ruins of a Roman temple from 7th–9th centuries in Vienna, in addition teeth were taken from five skeletal remains found in mass graves in Martigues about twenty-five km west of Marseilles which had been dated to 1720–1, and five teeth from three skeletal remains in a mass grave in Marseilles containing 216 victims who had been buried in May 1722, a mass grave that had been used also earlier and given positive identification of Yersinia pestis. Usual strict precautions were implemented in order to prevent contamination, material was also collected for negative testing, and the usual paleomicrobiological techniques were applied. All eleven negative controls proved negative, but five of thirtysix teeth yielded positive identification of Yersinia pestis in “2 of 4 persons’ remains from Vienna, 2 of 5 from Martigues, and 1 of 3 from Marseilles.” They exhibited total similarity with the genetic structures of Yersinia pestis Orientalis. The French scholars concluded that these results confirm the earlier detection of Yersinia pestis-specific DNA in the skeletal remains of plague victims from the first and second pandemics. After having demonstrated the presence of Yersinia pestis-type genetic material in Justinianic and medieval specimens, “we now have cumulative evidence using 2 different molecular approaches that Yersinia pestis closely related to the Orientalis biotype was responsible for the 3 historical plague pandemics.”25 Considering the comprehensive evidence available after ten years of paleomicrobiological research, there can hardly be any doubt that the three identified historical pandemics of plague were caused by Yersinia pestis, principally the Orientalis biovar. This constitutes also independent defining evidence based on identification of the microbiological nature of the contagion. 25

Drancourt, Signoli, Dang et al. 2007: 1–3.

dna of yersinia pestis from plague graves

389

This emphasizes the importance of presenting a complete survey of the most recent literature in studies which present positive identification of Yersinia pestis in biological material taken from historical plague graves with the objective of making them an indispensable part of future discussions of this subject. After 2002, new studies were published by scholars from quite a number of countries who reported the identification of Yersinia pestis in various localities at various times, all of them overlooked or ignored by all revisionists. Dental pulp, bones and other biological remains from plague graves were studied with improved or new molecular techniques which increased the range of usable biological material and determined the infectious agent with great certainty, even complete certainty since the spectre of laboratory contamination was eliminated.26 Soon, studies also provided identification of Yersinia pestis from plague graves dating back to the first pandemic/the Justinianic pandemic, from Sens about ninety km south-east of Paris, from Aschheim near Munich in Bavaria and from Vienna in Austria, thus, with great territorial spread.27 All studies providing identification of DNA or specific proteins of Yersinia pestis in material from historical burial sites are synoptically displayed in Table 6; the two first columns indicating the chronology of the papers and the development of this discipline as presented in fn. 28.28 26 27 28

Excepting the negative control samples which all were negative. See fn. 28, (5), (7), (8), and fns. 29–31. (1) Drancourt, Aboudharam, Signoli et al. 1998: 12637–40; Castex 2008: 29–34. (2) Raoult, Aboudharam, Crubézy et al. 2000: 12800–03; (3) McKeough and Loy 2002: 145; (4) Signoli, Séguy, Biraben et al 2002a: 821–47; (English ed.) Signoli, Séguy, Biraben et al. 2002b: 829–54. The material relating to Marseilles is taken from the same mass grave as no. 1, and as in nos. 8 and 9–10; the material relating to Martigues is taken from the mass grave at Le Delos, same as in no. 9–10. (5) Drancourt, Roux, Dang et al. 2004: 1585–92; Castex 2008: 25–34. (6) Pusch, Rahalison, Blin, et al. August 2004: 484–5. Cohn claims that this paper supports the revisionists’ rejection of the significance of the plague-related genetic research. Cohn 2008: 88. However, Pusch et al. maintain that they have succeeded in identifying both DNA and proteins specific to Yersinia pestis in skeletal material taken from a charnel house associated with the church of St Germanus in Stuttgart which can be dated to the seventeenth century but not to a specific plague epidemic among the several which ravaged the city in that century. True, in the opening statement they apparently disagree with the view that plague in the past was caused by Yersinia pestis which is clearly at variance with the substance of their paper. In a personal communication responding to me by e-mail of 30 December 2009 Professor Pusch states that the “confusion is due to the final editing process […] unfortunately, I had no influence on it.”

390

chapter ten

Table 6. Microbiologcal identifications of Yersinia pestis, year of publication, time of epidemic(s), and localities Paper No. Year 1

1998

2 3 4

2000 2002 2002

5

2004

1. Pandemic 2. Pandemic Locality 541–766 1346–1722 1590 1722 1348(–1400) 1348–9 1720–2

57129 1348 1348 1626–78

6

2004

7

2005

544/c. 56030

8

2007

600–76631

Lambesc: Provence Marseilles: Provence Montpellier: Languedoc London Aubagne, Cassis, PuySainte-Réparade, Marseilles, Martigues, Salon, Vitrolles: Provence Sens: 90 km south-east of Paris Dreux: 70 km north-west of Paris Montpellier: Languedoc Stuttgart: Germany, south-west Aschheim: Bavaria (near Munich) Vienna: Austria

(7) Wiechmann and Grupe 2005: 48–55; (8) Drancourt, Signoli, Dang et al. February 2007: 332–3; (9–10) Bianucci, Rahalison, Ferroglio, et al. October 2007: 747–54; Bianucci, L. Rahalison, E. Massa et al. March 2008: 361–7. These two papers are closely related, but the teams of scholars are not identical and the second paper appears to be an improved and expanded version of the first; I have therefore chosen to consider them together. 29 According to the sources and maps in J.-N. Biraben and J. Le Goff, “La Peste dans le Haut Moyen Age.” Annales Économies Sociétés Civilisations. 24; 1969: 1493–4, 1500– 07, bubonic plague epidemics could have reached Sens twice in the first pandemic, both times in epidemics occurring in the sixth century which is also the latest time limit of the radiocarbon dating: in 543 when the first epidemic of the Justinianic pandemic spread in France and next in 571 in the third epidemic. Castex 2008: 28. See also Little 2007: 20. 30 544 and c. 560 are the two years in the two first epidemics of the Justinianic pandemic when plague came geographically closest to Munich, Biraben and Goff 1969, 1493–4, 1500–07. This demonstrates that knowledge of the spread of plague epidemics can be increased or extended by paleomicrobiological studies. 31 The graves in Vienna are dated in two ways, by a 5th century coin, which allows dating to the sixth century, but dating by C14 indicates seventh or eight centuries.

dna of yersinia pestis from plague graves

391

Table 6 Cont. Paper No. Year

1. Pandemic 2. Pandemic Locality 541–766 1346–1722 1720–1

9–10 2007/8

1722 1590 1628–32 1649–50 1720–1 1720–1 1720–1 1722

Martigues: Couvent de Capucins32 Marseilles Lambesc Puy-St.-Pierre: Dauphiné,33 east Draguignan: Provence Martigues, Le Delos34 Martigues, Couvent des Capucins Berres L’Etang, near Martigues Marseilles

Table 6 shows that by March 2008, after mere ten years, ten studies had been published with twenty-six independent identifications of the DNA of Yersinia pestis relating to twenty different historical burial sites of plague victims. Among them were three geographically widespread graves from the Justinianic pandemic (near Paris, near Munich, in Vienna), twenty-three localities in the second pandemic comprising three relating to the Black Death 1348–9, i.e. Montpellier, Dreux and London, and also in widespread localities across southern, western and north-western Europe. Since French scholars pioneered this new discipline of paleomicrobiology developing techniques suitable for the identification of Yersinia pestis in biological material from historical graves and enthusiastically exploited the new opportunities, fifteen different sites of plague graves in France have so far yielded positive findings, one from the Justinianic pandemic in Sens, three from the

The two first epidemics of the Justinianic pandemic came closest to Vienna according to the sources and maps in Biraben and Goff 1969, 1493–4, 1500–07. 32 Le Couvent de Capucins de Ferrières; Ferrières is a section of the town Martigues in Provence west of Marseilles. See also Tzortzis and Signoli 2009: 749–60. 33 Region north of Provence; Briançon is situated in the north-eastern corner on the border with Italy. 34 Le Delos is another section of Martigues.

392

chapter ten

Black Death (two of them in Montpellier), one from 1590, two from seventeenth-century south-eastern France, and nine from the last epidemic in southern France in the years 1720–2. In addition, there has been one positive finding in biological material from seventeenth-century Stuttgart in south-western Germany situated at about the same latitude as Paris but in Central Europe. Consistently, the genetic characteristics of the same mortal pathogen have been identified, specifically the DNA fragments or specific proteins of Yersinia pestis of the biovar Orientalis, excepting in Stuttgart where the technique did not lend itself to identification of biovar. This demonstrates that bubonic plague spread in a dynamic broad epidemic form over large parts of Europe both in the first and second pandemic. It appears that Gilbert et al. are the only scholars in the field who have not succeeded in identifying DNA or proteins of Yersinia pestis in sites of plague burials. Is it true that this study is still valid in the face of so many and varied positive identifications by so many scholars from so many different academic institutions in so many countries? This puts in perspective the fact that Cohn in 2008 had only found more negative comments made by scholars associated with Gilbert et al., and claims to have found no new positive studies, i.e., finds of Yersinia pestis DNA in plague graves.35 He does however cite a study by Pusch et al. as supporting the negative stance of the rejecters,36 although they actually report positive findings of genetic material and proteins

35 In Cohn 2008: 100, footnote132, Cohn maintains that “Few have in fact, corroborated the findings of the Marseilles team; for the latest of these scientists’ results, see G. Aboudharam, M. Drancourt, O. Dutour, H. Martin, D. Raoult, and M. Signoli, “Validation de la saisonnalité des décés et authenticité biologique de la nature de l’épidémie,” in Bizot, et al. (eds.), op. cit., note 56 above, pp. 63–7 [= La Saison d’une peste].” This brief statement arguably contains five incorrect or misleading assertions: (1) it is not true that by 2008 “few have corroborated the findings of the Marseilles team, as can readily be seen from Table 6 (it would, nonetheless, have been useful if Cohn had specified the “few”; (2) that in 2008, the paper referred to by Aboudharam, Drancourt, Dutour, et al. 2005: 63–7, is the last which corroborates the findings of the “Marseilles team, as can be seen from Table 6, studies nos. 7–10, all published in the years 2005–07/8; (3) one must also add nos. 3–6 which Cohn has also overlooked; (4) this study cannot be said to corroborate earlier findings, since it does not include a new microbiological study of biological material taken from the cemetery at Lambesc, in this paper, the scholars present early research, microbiological techniques, and findings; (5) however, such microbiological studies performed on biological material taken from this cemetery are published in nos. 9 and 10 in Table 6. 36 Cohn 2008: 88–9, 100. He appears to suggest in fn. 122 that Aboudharam, Drancourt, Dutour et al. 2005: 63–7, have corroborated the DNA findings, this is not the case, since they have not made any attempt.

dna of yersinia pestis from plague graves

393

of Yersinia pestis in skeletal material from seventeenth-century Stuttgart (see above Table 6 and comments in footnote 28, no. 6). In a line of argument that at least comes close to the methodological fallacy of not fulfilling the principle of invalidatability, Cohn asserts in his monograph and paper of 2002 that the identification of Yersinia pestis in the two first studies cannot be correct because it is at variance with what he designates two “enigmas for biological evolution” based on central conclusions in his monograph, i.e.: “Why did a disease that once passed rapidly person-to-person become a rat disease dependent on a flea vector? Why did the human species once possess an ability to acquire immunity to this microbe and then lose it?” Cohn reiterates this stance in his paper of 2008.37 Although Cohn presents these purported enigmas as based on historical truth or fact established by his research, they are in my opinion due to combination of seriously flawed selections of material and misinterpretations which I believe have been brought to light in this monograph. The identification of the DNA of the ordinary biovar of bubonic plague in dental pulp from a plague grave in London dating back to the Black Death holds important implications. The spread of geographical locations of such finds were thus greatly expanded, roughly by 1000 km from south-eastern France to London in north-western Europe at 51° 30' North. Furthermore, the bubonic-plague contagion arrived in southern England from Bordeaux after having spread via Montpellier from the first French outbreak in Marseilles whence it arrived by ship from Kaffa in the Crimea via Messina or possibly via Constantinople. Thus, the contagion which reached England was in all likelihood the same that has been identified twice in Montpellier, Yersinia pestis Orientalis which in all likelihood must have been the original contagion which was shipped out of Kaffa with Italian galleys in the spring of 1347 and reached Marseilles at the latest in mid-September with subsequent epidemic outbreak around 1. November.38 The Black Death was spread from a port in south-eastern England (possibly London) to Oslo in south-eastern Norway late in 1348, and probably from King’s Lynn on the Wash (about 140 km north of London) to Bergen in western Norway with a(n identified) shipment of grain in the summer of 1349.

37 38

Cohn 2002a: 248–9; Cohn 2002b: 735–6: Cohn 2008: 88–9. Benedictow 2004: 72–3, 96–104, 123–37.

394

chapter ten

This makes it highly probable that the Black Death in Norway was also ordinary bubonic plague caused by the Yersinia pestis Orientalis. The Black Death spread from Norway into western Sweden and parts of Denmark in late 1349, and Denmark was also contaminated from northern Germany in 1350 but quite likely from the same original “source:”39 the Black Death was probably shipped from Oslo to Elbing/ Elblag in the south-eastern corner of the Baltic Sea in the early autumn of 1349 from whence it spread into Poland and northern Germany, northwards into the Baltic area and thence eastwards across Russia.40 This expands greatly the probable extent of the spread of the Black Death in the form of ordinary bubonic plague in the northerly and eastern parts of Europe and predicts similar identifications of Yersinia pestis Orientalis in biological material taken from putative plague graves relating to the Black Death in these parts of Europe. Considering the comprehensive evidence available after only ten years of paleomicrobiological research, there can hardly be any doubt that the three identified historical pandemics of plague were caused by Yersinia pestis, principally the Orientalis biovar/pathovar. This also constitutes independent defining evidence based on identification of the microbiological nature of the contagion. This means that the alternative microbiological theories can be considered invalidated on the basis of these paleomicrobiological studies on plague, according to usual criteria or tenets of methodology for invalidation. This means that the French paleomicrobiologists’ triumphant conclusion can be accepted: “Our results enabled us to resolve the long dispute over the aetiology of the Black Death by showing that the disease was in fact plague caused by Y. pestis.”41 These genetic studies also demonstrate, on the basis of an entirely independent platform, that Karlsson’s entirely speculative alternative theory from 1996 to the effect that the contagion of medieval plague was a mutant of Yersinia pestis which caused pure epidemics of primary

39 In English: Benedictow 2004: 146–78, 196–7, see also an earlier version in Benedictow 1993/1996: 75–94. The most detailed presentation and discussion of the arrival and spread of the Black Death in Norway are unfortunately or regrettably rather written in Norwegian, see Benedictow 2002: 44–57, 67–77; Benedictow 2006: 86–131, English summary pages. 161–2. 40 Benedictow 2004: see Map 1 between page xvi and I, and 161, 194–202, 209–15. 41 Drancourt and Raoult 2002: 105–09; Drancourt and Raoult 2008b: 153. Drancourt and Raoult 2008c: 182.

dna of yersinia pestis from plague graves

395

pneumonic plague can be discarded. The biovars of Yersinia pestis have now been genetically identified but no such mutant has been discovered in any of the samples, and Yersinia pestis orirentalis has proved to be the common pathovar of all three pandemics. Can it be accepted that all advocates of alternative microbiological theories have collectively failed to discover this development, especially since they must have known at least the two first genetic studies of this kind? Would it not be natural for serious scholars to look eagerly out for further developments and studies? Would it not be natural according to this material alone to take a strong renewed interest in how the alternative theories are argued, their material basis and use of the methodology of history and medical science? The triumph of the emerging new scientific discipline of paleomicrobiology is concordant with the triumph of another emerging scientific discipline, namely zoo-osteoarchaeology which, as shown above, by now has documented the broad existence of the black rat all over Europe, also Northern Europe and in the Nordic countries, in Sweden up to almost the 61st parallel and back to the Viking Period, in Norway almost up to the 63rd parallel and dating back to at least the early twelfth century (see above). Even if zoo-osteoarchaeology had not been established as a scientific discipline, the success of paleomicrobiology would have indicated that this was the case. Now, the triumphs of these two new scientific disciplines can be seen to be complementary and have a synergetic interrelationship or pattern of interaction which produce decisive evidence to the effect that historical plague epidemics were bubonic plague.42 Finally, the huge contribution these French paleomicrobiologists have made to historical science by the development of their techniques and to historical plague research by their very important findings must be emphasized.

42 A few years ago, Drancourt, Houhamdi, and Rault 2006: 234–41, presented a research project which could be misinterpreted as indicating that they considered the human flea a serious candidate as an important or the important vector of historical plague epidemics. As mentioned above, in a personal communication in an e-mail of 30 April 2009 Professor Michel Drancourt made it clear that this was not the case, and that any such notion had been abandoned, but that they still were looking into a possible role for the human louse. Drancourt, Houhamdi, and Rault 2006: 234–41. See above: 12, fn. 28.

CHAPTER ELEVEN

DEFINING FEATURE 5: SEASONALITY OF BUBONIC PLAGUE Introduction: Bubonic Plague’s Association with Moderately Warm Temperatures and Seasons Bubonic plague has a distinctive seasonal pattern. According to observations and studies performed in India and other developing countries with a more or less tropical climate, when humidity is reasonably favourable, favourable temperatures for plague epidemics are generally around 20 °C, while temperatures much above or below this range, generally above about 30 °C and below 10 °C, will weaken or suppress them. I have pointed out above that it is a fallacy of methodology to assume that these precise climatic limits apply in more northerly countries with the implication that bubonic plague is not possible in the north, since one must take into account the ability of rats and fleas to evolutionarily adapt to various climates and ecological niches.1 In the words of G. Lamb, Senior Member of the IPRC: “While plague can exist and spread under a great range of climatic conditions, it exhibits a marked seasonal prevalence, which is the most striking feature of the epidemiology of the disease.”2 Lamb considers the seasonality of bubonic plague in terms approaching the concept of defining feature; he also emphasizes that it can spread efficiently under “a great range of climatic variation.” This defining feature is mainly due to two central structural aspects of the epidemiology of bubonic plague springing from its basis in (black) rats and their fleas: (1) The natural mortality rate of fleas is high. Levels of temperature and humidity affect the reproduction of fleas, the rates of egg-laying and development of fertilized eggs, and the rates of survival and development of larvae and cocoons on the ground. This means that in adverse temperatures and conditions of humidity, the population of 1 2

See above: 116–22. Lamb 1908: 1, 85.

seasonality of bubonic plague

397

fleas will not be replenished by reproductive processes and their number will fall. This will affect the intensity with which a rat-flea population can transmit and disseminate plague and therefore the dynamics of the epidemic process. (2) Plague septicaemia in rats falls strongly at temperatures below 10 °C. Consequently, in chilly and cold circumstances rat fleas which draw blood from plague-diseased rats will become much less infected and will, therefore, develop blockage far more slowly and at much lower rates. Protraction of this process also implies higher death rates of fleas from other causes which will contribute to a corresponding reduction of infected fleas and the further weakening of the disseminative powers of the flea population.3 This means that the plague season will vary with temperature and humidity in various countries or within the same country if it covers two or more climate zones.4 In India and other countries with very warm summers bubonic plague epidemics will subside and disappear with the advent of the warm season. In India, for instance, epidemics normally attain their maximum severity in Bombay in October; in the Central Provinces in February; in the United Provinces and Bihar in March; and in the Punjab in April. In the remaining provinces, taken together, March is the month of maximum mortality.5

In Egypt, the plague seasons were March to May in Upper Egypt, April to June in Middle Egypt, April to July in the Nile Delta and Suez, and May to October in Mediterranean ports. In Peru, “as elsewhere the plague seasons fell into an earlier period in areas where the winter months were warm than in localities with a colder climate.”6 The same two basic factors also explain why historical plague epidemics in Europe are strongly associated with the warmer seasons and falter, subside or disappear with the advent of chilly autumn weather and cold winter weather. The use of words like “falter” and “subside” is not fortuitous. One should note that rat fleas are typical fur fleas (and not nest fleas),7 which means that they spend much of their adult lives 3 IPRC 1908c: 285–8; Lamb 1908: 88–90; Hirst 1953: 270–82, 340–5; Seal 1969: 288–9; Benedictow 1993/1996: 156–70, 227–64. 4 See, for instance, Pollitzer 1954: 20, 22, 24–5, 28, 33, 37, 43, 46, 48–50, 58, 60, 63, 65, 487–90. 5 Pollitzer 1954: 28, 487–90. 6 Pollitzer 1954: 33, 63. 7 IPRC 1908b: 245–6, 258; Liston 1924: 997; Pollitzer 1953: 321; Pollitzer and Meyer 1961: 461; Busvine 1976: 37.

398

chapter eleven

in the fur of their hosts, enjoying there a relatively warm microclimate even in chilly or cold weather and ample feeding opportunities. This explains why plague epidemics can produce cases in chilly or cold autumnal weather, although at a rapidly diminishing rate. The notion that plague epidemics stop abruptly with the advent of chilly or cold weather is erroneous. The notion of Shrewsbury (and some other scholars who have apparently picked up this notion from his monograph) that the usual flea of the black rat, Xenopsylla cheopis, hibernates in the winter is a misunderstanding. It is also a misunderstanding that it is a typical nest flea, although this is the case for most species of fleas.8 Consequently it is a double misunderstanding that this flea normally hibernates in the host’s nest.9 The same two basic factors explain also why historical plague epidemics tended to start earlier and to last longer in Southern Europe than in Northern Europe. Seasonality of Historical Bubonic-Plague Epidemics with Emphasis on the Transseasonal Form For the same basic two reasons, epidemics in the northerly parts of Europe will often not have taken their full course through the rat colonies when they are suppressed by cold weather. In many cases, plague contagion transported by rat fleas or (less often) by infected rats will arrive late in the plague season, often on merchant ships returning from abroad at the end of the sailing season, which will have the same effect. At the end of the plague season, there will therefore quite often remain a murine epidemic potential that can permit the epidemic to recrudesce with the advent of warmer spring weather (see below). As shown in my monograph on the Black Death, this pattern is very evident in the Black Death in central and northerly parts of Europe (see below).10 This alternative transseasonal pattern of bubonic plague associated with late arrival in the plague season, withdrawal with cold weather and recrudescence with warmer spring weather was also 8

Shrewsbury 1971: 3, 21, 62, 117; Scott and Duncan 2001: 26. It is another matter that when extra-mural rat colonies die out from plague, fleas from rats dying in the nest will be forced to stay in the nest, dependent on re-occupation by new rats for their survival. 10 See Benedictow 2004: 233–5, which contains a summary of these data and the page references in the index under “seasonality” (418). 9

seasonality of bubonic plague

399

studied in India at the beginning of the twentieth century, especially in the Punjab where this pattern was quite frequent: This recrudescence was not due to importation but apparently to an epizootic continuing below ground, progressing slowly during the off-season on account of a scarcity of fleas, or at least highly infective fleas, but quickening up with a return of conditions suitable for flea transmission.

The study of seventeen villages in the Pune (Poona) region roughly 100 km south-east of Mumbai revealed the following pattern: If infection of a village occurred early in the plague season the epidemic died out before the arrival of the off-season, but when a village was infected late in the season the disease was apt to linger through the offseason and to reappear the next season […] the important fact was established that all the 17 villages had been infected late in the preceding plague season.

On this background, a practical scheme was developed for “predicting the carrying over of epidemics, based upon (1) the size of the community and (2) the month in which it was primarily infected.”11 It is correct that bubonic plague in full epidemic form (in contrast to the endemic or sporadic occurrence) requires a certain minimum level of temperature in Europe and is dependent on the temperatures of the warmer seasons. But it is erroneous or fallacious, as has been emphasized several times, to assume that this level was exactly the same in Europe (and across Europe) as in India and to deny or ignore the possibility of evolutionary adaptation by natural selection of rats and fleas to various European biotopes or climatic zones. Also in the winter, the temperatures would in many areas in the southerly parts of Europe quite often allow a certain low-scale, lingering epidemic or endemic activity at least temporally, and this could also have overarching seasonal effects. One should also take into account the effects of oceanregulated and Gulf-Stream-affected coastal climates in western and north-western Europe that tend to produce relatively mild winters, which would no doubt dampen or restrain epidemic activities but not necessarily suppress them into an enzootic existence among rats or complete extinction. This is the case even along the coasts of Norway since the Gulf Stream raises average temperatures by 10 °C.12

11 12

Wu Lien-Teh 1936c: 397–9. See above: 139.

400

chapter eleven

With this background we may consider H. Dubois’s summary of the seasonal pattern of the Black Death in France: “Almost everywhere in France, the plague has taken on the bubonic form with secondary manifestations, and most often it has been inhibited or slowed down by the winter, staying away to re-emerge in the spring.”13 In Rheims, for instance, the Black Death arrived in the autumn of 1348, too late to develop an epidemic form, but after the disease had smouldered in the rat colonies during the winter the outbreak started in April at the latest, was raging in the summer and reached its “paroxysm” in August.14 Biraben generalizes this information from a historical perspective, pointing out that the epidemics of bubonic plague which dominate the scene in France “are arrested or diminished by the cold season.”15 Carmichael states: “Also characteristic was the season of the plague: throughout the fourteenth century, chroniclers reported a faithful May-to-September course of plague in each city epidemic.”16 In Northern Europe the plague took on a somewhat different but predictable version of this pattern. In my doctoral thesis I found no instance of a winter epidemic in late medieval Norway, and after having finished my history of Norwegian plague epidemics in 2002, ten years later, I could conclude that in the 300 years of Norwegian plague history, from the Black Death to the last epidemics in 1654, i.e., in the course of more than 30 (waves of) epidemics, there never was a case of a winter epidemic of plague.17 In his 2008 paper, Cohn maintains, nonetheless, that “the seasonality of the late medieval plagues does not resemble that of modern plague […] could occur at any time of year, including January in places as inhospitable to the subtropical rat flea […] as Norway.” He refers for support to my doctoral thesis and to Walløe 1982, the English translation of “199518 pp. 25 passim” maintaining that For the Black Death in Bergen, Norway, in January, see Ole Jørgen Benedictow, Plague in the Late Medieval Nordic Countries: Epidemiological Studies, Oslo, Middelalderforlaget, 1992, p. 44. For plague in Trondheim,

13

Dubois 1988: 316. My translation from French. Desportes 1977–2: 795–6. 15 Biraben 1975–1: 86. My translation from French. 16 Carmichael 1983: 514. 17 Benedictow 2002: 320. 18 Walløe mentions in the preface that it was mostly finished by 1977, Walløe 1995: 4. 14

seasonality of bubonic plague

401

Norway, that peaked in February 1566 and many other examples of winter outbreaks in Scandinavia, see Lars Walløe, Plague and Population: Norway 1350–750.19

Neither on page 44 in my doctoral thesis nor elsewhere in it, is it stated that the Black Death raged in Bergen in January 1350 simply because there is no evidential basis for it. The few dated or datable sources relating to the Black Death in Bergen are from September 1349, the earliest from briefly after 8 September and the last from 26 September. On page 44, the account in the Icelandic Lawman’s Annal is cited on the circumstances leading to the contamination of Bergen by a ship from England. In my Norwegian plague history, I have quite likely identified this ship together with the merchants from King’s Lynn who in early May, while the Black Death raged in the areas on the Wash, received royal permission to sail to Norway with 1000 quarters of grain,20 the most dangerous of all goods with respect to metastatic spread of rat-flea-borne plague. The time perspective fits nicely to a scenario where a ship sailing from King’s Lynn in the early summer of 1349 and putting into the harbour of Bergen in the first half of July with a cargo of grain infested with infective rat fleas which first unleashed a rat-epizootic. According to the usual development pattern of rat-flea-borne plague, it would produce an early epidemic phase among the human population about six weeks later and develop into a full-blown epidemic in September, when it would start to take its toll among the upper classes and scare them into making their wills. According to the mortality pattern of Table 7 showing the development of mortality in the plague epidemic in Bergen 1565–6, the Black Death would be expected to begin to diminish abruptly in November or perhaps in late October since it apparently arrived earlier in the season than the 1565–6 epidemic, and it would disappear around the turn of the year. Cohn refers also to Walløe 1995: 25 passim for support of the assertion that a plague epidemic peaked in Trondheim in February 1566. This assertion is also without basis in the text referred to. The historical source on plague in Trondheim on this occasion is a notice in the Diary of Absalon Pederssøn (Beyer),21 the highly regarded Norwegian humanist and ecclesiastic in Bergen, where it is stated in his entry for February 1566 that he had

19 20 21

Cohn 2008: 78 and 92, fn. 38. Benedictow 2004: 137–40, 149, 154–6. Absalon Pederssøn 1963. My translation of the title into English.

402

chapter eleven

received a letter from a priest in Trondheim informing him that “600 persons had died from plague in this town.” Walløe cites the source correctly, and there is no way it can be understood to the effect that the epidemic peaked in Trondheim in February or that it took the form of a winter epidemic.22 On the contrary, it is implied by the use of the past tense and by the rough estimate of the number of victims that the epidemic had been over in this small town for some unspecified time. Clearly, this indicates the normal seasonal pattern, the epidemic having broken in the early autumn, quite likely after importation from Bergen, and declined and disappeared with the arrival of cold weather. Moreover, during the plague epidemic in Bergen 1565–6, Absalon Pederssøn indicates in his diary the number of dead persons brought each day to the Cathedral in Bergen for burial in its function as a parish church. This information provides the opportunity to follow closely the development of the plague epidemic in detail, particularly as he specifies the few cases which were not caused by plague and because he provides increasing information on the number of plague victims being brought to the other three parish churches in the city. This information is summarized in Table 7 and Figure 2 below, which shows that the epidemic broke out in early September 1565, peaked predictably in November and then was rapidly diminishing until it disappeared, a pattern that was repeated the next autumn. The number of victims in February 1566 was only a small fraction of the number of victims in November. This seasonal pattern is, of course, inexplicable with respect to diseases spread by cross-infection and must almost inevitably reflect a disease transmitted and disseminated by insects on which chilly and cold weather have strong deleterious effects (above). Cohn’s further reference to “many other examples of winter outbreaks in Scandinavia” according to Walløe’s account is also not correct. Since Walløe mentions only Norwegian epidemics, this can be confirmed in my history of Norwegian plague where all epidemics are identified and all sources are presented and discussed extensively. In his Diary, Absalon Pederssøn provides information on the introduction of the contagion and the first cases which lends itself to epidemiological analysis and makes it possible to identify a period of latency which is a defining feature of ratflea-borne plague (see above).23

22 23

Benedictow 2002: 211–2. Benedictow 2002: 190–4. Above, Chapter 7.

seasonality of bubonic plague

403

In the period 1348–1599 plague was mainly imported into Norway from England, occasionally also from the Netherlands, probably from England:24 the microbiological basis would have to be the same. In Norway, the Black Death evidently arrived in Oslo in the autumn of 1348 with ship(s) returning from south-eastern England, was suppressed by cold weather, and broke out again in April, as it seems; a new introduction of plague from England took place in Bergen in the summer of 1349. From these two bridgeheads or epicentres the epidemic spread across Norway in 1349 and petered out and became extinguished at the end of the year with the advent of winter weather; there is no evidence of epidemic activity in the winter of 1350. Only one person is known to have died from the Black Death in Norway in 1350, namely the bishop of Stavanger who died 7 January, which confirms the seasonal pattern and the Black Death’s rapid disappearance with cold winter weather.25 In Sweden the Black Death was introduced into a few localities across the border in late 1349, from Halland (Denmark) whence the Black Death had presumably come by ship from Oslo to Halmstad, into Småland, from south-eastern Norway into Västergötland, and to Visby in Gotland Island in the Baltic Sea late in 1349 by a Hanseatic ship. In all three cases, the epidemic was suppressed by cold weather and broke out again in the spring to spread all over the country in 1350 from the bridgeheads in the west and disappeared at the end of that year. In Denmark, the Black Death was introduced in Halland in the summer whence it spread southwards along the coast to the cathedral city of Lund which it reached at the end of 1349, and was also introduced in the town of Ribe in the south-western corner of the country (Jutland) at the end of 1349. Also in these cases, the epidemic developments were arrested by cold winter weather and recrudesced with warmer spring weather, and from these bridgeheads spread all over Denmark in 1350, again to disappear with cold weather at the end of the year.26 This means that in the case of Oslo in Norway, and the points of introduction in Sweden and Denmark, the Black Death developed according to the transseasonal model or pattern. Probably in all these cases plague was introduced in Sweden and Denmark from Norway 24

Benedictow 2002: 103–8, 131, 139–43. Benedictow 2002: 47–82; Benedictow 2004: 149–58; Benedictow 2006: 86–123, 128–31. 26 Benedictow 2004: 159–78. 25

404

chapter eleven

which had received the contagion from England, and one should therefore expect that the disease was the same with the same basic epidemiological properties and that the seasonal pattern should be broadly similar when it is taken into account that England is situated south of Scandinavia and enjoys a milder Atlantic climate and the effects of the Gulf Stream. Predictably some subsequent plague epidemics took on this transseasonal form, being suppressed by chilly and cold weather but breaking out again in the spring, producing a bimodal curve of mortality showing two peaks. Some examples may be useful. At the end of August 1547 plague broke out in Oslo; around 20 September the epidemic had developed such a severe form that the commander of Akershus Castle in Oslo left the castle for his manor in a nearby island where he could isolate himself and his family. With the advent of cold(er) weather the plague declined and disappeared. However, 24 April the commander wrote to the Chancellor of the Realm Eske Bille that “the plague had broken out again and raged severely.”27 Importantly, this pattern does not manifest itself only in Northern Europe but also in the Alpine areas much further to the south where it is high altitude that makes for cold winter climate. Spreading northwards from its original epicentre in Venice, the Black Death crossed the Tyrolese Alps at the Brenner Pass in July 1348, reaching deep into Austria in some areas in the autumn of 1348, ravaging the inner mountain areas of the province of the Tyrol in September, and breaking out in areas west of Innsbruck, among other places. The distance from Innsbruck to the present-day German border is roughly twenty-five km which distance the disease should have been able to cover in (less than) a month. However, the Black Death did not advance further into the Alpine areas and did not break out in southern Germany until the following (late) spring. At lower altitudes the epidemic could continue its spread, although at a moderate pace: spreading westwards the Black Death reached Pfäfers about 200 km from the Brenner Pass in eastern present-day Switzerland in May 1349. Presumably the onset of cold winter weather is the reason that the Black Death did not proceed directly from its outbreak in November in Constance on the central Swiss-German border into Germany’s south-western province of Baden-Würtemberg. The Black Death was forced to postpone its

27

Benedictow 2002: 163–4.

seasonality of bubonic plague

405

invasion of south-western Germany from this advanced position until the arrival of spring brought warmer weather. Much the same appears to have happened with the Black Death’s spread out of the Swiss city of Basle on southern Germany’s south-western corner in the spring. Many German Hanseatic cities on the North Sea and the Baltic Sea were infected in the late autumn of 1349 with the return of the ships. However, except for a few recognized outbreaks that soon were suppressed by the advent of cold winter weather, it was not until the following spring that the Black Death broke out in force and formed a northern plague front spreading southwards which met the southern plague front which was moving northwards somewhere in central Germany.28 Thus, clearly the transseasonal pattern was an important feature of the Black Death in Austria, Switzerland and Germany. Since the plague contagion of the Black Death was introduced into England from France where, as underlined by Dubois and Biraben, the transseasonal form of the epidemic was usual, it is difficult to imagine why the Black Death should not tend to take on the same pattern in England when differences in climate are taken into account. Twigg takes another view: “high mortality in late spring and early summer would not be typical of bubonic plague and illustrates the point that the disease produced heavy loss of life when it first made contact in a new area, no matter what time of year that was.”29 This means that he has overlooked or ignored the transseasonal form of plague. Twigg uses as evidential support the sequence of plague events at the manor of Fingrith in south-western Essex where the outbreak manifested itself in an abrupt increase in the registered deaths among the tenants at the court of 23 March and raged during the following months.30 Interpretation of the events at this manor requires a much broader perspective. The Black Death broke out in London at the end of September and had by the end of 1348 broken out in various localities along the south-eastern coast up to the R. Stour, the border river between Essex and Suffolk/ East Anglia. Since Fingrith is situated only about twenty-five km from London, it appears quite likely that the manor was infected from London some time in the late autumn of 1348, and that the epidemic processes had been suppressed by cold weather but re-emerged with the advent of mild spring weather, according to a usual pattern of bubonic plague. 28 29 30

Benedictow 2004: 120, 181–2, 186–7, 194–201. Twigg 1984: 69. Fisher 1943: 13–4, 19–20.

406

chapter eleven

Table 7. Plague in Bergen 1565–6. Mortality in the Cathedral’s parish Year

Month

Deaths

1565

September October November December January February March April May June July August September October November December January

33 66 113 66 27 14 7 0 1 2 0 70 229 133 35 4 0

1566

1567

Schofield comments sensibly on such matters in his study of plague in Colyton in 1645–6 where plague first struck in the autumn but was soon wholly or mainly suppressed by cold autumn and winter weather, so that the level of mortality was quite modest until late spring or the early summer, when the plague epidemic took on a dramatic character. Schofield points out that there are “few examples of plague persisting as a human epidemic through the inhospitable north European winter months.” The ability of plague to carry episodically on through adverse climatic circumstances reflects that “the micro-climates of rodents’ habitats continue to provide favourable conditions regardless of seasonal changes outside,” which was, as shown above, also true for black rats in the Nordic countries. One should in this context keep in mind that the black rat’s fleas are fur fleas riding in the fur of their hosts, there enjoying a relatively warm micro-climate even in cold weather and easy access to nutriment, and that the black rat with its fondness for human habitats, including the housing of domestic farm animals

seasonality of bubonic plague

407

(where maids or farm-hands often slept), would tend to live in considerably higher temperatures than prevailed outside during Nordic winters. It is the reproduction of fleas that is seriously affected by chilly or cold weather and, thus, the size of the flea population and its collective vector capacity and also the level of septicaemia in rats (see above). Another point is that “if the winter were warm and wet, the persistence of plague through an English winter must be entertained as a serious possibility.”31 Thus, the view that Twigg and Scott and Duncan present as an absolute truth, that plague epidemics could never take place in the winters in England, is not warranted, and does not constitute proof that these epidemics could not have been bubonic plague. Episodically, higher temperatures and other circumstances could allow plague epidemics to continue through the mild English winter months, albeit at a relatively low level of intensity. Schofield emphasizes that the transseasonal pattern (without using the term) with bimodal mortality curve is typical of plague, referring to a number of later outbreaks of bubonic plague epidemics in England and Sweden as evidence.32 A beautiful instance of an epidemic with this transseasonal form is provided by Shrewsbury, namely the epidemic at Colchester 1665–6.33 This pattern is, of course, inexplicable for diseases spread by cross-infection, but easily explicable for rat-fleabased epidemics of bubonic plague. Other aspects of the seasonality of the Black Death in England will be discussed at quite some length below. The information Absalon Pederssøn gives on a daily basis in his diary on the number of dead persons brought to the Cathedral in the plague epidemic 1565–6 indicates an interesting alternative, the twoseasonal plague epidemic. In Table 7 and Figure 2 the development of mortality in the Cathedral’s parish is organized according to month and shows a very distinctive seasonal pattern. The surge in mortality was clearly checked by chilly autumn weather followed by moderately wintry weather typical of this south-western coastal town on the North Sea, which first produced a rapid fall which developed into a slower final phase of decline ending in no plague cases in April and insignificant or no plague mortality the following months. However, the plague 31 32 33

Schofield 1977: 101 and footnotes 33–4. Schofield 1977: 101. Shrewsbury 1971: 499–501.

408

chapter eleven 250 200

1565

1566

1567

150 100 50

Se pt

em b O er ct N ob ov er em b D ec er em b Ja er nu Fe ary br ua M ry ar ch A pr il M ay Ju ne Ju A ly Se ugu pt st em b O er ct o N ov b er em D be ec em r b Ja er nu ar y

0

Figure 2. Plague in Bergen 1565–6. Mortality in the cathedral’s parish.

broke dramatically out again in August and developed explosively until chilly autumn weather and increasingly wintry weather again caused a rapid decline; in December only four cases of plague mortality were registered, in January there was no case and the epidemic was finally over. Late autumn and wintry temperatures hit at the heart of the epidemic’s dynamic powers and set it on a more or less rapidly declining course that reflected the degree of chilliness or coldness of prevailing temperatures, in both cases ending with the complete disappearance of plague cases. The long interval of four months (April to July) with no cases or with one or two cases respectively, and no case in July at the height of warm summer temperatures, is conspicuous and indicates that the epidemic was extinguished by the winter weather of 1566 without having exhausted the murine epidemic potential and that the outbreak in August 1566 was due to re-importation. The epidemic clearly took up its course where it had ended and died out in the same order as it had broken out in the parishes. The two-seasonal pattern based on re-introduction draws support from the fact that there was one plague death in August and one in October 1567, eight to nine months after the last plague death in December 1566. These cases must also reflect independent re-introduction, however, at a time when the murine basis was exhausted in a city of 5000–6000 inhabitants,34 but suggest that in big urban centres a multi-seasonal pattern could occur.

34

Benedictow 2002: 197.

seasonality of bubonic plague

409

These epidemic case histories illustrate the deleterious effects of chilly and cold weather on plague epidemics: cold weather could either lead to the extinction of the epidemic or diminish it to the point that it would go underground and disappear from the human scene, smouldering in the rat colonies in a process that could be revealed by the occasional case. In order to understand the developments more fully, one should take into account the fact that there would be a delay of a couple of weeks from when chilly weather sets in and when the negative effects on the reproduction of fleas and the reduction in the levels of septicaemia in rats would start to affect the development of the epidemic, since the number of heavily infected and infective fleas will not fall instantaneously but in a gradual process. This characteristic temperature-dependent feature of plague epidemics was recognized by contemporaries. In November 1545, the Danish Chancellor of the Exchequer Joakim Beck wrote from Roskilde, Zealand Island’s cathedral city situated about thirty km north of Copenhagen, to the soon-to-be Chancellor of the Realm Eske Bille: “I will not advise you to go to Copenhagen before it begins to freeze and the plague stops to reign there in the city. I intend to pass the waiting time here in Roskilde.”35 In 1641, a Londoner claimed that a proposed day for religious humiliation to ward off plague was unnecessary, because “winter was coming on, and then the plague would be stayed.”36 The peculiar pattern of seasonality in historical plague epidemics can, as shown above, be explained by the properties of rats and rat fleas and their roles or functions when contaminated by plague contagion. All alternative theories of the microbiological nature of historical plague epidemics which cannot on empirical grounds explain why the mechanisms of transmission and dissemination would produce such a seasonal pattern and be compatible with this feature are ipso facto falsified. The central argument of this chapter has three main parts: (1) this seasonal pattern can only be explained by the epidemiological properties of rat-flea-borne bubonic plague; (2) this seasonal pattern is incompatible with diseases spread by crossinfection; and (3) none of the alternative theories can explain this pattern. 35 36

Benedictow 2002: 40. My translation from the source into English. Slack 1985: 239.

410

chapter eleven

The plague epidemics at Penrith in 1597–8 and Eyam in 1665–6, which both display a transseasonal pattern, are incompatible with any viral theory based on interhuman transmission, but are easily compatible with bubonic plague. Scott and Duncan’s discussion of these epidemics is peculiarly strained and untenable.37 Eyam has been studied by L. Bradley and M.P. Coleman on the basis of demographic parish reconstitution techniques and the disease has been shown by both scholars to be compatible with bubonic plague, including with respect to the seasonal pattern,38 a fact which is conspicuously difficult to discern in Scott and Duncan’s discussion of it. This seasonal pattern is incompatible with all epidemic diseases spreading by cross-infection because it does not comply with the central principle of epidemiology which is formulated so well by Burnet (and White)39: “no matter by what method a parasite passes from host to host, an increased density of the susceptible population will facilitate its spread from infected to uninfected individuals.” All infectious diseases spread by cross-infection flourish in chilly and cold weather: they gain strength from people’s intuitive and practical reactions which are to stay or huddle closer together, remain indoors more and restrict living space for better and more efficient heating. The net effect is to bring people closer together, in other words to increase population density at the micro-level of human behaviour, which means that all interpersonally communicable diseases will gain increasing powers of spread. By implication, all alternative theories based on assumptions that historical plague was spread by cross-infection must be untenable, namely the theories of Morris and Karlsson, Scott and Duncan and Cohn. This seasonal pattern is a defining feature of bubonic plague. How do the advocates of alternative theories address the compelling evidence on plague seasonality and defend their theories against its potentially devastating effects? They employ three strategies: (1) they attempt to reject the evidence of seasonality; (2) they argue that seasonality did not apply to their alternative infection for some special reason; (3) they argue that the Black Death did not exhibit seasonality, though subsequent plague epidemics did, but that the Black Death and 37 Scott and Duncan 2001: 114–48 (Penrith), 261–83 (Eyam); Scott and Duncan 2004: 5–8, 153–62 (Penrith), 191–206, 212–3 (Eyam). 38 Bradley 1977a; Coleman 1986. 39 Revised edn. of 1972.

seasonality of bubonic plague

411

subsequent epidemics were, nonetheless, the same disease, and that the pattern of the Black Death proves that historical plague epidemics were not bubonic plague. Although anthrax is not generally, or is only sporadically, transmitted by cross-infection between human beings, Twigg realizes the inherent danger to his theory posed by the question of compatibility with plague seasonality and presents some peculiar arguments which later are picked up by Scott and Duncan, while Cohn relies mainly on his own line of arguments and again more or less confines his attention to northern Italy and Italian chroniclers. Twigg’s first climatic argument against the possibility that the Black Death was bubonic plague is that the epidemic, he asserts, moved (freely) across the Alps into southern Germany in the winter of 1348–9, and Davis and Scott and Duncan pick up the argument in closely related wordings.40 As shown above, this is wrong. Twigg also launched the argument that the Black Death ravaged Greenland, which would, of course, have been a good argument if it were not fictitious.41 Since Greenland is not mentioned in Twigg’s index, the whole monograph must be read carefully in order to discover the argument and reveal its true character. Cohn starts his discussion of the seasonality of plague by citing Burnet’s prestigious monograph Natural History of Infectious Disease (3rd. ed.) to the effect that diseases of the past must be studied not only according to clinical indications but also according to their epidemiology. Of course, the seasonality of epidemic diseases is part of their epidemiology. However, Cohn passes again in silence by Burnet’s presentation of the central principle of epidemiology, the link between increasing density of (susceptible) population and the powers of spread of infectious diseases disseminated by cross-infection, whatever the means or mechanisms of transmission. The reason for Cohn’s neglect of this principle seems obvious: it would immediately reveal the untenability of his alternative theory based on a viral disease spread by crossinfection which would inevitably present itself as a disease thriving in cold weather when people stay closer together and the density of people is higher. All alternative theories on the microbiological and epidemiological nature of historical plague must satisfy the criterion of a

40 41

Twigg 1984: 57; Davis 1986: 460; Scott and Duncan 2001: 87. Above: 98–9.

412

chapter eleven

disease strongly associated with the warmer seasons and exhibit weak properties for spreading in chilly and cold weather. Cohn’s approach also to this matter of seasonality is characterized by his neglect of the work of historical demographers with their demand for quantifiable source material in order to secure a high level of empirical tenability. Instead, Cohn considers that the sources suited for the study of the seasonality of historical plague are chronicles, which however are characterized by their inaccuracy and subjectivity, especially in the relatively narrow perspective of Italian chronicles. However, plague’s typical association with the warmer seasons is a very conspicuous feature even of Cohn’s material and cannot simply be explained away: a summary of his citations of various chroniclers will show a very heavy preponderance of references to the warmer seasons.42 It is not correct that “a reading of the chronicles might suggest that the medieval bubonic plague had no season and could strike at any time.”43 The distribution of seasonal identifications of plague epidemics by chroniclers relates overwhelmingly to the warmer seasons. As underlined above, in Southern Europe weather conditions may occasionally allow plague in epidemic form in the winter, albeit at quite a low level of intensity. Sporadic outbreaks in chilly weather or winter months, which can reflect mild weather for the season, cannot override the fact that in the overwhelming number of cases historical plague epidemics are associated with the warmer seasons. It is erroneous not to take into account the fact that bubonic plague can arrive in the late autumn or winter with contaminated goods or luggage, progress slowly among the rats and produce sporadic human cases for some time, and with the advent of warmer spring temperatures develop into a serious epidemic form that would impress chroniclers. Also in the case of Italy, the results of studies on the seasonality of plague by historical demographers are very clear, but since Cohn has succeeded in avoiding all of them, some central findings shall be presented here. Herlihy and Klapisch-Zuber provide very strong material on the seasonality of plague in Tuscany. For the period 1251–1500 they succeeded in individualizing according to month the deaths of 939 persons who died in plague years and 1614 persons who died in plaguefree years. They found that 85.6 per cent of all deaths in plague years

42 43

Cohn 2002: 140–87, 209–10. Cohn 2002: 140.

seasonality of bubonic plague

413

occurred in the six months April to September, whilst 54 per cent of all deaths took place in these six months in plague-free years, near the normal distribution. They were also able to distinguish the cause of death for 4711 persons in the period 1424–30. Among these 4711 persons 3296 or 70 per cent died from plague, and among those who died from plague 3091 or 93.8 per cent died in the six months May to October.44 This reveals that 5.85 per cent of plague mortality in this southern European city occurred in the months January to March and almost the same percentage in the months November and December. In Southern Europe, plague cases can occur in any month, but the overwhelming majority take place in the warmer months or seasons. In fact, with the arrival of the Black Death and subsequent plague epidemics in the period 1348–75 nearly a quarter of all Florentine deaths took place in July, which contrasts sharply with the preceding period 1276–1347 when 9.4 per cent of all deaths took place in this month.45 Herlihy and Klapisch-Zuber conclude: “The concentration of the deaths in the summer months corresponds well to the description which contemporaries make on the great plague epidemics,” and go on to cite Giovanni Morelli, the chronicler, who writes that plague “begins to make itself felt in February and goes on to grow until it peaks in July […].”46 This seasonal pattern corresponds quite closely to that of the Black Death in Tuscany where the outbreaks were noted in Pisa in January, in Lucca in February, and in March in Florence where according to Matteo Villani the disease developed rapidly from April reaching its peak in the summer and lasting until the end of September.47 This pattern is strongly reflected in the dates at which many wills were written, if we take into account the usual delay between the outbreak and the time the will-producing social classes feel threatened.48 Del Panta provides other instances of transseasonal plague epidemics in Italy, in Mantua 1575–6, in many localities in Tuscany 1630–1, and in Genoa 1656–7. In all three cases, the original outbreaks were quite late in the autumn, in October, and seemingly disappeared with the arrival of winter weather, but recrudesced in the spring.49 In Rome,

44 45 46 47 48 49

Herlihy and Klapisch-Zuber 1978: 192, 465. Herlihy and Klapich-Zuber 1978: 193–4. Herlihy and Klpaisch-Zuber 1978: 192. My translation from French. Matteo Villani Cronica 1995–1: 13; Falsini 1972: 432–3; Benedictow 2004: 93–5. See Cohn 2002: 158. Cf. 150–71, 178–84. See above: 401; below: 431. Del Panta 1980: 50–1, 53–4.

414

chapter eleven

where the epidemic of 1656–7 broke out in July, the epidemic completed its course in the plague season, albeit with the peak skewed towards the autumn months, indicating that if the contamination of the city and the subsequent outbreak had been a little later, the epidemic process would not have been completed in the warmer seasons and could have taken on the transseasonal form. Del Panta also points out the association of bubonic plague with warmer seasons and underlines its connection with the role of rat fleas,50 the only viable explanation. This helps to explain why Cohn, who relies so heavily on Italian material, especially chroniclers and wills, passes in silence by this standard work by a leading Italian historical demographer. Whatever chroniclers wrote, the hard demographic statistical data speak loudly to the effect that a new disease had arrived in Italy that dramatically changed the usual seasonal pattern of mortality and produced a heavy preponderance of mortality in the summer months and adjacent relatively warm spring and autumn months. Only bubonic plague is characterized by this seasonal pattern of mortality and only in the case of bubonic plague can this pattern be epidemiologically explained. Importantly, Herlihy and Klapisch-Zuber and Del Panta have made both their data and their conclusions testable by other scholars. Italian chroniclers can be shown to provide valuable information on the matter: they overwhelmingly relate plague epidemics to the warm(er) seasons. Cohn’s citations of various types of statistics regarding wills and mortality in the form of figures associated with various hospitals and a couple of burial grounds of ecclesiastical institutions in the period 1348–1400, mostly in Italy but also in other regions, overwhelmingly show plague’s association with warm(er) months and seasons.51 Much of Cohn’s presentation of this material deserves serious criticism, but since he cannot get away from the pivotal point, historical plague epidemics’ close association with the warmer seasons or months, this can be dispensed with. There is much more severe criticism to come. However, seasonality is a material feature of epidemiology. Cohn starts his chapter on seasonality by citing Burnet to the effect that historical epidemic diseases must be studied according to their epidemiology, but in the presentation and discussion of his material he ignores this

50 51

Del Panta 1980: 48–9. Cohn 2002: 156–9, 161–73, 181–5.

seasonality of bubonic plague

415

crucial point. Instead, he attempts to explain away the strong seasonality of plague epidemics with some rather peculiar arguments on fleas and climate that he maintains prove that this seasonality, nonetheless, was not an epidemiological reflection of the central role of rats and their fleas.52 Cohn makes extraordinary comments on some of the developments of plague seasonality in England, and claims that there should be peaks in the late autumn and criticizes Slack and Schofield for maintaining the established view of plague seasonality.53 As underlined repeatedly above, the peaks of plague epidemics are affected by the time of arrival in the plague season, and especially under favourable climatic circumstances late arrivals would make for late peaks. A couple of late autumnal peaks in Bristol in the sixteenth century do not constitute a change of pattern, and Slack and Schofield, who know that plague epidemics in England continued to be overwhelmingly associated with the warmer seasons according to a long established systematic pattern, have no reason to change their views on the matter. There will be occasion to present much of this material below. Cohn tries to undermine the rat-flea theory when he asserts in the concluding pages of his monograph that plague epidemics in the Mediterranean regions strike consistently “during the hottest and driest months of the year” but “north of the Alps” broke out “in the cooler and wetter autumn.”54 This is not correct: all over Europe plague epidemics were associated with the warmer months or seasons. The point is simply that since warmer weather develops later north of the Alps, plague epidemics there will tend to rise later and not complete their spread in the rat colonies before later in the autumn, a pattern that is, of course, easily explicable on the basis of the rat-flea theory of plague. Cohn naturally does not make the point that this epidemiological pattern of seasonality which is so easily compatible with the rat-flea theory of bubonic plague is incompatible with his theory of a viral disease spread by interhuman cross-infection. Scott and Duncan enlarge on Twigg’s false arguments that the Black Death crossed the Alps into Southern Germany in the winter of 1348–9 and his statements about plague in Greenland. They assert that this “pandemic [the Black Death: my insertion] even reached the polar 52 53 54

Cohn 2002: 175–8. Cohn 2002: 185. Cohn 2002: 251.

416

chapter eleven

regions,” reiterating six times that also Greenland and Iceland were invaded by the Black Death and claim that this constitutes proof that the epidemic could not have been bubonic plague: “It is inconceivable that bubonic plague could have spread rapidly in winter, over alpine passes and through sub-Arctic regions including Iceland, Norway and Greenland.”55 The fact that I have written a monograph on plague in the Nordic countries in the Late Middle Ages is ignored. The juxtaposition and implied identity of the concepts “polar regions” and “sub-Arctic regions” are quite extraordinary: according to dictionaries the term polar means “of or near the North or South Pole,” hence “the polar regions.”56 No scholars other than Scott and Duncan have asserted that there ever was a bubonic plague epidemic on or near any of the poles, for obvious demographic reasons. As shown above, the Black Death never came to Greenland or Iceland, there is no factual basis for this assertion, it has been taken out of thin air. And as shown below, the two purported plague epidemics in Iceland in the fifteenth century cannot for several independent sufficient reasons have been plague. In short there never was an epidemic of plague in Iceland, neither bubonic plague nor primary pneumonic plague. Scott and Duncan also accept uncritically Twigg’s assertion that the climate in Northern Europe was too cold to allow fleas to breed and that for this reason there could not have been plague epidemics in England, Scotland or Norway. This contrasts sharply with the brief opening statement of the IPRC in a chapter on the “Distribution of Fleas, Geographically and on Animals”: “Fleas are found in all climates from the arctic regions to the tropical zones.”57 Scott and Duncan also add unreservedly as an objective fact: “It is important to remember that during the Little Ice Age, when the plague was rampaging most fiercely, the conditions would have ensured that flea breeding was absolutely impossible.”58 Obviously if flea-breeding was impossible in Northern Europe there could not have been any fleas there or bubonic plague. One may wonder how it could be that medieval and early modern Scandinavians, obviously inhabitants of Northern Europe were plagued by fleas in the period covered by the misnomer “the Little Ice Age” (see below). Colloquially, with an element of black humour, old-time 55 56 57 58

Scott and Duncan 2001: 57, 81, 98, 108, 109, 357, 376. Oxford Advanced Learners Dictionary 1990: 957. IPRC 1908b: 245. Scott and Duncan 2004: 178–9.

seasonality of bubonic plague

417

Norwegians called their beds “fleaboxes,” so as the English “hit the hay,” old-time Norwegians hit the “fleabox.” And how can it be that in the Nordic countries many types of wild animals and birds are plagued by fleas, although they do not live indoors in heated rooms but have to endure the cold winter climate in nests and lairs in the “woods so wild”? A shown above, this was also the case with rats, and the black rat was the only rat in the Nordic countries in the Middle Ages. The modern grey or brown rat, which was first described in the Nordic countries in Norway around 1750 (which is the reason it is called Rattus norvegicus), have substantial numbers of fleas in their nests in the Nordic countries. Scott and Duncan’s concept of the Little Ice Age is an exaggerated version of a misnomer. In the period ca. 1540–1830, there was indeed a slight fall in average temperatures in Europe, however, the tiny significance of this development is demonstrated by the fact that the first hundred years of this period saw the taking up of all lands all over Europe that had become deserted in the late medieval period and the recuperation of European populations after the precipitous decline of that period.59 In the period c. 1520–1666, the number of agricultural holdings in operation in such a northerly country as Norway increased from c. 23,500 to 58,000; in addition many thousands of new undersettlers/ sub-tenancies were established within their territories, and the number of both holdings and undersettlers continued to expand all through the so-called Little Ice Age: even the deserted mountain settlements were resettled and expanded. And this development took place even in northern Norway. In a broader European perspective, this subject should certainly be discussed in relation to E. Le Roy Ladurie’s sober works on the interaction of historical climate and historical change with emphasis on the period in question.60 The implication that Norway is situated in the “polar regions,” whatever the meaning of this term, even in the implied highly unconventional meaning of sub-Arctic, must be taken as an expression of great geographical and conceptual confusion. Norway is not situated in a sub-Arctic region, this is only the case for the northernmost parts of Norway containing only a tiny part of the Norwegian population; in 59 The exception is England, but this was not due to climate but to profound demographic changes. Hatcher 2003. 60 Le Roy Ladurie 1965: 899–922; Le Roy Ladurie 1967. Le Roy Ladurie 1974: 3–30.

418

chapter eleven

the Middle Ages this proportion was even smaller than it is today. It is an expression of great geographical and conceptual confusion also because the term is climatically and biologically determined and not mechanically associated with latitude.61 One should note that the Gulf Stream produces a climate in Norway with average temperatures about 10 °C. higher than would otherwise be the case.62 Central Norway (Trøndelag), situated roughly at latitudes 63–65°, corresponding to the southern half of Iceland and the region around Godthåb about 500 km north of the southern tip of Greenland, is a rich agricultural area producing, among other things, large amounts of Norway’s grain, vegetables and strawberries. In the Middle Ages Norway was generally self-sufficient in grain, and the central region of Trøndelag produced a surplus which was sold in the adjacent eastern county of Jemtland, in the western coastal areas of Namdalen and Fosen, and to some extent in southern parts of northern Norway.63 The situation was entirely different in Greenland or Iceland, in fact, early attempts at growing grain in those regions were rapidly given up. Only the tiny fishing population in villages along the coasts of northern Norway was largely dependent on importation of grain from abroad, exchanging stockfish for grain with Hanseatic merchants in Bergen. These fishing villages were mainly established on this economic basis, and at the time of the Black Death this development was in an early phase. Unfortunately, the fishers and fisher-peasants

61 It is also highly surprising that Norway should be thought to be part of sub-Arctic regions in the ordinary scholarly meaning of a border zone between the Arctic regions and the temperate climatic regions. Assuming that the point relates to the part of Norway situated north of the Arctic Circle and the population living there at the time of the Black Death, the following remarks will be relevant: this population consisted mainly of an ethnic Norwegian population living up to or quite near to the border of the most northerly county of Finnmark, on about 2400 individual agricultural settlements (subsisting mainly on a combination of animal husbandry and fishing) comprising a population of about 11,000 persons, and in addition those living in the few fishing villages in operation at the time. At the time, Finnmark was mainly inhabited by Saami people, nomadic hunter-gatherers numbering perhaps a couple of thousand persons (at the most). In all, the part of Norway situated north of the Arctic Circle contained some 14,000–16,000 persons or about 4–4.5 per cent of the national population. Thus this line of argument is untenable. See Sandnes, 1968: 289; Benedictow 1996b: 179–81; Benedictow 1996c: 155–6, 179–81; Benedictow 2003: 245, 248–9; Benedictow 2004: 147–8, fns. 5–6; Benedictow 2006: 125–7, 131–57, contains a new thorough discussion of the size and composition of the Norwegian population at the time of the Black Death, confirming, supporting and supplementing previous conclusions. 62 Eldevik 2006: 48. 63 Sandnes 1971: 69–70; Benedictow 2002: 161.

seasonality of bubonic plague

419

who sailed to Bergen in the spring with their stockfish returned with grain that could be contaminated with dangerous rat fleas, or Norwegian traders could bring contaminated Norwegian grain with them from Bergen or Trondheim. A few later outbreaks of plague in northern Norway are mentioned in the sources. The parson in Rødøy, a parish situated just north of the Arctic Circle, provides in his chronicle-like notes information on outbreaks of plague in Bergen and the devastating spread to Trondheim and northern Norway in 1599–1600 and 1618. In 1618, he specified the areas ravaged by plague in northern Norway as the contemporary bailiwicks of “Helgeland, Salten, Lofoten, etc.,” comprising most of the present-day county of Nordland; only the northernmost bailiwick of Andenes is not mentioned.64 The northern part of the bailiwick of Helgeland, where the parson’s parish of Rødøy is situated, and also Salten and Lofoten are situated north of the Arctic Circle. Since skeletal remains of black rats have been found in Trondheim (see above), and the climate in the inland city of Trondheim is considerably colder in the late autumn, winter and early spring than the coastal areas around the Arctic circle, there is no reason why the black rat should not have spread much earlier in sacks or barrels of grain or flour to northern Norway in fishing boats or in ships belonging to Norwegian traders from Bergen and Trondheim, and why black rats should not have thrived there and provided a basis for epidemics of bubonic plague. Some of the observations of the IPRC may here be usefully recalled: We would, however, like to draw attention to the ease with which rats with their fleas can be transported in certain kinds of merchandise. We have seen rats dive, as it were, into bags containing bran and disappear, so that the bags could be moved without any evidence of the presence of the rats within. M. rattus [= Rattus rattus, the black rat] from its habits is particularly liable to be transported in this way […]. From what has been said above it will be apparent that merchandise and grain, which have been visited by rats, may have fleas deposited on them and these fleas may be transferred with these articles to distant places.65

These are important points that should be kept in mind. Twigg’s and Scott and Duncan’s assertions on climate are arguably not the result of serious scholarly work. 64 65

Benedictow 2002: 234, 240–3, 258–60. IPRC 1908b: 254–5. Above: 105, 160.

420

chapter eleven The Seasonality of Plague and Mortality in England 1340–1666

Both Twigg and Scott and Duncan maintain that the Black Death spread in the south-western counties or dioceses of England in the winter months and that this constitutes proof that the Black Death could not have been bubonic plague. The Black Death was introduced into Norway from England and to the other Scandinavian countries probably mostly from Norway. It has been shown that the Black Death in these countries was temperature dependent, spreading only in warmer seasons and disappearing with cold winter weather. In Norway, it has been shown that there was never a winter epidemic of plague in the country’s whole plague history of over 300 years. It has been shown above that this was also the case with the Black Death all over Europe.66 In view of these facts, one should expect that the Black Death’s seasonal pattern in England was similar. Since Shrewsbury and especially Twigg and Scott and Duncan play such a central part in this discussion, English evidence tends to play a central and even disproportionate role. However, in defence of their theories Twigg and Scott and Duncan focus only on small and selected parts of the seasonal history of the Black Death’s spread in England and base their arguments on sources which are highly problematic for inference to the reality of these matters, as will be seen below. It is therefore important to construct a rather complete overview of the status of English research on the seasonal pattern of historical plague epidemics in England throughout the whole plague period of over 300 years and apply source-criticism in quantum satis (sufficient quantity). An overview which is complete for all practical purposes will provide the strongest possible basis for identification of the seasonal pattern of plague and for inference to the causal nexus underlying the particular form of correlation of plague epidemics and climate, i.e. their seasonality. Only a qualitatively secured and, for all practical purposes, complete overview can provide a holistic perspective and framework within which their arguments can be satisfactorily considered. A methodological and source-critical point that may appear selfevidently true must be stated for reasons that soon will be clear: only empirical evidence consisting of generally accurate identifications of 66 There may have been a case of a mixed epidemic of bubonic and primary pneumonic plague which spread also in the winter in the pneumonic mode, or just possible two cases. Benedictow 2004: 236–41.

seasonality of bubonic plague

421

day of death or burial of a sufficiently large sample of persons dead from plague can provide reliable information on the seasonality of plague, providing that the registration is seasonally independent. The reliability of information will decrease (1) with increasing temporal distance or uncertainty as to the time of death of plague victims and the registration of their demise, it will also decrease (2) as the number of persons included in the sample diminishes, and it will (3) lose its evidential power if the number falls under a critical minimum level. The arrival of the Black Death and subsequent plague epidemics caused a dramatic transformation of the seasonal distribution of mortality in England throughout the Late Middle Ages and well into the Early Modern Period, that is, for the duration of the plague period. Russell produced data on the seasonality of the time of death of tenants-in-chief, the noble class that held feudal land directly from the king, in the period 1340–1450 and 1476–1500.67 The high social class of the subject of Russell’s work will exclude direct influence from hunger, malnutrition or undernutrition associated with bad harvests which among the poorer classes would tend to cause increased mortality in the summer and early autumn of the following year as reserves of foodstuffs were being depleted and unavailable at affordable prices in the market. Since tenants-in-chief had large households and an active social pattern of behaviour, they would tend to be exposed to contagious diseases as much as or perhaps more than the average population without having normal consumption patterns of foodstuffs that would significantly increase resistance to disease. This material will therefore reflect more clearly the seasonal distribution of mortality caused by epidemic disease and be reasonably representative in this respect also for the general population. Tenants-in-chief lived at their manors or estates around the country, and thus the material is probably geographically well distributed. Assuming that historical plague was bubonic plague, this representativeness is negatively affected by the fact that tenants-in-chief tended to live in stone buildings which were less amenable to rats than ordinary housing at the time, and this fact would presumably tend to reduce this disease’s impact on this social class relative to peasants and burghers who lived in far more unfavourable dwellings in this respect. In principle, the representativeness would tend to deteriorate to the extent that the incidence and demographic

67

Russell 1948: 195–9.

422

chapter eleven

impact of plague epidemics became relatively more urban, a development that did not, however, become pronounced until about the mid1550s, and therefore does not affect Russell’s data here. As can be seen from Table 8, the temporal coverage is sufficiently large to provide good data.68 It should be noted that as outstanding medieval demographer as Hatcher, who often is very critical of Russell’s material and his handling of it, and rightly and fairly so, has no difficulty in accepting the usefulness of Russell’s data and the validity of the inferences drawn from it on this point of the seasonality of mortality.69 Russell found that before the Black Death, in the eight pre-plague years 1340–7, the “heaviest mortality was in the late autumn and winter months, in January and February, in October and November,” and he adds correctly: “The heavy mortality of the winter months requires no other explanation than winter severity.” Traditionally, the months of November and December were regarded as the first winter months, the “forewinter.” With the advent of the Black Death, the seasonal distribution of mortality changed dramatically. In the period 1348–1375 covering the Black Death and the subsequent three plague epidemics (1360–1, 1369, 1374), Russell’s data show an abrupt surge of mortality in July, the heaviest impact on mortality in September or more broadly the months August to October, with an abrupt tendency of decline starting in October. Conspicuously, the seven years of plague in this period accounted for twenty per cent more deaths than the remaining twentyone non-plague years taken together.70 Twigg’s efforts to render these findings harmless to his theory are curious: he divides his discussion of seasonality and Russell’s findings into two parts more than hundred pages apart, which means that important argumentative connections are severed, the critical reader is put at a disadvantage, and the problematic character and lack of real significance of his discussion in the second part tends to be veiled.71 Curious also is Twigg’s dismissal of Russell’s findings on the grounds that in the first plague period 1348–75, “the death rate is only four in

68

One should note that even in countries the size of the U.K. or U.S.A. national political Gallup polls are often based on a sample of about a thousand persons, which provide national polls with an uncertainty margin of about 3 per cent. It is all a question of reasonable or adequate representativeness. 69 Hatcher 1977/1987: 25–6. 70 Russell 1948: 195–8. 71 Twigg 1984: 59–69, 175–85.

seasonality of bubonic plague

423

January,”72 which reflects his usual carelessness: in fact it is the number of deaths that is four. If this figure is taken at face value, the death rate as proportion of deaths in this month in the period is 0.9.73 Some sort of numerical error is involved, since among the remaining seventy-one mortality datapoints distributed according to month and temporal subdivisions in the period February 1348 to December 1500 on which the data presented in Table 7 are based, the lowest figure is 18. However, on statistical grounds one should take heart from the fact that material for correction is available: for the other months of January in the respective subperiods the figures are 42, 47, 56, and 53. The fact that these numbers are quite closely bunched inspires confidence. The average is 49.5 deaths, and since there is a noticeable tendency of increase throughout the period as a whole from 42 to the mid-fifties, it appears reasonable, in our attempt to find the true figure for January in the first plague period of 1348–75, to weight this average in the direction of forty. Thus, it seems that the figure four is a slip of the pen for forty, a zero has slipped away, and forty can readily be substituted for four in the tables. This means that 52 per cent of total yearly mortality in the period 1348–75 was distributed on the four months July–October. This confirms that Hatcher’s use of Russell’s seasonality data is justified. One could also remark that it does not seem that anomalous figures concern Twigg much when they seemingly strengthen his case. Since he must try to reduce mortality in the Black Death as much as he can, Table 8. Percentage of mortality July–October 1340–1500 among English tenants-in-chiefs Period

Nos.

%

1340–7 1348–75 1376–1400 1401–25 1426–50 1476–1500

159 426/466 632 759 640 791

33 56/52 43 42 35 40

1348–1500

3248

43

72 73

Twigg 1984: 181. Russell 1948: 197.

424

chapter eleven

far more than anyone else has found possible, in order to make the facts fit his alternative anthrax theory,74 he accepts without objections Russell’s crude mortality data on the Black Death based on inquisitions post mortem as a realistic factual basis, and not only for mortality among the tenants-in-chief but also for the general population. In the age group 0–1, this material contains no infants, implying, consequently, a mortality rate of zero for this age, or alternatively, that there were no infants, neither of which is a realistic possibility. In ages 1–5, Russell’s material includes three young children, of whom one died. Thus, in ages 0–5, Russell’s total child population consists of three persons of whom one died, which he assumes permits the conclusion that the mortality rate in ages 0–5 was a ludicrous 33 per cent.75 The result is a very low mortality rate among the population of tenants-in-chief in the Black Death as a whole that suits his case, especially when Russell considers the mortality rate among tenants-in-chief representative for the general population. However, Life Tables Model West for populations with life expectancy at birth of twenty-five years show a normal infant mortality of 30.5 per cent for female infants and of 35 per cent for male infants, and of 21 per cent for young children of ages 1–4.76 It should have been impossible not to note that the mortality rates according to age imply that adult cohorts in this material were very much larger than child cohorts since far more adults die according to age cohorts in this social class than is warranted by the implied birth rates. This should make it clear that Russell’s data are out of touch with reality and do not allow any sort of statistical use but probably reflect interesting aspects of culture and mentality. There can only be one explanation for Russell’s registrations of children of these ages, namely that the mortality rates of infants and young children were so high that their deaths were taken for granted and parents quite generally did not bother to register the deaths of their youngest children, only of their somewhat older children who had greatly improved survival rates and were of greater interest for questions of inheritance and lineage. Thus, these data do not reflect realities of mortality in these age cohorts but cultural and practical attitudes of parents. The use of statistics and demographic sociology apart, Russell’s estimate of mortality among infants and young children is at gross variance with medieval

74 75 76

Below: 595–608. Russell 1948: 216. Coale and Demeny 1983: 43.

seasonality of bubonic plague

425

demography on these ages.77 This explains why Russell’s estimate of mortality in the Black Death has been generally rejected.78 Twigg’s peculiar efforts to reduce Russell’s mortality figure to c. 16.5 per cent for tenants-in-chief in the Black Death and to argue that they are representative for the general population will be commented on below. Russell made the same type of estimate of the seasonality of mortality for the subsequent subperiods 1375–1400, 1401–25, 1426–50, and 1476–1500. The central data are presented in a highly concentrated form in Table 8 which is so constructed that average mortality for a four-month period is, other things being equal, 33 per cent; higher percentages must reflect higher than average mortality, and vice versa. The average of 33 per cent was the case in the months July–October of the eight pre-plague years, importantly, in these years almost 45 per cent of all mortality occurred in the four months January–February plus October–November. This underlines the great change in seasonal mortality heralded by the advent of the Black Death better than the bare numbers in Table 8. In the period 1348–1450 and 1476–1500 as a whole and in all its constituent subperiods there was a consistent supermortality in the four-month period July–October. A reservation is called for in the penultimate subperiod 1426–50 as there was hardly a statistically significant supermortality in these months. The main reason is that a smaller or secondary peak had emerged in the months April–May which drained off some of the relative distribution of mortality.79 However, it is difficult to explain this as a real or factual change, because in the next subperiod for which Russell provides data, namely the last of 1476–1500, the seasonal pattern reverts by and large to the previous level of supermortality in these months. It is therefore more likely that there is some flaw in Russell’s material for 1426–50, which also saw some very serious plague epidemics (see below). This may also serve to explain the gap in the series caused by Russell’s inability to present data for the implied following sub-period 1451–1475: there seem to be serious problems associated with this specific material for the decades around 1450, at least as collected by Russell. The data may not be erroneous or skewed, but need further study, perhaps a heavier input of source-criticism, and increased substantiation. Only Russell’s data for the period 1340–1426 can be considered reliable and usable 77

Benedictow 2004: 246–56. See for instance Titow 1969: 68; Razi 1980: 100; Hatcher 1977/1987: 13. See also below: 596–602, 605–07. 79 Ibid. 78

426

chapter eleven

here. Fortunately, there are alternative sources of information on the distribution of mortality according to season for the fifteenth century which allow the development of an overview of the seasonality of mortality in this period on independent material, and also correction or adjustment of Russell’s data for the periods after 1426 (see below). The seasonal pattern of mortality uncovered by Russell does not mean that the incidence of mortality in the late autumn/early winter months and central winter months had decreased significantly, although, of course, persons with poor health now died from plague who would otherwise have died in the subsequent winter months. Mainly, it means that winter mortality now was overshadowed by new forces of death with their greatest impact in the late summer and early autumn as would be the case with bubonic-plague epidemics. The sudden transformation of the seasonal distribution of mortality from the pre-plague to the plague-era uncovered by Russell is a very important finding. Certainly, it is entirely compatible with bubonic plague with its basis in rats and fleas which would develop its highest epidemic intensity in the months of (late) summer and early autumn and subside and (almost) disappear with the advent of chilly and cold weather in the late autumn and winter, as has also been pointed out by several prominent historians.80 The easy explanation of this transformation of the seasonal distribution of mortality on the basis of central aspects of bubonic-plague epidemiology strengthens the positive assessment of Russell’s material and the good level of tenability of observations inferred from it. Its incompatibility with diseases spread by cross-infection should be clear: they would tend to increase winter mortality. The attainment of reliable general knowledge of the seasonality of plague in the fifteenth century requires that information be collected from several studies and pieced together. Hatcher has, as mentioned, published an important study of the mortality among the monks of Christ Church Priory, Canterbury. Obituary lists and other evidence permit a complete registration of the day of death of the great majority of monks who died there in the period 1395–1507, and to make good assumptions as to the time of death for the remainder.81 In this period,

80 81

Hatcher 1977/1987: 25–6; Slack 1979: 43. Hatcher 1986: 23–5; Hatcher 1977/1987: 17–8.

seasonality of bubonic plague

427

plague visited the priory in 1413, 1419–20, 1431, 1447, 1457, 1465, 1467, 1470–1, 1487, 1501, 1504, 1507.82 There were also a couple of epidemics there in the preceding eighteen years that could quite likely have been plague as indicated by high mortality at the very end of the fourteenth century and c. 1407, years corresponding to known or presumed national plague epidemics in the years 1400 and 1405–7.83 Since monks are a special social category and live in quite a different way from the various segments of the ordinary population, the representativeness and, thus, the usability of this material for the question must be clarified and corroborated before inference to society at large can be made. The monks were “exceedingly well fed, clothed and sheltered,” and “they benefited from levels of sanitation, hygiene and medical care which were wholly exceptional for the times.” On the other hand, the monks did not live reclusive or isolated lives. There were twice as many servants as monks, the priory housed an “unquantifiable” number of permanent and temporary lay residents and corrodians.84 There was also a “constant stream of visitors,” so monks made “frequent contact with the wider world,” and it was centrally located in a bustling market town containing a population of about 4,000–5,000 persons with which there was lively social exchange, townspeople visiting the monastery, and monks frequenting the town. In market towns there was a strong confluence of people and with them of various epidemic diseases which caused high urban mortality rates. Also Canterbury’s population was declining throughout the fifteenth century. Clearly, the monks were exposed to diseases transmitted by cross-infection both by visitors who would quite likely suffer from an unrepresentative incidence and array of diseases and by their own visits in the town. The problem of cross-infectious diseases must have been exacerbated by their communal living: the rank and file monks, the younger monks or ordinary cloister-monks, “invariably slept in common dormitories and ate the common meals,”85 which must have “further facilitated the transmission of a range of diseases.”86

82

Hatcher 1977/87: 17. Hatcher 1986: 26; Hatcher 1977/1987: 57; Shrewsbury 1971: 138, 141–3. Cf. Harvey 1993: 125. 84 See for instance Harvey 1993: 179–209. “A corrody was a special form of pension or annuity. Some corrodians enjoyed their privileges as a gift from the monks, but many, as will appear, paid for them.” 85 Hatcher, Piper and Stone 2006: 682; Harvey 1993: 77. 86 Hatcher 1986: 34–6; Bailey 1996: 2; Hatcher 2003: 97. 83

428

chapter eleven

The great similarity of the highly negative developments of life expectancy of monks and their risk of disease in such distant localities as Canterbury, Westminster and Durham (see below) to more general demographic developments in English society at the time are striking. Hatcher uses the terms “symmetry” and “synchronized” about this concurrence of similar demographic patterns of people and monks in the fifteenth century.87 Considering this concomitant demographic evidence Hatcher first concluded that the monks’ health was “likely to have been driven in major part by the same forces which were determining the health of the population at large.”88 In his latest paper, he argues that there may have been a certain supermortality associated with monastic life in the past, a view which tends to underline the importance of infectious diseases spread by cross-infection in this specific environment.89 This may have been the case, but Hatcher also argues convincingly that the size of the general population was falling in the fifteenth century, markedly after 1450 until some time in the early sixteenth century.90 It is therefore not clear that the possible difference between the levels of mortality of people and monks was pronounced, although the mortality profiles may quite likely have diverged. One point of importance could be that the monks lived in buildings of stone or bricks that would, presumably, be an environment less amenable to rats than ordinary housing at the time. This suggests that monastic buildings would tend to reduce the numerical incidence of rats and rat fleas in relation to monastic men compared to the situation in environments of the general population in town and country. The general analysis would therefore tend to suggest that these monastic communities may have been relatively more at risk of contracting infectious diseases spread by cross-infection and less at risk of contracting bubonic plague than the general population. And this seems to have indeed been the case. There is a clear increase of mortality in the winter months among the monks. However, in general terms the

87 Hatcher 2003: 97; Hatcher, Piper and Stone 2006: 667: “[…] no doubt, the symmetry that has been established between mortality in three monasteries located in different parts of the country has important implications for our understanding of the demographic history of late medieval England.” 88 Hatcher 2003: 97–8. 89 Hatcher, Piper and Stone 2006: 682–3. 90 Hatcher 1977/87: 43–57, 64–5; Hatcher and Bailey 2001: 31; Hatcher 2003: 95–9; Hatcher, Piper and Stone 2006: 683–5.

seasonality of bubonic plague

429

seasonal pattern of mortality among the monks at Christ Church Priory in the period 1395–1504 still shows heaviest mortality in the months July–October, a mortality profile that is clear all through the period, but markedly stronger after 1450 than in the preceding period,91 which may have been the case also for the “population at large” for the same (main) causal reason, namely an increased incidence of bubonic plague epidemics. Arguably, the supermortality among the monks in the months July–October as a reflection of bubonic plague would tend to understate the impact of bubonic plague on the ordinary population in the same months and as such the importance of bubonic plague as a demographic factor in the lives of the English population in the period. In a fine monograph, B. Harvey has studied the lives of monks at Westminster Abbey, London, in about the same period. Unfortunately, the material at her disposal for the demographic study of mortality is considerably weaker, because, among other things, the obituaries are lost, so that the day of death of the monks cannot be identified with the same accuracy as in the case of Christ Church Priory in Canterbury. However, other sources make it possible to address usefully the question of the seasonal pattern of mortality in the period 1390–515. It happens that 28 per cent of deaths occurred in winter or early spring, 69 percent in the late spring, summer, and autumn, and 3 per cent of deaths cannot be temporally accounted for. Furthermore, mortality in the warmer seasons “claimed more victims in the crisis years” than in years of “high mortality of the second order.” Importantly, in some of the crisis years the summer and autumn were actually the “dangerous seasons—and dangerous by any standards.”92 In a less specific and compelling way, this material shows much the same pattern as was identified in the case of Christ Church Priory, that the mortality among the community of monks, despite the particularly high level of exposure to cross-infection, was much the highest in the warmer seasons, especially in the summer and the autumn, and that this pattern is closely associated with known plague epidemics in this period, namely those in 1400, 1420, 1434, 1458, 1464, 1471, 1479, 1491, and 1500. Evidently these studies of monastic mortality accord completely with Russell’s findings, link up to his data around 1400, overlap his data

91 92

Hatcher 1986: 26. Harvey 1993: 135–8.

430

chapter eleven

for the periods 1401–26, and extend the seasonal overview up to about 1500, and as such also overlap and confirm the value of his data for the period 1476–1500. The similarity of these findings based on unrelated source materials is strongly corrobatory. They also strengthen the probability that Russell’s data for the subperiod 1426–50 are anomalous due to some unresolved source-critical problem and should, as maintained above, be left out of consideration.93 In his monograph on demographic developments in England in the period 1430–80, R.S. Gottfried discusses to the seasonality of mortality and its association with plague, especially in a chapter with the dramatic title “Season of Death.”94 In the period 1430–80 there appear to have been seven epidemics of plague in England of a national or extraregional scale, in 1433–4, 1438–9, 1452–3, 1457–9, 1463–4, 1467, 1471–3, and 1478–80; locally there were many more.95 However, his study is restricted to south-eastern England, more specifically to the counties Suffolk, Norfolk, and adjacent parts of Cambridgeshire and Hertfordshire, and it is mainly based on wills for its source material.96 The source-critical problems associated with the use of wills for demographic historical studies are many and must be taken very seriously. Wills are a highly unrepresentative category of historical sources: those who made wills belonged to the economic and social upper classes of the population; a substantial majority of the population had little or nothing to bequeath.97 Because of their “selective social coverage,” wills constitute a poor indicator of the levels of mortality in general populations in epidemics of plague, since levels of mortality are socially unequal, higher among the poor than among the well-to-do.98 In times of a perceived serious threat of mass death from plague many people would rush to make their wills. However, wills reflect more fear of death than death itself, and at the end of the epidemic usually the (great) majority of those who made their wills would still be

93 It is unfortunate that the study of the superior demographic material relating to the monastic community of Durham Priory in about the same period does not address the question of the seasonality of mortality. Hatcher, Piper, and Stone 2006. 94 Gottfried 1978: 107–7. 95 Hatcher 1977/1978: 17, 57; Hatcher 2003: 97; Harvey 1993: 125; Gottfried 1978: 35–51, 238. 96 Gottfried 1978: Chapter 6. 97 Hatcher 1986: 22; Hatcher 1977/87: 28–9; Hatcher 2003: 95–6; Slack 1979: 12–4. 98 Slack 1979: 14.

seasonality of bubonic plague

431

alive. The association between the making of a will and the day of death is tenuous at best; “the frequency of probate was overwhelming.”99 Use of wills as demographic sources for the study of levels of mortality is therefore fraught with difficulties that cannot be satisfactorily or usefully resolved. In the words of Hatcher: “It will never be possible to derive death rates from wills.”100 Nonetheless, wills are a usable source for the study of some aspects of mortality, for instance, for the identification of years of mortality crisis and the seasonality of mortality. However, this use also posesses significant problems that must be taken into account. In urban centres there was a social geography, a social differentiation of residential patterns according to economic and social conditions. The poor classes inhabited mainly the suburbs, while the central areas became more strongly middle-class quarters, and this social geography was changing in the direction of an increasing social polarization. Upper classes were used to epidemic outbreaks among the poor classes. Increasing social distance in residential patterns made for increasing time lag between the outbreak of epidemic disease among the poor and observation of and reaction to these events among the upper classes.101 Wills were made when the upper classes recognized to their horror that epidemic mortality among the poor was spreading and that also their own lives would probably soon be at risk. Thus, a sudden strong rise in the number of wills indicates quite a developed epidemic situation. This means that there is generally a time lag of several weeks between the outbreak among the poor and the surge of consternation among the will-producing classes that causes a sudden and strong increase in the making of wills. This is especially the case with plague because of the characteristic slow and protracted incipient development of its early endemic and epidemic phases.102 These source-critical comments must be kept in mind when Gottfried states that the “fewest testators in the sample died in the summer quarter, except during purported plague years, when mortality rose in late August.”103 Taking into account the time lag between the outbreak of plague and the time it began to impress itself on people in a way that

99 100 101 102 103

Gottfried 1978: 22–34. Hatcher 1986: 22. Cf. Slack 1979: 14. Slack 1979: 51; Slack 1985: 55–6. See Benedictow 2004: 81, 136–7, 197–8, 272, 336. Gottfried 1978: 107.

432

chapter eleven

persuaded many of them to make their wills, it can be seen that the plague season in general terms appears to have started in July, which conforms to the pattern Russell uncovered for the preceding hundred years. The severe plague epidemic of 1479–80 is clearly reflected in a great rise in the numbers of probated wills, starting in the summer in the town of St Albans; the epidemic then moved to Suffolk and Norfolk, as reflected in a delay in the rise of the numbers of wills, which began in August and September, reaching a sharp peak in the autumn, and then a rapid fall set in.104 A chronicler states that plague this year broke out in London in September and disappeared early in November.105 Quite likely, the epidemics of 1438–9 and 1479–80 took on a bimodal form and broke out again in the spring. The studies of Russell, Hatcher, Harvey and Gottfried cover among them the seasonal pattern of mortality throughout the fifteen century. Taken together they show a consistent and strong pattern with the heaviest mortality in the months July–October; this was the new pattern that emerged abruptly with the arrival of the Black Death and continued with the subsequent recurrence of plague epidemics in the following 150 years. This was also the characteristic seasonal pattern of mortality throughout the remaining 166 years of the plague era. In his study of plague in Tudor and Stuart England, Slack emphasizes that this was not only the case in England, but a general European experience, demonstrating that the same disease was at the heart of the matter all over Europe and that there could only be one and the same reason for this general epidemiological manifestation: outbreaks of bubonic plague have a characteristic seasonal incidence, dictated by the climatic conditions favouring the development of the fleas which carry the disease. All over Western Europe these epidemics were marked by a rapid rise in the number of deaths in the summer; burials normally reached their peak in the months between July and September, and then fell more gently with the onset of colder weather […].106

104 Gottfried 1978: 35–51, 107–25. I do not, however, understand on what grounds Gottfried 1978: 62, states that “the occurrence of bubonic plague in England is almost always in late summer and early fall,” referring in the accompanying footnote on page 79 to Hirst 1954: 238, for support, where nothing to this effect is stated. 105 Gottfried 1978: 45. 106 Slack 1985: 65. Cf. Slack 1979: 24.

seasonality of bubonic plague

433

The large epidemics in Devonshire in the years 1546–7, for instance, exhibited the characteristic seasonality of bubonic plague: the “number of burials began to increase in late spring and early summer of 1546 in several parishes,” “the disease continued to cause havoc in the county” even after the good harvest, and thus was not hunger-related. Only seven of thirty-five parish registers showed no evidence of the disease, while elsewhere there are all the characteristic signs of bubonic plague: “summer peaks in the number of burials where the disease was worst,” “the apparent slow movement of disease from place to place, burials rising in one village a fortnight or a month after they had done so in another a few miles away.”107 The last point is interesting in so far as it constitutes evidence of short-range metastatic leaps and the latent period conforming to and reflecting the rhythm of development of bubonic plague in the plague season. Finally, Slack also points out that people in London “noted the regular seasonal periodicity of plague and acted accordingly.”108 All through his monograph Shrewsbury is clear on this unique pattern of seasonality of plague and the reason for it, noting the winter intermissions and the typical onslaught of plague epidemics in the (late) summer which are characteristic of rat-flea-based transmission.109 However, he has little information on epidemic diseases for the period c. 1375–1500, and hardly any seasonal information at all, for the simple reason that little information was available at the time he wrote his monograph. As was seen above, all studies containing significant or important information on the seasonal pattern of mortality in the fifteenth century were published later except Russell’s. After 1500, Shrewsbury’s account expands greatly and contains much detailed material. Unfortunately, the term “seasonality” is not in his index, which makes the task of systematizing his quite detailed empirical information on this point very work-intensive. Fortunately, however, he is fond of systematizing his data in histograms (bar charts) and figures, which makes much information showing the progression of plague epidemics according to the monthly distribution of mortality easily identifiable and usable. Although concentration on this material omits the occasional piece of evidence noted by chroniclers on when the outbreak began and ended, and also not rarely when they raged most intensively, 107 108 109

Slack 1985: 84. Slack 1985: 239. See for instance Shrewsbury 1971: 117. Cf. Creighton 1891: 217–33.

434

chapter eleven

it provides quite a valuable and useful platform for insight. In all, his book contains fifty relevant histograms or figures (mostly the latter) on this topic, showing the seasonality of plague mortality according to month in various locations in England, from London to tiny rural parishes. In addition, a few tables show the time of the beginning and end of epidemics as reflected in plague deaths.110 Since display of the distribution of seasonal mortality according to month requires individualized data which for ordinary populations is mainly provided by parish registers or bills of mortality, all of this material relates to the period 1548–1666. This requirement for statistical identification of seasonality also ensures good data quality and important detailed information on the progression of epidemics and reliability of inference to the reality of such developments.111 This material shows a clear majority of urban epidemics, which should be expected for the last hundred years of plague when these epidemics increasingly became an urban phenomenon. The material consists of fourteen histograms and figures showing the distribution of plague mortality according to month (or season) for the period 1548–99112 and thirty-six figures or histograms showing mortality according to month (or season) for the remainder of the plague period, the years 1600–66.113 All fifty figures and histograms exhibit the same pattern without exception. All plague epidemics broke out in the warmer seasons and began to decline with the advent of the colder seasons in October, subsiding and disappearing in the following months, causing only episodically some deaths in January. Summing up, in the preceding pages substantial material has been presented on the seasonality of plague epidemics covering the whole European plague era from 1347 to 1666/1722, with a particular focus on the English evidence. The English material is based on diverse sources, inquisitions post mortem, monastic studies, wills, parish registers and bills of mortality, etc. The studies based on these sources produce a comprehensive, continuous and consistent account of the

110

Shrewsbury 1971: 396. I will make source-critical comments below on the use of institutions of parish priests during the Black Death. 112 Shrewsbury 1971: 176, 182, 183, 191, 197, 199, 214, 216, 238, 244, 249, 253, 396, 492. 113 Shrewsbury 1971: 267, 280, 296, 302, 310, 316–7, 320, 326, 328, 329, 350, 361, 364, (372), 374, 376, 378, 383, 386, 391, 396, 406, 411, 412, 417, 436, 438, 462, 463, 476, 500, 504, 511, 523. 111

seasonality of bubonic plague

435

seasonality of plague which unambiguously associates plague epidemics with the warmer seasons (spring, summer and autumn), with an emphasis on the late summer and early autumn months. They constitute together a powerful basis for inference that historical plague was an epidemic disease that is systematically and by innate, systemic properties dependent on warmer seasons for developing epidemic manifestations and functions. The occurrence of bimodal epidemics, epidemics that break out (late) in the warmer season of one year, subside and disappear with the advent of late autumnal and wintry weather, and then break out again in the same locality in the spring to produce another peak of mortality, is such a conspicuous and unique feature that it strengthens this conclusion even more, if possible.114 The plague epidemic at Colchester in 1665–6, exhibits a pattern as similar to that of the epidemic in the Cathedral’s parish in Bergen a century earlier as well-nigh possible in the real world. The epidemic started in September with a fulminant development which was abruptly reversed by the advent of cold weather which caused a rapid diminution and virtual disappearance of the disease, which reappeared in Spring and produced the last cases in December the following year, although, in the case of Colchester, without producing a complete winter intermission as it seems (if all deaths registered in Colchester were plague deaths), which could quite likely be associated with the fact that Colchester is situated over 900 km further to the south than Bergen with a correspondingly milder winter climate in ordinary years. This seasonal pattern was well known to contemporaries and is the basis of the title of John Taylor’s book published in 1625 and reprinted 1636: The Fearefull Summer: Or Londons Calamitie, The Countries Discourtesie, And both their Miserie. Printed by Authorities in Oxford, in the last great Infection of the Plague, 1625.115 In 1641, a Londoner claimed that a proposed day for religious humiliation to ward off plague was unnecessary, because “winter was coming on, and then the plague would be stayed.”116 This consistent seasonal pattern throughout the whole plague period, which is based on various types of relevant source material and independent studies, demonstrates that Twigg’s great efforts to discredit Russell’s findings about the seasonal incidence of plague for the period 114 115 116

See for instance Shrewsbury 1971: 500, 504, 523. Cox 1910: 149. Slack 1985: 239.

436

chapter eleven

1340–1500117 are untenable, and that the pattern Russell identified for this period was similar throughout the remaining 166 years of the plague era, 1501–1666. Twigg’s efforts reflect a great need springing from the fact that this pattern of seasonality is easily compatible with bubonic plague and incompatible will all the alternative theories of the microbiological nature of historical plague including his own. Finally when Twigg recognizes that his arguments are not convincing, he concludes rather lamely, but as enthusiastically as he possibly can under the circumstances: “I suggest, therefore, that the mortality patterns in the post-1348 period, whether of epidemic or endemic years, are not sufficiently different from the pre-1348 years as to allow us to believe that bubonic plague was present.”118 This is clearly not correct. Duration of Vacancies in Parish Benefices during the Black Death Since Twigg and Scott and Duncan assume such a central part in this discussion, English evidence tends to play an important and even disproportionate role. However, to my knowledge it is not possible to construct such a well-documented complete historical overview over the correlation of seasons and plague epidemics for any other country. Twigg and Scott and Duncan only address selected small parts of the relevant material, focusing on a part of the seasonal history of the Black Death’s spread in England, mostly based on a poorly suitable or, as we shall see, more likely unsuitable category of sources, namely institutions of parish priests. The time has come for an examination of this source material and its usability. Twigg was the first of the advocates of alternative theories to emphasize the importance of the material on institutions of new parish priests during the Black Death for the study of the seasonality of plague because, in his opinion, they show in the southern dioceses a winter incidence incompatible with bubonic plague.119 “The seasonal mortality pattern during the Black Death must be one of the most telling arguments against it being bubonic plague.”120 Twigg’s line of argument was enthusiastically picked up by Scott and Duncan who concluded

117 118 119 120

Twigg 1984: 181–4. Twigg 1984: 183. Twigg 1984: 60–2, 65–9, 176–85. Twigg 1984: 185.

seasonality of bubonic plague

437

triumphantly: “We can now abandon the idea, so firmly promulgated in the literature, that the Black Death was an outbreak of bubonic plague.”121 Remarkably, Twigg also states that “plague did not appear until late 1348.”122 Scott and Duncan accordingly state unreservedly: “In the diocese of Salisbury, the epidemic was rampant through December to February and reached its peak in March.”123 It is generally acknowledged that the Black Death broke out in Melcombe Regis (Weymouth) in the diocese of Salisbury shortly before 24 June,124 and spread in England throughout the whole second half of 1348. Since these are basic facts which are important for the discussion of the seasonality of the Black Death in England, there will be ample opportunity to produce the evidence below. Hypothetically, Twigg could correctly have meant that the effects of the Black Death did not appear in the form of institutions of parish priests until late in 1348, in which case a danger signal should start blinking with respect to the temporal connection between the spatio-temporal progression of the Black Death and its mortality effects and the reflections of this process in the form of institutions of parish priests into vacancies. This material on institutions of parish clergy in a few months of the Black Death in a small part of England, mainly the winter months of 1349, is supposed to undermine the consistent and strong link between plague epidemics and the warmer seasons demonstrated for the remainder of the Black Death and the remaining plague era of 320 years, i.e., 99.85 per cent of the history of plague in England in this period, a fact which they refrain from attempting to explain or in the case of Scott and Duncan even from mentioning. Twigg falsely attributes to Shrewsbury the view that the Black Death (and later plague epidemics) occasioned a different seasonal distribution of mortality from the pre-plague mortality pattern to the effect that the heaviest mortality now occurred in the three autumn months from August to October (see above). This distortion of research history prepares the ground for Twigg’s defence of his view that the Black Death and later plague epidemics could not have been bubonic plague: 121 122 123 124

Scott and Duncan 2001: 105–9. Twigg 1984: 181. Scott and Duncan 2001: 355. Benedictow 2004: 126–31.

438

chapter eleven Despite what Shrewsbury says about the creation of a single peak in August, September and October this fact does not emerge from the Institutions to vacant benefices in the several dioceses, all vacancies being generally but probably erroneously attributed to plague deaths.125

As shown above, it is not Shrewsbury but Russell who has documented this peak in August–October. To characterize this finding as a “creation” is misleading; it is also disquieting because it appears to serve a purpose. Next, Twigg goes on to use Shrewsbury’s extensive presentation of institutions of parish priests during the Black Death to argue against the view he has erroneously attributed to him, disparagingly implying that Shrewsbury has not noticed the gross contradiction between his data and a conclusion which in fact he never drew. One should also note the arbitrary assertion that “all vacancies being generally but probably erroneously attributed to plague deaths”:126 this is, to the best of my knowledge, not correct and is not substantiated by Twigg with any reference to the scholarly literature. A few pages earlier, he states that “some writers have assumed that all vacations during 1348–9 were due to death from plague,” which is very different from asserting that this has “generally” been the case, and again there is no substantiating reference that could clarify who “some writers” were.127 Are they serious scholars? However, identifications can be made: the “accusation” can only be relevant for F. Seebohm 1865128 and perhaps for some scholars up to the time Gasquet’s monograph was published in 1893. In that work Gasquet makes it entirely clear that vacancies were due not only to death, but also to “exchange, or resignation,”129 and he actually provides a rule of the thumb: “it is safe to say that twothirds were institutions to vacancies due to the plague.”130 It is another matter that Gasquet does not consistently take this into account131 (but then he was not a historian by training; nonetheless he made an impressive pioneering achievement in an important field of historical study). Twigg’s assertion on this point is untrue for all scholars who address 125

Twigg 1984: 65. Twigg 1984: 65. 127 Twigg 1984: 59. 128 Seebohm 1865: 150–60. 129 Gasquet 1908: 86, 88–9. (I have used the 2nd edition of 1908 which is identical to the 1893 edition for all practical purposes.) It should be remarked that Gasquet does not seem to have consistently taken this into consideration, see, for instance, Pickard 1947: 25. 130 Gasquet 1908: 188. 131 Ziegler 1970: 184. 126

seasonality of bubonic plague

439

the subject after Gasquet’s monograph was published and the appearance of A.H. Thompson’s two pioneering papers on institutions during the Black Death in the dioceses of Lincoln and York in 1911 and 1914—in other words, the assertion has not been true for at least a hundred years. Also, Twigg does not indicate the proportion of vacancies that have been “erroneously attributed to plague deaths” and provides, thus, no clue as to the possible (in)significance of the argument. In reality, Twigg pursues an anti-source-criticism line which serves to confuse the discussion and allows arguments to slip into the discussion that in the interest of its quality would better have been left out. In view of the great importance they attribute to institutions as evidence on the seasonality of the Black Death, one can legitimately be surprised by the scant source-critical interest Twigg and Scott and Duncan take in this type of source and especially in the crucial question of the temporal link between the deaths of incumbents and the institution of successors. Twigg is surprised by Shrewsbury’s remark that, according to J. Lunn’s thesis on institutions (see below), there was a time lag of about a month between deaths of incumbents and the institution of successors, but appears willing to accept it.132 Shrewsbury does not indicate that Lunn’s assumption had any empirical basis, and since Lunn’s thesis has been lost, the crucial scientific tenet of testability has vanished as well.133 However, since his assumption is identical with A.H. Thompson’s statement on this point in his paper on the institutions in the diocese of Lincoln in the plague period, Lunn’s statement may quite likely have come from this paper. Thompson’s view will be discussed below and found to be based on a misunderstanding or misconception. Scott and Duncan have not taken interest in this problem, presenting their case on the assumption of contemporaneity between the two events. Their figures or histograms show numbers of institutions according to month (taken from Twigg’s monograph) and are presented as if they provide direct information on the mortality among parish priests in time and space. This is erroneous and misleading. In his admirable and still useful account of the Black Death in England, Ziegler maintains that there was a “usual gap of a month to six weeks between mortality and replacement,” however, as there is no supporting footnote the statement is also arbitrary, though it may be based on

132 133

Shrewsbury 1971: 59; Twigg 1984: 65. Shrewsbury 1971: 59.

440

chapter eleven

Thompson’s statement on the matter.134 Therefore, this important point appears to have been largely neglected, but in the present context this question is at the heart of the matter and must be seriously and satisfactorily addressed. Only Thompson refers to a material basis for his statement on the matter and can as such be taken seriously. All others who express an opinion on the matter seem to base their view on his statement, without having tested the material basis. For this reason, it is of crucial importance to examine the basis for Thompson’s view and assess its tenability. If tenable, this will be an important fact, but its geographical limitation and specificity will limit its representativeness with regard to seventeen bishoprics and will also have a corresponding limiting effect on its significance. If it is untenable or problematic, a new study of the matter is called for. Thompson has produced two of the classic studies of institutions at the time of the Black Death, for the diocese of Lincoln (1911) and the diocese of York (1914). In his study of the diocese of York’s bishop’s register, he states that “It may be fairly assumed that the institutions in any given month represent deaths which took place during the previous three or four weeks,”135 however, he provides no evidence or even explanatory considerations for why this should be a reasonable or “fair” assumption. It is in his study of the bishop’s registers of the diocese of Lincoln that Thompson provides the material basis for his assumption on the time lag between the death of incumbents and the institution of successors and the method of estimation: by comparing the dates of institutions to benefices “which were at this time in the hands of the king […] and the death of tenants-in-chief, with the dates of the letters of presentation which fill the patent rolls for this year, one is lead to the conclusion” that the average period which elapsed between the death of an incumbent and the institution of his successor was “at least a month.”136 Unfortunately, four big problems immediately present themselves: (1) Thompson appears to have misstated his case on this point: this material does not reflect the time elapsing from “the death of an incumbent to the institution of his successor,” but covers the time elapsing

134 135 136

Ziegler 1970: 148. Thompson 1914: 105. Thompson 1911: 317.

seasonality of bubonic plague

441

from the day a candidate for the crown was presented to the bishop’s administration to the day of institution as entered in the bishop’s register. The question that can be answered on the basis of this material is therefore the average time which elapsed from the day the crown presented a candidate for a parish benefice until the institution of the presentee. It does not relate to the crucial question of the average period of time elapsing from the death of incumbents until the crown’s presentation of candidates for vacated parish benefices took place, which together with the average time elapsing from the presentation until the time the institution was entered in the bishop’s register, constitute the time elapsing from the death of incumbents to the institution of their successors. Thompson, an exemplary scholar, provides the source material on which his estimation is based in an appendix, which makes testing readily possible. The time of all presentations by the crown and the time of the corresponding institutions in the period 25 March 1349 to 25 March 1350 as supplied in Thompson’s Appendix II have been studied.137 There are in all sixty-nine presentations by the crown, and the time that elapsed from the day of presentation to the day of institution was, on average, 33.5 days or 4.8 weeks, which may be taken to support the assertion that this was the period of time which Thompson had in mind with his reference to “at least four weeks” and Ziegler’s statement of “a month to six weeks.” This means that the trust I placed in Thompson’s statement in my monograph on the Black Death was misplaced and that the standard assumption I developed based on his statement and on Ziegler’s statement on this matter138 falls apart. Thompson provides no evidence on the time elapsing from the deaths of parish priests to the institution of their successors. (2) Nothing is said about benefices in the king’s gift for which no candidate was found at the time of the epidemic, for which institutions were performed in the following couple of years. As will be shown below, this appears to have been the case with 15–30 per cent of the parish benefices for which the bishop had the right of institution, and one could reasonably surmise that much the same would be the case with the vacancies for which the king was in the position of the patron.

137 Thompson 1911: 339–56. No usable material of this kind is given in the bishop’s register of York diocese, Thompson 1914: 135–40, 148. 138 Benedictow 2004: 124.

442

chapter eleven

This perspective implies substantial additions to the average lapse of time as estimated for the plague period. (3) The type of source used by Thompson in this case is subject to very serious source-critical objections or reservations. In a small passage in Appendix III in the paper on the institutions of the diocese of York some formidable weaknesses with respect to this material are presented: “a crown presentation is no guarantee that the person presented actually received institution, as such presentations were frequently made without proper references to facts, and in such cases often proved inoperative or were actually revoked.”139 In his later monograph on the English clergy in the Later Middle Ages, Thompson actually emphasized the Crown’s role as a mess of such proportions that it certainly implies much confusion and reservations as to its practical usability for clarification of the present topic.140 (4) Since the crown’s candidates are presented by a parallel organization that was not specialized in religious functions, as is clear from the amateurishness that appears to characterize its functions in these matters according to Thompson, it might not function according to the same time schedule as the episcopal organization, which also introduces a serious source-critical problem of (un)representativeness. Ignoring for the moment the problematic source-critical nature of this material, the crucial question that remains to be answered, and which cannot be answered on the basis of Thompson’s data, is the average period which elapsed from the time of death of incumbents in cures to which the king had the right of presentation until a candidate for succession was presented to the bishop’s administration. The average period from the death of incumbents to the institution of their successors must have been much longer than 33.5 days. Twigg only touches the crucial problem of the average lapse of time between the monthly numbers of institutions in the histograms and these numbers’ spatio-temporal relationship with the deaths of the incumbents, and the basis for this “touch” has been shown to be untenable. Scott and Duncan do not address the issue at all. Since they adduce no testable material or study in support of their argument, their assumptions on this point appear arbitrary and their climatic or seasonal arguments can be dismissed. Evidently, here is a problem that needs elucidation. 139 140

Thompson 1914: 148. Thomspon 1947: 104.

seasonality of bubonic plague

443

A useful start could be to address some basic factors that affected the lapse of time between the two events, keeping in mind that this is only a start, and that other factors will be presented below: (1) When a parish priest died (retired, or resigned to exchange for another parish benefice), this set in motion a complex process leading to the institution of a successor. In this process, first the system of patronage on which the medieval church depended at every level was activated.. In the case of parish churches, the patrons were the possessors of church advowsons which gave the right of presentation to a benefice or living. The patrons of local benefices could be the bishop, the dean and chapter, heads of wealthy families, religious houses, the local ordinary, often the Crown, tenants-in-chief, or groups of local parishioners. The Crown’s important role should be emphasized and explained, in the words of Thompson: An immense number of presentations to rectories by the Crown are recorded on the patent rolls. These for the most part were benefices in the patronage of tenants-in-chief which escheated to the Crown during the minority of an heir or the vacancy of a religious hose, or in consequence of a forfeiture of estates. Such presentations did not always take effect: they were frequently made upon false information, and instances of two or more concurrent presentations to the same benefice through mere inadvertency are not uncommon. But they gave the Crown a good opportunity of providing for its clerks.141

Possession of an advowson and the consequent rights of presentation could be divided into shares or portions (medieties), in which case the grant of presentation could alternate in turn from one owner to another or the portioners could act as a collective patron in presenting a cleric to the cure. The bishop’s registers show that the king in many cases enjoyed temporary ownership of advowsons pending the inheritance of property or the filling of a vacancy.142 Then there are the problems of pluralism and absenteeism, and so on. Hopeful non-beneficed clergymen in the parish or district would take the initiative to start the process and take up contact with the possessor(s) of the advowson, but often the possessor(s) 141 142

Thompson 1947: 104. Dohar 1994: 26–9, 110–2.

444

chapter eleven

would take the initiative. The beginning of the process of replacement would therefore often be complicated and quite time-consuming, and might involve a considerable journey for the hopeful, or some prominent person in the parish, to the patron just to provide information about the vacancy, and in those days the whereabouts or identity of a patron might not be obvious and need clarification that could take some time. If the patron were local(s), the process would probably be simpler, but not necessarily in the case of multiple possessors of the advowson. (2) The patron would then be obliged to find a suitable replacement; this could take time, and the vacancy could be sought by various interests and candidates with consequently lengthy discussion and dispute. (3) When the patron had reached his decision, he would contact the archdeacon who might not be readily available and ask him to perform an enquiry into the legal circumstances of the vacancy and the suitability of the candidate, which could be a complex and time-consuming process, especially when, as in the time of the Black Death, there were many such requests, and numerous vacancies and candidates which needed to be screened or scrutinized. (4) If the candidate was suitable and the legal circumstances of the vacancy unproblematic, this would be made known to the bishop and his staff who would consider the candidate, especially if he was presented by the king or a tenant-in-chief. The candidate would then be notified that his candidacy was accepted and he could come to the bishop’s residence in order to be instituted in the vacancy. (5) The candidate would then prepare for the journey, find the bishop, whose whereabouts might not be readily known if he was circulating in his diocese or had sought refuge at some peripheral manor, and wait for the ceremonies of admission to the vacancy and of institution into the benefice to take place.143 (6) The size of dioceses varied greatly and affected the time required for the various processes of contact between the hopeful candidates, patrons and the bishop’s staff at a time when travelling also on horseback was quite slow and could also be dangerous.

143

See, for instance, Wood, Ferrell, and DeWitte-Aviña 2003: 430.

seasonality of bubonic plague

445

Taken together, the various elements of this process could evidently take months before being completed even at the best of times, and in a time of great distress and catastrophic mortality it could obviously take much longer time and the average lapse of time which is in focus here could be considerable (see below). As this introduction to the underlying problems of the topic should indicate, the use of registers of institutions for determination of the time and seasonality of deaths of incumbent parish priests during the Black Death is far more problematic than implied by Twigg and Scott and Duncan. In fact, to attempt to do so is to open a can of methodological and source-critical worms that would make Medusa’s head pale in comparison.144 The connection between the two crucial events, the death of an incumbent and the institution of his successor, is in sourcecritical terms very indirect and circumstantial: the institution may not be caused by the incumbent’s death, and when caused by his death may have quite a distant and variable relationship to the time of his death, especially at a time of almost incomprehensible mortality among the beneficed parish priests and high mortality in the bishops’ administrative staffs that should handle an enormously increased number of institutions and other types of ecclesiastical business. The crucial point or defect is, as there will be ample opportunity to consider, the lack of information on the time of death of incumbent parish priests. Only the bishop’s register of the diocese of Coventry and Lichfield registers time of death of the previous holder of the benefice, but in the present context the representativeness and significance of this are quite limited (see below). The lapse of time between the death of incumbent priests and the institutions of their successors and its effects on the usability of institutions for the study of the seasonality of the Black Death and plague epidemics more generally will be in focus in this subchapter, in accordance with the importance ascribed to this material by Twigg and Scott and Duncan. Importantly, the institution of a new parish priest could also be due to resignation or exchange of living. Resignations and exchanges must be deleted from the material for estimation of mortality rates or determination of time of the epidemic, since they are not caused by death 144 The following discussion of methodological and source-critical problems associated with the use of institutions is based on the quite detailed discussion in Benedictow 2004: 343–59.

446

chapter eleven

and will often relate not to the presence of the epidemic but to frightening hearsay of the epidemic’s ravages and clerical mortality in other districts or counties or dioceses. In fact, the number of resignations increased sharply in many dioceses under the Black Death partly or mostly but not only (see below) because of a wish to avoid dangerous priestly service. This also affects the time horizon of the epidemic as reflected in institutions. It is important to take into account the fact that resignations from fear of plague and the desire to move away before the arrival of the epidemic would have to be initiated significantly earlier, which means that there would tend to be a considerable or at least significant difference in time between the two causes of voidance, by resignation and by death, which would tend to affect the distribution of institutions over time and the time perspective of the process. The importance of a sharp increase in resignations in the face of the approaching epidemic is also due to another effect: it added many vacancies to those caused by the mortality among the parish priests. It increased the pool of vacancies in good cures for which not only nonbeneficed auxiliary parish clergy but also many incumbents would vie, since resignations could be prompted by a wish for an exchange of living into a better cure. According to Thompson, “in the course of the fourteenth century the custom of exchanging ecclesiastical benefices had reached serious proportions.”145 Great mortality among the parish clergy together with great fear of the plague triggered great clerical social mobility not only vertically in the form of the rise of clerics in auxiliary service into the ranks of beneficed parish priests but also diagonally, so to speak, in the form of exchange or preferment from poor to good livings.146 Unfortunately, the information on these matters provided by the bishop’s registers is of uneven quality (see below). There are still other problems with this material. The right to perform institutions was not the bishops’ prerogative, which is the impression conveyed by Twigg and Scott and Duncan. The right to institute parish priests was to a considerable but variable degree granted to other ecclesiastical dignitaries, and especially archdeacons quite often possessed this right in their archdeaconries. In the diocese of York, the

145

Thompson 1947: 107. Much the same social pattern of mobility took place in the manorial social system where not only landless men but also smallholders entered vacant customary tenancies and therefore improved their social standing by moving upwards vertically or diagonally. 146

seasonality of bubonic plague

447

number of parishes was somewhat below 1,000 but the bishop had the right of institution to only 536 benefices. Thus, a substantial proportion of the deaths of parish priests would not be reflected in the bishops’ registers. Inevitably, this weakens at least significantly and quite likely considerably the usefulness of the registrations of the bishops’ institutions as a source for identifying when exactly the Black Death entered and ravaged considerable parts of England. Further, as mentioned above, pluralism and absenteeism represent serious problems. It was quite usual that clerics in the service of the king or a noble patron held benefice in more than one parish and, by implication, a significant number of parish priests were absent from their livings for this reason. They would be represented in the parishes from which they were absent by non-beneficed clergymen who acted as their vicars. Also ordinary rectors who held only one benefice were quite often, for various reasons, allowed to be non-resident on condition that they arranged for non-beneficed clergymen to be their vicars and to perform their functions for pay or a share in the living’s income. Since the death of vicars and other clergymen acting on behalf of absent rectors would not be reflected in institutions, the effect of pluralism and absenteeism was to weaken the correlation between the spread of the Black Death in(to) parishes and institutions as reflections of clerical mortality and its seasonal distribution in the parishes. In addition, the bishops’ administrations did not escape unscathed from the onslaught of the Black Death. In considering this aspect of the problem one must take into account the fact that a bishop’s administrative staff had two forms, a complete household staff at his principal residence, the bishop’s palace, and a small one consisting of selected members of his household staff when he was circulating in his diocese. Bishops were assumed to be travelling round their bishoprics for a considerable part of the year in order to inspect or superintend religious matters, but also, to a considerable extent, in order to consume the bishopric estate’s local manorial incomes in the form of liveries in kind that were not carted or carried by pack horses to his palace in the cathedral city (prandial perambulations). This meant that it was usual that bishops, for a considerable part of the year, were travelling with a small staff and many institutions were performed in this context, while others were postponed until the return of the bishop to his cathedral city and residence. Thus even in normal times institutions occurred in circumstances that would often cause considerable delay for various practical reasons.

448

chapter eleven

In times of dramatic general mortality, the connection in time between an incumbent’s death and the performance and registration of the institution of his successor would tend to be seriously affected both when the bishop was resident at his palace and even more so when he was perambulating. Important reasons for delay were: (1) the bishop’s whereabouts were unknown and had to be ascertained and the bishop contacted before a patron could present his candidate for a vacant benefice and apply for his recognition as successor; (2) extraordinary mortality among the ordinary staff of the bishop’s administration would reduce its normal organizational capabilities, at least during some periods; (3) the bishop’s small travelling staff would tend to be overwhelmed by an exceptionally large increase in number of institutions which it was never designed to handle; (4) the functioning abilities of the small staff which travelled with the bishops were vulnerable to the loss of members, and also because replacement(s), if available at the bishop’s palace, would have to be called for, a process that would tend to take quite some time; (5) lack of suitable candidates for replacements of dead members of the staff. These points can be illustrated concretely. A prominent contemporary chronicler, William Dene, a monk of Rochester, relates that the Bishop of Rochester “out of his small household lost four priests, five gentlemen, ten serving men, seven young clerks, and six pages, so that not a soul remained who might serve him in any office.”147 Even though a rhetorical exaggeration can be noted, and it is difficult to believe that the bishop’s staff succumbed completely, the severity of the onslaught on the staff and the great administrative problems it must have caused can hardly be doubted. During the epidemic onslaught, these factors relating to bishops’ administrations would tend to affect seriously the temporal connection between the resignations or death of parish priests and the institution of successors. The concrete effects on the functioning abilities of the episcopal administrations as observable in the quality of their

147

Gasquet 1908: 120.

seasonality of bubonic plague

449

production of sources, as historians will call it, can be concretely demonstrated (see below). Furthermore, when the successor had eventually been instituted, the archdeacon would be given mandate to induct him into the living, which meant that the would-be successor would have to contact him with the mandate and ask for induction to be effected. One must also take into consideration the spatio-temporal aspects of the Black Death’s impact on the bishops’ administrations: the first dioceses which were attacked were taken completely by surprise and overwhelmed by the exceptional mortality of the epidemic, having no experience on which to base their reactions in order to cope with the onslaught and little or no time to prepare for the catastrophe. Further to the north, however, the bishops and their administrations could prepare themselves mentally and practically for the approaching disaster based on what had happened in the southern dioceses. One should therefore expect that the bishops’ administrations in central and northern dioceses would have coped considerably better with the disastrous events. In 1937, J. Lunn earned a PhD degree in Cambridge for a thesis on the study of eleven of the thirteen surviving registers (from a total of seventeen dioceses in England at the time) titled The Black Death in the Bishop’s Registers (the registers of the dioceses of York and Lincoln had already been studied by A.H. Thompson). Unfortunately, Lunn’s thesis has been lost because a copy was not deposited in the University Library, but some of the data are cited by G.G. Coulton and Shrewsbury who had the opportunity to read it before it was lost. Thus the work’s methodological and source-critical premises cannot be examined and the quality or problems cannot be clarified.148 Also importantly, the accuracy of citation cannot be tested at the source itself (see below). According to Shrewsbury, Lunn stated that the best kept and “most valuable registers are, in order of importance: Lichfield, Lincoln, and York, with Worcester and Hereford of considerably less value.”149 According to Shrewsbury, Lunn also asserts that five of the bishop’s registers, namely those of Bath and Wells, Exeter, Winchester, Ely, and Norwich, do not give the causes of the voidance of their benefices and that Lunn should have concluded that “included in the great number of

148 149

Coulton 1947; Shrewsbury 1971. See also Twigg 1984: 224, fn. 4. Shrewsbury 1971: 51.

450

chapter eleven

plague institutions must be many which were not caused by death.” However, Pickard asserts that resignations and exchanges are specified in the diocese of Exeter’s bishop’s register, and Ziegler that in the bishop’s register of “Somerset [Bath and Wells] about a quarter of the new institutions were the result of the resignation of the previous incumbent rather than his death.”150 Both K.L. Wood-Legh and J. Aberth who independently studied the bishop’s registers of the diocese of Ely also found resignations, Wood-Legh only one and Aberth three, of which the larger number must be accepted. The difference may appear surprising but gives little cause for concern, since the order of magnitude appears quite trustworthy, this was a small diocese, and the average yearly number of institutions before the plague was 3.5.151 I have previously had occasion to point out a tendency towards carelessness in Lunn’s work,152 but now I recognize that I may have been unfair: possibly Shrewsbury has cited Lunn’s thesis inaccurately and in a way that would support his own “campaign” to reduce the mortality rates among the parish clergy as estimated by Lunn. We will enlarge on this point below. The state of the Exeter episcopal registers in this period is described in very negative terms by (Rev. Prebendary) Hingeston-Randolph, as cited by Gasquet, and reflects strongly the impact of the Black Death on the diocesan administration: The Registrum Commune, which is wonderfully full before and after the fatal year, records scarcely anything during the year itself. The ordinary work of the diocese seems to have been all suspended, with a single exception. The register of institutions—a separate volume—is a record of incessant and most distressing work. Its very outward aspect for this period tells a tale of woe. The entries are made hurriedly and roughly, in striking contrast with the neatness and regularity of the rest of the Register. They are not longer grouped, as before, in years, but in months, and the changes in each month exceed the changes of a whole ordinary year, when there was no pestilence. The scribe leaves off the customary ‘vacant per mortem’, as if he dreaded to write the fatal word.153

This does not confirm that the diocese of Exeter’s register of institutions in this period did not indicate whether parish benefices were 150

Benedictow 2004: 344; Pickard 1947: 25; Ziegler 1970: 130, I have not been able to identify Ziegler’s basis for this assertion. 151 Benedictow 2004: 354. 152 Benedictow 2004: 353–4, 356–7. 153 Cited by Gasquet 1908: 100.

seasonality of bubonic plague

451

vacated by resignation, as stated by Lunn according to Shrewsbury, only that vacation by death was not specified. The register has also two sizeable lacunae that may reflect the deaths of the scribes who kept them. Lunn is cited to the effect that the lacunae could be reasonably filled in with an estimated two institutions per day.154 However, the general geographical outline of Lunn’s assessment of the bishop’s registers, the poor quality of those of the southern dioceses at or around the place of arrival of the Black Death and the better quality of those produced in northern dioceses, fits very well into the outlined spatio-temporal perspective on how the bishops’ administrations should be expected to cope with the disastrous events. In his study of the institutions entered in the diocese of Lincoln’s bishop’s register Thompson points out that The presentee could often have a long journey to make to reach the bishop; and again and again, in classifying the institutions, one is struck by the appearance on the same day of several candidates who had been presented to churches in adjacent parishes […]. This looks as though the clergy, who were largely drawn from the neighbourhood in which their parishes lay, waited until they could get one or more companions to make the journey with them.155

The practice of non-beneficed priests who wished preferment to a local benefice vacated by the Black Death of waiting to set out on the journey to the bishop until they could get one or more companions would certainly entail at least some delay. However, one may wonder if they would take the chance of postponing departure if they really had good prospects of being instituted, and this question raises that of the central role of patrons and advowsons. Thompson seems to have overlooked the fact that the real reason for the postponement was that these hopeful men needed to receive the support of the patron or group of medieties holding the advowson to the parish church in question, who would then contact the archdeacon and ask him to enquire into the legal circumstances of the vacancy and the suitability of the candidate. If the response was positive, the patron would present his candidate’s service to the authority who possessed the right of institution, the bishop or the archdeacon, and receive confirmation of the candidacy for the benefice. Next, this piece of news would be conveyed to the candidate,

154 155

Shrewsbury 1971: 59. Thompson 1911: 316–7.

452

chapter eleven

who only then would optimistically set out on a journey to be instituted in the benefice. This account of the process accords better with Thompson’s own wording, understanding the term “presentee” to apply to those who set out on the road to the bishop to be instituted, which implies that they had already been presented by a patron and officially approved, and had then received a notification, at which point they could prepare for the journey to the bishop to be presented and instituted. This means that several non-beneficed priests in a district where the Black Death was raging would be in this situation, awaiting eagerly confirmation of preferment, which also can explain that they could set out on the journey together. This process would obviously be quite time-consuming. Thompson also provides some material that indicates quite a long time lag between the occurrence of vacancies and the institution of new incumbents in the diocese of Lincoln, namely, that “some of the six institutions in September were to churches which had fallen vacant before the end of July.” In Nottinghamshire, “where we might expect to find the earliest ravages of the plague, there is only one such institution before July [1349]” and it is known “that on 15th May archbishop Zouche licensed the dedication of a cemetery at Newark, owing to the alarming growth of the pestilence.”156 Newark is situated deep in Nottinghamshire, and the Black Death must be assumed to have been spreading for a longish time before attacking this town. If we add to this time the usual time of the disease’s development among the rat colonies and unobtrusive endemic phase of about six to seven weeks before demonstrating its presence by a significant number of deaths, and the additional time before the disease had caused a great mortality necessitating the establishment of a new cemetery,157 we see that the Black Death had ravaged Nottinghamshire for at least several months before there was any reflection in the incidence of institutions. Cures vacated by the death of incumbents would quite often not be reflected in institutions for quite a long time of variable duration simply because the number of deaths among the beneficed parish clergy exceeded the number of substitutes competent to fill them, a point that there will be occasion to enlarge upon. Another closely related point that will also tend to distort the connection between the time and location of the death of parish clergy and institution of successors is that 156 157

Thompson 1914: 105–6. Benedictow 2004: 139–41.

seasonality of bubonic plague

453

the best cures would be taken up first whilst the poor cures would go begging, a fact strongly criticized and deplored by contemporaries.158 Studies of institutions which cover not only the period of the Black Death but also the pre-plague and the post-plague years exhibit some conspicuous features that have been generally overlooked. However, in this context they must be closely examined because they imply a much longer average lapse of time between vacancies and institutions than has been envisaged up to now. In particular the high numbers of institutions in the post-plague years deserve comment. In the diocese of Exeter, which comprises the two counties of Devonshire and Cornwall, Devonshire was invaded in the summer of 1348, and it is known that in August the Black Death was causing terrible mortality in religious houses on the River Otter about twenty-five km from the border of Dorset; Cornwall was invaded in the late autumn, implying that by this time the Black Death had spread across Devonshire.159 Exeter was a largish diocese with 642 parishes.160 Pickard found an average of twenty-five institutions for the period 1338–47 and the yearly variation was 8–31. Thus when the number of institutions in 1348 was twenty-eight, the difference from the average is not significant and cannot be taken as evidence of supermortality caused by the Black Death. In 1349, the number of first institutions was 331, in 1350 seventy-five, and twenty-nine in 1351. The fact that the Black Death raged in Devonshire in August, but that there is no noticeable increase in the number of institutions before January 1349, shows that there must have been a usual lapse of time between the death of incumbents and (the registration) of the institution of their successors of something of the order of five to six months. This must reflect the fact that the diocesan administration broke more or less down under the impact of the Black Death, as was suggested above would be the case for the dioceses that were attacked first and had scant time to prepare administratively and mentally for the ferocious onslaught. This shows that a large proportion of the vacancies caused by the Black Death was filled in after the epidemic had disappeared, especially in Devonshire. When this is not taken into account, the level of normal mortality among the beneficed parish clergy will be substantially underestimated 158 159 160

Benedictow 2004: 347; Campbell 1931: 138. Benedictow 2004: 128–9, 131–2; Shrewsbury 1971: 60. Pickard 1947: 22.

454

chapter eleven

and the spatio-temporal aspects of the epidemic process become strongly skewed. In the following period of 1352–60 the average yearly number of institutions diminished to 16.4, reflecting the fact that the normal mortality rate among the new and younger parish priests was much lower than the normal mortality rate among the elderly preplague incumbents; in fact it was almost halved. This implies that thirty-three of the 104 institutions in 1350–1 were due to normal mortality, resignations or exchanges and that about seventy-one were due to plague,161 many of them quite likely pertaining to Cornwall where the Black Death petered out in the autumn of 1349. Also some of the deaths in the plague period were, of course, due to other causes than plague, but many of those that would otherwise have died from such ordinary causes now died from plague instead, and this aspect of clerical mortality therefore loses much of its significance. This shows also that the real mortality rate among the parish priests in the Black Death was considerably higher than 51.5 per cent as estimated by Pickard. However, not all post-plague institutions were first institutions, some were successive institutions in the same living, second, third or even fourth. These successive institutions must be deleted in order to ascertain the pool or population of original incumbents which can serve as a base for estimation of mortality rate, the proportion of them who died, and for constructing an outline of the temporal progression of the epidemic throughout the parishes.162 The numerical relationship between first institutions and successive institutions in the same benefice is reasonably well known only in the case of the diocese of Coventry and Lichfield. Lunn and R.A. Davis agree that the period of the Black Death in this diocese was April to October of 1349. In this period 208 parish priests were instituted. Twenty-three of them were successive institutions to the same benefice; when this number is deducted, the number of first institutions was 185, and successive institutions constituted 11 per cent of the total.163 Assuming that this percentage is

161 Pickard 1947: 22–7. Gasquet 1908: 199–200, gives considerably higher figures, but they are dismissed by Pickard who asserts that they do not refer to first institutions in parish benefices but to all sorts of institutions, also successive institutions in the same living. 162 The size of the population of auxiliary priests from which new incumbents were recruited into the vacancies is not known and must therefore be deleted from the material. See also Davis 1989: 86. 163 Davis 1989: 86. According to Lunn, as cited by Shrewsbury 1971: 77, the number of first institutions was 188. Here Davis’s figures are preferred, since Lunn’s thesis has been lost and his premises cannot be tested.

seasonality of bubonic plague

455

reasonably representative of the proportion of successive institutions among the total number of institutions in the following couple of years in the diocese of Exeter, this indicates that of the seventy-one institutions in the years 1350–1 caused by plague, sixty-three were first institutions. This means that the total number of first institutions caused by plague was 331+63 = 394 first institutions performed in 642 parishes. Consequently, post-plague first institutions constitute 19 per cent of the number of institutions in the plague period and 16 per cent of the total number of vacancies caused by plague. It also means that 61.4 percent of all parish priests serving in the diocese of Exeter at the time it was invaded by the Black Death died in the epidemic. This indicates that the average lapse of time between incumbents’ death by plague and the institution of successors must be much longer than the average of the institutions that were being performed during the plague epidemic in the diocese. It must be underlined that the accuracy of these estimates is dependent on that the assumption that the proportion of successive institutions in the same cure in Coventry and Lichfield is reasonably representative also of this diocese. Taken together, the information relevant to the question of the time lag between deaths of incumbents and institution of their successors in the diocese of Exeter has uncovered a high proportion of long delays that considered together indicate an average time lag of at least several months between the death of incumbents and the first institution of successors, quite likely on the order of five or six months or longer. The considerable proportion of plague mortality related institutions in 1350–1 must reflect great difficulties in filling in many vacancies during the epidemic and a high incidence of long delays in the plague period that would not show in the bishop’s register. This is confirmed by another feature of the register. Gasquet remarks that It is curious to note in these years that numerous benefices lapsed to the Bishop. These must have been vacant six months, at least, before the dates when they were filled by Bishop Grandisson [of Exeter].164

The time perspective of the relationship between the death of incumbents and institution of successors should also be seen in the light of the frequency of lapses of benefices. The magnitude and importance of these problems can be seen in other dioceses as well. In the diocese of Ely (Cambridgeshire), the

164

Gasquet 1908: 200.

456

chapter eleven

number of institutions in 1349 was about eighty-five. In the pre-plague years, the average number of institutions was 3.5, but conspicuously, after the Black Death had disappeared, in 1350 and 1351, there were thirteen and eleven institutions respectively. Since the new parish priests tended to be considerably younger than the incumbents they succeeded, their natural mortality rate was, as could be expected, considerably lower than before the plague, a factor that would be concealed by the total figures of institutions during the immediate post-plague years. In the years 1352–5, the average number of institutions in the diocese of Ely was 1.75, down from 3.5 before the plague, in fact, halved.165 Thus, the twenty-four institutions of 1350–1 represent an “excess” of vacancies related to the plague period of twenty or twentyone parish priests (not seventeen), making the total number of plague mortality related vacancies 105–6. This constitutes strong evidence that a considerable proportion of institutions of successors to cures were performed in the two years after the plague had disappeared, in fact a proportion of 24 per cent of the institutions of 1349 or 19.5 per cent of the total number of plague-mortality related vacancies. Obviously, this implies that a significant or rather substantial proportion of voidances remained unfilled for many months in the plague period, but that this is concealed by the way institutions are recorded in the bishop’s registers, since they (with one exception) do not note the time of the incumbent’s death (or resignation). Taking into account the fact that the post-plague institutions do not reflect mortality in the dying days of the epidemic but rather a variable number of months earlier, the time lag between these institutions and the incumbents’ deaths was even longer, quite likely around 1.25–2.5 years later. Again, this shows that the average lapse of time between the death of incumbents and the first institution of successors must have been quite a number of months. In the diocese of Hereford the average number of institutions during the three pre-plague years was, according to Gasquet, thirteen, while in the plague year of 1349 175 institutions were recorded in the bishop’s register.166 According to W.J. Dohar’s count in his recent study of the Black Death in this diocese, the average number of institutions in the years 1345–7 was six,167 and in 1349 160, almost twenty-seven times 165

Benedictow 2004: 354–5; Aberth 1995: 278–9. Gasquet 1908: 165. 167 In 1348 the number was 11, affected by the intrusion of the Black Death into the southern districts of the diocese at the end of the year, and can therefore not be included in estimation of the pre-plague average. Dohar 1994: 41–2. 166

seasonality of bubonic plague

457

higher. The discrepancy is rather disquieting. Dohar’s figures include all sorts of reasons for vacancies, including death, retirement, resignation and exchange, and apparently also all subsequent institutions in the same parish in 1349, which means that no mortality estimate can be made. However, according to Lunn, as cited by Shrewsbury in a histogram, only about 127 institutions were performed in the months March to December,168 representing a yearly total of 132 when five institutions in January and February are added.169 Perhaps meticulous registration of the institutions would have allowed Lunn to delete successive institutions in the same benefice from the material, which might fit quite well with the difference and should perhaps have been accepted instead. All other explanations tend to be disquieting, and would tend to give the following simple calculations the character of guesstimates or indicative exemplifications. According to Gasquet and Dohar, there were forty-five more institutions in 1350,170 7.5 times the pre-plague average, while in 1351 and 1352 the numbers of institutions were twenty-five and twenty-six respectively, and in fact, the yearly number of institutions did not revert to the pre-plague figure until 1358 (7), then jumped to eighteen in 1359, to return to seven in 1360.171 Thus, in the decade 1350–9 there were 207 more institutions, an average of about 21. If, for the sake of comparability, it is assumed according to the previous data that the post-plague normal yearly attrition rate of the new and young(er) parish priests was roughly half of the level among the pre-plague incumbents, this suggests that thirty of the post-plague institutions resulted from normal deaths and that the remaining 177 institutions presumably reflected the ravages of the Black Death with the caveat in this special case that successive institutions to the same cure must be deducted. Data discussed above suggest that successive institutions in the same parish benefices could have constituted around 11 per cent of the total. On these premises, forty-two of the forty-five institutions in 1350 could be assumed to be due to plague, of which 11 per cent or five institutions may have been successive institutions, and thus the number of first institutions would be thirty-seven. In the

168

Shrewsbury 1971: 70. Dohar 1994: 46. 170 Gasquet 1908: 165; Dohar 1994: 42. This confirms that Gasquet tends to register all institutions whatever the cause of vacancy. 171 Dohar 1994: 42. 169

458

chapter eleven

case of the fifty-one institutions of 1351–2, the same considerations would provide a number of first institutions of forty. When normal mortality and successive institutions are deducted, this means that there were seventy-seven institutions in the years 1350–2, which constitute 58 per cent of the first institutions in 1349 and 37 per cent of the total number of first institutions of 209 in the years 1349–2. Again it must be clear that a substantial proportion of parish benefices vacated by the Black Death was not filled in until several years after the epidemic; in Hereford diocese, as it seems, not until the end of the following decade. If seventy-six institutions performed in the five years 1353–7 are also taken into account, fifty-four of these would on the same premises be first institutions vacated by the Black Death. This implies that the number of first institutions in the period 1349–57 was 263, and that in this diocese only half of the vacated parish cures were filled in during the epidemic. No matter which of these estimates are applied, a very long average lapse of time is implied between the death of incumbents and the institution of successors. The usability of institutions for following the process of epidemic spread of the Black Death is further undermined, or rather their unsuitability for this task is confirmed. Gasquet realizes that there is something important associated with his registration of forty-five vacancies that were filled up in the first post-plague year: this “points to the fact that many livings had probably remained for some months without incumbents.”172 Importantly, he goes on to add: This suspicion is further strengthened by the frequent appearance of the words “by lapse” in the record of institutions at this period, which shows that for six months the living had not been filled […].

Gasquet’s comments show an incomplete understanding of the real significance of his findings, but the pioneering character of his work must be underlined. One might also consider the effects of the bishop’s antiepidemic strategies: he did not stay much at his palace in Hereford, he moved away from the progress of the epidemic to episcopal manors in his diocese, and next to manors belonging to his diocese in the neighbouring diocese of Worcester.173 For all parties concerned this would inevitably cause considerable additional delay and extra difficulties in the process of filling in the vacancies. 172 173

Gasquet 1908: 165. Dohar 1994: 56–7.

seasonality of bubonic plague

459

At the episcopal level of analysis, the Bishop of Bath and Wells conveys relevant comments and views in a circular letter to his clerical personnel in the diocese of 17 January 1349: the pestilence which is spreading itself far and wide has left many parish churches and other cures, and consequently the people of our diocese, destitute of curates174 and priests. And inasmuch as priests cannot be found who are willing out of zeal, devotion, or for a stipend to undertake the care of the foresaid places, and to visit the sick and administer to them the Sacraments of the Church (perchance for dread of the infection and contagion), many, as we understand, are dying without the Sacrament of Penance.175

Thus the bishop conveys information and impressions which in his religious perspective imply that in mid-January 1349 dramatic and unacceptable duration of voidances of priestly benefices was usual in the parishes of the diocese which covered most of the county of Somerset, which in the Middle Ages stretched all the way to the River Avon and Bristol. Since this was a circular letter to his clergy, its contents would not be mere rhetorical imaginings, and it seems likely that the recipients would accept its main thrust on this point, that there was a great dearth of clergy and priestly services and that many people were dying in the diocese without priestly spiritual services in their dying hours. At a time of great religious devotion and the belief that the last rites were a necessary condition for salvation, this was an extremely grave situation indeed. The time perspective of this letter makes it clear that, in the autumn of 1348, the Black Death had raged so severely in Somerset that the situation was critical at the latest at the end of the year. This corresponds perfectly well with the fact that most of the tenants at manors in the south-eastern part of the county and at Frome Braunch in the north-eastern part of the county were dead by the beginning of August and that the Black Death broke out in Bristol 15 August.176 If institutions followed “some little time” after the deaths of incumbents, how could it be that the spread of the Black Death all over the diocese or county in the autumn of 1348, which caused a widespread and grave lack of parish priests by the end of the year, an increase in the number of institutions was noticeable in November at

174 The term “curates” refers to the positions of parish priests who had “the actual cure of the souls.” 175 Gasquet 1908: 92–3. 176 Rees 1923: 29; Benedictow 2004: 128. See also below.

460

chapter eleven

the earliest?177 However, this small increase in November is quite likely not significant: it is independently explicable by Russell’s finding of a normal pre-plague peak of mortality at this time of the year and at the beginning of winter weather when vulnerable persons with poor health were more likely to die than in the warmer seasons (see above). And in view of the early outbreak in Bristol and shortly thereafter in Gloucester, how can it be that there is not an indisputable clear plague-related increase in the institutions of the diocese of Worcester until May of 1349?178 The small increase in December 1348 and January 1349 is also explicable by Russell’s finding which means that such an increase in this month was normal. Independently, other contemporary observers made the same point as the bishop, and as early as 1348 a chronicler asserted that “there is such a scarcity of priests and others serving churches that many of the latter remained without incumbents.”179 Again it must be asked, why is this situation not reflected in the registers of institutions? Can it be any other explanation than that there is a usual time lag of around six months, quite likely significantly longer, between the death of incumbents and the institution of successors, at least in the southern dioceses that were attacked first, unprepared and terror-stricken? A recent paper offers a fresh discussion of the bishop’s register of the diocese of Coventry and Lichfield. This is, as mentioned above, the only such register that provides information both on the dying day of the incumbent and the day of the institution of his successor. It is important to note that this diocese’s bishop’s register is generally characterized as the best, most detailed and most neatly kept bishop’s register (see above). Impressively, this was also the case throughout the epidemic period, thus, the staff managed to maintain these standards under circumstances of immense distress and workload. In a sourcecritical perspective, this reflects the workings of a diocese with a strong tradition for high administrative standards and indicates that the bishop and his staff put, accordingly, a special emphasis on being well prepared for the coming onslaught and being able to uphold their standards, which was not the case with the bishops’ registers of the south-western dioceses. This paper shows an average time lapse between the death of incumbents and the institution of their successors 177 178 179

Gasquet 1908: 96; Shrewsbury 1971: 64; Benedictow 2004: 128. Shrewbury 1971: 66, 68. Campbell 1931: 137.

seasonality of bubonic plague

461

of 39.4 days for the first eight months of the epidemic.180 As should be clear by now, such a time perspective for the study of this subject is insufficient and will not cover a substantial proportion of institutions caused by plague deaths among incumbents. One may wonder why there were no lapses of cures into the hand of the bishop in this diocese and why or how, in contrast to other dioceses, substitutes could be so readily found for all incumbents who died in the epidemic.181 One should note that only those vacancies which were filled and for which institutions were performed were entered in the bishop’s register, and that those which remained vacant for the duration of the epidemic or which lapsed to the bishop are not mentioned. This means that the estimate of the average lapse of time between the death of incumbents and the institution of successors provided by these scholars are not relevant for the present discussion. According to the course of events in other dioceses, a longer perspective of several years would presumably have uncovered further important information. Assuming that the proportion of institutions which was performed in the following four months and the proportion in the following two or three years resemble those of other dioceses for which data are available, the complete average lapse of time was no doubt considerably longer. This paper also reflects some of the misconceptions with respect to the spread rates of plague and the reasons for the differences between historical plague and modern plague that have been thoroughly discussed above. These misconceptions reflect the fact that the authors have not acquainted themselves with the primary studies or standard works on bubonic plague.182 Fortunately, R.H. Davis and also Lunn, as cited by Shrewsbury, provide valuable information on the Black Death related developments in this diocese on the basis of this bishop’s register (see above). Also from a source-critical perspective there is truth in Shakespeare’s words: “When sorrows come, they come not single spies,/but in battalions!” Twigg is surprised by Shrewsbury’s remark that, according to Lunn, the peak in institutions in March in the diocese of Salisbury indicated that the epidemic reached its peak in February, implying that this, in his opinion, was an unexpectedly long average lapse of time 180

Wood, Ferrell, DeWitt-Aviña 2003: 441, 439. Wood, Ferrel, DeWitt-Aviña 2003: 445. 182 See also Wood and DeWitt-Aviña 2003: 327–8, and Wood and DeWitt-Aviña 2004: 485. 181

462

chapter eleven

between the deaths of parish priests and the institutions of their successors.183 As should now be clear, this assumed duration of the average lapse of time between the death of a parish priest and the institution of his successor must be considered unrealistically brief; and as shown above, the reason is that it is based on a misconception or misunderstanding by Thompson. Certainly, in the case of the southern dioceses there is much evidence for assuming average delays of quite a number of months and much longer delays for a substantial proportion of the parish benefices vacated by the Black Death. The central insights that can be learned from this discussion are that there was apparently great variation in the standards of the diocesan staffs or administrations, that there was great dissimilarity in the opportunities to prepare for the onslaught, and that the interaction between these main structural factors caused great variation in the lapse of time between the death of incumbents and the institution of their successors. Another factor is the size of the dioceses, which varied greatly and affected the processes in co-variation with the bishops’ various strategies in the face of the threat of the spread of the Black Death, particularly their strategies of taking refuge on peripheral manors or being on the move away from the approaching plague, settling provisionally on various episcopal manors, and if necessary even moving into a neighbouring diocese. Each diocese must be considered individually, there is no such thing as a usable standard average lapse of time for all dioceses in this respect. It has been well documented above that a flexible time horizon of around half a year is relevant for several dioceses, especially the southern dioceses closest to the Black Death’s landing ground in Melcombe Regis/ Weymouth, which are central to the present discussion. This implies that Twigg’s and Scott and Duncan’s use of institutions to determine the time of mortality in the parishes on the basis of an assumption of contemporaneity or proximity in time between mortality and institution is untenable (also within wide margins of uncertainty). The substantial incidence of long lapses of over six months and of one to two years indicates that the usual estimates of the mortality among parish priests on the basis of institutions in assumed close association with the epidemic will tend to be substantial underestimations and that the real mortality rate of parish priests quite likely was

183

Shrewsbury 1971: 59; Twigg 1984: 65.

seasonality of bubonic plague

463

considerably higher than usually assumed, on the order of 50–60 percent. This supports the direction of my discussion of the various source-critical problems associated with the use of bishop’s registers for estimating mortality rates among parish priests in my monograph on the Black Death.184 Temporal Relationship between the Territorial Spread of the Black Death and Increase in Institutions At the present state of research, this conclusion based on the study of bishops’ registers can only be further tested by examining independent data on the spread of the Black Death in time and space and by comparing these data with the reflections of the mortality among the parish priests in the form of institutions of successors. Twigg’s brief account of the arrival and spread of the Black Death in England and, consequently, also of Scott and Duncan who follow Twigg’s account closely and dependently, are quite misinformed and misleading (see below).185 Instead, the discussion will be based on the most recent synthetic and fully documented presentation of this important historical event which is given in my monograph on the Black Death and supplemented with additional information.186 Given this background, the discussion of this topic will focus directly on the dioceses where they assert on the basis of institutions that the beneficed parish clergy exhibited high mortality in the winter months, and that these months coincided at least mainly with the time the ordinary population there were visited by the Black Death. If this view can be shown to be reasonably tenable, the epidemic would have to be something else, since bubonic plague does not spread efficiently in the winter. The dioceses that have been central in the previous discussion exactly for the same reason are the south-western dioceses of Salisbury, Exeter, Bath and Wells, and the south-western part of Winchester (county of Hampshire). Twigg and Scott and Duncan are completely dependent on Shrewsbury for their material on institutions, so their data is a secondary selection of data from Lunn’s lost and untestable thesis, which also means that Shrewsbury’s rendering of it is untestable. As repeatedly shown above, there are serious grounds for concern with respect 184 185 186

Benedictow 2004: 242–59. Twigg 1984: 58–69; Scott and Duncan 2001: 88–91. Benedictow 2004: 123–43, 342–60.

464

chapter eleven

to this important point (which, unfortunately, has dawned upon me quite belatedly). Twigg purportedly cites Shrewsbury’s data by month. Scott and Duncan do it differently and more inaccurately in the chapter where they discuss the seasonality of the Black Death in England: they indicate only the month when the epidemic started and the months of the peak of the epidemic, in both cases according to an assumption of identity in time between institutions and the progression or main phases of epidemic developments.187 These approaches to the material and their dependence on Shrewsbury’s monograph will shape much of the discussion here, because also Shrewsbury has a negative agenda. His objective is to reject the conclusion that plague could cause high mortality in medieval England because the densities of people and rats and rat fleas in his opinion were too small to allow efficient powers of spread, and for the same reason mortality rates would have to be very much smaller than ordinarily assumed by demographers and agricultural historians at the time he wrote his monograph. This agenda suits Twigg’s and Scott and Duncan’s objectives, namely to deny that the epidemic could have been bubonic plague, which clears the way for an alternative theory that also involved very much smaller mortality rates. In their opinion, the epidemic was, as mentioned, anthrax or the filoviridal Ebola or Marburg diseases, diseases that are so extremely different that apparently very little of an empirical nature restricts their choice of microbiological alternative: in this situation choice of alternative can be made quite arbitrarily, which undermines their validity. It has been shown above that Twigg’s, Scott and Duncan’s and Cohn’s assertions to the effect that bubonic plague spreads only contiguously between rat colonies are not based on the research literature and are at variance with the studies in India and elsewhere; they are, in short, erroneous. On the basis of my quite complete analysis of the Black Death’s spread in England, average spread rates of 1–1.5 km a day by land,188 corresponding to spread rates elsewhere in Europe, including in Norway,189 will be assumed as normal under not unfavourable conditions. This range of spread rates should be considered within a wider registered range of spread rates of c. 0.5–2.5 km a day, with the caveat 187

Twigg 1984: 65–7, 175–80; Scott and Duncan 2001: 88–90, 105–7. Benedictow 2004: 142. 189 Benedictow 1993/1996: 78–80; Benedictow 2004: 227–31; Benedictow 2002: 33–8; Benedictow 2006: 90–4, 107–8. 188

seasonality of bubonic plague

465

that in chilly or cold weather epidemic spread would be greatly reduced or halted altogether.190 One should also take into account bubonic plague’s ability to spread easily by metastatic leaps. In the history of the Black Death in England it is possible to identify a number of metastatic leaps over considerable distances by ship transportation both along the coasts and along estuaries and rivers which established new centres of spread. Among the most important are the early leaps by ship from Melcombe Regis to the Pale in eastern Ireland, to Bristol, to London, to East Anglia and up the River Stour to Sudbury, perhaps from an original infection at Harwich, which can explain why Cambridgeshire was invaded several months earlier than Oxfordshire and Buckinghamshire, and by ship from south-eastern England to Grimsby (or possibly Hull) in the autumn of 1348,191 and so on.192 The diocese of Salisbury is where discussion of the Black Death’s seasonality in England starts. The point of departure must be the original outbreak of the Black Death in England shortly before 24 June 1348 in Melcombe Regis (Weymouth), a town situated on the coast of the county of Dorset in the diocese of Salisbury which also included the inland counties of Wiltshire and Berkshire. This makes it very difficult to understand the reality or substance of Twigg’s assertion that “plague did not appear [in England] until late 1348”193 or Scott and Duncan’s corresponding and dependent assertion to the effect that “In the diocese of Salisbury, the epidemic was rampant through December to February and reached its peak in March.”194 Dorset comprises an area of 2559 sq. km; the maximum distance along the west-east axis is slightly above ninety km, and slightly above fifty km along the south-north axis. Melcome Regis where the Black Death was introduced into the county (and England) is situated at the most about fifty-five km from the borders of the county in any direction. This implies that the epidemic should or could have spread to all corners of the county around mid-August, if the time of the outbreak is taken as the point of departure and not the time of introduction which

190

Benedictow 2004: 230–1. Benedictow 2004: 128, 127–34, 139–40, 144. 192 At the end of September, the prior of Christ Church Priory in Canterbury wrote an alarmed letter to the Bishop of London informing him about various invasions of the Black Death in the diocese. Benedictow 2004: 134. 193 Twigg 1984: 181. 194 Scott and Duncan 2001: 355. 191

466

chapter eleven

is followed by the latent period when contaminated rat fleas could unobtrusively have been transported in goods by land and sea. Importantly, there was great mortality in religious houses on the River Otter in the south-eastern corner of Devonshire about sixty-five km west of Melcombe Regis in August.195 Gillingham is situated at the very northern end of central Dorset, in a longish territorial protrusion between the southern parts of Somerset and Wiltshire. At the sitting of a manorial court held at the royal manor of Gillingham on the Wednesday after the feast of St Lucy (13 December) 1348 it was recorded that heriots (“death duties”) were paid on the deaths of about twenty-eight tenants, furthermore, the bailiff noted that he had in hand the lands and tenancies of about thirty tenants, which means that they had died without heirs who could succeed into their holdings. In many cases, it was declared that no heriot had been paid, although receipts of this kind at the court were unusually numerous.196 This means that the Black Death had raged there for quite some time, since such a large number of heriots was being paid on tenants who had died since the previous sitting of the court, and since at this time about thirty holdings had reverted into the hand of the lord, and since there was already a large backlog of unpaid heriots, which must be assumed to reflect the cumulative process over some significant length of time.197 Consequently, at the latest in the first half of November, and quite likely considerably earlier, the Black Death had broken out in this district almost as far away from Melcombe Regis as one could possibly get in any direction within the county and about as deep inland as one could possibly get. There is no reason to assume that this was the first manor in the area or in the northern parts of the county to be attacked. On the contrary, the survival of medieval manorial records is quite fortuitous; as is, to some extent, the concrete information in this case, since it is a result of Gasquet’s personal request for permission from the Squire of Gillingham to have a look at them. One hopes that more manorial material waits to be studied that can shed more light on these events. This analysis is confirmed by the large number of institutions performed in Wiltshire in 1348, over seventy (see below), which shows that the Black Death had crossed Dorset’s border in the north and spread devastatingly there for a considerable period of time in the autumn. 195 196 197

Benedictow 2004: 129. Gasquet 1908: 194. Ibid.

seasonality of bubonic plague

467

This evidence indicates that the whole of Dorset was engulfed by the Black Death by November at the very latest, probably considerably earlier, although there were no doubt districts or territorial pockets that remained to be invaded or were passed over by the epidemic. This view is supported by the fact that the experienced ecclesiastical historian J.C. Cox found 140 institutions in the diocese in the years 1345–7, a yearly average of c. 47, but registered 190 institutions in 1348 and 140 in 1349. When the average number of institutions in the preceding three years are deducted from the 190 institutions performed in 1348, this produces a net number of 143 institutions that must reflect quite closely the effect of the Black Death in the second half of 1348, representing twelve times the normal average for half a year.198 In fact, the number and proportion of plague-related deaths must be higher, around 155, since incumbents that would have died from ordinary causes in the previous years, now died from plague instead. This makes it rather disquieting that Lunn, according to Shrewsbury’s histogram, found only c. sixty institutions in the last six months of 1348 for the whole diocese, and not a noticeable rise until November.199 Cox’s registration means that the peak period of vacancies and institutions in the diocese of Salisbury was the last six months of 1348, which is corroborated by the large number of institutions in Wiltshire. In fact, Gasquet and Fletcher found seventy-three and seventy-two institutions respectively in Wiltshire in 1348, higher numbers of institutions for this county alone than Lunn registered for the whole diocese according to Shrewsbury, which is even more disquieting.200 One should note that in the diocese of Salisbury there were thirty institutions in 1345 and fiftysix in 1346, so the normal yearly variation is at least hundred per cent,201 since there is no reason to believe that the figures for these two years represent maximum variation in numbers of institutions in the preceding decades. This means that seventy-two or seventy-three institutions in Wiltshire in 1348 represent a level of mortality among incumbents corresponding to the normal attrition of incumbents for two years for the whole diocese. The high number of institutions in Wiltshire in 1348 must reflect the fact that this county to the north of Dorset was invaded in the early 198 199 200 201

Cox 1907: 13. Shrewsbury 1971: 59. Gasquet 1908: 189; Fletcher 1922: 11; Shrewsbury 1971: 59. Cox 1907: 13.

468

chapter eleven

autumn at the latest and that the disease had spread widely, which conforms to the prediction of the of normal spread rates of bubonic plague as presented above. This makes it quite inexplicable that Dorset should not have been engulfed by the Black Death in these months, and demonstrates that the tiny number of institutions registered by Lunn (according to Shrewsbury) before November cannot reflect the real number of victimized incumbents in this period but can be explained as normal attrition by death although within the higher reaches of the range of normal variation. Thus, from the outset of this examination of the relevant data, Twigg’s and Scott and Duncan’s assertions and assumptions crumble. How does this spatio-temporal picture of the spread of the Black Death in Dorset correlate with known institutions? In his paper on the Black Death in the county of Dorset which is mainly based on the study of institutions, Fletcher states that he had found four institutions in Dorset in October, but he seems to have included one of 30 September in West Chickerell “which appears to have been the first parish to be deprived of its incumbent.”202 Does this not appear very surprising? Should not the first institutions have occurred in Melcombe Regis where the Black Death first broke out shortly before 24 June? If the Bishop’s register is reliable and institutions followed incumbents’ death after a month’s time, how can it be that the local incumbents seemingly escaped unscathed at least until the end of the year (and possibly later, as no institution in Melcombe has apparently been identified)? One institution elsewhere at the very end of September and three in October constitute an incidence within the confines of normal variation. The registered institutions occurred 30 September, 9 October, two on the 19th, and then nothing occurred until the beginning of November and again, as it seems, on 9 November (Bridport).203 Institutions are part of the normal clerical events and business of the diocesan organization. There is no reason to consider these four institutions as being due to the Black Death, since they do not represent a statistical incidence outside of normal variation. Neither is there a territorial relationship between these institutions, which display great territorial dispersion, a haphazard distribution unconnected by the movement of an epidemic disease. These institutions do not suggest an epidemic pattern or

202 203

Fletcher 1922: 7. Fletcher 1922: 7–11.

seasonality of bubonic plague

469

rhythm but an ordinary episodic character of clerical deaths. There is no clustering of institutions in Dorset until after mid-November when there were eight from the 17th to the 20th, which makes it likely that the remaining seven institutions for November (out of 17 in all) occurred in the following ten days. In December, there were twentyeight more institutions, which indicate a strong acceleration in the rate of registrations of institutions from about mid-November. Thus, the effects of Black Death appear not to be reflected in the institutions until almost five months after the outbreak at Melcombe Regis, until it had spread all through the county and crossed the borders into the neighbouring counties and had raged there throughout the autumn. Remarkably and rather suspiciously, the number of institutions in Dorset in the second half of 1348 was only a fraction of the institutions in the county situated north of it, namely Wiltshire, which raises serious doubts as to the administrative process by which institutions were entered in the bishop’s register at the time. Taken at face value, this should mean that the Black Death reached this county to the north of Dorset at a time which allowed it to spread according to a pattern of pace and intensity which caused a much higher level of mortality among incumbents than in Dorset. Certainly, this feature needs explanation since it may seem rather farfetched or unrealistic, and as such must rather be taken as evidence to the effect that the bishop’s register does not reflect the reality of mortality among the parish priests in Dorset. And why are there, as it seems, no data for Berkshire? Perhaps it would be useful to take a much closer look at the bishop’s itinerary and, if possible, what happened to the bishop’s staff, and identify possible difficulties of effectuating and completing the process leading to institutions (did he flee away early to Wiltshire?). The main thrust of the evidence is that it took almost five months from the outbreak of the Black Death in Melcombe Regis before effects of the Black Death were reflected in institutions in Dorset; any possible deviation from this conclusion must have been insignificant. This demonstrates that institutions as reflections of and evidence of the process of spread and the mortality among parish priests in the Black Death are only distantly related or correlated to the actual epidemic process or at least that this was the case in this southern diocese. This indicates that parish priests died in great numbers through the summer and autumn, but that this tragic and disastrous development was not reflected in the bishop’s register until much later, and probably imperfectly and in an order that did not reflect in any clear-cut way the

470

chapter eleven

territorial progression of the epidemic. The institutions recorded in the bishop’s register of this diocese are clearly unusable for the purpose of identifying the Black Death’s spatio-temporal pattern of spread in Dorset. Twigg’s and Scott and Duncan’s use of institutions for this diocese is untenable and reflects the absence of source-criticism. Also, the fact that Gasquet and Fletcher registered far more institutions in Wiltshire than in Dorset in 1348 reflects badly on institutions as sources on the spread and mortality effects of the Black Death in this diocese. According to Shrewsbury, Lunn registered about sixty institutions for the whole of the diocese in the months June to December. This means that Lunn found a much smaller total number of institutions for all three counties than Gasquet and Fletcher found independently of each other for Wiltshire alone, and Fletcher is very clear on the point that he has excluded all vacancies “caused by resignation or exchange” from his material.204 Either Lunn’s registration is very deficient or, as there has repeatedly been occasion to point out, Shrewsbury’s rendering of his data is highly inaccurate. This is unfortunate for Twigg and Scott and Duncan who base their cases on Shrewsbury’s rendering of Lunn’s results—“purported results” would now seem a more appropriate choice of words. The registration of such a large number of institutions for Wiltshire in 1348 indicates that the Black Death must have spread widely and ravaged a large part of the county in the autumn of 1348. Fletcher registered 103 institutions in Wiltshire in 1349, which also proportionally indicates that quite a large part of the county was ravaged in the autumn of 1348. However, since it must be assumed that a substantial portion of the parish benefices vacated by the Black Death in 1348 was not filled in before the next year, an even larger part of the county must be assumed to have been ravaged in these months, half or more. This is not at all reflected in the numbers and seasonal distribution of institutions presented by Twigg and Scott and Duncan, which means that their case again breaks down. It also appears rather incomprehensible how the pattern or rhythm of spread should in any way be compatible with anthrax or any viral disease spread by physical contact and the direct transmission of infected living cells as required by filoviridal diseases. The diocese of Exeter lies immediately to the west of Dorset. It is England’s south-westernmost diocese comprising the two counties

204

Fletcher 1922: 7.

seasonality of bubonic plague

471

Devonshire and Cornwall. According to Twigg’s and Scott and Duncan’s account of the events there, the number of institutions in the diocese of Exeter did not begin to rise until January of 1349 and the Black Death continued unabated through the winter months and into the spring and summer of 1349. Twigg’s figures for monthly institutions in the diocese deviate quite markedly from those given by Shrewsbury, they are considerably higher, although he asserts that they are “after Shrewsbury 1971.”205 The poor state of the diocese of Exeter’s bishop’s register cannot explain the gross disparities between the number of institutions in the months November 1348–September 1349 produced by HingestonRandolph, as cited by Gasquet, and Lunn’s number of institutions, as cited by Shrewsbury in a histogram (bar chart), namely 361 and c. 257 respectively.206 Later in his monograph, Gasquet states that the number of vacancies in 1349 was 382.207 Pickard, who has made a new and independent study of the institutions of this diocese, dismisses Gasquet’s figure, asserting that it must include all sorts of institutions, for example those to non-parochial benefices as well as exchanges and resignations. He found 331 first institutions in 1349,208 which means that he very disquietingly found seventy-four more first institutions than Lunn, almost 30 per cent more. Again these considerations raise serious doubts as to the quality and usability of Lunn’s work or perhaps rather Shrewsbury’s rendering of it, and consequently serious doubts over Twigg’s and Scott and Duncan’s use of it. Devonshire is conterminous with Dorset 35–40 km west of Melcombe Regis where the original outbreak occurred shortly before 24 June 1348.209 At the heart of Twigg’s and Scott and Duncan’s argument is a willingness to accept as fact that when the incidence of institutions does not begin to rise until January 1349 this proves that the Black Death began its ravages at or around this time, half a year later, instead of taking it as evidence of the problems in using institutions as sources for this purpose. Assuming a normal spread rate by land of 1.25–1.5 km,

205 206

Twigg 1984: 179–80. I again have an uneasy feeling about Shrewsbury’s figure which seems out of

line. 207

Gasquet 1908: 199. Pickard 1947: 24–5. 209 Grandsen 1957: 274: “Isto anno apud Melcoumbe in comitatu Dorsate parum ante festum nat’ sancti Iohannis Baptiste […].” 208

472

chapter eleven

the Black Death would have crossed the border into Devonshire 14–20 July. Two religious institutions in the south-eastern corner of Devonshire suffered heavy losses in August, namely the canons of the collegiate church of Ottery St Mary and the Cistercian house of Newenham in Honiton about 10 km north-east of Ottery. The time perspective leading to full-blown outbreaks in the second half of August suggests metastatic leaps, either by land, perhaps by pilgrims seeking comfort in the religious institutions, or perhaps the contagion had been transported by ship from Melcombe Regis to the estuary of the River Otter, possibly to the small town of Budleigh Salterton and from there by boat or barge some way upstream. One must also take into account the possibility that the spread of the contagion started before the outbreak in Melcombe Regis by transportation in merchandise loaded from a contaminated ship in the harbour and carried by ship, cart or pack horse. The account of the Grey Friars’ Chronicle that contagion was transmitted in the harbour from the contaminated ship which had arrived from Gascony to a ship from Bristol210 is a sharp reminder of this possibility. The process of spread could also have been accelerated by people fleeing from the outbreak in Melcombe Regis, transporting infected rat fleas in their clothing or luggage, which is an ordinary feature of bubonic plague’s epidemiology. Like many other counties, Devonshire was apparently invaded from several directions, by epidemic spread over land, by carriage of goods or by the movement of people and their luggage over land, and in this case also by people fleeing from Melcombe Regis, or by metastatic leaps by ship or boat. Gasquet and Ziegler both comment that transportation by fishing boats and ships along the coast and up the estuaries and navigable rivers played a major role in the process of dissemination of the Black Death.211 Coulton, who also had the opportunity to read Lunn’s thesis, cites him to the effect that “navigable rivers and estuaries did much to disseminate the plague.”212 More instances will be presented below. Gasquet cites a source which states that the Black Death was raging in the area of the modern district of North Devon on the Bay of Barnstaple: it was raging 7 November at Northam on the estuary of River Torridge, the same day also in the parish of Alverdiscott about

210 211 212

See for instance Benedictow 2004: 126–7. Benedictow 2004: 131. Coulton 1947: 496.

seasonality of bubonic plague

473

five km south-east of Northam, the next day it is mentioned in the village of Fremington situated on the estuary of River Taw at the northern end of the Bay about ten km from Northam, 23 December it was present also in the small town of Barnstaple situated also on River Taw a little over one km east of Fremington. All of these localities are situated about fifty to sixty km north-west of Exeter (as the crow flies).213 This pattern is entirely compatible with the marked tendency of bubonic plague to linger in the same area for five to eight months, because it needs to develop through phases taking around twenty-three days at each place or house of arrival before the first death occurs, and almost six weeks to develop into a local epidemic. Thus, the datings of the epidemic presence in these neighbouring localities reflect a timeconsuming process of arrival and local spread, and imply that the disease had first broken out in the area at least several months earlier and that the contagion had reached there almost six weeks before the first outbreak, a pattern or process which would be repeated in all the subsequent outbreaks in the area. Barnstaple and Northam could easily have been contaminated by ship and have been included in a more comprehensive spread along the coast that started in the summer and caused the outbreak which was recognized at Bristol 15 August. The Black Death was also raging in villages on the River Exe in November,214 a river that is navigable for a long part of its course, far north of Exeter, all the way to Tiverton in north-eastern Devonshire, only about fortyfive km south-east of Barnstaple. Again transportation by ship or boat may have played an important part, in this case from the south. These data on the spread of the Black Death in Devonshire indicate that the whole of Devonshire had been engulfed by the Black Death by the late autumn and that the county had been invaded from several quarters, by landings from ships or boats sailing along the coasts, especially in villages or small towns on the estuaries of major rivers, from where the epidemic leapt inland by river transport and by spread over land. This makes it rather incomprehensible that there is no sign of any increase in institutions before January 1349, if institutions were useful sources for determination of the spatio-temporal progression of the Black Death. The validity of the assumption that institutions were useful in this regard should be considered in light of the distance from

213 214

Gasquet 1908: 102. Ibid.

474

chapter eleven

Melcombe Regis deep into Wiltshire where the Black Death caused over seventy institutions in the autumn of 1348. How could it be that parish priests in Devonshire should collectively have remained unscathed in the autumn of 1348, although outbreaks and great mortality are documented in August and the epidemic raged in northern Devon later in the autumn, while the parish priests of Wiltshire were exposed to catastrophic mortality? And how could it be that much the same must have occurred in the county of Somerset north of Devonshire (see below)? Instead, this outline of the spatio-temporal progression of spread of the Black Death according to institutions appears highly unlikely or inexplicable, at variance with other independent types of sources constituting further proof that institutions are at best poor sources or rather unusable or misleading sources regarding the spread of the Black Death, especially in the early phase of the epidemic. This means that they do not constitute evidence of a winter epidemic of plague in Devonshire. It is also important to note that no winter epidemic of plague was recorded in this county after the introduction of parish registers which allows a closer examination of plague seasonality for the period 1546–645.215 By failing to consult Hatcher’s fine monograph on late medieval Cornwall, Twigg and Scott and Duncan lost the opportunity to study his specification of numbers of institutions by month for this county, which is at variance with their assertion of a winter pattern: in Cornwall, the incidence of institutions does not show significant increase until March 1349, the highest figures for institutions occur in the months April to July, and then numbers begin to fall, reaching quite ordinary levels in the late Autumn.216 Thus, it is erroneous to include Cornwall in their argument for the spread of the Black Death in the winter according to institutions. On the same assumption of normal spread rates, the Black Death should have moved across Devonshire the c. 100 km from the border with Dorset to the border with Cornwall in sixty-seven to eighty days, that is, some time between about 20 September and early October, a pace of westwards spread of plague across the county that is recorded also later.217 The whole of Devonshire should have been ravaged by the Black Death in the summer and autumn of 1348. This is by and large

215 216 217

Oswald 1977: 77–81, 87–91. Hatcher 1970: 103. Oswald 1977: 78.

seasonality of bubonic plague

475

confirmed by an entry in the register of the Church of Friars Minor at Bodmin where it is stated that the Black Death broke out there shortly before Christmas,218 which means that epidemic manifestations occurred about thirty km into Cornwall from Devonshire by the end of the year and that most of this county presumably was ravaged in 1349. Importantly, Pickard registered seventy-five institutions in 1350 and twenty-nine in 1351, which compared with the average of twenty-four institutions in the pre-plague decade show that the diocesan organization did not succeed in filling in the vacancies caused by the Black Death until 1351; in the following years the situation normalized. Since the average number of institutions in the following nine years 1352–60 was eighteen due to the lower age of the new incumbents who had a correspondingly lower normal attrition rate, it appears that sixty-eight of the institutions in 1350–1 were replacements of incumbents killed by the Black Death. This means that 331+68 = 389 institutions in the years 1349–51 were caused by the Black Death and that the mortality rate among the 642 parish priests at the start of the Black Death was 60.6 per cent. This estimate will only be marginally affected by some minor factors that are not accurately accounted for. It is unlikely, for instance, that all parishes had their formal incumbents in place and were not represented by vicars who would not be replaced by institutions after their death, which would tend to reduce the mortality rate among the pool of functioning priests. The diocese of Bath and Wells comprised the medieval county of Somerset which stretched from the borders of Devonshire and Dorset in the south all the way to the River Avon. Bristol is situated on the other riverside where the county of Gloucestershire and the diocese of Worcester began. According to the data furnished by Shrewsbury, there was a small increase in institutions in November followed by quite a strong increase in December. One should note Russell’s finding of a general pre-plague mortality increase in November, which means that the small increase in November has an alternative explanation and that there is no clear plague-related evidence of an increase of institutions before December. A higher level of institutions prevailed through the winter months and the early spring months (January–April). The crucial question is: How can this temporal pattern of institutions reflect the spatio-temporal spread of the Black Death in the 218 Creighton 1891: 116: “parum ante nativitatem Domini intravit villam Bodminiae.”

476

chapter eleven

diocese? The distance from Melcombe Regis to the border of Somerset is about thirty-five km. Taking as the point of departure the original outbreak of the Black Death in Melcombe Regis shortly before 24 June and applying normal spread rates of 1.25–1.5 km a day, the Black Death would cross into Somerset about twenty-three to twenty-eight days later, 14–19 July. However, the process of spread could have started earlier, before the outbreak, through transportation of contaminated goods by ship, cart or pack horse. The process of spread must also be assumed, as mentioned above, to have been accelerated by people fleeing from the outbreak in Melcombe Regis and surrounding areas who transported infected rat fleas in clothing or luggage, since this is an ordinary feature of bubonic plague’s epidemiology. It is as should be expected, therefore, that “by the beginning of August, most of the tenants of Frome Braunch in Somerset were dead and there were other deaths in North and South Cadbury.”219 The two manors and villages of Cadbury are situated in the south-eastern corner of Somerset around forty-five km north of Melcombe Regis, and Frome about thirty km further to the north, in the north-eastern part of Somerset. In the area between these three localities, the Black Death is reported to be raging 19 November in Evercreech, a village situated a couple of km north of Castlecary, and a fortnight later in Castlecary itself and the adjacent village of Ansford.220 This is the same pattern noted above for North Devon. It is entirely compatible with the marked tendency of bubonic plague to linger in the same area for five to eight months for easily explicable epidemiological reasons, and with late arrival in the plague season, the epidemiological processes could be suppressed by cold winter weather to recrudesce in the spring and complete their course among local populations of rats and human beings. This means that it can be shown that the Black Death was raging in quite a large area in eastern Somerset from early August at the very latest, which means that it must have broken out in the second half of July in order to have attained a serious character in early August and maintained it throughout the autumn. North and South Cadbury are situated about fifteen km west of Gillingham, which broadens the documented area for the Black Death in this part of the country. Very serious developments in Somerset by early August at the latest can explain

219 220

Rees 1923: 29; Benedictow 2004: 128. Gasquet 1908: 97; Holmes 1911: 25–6.

seasonality of bubonic plague

477

that that the Bishop of Wells and Bath issued prayers for general use in the diocese in August.221 One might like to surmise that Frome Braunch was contaminated so early by goods from Bristol loaded on boats moving up the River Avon to be unloaded at various places and transported to various destinations. However, the recognized outbreak in Bristol is dated to 15 August,222 more than a week after the plague is known to have been raging at Frome Braunch which may appear a problem for the chronology of the epidemic’s development. One could realistically assume that the epidemic had reached an early phase among poor people living in the harbour area before its extreme mortality caught the attention of chroniclers among the social elites. Assuming a normal time horizon for the development of bubonic plague epidemics from the arrival of contagion to the recognized epidemic outbreak in the city, i.e. seven weeks, it must have arrived at the end of June. Since ships in those days sailed at an average pace of about forty km a day,223 the voyage from Melcombe Regis of around 700 km would normally take about seventeen days, thus, the ship transporting the contagion must have left Melcombe Regis around 10 June, almost a fortnight before the recognized outbreak in this town. Interestingly, in the chronicle providing the best account of the first phase of events there, it is stated that two ships came alongside in Melcombe Regis’s harbour, one from Bristol, one from Gascony, presumably the ship that originally brought the contagion from Bordeaux, although the account is dramatically condensed in time as was so typical of medieval chroniclers. Since the Black Death broke out in the Pale in Ireland at the very beginning of August, the same type of analysis of the time horizon of epidemic developments suggests that the ship transporting the contagion from Melcombe Regis to towns on the coast of the Pale must have put to sea around 1 June.224 This means that it is quite possible that Frome Braunch was contaminated with goods shipped upstream from Bristol before the outbreak in the city itself. This accords with Gasquet’s assertion that small towns along the coast of Somerset, namely Bridgewater, Clevedon, Weston-super-Mare, Portishead and also Bristol, “were among the

221 222 223 224

Holmes 1911: 25. Boucher 1938: 34. Benedictow 2004: 102, fn. 20. Benedictow 2004: 127–8, 143–4.

478

chapter eleven

earliest places in the county to be attacked,” and that this demonstrated that “the contagion was carried to these coast towns by a boat passing up the Bristol Channel.”225 This outline accords with the pattern that was observed in North Devon in localities in the vicinity of or on Barnstaple Bay. Thus, the Black Death spread in cargo by ship to many localities along the coast and up the estuaries and rivers, producing multiple contaminations of towns and villages. One should also envisage how the epidemic was spread with more and more broadly by goods and by people fleeing from these localities, the powers of spread developing almost according to a multiplicative pattern of progression. On this basis of all available data on the spread and whereabouts of the Black Death in Somerset and the possible origins of contagion I cannot see how they can be made compatible with the temporal perspective provided by institutions. The Black Death had broken out in the north and south of eastern Somerset by some time in July, presumably in the second half of the month, and was raging from the early August at the very latest. The Black Death can be shown to be present in quite a number of other localities later in the autumn. The early outbreak in Bristol must have functioned as a powerful centre for the spread of the epidemic into Somerset, not only by goods, but certainly by people who fled the city when they saw the horrors and likely death awaiting them if they stayed. On the premise that institutions should be suitable for spatio-temporal determination of the spread of the Black Death, the time perspective inherent in these data makes it rather impossible to understand that there was no institution in September, and that a clear plague-related increase in the number of institutions first occurred in December. Obviously, one would like to have more data. Interestingly, a number of mortality studies has been performed on manors in the eastern half of Somerset, for Walton, Mells, Pilton, Batcombe, Ditcheat and High Ham (and for Marnhull in Northern Dorset).226 One may hope that the manorial sources from which these mortality estimates are produced can provide information on the arrival and spread of the Black Death in the eastern parts of the county and diocese. Razi for instance has shown that the Black Death invaded the parish of Halesowen in May 1349 on the basis of information given in the court rolls.227 225 226 227

Gasquet 1908: 97; Holmes 1911: 26. Benedictow 2004: Map 361, 364, 375. Razi 1980: 102.

seasonality of bubonic plague

479

The diocese of Winchester is the last area to be examined in this way in order to study the relationship between the temporal distribution of institutions and the time of the Black Death’s spread. The diocese of Winchester is constituted by the counties of Hampshire and Surrey. Then as now, Hampshire was conterminous with Dorset’s eastern borders. According to Shrewsbury, for 1349 Lunn registered 228 institutions in Hampshire and thirty-one institutions in the county of Surrey.228 Gasquet found both 204 and 228 institutions in Hampshire and, confusingly, eighty and ninety-one institutions in Surrey, 2.5–3 times more than Lunn found there, according to Shrewsbury. Although the lower figures presumably reflect unspecified deductions for institutions not caused by plague,229 something must plainly be erroneous. The temporal distribution of institutions does not show a tendency of extraordinary increase until January 1349;230 the slight increase in the previous month is so modest that it may reflect the ordinary late autumn–early winter mortality increase identified by Russell. Unfortunately, in the case of Hampshire there are few secular data with which to test the incidence and temporal distribution of the institutions which is at the heart of the matter in this subchapter. Melcombe Regis is situated about sixty km from the border with Hampshire, and at a normal spread rate by land of 1.25–1.5 km per day it should have taken the Black Death forty to forty-eight days to the border into Hampshire. Assuming that the spread started at the time of the recognized outbreak, the crossing of the border should have occurred sometime between 29 July and 6 August, though as mentioned above, the spread could have started earlier and the border have been crossed earlier. Since Hampshire is a little over sixty km along the west-east axis to the border with Sussex, this distance should have been covered by about mid-September. However, it is hard to imagine that the Black Death should not have been introduced quite early in localities along the coast of Hampshire as has been shown to have occurred in Devonshire and Somerset. This was in fact the case, the Black Death was spread efficiently by ship also eastwards along the coast: at the end of September, the prior of Christ Church Priory, Canterbury, wrote in alarm to the bishop of London about the outbreaks of the Black Death

228 229 230

Gasquet 1908: 130, 208–9; Shrewsbury 1971: 90–1. Gasquet 1908: 209. Cf. Watts 1998: 22.

480

chapter eleven

in the latter’s diocese,231 at the same time the outbreak in London was recognized. The bishopric of London included also the county of Essex and the Black Death had spread further up the south-eastern coast at least as far as the estuary of the River Stour on the border between Essex and Suffolk and had been transported up the river at least as far as Sudbury.232 This makes it rather unreasonable to assume that the coasts of Hampshire were passed by. Against this background, it seems reasonable to mention that Henry Knighton, a contemporary chronicler, asserts that the Black Death first broke out in Southampton, which could be taken as an indication of a very early outbreak there.233 Fortunately, in recent years some concrete evidence of this process has been provided by preliminary studies of transactions at manorialcourt sessions at the manor of Titchfield on the coast of Hampshire. Titchfield is a village and small port on the estuary of River Meon which empties into the Solent around twenty km south-east of Southampton. In 1347, five heriotable deaths among the villains were recorded at the sittings of the manorial court, and in the first seven months of 1348 another five cases were recorded, which in itself is a suspect increase bringing to mind the outbreaks in the second half of July at manors in Somerset which had caused great mortality by the beginning of August. Next, there was a long break from the July session of the court until eight heriotable deaths were recorded at the court held 31 October. Very unusually, only a week later there was a new sitting of the court in which twenty-five more deaths were reported, which suggests a weakly functioning court organization that did not manage to carry out much work at the previous sitting. Since the normal rhythm of the court’s sittings is not known, the analysis of the events becomes uncertain. However, in the last seven months of 1349 there were four sessions of the court, a court session being, on average, held each seven weeks. Against this background, the eerie silence in the over three months between the implied July session of the court and the last day of October suggests that two sessions of the court would ordinarily have been held in this period. This also suggests that the manorial scribe was an early victim and that the onslaught of the Black Death temporarily broke down the manorial organization and that this could have occurred

231 232 233

Ziegler 1970: 161. Benedictow 2004: 134–5, 137–8. Benedictow 2004: 132; Ziegler 1970: 123.

seasonality of bubonic plague

481

before the expected court in the second half of August. Under the catastrophic circumstances, the court could only be workably reconstituted after several months when two court sessions were hastily held, before it broke down again and no session of the court was held again until over four months later, on 11th March.234 This reflects the fact that great amounts of court business were accumulated and hastily taken down in the records at very uneven intervals in catastrophic circumstances making the temporal links between the recording and the events tenuous. The two sittings on 31 October and 7 November may quite likely have recorded mortality effects of the Black Death in September, possibly also from August, and we cannot assume that these two courts actually managed to bring the records up to date: it is possible that many deaths which actually occurred in the autumn of 1348 remained unrecorded until the next court in mid-March. The events on the small neighbouring manor of Swanwick are even more clouded, but it appears that the Black Death certainly was making its presence felt in the late autumn when two deaths were reported in the court held 25 November, but then another court was not held for 3.5 months, which could be taken to suggest that this manorial organization had also broken down.235 As can now be seen, court rolls and other manorial records also tend to be quite problematic sources for determination of the time the Black Death visited a given location. They are also problematic because a tenancy could have changed hands several times owing to the death of subsequent holders as they died in rapid succession without being formally noted in the court’s records.236 The pace of change of hands of tenancies could easily have been increased when new tenants moved into the houses of the previous holders before the epizootic process had come to an end and infective rat fleas had died. Obviously, this is a process which would tend to distort the time-link between the epidemic impact and the recording of heriots, lending the process some disquieting resemblance to the temporal and organizational process occurring between an incumbent’s death and the institution of his successor. However, no other types of sources seem to be available that could help detail the spatio-temporal progression of the spread of the

234 235 236

Watts 1998: 23–4. Watts 1998: 25. Benedictow 2004: 376.

482

chapter eleven

Black Death in this county. Fortunately, there appears to be interesting manorial material available, and mortality studies have been performed for some Hampshire manors, for Bishop’s Waltham, Corhampton and Damerham, and more in-depth studies of the extant sources of Titchfield and other manors in the surrounding districts seem to offer some promise.237 Recently P. Arthur has written an outstanding thesis on the study of eleven of the Bishopric of Winchester’s manors in Hampshire providing, among other things, valuable mortality data, but without paying attention to the temporal aspect of the Black Death with respect to arrival and spread.238 At least some of the records of these manors which could be used for mortality estimates of customary tenants and social classes paying money heriots in the Black Death must be assumed to contain valuable indications of the time of their death. Admittedly, this is not much evidence with which to test the usability of institutions for determination of the time the Black Death’s spread in Hampshire. However, the available evidence indicates that the Black Death spread in the county in the early autumn of 1348 and that this process is not reflected in the number or spatio-temporal distribution of institutions. Summary and Conclusion This chapter’s objective has been to examine all material bearing upon the connection between seasonality and the spread of the Black Death and later plague epidemics in England. It has appeared that through the whole plague era of 1348–1666 plague epidemics spread efficiently only in the warmer seasons and subsided and more or less disappeared with the advent of chilly and cold weather. This pattern is incompatible with all diseases spread by cross-infection, by droplets or by personal contact, which flourish in cold weather when people stay closer together and droplets last longer and drift further. All ascertained facts and conclusions are consistent and compatible with the conclusion that the epidemics were bubonic plague. Twigg and Scott and Duncan argue that institutions of beneficed parish priests in the period of the Black Death show a clear winter 237 238

Benedictow 2004: Map 361, 364–5; Watts 1998: 25–6. Arthur 2005.

seasonality of bubonic plague

483

incidence in the south-western counties which disprove that the Black Death was bubonic plague. However, they have neglected to exercise source-criticism and to examine critically the evidence for a temporal link between the death of incumbents and the institution of successors which in this case is the crucial piece of information. Instead, this task has been performed in this chapter. It has appeared from the critical examination of sources and studies on the matter that the use of institutions to determine the spread of the Black Death in time and space is highly problematic for several serious reasons. The study of the intermediate process between an incumbent’s death and the institution of his successor has uncovered a time-consuming and complex system often taking several months or longer. A significant amount of secular evidence reflecting the time and whereabouts of the Black Death in the south-western counties has revealed that the epidemic was widespread and causing great mortality in the southwestern counties and dioceses without being reflected in institutions. Despite the fact that the Black Death broke out in Melcombe Regis in Dorset shortly before 24 June, there is no reflection of the widespread severe mortality which it must have caused among the beneficed parish priests until the turn of the year, the second half of November being the earliest time such a mortality process can be discerned, but in most cases not until January 1349. A similar situation appears also to have been usual in other southern dioceses around the epidemic epicentre in Melcombe Regis (Weymouth). This shows that institutions in these counties and dioceses reflect incumbents’ death in the Black Death in a clearly discernible way with a time lag of five to six months. However, it has also been shown that that lapses of six months or longer were frequent, and that a substantial proportion of vacancies was not filled until one or two years after the incumbents’ death. Taken together these data indicate a long average time-lag but also suggest that more focus should be placed on the process of filling in vacancies after the Black Death. This study has uncovered a serious lack of congruence between our source-based knowledge on the outbreak of the Black Death in Melcombe Regis shortly before 24 June 1348 and the epidemic’s spread in the south-western dioceses in the following six months and the spatial and temporal reflections of mortality among parish priests in the statistics of the institutions of parish priests according to Shrewsbury’s rendering of Lunn’s data, which constitutes the material used by Twigg and Scott and Duncan. This makes it an even larger scholarly tragedy

484

chapter eleven

that Lunn’s thesis was lost at least a couple of years before Shrewsbury’s monograph appeared,239 with the serious consequence that the correctness of Shrewsbury’s use of it or Lunn’s application of source-criticism cannot be examined or tested. Taken together, the many problems which have been uncovered with respect to the data rendered by Shrewsbury which are purportedly taken from Lunn’s thesis, the gross incongruence between these data on institutions and the facts on the ground with respect to the Black Death’s arrival and spread in time and space in south-western England, as well as the loss of testability, mean that Twigg’s and Scott and Duncan’s reliance on this lost study of institutions for their argument of seasonality appears materially untenable and methodologically invalid. Their use of this material in order to prove that the Black Death spread in these regions in the winter breaks down as untenable. One can only hope that the institutions in the bishop’s registers for this period will be studied again and now with a keen eye to possible information on the lapse of time between the time of death of incumbents and the time of institution of their successor and an awareness that this requires a study of the entries in at least a tenyear perspective comprising the years preceding and following years of the Black Death. Using institutions as sources for the seasonality of the spread of the Black Death in England is not for faint-hearted medievalists, and scholars of other disciplines are respectfully advised to avoid them.

239

Ziegler 1970: 297, fn. 22.

PART FIVE

THE ALTERNATIVE THEORIES

INTRODUCTION: THE HISTORY AND ESSENCE OF THE ALTERNATIVE THEORIES In the history of alternative theories of the identity of historical plague epidemics, the two first and the fourth, those put forward by Shrewsbury (1971), Morris (1971), and Karlsson (1996), respectively, are closely connected in two important respects. Firstly, Morris’s theory reflects or represents a strong negative reaction to Shrewsbury’s theory and Karlsson’s theory is very much inspired by Morris’s theory. Secondly, they have in common that they all accept that the microbiological agent was Yersinia pestis, albeit in the case of Karlsson’s theory an unspecified mutated variant. This chain of development of alternative theories reached a dead end with Karlsson’s theory. Nonetheless, Karlsson’s theory represents a sort of link to the following theories in so far as he is the first to make use of the arguments against the bubonic-plague theory that Twigg presented in the third alternative theory (1984) on which I will comment next among the alternative theories. The three other alternative theories have in common that they are based on other microbiological pathogens. An abrupt and sharp process of radicalization took place that started with Twigg’s anthrax-based theory, was followed by Scott’s and Duncan’s theory of a filoviridal virus, the type of microbiological agent causing Ebola disease and Marburg disease (2001) or, perhaps, even a disease that has since disappeared (2004) and therefore is caused by an unknown and microbiologically unverifiable and unidentifiable virus. Similarly Cohn argues in his alternative theory for a viral disease spread by cross-infection that has since disappeared and is therefore also caused by an unknown and microbiologically unverifiable and unidentifiable virus (2002). These theories are in the process of being overtaken by the rapid development of paleomicrobiology (see above). Firstly, because paleomicrobiologists have developed fully-fledged techniques for the testing of skeletal remains in historical graves for bacterial causes of death and on this basis several studies have been published which show that all the great historical pandemics of plague have been caused by a genetically stable unmutated variant of the biovar Yersinia pestis Orientalis. This leaves Scott and Duncan’s and Cohn’s theories only the faintest hope for survival, that their purported pathogen(s) may have spread

488

introduction

concomitantly with bubonic plague without having been revealed by the presently available techniques. However, these diseases are so different from bubonic plague in their transmission and pattern of spread that they can for all practical purposes be excluded as alternatives by traditional historical and medical sciences. All six advocates of alternative theories have in common that they flatly reject all other alternatives in addition to the established bubonicplague-cum-Yersinia-pestis theory, and since they are incompatible at least five of them must be untenable and massively erroneous, and why not all six? However, there is a close and cordial connection between Twigg and Scott and Duncan, the only instance of open mutual respect and co-operation within this field of study. The relationship is principally shaped by Scott and Duncan’s ambition to develop their own alternative theory, but they take over lock, stock and barrel Twigg’s arguments for rejecting the bubonic plague theory, which spared them the effort of developing their own platform but also exposed them to very serious problems. Much the same goes for Cohn who also eagerly grasps Twigg’s arguments against the bubonic plague theory, but otherwise is much more independent in his approach. As now can also be seen, Twigg is the central scholar in the later developments of alternative theories of historical plague; his anthrax theory is apparently generally rejected, but his arguments against the bubonic-plague theory are eagerly employed by all later advocates of alternative theories. Twigg’s central arguments against the bubonic-plague theory have been discussed above in various chapters and have been shown to be untenable, specifically his denial of the broad European presence of black rats, the implications of the mortality rates in the Indian plague epidemics, and with respect to the importance of metastatic spread in the epidemiology of bubonic plague. Karlsson’s theory will be discussed first, since it is closely associated with Morris’s paper.

CHAPTER TWELVE

THE BEGINNING: THE ALTERNATIVE THEORIES OF SHREWSBURY AND MORRIS Shrewsbury: the Composite, Low-Intensity Theory It is often overlooked that J.F.D. Shrewsbury is the pioneer of alternative theories of the microbiological nature of the Black Death and later plague epidemics in his monograph A History of Bubonic Plague in the British Isles of 1971. He did not reject the role of bubonic plague altogether. He argues that rat-borne bubonic plague was introduced into England with the Black Death, but that it caused a specific mortality rate of only about 5 per cent at the most. Instead, he asserts that the fact that there were numerous plagues other than bubonic plague in fourteenth-century England is commonly ignored; but smallpox, measles, diphtheria, pertussis [= whooping cough], influenza, and dysentery undoubtedly occurred in widespread and deadly epidemics, and the “burning ague” in Langland’s list was almost certainly typhus fever […] it is obvious that he was acquainted with a variety of communicable diseases and other disorders, as anyone would expect who was not obsessed with the notion that bubonic plague was omnipresent in fourteenthcentury England.1

Thus, Shrewsbury addresses the problems posed by the advent of plague and the abrupt and long-lasting late medieval population decline by underscoring the epidemiological and demographic importance of other microbiological agents which caused other serious or severe epidemic diseases, but which had been around all along. The central line of argument throughout his monograph is that the introduction of bubonic plague meant only a small but significant increase in the prevailing generally high level of epidemic mortality of those times. Shrewsbury’s monograph is characterized by his huge and systematic efforts to play down the significance of the Black Death and subsequent epidemics of bubonic plague.

1

Shrewsbury 1971: 36, 42.

490

chapter twelve

It is, therefore, misleading when Twigg and Scott and Duncan portray Shrewsbury as an irrational, incompetent and rigid defender of the bubonic plague theory of historical plague epidemics.2 They have completed his line of argument by rejecting the possibility that there could have been epidemics of bubonic plague in England excepting, perhaps, the sporadic incidence in port cities, particularly London. However, since their lines of argument are strongly restricted to England, they needed to use his monograph but must argue that he systematically misunderstood the obvious microbiological and epidemiological facts on the ground and claim that the epidemics he designated bubonic plague either were anthrax or “haemorrhagic plague” respectively. At the same time, they miss no opportunity to avail themselves of Shrewsbury’s efforts to minimize the significance of bubonic plague. In contrast to Karlsson, Cohn, and Scott and Duncan, Shrewsbury does not invent or introduce new or unknown diseases or mutated forms of other diseases unknown to modern medicine, but presents a composite alternative theory in which plague plays only a minor contributory role. I cannot see how it was possible at that time (the early 1970s) to assert that the Black Death caused relatively high mortality only in urban centres and that the mortality rate for the whole country was at most 5 per cent. At the time, quite a number of manorial studies were available to him showing, on average, at least ten times higher mortality in the countryside than his estimate of 5 per cent, but not a single mortality estimate for any English urban centre was available to him and is still not available.3 Another independent and sufficient reason for rejecting his theory is that the main alternative diseases of his composite theory, such as exanthematic typhus and also probably smallpox, apparently did not arrive in Europe until around 1490.4 Although he cites H. Zinsser’s authoritative monograph on typhus where it is concluded that this disease did not arrive in Europe until the end of the fifteenth century,5 Shrewsbury emphasizes on the

2

Scott and Duncan 2001: 14, 16–15, 94, 98–100, 102, 110–1, 149, 151–4, 166–8, 202, 209, 212. 3 Benedictow 2004: 360–77. 4 See, e.g., Zinsser 1985: 71–6, 241–53, 278–9; Copeman 1960: 127–8; Cartwright 1977: 76–8; Snyder 1965: 1059–60; Greenwood 1935: 172–4, 227; Ackerknecht 1963: 67. 5 Zinsser (1934)1985: 241–4.

the alternative theories of shrewsbury and morris 491 same page the importance of this disease during the Black Death and subsequent plague epidemics.6 And there are other serious objections to his conclusions. Morris: the Primary Pneumonic Theory In a sharply critical review paper of Shrewsbury’s monograph, C. Morris launched another alternative theory, namely that the Black Death and later plague epidemics were primary pneumonic plague, i.e., caused by the same pathogen Yersinia pestis but disseminated by interhuman spread of infected droplets. He makes this contention for British plague history but the implications for other countries are clear.7 Morris’s review is the basis of Karlsson’s paper to the same effect and will be discussed briefly as part of a thorough analysis of this paper. However, it must be pointed out that Morris confuses secondary pneumonic plague with primary pneumonic plague. He castigates Shrewsbury, for example, for citing the Irish friar of Kilkenny John Clyn’s clinical description of plague cases in the Black Death without including the element “some died spitting blood”. However, even these few words must reflect that the majority of plague cases did not spit blood and therefore, presumably, were bubonic cases, and that the clinical characteristics of the Black Death in this area had the normal incidence of cases which developed secondary pneumonia and were “spitting blood” before they died. Morris avoids citing the part of John Clyn’s clinical description that would make this absolutely clear and justify Shrewsbury’s view on the medical and epidemiological nature of the Black Death in the British Isles: […] many died of boils and abscesses, and pustules on their shins [= legs] and under their armpits; others frantic with pain in their head, and others spitting blood […].8

As can be seen, the references to buboes and pustules and carbuncles dominate the clinical picture, and the extreme headache which often

6

Shrewsbury 1971: 125. See also register ibid: 660, typhus fever and smallpox. Morris 1971: 205–15. 8 Hirst 1953: 13. There is an insignificant deviation from Hirst’s translation in Morris’s citation, substituting “others” with “some.” 7

492

chapter twelve

drives patients to irrational, desperate action is a typical clinical feature of bubonic plague. John Clyn’s observation that some were spitting blood indicates a normal proportion of cases of secondary pneumonic plague in epidemics of bubonic plague. This account contains quite a good description (for the time) of an ordinary epidemic of bubonic plague and as such constitutes empirical evidence to this effect. Morris is also sharply critical of Shrewsbury for denying the existence of pure epidemics of primary pneumonic plague,9 a modality of plague that is not dependent on a basis in bubonic cases which develop secondary pneumonia. Morris’s erroneous assertion on the existence and importance of pure epidemics of primary pneumonic plague is commented on below in the discussion of Karlsson’s alternative theory, and urgently raises the question of the origin of the epidemic.10 However, in contrast to the more recent advocates of alternative theories of the nature of historical plague epidemics he recognizes that “a rodent migration is not necessarily required for the spread of plague since infected fleas, and occasionally infected rats, can travel long distances in grain, clothing or other merchandise.” In other words, he acknowledges the importance of metastatic leaps in the epidemiology of bubonic plague.11 I cannot see how the notion of plague-infected rat fleas can be separated from the notion of bubonic plague cases and the spread of epidemics of bubonic plague.

9 10 11

Morris 1971: 207–9. See below: 502–14. Morris 1971: 206–7.

CHAPTER THIRTEEN

GUNNAR KARLSSON’S ALTERNATIVE THEORY: THAT HISTORICAL PLAGUE WAS PURE EPIDEMICS OF PRIMARY PNEUMONIC PLAGUE Introduction G. Karlsson presented his alternative theory to the international community of scholars in a paper published in Journal of Medieval History in 1996 where he argues that two late medieval epidemics in Iceland and more generally that plague in medieval Europe were pure epidemics of primary pneumonic plague.1 For his epidemiological interpretation, Karlsson bases his alternative theory directly on Morris’s assertion of the occurrence of pure epidemics of primary pneumonic plague, a modality of plague disease spread by interhuman cross-infection by droplets. The concept of a pure epidemic of primary pneumonic plague implies that the origin of the epidemic is not a case of bubonic plague which develops secondary pneumonia but a case in which the first victim contracted pneumonic plague directly by inhalation of infected droplets into the lungs. Karlsson’s paper follows quite closely and draws heavily on a paper he published together with S. Kjartansson in an Icelandic journal in 1994 on two supposed plague epidemics in Iceland in 1402–4 and 1494–5 respectively.2 He is clear about its objective: “The present article [as the first in Icelandic] can be seen as a defence of the late Jón Steffensen against Benedictow’s critique of his conclusions,” namely, that these epidemics, and also the Black Death of 1348–9 in Norway were primary pneumonic plague.3 Thus, the central feature of Karlsson’s (and Karlsson’s and Kjartansson’s) paper on the two supposed plague epidemics in fifteenth-century Iceland is a comprehensive and sharp criticism of my doctoral thesis (1993, repr. 1996). The apparent objective was to clear the way for his own theory that the epidemics were

1 2 3

Karlsson 1996: 263–84. Karlsson and Kjartansson 1994: 11–74. Steffensen 1973. 40–55.

494

chapter thirteen

pure epidemics of primary pneumonic plague: the epithet “pure” determines that they were without any basis or origin in flea-borne plague from rats (or other rodents) or cases of human bubonic plague.4 Thus he thinks that the contagion was the bacterium Yersinia pestis, as in the case of bubonic plague, but the process of dissemination was interhuman cross-infection by droplets and not transmission by rat fleas at any stage of the epidemic process. This immediately presents the insurmountable problem of how primary pneumonic plague could arise in the complete absence of bubonic plague and in the complete absence of rats, a problem he surprisingly does not identify or try to explain (and the editors and consultants of the Journal of Medieval History did not find significant). Alternatively, he might have launched a theory of importation, which he conspicuously fails to do and, as we shall see, for the very good reason that this would disclose another insurmountable problem, which is that there is no place abroad whence plague in any form could have been imported into Iceland in these years (another problem which the editors and consultants of the Journal of Medieval History did not find significant). The Icelandic epidemics exhibit such peculiar features that Karlsson, as the first of the advocates of alternative theories, has to invent some suitable mutations in order to defend his theory. He does not consider that his assertion as to the occurrence of these mutations can move from the status as arbitrary or speculative to the status as tenable (at any level of validity) only by meeting some elementary methodological requirements, namely to explain to the scholarly community: (1) why and how and by which process of evolutionary selection this mutant strain or biovar came into being; (2) when and where, in Iceland or abroad, this mutant strain of primary pneumonic plague originated and developed; (3) whether this mutated variant miraculously came into being twice; and (4) where on earth (literally) it had been in the meantime (another problem which the editors and consultants of the Journal of Medieval History did not find significant). Undaunted by these formidable problems, Karlsson expands the perspective of his theory from its tiny and isolated Icelandic territorial base in the middle of the North Atlantic to argue that historical 4

Karlsson 1996: 265.

gunnar karlsson’s alternative theory

495

plague in Europe generally was pure epidemics of primary pneumonic plague. On this basis, Karlsson concludes triumphantly that by having removed the black rat from the medieval plague he has more generally paved the way for asserting that the medieval plague epidemics in general, all over Europe, were primary pneumonic plague, presumably caused by that unknown mutated variant. These assertions will be addressed in this chapter. The principal interrelationship between the advocates of alternative theories is the usual one in this case: that they accept his view that there were not rats in Iceland and that the fifteenth-century epidemics consequently could not have been rat-borne, which suits their alternative theories, but they flatly reject his theory that these epidemics or the medieval plague epidemics generally were (pure) primary pneumonic plague.5 The gist of these counterarguments is, thus, that there never was a plague epidemic in Iceland, neither bubonic nor pneumonic, and Karlsson’s assertion that there were not rats in Iceland offers an excellent explanation. The obvious implication is that the severe epidemics in Iceland were another epidemic disease or other diseases. To my knowledge, no other scholar has supported Karlsson’s view, at least not outside the Icelandic scholarly community where opinions apparently differ sharply.6 One should note that there is a remarkable qualitative difference between the way Cohn and Scott and Duncan argue their rejections of Karlsson’s theory, and in my opinion, only Cohn makes his case on this point in a scholarly and scientifically tenable way.7 Karlsson and Benedictow I consider Karlsson’s reading of my thesis so bizarre and skewed that it is, in my opinion, grossly misleading and I hope I may be excused for considering it an expression of the weakness of his case.8 In my

5

Cohn 2002: 23, 51; Scott and Duncan 2004: 182. See also Twigg 1984: 68, 161–8. Karlsson’s (and Kjartansson’s) paper’s were discussed at a conference in Iceland and met with much criticism; papers from this conference are published in Sagnir 1997. 7 Cohn 2002: 22–3. 8 This is even more the case for the original paper in Icelandic, Karlsson and Kjartansson 1994, but since very few read Icelandic or Icelandic scholarly journals, this is not important in this context, only to the Icelandic scholarly community. Also the offensive comments on my work can, therefore, be ignored. 6

496

chapter thirteen

thesis, I presented a detailed account of the scholarly literature on primary pneumonic plague, however, to no avail so far as Karlsson was concerned. This highlights another feature of Karlsson’s paper: although he argues very strongly for a theory to the effect that the Icelandic epidemics of 1402–4 and of 1494–5 were pure primary pneumonic plague and ends up with a triumphant conclusion with a much wider territorial sweep, linking the nature of “medieval plague” to this disease, he has not made any attempt to acquire scholarly knowledge of primary pneumonic plague. Not a single medical study on primary pneumonic plague can be found in his footnotes. According to traditional academic principles, this ought to mean that he cannot discuss the disease that constitutes the cornerstone of his theory with the competence that only familiarity with the primary research studies and standard works on this disease can provide. The reason for this extraordinary approach by a scholar is presumably that the Icelandic epidemics exhibit many epidemiological characteristics or features that are not compatible with the studies on primary pneumonic plague. This is where wishful thinking about mutations is introduced into his arsenal of arguments. For the same reason, he cannot avail himself of the fact that I provided a comprehensive summary of all primary studies on primary pneumonic plague and the presentation of this disease in the standard works in my thesis. My endeavours to track down and present the gist of these studies does not earn me any praise, it represents, on the contrary, a significant problem that has to be managed. Since Karlsson cannot use the corpus of scholarly works on primary pneumonic plague in order to form a basis for his theory and likewise cannot use my complete presentation of it, he must find a way out of this problem. His solution is to base his arguments on a secondary paper which is profoundly flawed, namely Morris’s sharply critical review article of Shrewsbury’s monograph where Morris was the first scholar to launch a theory that the Black Death was an epidemic of primary pneumonic plague. Karlsson starts in this way: “Other diseases [than bubonic plague] are hardly considered by him [Benedictow], and all other forms of contagion are excluded, mainly because they are said to be insufficient to explain epidemics of the dimension under discussion here.”9 Firstly,

9

Karlsson 1996: 264.

gunnar karlsson’s alternative theory

497

one should note the logical and factual contradiction in the opening part of the statement, that “other diseases are hardly considered by him” and that “all other forms of contagion are excluded:” since all other forms of contagion unavoidably relate to many other diseases, I cannot have excluded other forms of contagion without having discussed other diseases.10 Secondly, he fails to mention that I made a complete presentation of the corpus of primary research on primary pneumonic plague, and this omission allows him to present a spurious explanation as to why I reject his theory. Thirdly, one should also note that in the second part of the statement he sharply criticises my approach, saying that I exclude all other forms of contagion “mainly because they are said to be insufficient to explain epidemics of the dimension under discussion here.”11 Thus, the truth shows through, albeit indirectly and involuntarily, that I have discussed other alternative diseases based on other forms of contagion, but have found that they have, inter alia, insufficient mortality-generating properties. Notably, Karlsson acknowledges in his paper that the Icelandic annals do not contain any clinical or diagnostic information that would permit the microbiological identification of these Icelandic epidemics. However, he contends that these chronicles provide information that can be used for producing estimates of the population loss in both epidemics, and that the extreme estimated mortality level could only have been caused by primary pneumonic plague.12 In other words, in practice he avails himself of exactly the same approach that he criticizes me sharply for using (although I do not use it as a fundamental argument but only as an additional argument). Later in Karlsson’s paper, there is another sudden but indirect indication that he has read my presentation of primary pneumonic plague. This occurs with a parenthesis within a citation from Morris’s paper to the effect that the great pneumonic epidemic in Manchuria would have spread much more, “but for the heroic counter-measures taken by the great Chinese

10

Benedictow 1993/1996: 121–5, 214–27. Benedictow 1993/1966: 16, 125, 266–74. As this statement is inaccurate and could produce misconceptions about my view, I would like to point out that I have discussed not only the size of the epidemics, as Karlsson may be taken to state, but also properties that combine tremendous powers of spread with tremendous lethal powers, and I argue explicitly why that is a rare combination (see also above). 12 Karlsson 1996: 265, 268–84. 11

498

chapter thirteen doctor Wu Lien Teh [one of Benedictow’s greatest authorities on plague] who most fortunately was put in charge.”13

However, Morris continues, unquoted by Karlsson: Wu Lien-Teh’s classic treatise on pneumonic plague is significantly absent from Shrewsbury’s very extensive bibliography.14

This treatise is also “significantly absent from” Karlsson’s few footnotes. One could also note the distortion inherent in Karlsson’s combined reference to me and “Wu Lien-Teh [one of Benedictow’s greatest authorities on plague],” since Wu Lien-Teh is the indisputable and uncontroverted towering expert on primary pneumonic plague, not on “plague.” Morris’s aim was to reject Shrewbury’s theory to the effect that the Black Death and later plague epidemics in Britain could have caused only a minor part of the national mortality rate, about 5 per cent, and that exanthematic typhus, smallpox and other serious epidemic diseases caused most of the mortality (see above). Because Morris has insufficient knowledge of bubonic plague to effectively counter Shrewsbury’s arguments, he launched another and apparently relevant alternative theory, namely that plague in Britain was primary pneumonic plague. However, he had poor knowledge also of primary pneumonic plague, and many of his central assertions are unfounded. This subject is discussed below after the substance of Wu Lien-Teh’s and other researchers’ studies on this modality of plague have been presented, in order to perform a systematic comparison between these studies and Morris’s and Karlsson’s assertions. Karlsson bases his paper and theory on Morris’s ten-page review of Shrewsbury’s monograph instead of on the primary research studies on primary pneumonic plague because they in important respects have the same ambition, namely to prove that the medieval plague epidemics, at least in Britain and in Iceland, were pure epidemics of primary pneumonic plague. However, Shrewsbury’s rejection of primary pneumonic plague as a significant causal factor of mortality is in full accordance with all primary research on this modality of plague, the same research that persuaded me to reject in my thesis the theory that the Black Death or subsequent plague epidemics could have been primary pneumonic plague. Apart from the fact that Morris referred to

13 14

Karlsson 1996: 283. Morris 1971: 208–9.

gunnar karlsson’s alternative theory

499

Wu Lien-Teh in his text and mentioned his monograph in a footnote, it can hardly be demonstrated that he has read his work or knows more about primary pneumonic plague than Karlsson. Karlsson based his case on the quotation from Morris’s paper for two crucial reasons: (1) because it provided an impression that primary pneumonic plague has great powers of spread, but in this case was halted by the countermeasures introduced by Wu Lien-Teh; (2) because Morris introduced the concept of pure pneumonic plague, which Karlsson makes the cornerstone of his theory. Both assertions are, as we shall see, at complete variance with Wu Lien-Teh’s presentation of primary pneumonic plague, where it is emphasized that epidemics of this disease arise from cases of bubonic plague which develop secondary septicaemia with subsequent lung consolidation and a bloody cough spreading infected droplets. Thus, Wu Lien-Teh maintains that epidemics of primary pneumonic plague never are pure, never arise de novo from a first or original case of primary pneumonic plague droplet infection. The heart of the present monograph is the identification of epidemic diseases of the past. This objective requires that some elementary methodological rules are followed in order to ensure the validity of identification of diseases, otherwise any mention of a severe or disastrous epidemic in the sources can be arbitrarily taken as evidence of plague (or any other serious communicable disease). An illustration of the consequences of an approach unguided by methodological considerations is provided by Scott and Duncan who assert that “there are said to have been 233 outbreaks [of bubonic plague] in China between AD 37 and 1718.”15 They have used Wu Lien-Teh’s general list of epidemics in China, for some reason leaving out the first of 224 BC.16 However, Wu Lien-Teh does not at all suggest that all these epidemics were or could have been bubonic plague. He emphasizes that it is possible to identify only a couple of these 233 epidemics as bubonic plague. He has not succeeded in finding clinical or epidemiological evidence of bubonic plague in chronicles or literary accounts, only in three medical works. Two of these medical works were from the first half of the seventh century; their clinical descriptions are unambiguous but cannot be

15 16

Scott and Duncan 2001: 171. Wu Lien-Teh 1936a: 43–51; Benedictow 2004: 40–2.

500

chapter thirteen

correlated or associated with any specific epidemic(s) in China. Only in a medical work of 1642 is a clinical description of bubonic plague given within an epidemic context, obviously referring to the epidemic of 1641–2.17 Identification of an epidemic disease, in this case as plague (either bubonic or pneumonic), requires specific evidence of at least one defining epidemiological or clinical feature or a combination of features that are unique (see above). In weak or inconclusive cases, it must be possible to demonstrate at least a possible link of dissemination from a known epidemic of plague to the epidemic under study which may allow formation of a hypothesis to the effect that it may have been plague. This does not, of course, constitute any proof that it actually was the plague; the function of a hypothesis is to legitimate research and direct the search for corroborative evidence. This requirement is of particular importance in the case of epidemics in a highly isolated island like Iceland. This clarifies the basic methodological, empirical and source-critical requirements that Karlsson should meet in order to justify his theory of the aetiology of the purported fifteenth-century plague epidemics in Iceland. The Icelandic sources that provide information on these epidemics consist mainly of brief accounts in two chronicles for each epidemic; translations of these accounts into English are supplied in my thesis and by Steffenson. My translation into English is provided in Appendix 2 below.18 As is most often the case with this type of source, the quality of the information they provide is quite deficient (in the eyes of modern scholars). They have nothing to say about whence the contagion arrived in Iceland or about defining or weaker indicative clinical features, excepting perhaps on the typical duration of the illness. They contain some comments on spread and mortality that are incidental and sensational in character as would be expected from this kind of source. Since Karlsson asserts that this “information” can be used for 17 Wu Lien-Teh 1936a: 10–3; Benedictow 2004: 35–42. This means that also McNeill’s use of the same list is unfortunate, and his choice of a Chinese epidemic of 1331 as the origin on the Black Death that subsequently spread all the way to the Crimea is completely unsupported by clinical or epidemiological evidence; see McNeill 1979: 152–4. Instead, McNeill let himself be victimized as a scholar by “the overwrought imaginings and hopelessly inaccurate quantification of the chroniclers,” to cite yet again Hatcher’s apt description (1977/87: 21). His theory is also contrary to a number of other empirical facts, for instance, the fact that the communication lines between China and the Crimea were severed long before the Black Death broke out in the Crimea or Constantinople. See Benedictow 2004: 44–51. 18 Benedictow 1993/1996: 211–2; Steffensen 1974: 457, 50–1.

gunnar karlsson’s alternative theory

501

estimates of mortality which are indicative of plague, this point will be discussed below. An intriguing question presents itself immediately and with great urgency: how can it be possible in such evidential circumstances to identify with a (very) high level of certainty the aetiology of the fifteenth-century Icelandic epidemics, in this case specifically as pure primary pneumonic plague caused by some mutant variant of the contagion Yersinia pestis? This problem is exacerbated by the fact that in his paper Karlsson does not perform source-criticism in accordance with scholarly standards, stating only with reference to his and Kjartansson’s paper that: “It would be tedious here to repeat all the arguments and reservations concerning our use of Icelandic sources, let alone all the references to sources and literature that only people who read Icelandic could use.” Inevitably, it means that his paper, on this crucial point, represents incomplete methodology and scholarship. There is also another serious matter of deficient methodology of sourcecriticism that will be discussed below. Karlsson’s theory is characterized by at least three independent fatal flaws of both empirical and methodological nature, in the sense that each represents a sufficient condition for rejecting it as untenable or invalid. (1) In the circumstances, when the two requirements for identification of epidemic diseases outlined by Shrewsbury cannot be met by the Icelandic sources, it is a serious deficiency that Karlsson has completely neglected to investigate the possible provenance, the possible territorial origin of the contagion that was introduced into Iceland and that unleashed the purported plague epidemics there in the years 1402–4 and in 1494–5. In reality, this question is composed of two independently decisive parts that must each be satisfactorily resolved in order to keep the theory afloat: he must for each epidemic be able to identify at least (1) one contemporary plague-stricken port town in Europe which (2) was sending ships to Iceland at the time these epidemics arrived there. These two crucial questions or problems for the tenability of his theory are passed by in silence. In 2002, I published a complete Norwegian plague history from 1348–1654 which covers more than thirty waves of plague epidemics, without finding evidence of any epidemic of primary pneumonic plague, let alone of a pure epidemic of primary pneumonic plague; in fact all epidemiological evidence is compatible with bubonic plague.19 19

Benedictow 2002. See also Benedictow 2006.

502

chapter thirteen Could Plague Have Come to Iceland from Anywhere?

Only a few ships came to Iceland from abroad at the beginning of the fifteenth century, only Norwegian ships or Icelandic ships returning from Norway, normally from Bergen. The first English fishing ship is reported to have arrived in Icelandic waters in 1412.20 It was prohibited by law for the Icelanders to trade with foreigners. In order to illustrate this point one could note that in 1409, there was an intensive discussion at the Icelandic all-moot (‘Alþingi’) about what to do with all the royal incomes that had piled up in the island.21 Iceland was part of the Norwegian kingdom, normally administered by a royal governor (‘hirðstjóri’), and taxes were mostly paid in homespun woollens and, to some extent, in stockfish (wind-dried cod). Evidently, the cause of the problem was that too few ships arrived from Bergen, and that not even the commander of the King’s Mansion22 in Bergen who was responsible for collecting the royal incomes in Iceland, regularly sent a ship there to collect them. In the following years the New Annals (Nyi Annáll) occasionally provide telling pieces of information, for instance, under the year 1412 we are told that “No news came from Norway to Iceland,” i.e., no ship arrived from Norway; next year we are told that “A ship came from Norway,”23 a fact that the annalist finds worth mentioning. In 1419, the Icelanders wrote a letter to the king complaining that for several years no ships had arrived from Norway according to the old agreement with the Crown, which had been gravely detrimental to their poor country. They therefore considered it unreasonable that the old prohibition against trading with foreigners was still in force.24 British sources tell the same story. Ships from Britain were sailing to

20

Carus-Wilson 1966: 161. Steffensen 1974: 48. 22 The ‘King’s Mansion’ is a translation of ‘Kongsgården,’ the royal administrative centre of western Norway in Bergen. At the time, this was not a castle built in stone, but consisted of wooden buildings surrounded by a wooden palisade and had no real defensive capabilities. 23 Annales islandici posteriorum sæculorum. Annálar 1400–1800: 18–9. Also the Icelandic Vatnsfjarðarannáll hinn elzti relates to this epidemic but it is written so long after the event and is so infested with source-critical problems that it is not mentioned by Gunnar Karlsson (or Jón Steffensen) who in other works shows good knowledge of these important types of sources to Icelandic medieval and early modern history. Annales islandici postseriorum sæcolorum, 1933–8: 22. 24 Diplomatarium Norvegicum, vol. 2, no. 651; Diplomatarium Norvegicum, vol. 4, no. 330. 21

gunnar karlsson’s alternative theory

503

Iceland at the time: the first English fishing ship arrived in 1412 to be followed by many others in the subsequent years. However, throughout the fifteenth century only English fishing ships and merchant ships sailed to Iceland; Scottish ships do not seem to have been engaged in fishing in Icelandic waters or trading with Iceland during this century.25 Crucially, there is not a single account of plague in these countries in 1402. Not a single plague epidemic has been registered in England between 1400 and 1405–7, nor was there any outbreak of plague in Ireland or Scotland during this period,26 nor for that matter in Northern Germany between 1396 and 1405–6, nor in the coastal commercial cities of the Netherlands between 1400–1 and 1409.27 Since the epidemic broke out in the autumn of 1402, after the return of an Icelandic ship,28 it is also clear that the disease would have to have been imported from a city or region where it was spreading in this year.29 In Norway, the sources provide no certain information of plague between 1391–2 and 1452, although there are some indications that there could have been plague in 1438–9. Norwegian sources are particularly sparse in these decades, and it is likely that one or more plague epidemics may have gone unnoticed. However, it is improbable that plague contagion could have been imported into Norway and re-exported to Iceland in years when there was no plague epidemic in the countries whence plague was imported to Norway, and this was throughout the Late Middle Ages mostly England, and at least once the Netherlands.30 There is no evidence that plague was imported from Northern Germany before 25

Carus-Wilson 1966: 155–82. Shrewsbury 1971: 149–50, mentions that “some time in 1402 there was ‘some disease in Scotland that ‘caused several deaths’ in Dundee.” Evidently, he does not consider it to have been plague, referring to it only as “some disease,” and since the only concrete information on mortality is restricted to the statement that it “caused several deaths” no impression is conveyed of a dramatic epidemic situation. And one must keep in mind that no ships from Britain were sailing to Iceland at the time and that also later in the century only English fishing ships and merchant ships sailed to Iceland, Scottish ships do not appear to have been engaged in fishing near or trading with Iceland. Carus-Wilson 1966: 155–82. 27 According to Blockmans 1980: 854, there was an outbreak of plague in Guelders, an inland city situated in the south-eastern part of the Netherlands near the border of Germany. 28 “Nýi Annáll,” in Annales islandici postseriorum sæcolorum, 1922–7: 9–10; “Lögmanns-annáll” in Islandske Annaler indtil 1578: 286. 29 Benedictow 2002: 102–11. 30 Benedictow 2002: 102–11. Evidently the reason is that Denmark’s pattern of international trade was very different from Norway’s. 26

504

chapter thirteen

1500 (or more accurately before 1628), and for the year 1402, with a substantial margin of safety of years around it, plague is not recorded in this area.31 According to the extant sources, plague was never imported from Denmark in the whole plague history of Norway, and no plague epidemic has been registered in Denmark from the end of the fourteenth century until possibly in 1405.32 Steffensen, who recognizes that notions on provenance cannot be dispensed with and that this question therefore cannot be ignored, asserts that the supposed plague contagion came to Iceland with a ship from England. His source is Sticker’s old pioneering standard work on plague of 1908, where plague is mentioned as having occurred in England in 1402, but without indication of his source.33 Probably Sticker has misunderstood a reference to the epidemic in Iceland in the Danish scholar F.V. Mansa’s proto-scientific monograph of 1875 on the epidemic history of Denmark.34 It is a mistake or rather a slip of the pen on the part of Sticker that Steffensen could easily have corrected by using Shrewsbury’s recent monograph on the history of plague epidemics in Britain and, as we shall see, Steffensen knows the work and has consulted it, which makes his silence on this point the more remarkable. In fact, in another context Steffensen remarks that Sticker’s mention of a plague epidemic in Denmark in 1402 with reference to Mansa’s monograph is erroneous,35 apparently he knows that this passage in Sticker’s work is not correct. Furthermore, Steffensen does not attempt to assert that ships sailed directly from Denmark to Iceland at the time which also can be checked and corroborated in Icelandic annals and other sources. The staple36 was in Bergen and the Iceland trade a privilege for Norwegians. At the time of this epidemic, Icelanders were living in isolation with only sporadic contacts abroad and, for all practical purposes, abroad was Norway. 31

Shrewsbury 1971: 138, 141, 149–56; Ibs 1994: 206; Blockmans 1980: 836–45; Benedictow 2002: 102–5, 354–5, see especially Table 2A showing all known plague epidemics in Norway, England, Northern Germany and the Netherlands in the period 1348–1500 organized so as to facilitate comparison and discussion of territorial origin. Also see the references on this subject cited just above. 32 Mansa 1873: 92–100. 33 Sticker 1908: 8; Steffensen 1974: 47–50. 34 Mansa 1873: 99. 35 Steffensen 1974: 47. 36 The Shorter Oxford English Dictionary, vol. 2, p. 2109 gives the following definition “staple:” “A town or place appointed by royal authority, in which there was a body of merchants having the exclusive right of purchase of certain classes of goods destined for export; also the body of merchants so privileged.”

gunnar karlsson’s alternative theory

505

Thus, 1402–4 were years with unusually few outbreaks of plague in Europe and they occurred far away from the northerly parts of Europe and commercial centres that could serve as the point of departure for transportation of plague by ship to Iceland. These findings permit a secure conclusion. No doubt there was a serious or severe epidemic in Iceland in the years 1402–4, but plague in any form based on the contagion Yersinia pestis appears to be excluded: there was no plague epidemic in any of the countries or regions with shipping activity with Iceland whence it could have been transported there. Another point which excludes primary pneumonic plague is the long duration of an epidemic which requires continuous and rapid spread in such a tiny population (probably 30,000–40,000 inhabitants37), and this duration would by far be the longest on the record. At the time, Iceland was a long voyage from any port in the northerly parts of Europe. The voyage from western Norway to Iceland would under favourable circumstances and with suitable wind usually take a couple weeks of sailing. However, ships from Bergen or Nidaros/ Trondheim would first sail along the coast approximately to the northwestern point of Stad, which would normally take about five days, before they could turn and with an easterly wind sail westwards to Iceland.38 Waiting periods for useful winds could easily take much more time than the actual sailing.39 This would very much be the case for ships waiting for the easterly winds necessary for sailing westwards to Iceland, since Norway is situated in the so-called west wind belt which is dominated by westerly winds. In the twentieth century, easterly winds constituted only 2.2 per cent of all wind measurements in the sailing season 1 April–30 September40 in western Norway.41 Obviously, any ship with primary pneumonic plague on board among the cramped conditions for crew and passengers after cargo had been given strong priority would be rapidly heading for disaster. 37

See below, fn. 68. Helle 1982: 68. Cf. Steen 1934: 227. 39 Steen 1942: 306. 40 The maximum sailing season is given in the important Norwegian source Kongespeilet [The King’s Mirror] written around 1250. Here I have used the recognized translation Kongespeilet 1947: 53, 55. 41 Since the prevailing distribution of wind direction is heavily affected by the direction of the earth’s rotation, the distribution of wind directions has probably not varied greatly over historical time. The crude data of all wind-force measurements registered by the wind-gauge stations in Bergen are published by the Norwegian Meteorological Institute: www.met.no 38

506

chapter thirteen

Since no epidemic of primary pneumonic plague has been identified in Norwegian sources, and in the year in question (1402) not even a plague epidemic, Steffensen’s theory is only a speculative flight of imagination. In the case of the supposed plague epidemic of 1494–5, the situation is much the same. Karlsson has not attempted to identify the provenance of the contagion and passes in silence by the problem of whence plague contagion could have been transported to Iceland. In the meantime, shipping activities in northern Europe had increased greatly. Although the small island of Iceland with its tiny population situated in the middle of the North Atlantic Ocean on the northwestern outskirts of Christendom was a destination with limited attraction, it was by now less isolated and to some extent linked to northern Europe through trade in stockfish. At the time, English interest in fisheries in Icelandic waters and commercial interests in the island had been sharply reduced, due largely to strong efforts by Hanseatic cities to drive the English away and assert their primacy and the importance of the staple of stockfish in Bergen. By the end of the fifteenth century, Iceland was apparently quite regularly visited by a ship sent there by the commander of the King’s Mansion in Bergen in order to collect the royal taxes, and stockfish may at least occasionally also have been purchased in order to fill up the ship and earn some extra income. This pattern can be discerned in a sprinkling of fifteenth-century sources and is confirmed by the records of Bergenhus Castle, the new royal castle in Bergen, which are extant from 1514, and where also the occasional Icelandic ship is mentioned.42 The sources reveal that Iceland at this time had some regular commercial contacts with Norway and was now more exposed to the importation of contagion than at the beginning of the century. This puts the epidemics of 1494–5 in a somewhat different light. However, as can be seen from Table 2A and the comprehensive comments in my Norwegian plague history, there was no plague epidemic in these years in Norway, England, Northern Germany or in the coastal commercial cities of the Netherlands.43 In 1494, epidemics are mentioned in Gouda and Guelders as typical localized outbreaks and in inland cities without shipping contacts or commercial connections

42 43

Norske Regnskaber og Jordebøger. See the very good index. Benedictow 2002: 102–11.

gunnar karlsson’s alternative theory

507

with Norway or Iceland.44 Gouda and Guelders are the only places where there may have been outbreaks of plague this year.45 Nonetheless, Steffensen asserts again that the contagion that triggered the purported Icelandic plague epidemic was imported from England. This conclusion is seemingly the outcome of a process of elimination. He admits that plague is not mentioned in “Scandinavia or Denmark” in 1494. He has again consulted Sticker, who in the crucial year of 1494 in the whole of Europe has registered plague only in Nuremberg, and in 1495 more or less probable or possible plague epidemics in Landshut (Bavaria), Erfurt and in Lower Austria.46 Since Steffensen does not specify these localities he can state rather inaccurately that plague “is mentioned in many German towns.”47 Obviously, the contagion that unleashed the Icelandic epidemic could not have originated in any of these localities which were not Hanseatic commercial cities on the North Sea or Baltic Sea. Since Sticker cannot help him with a plague epidemic in England, not even by a slip of the pen, Steffensen must look elsewhere for support of his theory of provenance. He now mentions that he has consulted Shrewsbury’s recent monograph, thus admitting that he knows it, but was confronted with the fact that Shrewsbury does not consider that there has been any pestilence in England in the last decade of the 15th century.48 Since he is not willing to draw the scholarly conclusion that there was no plague epidemic either in England (or anywhere in the British Isles) or elsewhere in northwestern or northern Europe that could have served as an origin of the contagion which was transported to Iceland in 1494, he looks elsewhere for support. He turns to Creighton’s monograph of 1891, A History of Epidemics in Britain, where “minor

44

Noordergraaf and Valk 1996: 225; Blockmans 1980: 854. In the following year, 1495, there appears to have been a plague epidemic in southeastern Sweden, as the convent of Vadstena and the city of Stockholm on the Baltic Sea is reported in contemporary chronicles as being seriously visited by pestilence. Moseng 2006: 314–5. Since an outbreak of plague in Sweden in 1495 cannot be the origin of plague in Iceland in 1494 and Sweden had no contact with Iceland by ship, this epidemic is not significant in the present context. It is also noteworthy that eastern Sweden was exposed to importation of plague across the Baltic Sea and had, like Denmark, a different temporal rhythm of plague epidemics than Norway which imported plague from England and northwestern Europe more generally, but never from Sweden or Denmark. 46 Sticker 1908: 87. 47 Steffensen 1971: 53. 48 Shrewsbury 1970: 149, 155. 45

508

chapter thirteen

epidemics are mentioned in Oxford 1486, 1491 and 1493, and it appears that the pestilence was close to Edinburgh in March 1493.”49 Although Creighton does not use the term “plague epidemics,” but only the unspecific term “epidemics,” this statement is taken to constitute justification for an unqualified assertion to the effect that Shrewsbury took no interest in minor plague epidemics and “presumably means only large-scale epidemics.” Every reader of Shrewsbury’s highly detailed work will know that this assumption is groundless: no epidemic is too small to escape his acute interest, neither can Shrewsbury’s numerous references to and detailed knowledge of Creighton’s work escape notice. In fact, Steffensen’s assertion in relation to Shrewsbury work is at variance with Shrewsbury’s presentation of his research program on fifteenth century plague epidemics: “As this work is primarily a history of bubonic plague, an attempt must now be made to pinpoint the possible outbreaks of that disease in the British Isles during this century,”50 making it clear that his objective is to identify every possible outbreak of plague. This does not exclude the possibility that he overlooked epidemics, especially local outbreaks.51 Scrutiny of the sources or research literature for more information is always warranted but Steffensen did not succeed in identifying any plague epidemic and did not accept the consequences. The reason Shrewsbury does not mention the epidemics in Oxford in these years is that he did not find any evidence to the effect that they were plague. In fact, Shrewsbury has not registered a single epidemic of plague in England “after November 1480 until an epidemic erupted at Oxford in 1499” which he considers a “doubtful exception.” Thus, Shrewsbury is clear in his view that in the sources there is no indication of plague in England in the period comprising the epidemics in Oxford and the purported Icelandic plague epidemic. It can also be shown that he was certainly not averse to mentioning small possible outbreaks of plague in Oxford.52 J. Hatcher and P. Slack, prominent English scholars who, in important subsequent studies of plague in England, have fine-combed the sources for epidemics, including the sources relating to the last two decades of the fifteenth century, did not find any credible information 49 50 51 52

Creighton 1891: 283; Steffensen 1974: 53. Shrewsbury 1971: 155. See Gottfried 1978: 238–40. See Shrewsbury 1971: 149.

gunnar karlsson’s alternative theory

509

to the effect that the small epidemics in Oxford mentioned by Creighton were plague.53 The reason may quite safely be assumed to be that there is no such evidence. Another insurmountable problem is how contagion from this small inland outbreak of an epidemic disease should have been moved to Iceland, as the continuous lines of communication presumed by such an event appear to be completely unknown to either contemporaries or to modern historians. Another insurmountable problem is that even the last mentioned epidemic in Oxford occurred in 1493 and cannot be linked to the outbreak of an epidemic in Iceland 1494. Steffensen appears to assume that he can brush aside Shrewsbury’s recent work, written by a modern bacteriologist, and substitute it with Creighton’s proto-scientific work of 1891. Creighton’s monograph is, as noted above, written according to the spirit of an ardent protagonist and defender of miasmatic epidemiological theory in the face of the rise of the new science of bacteriology. This means that Creighton denied that each epidemic disease was caused by a specific microbiological agent and believed instead that miasma could take on various forms and could develop into plague from other manifestations of miasmatic disease (i.e., other epidemic diseases), especially from typhus and dysentery; he also claimed that plague was due to a poison emanating from putrescent corpses.54 According to miasmatic theory, an outbreak of any epidemic disease could therefore be of interest to a study of plague since it could develop into plague. This is also the reason for Steffensen’s sudden use of the term “pestilence” in the citations above. It reflects the miasmatic assumptions that have now been inserted at the core of his argument, although nothing is explicitly said about this extraordinary turn of his argument away from modern scientific bacteriological and epidemiological premises of analysis to untenable proto-scientific miasmatic medical theory. Besides the fact that Creighton has not suggested that the epidemics in Oxford were plague, it must be emphasized that Creighton does not assert that there was an epidemic at Oxford or anywhere else in England in 1494. Nonetheless, Steffensen sticks to his theory, although it is untrue that Shrewsbury only took interest in major plague epidemics and ignored minor epidemics, so that plague could have been imported from

53 54

Hatcher 1977/1987: 17–8; Slack 1985: 53–65. See, e.g., Hirst 1953: 74–5, 87, 89, 93–4, 285; Shrewsbury 1971: 150.

510

chapter thirteen

England to Iceland in 1494 in connection with some minor outbreak of plague which Shrewsbury ignored, Creighton did not know, and which Hatcher and Slack overlooked. According to all accumulated scholarly knowledge on English plague history no plague contagion could have been transported from England to Iceland in 1494. Steffensen also mentions a possible plague epidemic “close to Edinburgh” in 1493, referring again to Creighton as his source. Shrewsbury takes seriously the possibility of an outbreak of plague in Edinburgh and outlying townships in 1493 which led to the isolation of the town, but thinks that it probably was an epidemic of typhus. He concludes therefore his chapter on plague in Scotland in the fifteenth century by stating: “There does not seem to be any outbreak of epidemic disease in Scotland that presents any circumstantial evidence for its identification as an outbreak of bubonic plague, with the doubtful exception of 1499.”55 Significantly, this epidemic did not spread to any other place in Scotland, which makes it a very local outbreak of whatever disease it might have been. Furthermore, an epidemic outbreak in 1493 is out of chronological co-ordination and cannot serve even as a hypothetical origin for the Icelandic epidemic. Edinburgh was not a commercial shipping centre, and it is rather unsurprising that it had no known connection by ship with Norway, and certainly not with Iceland. Again, it is not possible to construct any case for transportation of plague contagion from Scotland to Iceland in 1494. Thus it is not possible to adduce empirical support for the theory that the epidemic outbreak in Iceland in 1494 was primary pneumonic plague or bubonic plague for that matter, since there was no area or city which was visited by plague whence plague could have been shipped to Iceland. Undoubtedly this epidemic in Iceland was a serious outbreak of a contagious disease or multiple contagious diseases taking a high toll of lives. One should take note that there are numerous accounts in the Icelandic annals of serious or severe epidemics, including accounts that pre-date the advent of plague in Europe and also subsequent epidemics that typically are out of rhythm with known European plague epidemics. Some examples may be useful: in 1292, “Came such a big disease over all the country […] and caused great mortality”; in 1306, “Big epidemic in Iceland and high mortality in the south of the country”; in 1309, “Big killing disease in the north of the country”; in 1310, “Killing disease and mortality in all the Vestfjord area and the 55

Shrewsbury 1971: 151, 155.

gunnar karlsson’s alternative theory

511

Southerners’ area and boil disease”; or in 1380 and 1382: “Huge boil disease all around the country and great mortality […] disease over all the country and huge mortality.”56 Thus, also 1494 was a year with particularly few plague epidemics in Europe and they occurred far away from the northerly parts of Europe and from commercial sea ports that could serve as a point of departure for transportation of plague contagion by ship to Iceland. Steffensen’s assertion that plague contagion came from England has been shown to have no evidential underpinning, essentially it is an arbitrary assertion, and likewise not a single plague epidemic was registered in these years in Norway. Again, the intensive and comprehensive discussion permits a clear conclusion: no doubt there was a serious or severe epidemic in Iceland in the years 1494–5, but it appears impossible that it could have been due to plague in any form based on the contagion Yersinia pestis. Steffensen sees the problem of provenance clearly and appreciates the fact that positive identification of at least one case of plague in one sea port with at least some evidential support for possible shipping to Iceland is crucial to instil his theory with any (level of) tenability, however low. However, he cannot come to terms with the the complete lack of supporting evidence on both points for both epidemics. Karlsson has chosen the option of passing the problem by in silence, although this undermines the very foundations of his theory, quite possibly because he recognizes that there is no supporting evidence. This exhaustive discussion of a possible provenance of plague contagion (Yersinia pestis) for the purported plague epidemics in Iceland in the years 1402–4 and 1494–5 has been completely negative. This finding constitutes a sufficient condition for characterizing the theory as materially untenable and for the conclusion that it must be rejected. This does not mean that there cannot be other independent and sufficient conditions for rejecting the theory. Pure Epidemics of Primary Pneumonic Plague: Fact or Fiction? A thorough and for all practical purposes complete presentation of the medical and epidemiological studies of primary pneumonic plague is presented in my thesis in order to provide the broadest possible basis

56

Annales Islandici 1888: 71, 53, cf. 75, 364. My translation from Icelandic Norse.

512

chapter thirteen

for my discussion of the nature of the late medieval plague epidemics in the Nordic countries. It was also motivated more specifically by my desire to provide a background for discussion of Steffensen’s paper,57 since his theory of epidemics of primary pneumonic plague in Iceland is not supported by a single reference to any medical or epidemiological study of primary pneumonic plague. Karlsson who defends his theory intensively fails to include any reference in his paper to a primary study of pneumonic plague or to the broad summaries of such studies provided in the standard works on plague, not even to K. Meyer’s brief and succinct paper. However, according to the methodological tenets of medical and historical science, their theory of the nature of these Icelandic epidemics as being primary pneumonic plague or some mutant variant of this disease can only be adequately discussed in relation to modern medical and epidemiological knowledge on this modality of plague, implemented in the form of a systematic comparison between historical data and modern data. The better and more comprehensive the correspondence or correlation between modern medical data and historical data, the more tenable the inference of the identity as primary pneumonic plague. Fruitful discussion requires a satisfactory empirical knowledge of the medical characteristics, epidemiological structures, lethality and demographic effects (population mortality) of primary pneumonic plague. Since Karlsson denies that there were any rats in Iceland, he is obliged to, launch a theory of pure epidemics of primary pneumonic plague, which requires that he consistently avoids the medical literature on primary pneumonic plague and instead makes his case depending entirely on an assertion in a review paper by Morris. This assertion occurs in a passage where Morris scathingly and disparagingly attacks Shrewsbury for denying the existence of this form of plague: What is the cause of Shrewsbury’s myopia?58 Perhaps it came upon him at the moment when (on page 6) he delivered himself of the dictum “pneumonic plague cannot occur in the absence of the bubonic form and it cannot persist as an independent form of plague.” This is untrue […]. The Manchurian epidemic was indeed exclusively pneumonic, as was the slightly less destructive outbreak of 1920–1; […] Wu Lien-Teh’s classic

57

Benedictow 1993/1996: 25–31, 214–27. “Myopia” means shortsightedness in a medical sense or figuratively narrowmindedness. 58

gunnar karlsson’s alternative theory

513

treatise on pneumonic plague is significantly absent from Shrewsbury’s very extensive bibliography.59

This basic idea and crucial premise of Morris’s theory of the nature of plague in England and Karlsson’s theory of plague in Iceland, the notion of pure epidemics of primary pneumonic plague, can usefully be addressed first. Theoretically, pure epidemics of primary pneumonic plague are possible in the technical meaning that they could start de novo from an original case of primary infection: hunters could, for instance, be infected by droplet infection when skinning or cutting up a sick animal with plague septicaemia; American veterinary personnel have contracted primary pneumonic plague directly from pet cats which had inhaled contaminated droplets in the process of killing rodents with plague septicaemia. These cases relate to a rodent basis in the form of a plague reservoir where plague circulates continuously, which is excluded in the case of Karlsson’s Icelandic theory. Furthermore, these very few cases have never caused spread to any other person, thus, they have never given rise to an endemic development (with possible consequent epidemic forms).60 Morris refers to Wu Lien-Teh’s monograph on primary pneumonic plague for empirical support of the existence of pure epidemics of primary pneumonic plague, and Karlsson does so indirectly by citing parts of the citation including the explicit reference to this work. However, Wu Lien-Teh states the contrary unequivocally: It is generally agreed that the pneumonic form of plague is not directly traceable to the epizootics [i.e., does not originate by cross-infection with plague-infected droplets from rodent to man] but arises from human cases of bubonic plague with secondary lung involvement.61

Wu Lien-Teh states here emphatically, and repeatedly, that primary pneumonic plague develops only from cases of secondary pneumonic plague, i.e., human victims of bubonic plague who have developed septicaemia. He argues that the term ‘pure epidemic of pneumonic plague’ “should be avoided as it is misleading as far as the origin of the outbreaks is concerned.”62 This puts Karlsson’s theory of pure

59 60 61 62

Morris 1971: 208. Benedictow 1993/1996a: 215–9. Wu Lien-Teh 1926: 162–4. Wu Lien-Teh, Chun, Pollitzer 1934: 83. Wu Lien-Teh 1936b: 418–9.

514

chapter thirteen

epidemics of pneumonic plague in Iceland in perspective, disclosing in another way the arbitrary nature of his theory and its lack of empirical underpinning in primary studies on pneumonic plague. It also puts in perspective the fictitious support Karlsson draws from Morris who insists that the Manchurian epidemics were pure epidemics of primary pneumonic plague without basis in bubonic plague and incorrectly refers to Wu Lien-Teh’s monograph for empirical support.63 The arguments on this point can now be summed up: researchers have not succeeded in identifying a single epidemic of pure primary pneumonic plague. If empirical evidence is for methodological reasons considered essential for establishing factual data with any level of validity or tenability that can be used for construction of explanatory theories, epidemics of primary pneumonic plague do not develop de novo. There is no such thing as pure epidemics of pneumonic plague, and all assertions to the contrary are arbitrary.64 Since there is no such thing as a pure epidemic of primary pneumonic plague, there cannot have been pure epidemics of primary pneumonic plague in Iceland. According to ordinary methodological considerations, the discussion of this point has produced another sufficient independent condition for rejecting Karlsson’s theory. Primary Pneumonic Plague in Manchuria: A Model for Iceland? According to Steffensen and Karlsson, the Icelandic epidemics were large-scale, sweeping away a large part or even most of the Icelandic population. This view should be seen in the light of the fact that only one fairly large epidemic of primary pneumonic plague has so far been identified with certainty in the history of plague, namely the epidemic of 1910–11 in Manchuria and adjacent regions that took around 60,000 lives, with 10,000 deaths occurring in the Russian Vladivostok area. This is by far the largest epidemic of this modality of plague ever recorded, and was followed by the second largest epidemic in the same area a decade later. The first of these epidemics are cited enthusiastically by protagonists of the importance of large-scale epidemics of

63 64

Morris 1971: 208–9. See especially Wu Lien-Teh 1926: 162–95; Wu Lien-Teh 1936b: 401–3.

gunnar karlsson’s alternative theory

515

primary pneumonic plague, also by Steffensen and Karlsson. This is only possible because they avoid taking into account: (1) the tiny rate of population mortality in these epidemics which has no explanatory potential for the Icelandic case; (2) the exceptional circumstances of these two epidemics; (3) the medical and epidemiological evidence provided by scholarly studies of primary pneumonic plague when it does not suit their case. A brief summary here may therefore be of use. A fresh presentation of the central structural circumstances that gave these two Manchurian epidemics of primary pneumonic plague their exceptional dynamics is needed in order to permit a concrete comparison of basic and epidemiologically relevant social structures between Manchuria at the beginning of the twentieth century and late medieval Iceland (or Europe more generally): (1) At the time, Manchuria’s population underwent exceptional growth through the immigration of adult males from China for work, and increased from 12.7 million according to the Chinese Census of 1912 to 22 million in 1922.65 The great majority of the Manchurian population was Chinese coolies working in the mines and along the rivers Sungari and Amur. Some 10,000 hunted large rodents called tarabagans (marmots) for their valuable fur, and since plague infection circulated among these rodents, hunting was the origin of quite frequent cases of bubonic plague that were the origin also of the primary pneumonic epidemics. This means that the social structure and the age and gender dimensions of the population were extremely skewed and entirely unrepresentative of any normal population. When the epidemic of 1910–11 broke out, there was no anti-epidemic organization which could combat it. When the second epidemic broke out in 1921, an organization had been built to deal with such an event and thus much better records are available which provide more detailed knowledge also of the population’s social composition and its extremely skewed character compared with normal populations: for instance, among the patients at the hospital in Harbin there were 1139 labourers out of a total of 1252 patients (91 per cent), 67 women as against 1243

65

Wu Lien-Teh 1922–3: 262.

516

chapter thirteen

males (5 per cent), and 21 children of ages 0–10 constituting 1.67 per cent of the patients.66 The immense inrush of poor migrant workers created a gigantic market for miserable accommodation. They stayed mostly in incredibly overcrowded inns and lodging houses of a kind completely unheard of in normal populations whether in Iceland or elsewhere in medieval Europe: The accommodation in both types of inns is based upon much the same plan. Two, and sometimes three, tiers of berths for the lodgers are present, there being just room enough between the tiers for a man to sit up […]. Dr Ch’uan visited some of these inns in the winter. His report showed the conditions to be bad in the extreme: “in one hut, 15 ft. square and 12 ft. high [20.9 sq. metres or 76.4 cu. metres], there were packed in three tiers of berths, one above the other, more than 40 people,” thus, each having at his disposal less than 1.9 cu. metre of space. For protection against the cold in the winters, when the temperature “as a rule reaches −30°C to −40°C,” the lodging-houses were constructed either entirely underground or at least partly underground. The windows were closed during the winters, and “even in May the rooms were ill-ventilated and stuff y.” “The men eat, sleep and very often cook in the same room. They sleep in rows with the head against the wall and the feet towards the central passage. There is no partition between adjoining berths so that they can easily breathe and cough into each other’s faces.67

These men were living in incredible density in extremely ill-ventilated housing, breathing, sneezing and coughing in the immediate proximity of the face of the next man. For a very large proportion of the population, the social circumstances were extreme, in the sense of extremely favourable to propagation of disease by droplet infection, much more favourable than in the case of any normal medieval population. The contrast to Iceland is extreme: an isolated island society with slight contact abroad, with very sparsely and highly dispersed settlements and a largely stable population distributed on (probably) 5000–6000 detached tenancies or free holdings.68 The inhabitants were

66

Wu Lien-The 1926: 82; Chun 1936: 320–1. The change in the total number of patients from 1252 to 1310 in the information on the gender incidence is due to a category of 60 persons with unknown age which means that the total number of patients actually was 1312, but these inaccuracies do not significantly affect the estimates. 67 Wu Lien-Teh 1913: 248–9. 68 Benedictow 1996b: 182–4; Benedictow 2003: 34; Orrman 2003: 438. According to Orrman, the maximum number of peasant holdings in operation in Iceland at the time was 3800–4500, but according Jón V. Sigurðsson 5000–6000. In my view, Orrman’s use

gunnar karlsson’s alternative theory

517

overwhelmingly making their living by subsistence economy, mostly extensive domestic husbandry more or less in combination with some fishing, gathering and small-scale hunting, which means that the agricultural units needed large territories and the farmsteads were greatly dispersed. There was, consequently, relatively little social exchange and commercial contact between these constituent parts of the Icelandic population, quite likely less than among any other European population. (2) The railway played a pivotal dynamic and entirely unmedieval role in the process of disseminating the epidemic: it was first spread from Manchouli69 “along the railroad, westwards into Siberia again and eastwards into China” and “the Chinese Eastern Railway conveyed the infection broadcast.”70 Because primary pneumonic plague is spread by interhuman dissemination, Wu Lien-Teh, points out that “such spread will be slow in sparsely populated territories […] an epidemic will cover wide distances with almost lightning rapidity as soon as modern means of communication are available.”71 The last observation reflects the process of dissemination in the Manchurian epidemics and ought to put the dynamics of the Manchurian epidemics in an instructive perspective, particularly in relation to medieval Iceland. (3) The epidemic ran its course from April to the end of 1910 without significant countermeasures. On Christmas Eve, the Cambridgetrained Chinese physician Wu Lien-Teh arrived in the provincial capital of Harbin under orders from the Imperial administration to

of these figures reflects incomplete source-criticism: the actual figure must be higher and Jón Sigurðsson’s estimate seems more credible. There is no evidence on contemporary household size and thus on household multiplier, except some indications that multiple households were not unusual. The Icelandic Census of 1703 shows an average household size of 6.5 persons. If this can be taken as fairly representative also of early fourteenth-century household structure, and in the meantime there had been little change in the economic basis or structures regulating population size according to Malthusian principles, Jón Sigurðsson’s estimate indicates a population size of 30–40,000. It is highly unlikely that medieval population was at any time larger than recorded by the Census of 1703, namely 50,400 inhabitants, which also is the figure suggested by Orrman, implying a much higher average household size than that found by Jón Sigurðsson. See the discussion in Benedictow 1996b: 182–4. 69 Situated in northern Manchuria at the junction of the Chinese Eastern Railway and the Trans-Siberian Railway. 70 Wu Lien-Teh 1926: 71; Wu Lien-Teh 1936a: 32. The Manchurian Plague Prevention Service was established in 1912. Manchurian Plague Prevention Service. Memorial Volume. 1934. 71 Wu Lien-Teh 1926: 182–3, cf. 74.

518

chapter thirteen

take charge of combating of the epidemic. One should recognize that what this excellent scholar could achieve was quite limited. At the time, very little was known about primary pneumonic plague. He had at his disposal a minimal sanitary administration or medical staff which was responsible for a vast region with c. 12 million inhabitants spread over 939,000 sq. km (363,000 sq. miles), more than six times the size of England and Wales, with the possible support of only a rudimentary Chinese Imperial administration and with military occupation of sizeable areas by Russian and Japanese forces.72 Wu Lien-Teh had at his disposal only the most rudimentary medical facilities, a situation that was much improved only after the establishment of the Manchurian Plague Prevention Service in 1912 with him as director and the appropriation of substantial funds for hospitals, laboratories and staff.73 Importantly, Wu Lien-Teh does not in any of his copious and detailed writings on the Manchurian epidemic make any claim to the effect that his actions had significant effect on the further course of this epidemic. Morris’s claim to the contrary on his behalf is groundless. Nonetheless, by April 1911, the epidemic had faded away. The Spontaneous Decline of Epidemics of Primary Pneumonic Plague Wu Lien-Teh, who led the campaigns against both Manchurian epidemics of primary pneumonic plague, has written most of the medical and epidemiological studies on this disease, including the only monograph, a fact that also reflects the relative rarity of this disease. He has clear opinions on the reasons or mechanisms causing the decline: the main reason for the fading away of the epidemic was not his personal efforts but the characteristic tendency of epidemics of primary pneumonic plague to undergo “spontaneous decline.”74 In a later work, Wu Lien-Teh relates that when he first came to Harbin, “many of the inhabitants with whom I conversed informed me that this epidemic was quite an ordinary visitation, to which they had been accustomed. It never killed many, and would stop of itself, if no attention were paid to it.”75

72 73 74 75

Wu Lien-Teh 1913, 1926. Wu Lien-Teh 1934a: 1–3. Wu Lien-Teh 1926: 188–92; Wu Lien-Teh, Chun, Pollitzer 1934: 85–6. Wu Lien-Teh 1934b: 16.

gunnar karlsson’s alternative theory

519

Obviously, something new had happened that gave the outbreak of primary pneumonic plague much enhanced powers of spread, namely the immense influx of coolies living in exceptional density in the lodging houses or inns, the extreme cold that kept them indoors, and the disseminative effects of the railway. Nonetheless, also in the new conditions with much strengthened epidemic dynamics and higher rates of spread and mortality the disease’s tendency to self-limitation and spontaneous decline still prevailed. The fact that spontaneous decline can be such a prominent feature of epidemics of primary pneumonic plague despite exceptionally favourable conditions for respiratory transmission compared with the medieval social scene explains why population mortality in much the largest of all known epidemics of primary pneumonic plague was only a minute fraction of the rates ordinarily wrought on populations by medieval plague epidemics. The Manchurian epidemic of 1910–11 claimed about 50,000 lives in Manchuria, which means that population mortality was only a tiny 0.4 per cent, not at all compatible with or comparable to the mortality rates assumed by Steffensen and Karlsson for the Icelandic epidemics under discussion or by Morris for England. Since Karlsson had read parts of my doctoral thesis, he saw the threat that these facts presented to his theory and argues that the same problem, or “riddle” as he calls it, of minimal mortality also prevailed in the bubonic plague epidemics in India around the turn of the previous century, and asserts that this must have escaped my notice.76 That is not correct. As pointed out above, the mortality in the Indian epidemics of bubonic plague was small because they were from the outset combated intensely with efficient anti-epidemic countermeasures, which conspicuously was not the case with the Manchurian epidemic of primary plague of 1910–11 or with the Black Death or subsequent plague epidemics.77 If Wu Lien-Teh’s observation of a marked tendency of self-limitation and spontaneous decline of epidemics of primary pneumonic plague is correct, it implies that it is a characteristic feature of such epidemics to be small. This proposition can be tested by collecting and collating all evidence on all known epidemics of this mode of plague, a task Karlsson

76 77

Karlsson 1996: 283. See above: 194–202.

520

chapter thirteen

neglected. This material makes it clear that the two Manchurian epidemics are the only instances of fairly large epidemics of primary pneumonic plague, and that even they caused miniscule population mortality rates. The corpus of scholarly studies on primary pneumonic plague contains only one probable and one possible instance of epidemics designated primary pneumonic plague (other than the two in Manchuria) with as many as one thousand cases: (1) in 1905, an epidemic with around 1000 cases occurred, according to Wu Lien-Teh, in the Bukeëf Horde of the Kirghiz Steppes of the (Imperial Russian) Astrakhan Government (“guberniya”); however, according to Klimenko, there were 659 cases with 621 deaths, which means that the epidemic was considerably smaller, included about190 bubonic cases,78 and should rather be designated a mixed epidemic. In 1920, 1056 pneumonic cases were registered in the northern Punjab province of India.79 Scholars have registered a small number of epidemics designated primary pneumonic plague with over one hundred cases, the largest comprising 416 cases.80 Thus, the overwhelming majority of known outbreaks of epidemics designated primary pneumonic plague are quite small or even tiny, most of them restricted to the social level of household, relatives or neighbours, the great majority of outbreaks comprising from a couple of cases to a few tens of victims. This is a general feature covering all areas where epidemics designated primary pneumonic plague have been medically verified, whether in Russia, Central Asia, India, China, Manchuria, Egypt, Madagascar, Vietnam or Indonesia, or elsewhere.81 Arguably, this could be taken to mean that primary pneumonic plague in the overwhelming majority of outbreaks assumes an endemic character, becoming extinguished without having developed an epidemic form comprising a significant number of cases. Similarly, it appears impossible to identify any certain or likely historical epidemic of primary pneumonic plague. Sticker, who was an impressive pioneer in the field of plague history, attempted to collect all 78 The estimate is based on assumptions of a 100 per cent lethality rate in cases of primary pneumonic plague and 80 per cent in cases of bubonic plague. 79 Wu Lien-Teh 1913–4: 244; idem, 1926: 56; Klimenko 1910: 660; Wu Lien-Teh 1927–8: 58. 80 Klimenko 1910: 660. Cf. Wu Lien-Teh 1913–4: 244. 81 Studies presenting epidemics of primary pneumonic plague include Klimenko 1910: 657–63; Wu Lien-Teh 1913: 237–52; Wu Lien-Teh 1926: 9–99; Wu Lien-Teh 1927–8: 55–92; Tieh, Landauer, Miyagawa et al. 1948: 52–8; Pollitzer and Li 1943: 212– 6; Brygoo 1966: 51–2; Trong, Nhu and Marshall 1967: 93–7; Narkevich, Onishchenko, Naumov et al. 1991: 32.

gunnar karlsson’s alternative theory

521

relevant historical evidence on pneumonic plague, but managed to find only a few interesting possible cases of such epidemics, six before 1800. Importantly, he cautiously designates them as being characterized by “predominant [“vorherrschende”] lung disease,” which presumably should be taken to mean that, in his view, they were mixed epidemics that also included significant proportions of bubonic cases.82 One should also note that he does not (because the sources will not permit it) differentiate between secondary and primary pneumonic plague.83 Wu Lien-Teh, who took a strong interest in plague history, succeeded in adding a few epidemics to the list, but also in his case all epidemics are mixed.84 In his excellent study of plague and other epidemic diseases in Early Modern Central Europe (1560–640), E.A. Eckert discusses some evidence based on parish registers relating to plague epidemics in seventeen communities in southern central Europe and the Rhenish region in the years 1563–4. The clinical evidence provided by contemporaries does not discern between secondary and primary pneumonic plague, but the fact that 11 of 17 communal epidemics reached their peaks of burials in the winter months merits attention. However, the author concludes his discussion by stating that these and other outbreaks of winter epidemics probably were mixed epidemics, pointing to the Madagascan epidemics for an analogous model.85 In my monograph on the Black Death, doing my very best to collect and collate all relevant studies for the whole of Europe, I similarly found no evidence implying epidemics of primary pneumonic plague, only two possible cases of mixed epidemics, namely in Avignon and only (just) possibly in Novgorod. And this outcome was strongly confirmed by the seasonality and pattern of spread of the Black Death.86 Despite much effort, it has so far not been possible to identify a likely historical case (before c. 1850) of an epidemic of primary pneumonic plague. The notion of pure epidemics of primary pneumonic plague is, as shown above, fictitious, an epidemic of this type has never been 82 Mixed epidemics comprising (for social and cultural reasons) an increased incidence or level of pneumonic plague have been studied by modern scholars in Madagascar 1924–40 (20 per cent), Upper Egypt 1904–22 (31 per cent), Java (4–8 per cent) and episodically in Vietnam. Brygoo 1966: 45–7; Wu Lien-Teh 1926: 33, 23; Trong, Nhu and Marshall 1967: 93–7. 83 Sticker 1910: 246. 84 Wu Lien-Teh 1926: 7. 85 Eckert 1996: 83, 85–6. For the Madagascan plague epidemics, see fine and comprehensive overview by Brygoo 1966. 86 Benedictow 2004: 214, 233–41, 238–9.

522

chapter thirteen

observed in the research history of plague. Steffensen’s and Karlsson’s assertions that there were epidemics of primary pneumonic plague or pure epidemics of primary plague in Iceland and Karlsson’s view that that the Black Death in general was primary pneumonic plague, are without empirical support. This may explain that there is no indication in Karlsson’s paper of any effort to obtain relevant information on the matter. This discussion has established another independent sufficient condition for rejecting their assertions. The epidemiological effects that could be expected if Wu Lien-Teh’s observation is correct, that the course of epidemics of primary pneumonic plague are characterized by “spontaneous decline,” have now been tested on the complete record of registrations of epidemics of this modality of plague and the outcome has been found to conform entirely to his prediction: generally, outbreaks in normal populations are quite small or tiny, rarely exceeding a hundred cases. Neither in the past nor in recent history is there any instance in the records of an epidemic of primary pneumonic plague in a normal population comprising the number of cases (mortality) or sweeping away the proportion of the population (population mortality) corresponding to Steffensen’s and Karlsson’s assertions as to the mortality effects of the Icelandic epidemics of 1402–4 and 1494–5, and by very large margins. This outcome of the discussion of this epidemiological aspect, the highly limited powers of spread of primary pneumonic plague, suffices as another independent sufficient condition for rejecting Steffensen’s and Karlsson’s theory. It would, however, be unsatisfactory to leave this subject without identifying the main reasons for the three very important characteristic epidemiological features of epidemics of primary pneumonic plague, namely to undergo “spontaneous decline,” be small or tiny, and to give rise to a relatively small number of outbreaks—three epidemiological manifestations of the disease that are, presumably, closely causally linked. There are three main reasons: (1A) Contrary to what is asserted surprisingly often, primary pneumonic plague is not strongly contagious and does not easily “recruit” new infective agents who assure the continuation and dynamic development of the epidemic process, except, as underscored above, under exceptional social circumstances of extreme overcrowding. Again, in the words of Wu Lien-Teh:

gunnar karlsson’s alternative theory

523

Inasmuch as, in our opinion, an overwhelming majority of cases receive infection through being in the direct range of a cough, we wish to lay stress upon overcrowding,

and he goes on to illustrate the point: At Dalinor mines, though the population consisted of 4,000 Chinese and 2,000 Russians, the 1921 epidemic claimed only four Russians out of a total mortality of 1,017. The Russians were better housed on level ground, while the Chinese lived in crowded semiunderground dwellings.87

The crucial importance of close physical proximity is still the prevailing view. The American scholar J.D. Poland makes this point: Primary plague pneumonia occurs primarily in persons in close and prolonged contact with another person with pneumonic plague. Hence, respiratory transmission occurs most frequently to medical personnel or household contacts who are directly involved with the care of the patient.88

(1B) Presumably, this feature is at least to a large extent due to the fact that plague is a bacterial disease and bacteria, being hundreds of times larger than viruses, need much larger and heavier droplets for aerial transportation and will, consequently, normally move much shorter distances through the air. Hirst summarizes recent research showing that droplets of sputum ejected from the mouth tend to fall rapidly towards the ground and that, even when people cough, a surprisingly small number of bacterial colonies develop on culture plates placed only a foot directly opposite the mouth.

This corresponds well with the fact that most patients give a history of association with a previous case for a period of hours, or even days.89

(2) Another crucial reason for the weak powers of transmission and dissemination of primary pneumonic plague is that this disease is an extraordinarily fast killer, leaving little time for interhuman spread. In 1921, in Harbin (Manchuria) mean duration of the

87 88 89

Wu Lien-Teh 1926: 180–1, 298–302. Poland 1983: 1230. See also Meyer 1961: 252. Hirst 1953: 226–7.

524

chapter thirteen

disease in 1,128 patients was 1.8 days.90 This characteristic is confirmed by observations made during smaller epidemics, for instance, during an epidemic in Vietnam in 1915 comprising twenty-four persons including three medical personnel, all of whom died. It was documented that “death occurred within forty-eight hours of the onset of primary symptoms,” which must be taken as a more inaccurate way of expressing an identical observation. Also in a study of another plague epidemic of about the same size in Vietnam in 1941 it was documented that all cases were dead within forty-eight hours of the onset of the symptoms.91 Importantly, it takes, on average, twenty-four hours before the contagious cough with bloody expectoration develops, which leaves only 0.8 day for transmission.92 Also this clinical feature explains why outbreaks of this disease normally comprise only a small number of cases and will tend to be quite easily extinguished in the incipient or early endemic phase or, quite rarely, early in the epidemic process. Arguably, this clinical feature also represents an independent sufficient cause. (3) However, the causation of “spontaneous decline” is more complicated; it results from the combined effect of three usual clinical forms of the disease that do not (or only slightly) lead to development of the cough with bloody expectoration which is the principal vehicle of dissemination of primary pneumonic plague: (3A) As suggested by the extremely rapid course and brief duration of the disease, one such form is quite a frequent incidence of a fulminant course of ordinary cases of primary pneumonic plague leading to the rapid demise of the patient before the contagious cough with bloody sputum has had time to develop. (3B) When larger droplets are inhaled (and as pointed out above, this will quite often be the case, see 1B), they tend to impinge on the upper parts of the respiratory tract where they infect the tonsillar region, causing pharyngeal and primary septicaemic plague with extremely rapid death of the patients who will not become contagious since the droplets are not 90

Chun 1936: 318–9. Trong, Nhu and Marshall 1967: 93. 92 Wu Lien-Teh 1922–3: 274; Wu Lien-Teh 1926: 297; Wu Lien-Teh, Chun, and Pollitzer 1934: 80. 91

gunnar karlsson’s alternative theory

525

deposited in the lungs and cannot give rise to the cough with bloody sputum. (3C) Wu Lien-Teh stresses in particular the importance of a third type of fulminant case called pulmonary plague. Dissection of lungs of such cases did not show the usual pneumonic foci [which produce the cough with bloody sputum: my insertion] but presented—though undoubtedly infected through the respiratory tract—only hyperaemic93 and oedematous94 changes in the lungs as well as marked septicaemic features. We designated these cases pulmonary plague because, though they were anatomically similar to the septicaemic cases encountered in bubonic plague, they were etiologically different from them, the infection having entered through the respiratory tract.

Conspicuously, the incidence of pulmonary plague increased sharply towards the end of the epidemics, while pneumonic cases, i.e. cases with pneumonic foci in the lungs (which give rise to the cough with bloody sputum), became relatively scarce. In Wu Lien-Teh’s opinion, these cases were probably due to an enhanced virulence of the B. pestis developing through passage from lung to lung. We assumed that through such repeated passages the invading organism finally became so virulent as to cause mainly pulmonary cases. These—though very fatally infected—are comparatively little infectious, because the disease runs a rapid course. As a consequence, the principal medium of infection, namely, the sputum, is absent. In other words, our post-mortem findings at the end of the 1920–1 outbreak give a scientific reason in favour of a spontaneous decline of pneumonicplague epidemics […]. Being thus rendered less infectious, the “spontaneous decline” of the epidemic, even in foci unattended by sanitary organizations, might be easily explained.95

R. Pollitzer, who was among the medical staff working in the epidemic of 1920–1 and made “a fairly large number of postmortems on lung pest victims,” later confirmed that he made exactly the same observations as

93

Denoting hyperaemia: an excess of blood in a part, engorgement. Pertaining to, or of the nature of, oedema, affected by oedema. Oedema: the presence of abnormally large amounts of fluid in the intercellular tissue spaces of the body, usually applied to demonstrable accumulation of excessive fluid in the subcutaneous tissues. 95 Wu Lien-Teh 1926: 189–92; Wu Lien-Teh, Chun, Pollitzer 1934: 86; Wu Lien-Teh 1936b: 420–1. 94

526

chapter thirteen

Wu Lien-Teh. Importantly, this was also the case with respect to the rhythm of developments, that dead bodies showing no pneumonic foci were mainly met with at the end of the epidemic. It was therefore tempting to assume that there might be a causal connection between the preponderance of this “non-pneumonic” form of lung pest and the decline of the outbreak.96

In 1942, Pollitzer and Li conducted a complete investigation of an outbreak of quite a usual size of primary pneumonic plague, comprising sixteen cases, which had taken place in a district in North Hunan (China). They made the following observations: (1) “The last patient in each of the two first affected families had no more bloody sputum.” (2) “In five of the six instances where the infection was carried from these two households into other families, no further spread took place, evidently because the secondary victims had no bloody sputum, in three instances even no cough.” (3) “Further inquiries showed that infection never resulted from contact with patients having neither bloody sputum nor cough. In only two out of fifteen instances was infection due to contact with patients having cough but no bloody sputum.” (4) Of particular importance in the present context are the following assertions: (a) the outbreak came to an end before measures taken by us could have any effect: (b) this decline took place during a rainy spell, when the temperature was comparatively low.

The first point of the last citation confirms the spontaneous decline at an early stage that characterizes outbreaks of primary pneumonic plague in which no countermeasures are applied, the second point is of relevance to some extraordinary assertions by Steffensen and Karlsson as to the importance of the climate in Iceland (see below). Pollitzer and Li make the following general conclusion: More or less rapid evolution of a “non-pneumonic” type of lung pest, characterized by absence of the usual vehicle of infection, the bloody sputum, and often also of cough, appears to be of causal importance in the decline of pneumonic plague epidemics.97

96 97

Pollitzer and Li 1943: 215. Pollitzer and Li 1943: 212–6.

gunnar karlsson’s alternative theory

527

Outbreaks of primary pneumonic plague have been shown above to be generally small or tiny, comprising only a paltry fraction of the number of cases or level of population mortality envisaged by Steffensen and Karlsson. The medical and epidemiological reason for this feature are also clear: the high frequency of various types of fulminant noncontagious forms that do not contribute to further dissemination of the epidemic and therefore break the chain of transmission. Most important among these forms is the appearance at an early stage of outbreaks of a strong increase in the incidence of cases of pulmonary plague that leads to a rapid decline and disappearance of the epidemics, a phenomenon designated “spontaneous decline.” These non-contagious forms arise from a combination of the virulence and size of the plague bacterium and the mode of respiratory transmission. Thus, they constitute a basic property and characteristic feature of this modality of plague which mould all known outbreaks in the past and in modern times into clearly defined medical, epidemiological and demographic patterns. These patterns diverge radically and decisively from the patterns envisaged by Steffensen’s theory that the two Icelandic epidemics of 1402–4 and 1494–5 were primary pneumonic plague and Karlsson’s theory to the effect that these two Icelandic epidemics were pure epidemics of primary pneumonic plague and that this was a general feature of the Black Death in Europe. Their theories are incompatible with the corpus of knowledge of the medical and epidemiological causes of the rise and course of the outbreaks of primary pneumonic plague. This explains also why there is no epidemic of primary pneumonic plague on the record with a duration of two or three years as in the case of the Icelandic epidemics of 1402–4 and 1494–5: the clear and systematic tendency of spontaneous decline would prevent this from happening. Thus also the duration of the Icelandic epidemics is a strong argument against their being primary pneumonic plague; that the notion of pure epidemics of primary pneumonic plague is fictitious is another matter. Finally, I would also like to point out that in the plague history of Norway from 1348–654, covering more than thirty waves of bubonicplague epidemics, there is not a single instance of an epidemic that lasted so long in the same region, which is also a strong argument against this Icelandic epidemic having been bubonic plague.98

98

Benedictow 2002.

528

chapter thirteen The Icelandic Climatic Theory of Primary Pneumonic Plague

Steffensen, who bases his theory on the hypothesis that the supposed Icelandic plague epidemics started from bubonic plague victims who developed secondary pneumonia, accepts the fact that there were rats in Iceland and thus avoids the impossibilities and absurdities of Karlsson’s theory as to the origin of epidemics of pure primary pneumonic plague. However, he cannot avoid the issue of the exceptional powers of spread that are not observed anywhere else, and must construct a unique Icelandic case based on assumptions of climate. Steffensen argues that bacteria harboured in the mucus of the respiratory tract derive from it some protection against dryness. In damp and cold air, such drops of moisture can preserve living bacteria for months on end, especially if there is frost. Under Icelandic conditions, therefore, it is quite possible for living plague bacteria to remain in tiny drops of moisture on, for example, bedclothes and personal clothing, long after the patient’s death, and for drops to be stirred up again and carried down into the lungs of the person, for example, who is about to bury the body […] there is, therefore, no apparent biological reason why an epidemic of primary pneumonic plague could not have occurred in Iceland.99

Steffensen does not consider this statement a composite working hypothesis constituted by several hypothetical elements each dependent on empirical support or corroboration for its viability. In his understanding of scholarly or scientific work the mere proposal of a hypothesis confers tenability on it without empirical support or references to research literature. This is obviously fallacious. The research literature on primary pneumonic plague contains no support, not even a unique case or sporadic case histories of this type of dissemination. No case has been observed of a person who has contracted primary pneumonic plague from plague-contaminated droplets in clothing or bedclothes left by patients at any time or in any climatic zone. This might constitute a pure epidemic of primary pneumonic plague which, as shown above, has never been observed or ascertained in any scholarly study of this disease. “Damp and cold air” is very far from being a unique Icelandic type of climate, as the circumstances of the epidemic of primary pneumonic plague studied by Pollitzer and Li in Hunan Province show (see above). The coasts of western and northern Norway 99

Steffensen 1974: 41.

gunnar karlsson’s alternative theory

529

are also characterized by “damp and cold” climate for a large part of the year, but no epidemic of primary pneumonic plague can be ascertained from the sources; all Norwegian plague epidemics conform to the pattern of spread and seasonality of bubonic plague. There is also another crucial point that Steffensen has failed to consider and which undermines or even invalidates his theory, namely, the effect of extraneous conditions on the virulence of plague bacteria. As stated by Pollitzer and Meyer: it is generally agreed that, although […] plague-contaminated objects may remain infected for some time, the chances of their proving infective, thus becoming responsible for the spread of the disease, are usually remote. Plague […] in its pneumonic form […] is almost always the result of a direct infection contracted in the immediate vicinity of patients suffering from secondary or primary lung involvement.100

Similarly, Wu Lien-Teh states specifically in relation to primary pneumonic plague that: the unsuitability of the plague bacillus for prolonged existence as a saprophyte and the unlikelihood of rodent or man contracting direct infection from contaminated inanimate objects, rule out the free existence of the causative organism as a means for preservation of the disease.101

This quotation is also given in my doctoral thesis102 in the discussion of this matter, however, to no avail, as Karlsson simply ignores it. Steffensen argues his case for primary pneumonic plague in Iceland in terms of what is possible under particular Icelandic climatic conditions: his concluding sentence is couched in the formal language of hypothesis formation. But he has built a model which cannot be tested, because no Icelandic material is available that allows the identification of the form of plague or epidemic disease afflicting the population. For this situation the following methodical rule applies: the inability to test an explanatory model does not invalidate it, but does render it useless as a scientific hypothesis. The justification for constructing this explanatory hypothesis, model or working hypothesis would have been strengthened if at least a sprinkling of this type of endemic cases had been observed elsewhere. But Steffensen’s is based on pure speculation, it has no evidentiary basis, no validity, no tenability. Its use in the

100 101 102

Pollitzer and Meyer 1961: 434–5. Wu Lien-Teh 1936a: xxviii. Benedictow 1993/1996: 216.

530

chapter thirteen

construction of an alternative theory of plague in Iceland can only serve to undermine the theory, and claims that such a theory of plague is superior to other empirically supported theories are obviously invalid.103 Conspicuously, later in his paper, Steffensen argues that the clinical elements in the account of the Lawman’s Annal on the Black Death in Bergen in 1349 show that it was an epidemic of primary pneumonic plague, an argument that will be addressed below and shown to be untenable. Here the following point shall be made: by turning to Norway, Steffensen greatly extends the scope of climatic conditions that allow large-scale epidemics of pneumonic plague. Whilst he originally stresses the uniqueness of the Icelandic climate, making a claim for Iceland as a unique case, the extreme weakness of his case has led him to a line of climatic argument which includes a much wider range of territorial relevance, covering quite large parts of northerly Europe including northern England and Scotland. This makes the rarity of epidemics of primary pneumonic plague, if indeed any occurred, even more hard to explain, as no such epidemic, as mentioned above, has been confirmed in any pre-industrial society. Steffensen’s and Karlsson’s assertions are without empirical medical or epidemiological support in the most accurate meaning of the terms. It has been possible to identify several independent sufficient causes for rejecting their theories. Mortality Rate of the Purported Plague Epidemics in Iceland Karlsson makes two central assertions with respect to the mortality caused by the Icelandic epidemics: (1) that the mortality rate in the epidemic of 1402–4 was 60 per cent and in the next epidemic of 1494–5 it was 53 per cent, and (2) that these mortality rates constitute definite proof that the epidemics were primary pneumonic plague.104 The massively documented fact is that no epidemic of primary pneumonic plague is known which has caused a population mortality exceeding 1 per cent. This is the case for very concrete and strong

103

Benedictow 1993/1996: 223–5. Karlsson 1996: 268–76. In the second case, Karlsson quite arbitrarily moderates his mortality estimate for the second epidemic to 30–50 per cent, since he recognizes that the evidence is very poor to put it mildly. 104

gunnar karlsson’s alternative theory

531

medical and epidemiological reasons. A level of population mortality of 60 per cent thus constitutes certain proof that the Icelandic epidemics must have been a different disease or conjunction of diseases. However, Karlsson’s estimates of mortality must be rejected. The texts of the Icelandic annalists or chroniclers on which these estimates are based are cited in English translation in Appendix 2. The suggestion that medieval chroniclers provide accurate information on distribution, mortality rates and areas affected cannot be taken seriously, as shown repeatedly above and again below.105 Hatcher disregards the “overwrought imaginings and hopelessly inaccurate quantification of the chroniclers.”106 Just to take a couple of illustrating examples of the nonsense of figures in Icelandic annals: in the Annal of Skálholt, it is related that in 1305 that King Håkon V of Norway went to war with Sweden with an army of 40,000 warriors, which is without any basis in the known facts on Norwegian military manpower at the time, to put it mildly. Compared with England’s contemporary population of around six million, it would correspond to an assertion that the king of England went to war with 700,000 warriors. The Lawman’s Annal asserts that only fourteen persons survived the Black Death in London.107 Instead, as Hatcher states, “advances in knowledge and technique have enabled us to proceed […] to a position where the majority of historians are agreed upon a reasonably narrow range of probabilities.” Only mortality figures based on population records that can be examined and evaluated according to the principles of demography are used in my monograph on the Black Death.108 Chroniclers’ assertions cannot be accepted, especially their assertions of numerical and demographic data, if source-criticism cannot be applied and the possible tenability at any level can be ascertained by independent material evidence. In this perspective it could be of interest that there are numerous

105

See, for instance, above: 78–84, 219–22, below: 589–92. Hatcher 1977/78: 21. 107 Islandske Annaler 1888: 200, 275. 108 One partial exception is the chronicle of Giovanni Villani. which can be considered usable, because it can be shown that he takes real interest in collecting statistical information on his beloved city of Florence and that the city’s authorities produced statistically usable population registers, for instance of taxable householders, that he has real competence with regard to statistical data, that his estimates are based on empirical material of various kinds, and because his estimate of mortality in the Black Death can be tested against various types of population records. His approach is protoscientific, reflecting his central background in the Early Renaissance in Florence, and therefore contains valuable empirical and statistical material. 106

532

chapter thirteen

demographic studies showing that epidemics of bubonic plague produce mortality rates at the level of 60 per cent.109 Karlsson does not mention that Steffensen, on the basis of the same sources, conjectures a population mortality of one-third,110 about half of Karlsson’s estimate. Since Steffensen honestly characterizes his estimate as a conjecture, i.e., a guess or guesstimate, the margins of error are obviously huge. Thus, Karlsson asserts that he has found solid ground for an accurate mortality estimate on the basis of sources that Steffensen thinks permit only a conjecture or qualified guess of a much lower level of population loss. This puts in perspective Karlsson’s contention that the margin of error could be a ludicrously low 10 per cent and the fact that this has been accepted by the editors and consultant(s) of the Journal of Medieval History.111 The difference between Steffensen’s and Karlsson’s estimates is 100 per cent, representing a corresponding margin of error. Karlsson incredibly maintains that the annals’ indication of area affected, distribution and level of mortality rates are accurate within margins of a couple of per cent, which soundly beats the margins of error associated with modern population censuses based on statistical data systematically collected by trained personnel. In view of the fact that margins of uncertainty associated with the various elements that constitute estimates relate multiplicatively to each other, the margins of error are much higher. Any scholarly critical examination of the annals and other evidence cited by Karlsson will demonstrate the justification for at least a modicum of prudence as shown by Steffensen. In my opinion, they permit no useful quantification of a specific mortality rate at all, only the impression of serious and locally also severe mortality (see below, Appendix 2). This perspective is corroborated in the most recent evaluation of population losses in the two fifteenth-century epidemics based on agrarian studies relating to northern and eastern Iceland where it is stated that they indicate a limited abandonment of farms in 1420–50 and 1495–1550 when some 20–25 per cent of the farms were deserted. The effect was particularly notable on the coast but it was temporary and probably caused by

109 110 111

Benedictow 2004: 245–384. Steffensen 1971: 54. Karlsson 1996: 276.

gunnar karlsson’s alternative theory

533

outbreaks of plague in 1402–4 and 1494–5. In the fifteenth century climatic deterioration should also be taken into account, the westernmost parts of Iceland, on the other hand, saw population growth and settlement expansion from about 1300 and show no signs of recession at all in the three following centuries.112

Clearly, Karlsson’s “estimates” fly in the face of the sources and empirical studies on settlement developments. The settlement studies suggest a population loss which is much lower; this shows that Karlsson’s “estimates” are wildly exaggerated, the predictable outcome of a basically arbitrary approach. Mortality at the level of 15–20 per cent can be caused by a number of epidemic diseases or conjunction of more or less concomitantly spreading epidemic diseases, especially in the epidemiological circumstances characterizing Iceland at the time.113 Summary: Why There Never Was a Plague Epidemic in Iceland The presentation of the characteristic medical and epidemiological features of primary pneumonic plague based on the complete corpus of relevant research constitutes a broad basis for comments on Morris’s alternative theory of late medieval plague as being primary pneumonic plague and on Karlsson’s use of this theory in his paper on the epidemics that ravaged Iceland in 1402–4 and 1494–5. It has been shown that their assertions are unfounded and erroneous on the following main points: (1) There is no such thing as pure epidemics of primary pneumonic plague, i.e., independent of an infected murine basis. No case of an epidemic of pure primary pneumonic plague has been identified in the entire corpus of historical studies of plague. All assertions to the contrary are empirically unfounded and arbitrary. (2) Since there were no rats in Iceland, according to Karlsson, no epidemic of plague of any kind could have arisen in the island, pure or not. (3) It is not correct that assertions in the sources to the effect that plague victims typically died in the course of three days of illness are indicative of primary pneumonic plague. The average duration

112 113

Vahtola 2003: 575–6. Cf. Cliff and Haggett 1985; McArthur 1968.

534

chapter thirteen

of the course of primary pneumonic plague is 1.8 days, and patients normally die within 48 hours. One would also expect that the frequent incidence of even much shorter fulminant cases would attract attention by their frightening character and tend to acquire prominence in contemporary accounts. Three days are within the normal range of the course of illness of bubonic plague, namely three to five days,114 and an average duration of plague disease within this range is therefore a clear indication of bubonic plague.115 (4) It is not correct that all victims of primary pneumonic plague develop infectious cough with bloody expectoration. On the contrary, epidemics of primary pneumonic plague are characterized by large and increasing proportions of cases of several clinical types which do not cause development of a cough with bloody expectoration in the diseased, who therefore do not pass on the infection.

114

Chun 1936: 313. Above: 279–80. Morris 1971: 206–7, maintains erroneously that the average duration of cases of primary pneumonic plague is three days and of cases of bubonic plague is five days. Since he does not support his view with a footnote, the basis or source of this assertion cannot be ascertained and examined. He refers to Gui de Chauliac’s account of the Black Death in Avignon where this contemporary observer discerns between a first phase, in which the course of illness lasted three days, and a second phase where it lasted five days, as proof that the first phase was primary pneumonic plague. However, this is not evidence to this effect, since both indications of duration of illness are within the normal range of bubonic plague. Since cough and bloody expectoration of secondary pneumonic plague cases normally constitute a significant but variable proportion of cases of bubonic plague, there cannot have been any phase without a noticeable incidence of this clinical feature, but there can have been substantial variation or change in the incidence. It is also not correct, as Morris contends or implies, that primary pneumonic plague can be the origin of epidemics of bubonic plague; the incorrectness of this assertion is demonstrated by the experience in the Manchurian epidemics. Although there were 50,000 cases in Manchuria itself and the dwellings of the Chinese coolies that constituted the great majority of cases swarmed with fleas and other blood-sucking parasites, bubonic cases that could have been caused by fleas infected by pneumonic cases were extremely few and isolated and only one case can be considered quite certain; in the words of Wu Lien-Teh: “practical experience has shown that pneumonic plague rarely caused the bubonic form,” and “Not so much the existence as the rarity of such cases calls for comment.” 1926: 186–7. The first phase of plague in Avignon was, therefore, probably a mixed epidemic in which the primary pneumonic part faded away due to the characteristic “spontaneous decline” of this modality of epidemic plague and a more usual epidemic of bubonic plague emerged. Benedictow 2004: 236–8. No instance of a primary plague epidemic that develops into a bubonic plague epidemic has ever been recorded. 115

gunnar karlsson’s alternative theory

535

(5) It is therefore not correct that epidemics of primary pneumonic plague have great powers of spread. On the contrary, epidemics of primary pneumonic plague are characterized by low diffusibility and “spontaneous decline.” Outbreaks of primary pneumonic plague are small or tiny, population mortality rates are consistently minuscule, and even the largest epidemic of this type, the first Manchurian epidemic of 1910–11, occasioned a population mortality rate of only 0.4 per cent. Mortality rates of the size asserted by Morris for England and by Karlsson (and Steffensen) for the Icelandic epidemics of 1402–4 and 1494–5 are unknown in the complete corpus of research on primary pneumonic plague, and by wide margins. Their assertions to the effect that the English or the Icelandic epidemics swept away large parts of the respective populations are powerful arguments against the notion that they could have been primary pneumonic plague. (6) No epidemic of primary pneumonic plague or of bubonic plague has been identified in the northerly parts of Europe 1402 or 1494, the years when the two epidemics broke out in Iceland or in the preceding years. There is therefore no way plague contagion in any form could have been transported to Iceland in these years. (7) Karlsson’s theory of a mutant version of plague disease specifically designed to suit his arguments is arbitrary, and it is also fallacious, since it is not developed according to the requirements of evolutionary theory and the obligation to uncover and present the mechanisms of selection. The territorial origin of a specific mutant version of primary pneumonic plague of the purported Icelandic epidemics is a crucial question left unanswered; its origin is also therefore arbitrary. Also unexplained is the crucial question of whether the same mutant strain really could have arisen twice, or where on earth it took refuge in the meantime. No such mutant strain has been identified by modern DNA studies of genetic material taken from plague graves. All of these crucial assertions by Stephenson and Karlsson are arbitrary and untenable. According to the normal methodological and empirical considerations and assumptions of scholarly work, these seven medical and epidemiological points settle the case, as they contain as many independent sufficient grounds for invalidating the theory. There never was a plague epidemic without rats in Iceland. There never was a plague epidemic in Iceland.

536

chapter thirteen Was the Black Death in Bergen (Norway) 1349 Primary Pneumonic Plague?

Karlsson states explicitly, as mentioned above, that the central objective of his paper is to defend Steffensen’s paper against my criticism of it and his theory that plague in Iceland was primary pneumonic plague. He is especially outraged at my criticism of Steffensen’s presentation and analysis of the clinical description of plague cases given in the Lawman’s Annal’s account of the Black Death in Bergen in 1349 and of his conclusion that it describes an epidemic of primary pneumonic plague. This account and another given in the so-called Fragment of the Annal of Skálholt, which is closely related but not identical,116 are normally and reasonably assumed to be based on accounts of two prominent Icelandic prelates who stayed in Bergen at the time of the Black Death and returned in 1350 and 1351, respectively.117 However, other Icelanders who returned, some quite likely in 1350,118 may have added independent information. Karlsson aggressively defends Steffensen’s views; I consider some of his arguments personally offensive, but will refrain from commenting on them, as the facts speak for themselves clearly and loudly. One should note that there are crucial problems not only with regard to the interpretation of the clinical descriptions of the Black Death in Norway provided by these Icelandic chronicles. Tacitly, Steffensen assumes that it is unproblematic to use the Lawman’s Annal’s account of the Black Death in Bergen in 1349 for the purpose of corroborating his views on the nature of the epidemics that spread in Iceland in 1402–4 and 1494–5 as primary pneumonic plague (see Appendix 2). This inevitably implies, as pointed out above, a sudden abandonment of his argument of the specificity of Icelandic climate as a necessary condition for the spread of large-scale epidemics of primary pneu-

116 Islandske Annaler 1888: 224: “þat uar kyn sottarinnar at menn lifdu iij dægr med hardan stinga þa toku menn blodspyu ok for þar med onndin.” The text is cited without indicating the expansion of abbreviations. Cf. below: 551 and fn. 151. 117 Benedictow 2006: 88, 101–2. 118 In the Lawman’s Annal it is mentioned that Thorlak’s ship at quay in Bergen was ready to leave for Iceland with a number of named Icelanders on board, but was so severely hit by the Black Death that it was prevented from putting to sea. Quite likely, this ship returned to Iceland in the shipping season of 1350 with survivors and other passengers and crew members on board who had their own stories to tell. Benedictow 2002: 67–72.

gunnar karlsson’s alternative theory

537

monic plague. In addition, his approach is problematic in several other important respects that he does not address: (1) The Icelandic annals give no clinical information about the two purported fifteenth-century epidemics of primary pneumonic plague. Consequently, there is no basis for valid comparison with the Black Death in Bergen or elsewhere, they are not in pari materia. Steffensen’s use of comparative analysis is fallacious. (2) Steffensen gives a highly problematic translation of a crucial part of the text which in a decisive way seemingly strengthens his case. This can be demonstrated by citing both the original text from the Lawman’s Annal,119 as I did in my thesis,120 and Steffensen’s and my translations, italics showing the crucial bit of contested translation relating to the two original Norse words “hordum stinga,” with the basic meaning of sharp, pricking, painful sting (literally “hard sting”), which is here associated with the clinical manifestations of the Black Death in Bergen. – Benedictow: The disease was such that men did not live for more than a day or two with sharp pangs of pain, then they began to vomit blood, and then they expired.

– Steffensen: The nature of the sickness was such that men lived not more than one day or two, with great pleuritic pain, whereupon they began to vomit blood and then the spirit passed on its way.

Steffensen uses the medical word “pleuritic” in his translation, although no word with this meaning occurs in the source. To add one or more crucial words to the translation of a text, without making it clear to the reader and providing a persuasive reason for it, violates one of the basic methodological conventions of historical science. Conceivably, it could be a matter of interpretation or connotations, but then, according to the conventional principles

119

Islandske Annaler 1888: 275–6: “þat var kyn sottarinnar at menn lifdu eige meirr en eitt dægr edr tuo. med hordum stinga. eftir þat sætte at blod spyiu ok for þar ondin med sinn vegh.” The text is cited without indicating expansion of abbreviations. 120 The text is almost identical with the text of the Fragment of the Annal of Skálholt; see above: fn. 116, and below: 551 and fn. 151.

538

chapter thirteen

of historical methodology and source-criticism, the reason should be explained and discussed openly, and not, as in this case, introduced tacitly or covertly. I simply cannot understand how Karlsson or other Icelandic scholars can defend this procedure. It is precisely the addition of the medical term “pleuritic” which permits him to identify the Black Death in Norway as an epidemic of primary pneumonic plague. He believes that he can assert that primary pneumonic plague is directly and normally associated with great pleuritic pain without any reference to the medical literature on primary pneumonic plague which confirms or supports that this is the case. (3) Steffensen and Karlsson do not consider it necessary to base assertions regarding the clinical and medical manifestations of (primary pneumonic) plague on the primary research literature or the standard textbooks on plague. Their unflinching confidence in their assertions that cases of primary pneumonic plague are clinically characterized by “great pleuritic pain” stand completely unsupported by any reference to the medical literature on primary pneumonic plague. As such, these assertions are arbitrary according to the standard conventions of methodology of historical, social and medical sciences. If empirical facts count, the medical research literature on primary pneumonic plague should be consulted. In his excellent treatise on primary pneumonic plague, the only monograph on this disease, Wu Lien-Teh discusses relevant points in this connection at some length. He does not state that cases of primary pneumonic plague are characterized by “great pleuritic pain.” He points out that there may initially be “no pain in the chest, only a feeling of constriction when breathing and coughing” and that “later on, these pains are usually more marked,” but that the pain is “never so severe as in ordinary pneumonia.”121 Thus, according to Wu Lien-Teh, some pain, but not great pain, is characteristic of cases in advanced stages of primary pneumonic plague. However, importantly, this element of pain is not associated with pleuritic pain caused by inflammation of the pleura, the membrane of the thorax and lungs. This description, some pain but not pleuritic pain, conforms and accords with other relevant comments. He underlines also that in cases of primary pneumonic plague there is

121

1926: 255, 259.

gunnar karlsson’s alternative theory

539

a “marked disproportion” between slight lung changes and serious general signs (of illness) which is “of great diagnostic value.” The crucial point is that pleurisy is characterized by “inflammation of the delicate membrane of the thorax and the lungs, causing severe pain in the chest or sides,” which is not a characteristic clinical feature of primary pneumonic plague.122 Instead, Wu Lien-Teh associates the small elements of pain in primary pneumonic plague with dyspnœa (difficulty of breathing) caused primarily by “the action of plague endotoxins upon the respiration” and “changed blood circulation.”123 In the most important general standard work on plague which is coauthored by Wu Lien-Teh, Chun, Pollitzer and C.Y. Wu, undoubtedly the most competent group of experts on primary pneumonic plague ever to come together on the same plague-related project, Chun, who wrote the part on clinical manifestations, states: “The patient complains of pain and a restricted feeling in the chest, but this is not severe […] he appears to suffer little,” and goes on to summarize the point clearly and unambiguously: There is not much pain in connection with plague pneumonia in contrast to ordinary pneumonia, though a few exceptions were observed.124

Chun stresses also, in accordance with Wu Lien-Teh’s description, that the “physical signs in the lungs are often slight, even in cases well advanced in the disease,” which, as pointed out, contrasts sharply with the condition of pleurisy. These statements by Chun must be assumed to have been accepted as adequate by his co-authors and are compatible with Wu Lien-Teh’s statements. This is confirmed by Pollitzer who in his own general standard work on plague of 1954 explicitly agrees with Chun’s views on these points, and even cites him quite extensively.125 As shown above, Pollitzer had a leading role in the combat of the second Manchurian epidemic of primary pneumonic plague and also performed numerous autopsies. He also carried out studies of later outbreaks of this disease. The fact that there are rare victims of pneumonic plague who suffer considerable pain cannot be assigned significance in this context in connection with 122 123 124 125

Oxford Advanced Learner’s Dictionary of Current English 1989: 950. Wu Lien-Teh 1926: 259. Chun 1936: 318–20. Pollitzer 1954: 441–2.

540

chapter thirteen

the quite generalized accounts of the Icelandic annals. Furthermore, this pain does not at all accord with the character of the two Icelandic scholars’ assertion with regard to “great pleuritic pain.” The slight significance of pain associated with lungs or the chest in normal cases of primary pneumonic plague finds also an indirect expression in the fact that several of the leading standard works on plague do not mention this subject at all, presumably because it is not a significant clinical feature.126 Consequently, Steffensen’s addition of the word “pleuritic” and Karlsson’s defence of this addition are not only flagrant breaches of the basic principles of source-criticism and scholarly work, but their interpretations that this pain indicates the presence of primary pneumonic plague are factually wrong according to the corpus of primary studies on primary pneumonic plague and the summaries given in standard works. I do not understand on what grounds Karlsson accuses me of not recognizing that “stinga” can refer also to strong pleuritic pain caused, for instance, by pneumonic tuberculosis or pneumonia.127 My point is that the clinical picture of primary pneumonic plague is not characterized by great pleuritic pain or sharp pain in the lungs or chest more generally, and that the term “hordum stinga” for this reason cannot refer to primary pneumonic plague and “great pleuritic pain” caused by this disease. “Stinga” just means “sharp pain,” and can refer to such pain in any part of the body. It is the same word as the English “sting” and has in medieval Norse much the same meaning as in modern English. Sting or “stinga” can be felt any place on the body that is stung by an insect, for example. Karlsson mentions a source that refers to “stinga” “under the arm,” which certainly could refer to a plague bubo in the second most usual site, namely an axilla. However, since the source is earlier than the arrival of the Black Death in Europe, this cannot be the case. Instead, this source reflects the elementary fact that infections of almost any origin can in special circumstances be drained through a lymph tract to one of the sites of clusters of lymph nodes and can there give rise to sharply painful or intensely tender swollen lymph-nodes of the type called bubo or boil. It is the epidemic incidence of swollen lymph-nodes in the form of buboes that is a defining feature of bubonic plague.128 Clearly, according to the principles of source-criticism, only 126 127 128

See for instance Hirst 1953, Langen and Lichtenstein 1936. Karlsson 1996: 281. Above: 203–05.

gunnar karlsson’s alternative theory

541

the use of the word “stinga” in sources produced after the arrival of the Black Death or subsequent plague epidemics can be of value for understanding the meaning and connotations of this word associated with plague disease. Karlsson has found only one instance, which occurs in a fifteenth-century Icelandic manuscript in a text about the treatment of plague which refers to “stinga” with “extreme pain and a boil/bubo.” Karlsson passes easily, even hastily, by it and prefers to emphasize the significance of the few pre-plague uses of the word.129 However, this is strong evidence to the effect that extreme pain is associated with the buboes of bubonic plague and that the word “stinga” at the time was considered suitable in Iceland for the description of the pain in plague buboes. Karlsson is extremely critical of my translation of “hordum stinga” with an expression using the plural form “pangs” of pain when the original is in the singular form. He accuses me of making a deliberate mistranslation in order to construct a false basis for a theory that this pain could be associated with other parts of the body than the lungs and, thus, that the clinical descriptions of the Icelandic annals could reflect bubonic plague.130 I am not a native speaker of English, but a foreigner who has worked hard to achieve a usable knowledge of academic English for the purpose of communicating with the international community of scholars in the field of the history of disease and demography. I may not make accurate translations in all contexts which successfully incorporate the right connotations and nuances whatever my ambition and endeavours. However, the point for me in using the plural form was to indicate continuous sharp pain in order to avoid what I assumed would be the implication in English of using the singular form, namely that there was one sharp pang of pain which then disappeared. Notably Cohn, who is an (American) English speaker, uses the same plural form of the term when describing the type of pain associated with plague buboes, namely “sharp pangs.”131 However, some central points still await full clarification. Now for the hard evidence. Steffensen and Karlsson ignore standard medical works on plague, although the crucial question of whether or not the descriptions provided by the Icelandic annals of the clinical manifestations of the Black Death in Bergen in 1349 is compatible with primary pneumonic plague 129 130 131

Karlsson 1996: 282. Ibid. Cohn 2002: 24.

542

chapter thirteen

or bubonic plague and buboes can only be decided according to the information provided there. It has been shown that the expression “hordum stinga” cannot relate to pleuritic pain in cases of primary pneumonic plague, and Steffensen’s and Karlsson’s assertions to this effect are arbitrary and untenable. However, it remains to be seen whether or not the standard works on plague which summarize the great mass of clinical evidence on bubonic plague confirm my opinion that plague buboes are extremely painful in a way that corresponds with the clinical descriptions given in the Icelandic annals on the Black Death in Bergen 1349 and can be responsibly translated by “sharp pangs of pain” indicating repeated or continuous sharp pain as a normal clinical manifestation. The following citations are arranged according to the chronology of modern scientific standard works on plague and represent to my knowledge a complete and therefore also a representative collection of statements on the matter: (1) Simpson 1905: If a bubo appears it is usually ushered in by intense pain in the groin, arm-pit, or neck which is increased by movement or pressure. The pain at first is so severe that the attention of the patient is mainly directed to it, all other symptoms being considered insignificant compared to the suffering experienced in the gland affected. The pain is followed by a swelling which constitutes the bubo. Pain, tenderness and swelling are the general characteristics of the bubo. The pain may be dull and aching or sharp and stabbing […] and is independent of the size of the bubo. The smaller the size of the bubo the more painful is it likely to be […]. Sometimes the tenderness is so acute that pressure over the bubo will cause wincing and moaning from pain even when the patient is in a comatose condition.132

Simpson describes buboes as generally intensely painful to a degree that dominates completely the patient’s attention. Obviously, this is a clinical manifestation which could be observed by ordinary medieval persons. In fact, the pain is so intense that even light pressure on the bubo will make patients in coma and therefore deeply unconscious wince and moan. The pain is characterized by being intense, sharp and stabbing and is triggered by movement or pressure, which, in my opinion, justifies the use of 132

Simpson 1905: 263, 274.

gunnar karlsson’s alternative theory

543

the word “sharp” and, because it almost inevitably will by triggered repeatedly, use of the plural form “pangs” of pain is also justified. (2) Chun 1936: The glandular mass [of a bubo: my insertion] is very painful and tender to the touch.

For this reason, in order to avoid pain caused by movement of the limbs “If the bubo is in the groin, the leg on the affected side is drawn up, somewhat abducted and twisted outwards; if it is in the axilla, the affected arm is abducted from the trunk; during examination it is often supported by the sound arm.”133 According to Chun, plague buboes are “very painful.” His description of how patients keep arms or legs out from the trunk of the body in order to avoid pain by movement justifies my translation in plural, “pangs” of pain, since it means that patients will experience strong pain every time a limb associated with a bubo is moved, as will inevitably occasionally occur. The characteristic position of limbs associated with buboes would easily be noted also by medieval contemporaries and induce questions as to the reason. (3) De Langen and Lichtenstein 1936: The buboes are usually visible on the second or third day and are as a rule very painful. If the patient is lying down, we can often see from a distance whether there is a bubo or not, and where, because of the typical but unusual position (according to the place of the bubo) of the arm, head or leg, which is so held as to give the least pain. […] it is usually most painful as long as it is small and hard and the expressive movements of the patient during examination betray his fear that the bubo will be touched […]. The pain of the bubo is greatest during the first days when it is still small.134

Thus, these two Dutch scholars with their background in the plague epidemics in Indonesia entirely agree with Simpson and Chun who draw on research in India and China respectively. Again the point is made that repeated intense pain of buboes is caused by movement of associated limb or by touch, which justifies my use of the plural form “pangs” (of pain). 133 134

Chun 1936: 316. De Langen and Lichtenstein 1936: 192–3.

544

chapter thirteen

(4) Hirst 1953: The size of the bubo varies from that of an almond to an orange, and, until it begins to discharge, may give agonizing pain.135

Thus Hirst, with his enormous experience with cases of bubonic plague, gives a description of buboes that justifies the description “pangs of pain” in the plural form, since Hirst clearly has not in mind the single sharp sting as that of a wasp or gadfly but continuous agonizing pain. De Langen and Lichtenstein and Hirst, who do not mention pain associated with pneumonic plague, presumably because they considered this clinical feature insignificant, both emphasize that buboes are continuously very painful or agonizingly painful which they consider a significant clinical point. (5) Pollitzer 1954: As is unanimously stated in the literature and has been borne out by the fairly ample field observations made by the present writer, manifestations on the part of the primarily-affected lymph-nodes appear, as a rule, quite early in the disease, simultaneously with or even before, the onset of fever […]. Even when seen within the first hours of illness, as a rule the patients already complain of discomfort or even of some pain at the site of the future buboes. The subjective sensations produced in the patients by the presence of plague buboes may vary considerably, some complaining of constant dull or even stabbing pains, others feeling little or no local discomfort as long as they do not move and keep in a position which lessens pressure on the affected parts of the body. Patients with a groin bubo keep for this purpose the corresponding thigh flexed, those with axillary buboes lie on their back and hold the affected arm away from the trunk, and those with cervical buboes hold their head still and inclined to the affected side. Generally speaking, pain is more marked in the case of smaller buboes than in that of larger ones […] during the acute stage of the disease the buboes are invariably sensitive to touch, often to such a marked degree that even comatose patients react when the affected lymph-nodes are touched. This marked tenderness to touch, which as a rule, appears in the earliest stage of illness […] forms one of the most outstanding clinical features of bubonic plague.136

Pollitzer uses the plural form “stabbing pains,” which puts in perspective Karlsson’s offensive accusation. Also Pollitzer describes 135 136

Hirst 1953: 29. Pollitzer 19954: 421–2.

gunnar karlsson’s alternative theory

545

buboes as intensely painful, and says that as a result patients keep limbs associated with buboes out from the trunk of the body in order to avoid as much as possible pain from movement, and he also makes the same comment as Simpson to the effect that the pain is so intense that patients in coma will react when their lymph-nodes are touched. Again my use of the plural for “pangs [of pain]” is justified. (6) Cantey 1974: Thirteen [Vietnamese] patients were hospitalized with bubonic plague […] The [lymph] nodes were exquisitely tender to palpation […].137

This refers to studies of Vietnamese patients during the Vietnam War, when the last large-scale epidemics of plague (with as many as 10,000 deaths a year138) gave American physicians the last opportunity up to now of studying great numbers of patients. Butler also has his personal experience from this context. (7) Butler 1983: Patients are typically affected by sudden onset of fever, chills, weakness, and headache. Usually, at the same time, after hours, or on the next day, patients notice the bubo, which is signaled by intense pain in one anatomic region of lymph nodes, usually the groin, axilla, or neck. A swelling evolves in this area that is so tender that the patients typically avoid any motion that would provoke tenderness of the affected lymph nodes. For example, if the bubo is in a femoral area, the patients will characteristically flex, abduct, and externally rotate the hip to relieve pressure on the area and will walk with a limp. When the bubo is in an axilla, the patients will abduct the shoulder or hold the arm in a splint. When a bubo is cervical in location, patients will tilt heir heads to the opposite side. This extreme tenderness of the buboes naturally causes patients to resist physicians’ attempts to palpate and aspirate their buboes […]. Palpation will typically elicit extreme tenderness.139

(8) Butler 1993: At about the same time [the onset of disease], patients notice the bubo, which is accompanied by intense pain in the affected lymphatic region […]. Palpation typically elicits extreme tenderness.140 137 138 139 140

Cantey 1974: 281. Butler 1993: 887. Butler 1983: 73, 75. Butler 1993: 884, 885.

546

chapter thirteen

This complete collection of evidence taken from all leading standard works on bubonic plague demonstrate that relevant statements on the extraordinary painfulness and tenderness of buboes can be readily found in the scholarly literature on plague. This material has been published over a period of eighty years, covering the whole period of scientific studies of plague, and given by authors who have great personal experience with cases of bubonic plague and great knowledge of the scholarly plague literature available at the time, has great evidential force in the matter under discussion. It is highly significant that they exhibit very similar clinical descriptions of the intense pain associated with buboes: it is great, agonizing, sharp, stabbing, will occur repeatedly with the movement of the associated limb or neck, and is so intense that even comatose patients wince and moan at the touch of the bubo. This intense pain is considered to form “one of the most outstanding clinical features of bubonic plague,” which can be taken to mean a defining clinical feature of bubonic plague. Only bubonic plague is characterized by the usual clinical manifestation of buboes which are also intensely or excruciatingly painful, and characterized by sharp “stabbing pains.” In my thesis I also refer to more recent primary studies on bubonic plague, citing the scholars’ descriptions of buboes as “painful and exquisitely tender” or characterized by “extreme tenderness.”141 This presentation of the subject is therefore complete and updated. Thus, all the prominent authors of the standard works on plague who also have great personal experience with plague patients emphasize that plague buboes are characterized by intense, piercing, stabbing and agonizing pain and that this feature is readily observable and can readily be clinically characterized as repeated sharp pangs of pain. This justifies my translation of the element in the Icelandic annals’ clinical description of the Black Death in Bergen referring to intense pain, “hordum stinga” as “sharp pangs of pain.” It corroborates also my understanding of it as referring to the characteristic sharp, stabbing, agonizing pain of plague buboes and, consequently, that this is a strong indication that the Black Death in Bergen in 1349 was bubonic plague.

141 See, for instance, Reed, Palmer, Williams et al. 1970: 479; Welty, Grabman, Kompare et al. 1985: 641–3; Owens 1990: 155.

gunnar karlsson’s alternative theory

547

If the Icelandic scholars Steffensen or Karlsson, who reject this understanding of the Lawman’s Annal’s clinical description of the Black Death in Bergen (see Appendix 2) had, according to conventional standards of methodology and scholarly work, consulted any of the standard works on plague, they would readily have ascertained the central facts of this topic. Instead, their will to ignore all the medical standard works on plague constituted the basis of offensive accusations against my view which is squarely based on the scholarly studies and standard works of plague. The authors of the standard works on plague consider the intense pain of plague buboes to be a predominant clinical feature of bubonic plague, so conspicuously characteristic that it in itself provides a strong indication of bubonic plague to observers. It should be easily observable also to persons without scholarly training and should be expected to be mentioned by medieval chroniclers when they choose to mention the Black Death and give some clinical detail, including the informants of the Icelandic annals. In fact, there is a surprising number of contemporary descriptions of the extraordinary painfulness of plague buboes. It must again be underlined that historical accounts must be seen in historical and source-critical perspectives. They are normally given by chroniclers without real scientific education and with rather confused ideas about disease, generally prone to accept notions of other-worldly intervention or misleading miasmatic notions and to express their views with great rhetorical exaggeration. As in the case of the Icelandic annals, ecclesiastics would often avoid specification of anatomical sites of buboes with sexual connotations like the groin.142 There are quite frequent contradictions, misunderstandings and other indications in the texts of contemporaries, including those who are most often cited, which show that they have quite likely not observed persons suffering from or having died from plague. Certainly, there is no indication that any of them have performed anything like a medical examination of plague victims. The usual impression is that they render more or less generalized second-hand or third-hand descriptions or accounts, rumours or hearsay. This explains why blood spitting is mentioned probably as often as buboes and that buboes also can be indicated only indirectly by reference to the intense or excruciating pain associated

142

See for instance Benedictow 2004: 192–4.

548

chapter thirteen

with them (see below). This is the case, for instance, with the Icelandic annals’ descriptions. The Franciscan friar Michael of Piazza’s (Michele da Piazza) account of the Black Death’s arrival and spread in Sicily is one of the most frequently cited, but features calling for source-criticism are generally overlooked. The central clinical features of the disease as it appeared in Catania, according to Friar Michael are that there developed gland boils on the sexual organs, the thighs, the arms, or on the neck. At first they were of the size of a hazel nut […]. Soon the boils grew to the size of a walnut, then to that of a hen’s egg or a goose’s egg, and they were exceedingly painful, and irritated the body, causing the sufferer to vomit blood […]. The sickness lasted three days, and on the fourth, at the latest, the patient succumbed.143

As can be readily seen, Friar Michael or rather his informants emphasize the sharp penetrating pain, the formation of “boils” or “gland boils” (= buboes) in the ordinary places for plague buboes, the ordinary size of plague buboes in various phases of development, the “vomiting” of blood, and the ordinary duration of the course of bubonic plague disease, that is three to five days.144 These pieces of clinical information, together with the additional terrified statements of extremely high mortality, constitute a very strong case for identifying the disease that spread in Messina and Sicily with bubonic plague. Sticker cites Gabriel de Mussis’s account of the clinical features of the Black Death in Piacenza in northern Italy. In accordance with modern standard works on bubonic plague, de Mussis starts by stating that completely sound persons suddenly were hit by piercing pains. Next, they were overwhelmed by great frost that made them shiver with fever and they felt stinging spikes, as if they were pierced by arrowheads. Some were cruelly hit under the clavicle [a phrase that probably means “in the armpits:” my insertion], others where the belly and thigh meet [a euphemism for the groin or nearby femoral area]. Here grew a smaller or larger lump and, then, soon fulminant fever with head pains […]. Many died on the first day of illness or on the second, most on the third or fifth day. The spitting of blood was always deadly […]. Those who had hardened glands died unless they did not turn soft […].145

143

Cited after Nohl 1961: 7–8. In secondary septicaemic cases, it will take a couple of days before the condition with bloody expectoration develops; a duration of this phase of three days indicates an ordinary duration of the whole course of this type of illness of five days. 145 Sticker 1908. 52–3. My translation from German. 144

gunnar karlsson’s alternative theory

549

De Mussis’s use of the plural forms “piercing pains, “stinging spikes,” “pierced by arrowheads” is interesting. De Mussis provides much the same clinical information as Michael of Piazza regarding the sudden onset of disease, the piercing pains associated with buboes in the armpits and the groin, fulminant fever, the severe headache, that secondary pneumonic plague accompanied by blood spitting which was always deadly, which conforms with modern observations, and information on the duration of illness that fits the modern standard works on bubonic plague perfectly. In his excellent monograph on the Great Plague in London in 1665, W.G. Bell provides a succinct summary of the clinical features mentioned by contemporaries, inter alia: “the rising of plague buboes was attended by such severe pain, and a feeling as of intolerable burning as the time for suppuration approached that the sufferers often became raving mad.” Other usual features were that people became comatose,146 which accords with the descriptions given in modern standard works on plague cited above.147 This analysis can be completed by citing the impressive protoscientific presentation of the plague epidemic in the Swedish city of Norrköping in 1710–1 given by the local physician M.G. Block who for his time was well educated and certainly had a clear and observant mind. Over three pages, he gives a detailed clinical description of bubonic plague, and towards the end of his book he provides numerous detailed case histories. This comprehensive proto-scientific clinical information conforms closely to the sections on clinical features given in modern textbooks on bubonic plague, and it is much more detailed than that given by late medieval chroniclers or physicians but also provides information which is similar to that given by late medieval informants. He mentions the headache, shivering and strong fever, and a number of other physical manifestations of the disease, but underscores that some features are more important than others, among them: That it pricks like needles everywhere in the glands and particularly under the shoulders and in the groin. Swellings in those places, swellings that eventually, though quite slowly mature into buboes […].148

146 147 148

Bell 1951: 127. Bell 1951: 125. Block 1711: 21. My translation from Swedish.

550

chapter thirteen

The plural form should also be noted. Thus, also in connection with the last wave of epidemics in Scandinavia (only Sweden and Denmark) the same clinical information is met with again, this time as systematically and acutely observed by a dedicated proto-scientific physician. Summary and Conclusion (1) It has been documented that modern studies of plague emphasize that primary pneumonic plague is normally associated with little pain and is not characterized by pleurisy or pleuritic pain. This proves that Steffensen’s understanding of the term “hordum stinga” as reflecting pleuritic pain associated with primary pneumonic plague is erroneous and arbitrary. It also proves that his addition of the word “pleuritic” in his translation of this term, “great pleuritic pain,” is unjustified and misleading. (2) It has been demonstrated that, according to the corpus of scholarly studies of plague, bubonic plague is consistently associated with intensely painful buboes, and that movements of an associated limb or the neck or touch will cause sharp pangs of pain. This justifies and vindicates my translation of “hordum stinga” with “great pangs of pain” and the use of plural form. Plural form is used also by authors of standard works on plague. This means that it is justified to associate the Annal’s clinical description of plague cases as characterized by sharp pangs of pain with the characteristic sharp pangs of pain of plague buboes and take this as a strong indication that the Black Death in Bergen was bubonic plague. Karlsson’s accusations are unfounded. (3) In addition it has been shown that contemporary chronicle(r)s emphasize the intense or excruciating painfulness of buboes, which are characterized by piercing, sharp, stabbing pains, which justifies my translation of the intense stabbing painfulness associated with plague cases in Bergen in 1349 in the plural form and its association with buboes. (4) It has been shown that the Icelandic annals’ clinical description of plague cases as associated with “vomiting” of blood conforms to contemporary and modern medical descriptions of bubonic plague cases with secondary pneumonia.149 149

See also above: 7–8; below: 491–3.

gunnar karlsson’s alternative theory

551

(5) No evidence supports the notion that the epidemics in Iceland 1402–4 or 1494–5 spread in the primary pneumonic modality. On several independent grounds it can be ascertained that these epidemics were not caused by plague in any form. There never was a plague epidemic in Iceland. The clear outcome of this discussion constitutes an important element in the process of identifying the epidemic disease that ravaged Bergen and Norway in 1349. Next, the other clinical elements of diagnostic value provided by the Icelandic annals must be considered in the light of modern knowledge of bubonic plague in order to ascertain whether or not they conform to the clinical manifestations of this epidemic disease. Clinical descriptive elements of diagnostic value are provided in the independent contemporary Icelandic fragment of the Annal of Skálholt.150 The disease was such that men lived for three days with sharp pangs of pain, then they began to vomit blood and next they expired.151

As can be readily be seen, this clinical description is so closely related to that given in the Lawman’s Annal that it could come from the same informant but deviates on one point of importance: (1) Both annals testify that the sharp (pangs of) pain set in from the beginning of the outbreak of the disease in humans. As copiously documented above, this is characteristic of the pain of plague buboes that starts before or at the beginning of the formation of buboes. Thus, this feature also supports the case that the onset of intense sharp or piercing pain reflects the onset of bubonic plague disease and heralds the development of one or more buboes. The point can be illustrated with a Norwegian case history associated with a plague epidemic in the region of Hardanger in 1600. A young girl who was soon to be married returned one evening from the cowshed; suddenly she let down her buckets and said: “Now the plague stung me,” and the next day she was dead.152

150 Islandske Annaler 1888: XVIII–XX; Benediktsson 1970: 390–1: “it is quite independent, even though some similarities with other annal redactions occur. It is an important primary source for the period it covers” [namely 1328–72]. 151 Islandske Annaler 1888: 224. Cf. above: 536, fn. 116. My translation from Icelandic Norse. 152 Benedictow 2002: 238. My translation from Norwegian.

552

chapter thirteen

(2) The duration of the course of illness accords fully with modern medical descriptions of the development of bubonic plague in victims who also develop secondary pneumonic plague, which is normal, occurring in about a quarter of all plague cases. The bubonic phase lasts three days before the development of secondary pneumonia manifests itself with the onset of bloody expectoration, and then the patient (almost) invariably dies. (3) Jón Steffensen’s rejection of Shrewsbury’s assertion that “primary pneumonic plague cannot develop independent epidemics to any degree” is not supported by documentation from the scholarly literature on primary pneumonic plague, and must therefore be considered arbitrary and untenable. Shrewsbury’s view stands vindicated. The evidence supports unconditionally and without exception a conclusion to the effect that the Black Death in Bergen and Norway more generally was bubonic plague.

CHAPTER FOURTEEN

TWIGG’S ALTERNATIVE THEORY Introduction Twigg is the central scholar in the brief modern history of alternative theories of the microbiological identity of historical plague epidemics. In his monograph of 1984, he was the first scholar to reject any role for the plague pathogen of Yersinia pestis, whether disseminated by rats and fleas or by droplets, and who introduces a microbiological alternative. In order to clear the way for their own alternatives, the subsequent advocates of alternative theories to a very large extent base their rejections of any role for Yersinia pestis on Twigg’s arguments. Thus, Twigg’s arguments for complete rejection of the Yersinia pestis theory of historical plague epidemics must be central in the critical discussion of the alternative theories in this monograph. Several of his main arguments have been thoroughly discussed above and shown to be untenable, namely the arguments relating to the presence and role of rats, the comparative implications of the mortality rates in the Indian plague epidemics of the late nineteenth and early twentieth centuries, and his confusing discussion of metastatic spread of bubonic plague, which at least implies the denial of the importance of this phenomenon in the epidemiology of bubonic plague. The time has come to consider his microbiological theory and his historical line of arguments, the main arguments which have so far not been the subject of intensive discussion. Twigg is the first advocate of an alternative theory of historical plague epidemics who has chosen not to fulfil one of the central requirements for scholarly work, namely that of systematically providing footnotes for all facts and for all data or ideas from the works of other scholars in the text. This contrasts unfavourably with the three monographs he has used most for his account of the Black Death, namely F.A. Gasquet’s of 1908, P. Ziegler’s of 1969, and Shrewsbury’s of 1971, which contain 375, 532, 466, footnotes respectively; Shrewsbury’s monograph contains in all 3290 footnotes for the whole plague history of the British Isles until 1666. All three scholars conscientiously fulfil the scholarly requirement of systematic and complete testability, the difference in the number of

554

chapter fourteen

footnotes between these three works reflecting differences in size and scope and the significant number of relevant studies which had appeared in the sixty years that divide them, and also Ziegler’s longish introduction on the Black Death in Europe until the landing in England. In all, Twigg’s monograph contains just twenty-one footnotes, but he mainly provides indications of author and work in the running text, and for each chapter a list of bibliographical references of works purportedly used in writing it, without indication of the relevant pages. In addition, at the end of the monograph comes a brief curious list called “Major Works on Plague and Disease,” and an even briefer and more peculiar list called “Secondary Works Not Mentioned in Text,” which reflect the fact that he has refrained from providing more than episodic footnotes or references. Certainly, this is at variance with a basic necessary condition or requirement for producing scholarly work, namely to assure ready testability. It is not practicable to read the whole length of a number of the large monographs and papers mentioned in the text or in the bibliographical list associated with a chapter in order to check or test the numerous points in his text which occasion disbelief or surprise. When Twigg refers to, for instance, “Wu Lien-Teh et al. (1936),” this is a standard work of 530 pages; “Sticker (1908)” is over 500 pages; “Hirst (1953)” comprises 467 pages; “Pollitzer (1954)” contains almost 700 pages, and so on. I have repeatedly given up trying to identify references that I consider desirable to check. Twigg mentions, for instance, that Simpson (1905) states that the “Great Plague of London took six months to travel from St Giles’ to Stepney,” but since neither St Giles nor Stepney is mentioned in the Index, even under London, I had to give up identifying the reference, but luckily eventually found it by chance while looking for something else. It is useful to compare Twigg’s assertions with the texts of his references for critical examination. Although I have the great advantage of having over many years endeavoured to read all relevant medical, historical and demographic studies on plague, I must throw in the towel and admit that Twigg’s monograph is not really testable for me, at least not within the boundaries of reasonably hard work. Unfortunately, the same practice has been picked up by Scott and Duncan, his close scholarly friends and associates and producers of another alternative theory of the nature of historical plague which is based on his arguments for rejecting the bubonic-plague theory (see below).1 1

Scott and Duncan 2001: xiii; Scott and Duncan 2004: viii.

twigg’s alternative theory

555

The Alternative Theory of Anthrax Twigg’s theory is that the plague epidemics of the past were caused by anthrax.2 His alternative theory is a known disease with known properties that lends itself to scientific discussion and for this precise reason can be easily rejected, and to my knowledge has been generally rejected. Twigg’s anthrax theory contains three central assumptions: (1) that anthrax can cause sufficient levels of mortality to have explanatory potential for the demographic effects of the Black Death; (2) that the Black Death’s pattern of spread can be correlated with the spread of epizootics which can be shown with reasonable probability to be caused by anthrax; (3) that the clinical descriptions of human plague cases are similar to human anthrax and not bubonic plague. Twigg comments on the decisive question of human mortality twice, both times basing his argument on arbitrary assertions and assumptions,3 for instance (my enumeration): It [anthrax] is, though, [1] probably equally fatal to man [as to cattle and sheep] and this, coupled with its [2] symptoms and its [3] high mortality rates, means that [4] it must be a prime contender for the alternative position [as the cause of plague/Black Death]. Furthermore it needs no vectors, [5] the spores being the agent of infection and [6] easily carried in the air or on skins, furs and wool and it is for this reason that anthrax has been known as “wool sorters disease.”4

As can readily be seen, this crucial passage is completely unsupported by footnotes or references to demographic and medical evidence or scholarly literature. It is, of course, true that anthrax is spread by spores, as stated in point 5; however, it is also true that anthrax is mainly spread to human beings in the form of anthrax bacteria, especially in the case of people who have ingested contaminated meat, and it is also true that this is by far the most common way human beings contract anthrax (see below). Twigg is attempting here to strengthen his case by making an implicit case for the importance of cross-infection which is erroneous and may be one of the reasons for the absence of supporting

2 3 4

Twigg 1983: 211–22. Twigg 1984: 214, 217. Twigg 1984: 217.

556

chapter fourteen

footnotes or references. As stated by Brachman: “Human-to-human or insect transmission has not been proven.”5 As a basis for discussion of this alternative theory, a brief summary will be given of recent medical discussions of anthrax in relation to human beings.6 Anthrax is “primarily a disease of sheep, cattle, horses, and many other animals; humans are affected only rarely.”7 There are three forms of anthrax: (1) gastrointestinal tract anthrax, (2) pulmonary or inhalational anthrax, and (3) cutaneous anthrax. Gastrointestinal tract anthrax is the only form of anthrax that can take on an epidemic character, as the other two forms occur only individually or endemically, that is episodically or incidentally and dispersedly. Gastrointestinal tract anthrax “usually follows the consumption of raw or undercooked contaminated meat.”8 Importantly, this epidemic form of anthrax is quite rare. The main reason for this is that human beings do not graze: “In animals the portal of entry is the mouth and intestinal tract by the ingestion of spores on vegetation.” “While animals often acquire anthrax through ingestion of spores and spread of organisms from the intestinal tract, this is exceedingly rare in humans. Thus, abdominal pain, vomiting, and bloody diarrhoea are rare clinical signs.”9 In other words, whilst animals ingest anthrax spores, human beings usually ingest anthrax bacteria with meat. For obvious methodological reasons, it is not permitted to infer that mortality rates among human beings and farm animals from ingestion of anthrax contagion are the same; it must be formed as a hypothesis that can be tested and confirmed by corroborative evidence, if possible, which Twigg does not do. However, according to Manson’s Tropical Diseases, gastrointestinal tract anthrax commonly occurs in epidemics when cattle which have died from anthrax in heavily infected areas are eaten by large numbers of people. Such epidemics are apparently associated with parts of Africa. This is explained by the mass consumption of “raw or

5

Brachman 1990: 880. This discussion of anthrax is based on the following works: Jawetz, Melnick, Adelberg 1982: 207–8; Manson’s Tropical Diseases 1982: 393; Brachman 1980: 83–93; Sternbach 2003: 463–7; WHO, Media centre, Fact sheet no. 264, October 2001: 1–2. www.who.int/inf-fs/en; Centers of Disease Control, www.cdc.gov./ncidod, FAQ’s – Medical Facts About Anthrax 1–2. 7 Jawetz, Melnick, Adelberg 1982: 207. 8 www.cdc.gov./ncidod FAQ’s – Medical Facts About Anthrax 1–2. 9 Jawetz, Melnick, Adelberg 1982: 208. 6

twigg’s alternative theory

557

undercooked contaminated meat,” especially among pastoral nomads who suddenly are confronted with mass death of their cattle and wish to use as much as possible of these animals as food before the meat spoils. Importantly, this book provides data on lethality rates (= case fatality rates). According to this standard medical work, “The mortality rate is low and the great majority recover in a few days.”10 This conclusion of low mortality among human beings from gastrointestinal tract anthrax, the only form of anthrax that can take on an epidemic form, is incompatible with Twigg’s assertion of population mortality or level of lethality for past plague epidemics. It can, therefore, serve as evidence of why he does not support his assertion on this point by evidence readily obtainable in the scholarly literature. Both cutaneous and pulmonary anthrax are strongly associated with individual occupational exposure to contaminated hides or wool, while the pulmonary form is often called “woolsorter’s disease,” as also mentioned by Twigg (see above). However, pulmonary anthrax, which is caused by inhalation of contagion into the lungs, occurs only rarely,11 which contrasts sharply with Twigg’s undocumented assertion above of easy dissemination by cross-infection and considerable numbers of cases. Pulmonary anthrax is characterized by high mortality, however, high mortality among a tiny incidence of cases among woolsorters entails negligible population mortality. The cutaneous form of anthrax, caused by the entry of contagion through a cut or an abrasion in the skin (cutis), accounts for 95 per cent or more of human cases globally. When Twigg argues that (the English) Galfrid le Baker’s mention of a highly mortal form of plague “characterized by small black pustules on the skin” refers to cutaneous anthrax, he implies arbitrarily that it was usual or normal at the time that persons had numerous abrasions and cuts which were contaminated by anthrax contagion. Why does he not consider the possibility that this description refers to bubonic-plague pustules, a feature also mentioned by the often cited Irish chronicler John Clyn? This is a clinical feature that will be discussed comprehensively below.12 Twigg again ignores the question of mortality, however, this is not unknown: the lethality (case fatality) rate of untreated cases of cutaneous anthrax

10 11 12

Manson’s Tropical Diseases 1982: 393. Jawetz, Melnick, Adelberg 1982: 207. On plague pustules, see above: 364, 368–78.

558

chapter fourteen

is about 20 per cent.13 In contrast, the lethality rate of bubonic plague is 80 per cent.14 Importantly: “There are no documented cases of person to person transmission”15 of anthrax. Anthrax has only one genuinely epidemic form, namely gastrointestinal tract anthrax. Thus there are several independent sufficient conditions for rejecting the anthrax theory on epidemiological and medical grounds alone. To my knowledge, historical sources do not provide believable descriptions of any epidemic of gastrointestinal tract anthrax among human beings, which is the only form that possibly could take on an epidemic character. This corresponds to the concluding statement on mechanisms of spread in the standard work on microbiology by Jawetz, Melnick and Adelberg: “Contact with infected animals or with their hides, hair, and bristles is the source of infection in humans.” Thus, in an historical perspective, sources of incidence of the disease would only include tanners’ risk of contracting this disease from work with hides and possibly the risk to people from wearing clothing made from contaminated hides, which will occasion episodic cases of cutaneous antrax, and the sporadic individual incidence of “woolsorters’ disease” in export centres of wool like London, or in the proto-industrial centres of wool cloth production like Florence, Ghent, and so on. Taking into account the lethality rate of 20 per cent associated with untreated cases of cutaneous anthrax, one seems justified in losing interest in mortality rates in possible historical cases of anthrax among human beings in the present context. The enormous mortality caused by the Black Death and the dramatic population decline it caused are incompatible with the incidence and mortality of human anthrax. One of the most conspicuous features of Twigg’s monograph is his efforts to play down the level of mortality caused by the Black Death (see below) and to play up the level of mortality causable by anthrax. He does not discuss in a serious way the relative rarity of this disease among human beings and the fact that the vast majority of anthrax cases have the cutaneous form with a relatively moderate lethality level. He makes no attempt to adduce an evidential platform that would allow

13

www.cdc.gov./ncidod FAQ’s – Medical Facts About Anthrax 1. I believe all useful data on lethality rates in historical bubonic plague epidemics still can be found in Benedictow 1993/1996: 146–9. 15 WHO, Media centre, Fact sheet no. 264, October 2001: 1. www.who.int/inf-fs/ en,fact. 14

twigg’s alternative theory

559

him to argue that the rare type of epidemic gastrointestinal anthrax ever caused large human population mortality rates at a regional or national level in medieval Europe and continued to ravage Europe for 300 years. Instead, Twigg makes the following three misleading assertions which will be commented on in the order 2, 3, 1: [1] the introduction of antibiotics has reduced the death rate from cutaneous anthrax to a very low level but [2] visceral anthrax is little affected by antibiotic treatment and [3] the death rate may be as high as 90 per cent.16

(2) Twigg’s assertion that the mortality rate of “visceral anthrax,” a curiously expanded term that presumably corresponds closely to the concept of gastrointestinal tract anthrax, “may be as high as 90 per cent” is not supported by reference(s) to scholarly work(s) in the text or an accompanying footnote, it must be rejected as arbitrary. His assertion on this important point is incompatible with the level of normal lethality given in Manson’s Tropical Diseases (cited above), namely that the “mortality rate is low and the great majority recover in a few days.” (3) According to standard works on microbiology, antibiotics are effective against gastrointestinal tract anthrax,17 thus Twigg’s undocumented assertion to the contrary is disappointing. (1) When Twigg states that antibiotics have today reduced the lethality (case fatality) rate of cutaneous anthrax to a very low level without informing his readers about the normal mortality rate of untreated and unmedicated cases, he leaves his readers with the impression of a very high normal lethality rate in cases of cutaneous anthrax in the past. However, although a lethality rate of about 20 per cent in untreated cases of cutaneous anthrax is moderately high, it compares unimpressively with bubonic plague’s normal lethality rate of around 80 per cent.18 Certainly much can be said about contemporary chroniclers’ clinical descriptions of the Black Death, but they never mention as symptoms of the disease the “abdominal pain, vomiting, and bloody diarrhoea” that characterize gastrointestinal tract anthrax. Thus, Twigg’s anthrax theory has no significant historical foundation. It is medically and epidemiologically untenable and cannot

16 17 18

Twigg 1984: 214. Jawetz, Melnick, Adelberg 1982: 206. Benedictow 1993/1996: 146–9.

560

chapter fourteen

explain the mortality rates caused by the Black Death—something that Shrewsbury’s theory also fails to do. The Historical Basis: The Use of Obsolete and Peripheral Studies A curious feature of Twigg’s monograph is his predilection for obsolete works based on miasmatic and astrological theories of epidemic disease. This is particularly the case in the final and crucial Chapter 11 where he summarizes his evidence and argues the case for his anthrax theory: “Clinical symptoms in the Black Death and in some other diseases. The case for anthrax” (pages 200–22). In this chapter, J.F.K. Hecker’s (1795–1850) monograph on The Epidemics of the Middle Ages which was first translated into English in 1837 and reprinted in 1844 and posthumously in 1859, is referred to eleven times (and repeatedly elsewhere).19 Hecker is also referred to indirectly through Twigg’s use of Gasquet’s references to Hecker’s work, for example on the clinical features of the Black Death.20 Hecker is even cited on an important point of the Black Death’s epidemiology in England, although Creighton has made it clear that Hecker’s superficial and deficient knowledge on the Black Death in England is taken from J. Barnes’s monograph the History of Edward III of 1688.21 Creighton refers disparagingly also to Hecker’s “a priori habit of mind” for making assertions of fact without support from sources.22 It would be surprising if Twigg has not noticed these relevant comments, since the main work of Creighton, the last champion in England of the miasmatic theory of epidemic causation, predictably is frequently cited in support of his argument, for example three times in Chapter 11. The skilful ecclesiastic amateur historian F.A. Gasquet (Abbot President of the English Benedictines) and his pioneering work on the Black Death in England is referred to ten times in Chapter 11. This work was originally prepared in the 1880s23 and first published in 1893; the edition of 1908 used here by me and by Twigg is a reprint “with one

19

Twigg 1984: 204–7, 211. See also pages 46–7, 60–1. Twigg 1984: 202–3. See Gasquet 1908: 8–9. 21 Creighton 1891: 144, fn. 1. Here Creighton refers to the English translation of 1837 of Hecker’s work on the Black Death of 1832, but Hecker had not improved his knowledge of the Black Death in England between 1832 and 1837. 22 Creighton 1891: 144, fn. 1, 200. 23 Gasquet 1908: xxi. 20

twigg’s alternative theory

561

or two minor corrections, and a few additions.” The text of Gasquet’s monograph represents pre-scientific miasmatic notions of the cause of epidemic disease, and all medical and historical works he refers to represent this miasmatic view and pre-scientific epidemiology and medicine more generally. In addition R. Mead’s view on the clinical symptoms of plague published in 1720 is taken seriously by Twigg;24 although Mead was born in 1673, he had never seen a case of plague in his life. This does not end the list of miasmatic and obsolete works Twigg refers to in chapter 11, which include W. Wood’s monograph of 1842/1865, H. Harrod’s paper of 1867, and so on. Within this framework which mainly is of interest and relevance for the history of medicine, a number of contemporary chroniclers are cited and referred to on the clinical features of the Black Death without any attempt at explaining their social, cultural or medical framework. Source-criticism is not mentioned or applied. Without the sourcecritical training of medieval historians, Twigg inevitably becomes a victim of what Hatcher calls “the overwrought imaginings and hopelessly inaccurate quantification of the chroniclers.”25 There will be occasion below to address this point more specifically. Twigg, who apparently neither likes source-criticism nor medieval demography, inevitably subjects himself to this process of scholarly victimization at the hands of medieval chroniclers whose assorted utterances of “overwrought imaginings and hopelessly inaccurate quantification” are, thus, passed on and given a new lease of life long after most of them should have been laid gracefully to rest. In his discussion of the last plague epidemic in the village of Eyam in Derbyshire in 1665–6, Twigg relies on W. Wood’s monograph first published in 1842 and also for one point of importance on the ninth reprint of 1744 of Mead’s monograph.26 L. Bradley’s fine modern familyreconstitution-based demographic study of 1977 on the epidemic at Eyam27 is mentioned only indirectly in a comment to the effect that

24 Twigg 1984: 214–5. Another of Twigg’s pervasive inaccuracies crops up here: the title of the work cited in the references on page 245 under Mead’s name was not written by him but rather by Joseph Browne (whose book was also published 1720). Browne, like Mead, had never seen a plague case in his life, so the comments are irrelevant in both cases. 25 Hatcher 1977: 21. 26 Twigg 1984: 192–5. 27 Bradley 1977a: 63–94.

562

chapter fourteen

Bradley disagrees with Wood’s analysis, without indicating why, which might have revealed very good reasons. However, it shows that Twigg knows Bradley’s fine demographic study, but like Cohn and Scott and Duncan, does not take its findings into account. Shrewsbury’s useful 1971 demographic discussion of the same material28 is passed by in silence. Bradley and Shrewsbury agree on the basis of modern medical, epidemiological and demographic analysis that the epidemic at Eyam was indeed bubonic plague.29 Twigg’s monograph abounds in such examples. His prolific use of obsolete pre-scientific studies is obviously contrary to central tenets of scholarly work and unavoidably raises the question: why does Twigg to such an extent build his case on long obsolete studies, scholarly antiques based on miasmatic epidemiological theory with characteristic astrological and telluric aspects? The reason can hardly be any other than because he needs them, because in the end Twigg has to resort to miasmatic theory himself, albeit in a slightly modernized version, in the futile hope that it can save the last vestiges of credibility of his theory. In his final chapter, it becomes obvious that a theory to the effect that the European populations should have been eating the Black Death both on the Continent and in England or that herds of sheep and cattle should have been transported by galleys from Constantinople to Mediterranean ports and been driven across the Continent whilst people eagerly devoured the flesh of obviously sick, moribund or dead animals was simply untenable and impossible to take seriously. The Telluric-Miasmatic Theory of Anthrax Eventually, it becomes clear to Twigg that there had to be another very dynamic mechanism of the spread of anthrax. At this point, central aspects of the miasmatic theory of epidemiology seemingly offered him a solution. He takes as his point of departure experimental studies on the possible airborne passage of the foot-and-mouth virus under some specific meteorological conditions relating to or inspired by an outbreak of foot-and-mouth disease in livestock in 1967–8. This mechanism of spread is not mentioned in later standard works on medical microbiology, for instance, by Jawetz, Melnick and 28 29

Shrewsbury 1971: 522–9. Bradley 1977a and 1977b.

twigg’s alternative theory

563

Adelberg.30 Airborne contagion connected with specific meteorological conditions accords completely with classical Greek miasmatic theory of the causation of epidemic disease and miasmatic epidemiology’s central tenets on the dissemination of epidemic disease. Against this background, Twigg argues that the extraordinarily rapid dissemination of the Black Death suggests pulmonary anthrax moving in a similar way […] this form of the disease could very likely have been the illness which has hitherto been identified with pneumonic plague.31

These few words contain a number of fallacies of methodology and neglect of facts. Firstly, Twigg uses a hypothetical mechanism of aerial spread of foot-and-mouth disease to suggest by analogy that this could also be the case with pulmonary anthrax, which he arbitrarily compares with pneumonic plague, and goes on to build on these analogies as if they were materially established by empirical evidence. According to modern scientific methodology, analogies can only be used for construction of working hypotheses, all use of analogies for inference to fact or reality is fallacious. It is true that classical Greek scholars and physicians used analogies for evidentiary purposes in this way, in accordance with their incompletely developed scientific methodology, but that was over two thousand years ago. According to the tenets of modern scientific methodology, Twigg must first adduce good evidence showing that pulmonary anthrax can spread by air in epidemic form according to the pattern of the viral foot-and-mouth-disease and the bacterial primary pneumonic-plague disease. If he were able to do this, he would also be obliged to document that pulmonary anthrax can spread with extraordinary rapidity, faster than any other epidemic disease which is dependent on interhuman transmission, before he could single it out as a possible candidate for the epidemic disease in question. However, Twigg does not attempt to satisfy these premises or basic conditions, and his inference from rapidity of spread to pulmonary plague is, therefore, a circular type of argument based on a purely hypothetical analogy. Indeed, earlier in his monograph, in accordance with the modern scientific literature on anthrax, Twigg restricted pulmonary anthrax to the episodic and largely individual occurrence among woolsorters, which has no epidemic form. There is no spread 30 31

Jawetz, Melnick and Adelberg 1982: 395–6. Twigg 1984: 220–1.

564

chapter fourteen

rate characteristic of the Black Death that can “suggest” that it was (primary) pneumonic plague; this conclusion is literally taken out of thin air. For the same methodological reason, an analogy cannot be used to “suggest” a factual condition, since use of the term “suggest” indicates a level of tenability, albeit low. Conspicuously, Twigg transforms the level of tenability associated with the concept of “suggest” into the level of tenability of “very likely” without the mediation of evidence. Scholarly work is associated with the principle of fallibility, which dictates that on principle no scholarly statement can be absolutely true. There is always, as a matter of principle, at least a tiny element of doubt or uncertainty associated with scholarly or scientific statements. The level of tenability of “very likely” is therefore about as certain as a scholarly statement can be and is correspondingly demanding with respect to its evidential basis, presupposing a solid empirical material. In this case, Twigg has not adduced any evidence, so not only is the asserted level of tenability of “very likely” untenable, it is also methodologically invalid and can be characterized as fallacious. Twigg goes on to use term “speculate” to describe his reasoning, which in scientific methodological parlance means not based on facts, only on logical inference. Twigg apparently does not know that analogies, like definitions and concepts, cannot be used for evidential purposes or for inference to fact or reality, and consequently cannot be associated with tenability, but can only be discussed in methodological terms of usefulness as intellectual tools for analysis. He treats levels of tenability along the whole register from the very lowest level of speculation, via suggestion up to almost the highest level of very likely as if they are interchangeable and independent of evidence. Also this part of Twigg’s work is methodologically confused and comprehensively at variance with the basic tenets of (social) science. To my knowledge, Twigg is the only modern scholar who has been inspired by miasmatic epidemiological theory to a degree that he also cites telluric aspects of this theory, that is, the idea that miasmatic contagion is let out from the ground after it has been disturbed by volcanic activities, earthquakes or astrological constellations, to be spread by the wind and cause epidemics when it reaches human settlements:32

32 See Hirst’s excellent presentation of these aspects of miasmatic theory in Hirst 1953: 22–72.

twigg’s alternative theory

565

It is tempting to speculate yet further and to suggest that the sequence of earthquakes and floods in the East before the Black Death might have disturbed anthrax in the soil and the spores were then carried by air currents to the Mediterranean and Europe.33

Telluric-miasmatic explanations for outbreaks of serious epidemic disease are a clear feature of Hecker’s epidemiological thinking in his works of the 1830’s,34 which Twigg refers to eighteen times,35 and of Gasquet’s monograph, which he refers to twenty-three times.36 Seen against the background of Twigg’s prolific use of these works and other miasmatic works (see above) in support of his anthrax theory, it can be legitimately assumed that this is his source of inspiration. By accepting long-discarded explanations of a serious epidemic outbreak, in this case the principle of telluric explanation of the origin of airborne miasma for the Black Death, Twigg has crossed a crucial line between scientific and unscientific work. He goes on to state that: Anthrax is widely known in African mammals, however, and air currents bearing spores of anthrax could easily reach northern Europe, as shown by the deposition of Saharan dust in England in recent years.37

Again Twigg uses an analogy, in this case based on the relatively rare instances of air transport of Saharan sand to England, which does occur, to assert that this easily could be the case for anthrax spores, an assertion for which he offers no evidence. How can he know that airborne anthrax spores from Africa “could easily reach northern Europe” when he is unable to provide any evidence for the factual occurrence of such transport at all? In ordinary scholarly or scientific discourse, the phrase “could easily reach northern Europe” should imply substantial empirical evidence for this phenomenon, quite a lot actually, in order to be able to differentiate between the rare occurrence, the sporadic occurrence and the quite regular occurrence that alone can prove that this could easily be the case. Instead, the fact is that he has no evidence to show in support of his assertion: it is based on the implication, the methodological fallacy, that an analogy can provide or constitute empirical evidence allowing inference to fact or reality. 33 34 35 36 37

Twigg 1984: 221. Hirst 1953: 41. Twigg 1984: 46–7, 60–1, 204–7, 211. Twigg 1984: 45–7, 56–7, 60–1, 70, 103, 202–4, 207. Twigg 1984: 221.

566

chapter fourteen

The analogy is false for several reasons: (1) the assertion that sand and anthrax spores have much the same properties in relation to airborne transport requires evidentiary support, without which it is an arbitrary assertion. (2) the assertion that Saharan animals could be the source of anthrax spores that could be transported by wind to northern Europe in the same way as Saharan sand requires evidentiary support. When it is maintained without evidence that this can, in fact, occur, also this assertion takes on the character of an arbitrary argument. (3) anthrax epizootics among cattle are not uncommon in parts of Africa (see above), and it is well known that Sahara is full of sand, but cattle are not common in the sand oceans of the Sahara, and large, numerous herds of contaminated cattle are required to create significant amounts of spores. It is the parts of Africa south of the Sahara that are inhabited by more or less nomadic pastoral people with large herds moving through large areas which are at the heart of the matter, and it is the question of whether or not air currents could transport anthrax spores from these areas which is the real problem Twigg should have addressed with energy and dedication. The conclusion he would have reached can be stated: that there is no historical evidence that air currents with spores from these areas have reached the northerly parts of Europe. Twigg resorts to unscientific miasmatic-telluric theory in order to defend his theory. This can only be taken to reflect the obvious untenability of his theory and the length to which he is willing to go in order to construct a basis for it. The Pace of Spread of Plague There is another reason for Twigg’s attraction to miasmatic theory. This is the distant thunder of the works of modern scientific plague researchers with excellent medical education from Cambridge and Oxford in England as well as leading universities in France and the U.S.A. who made such tremendous progress in the scientific study of bubonic plague in India, China, Madagascar, Vietnam, and elsewhere in the twentieth century. Many of them put great emphasis on the history of plague and comparison between the old clinical and epidemiological descriptions and accounts of plague and their modern observations of

twigg’s alternative theory

567

thousands of plague patients and plague’s epidemiology. On this basis and without exception they reached the conclusion that the disease they studied and the historical plague epidemics were the same. If Twigg had wished in earnest to learn from modern scientific discussions of this topic, he could have studied the works of Simpson of 1905, Sticker of 1908 and 1910, Wu Lien-Teh of 1926, Wu Lien-Teh, J.W.H. Chun, R. Pollitzer, C.Y. Wu of 1936, Hirst of 1953, Pollitzer of 1954, and papers by other leading plague researchers like Greenwood and Liston of the IPRC, just to name the most important in this context. Twigg mentions most of them in his text, but not on central points of epidemiology or clinical features, only on points that do not bear seriously on his theory. As shown above, his assertions on the mechanisms and patterns of spread of bubonic plague are untenable and are based on highly selective references and peculiar interpretations. Simpson’s monograph, the first but necessarily “immature” modern scientific work to emerge from the studies of British physicians and epidemiologists in India, is, for instance, referred to twice. Twigg correctly points out Simpson’s view that the Black Death, in relation to earlier plague epidemics, “was distinguished by its rapid spread and destructiveness,” “Never before had it shown such diffusive qualities.”38 Twigg takes this in support of (1) his view that the Black Death could not have been bubonic plague and (2) compares it with a purported slow pace of spread in India and cites again Simpson who points out that (3) the “Great Plague of London [of 1665] took six months to travel from St Giles’ to Stepney.”39 What Twigg describes here is, of course, contiguous spread of plague by contact between rat colonies, and the example from London 1665 is similar to the observation of IPRC that “the infection in the rats took six weeks to travel 300 feet” in a section of Sion village outside Mumbai.40 This means, of course, that the plague in London 1665 and in India of the early 1900s had a very important feature in common, namely that they could spread very slowly in a contiguous way. However, given this comparison I do not understand why a structural similarity of pace of spread of bubonic plague in India

38

Simpson 1905: 23. Twigg 1984: 135. He does not identify where in Simpson’s work he has found this instance; see, however, Simpson 1905: 70. Similarly, plague took over five weeks to move from Westminster to the city parish of St Olave, Hart Street. Cox 1910: 153. 40 IPRC 1907h: 827, cf, Map IV; Lamb 1908: 19. 39

568

chapter fourteen

and the Great Plague of London does not constitute evidence that the Great Plague in London was the same disease as in India, namely bubonic plague. Twigg overlooks the fact that if his point was correct, there would not have been any Great Plague in London; only a few small patches of the great city would have been ravaged. Since Twigg has used Simpson’s monograph, another important question remains unanswered: why Twigg ignores Simpson’s information on the great importance of metastatic spread by leaps,41 for instance, that “in Canton, many persons, especially the well-to-do, removed to the country, thus forming fresh foci for its dissemination; and in the same way the outbreak in Hongkong no doubt arose from persons having migrated from Canton to Hongkong.”42 In China as well “the infection on land has followed chiefly the routes of busiest intercourse.”43 Simpson also provides much information on spread by leaps in India, for instance, in connection with the mass exodus out of Mumbai when the plague epidemic suddenly blazed up: “Fugitives from Bombay and the Bombay Presidency were not long in carrying infection to the other provinces of India.”44 Twigg also passes by in silence the conspicuous phenomenon of metastatic leaps in the Great Plague of London, as can bee seen from Bell’s fine study of it, for instance: the spread of the disease by leaps in the city and in the outparishes and liberties, establishing numerous new centres of spread in the rat colonies more or less according to a geometrical progression of incidence. Bell has no difficulty in showing that the epidemiological and clinical features of this epidemic in London correspond very closely to those of bubonic plague.45 Twigg’s obligation to ignore the typical metastatic patterns of spread of bubonic plague in clothing or luggage or goods that lent the Black Death and subsequent plague epidemics dynamic powers of spread and was also such a conspicuous feature of bubonic plague in India, reflects the fundamental weakness of his theory. It is important to recognize that the diffusive powers of the Black Death were so strong in Europe in the middle of the fourteenth century because it arrived in a territorially interconnected and integrated

41 42 43 44 45

Above: 153. Simpson 1905: 62. Simpson 1905: 65. Simpson 1905: 71. See Bell 1951.

twigg’s alternative theory

569

civilization which offered epidemic disease in general entirely new powers of spread. My brief introduction to this aspect of medieval society in a journal of popular history runs like this: The extent of the contagious power of the Black Death has been almost mystifying. The central explanation lies within characteristic features of medieval society in a dynamic phase of modernization heralding the transformation from a medieval to Early Modern European society. Early industrial, market-economic and capitalistic developments had advanced more than is often assumed, especially in northern Italy and Flanders. New, larger types of ships carried great quantities of goods over extensive trade networks that linked Venice and Genoa with Constantinople and the Crimea, Alexandria and Tunis, London and Bruges. In London and Bruges the Italian trading system was linked to the busy shipping lines of the German Hanseatic League in the Nordic countries and the Baltic area, with large broad-bellied ships called cogs. This system for long-distance trade was supplemented by a web of lively short and mediumdistance trade that bound together populations all over the Old World. The strong increase in population in Europe in the High Middle Ages (1050–1300) meant that the prevailing agricultural technology was inadequate for further expansion. To accommodate the growth, forests were cleared and mountain villages settled wherever it was possible for people to eke out a living. People had to opt for a more one-sided husbandry, particularly in animals, to create a surplus that could be traded for staples such as salt and iron, grain or flour. These settlements operated within a busy trading network running from coasts to mountain villages. And with tradesmen and goods, contagious diseases reached even the most remote and isolated hamlets. In this early phase of modernization, Europe was also on the way to “the golden age of bacteria” when there was a great increase in epidemic diseases caused by strong increase in population density and in trade and transport while knowledge of the nature of epidemics, and therefore countermeasures to them, was still minimal.46

The point is that epidemiology is a subdiscipline of sociology in that it focuses on the study of the effects of social interaction, and that the powers of spread of epidemic diseases vary greatly with different types of social formations and must be seen within a societal framework of analysis. The powers of spread of the Black Death in the form of bubonic plague were much stronger than before because it reached a European society that offered new mechanisms and much stronger opportunities for dynamic spread, as was the case also for other microbiological

46

Benedictow 2005: 46–7.

570

chapter fourteen

pathogenic agents.47 While Simpson can be excused for not placing his correct observation in this historical societal perspective, since the development of medieval economic history was only in its infancy at the time, there is no such excuse for Twigg. Twigg again produces a fallacy of methodology by not comparing like with like, but comparing things that are not in pari materia to infer from dissimilarity of (epidemiological) manifestations to dissimilarity of (microbiological) causation. He compares plague’s pattern of spread in the form of the Black Death in a helpless medieval Europe around 1350 with plague developments around 1900 in the Indian subcontinent governed by British colonial authorities “armed” with European historical experience, modern organizational abilities and modern medical science, albeit in an early stage of development. As shown also above, Twigg ignores, among other things, the fact that the British colonial administration in haste built the largest anti-epidemic organisation the world has ever seen on the basis of a long and largely successful tradition of epidemic countermeasures that had successfully defeated bubonic plague in Europe as early as in the seventeenth century and also on the basis of the new bacteriological understanding of disease and increasingly on a real understanding of the mechanisms of dissemination of plague.48 Given that European authorities succeeded in stamping out plague at the middle of the seventeenth century, it is a strange notion that they, with a gigantic well-organized anti-epidemic effort based on superior medical and epidemiological knowledge at their disposal, should not have succeeded in keeping spread and mortality of bubonic plague to a minimum around 1900 and in the early twentieth century. The second time Twigg refers to Simpson’s work concerns a minor point regarding which animals may contract plague.49 As can now be readily seen, Twigg avoids discussing Simpson’s quite large historical section where historical plague is compared with bubonic plague in India and identity is concluded. Sticker’s work on historical plague and modern scientific countermeasures is treated in the same manner: these two volumes are referred to only once, for a peripheral speculative assertion of the mortality rate

47 48 49

Cf. Benedictow 2004: 387–9. See above: 194–204. Twigg 1984: 212.

twigg’s alternative theory

571

in the plague epidemic in Cairo 1574.50 Chun, who has written very usefully on the presentation of the clinical features of bubonic plague, is also mentioned once, in relation to the average duration of the course of illness in cases of primary pneumonic plague.51 Twigg refers to Pollitzer’s monograph in connection with questions relating to the historical origin of the Black Death and the understanding of the headstones in the Nestorian graveyard at Issyk-Kul.52 Hirst is mentioned in connection with a discussion of the history of the black rat in England,53 but his broad historical discussion of epidemiological and clinical features characteristic of bubonic plague, which represents a fatal threat to Twigg’s theory, remains unused. These are representative examples of how restrictively and selectively Twigg discusses the modern standard works on plague in contrast to his predilection for obsolete miasmatic works and his problematic relationship with methodology. Anthrax and the Name Black Death Twigg maintains that in order to determine the microbiological nature of the Black Death a “good starting point is the name Black Death.”54 The intention is to link the term Black Death with anthrax, a Greek word that means coal and conveys connotations of black, because this would signify that the use of the word black had a concrete clinical descriptive purpose associated with anthrax.55 This is unacceptable for several reasons. Firstly, Gasquet, to whom he first turns,56 makes it entirely clear that the name Black Death is not contemporary with this epidemic or subsequent plague epidemics but appears sometime after the last outbreak of plague in Britain.57 Secondly, the characteristic black associated with the name anthrax refers to the anthrax pustules of cutaneous anthrax which usually develop a black colouring.58 It has

50 Twigg 1984: 46–7. See Sticker 1908: 106. Sticker is the only of these scholars who contracted plague in India and, fortunately, survived. 51 Twigg 1984: 20. 52 Twigg 1984: 39. 45. Cf. Benedictow 12004: 48–9. 53 Twigg 1984: 77–8, 81–2, 85. 54 Twigg 1084: 202–13. 55 Twigg 1984: 213. 56 Twigg 1984: 202–3. 57 Gasquet 1908: 7–8. 58 See Manson’s Tropical Diseases 1982: 393 with picture.

572

chapter fourteen

nothing to do with the only epidemic form of anthrax, namely gastrointestinal tract anthrax, on which Twigg’s theory in reality relies or with the only form with high lethality rates, namely the rare pulmonary or inhalational anthrax, although Twigg refrains from mentioning it. Cutaneous anthrax is, as mentioned earlier, ordinarily an occupational disease of tanners and other craftsmen or labourers working with hides and has a lethality rate of about 20 per cent (in unmedicated cases). This form of anthrax disease, which is the only one that is associated with black pustules, can at most cause population mortality of some tiny fraction of 1 per cent. It does not have explanatory potential for the mortality rates caused by the Black Death of 1346–53. Thirdly, by focusing on Gasquet’s obsolete account, Twigg can neglect S. D’Irsay’s paper of 1926 on “The Origin of the Expression: Atra Mors” in which he convincingly shows that the term “Black Death” is a mistranslation of the term “atra mors” where atra can mean both “terrible” and “black,” thus, the “terrible death” by mistranslation was changed into the even more graphic term the “Black Death.” This explanation appears otherwise to be generally accepted and to have been so for quite a long time. D’Irsay argues also convincingly that this mistranslation originated in Scandinavia, where it was first registered in Sweden in 1555 and about fifty years later in Denmark. It may seem that this was a mistranslation that was quite likely to occur, especially for persons without a good Latin education, and it may have occurred repeatedly and independently before the sinister and frightening connotations caught the imagination. This happened much later: according to Hirst and Shrewsbury, the term the “Black Death” is used in history-oriented literature59 in England for the first time in 1823, and was, according to Shrewsbury, for the first time introduced in English medical literature in 1837 with the translation of Hecker’s monograph The Black Death in the Fifteenth Century.60 Clearly, the term the “Black Death” was introduced into English by persons and adopted by a population who had never seen a case of plague or its clinical manifestations. In normal scholarly discourse, this would be taken as decisive proof that plague does not have a clinical feature characterized by the colour black and that the origin of the adjective “black” must have a non-clinical origin. Twigg knows well and refers repeatedly to Ziegler’s monograph where

59 60

Hirst 1953: 32. Shrewsbury 1971: 37.

twigg’s alternative theory

573

this mistranslation of atra mors is underlined as “the most likely explanation,” its Scandinavian origin is mentioned, and where all alternative explanations of the term the “Black Death” are rejected because they are later than the plague period.61 Twigg refers to D’Irsay’s paper in the bibliographical list at the end of this Chapter 11,62 but ignores it in the text. Twigg’s attempt to link the (misnomer) “Black Death” with the black colour of (cutaneous) anthrax pustules is unsuccessful and misguided.63 Surprisingly, in support of his view on this point Twigg cites the French veterinarian E. Leclainche’s work on veterinary medicine of 1936: “In the terrible epidemic of smallpox of 1345–50 (la mort noire, der Schwarze Tod), the horses, the sheep and the goats died in thousands.”64 Thus, highly unusually, Leclainche asserts that the Black Death was an epidemic of smallpox that also caused high mortality among domestic animals. However, according to modern standard works on microbiology, “variola [= smallpox] infects only humans and monkeys,”65 consequently, the concomitant epizootic must have been another disease. One could have expected that this rather far-fetched and microbiologically untenable view which also runs contrary to Twigg’s anthrax-theory, would have induced him to take a rather sceptical attitude toward the competence and quality of Leclainche’s work. Instead, he states enthusiastically: “Variole is smallpox (Latin variola) and not only did this great outbreak kill domestic animals but it was referred to as the black death.”66 He has a motive for doing so: suddenly, many pages after he has discussed the origin and meaning of the term the “Black Death” and despite much effort had not succeeded in adducing evidence that the name was contemporary, he triumphantly quotes Leclainche’s assertion that the epidemic at the time was called the Black Death, “la mort noire, der Schwarze Tod.” However, he cannot provide his readers Leclainche’s source for this sensational find and potentially important contribution to the history of the Black Death, because there is none. This is also the reason neither French historians nor German historians have picked up Leclainche’s assertion. In modern French

61 62 63 64 65 66

Ziegler 1970: 18. Twigg 1984: 245. Twigg 1984: 204–7. Twigg 1984: 211. My translation from French. Jawetz, Melnick, Adelberg 1982: 437. Twigg’s italics.

574

chapter fourteen

scholarly work on the Black Death, the epidemic is unequivocally identified as bubonic plague. In the words of Dubois in the most recent summary of French research on the Black Death: “almost everywhere in France, the plague has assumed the bubonic form with secondary manifestations” (the small reservation relates to primary pneumonic plague).67 Leclainche was a veterinarian without training in the craft of the historian and the historical aspects of his work are fatally flawed by his lack of historical knowledge of medieval society and of training in historical source-criticism and the application of historical methodology more generally. Anthrax’s Historical Association with Other Epizootics among Domestic Animals and Plague The same fundamental problems can also be readily seen in Twigg’s use of Leclainche’s supposed information that “in 801 there was plague in Charlemagne’s empire which took men and animals alike and in 840 there was plague in men and horses.” Anyone who has taken a serious interest in the history of plague will know that there were no plague epidemics at the time of Charlemagne. The last possible outbreak of plague in the Justinianic plague pandemic was in 766 in Rome or perhaps in Naples and Sicily in 750.68 The last epidemic within the area of present-day France may have occurred in 694, and the last quite certain French epidemic of plague in this pandemic took place in Southern France in 655. All epidemics of this pandemic with their geographical extension are presented in a paper by Biraben and Le Goff of 1969; they are presented systematically over twenty-two pages which include a table with geographical information and individualized maps in Biraben’s monograph of 1975 which Twigg has entered in his bibliography.69 Twigg could easily have determined that Leclainche’s assertions were unhistorical and left his work aside. Leclainche could have used Sticker’s valuable presentation of the Justinianic pandemic in his first volume (1908).70 So could Twigg, who must be assumed to know 67

Biraben 1975: 7–18; Dubois 1988: 313–6. My translation from French. Little 2007: 14; Sallares 2007: 288; McCormick 2007: 292. 69 Biraben and Le Goff 1969: 1484–510; Biraben 1975: 26–48. They have missed the spread to England by some of the epidemics. See for instance Maddicot 2007: 171–214. 70 Sticker 1908: 26–35. 68

twigg’s alternative theory

575

Sticker 1908 since he refers to it once, albeit on a peripheral point of mortality in the plague epidemic in Cairo of 1574–6 (above). Serious or severe epidemic diseases among human beings were usual in the Middle Ages. As Twigg correctly states: it “is very likely that the people of the Middle Ages suffered from a wide variety of diseases.”71 However, contagious diseases among cattle and sheep and other domestic animals were also a general feature of life and these animals suffered from a variety of diseases, anthrax and foot-and-mouth disease, which are commented on by Twigg, but also sheep scab, sheep pox (variola ovina), brucellosis and trichinosis. Leading English agricultural historians agree that epizootics frequently took a serious toll of English livestock in medieval England: “Major epidemics of disease caused serious losses to the sheep population in England in the late thirteenth and early fourteenth centuries. Some flocks were reduced by as much as two-thirds.”72 This means that it was quite usual that epidemics among human beings and epizootics among domestic animals took place more or less concomitantly and that there was no pathogenic or disseminative connection between them. Contemporaneousness of events does not constitute proof that they are causally related, it justifies only the establishment of a working hypothesis to the effect that this could have been the case, with the function to induce the scholar to look for corroborative evidence. Consequently, it is a fallacy of methodology to conclude without further specific investigation that livestock and human population were hit by the same disease, as Twigg usually infers. Specific corroborative evidence must be adduced. And anthrax is not the only disease that can affect both farm animals and local populations in quite close epizootic and epidemic developments; this is also the case with brucellosis and trichinosis.73 Also for this reason it would be a fallacy of methodology to conclude that concomitant epizootic and epidemic developments must reflect anthrax—specific evidence would need to be adduced. If specific evidence cannot be produced, Twigg must admit that he has raised a working hypothesis that he is not able to prove and thus has no case. Twigg enthusiastically writes repeatedly about the numerous epizootics among domestic animals reported in the chronicles and other 71

Twigg 1984: 210. Trow-Smith 1957: 153–7, 240–1; Dyer 1988: 29; Grant 1988: 154, 185; Astill and Grant 1988: 216–7. 73 See, for instance, Manson’s Tropical Diseases 1982: 348–55, 191–4. 72

576

chapter fourteen

sources from the Early Middle Ages into the Late Middle Ages.74 The readers must be excused for assuming that Twigg considers this to be evidence of anthrax, since the accounts on this point cannot serve any substantial purpose for his project if they reflected a considerable number of other epizootic diseases. However, eventually a major problem confronts Twigg: if anthrax had been around for many centuries before the Black Death, it becomes impossible to explain the exceptional mortality caused by the Black Death. So, he must introduce a new disease into Europe, namely anthrax in the form of the Black Death. This flies in the face of what is known about the history of anthrax, which is usually assumed to be mentioned in the Bible and in sources from Antiquity,75 and English agricultural historians are certain that it was present in pre-plague England.76 It also flies in the face of what is known about the level of mortality rates caused by the Black Death (see below). Actually, Twigg’s line of argument turns out to be circular: “Although recorded on many occasions before 1348, murrains had never been accompanied by such an unprecedented human epidemic and this leads me to think that the Great Pestilence was caused by an organism not only common to man and animals, but because of its severity, perhaps new to both of them.”77 Thus, anthrax must be a new disease to fulfil Twigg’s preconceived idea that the Black Death could be anthrax. Twigg does not make a serious attempt to demonstrate the tenability of his second central assumption, namely that the Black Death’s pattern of spread could, even by the most creative exercise of imagination, have resulted from the fact that from Spain to Norway, from England to Russia, European populations were consuming “raw or undercooked” meat contaminated by anthrax and according to a temporal and spatial pattern co-ordinated with and compatible with the spread of plague. At the time, livestock was not a usual cargo, certainly not over considerable distances, and because the epidemic outbreaks in seaports were normally not preceded by epizootics among cattle and sheep, the crucial role played by ship transportation of the Black Death at long or intermediate distances is incompatible with the spread of anthrax. Nor was meat such a major part of diet (see below). 74 75 76 77

Twigg 1984: 200–1, 211, 217. Sternbach 2003: 1–3; Brachman 1990: 877. Grant 1988: 185; Smith 1988: 208. Twigg 1984: 217.

twigg’s alternative theory

577

Twigg’s assumptions take on an increasingly hypothetical and speculative character: “The route by which plague is reputed to have reached Europe could be the very same one that anthrax used.” “If anthrax had come from the East it could have been swiftly spread across Europe from Marseilles and other ports.”78 Thus, it is a fantastic scenario Twigg outlines for his readers of big herds of cattle being transported by galleys first from Kaffa to Constantinople, from Constantinople to Mediterranean ports, especially Marseilles, from whence they were driven across Europe, disseminating spores and contagion and producing instant mass mortality everywhere. Everywhere people gladly devoured contaminated meat from slaughtered sick animals or animals having died from “murrain” without ever or anywhere coming to suspect that it could be dangerous, although they saw people dying everywhere in droves, people that only had in common the fact that they had eaten meat from animals killed by “murrain.” Inexplicably, poor people who usually could not afford meat but had to do with porridge and coarse bread had even higher mortality than the affluent and rich.79 In fact, Twigg is unable to show that concomitant epizootics and epidemics were usual even in England. For this reason, B.M.S. Campbell points out in his review of Twigg’s monograph that Twigg’s theory is undermined by the absence of detectable abnormal mortality among demesne livestock during the Black Death.80 Campbell is not impressed by Twigg’s attempts at documenting the contrary by basing his account on Hecker’s pre-scientific work of 1837 which for plague is based on Barnes’s monograph on the History of Edward III of 1688 (see above): “Hecker says that the plague in England was soon accompanied by a fatal murrain among the cattle, which, left without herdsmen, fell in their thousands.”81 Why does Twigg base his theory on a long obsolete work, and why does he not provide Hecker’s source, since it is of such vital importance to the viability of his theory? Instead, Twigg goes on to cite a small part of a chronicle-based sentence by Rees about the Black Death in London in 1348 to the effect “that animals as well as men were affected.” However, Twigg refrains from citing the following part where Rees applies source-criticism and

78 79 80 81

Twigg 217–8. Benedictow 2004: 262–6, 368, 375–7. Campbell 1985: 314. Cf. Smith 1988: 208. Twigg 1984: 211.

578

chapter fourteen

adds cautiously: “but accurate evidence is not easily obtained,”82 which, in my view, makes the statement practically valueless. Medieval chroniclers must be used with great caution even when their accounts or information are not obviously incredible or unreliable. Their information must be testable by similarity of independent accounts or other forms of source material. This point can be further demonstrated by citing the first part of Rees’s chronicle-based statement left out by Twigg: “scarcely one-tenth survived [in London],”83 which should be impossible even for bubonic plague with a lethality rate of 80 per cent of those infected. Are the views of a chronicler who makes such an evidently hopelessly exaggerated assertion really credible? Is it true that Rees’s account on this point can serve to support a case for a concomitant epizootic and epidemic in London? How can it be made compatible with Ziegler’s correct observation that the Black Death broke out in London earlier than in the surrounding districts, actually by a margin of several months?84 This can only serve to illustrate the great caution with which medieval chroniclers should be treated. Icelandic chroniclers assert that only fourteen people survived in London.85 Twigg’s attempt to take refuge in the international trade of hides, furs and wool on the basis of E.M. Veale’s fine, but quite narrowly England-oriented monograph, is unconvincing.86 Nothing is said in this study about skins or furs as vehicles of the spread of zoonoses to human populations at the time, nor about anthrax, nor about any other animal disease,87 which shows that Twigg is forced to proceed by speculation. Assuming speculatively that anthrax was actually spread by this trade, this scenario would only result in the sporadic incidence of cutaneous anthrax with a lethality rate of about 20 per cent and rare cases of pulmonary anthrax, two forms of contagious disease that, taken together, can cause population mortality rates of fractions of 1 per cent (see above). It cannot be accepted as a serious proposition that

82

Rees 1923: 29. Ibid. 84 Ziegler 1970: 135; Benedictow 2004: 134–7. 85 Islandske Annaler 1888: 275–6. 86 Twigg 1984: 217–8. Nothing negative is meant by my characterization of Veale’s monograph as narrowly England-oriented (its title is The English Fur Trade in the Later Middle Ages), only that its focus or perspective poorly serves Twigg’s sweeping Europewide line of argument. The same goes for its temporal perspective which, as the title shows, is strongly oriented towards the post-Black Death period. 87 Veal 1966. 83

twigg’s alternative theory

579

these forms of anthrax could have spread in large waves over the continent and across England, causing havoc everywhere. This is why it has not been possible to adduce evidence to this effect. Since Twigg is not able to provide evidence demonstrating the concomitant spread of mortal epizootic disease among manorial herds during the Black Death, he is lead to emphasize his speculative approach. A few pages later he resorts to another pre-scientific work, this time by H. Harrod of 1867, which also speaks clearly for itself: “On the Manor of Heacham, Norfolk, there was murrain from 1346 to 1411 without pause and it attacked horses, cattle, sheep, pigs, chickens, ducks, geese, swans, pea-hens and even hives of bees.” It is, of course, impossible that the same zoonose should be the cause of an epizootic among all these animals. At the basis of this statement lies the miasmatic theory which is mono-causal and also can explain why birds and bees are severely hit, since miasma is spread by contaminated air. Finally, Twigg refers to E.L. Sabine’s paper on “Butchering in Medieval London” in which it is stated that the “periods of 1314–20 and 1346–89 were times of murrain among domestic animals,” in the second period also among poultry and wild birds, and specifically among sparrows in 1366.88 This should make it clear that “murrain” is a word used to designate any or at least a large number of diseases among animals and that murrains in this more general meaning of zoonoses were an ordinary part of medieval life, before the Black Death and after the Black Death. Murrain is the contemporary concept of epizootic, equivalent to the contemporary concept of pestilence for epidemic; in the case of pestilence bleeding of human victims was usual, and in the case of murrain bleeding of livestock was usual.89 Importantly, Harrod and Sabine do not maintain that there was concomitant spread in time and space of murrains among domestic animals and mortality among people in the Black Death. Twigg has not produced evidence to the effect that anthrax spread concomitantly with the Black Death in England, as Campbell correctly points out. The scholarly literature on the Black Death and subsequent plague epidemics typically consists of studies of outbreaks that are not preceded by any epizootic among cattle and sheep. One important reason that epizootics among livestock did not usually develop on a grand

88 89

Twigg 1984: 215. Trow-Smith 1957: 153–7, 240–1; Astill and Grant 1988: 216.

580

chapter fourteen

scale comparable with the Black Death is that medieval people were not so helpless as Twigg must assume. They had learned from long experience and made strong efforts to contain the spread of murrain. “For example, animals that died of murrain were burnt, and their heads placed on stakes to tell travellers to avoid the area.”90 Thus, medieval people employed some of the main methods used today to eradicate epidemics of anthrax, foot-and-mouth-disease and scrapy. For the same important reason, medieval people did normally not eat domestic animals which had died from outbreaks of murrain, i.e., from dangerous epizootic diseases. The Black Death’s Origin and Spread and the Anthrax Theory Twigg puts much emphasis on an account of the Black Death’s spread, especially the early phase, and he has an important reason or objective for doing so: “It is essential to examine the biological logistics of the Black Death in order to attempt to determine whether this particular epidemic could have been bubonic plague.” In his third chapter, titled “The Black Death – Origins and Spread to Europe” he says that his goal is “to examine the origin of the Black Death and the way it reached Europe, in the light of modern knowledge of plague biology.”91 Twigg wishes to use the history of the Black Death’s origin and spread to show that it is incompatible with bubonic plague but compatible with anthrax. This is a legitimate and potentially useful way to address the question of the microbiological identity of the Black Death and to consider possible alternatives. However, Twigg’s quite poor knowledge of medieval history and source-criticism and limited reading of the available modern accounts of the history of the Black Death combine to result in various assertions and discussions which are out of line with reason and reality. Because so much of his account is factually wrong, for practical reasons only a small representative sample of data and arguments with relevance for his objective can be discussed. Several contemporary chroniclers assert that the Black Death started in the lands of the Golden Horde in south-eastern Russia, in a region containing a large plague reservoir where people still contract bubonic plague today. They also assert that it was spread by galleys from the 90 91

Astill and Grant 1988: 216–7. Twigg 1984: 43–4.

twigg’s alternative theory

581

Italian trading station at Kaffa in the Crimea to Constantinople and seaports on the Mediterranean littoral. This outline of the origin of the Black Death can be safely confirmed by the early history of outbreaks.92 It is correctly recognized as a serious threat to several of the alternative theories, because it establishes a continuous line from an area of a known plague reservoir to the introduction of plague in Constantinople and in important commercial hubs of the Mediterranean littoral. The threat to Twigg’s theory is especially great, since the chroniclers have nothing to say about epizootics among livestock spreading concomitantly with the Black Death in the regions where it broke out in the spring of 1346 and until it reached the camp of the army besieging Kaffa.93 Twigg and Scott and Duncan endeavour on erroneous grounds to claim that the Black Death could as well have come to Mediterranean Europe from Alexandria or Syria, and Scott and Duncan have produced a map showing as established fact that the Black Death spread from Alexandria to Messina in Sicily.94 For Scott and Duncan it is crucially important to link the origin of the Black Death to Africa, since the haemorrhagic diseases of Ebola and Marburg are closely associated with Western Africa; the fact that these diseases have no known history in north-eastern Africa or the Middle East is ignored. They also present a completely outdated and misleading map of the spread of the Black Death that does not show the origin in south-eastern Russia and the spread out of Kaffa (see below). A central aspect of this topic is obviously the issue of the spread of plague over long distances. To his credit, Twigg is the only advocate of an alternative plague theory who attempts to do this explicitly in relation to the Black Death’s first phase of spread: most of the other advocates of alternative theories ignore the problem or accept unquestioningly Twigg’s discussion of the problem as Scott and Duncan do.95 Twigg rejects the possibility of long-distance transportation of bubonic plague by ship from Kaffa by agency of the nexus of rats and fleas on untenable grounds.96 However, a hundred pages later Twigg asserts that when bubonic plague was raging in India a hundred years ago, it was repeatedly transported from there by steamship all the long

92 93 94 95 96

Benedictow 2004: 44–73. Benedictow 2004: 50–2. Scott and Duncan 2004: 231, 242. Scott and Duncan 2004: 241–2. Twigg 1984: 47–55; Benedictow 2004: 17–21, 51–73. See also above chapter 4.

582

chapter fourteen

and time-consuming way to England. In this connection he states correctly that “Ships represent the greatest danger of introducing plague, mainly by means of rats and fleas in the cargo,” and goes on to mention a number of occasions when this occurred.97 In this passage, Twigg reveals that he is fully aware of the fact that bubonic plague spreads easily by ship over long distances, i.e., by metastatic leaps (per saltum), although he systematically refrains from taking it into account in his epidemiological analyses of the Black Death. The reality of metastatic leaps reflects the fact that rat fleas can survive away from their rat hosts for quite a number of weeks in humid and moderately warm climate typical of much transportation by ship, much longer than Twigg asserts, again without a substantiating footnote: “although in ideal conditions X.98 cheopis may live for a month without its host it is doubtful if at the end of that time it could transmit plague.”99 This is strongly at variance with Hirst’s statement that in favourable circumstances, “at temperatures below 15° C. the chief vector of bubonic plague, X. cheopis, can certainly survive in a very heavily infected state for at least fifty days,” and this is not the limit: “it is highly improbable, however, that the maximum longevity of unfed, infected rodent fleas is known.”100 It can be usefully added that this rat flea survives unfed in a very heavily infected state for 23 days at 27 °C. In Madagascar, researchers discovered that this rat flea could survive for months on grain debris,101 which demonstrates the significance for the spread of plague of the transportation of corn and farina, which were the most common goods in medieval transportation. The length of time dangerous rat fleas can survive a voyage is further extended by the period of the epizootic among the ship’s rats that eventually leads to the release of infected fleas from dead rats in a situation where many of these fleas do not find new rat hosts. In this perspective, the number of rat colonies on board large ships such as galleys (and cogs) and also the relative localization of their territories in the ship take on significant interest,102 since the strong reduction of a rat colony to this point takes ten to fourteen days (see above). This is at the

97 98 99 100 101 102

Twigg 1984: 47–54, 147. X. = Xenopsylla. Twigg 1984: 85. Hirst 1953: 324, 330–1. Hirst 1953: 330–1. Pollitzer 1954: 387.

twigg’s alternative theory

583

heart of the matter when Twigg correctly writes that the “galleys could therefore presumably support many rats,”103 because the presence of two or more rat colonies that were successively attacked by plague would readily add four or more weeks to the time preceding the point when rat fleas would be on their own. The point is the following: rats defend their territories and the food resources within them and they respect the boundaries of adjacent rat territories in order to avoid being attacked, which means that another rat territory will not be invaded until its rat colony is severely reduced and unable to defend it. When the rats of an unaffected rat colony invaded the territory of such a defenceless rat colony, they would pick up their fleas, and thus the process would be repeated and the time horizon of the epizootic would be further extended and potential epidemic developments would be correspondingly postponed. Thus, there is a clear potential for a substantially expanded time horizon before plague epidemics break out on galleys. For the same reason the long-term survival of infected rat fleas will tend to be much longer than Twigg assumes. If Twigg’s objective was to give a tenable, updated account of the early phase of the Black Death’s spread on the basis of best possible facts, it is difficult to understand the scholarly grounds for his prolific use of Hecker’s pre-scientific work on medieval epidemics of 1837 (posthumous reprint of 1859) and of Gasquet’s account written around 1890,104 and for his neglect of M.W. Dols’s fine monograph on the Black Death in the Middle East of 1977, or Biraben’s monograph on plague of 1975 or his paper of 1979,105 and several other excellent works that were available at the time he was writing his monograph. The vast majority of works on the Black Death were written not only after Hecker’s work but also after Gasquet’s, and this is the case for all works written after modern medicine, epidemiology and bacteriology were established. Inevitably, Twigg’s temporal outline of the Black Death’s spread from the Crimea to the Mediterranean coasts is wrong, as is his outline of its further spread over Europe, even for his native England. Inexplicably, he provides a map of the Black Death’s spread across Europe that he informs his readers is taken from a small paper on the Black Death by

103

Twigg 1984: 51. Twigg 1984: 45–7, 60–1. On these few pages, Hecker and Gasquet are referred to five and seven times respectively (and many more times elsewhere). Cf. Above: 565, fns. 35, 36. 105 Biraben 1975–1: 48–92; Biraben 1979: 30–40. 104

584

chapter fourteen

W.L. Langer in Scientific American of 1964. However, Langer has not drawn it. It is also published in Ziegler’s monograph106 which he has used extensively, referring to him by name twenty times in his text.107 This map is taken from a general paper on famines and epidemics in the fourteenth century by É. Carpentier published in 1962, two years before Langer’s paper.108 In this paper, she makes a pioneering attempt at sketching an outline of the spread of the Black Death at an early stage of plague research based on quite a small sample of studies, which was due to her limited access to studies in other languages. The result was seriously flawed, and it does not show the spread from the Crimea, which should have been important to Twigg given his point of departure, but starts in Southern Europe. It is so inaccurate or erroneous for the spread of the Black Death in the British Isles that it is difficult to understand how a British scholar was not struck by it. How profoundly flawed the map is can be easily ascertained by comparison with the map I provide in my monograph on the Black Death109 and is reprinted on page 2 above which is based on a detailed description of its spread over almost 200 pages taking into account the national research from all countries that were ravaged by it.110 Scott and Duncan also chose to republish Carpentier’s map, but since they too have chosen to ignore the standard requirement for scholarly monographs to provide footnotes, nothing is said of the map’s origin or background, and they let their readers believe that it could be of their own making.111 Ten years before Twigg published his monograph, Biraben had published a much improved, although still deficient, map of the Black Death’s spread across Europe.112 Twigg mentions this work in the two lines preceding Carpentier’s map, but on a point regarding the Black Death’s arrival in Bordeaux. Biraben’s very different and much improved map shows the Black Death’s origin in the Crimea. In 1979, Biraben published a much improved map on the spread of the Black Death in the Middle East which should have been of particular interest to Twigg at the time he wrote his monograph, but it remains unmentioned.113

106 107 108 109 110 111 112 113

Ziegler 1970: 106–7. Twigg 1984: 48–2, 49, 54, 55–3, 62, 78, 79–2, 82, 85, 90, 175, 189–4, 220. Carpentier 1962: 1062–92. Benedictow 2004: 1–2. See also the map in Benedictow 2005: 44. Benedictow 2004: 44–224. Scott and Duncan 2004: 29. Biraben 1975: 88–9. Biraben 1979: 30–40, map on p. 34.

twigg’s alternative theory

585

Also Dols renders a much better map than Carpentier’s in his fine monograph on the Black Death in the Middle East of 1977.114 What makes Carpentier’s map so attractive? Is it that it shows the spread of the Black Death at six-monthly intervals in long curved lines without reflecting the important part that ship transportation played in the process of dissemination and thus “conceals” the role of metastatic leaps. The numerous indications of metastatic leaps by ship are exactly the conspicuous aspect of the map I have drawn, fully supported by evidence in my text. Carpentier’s map does not show the Black Death’s spread out of south-eastern Russia from Kaffa on the Crimea by ship. Twigg can therefore indicate a theory of the Black Death’s geographical origin and route of spread to Europe very different from the established view that it broke out in southern Russia and was spread from Kaffa by Italian galleys. Instead, he cites Hecker’s pre-scientific work of 1837115 where it is stated that “before the plague reached Europe it had killed daily, in Cairo, between 10,000 and 15,000 people.”116 This is wrong. In Egypt, the Black Death first reached Alexandria in the early autumn of 1347 by a major metastatic leap from Constantinople, and this was the decisive epidemic event in this part of the world, which established the great epicentre of spread in the Middle East and North Africa. The Black Death’s spread out of this great and bustling city did not start until the late autumn, and by normal spread rates it did not reach Cairo until, as it seems, the summer of 1348,117 since the epidemic raged at its worst there in October–December.118 This also means that the Black Death had reached southern England and north-western France shortly before or at about the same time it reached Cairo, and had already ravaged a large part of Europe. Mortality rates by plague cannot be discussed on the basis of the type of information provided by Hecker. Dols’s careful specialist discussion of mortality rates is valuable. All this is uncritically taken over by Scott and Duncan. Twigg’s assertion that the Black Death could have been shipped to Europe from Syria at the same time it was shipped from Kaffa is

114

Dols 1977: 36–7. Although Twigg has used the posthumous edition of 1859, 1837 is the real historiographic age of the work. 116 Twigg 1984: 46. 117 Benedictow 2004: 63–4. 118 Dols 1977: 182. 115

586

chapter fourteen

unfounded and untenable. Scott and Duncan accept this view, since it somewhat shortens the distance to West Africa which is the only known region where Ebola disease and Marburg disease occur. Thus, the Crimea is an impossible origin for their alternative contagion for shipment to Constantinople and the Mediterranean littoral. The fact is that the Black Death spread from Alexandria to Syria, was raging in Gaza in April and May of 1348 and in Damascus in July, a year after the outbreak in Constantinople, and at the time when the Black Death had ravaged large parts of Southern Europe and had even begun spreading in England out of Melcombe Regis (Weymouth) and was closing in on Paris from Rouen. Twigg’s extensive use of Hecker’s pre-scientific work of 1837 for his account of the early spread of the Black Death is intriguing.119 At the time he was writing his monograph, Twigg should have used Dols’s excellent study of 1977, also Biraben’s monograph of 1975 and his paper of 1979120 which have much valuable information to offer on this topic. However, Dols and Biraben are able to write their monographs on the assumption that the Black Death was bubonic plague without landing in any obvious epidemiological difficulties. Metastatic leaps of bubonic plague by ship play a central role, in the words of Dols, for instance: “Al-Maqrizi informs us that the Black Death reached Egypt in the early autumn of 748/1347—about the same time that it arrived in Sicily. It may have been spread simultaneously to Asia Minor and the Levant by merchant ships.” “The fact that the Black Death arrived in Egypt at approximately the same time that it reached Sicily would strongly suggest its transmission by the brisk Christian maritime trade from the Black Sea and Constantinople.”121 Twigg’s efforts to prove that the Black Death cannot have been bubonic plague are undermined by other serious weaknesses of facts and assumptions. Twigg states that the “Genoese would, at the earliest, have left Kaffa during October and at the latest by December,” and assumes arbitrarily that the Genoese galleys which he claims arrived in their home city in January had been sailing directly from Kaffa.122 This is wrong: in Constantinople the outbreak was recognized in early July, which in the case of bubonic plague means that the contamination was introduced in early May. Actually, chroniclers mention that Genoese 119 120 121 122

Twigg 1984: 46–7. Biraben 1979. Dols 1977: 57–60. Twigg 1984: 51, 54.

twigg’s alternative theory

587

galleys fled from Kaffa in the spring of 1347 and contaminated the metropolis, which as can easily be seen fits the facts.123 It can be shown that Twigg knows these accounts.124 The temporal progression of these accounts also fits with the central facts of the further spread: the outbreaks in Alexandria in early autumn 1347, in Messina on Sicily at the end of September and in Marseille by 1 November,125 not in February, as Twigg asserts.126 These facts are related in considerable detail in Dols’s monograph.127 In this way, Twigg clears the ground for an argument to the effect that “Flea breeding must have been very low at that time both on ship and ashore.”128 On the contrary, many of these events took place at the height of the flea-breeding season. Twigg is very reluctant to take into account the fact that Constantinople was contaminated in the Black Death’s first phase of spread by galleys that had fled from Kaffa, making only an off-hand comment that Gasquet (1908) thinks that plague was “probably carried” from Kaffa to Constantinople.129 Twigg attempts to avoid or downplay the point that Constantinople could function as an intermediary base for further dissemination into the Mediterranean littoral by other ships contaminated in the harbours of the metropolis, and that they could even have been contaminated before the outbreak by exchange of goods, in a similar way to what was reported to have occurred in the harbour of Melcombe Regis (Weymouth) in England.130 Twigg needs to adduce evidence to the effect that long voyages are incompatible with plague biology and argues his case on the assumption that all ships from Kaffa sailed directly to their Mediterranean destinations, mainly Venice and Genoa, which makes the continuous voyage at sea (i.e., without stops for trade or to acquire supplies) as long as possible. It enables him also to ignore the notion that many of the ships which spread plague along the Mediterranean coasts in the autumn of 1347 could have been contaminated in Constantinople.131 Crucially, Twigg does not mention that the Genoese and Venetians

123 124 125 126 127 128 129 130 131

Benedictow 2004: 60–5, 69–73; Dols 1977: 53. Twigg 1984: 46. Benedictow 2004: 53, 63–4, 69–73, 96–101. Twigg 1984: 55. Dols 1977: 53–61. Twigg 1984: 54. Twigg 2984: 47. Benedictow 2004: 127. Benedictow 2004: 61.

588

chapter fourteen

along the shipping lanes had quite number of other minor trading stations and ports that they used for rest and provisioning. In the words of N.J.G. Pounds, there was “a ring of trading stations along its [the Black Sea’s] coastline,” for instance, Mauro Castro on the estuary of the Dnestr and Trebizond,132 and after having left Constantinople, for instance, Chios, Nauplion, Coron, Modon and Monemvasia, Corfú (Kerkyra) on the shores of Greece, and on the last stretch homewards up the Adriatic the Venetians used the ports of Ragusa (Dubrovnik), Spalato (Split) and Zara (Zadar), whilst the Genoese especially used the ports of Messina and Naples for their last stretch homewards.133 This also means that they had the opportunity to halt the voyage for shorter or longer periods of time and to hire additional sailors. Even an elementary introduction to the commercial history of the Middle Ages like R.S. Lopez’s fine little monograph The Commercial Revolution of the Middle Ages, 950–1300 mentions that “the Genoese established a cluster of colonial outposts all around the Black Sea.”134 Thus, Twigg’s presumption that returning Venetian and Genoese galleys would have to sail directly to their patriae is without basis in elementary facts of medieval trade history. In this way, Twigg has construed an artificial argument against bubonic plague being shipped out of a region where there is a permanent plague reservoir in order to clear the ground for his own theory, although no concomitant epidemic of anthrax is mentioned in the lands of the Golden Horde by the chroniclers (see above).135 For his presentation of the routes of the Italian galleys homewards from their easternmost trading station at Kaffa Twigg refers to E.H. Byrne’s small monograph on Genoese shipping in the High Middle Ages. However, this work is oriented towards their western trade routes, towards Barcelona, Málaga, Tunisia and Ceuta, and towards the Levant. It focuses on topics relating to shipping and business and relates rather peripherally to actual sailing and the system of sea lanes and ports used along the routes. Nonetheless, Byrne gives some pieces of information on ports of call along the sailing routes.136 As can be seen, much more useful information on this topic can be found in modern standard

132 The ancient Greek colony of Tyras, later called Akkerman, from 1946 with the Slavic name of Belgorod(-Dnestrovskiy), in Romanian Cetatea Alba. 133 Pounds 1974: 360–7. 134 Lopez 1976: 109. 135 Bratianu 1929; Pounds 1974: 360–8. 136 Byrne 1930/1970: 36–7, 44, 52.

twigg’s alternative theory

589

works on medieval economy like Pound’s still very useful monograph of 1974 which has also a rich standard apparatus of footnotes as well as fine bibliographical entries at the end of each chapter—as scholarly books should.137 Medieval chroniclers’ rhetorical exaggerations and loose relationship with facts are some of their most obvious features. What medieval chroniclers assert and what they do not mention are a rich source of great surprises to modern scholars.138 For this reason, assertions of the pace of spread that cannot be tested against independent sources, and in cases of data relating to cities, against local population records, cannot be accepted. Twigg considers it appropriate, on the contrary, to cite the chronicler Gabriele de Mussis, but he cites him indirectly, according to Creighton’s summary,139 who was, as pointed out above, the last champion of miasmatic theory in England. Twigg cites Creighton to the effect that, there were no cases of plague on board ships, although the very atmosphere or smell of the new arrival seemed sufficient to taint the whole air of Genoa and to carry death to every part of the city within a couple of days.140

Firstly, as already pointed out by Gasquet, it is not true, as Creighton repeatedly asserts, that Gabriele de Mussis had himself been in Kaffa and left with a Genoese galley for his home town and that his account therefore is based on personal observation. In fact, de Mussis stayed in his home town of Piacenza and pieced together his account on the basis of what he heard from sailors or merchants and other sources of hearsay. His account can readily be shown to be based on misinformation and misconceptions and miasmatic notions.141 It is also not true that there were no cases of plague on board: “It so happened that when the ships left Caffa—some bound for Genoa, some for Venice, and some to other parts of the Christian world—a few of the sailors were already infected.”142 Obviously, Creighton shapes his summary of de Mussis’s account in a way that serves his campaign for miasmatic theory against the rise of the new science of bacteriology or microbiology and puts 137 138 139 140 141 142

Twigg 1984: 52, 54. See above: 78–82, 219–24. Creighton 1894: 144–9. Twigg 1984: 52, cf. 54. Twigg’s italics; Creighton 1891: 148–9. Benedictow 2004: 52–3. Cited after Gasquet 1908: 19–20.

590

chapter fourteen

special emphasis on the theory that the ships carried merchandise contaminated with miasma. And in fact de Mussis’s account is formed according to contemporary miasmatic notions of epidemic disease.143 Creighton’s presentation of this material is therefore doubly imbued by miasmatic notions. Twigg neglects the basic approach of the historian’s craft, namely to identify the original source and start source-critical work from there, or he would have noted Gasquet’s correct rendering of de Mussis account, a work he knows well and refers to by the author’s name twenty-three times in his running text.144 Miasmatic notions can imply extreme contagiousness by touch and extreme spread rates since spread is not dependent on contact but is effected by wind. On this basis, Twigg can conclude that the disease introduced from Kaffa to Genoa could not have been bubonic plague. However, would any epidemic disease known to modern medical science spread across Genoa in a couple of days, even intensely infectious diseases like smallpox or influenza, since they are dependent on interpersonal contact for transmission? Is it not only miasmatically contaminated air that can spread an epidemic disease in this way, because people will inhale it as it blows down their streets and in through their windows? Is it really a medically and epidemiologically qualitative difference between de Mussis’s, Creighton’s and Twigg’s accounts? Are they not all based on miasmatic assumptions? Scott and Duncan take great interest in much the same events, namely the Genoese galleys’ arrival in Messina on Sicily, and subsequently in their home town. They take over wholesale Twigg’s arguments which can seemingly serve to undermine the bubonic-plague theory and as such clear the ground for their own alternative theory. De Mussis’s account is in fact yet another definite proof that the disease was not anthrax. It cannot be accepted that the galleys arrived in Genoa from Kaffa with herds of cattle or sheep on board which were seriously sick from or had recently died from anthrax and that the population of Genoa eagerly consumed the flesh of these animals all across the city with extraordinary epidemic speed, actually in two days.145 143

Benedictow 2004: 52–3. Twigg 1984: 45–7, 56–7, 60–1, 70, 103, 202–4, 207. 145 I have assumed that Twigg did not believe that the galleys arrived from Kaffa full of contaminated wool that was immediately spread all over the city and that the great majority of Genoa’s inhabitants were woolsorters who en mass contracted anthrax by inhalation, and even this flight of fancy would be insufficient for explanation, since we also must assume that the woolsorters did not early detect that work with wool at the 144

twigg’s alternative theory

591

According to elementary scientific principles, Twigg should be obliged to demonstrate in concrete detail how this could have been possible and on this basis form a realistic and tenable explanatory model; the fact that he has declined to do so means that his assertion is unfounded and can be taken as evidence that such modelling is impossible. Even if every inhabitant of Genoa were infected, the lethality rate would only have been about 20 per cent, only a fraction of Italian mortality rates in the Black Death estimated on the basis of population records and other types of demographic sources, for instance one-third of the mortality rate in Florence.146 Also Scott’s and Duncan’s alternative theory of a filoviridal disease is excluded, since these diseases spread only by direct physical contact and transmission of living contaminated cells, which makes for an exceedingly slow spread and tiny outbreaks (see below). The outbreak in Genoa appears to have been recognized at the end of 1347, not in January, as Twigg states.147 Assuming that it was bubonic plague, the contamination would have been introduced into the city about seven weeks earlier and would have had much time to prepare the ground for an outbreak in January after having developed for at least a couple of months, provided that the temperature was moderately chilly for the season. However, there is no source material available which can provide an empirical basis for a spatio-temporal outline of the Black Death’s spread across the city. The inherent dangers of accepting the “overwrought imaginings” and “hopelessly inaccurate quantifications” of medieval chroniclers can be further illustrated. Twigg’s monograph exhibits no trace of the scepticism of medieval sources and the great importance of source-criticism that is uppermost in the minds of all medievalists worth their salt. Twigg claims, for instance, that 56,000 persons died from the Black Death in Marseilles.148 This figure is taken from Ziegler’s monograph, and since Ziegler, according to the ordinary standards of scholarly work, provides a supporting footnote it can be ascertained that it comes from a prescientific149 study of 1869,150 which allows identification of the original source as a contemporary chronicle. However, Ziegler took this figure time was extremely dangerous. Of course, significant epidemic outbreaks of pulmonary anthrax have so far not been discovered. 146 Benedictow 2004: 285–91. 147 Benedictow 2004: 71; Twigg 1984: 55. 148 Twigg 1984: 55. 149 Anglada 1869. 150 Ziegler 1969: 64, 293, 312.

592

chapter fourteen

and its footnote from Gasquet’s monograph who more accurately informs his readers that the figure is 57,000, represents the death toll for a month and, therefore, constituted only a small part of the total mortality which according to the implied information must in the end have numbered hundreds of thousands of victims.151 Thus, this is a case of serial uncritical and careless copying of information in which only the first author has read the original study and none has read the original source or applied source-criticism. This type of serial dependence characterizes Twigg’s historical account as a whole (far more than Gasquet’s and Ziegler’s monographs). The demographic history of Provence has been written, although Twigg has not taken account of this. According to E. Baratier, the expert on Provence’s medieval and early modern demography, the city of Marseilles contained only about 15,000 inhabitants in 1315, and presumably also on the eve of the Black Death,152 a piece of information that at the time Twigg wrote his theory had been available for almost a generation, and was also available to Ziegler. Thus, Twigg is prepared to accept and to convey to his readers the suggestion that five times as many people died in the Black Death in Marseilles in one month of the epidemic as actually lived there. According to Baratier’s study, 52–3 per cent of the householders in Provence died in the Black Death, both in the urban centres and in the countryside,153 which corresponds to a population mortality rate of about 60 per cent.154 This means that Twigg by ignoring Baratier’s work avoids citing this order of population mortality for a large region and explaining how it can be compatible with the mortality rates of anthrax. He has also failed to find empirical data showing or at least suggesting the concomitant raging of an anthrax epidemic among cattle and sheep and to demonstrate that there is close contemporaneity between the spread of the Black Death among human beings and the spread of an anthrax epizootic. Twigg’s account of the Black Death’s spread out of Marseilles, a milestone in its history, and its extension into a much broader picture of its spread across large parts of Europe is also wrong.155 The crucial point is 151

Gasquet 1908: 39. Baratier 1961: 66–7. 153 Normal demographic adjustments with respect to the population growth in the time between the end of the epidemic and the writing of the registers indicates rather a mortality among the householders of 54–55 per cent. 154 Benedictow 2004: 308–15. 155 Twigg 1984: 55–62; Benedictow 2004: 126–45. 152

twigg’s alternative theory

593

his untenable assumption that bubonic plague spreads only by contact between contiguous rat colonies: “If it is assumed that rat populations were contiguous throughout the region—and they would need have been—the rate of spread across France is as follows […].” It is this false premise, the denial that bubonic plague spreads over distances by metastatic leaps by rat fleas in clothing, luggage or merchandise, which permits Twigg to construct obviously untenable spread rates from Marseilles to Carcassone or from Carcassone to Bordeaux or from Marseilles to Avignon or from Avignon to Lyon, or from Marseilles to Paris, thus producing phoney proof that the Black Death cannot have been bubonic plague. All his indications of the Black Death’s time of arrival at these locations are systematically erroneous and his spread rates correspondingly misleading. According to Twigg’s account, the Black Death spreading northwards from Lyon should have broken out in Burgundy in July and August and inexplicably have reached Paris in time to break out there in June. However, the Black Death did not break out in Paris in June, but towards the end of the third week of August.156 This highlights the important fact that the Black Death did not spread from Marseilles to Paris, but from Rouen to Paris,157 because it arrived in Rouen with a ship from Bordeaux by an instance of a metastatic leap, and produced an outbreak which began 24 June.158 Twigg’s rejection of the notion that bubonic plague spreads by leaps and acceptance of obsolete miasmatic and erroneous information on the spatio-temporal progression of the Black Death across Europe combine to make his discussion of the events in his own country quite absurd. He seems to accept that the Black Death broke out first in the southern seaport of Melcombe Regis (Weymouth), shortly before 24 June, referring indirectly to the Grey Friars Chronicle which provides this information, but then all reason evaporates. “There can only be speculation about where it came from,” he asserts, although it is unequivocally stated in the Chronicle with some concrete detail that it came with a ship from Gascony.159 This is normally and reasonably taken to mean that the Black Death was brought to England by a ship from 156

Benedictow 2004: 107–8; Dubois 1988: 316. Benedictow 2004: 97–9, 101–8. Cf. Dubois 1988: 314–6. 158 Twigg states that the source for his (misleading) presentation of the Black Death’s spread out of Paris is Gasquet’s monograph of 1908, however his text is very close, almost a verbatim, rendering of Ziegler’s account which is largely but not entirely based on Gasquet’s account. Twigg 1984: 56–7; Ziegler 1969: 64–5. Cf. Gasquet 1908: 39–53. 159 Benedictow 2004: 126–8. 157

594

chapter fourteen

Bordeaux where the Black Death had been raging for several months.160 Rouen was infected by a ship from Bordeaux which caused an outbreak there almost simultaneously with the outbreak in Melcombe Regis (Weymouth). However, Twigg speculates that the contagion could have been shipped from Calais to Melcombe Regis, although the Black Death broke out in Calais in December, half a year later than in Melcombe Regis.161 He also speculates that the Black Death could have arrived in Melcombe Regis from northern French ports or the Channel Islands. The earliest outbreak in a northern French port is the outbreak in Rouen which does not precede but is about simultaneous with the outbreak in Melcombe Regis, which could suggest that these two seaports were contaminated by ships sailing from Bordeaux in the same convoy, as merchant ships often did at the time.162 The suggestion of an origin in the Channel Islands is not based on a dateable source and cannot be used for determining the Black Death’s time of arrival.163 Twigg assumes also that the Black Death could have been on board ships sailing directly from the Mediterranean. This implies that at a time of unique disaster and immense difficulties for organizing great trade expeditions, galleys should have left Genoa or Venice unusually early for a voyage of roughly 4500 km for the Genoese with a duration of roughly three to four months and substantially longer for the Venetians. If the disease they brought with them had been anthrax, the voyage would have taken place with contaminated herds of live cattle or sheep on board which immediately on arrival alongside the quay of the harbour of Melcombe Regis would have to be driven through England. I cannot imagine how this disease could function on board among animals and men for such a long journey, but the burden of proof is on Twigg. Twigg goes on to cite other chroniclers with later datings of the original outbreak in England and other ports of arrival, although none of these alternatives are compatible with the known pattern of early spread in England which is based on the sources.164

160

Benedictow 2004: 101–4, Biraben 1975: 74; Dubois 1988: 316; Benedictow 2004: 108. 162 According to the information provided by the chroniclers, plague broke out in Melcombe Regis shortly before 24 June, in Rouen about 24 June, a small difference in time which probably reflects the fact that Rouen was a considerably larger urban centre, a city of some 30,000 inhabitants; quite likely these two urban centres were contaminated at the same time. 163 Ziegler 1970: 125. 164 Benedictow 2004: 126–34, 137–40. 161

twigg’s alternative theory

595

Twigg’s account of the spread of the Black Death in England is untenable, as shown also above in the chapter on seasonality.165 The main reason is that Twigg bases his account of the Black Death’s spread across England on the false assumption that spread over land was dependent on rat-to-rat contact, according to the scholarly myth he pioneered that bubonic plague spreads only between contiguous rat colonies. This enables him to assert correctly that this mechanism of spread could not produce the observed pace of spread, “not even one and a half miles per day.” Actually the average pace of spread on the ground of the Black Death in England was substantially slower, about 1–1.5 km a day, which still is much faster than the spread rate between conterminous rat colonies.166 Twigg denies that human beings perform the central role in the spread of plague by transporting infected rat fleas in clothing, luggage or goods, by ship or by land, bringing about metastatic spread. His conclusion is therefore based on the denial of fact. This argument is taken over by Scott and Duncan: they accept unconditionally his account of the spread of the Black Death in England. Twigg’s Demographic Argument It is important for Twigg to argue for the lowest possible level of mortality in the Black Death in the hope that it will not be obviously incompatible with his highly exaggerated and speculative assertions of mortality causable by anthrax (see above). In his view, the “mortality in the years 1348–9 has frequently been exaggerated and treated as though no other epidemic periods could be compared to it.”167 For this view he provides no reference. At the time Twigg was writing his monograph, there was a broad consensus on the level of mortality caused by the Black Death, namely Hatcher’s estimate of 1977 in a small but outstanding book on the interaction of economic, demographic and plaguerelated developments in late medieval England. Highly conscious of the fact that the vast majority of the population was constituted by peasants in the broadest sense of the term Hatcher based his estimate mainly on manorial and other types of local mortality data. However, due to a certain paucity of data he also underlines the significance of the

165 166 167

Twigg 1984: 57–68; Benedictow 2004: 126–45. Twigg 1984: 58; Benedictow 2004: 142, cf. 229–31. Twigg 1984: 72.

596

chapter fourteen

mortality rates for the beneficed clergy who had much the same territorial distribution but highly different characteristics as a social category. He concludes that this material bears “testimony, with a lack of precision but a compelling force, to a death rate of at least 30–5 per cent,” and that the “most judicious estimate of the national death-rate in 1348–9 in the present state of knowledge: 30–45 per cent.”168 In Hatcher’s view, the minimum mortality level was thus about a third of the population, the average apparently nearly 40 per cent. One should note that Hatcher in the gentlemanly tradition of Oxbridge academics seeks a cautious balance of the facts with respect to the mortality estimate, which makes J. Titow, the highly regarded English agricultural historian, remark in his review of the book that “it is difficult to see on the evidence here assembled, how it could have possibly been any lower.”169 Obviously, this level of mortality was much too high to be compatible with Twigg’s theory. Presumably, this is the reason Twigg turns instead to Russell’s pioneering monograph British Medieval Population of 1948 for his mortality data. This means that he must pass in silence by the comprehensive and sharp criticism of this work and also much fine new research that had been published in the following thirty-six years. Russell engages in little source-criticism and he makes a number of assumptions with respect to central demographic structures and developments that have been quite generally rejected in the discussion following the monograph’s publication. In 1969, T.H. Hollingsworth generously concluded that “Russell’s chief virtue, in fact, is that he gives others something to refute. All his figures may be altered eventually, but the debt to him will remain.”170 Or as Hatcher also elegantly formulates his view: “One of the major sources of nonconformist beliefs is the work of J.C. Russell.”171 For quite a number of solid scholarly reasons, the mortality figures have been subjected to particularly damaging criticism, for instance by M. Postan, G. Ohlin, and Hatcher.172 In this context, the very special nature of Russell’s material on mortality in the Black Death must be strongly emphasized. It relates to the mortality among tenants-in-chief, the supreme and extremely

168 169 170 171 172

Hatcher 1977: 21–6. Titow 1978: 466. Hollingsworth 1969: 58. Hatcher 1977: 13. Postan 1966: 561–2; Ohlin 1966: 78–80; Hatcher 1977: 23–4.

twigg’s alternative theory

597

exclusive class of feudal nobles who held land directly from the king, the barons of the realm; he based his research on a category of documents called inquisitions post mortem which effectuated the transfer of such feudal land following the death of the possessor (in the epidemic).173 The social unrepresentativeness for inference to general mortality and distribution of mortality according to age, gender and social class more generally is overwhelming. It contrasts sharply with Hatcher’s endeavours, in accordance with the basic tenets of sociology and demography, to base his general mortality estimate as much as possible on data representative of the social classes constituting the vast majority of the population. Technically, Russell used a population of tenants-in-chief of 505 persons of whom 138 or just over 27 per cent died, but this figure is beset by severe problems.174 The mortality of 138 tenants-in-chief is much too small to constitute a base for reliable statistical inferences and too unrepresentative both with respect to social class and with respect to age to be of any use for generalizations with respect to general mortality or mortality according to age or gender.175 Conspicuously, 23 per cent of the population of tenants-in-chief died in the following plague epidemic of 1361–2, despite general agreement that this was a much smaller epidemic: Hatcher is obviously right in his conclusion that this reflects the fact that the samples are too small to provide useful statistics.176 With respect to the younger age categories, this material is so tiny that estimates of mortality based on it or including it must be rejected as useless. It comprises no infants who, in the case of males according to Model West life table, level 4 (life expectancy at birth of 25 years), are liable to a normal mortality rate of 32 per cent,177 but according to these statistics astonishingly suffered no case of mortality in the year of the Black Death. Ages 1–5 are represented by three children of whom one died making for a mortality rate of 33 per cent for these five age categories, which is, of course, a valueless exercise in statistics. Only one of thirteen children of ages 6–10 died, producing an incredibly low mortality rate of 7 per cent in the Black Death, whilst, according to the

173 174 175 176 177

Russell 1948: 214–8. Russell 1948: 216. See, for instance, Hatcher 1977: 24. Cf. above: 421–2; Benedictow 2004: 342. Hatcher 1977: 23–4. Coale and Demeny 1983: 43. See, also, Benedictow 2004: 249, 350.

598

chapter fourteen

life table, normal mortality in these ages would be 19.5 per cent.178 According to Russell’s material, children of these ages had the luck to have only a small fraction of their normal mortality in the year of the Black Death. This is the reason I have previously rejected using the material gathered by Russell for mortality estimates.179 Hatcher points out that, according to evidence from the chronicles, the Black Death “struck mainly at people in the prime of life” but underlines carefully the great uncertainty associated with this type of evidence.180 However, a few years later Z. Razi’s study of the manor of Halesowen appeared, which Twigg could have put to good use. Here Razi concludes that “the child mortality in the Black Death was very heavy,” that, in fact, “child mortality in the plague must have been catastrophic.”181 Quite a number of pages away from his table, Russell points out that the “chroniclers have to tell of very heavy mortality of children.”182 However, using a wording echoing Russell’s own endeavours to minimize the impression of seriously flawed material183 and ignoring the severe criticism of it, Twigg notes with considerable understatement that this material constitutes “an unfortunately small sample,”184 (unfortunately) without specifying the methodological and source-critical implications of the characteristic “unfortunately.” This permits Twigg to proceed to use Russell’s material as if the sample is not “unfortunately small,” as if it is not too small and mortally flawed for almost any demographic use. Undaunted, Twigg goes on to use Russell’s estimates both of general mortality and age-distribution of mortality in the Black Death. He starts with age-distribution which, according to demographic science, is particularly demanding with respect to the quality of material. His point of departure is the valid argument that diseases vary in the mortality rates they inflict on specific age classes and “if this information is available and is accurate it can be of some assistance in helping to narrow the field in the identification of past epidemics.”185 Surprisingly,

178

See Benedictow 2004: 350. Benedictow 2004: 342, 350. 180 Hatcher 1977: 24. 181 Razi 1980: 104. 182 Rusell 1948: 231. 183 Russell 1948: 262. “The information from the table (10.13) suffers from being a relatively small sample.” 184 Twigg 1984: 63. 185 Twigg 1984: 63. 179

twigg’s alternative theory

599

Twigg pretends that such information is “available” and “accurate” in the form of Russell’s figures, which is at variance with all comments by other scholars. Russell concluded that the plague fell more heavily on older men than on the young.186 G. Ohlin, the demographer, challenged this conclusion, and demonstrated that Russell’s source-critical and statistical approaches were flawed and that age, according to this source material, made no difference to this particular risk of death in this social class,187 a piece of important information that was available to Twigg but is ignored or overlooked. This means that Twigg’s agespecific premise is untenable. However, this is only a disappointing beginning. Twigg goes on to argue that the Black Death and bubonic plague in India around 1900 were different diseases. He asserts that this can be demonstrated by comparing Russell’s table showing the age-distribution of the mortality in the countryside among the English baronial class in the Black Death in 1348–9 and a table produced by the IPRC in 1907 showing mortality in bubonic plague in Mumbai City among a caste-structured population consisting mainly of poor and destitute social classes.188 On this basis, he concludes that it is “clear without any elaboration that there is considerable difference between these two disease mortality patterns”189 and that this constitutes evidence that the Black Death could not have been bubonic plague, but must have been some other disease. Ignoring for the moment the devastating criticism of Russell’s material, this represents neglect of basic sociology and social science as integral parts of demography and epidemiology. It would have been sensational at least or rather inexplicable if these two tables had showed similar distribution of age-related mortality. The only acceptable usage of such a comparison is to demonstrate the differentiation of mortality pattern caused by great disparity in social, economic, political and cultural circumstances. It is exactly the absence of “elaboration” according to social science that permits Twigg to make this inference. On the same page, the IPRC gives mortality figures distributed according to religion showing strong differentiation of mortality according to this criterion 186

Russell 1948: 216–7. Ohlin 1966: 78–80. 188 Since Twigg does not provide a footnote to this comprehensive material published by the Commission this year (which may suggest a secondary source of information), I will give it: IPRC 1907g: 763. 189 Twigg 1984: 63–4. 187

600

chapter fourteen

alone.190 This use of Russell’s data is uncritically taken over and presented by Scott and Duncan as proof that the Black Death could not have been bubonic plague because in comparison to the epidemic realities in India “the overall mortality of bubonic plague is much lower” and “killed predominantly those in the 6–40 year age group.”191 If Scott and Duncan had taken interest in English medieval demography which is at the heart of the matter here, they would have known that in a population with an average life expectancy at birth of around 25 years the “6–40 year age group” constituted the predominant proportion of the population.192 Next, Twigg turns to the question of general population mortality. Russell dares to claim that the mortality of the nobility is representative of general population mortality. This assertion must be dismissed out of hand, which has been emphatically done by several scholars.193 Inference to general population mortality on the basis of this material is an obvious fallacy of the methodology of social science. The assertion flies in the face of one of the central findings of demography, namely that mortality across European society in time and space tends to be strongly skewed according to age, gender and social class. The general predilection of the Grim Reaper for infants, young children, poor and destitute people, and his relative lenience with the upper classes, are documented beyond all reasonable doubt or dispute. Russell argues, also erroneously, on the basis of the skewed age-structure of his data that real mortality must have been lower than the 27 per cent shown by his material (138 deaths among 505 tenants-in-chief).194 Using in addition the Poll-Tax registers of 1377 for retrospective analysis, in a way that has also been severely criticized,195 he concludes with a mortality rate for tenants-in-chief of 20 per cent, which is directly transformed into an estimate of general population mortality. This estimate is enthusiastically accepted by Twigg as the point of departure for his own discussion of the level of mortality, disregarding Hatcher’s serious

190 191 192 193

IPRC 1907g: 763–4. Scott and Duncan 2001: 111–2. See, for instance, Benedictow 2004: 249. See. e.g., Titow 1969: 68; Hatcher 1977: 22–4; Razi 1980: 100; Benedictow 2004:

342. 194

Russell 1948: 216, 230. Postan 1966: 561–2; Hatcher 1977: 13–4; Titow 1969: 67–8, 84–5; Benedictow 2004: 259–60. 195

twigg’s alternative theory

601

warning: “there are strong reasons for believing that Russell’s estimates of English population in 1348 and 1377 are gross understatements.”196 Russell’s estimate can be dismantled in various ways, not only on the basis of the small size of the material and of its lack of social diversity and representativeness. Twigg must be the only scholar in the last sixty years who accepted Russell’s contention that average household size in medieval England was 3.5 persons, and not 4.5, which alone makes for a difference of almost 30 per cent in population size. On this basis, Russell estimates England’s population on the eve of the Black Death at 3,757,000 inhabitants. This estimate differs sharply from Hatcher’s estimate in his widely admired account of 1977, a generation later, of “4.5–6 million, with the balance of possibilities pointing to the higher reaches of this range.” Already the following year, in a study therefore also available to Twigg, the minimum side of this estimate was revised upwards by E. Miller and Hatcher to 5–6 million people, an estimate with which R.M. Smith agreed a decade later.197 This development regarding pre-plague population estimates casts sharp light on the weakness inherent in Russell’s pre-plague population estimate. This is also the case with later estimates of late medieval English population size. In 1988, Hallam revised the population estimate further upwards to about six million inhabitants on the eve of the Black Death, with which again Smith agreed a few years later,198 and this is the present status of research on which there is broad agreement among British scholars in the field of medieval demography; Hatcher and Bailey also appear close to accepting this figure in 2001.199 On the ground of population estimates alone, mortality in the Black Death must have been very much higher than Russell claimed. According to Russell, the English population was around 2.25 million immediately following the Black Death,200 an estimate which is quite close to prevailing scholarly opinion. This means that, at the time Twigg wrote his monograph, combining the prevailing scholarly opinion on pre-plague population size and Russell’s post-plague population estimate, the mortality caused by the Black Death had reduced the population from 5–6 million to

196

Hatcher 1977: 13. Hatcher 1977: 68; Hatcher and Miller 1978: 29; Smith 1988: 191. Cf. Miller and Hatcher 1995: 393; Hatcher and Bailey 2001: 31. 198 Hallam 1988: 536–7; Smith 1991: 48–9. 199 Hatcher and Bailey 2001: 31. 200 Russell 1948: 263. 197

602

chapter fourteen

2.25 million, or by 46–62.5 per cent. Shortly afterwards, the population estimate of about six million on the eve of the Black Death was confirmed and accepted, meaning that the figure of 62.5 per cent was confirmed according to the premises laid down here. This is exactly the figure at which I arrived on the basis of my analysis of seventy-nine manorial studies,201 most of which were available to Twigg at the time he wrote his monograph. Why did Twigg not collect the data on manorial mortality rates as I did, providing a broad picture of mortality among the peasant classes who constituted the vast majority of the English population? As my data unequivocally show, the mortality rate among the customary tenants who represent the upper classes of peasant society must have been in the order of 55 per cent. Supermortality among the rural proletariat, the all-but-landless classes and among children and women means that the real population mortality rate must have been significantly higher.202 In addition, at the time Russell and Twigg wrote their monographs the mortality rates of the beneficed parish clergy was known to be at least or close to 40 per cent, which Russell in reality gives up on explaining.203 Twigg makes considerable efforts to undermine the mortality studies based on institutions of the beneficed clergy during the Black Death. He starts by asserting erroneously: “It is generally accepted that the vacation of a benefice automatically implies the death of the incumbent and some writers have assumed that all vacations during 1348–9 were due to death from plague.”204 This has, as mentioned, certainly not been true since Seebohm’s work of 1865 and possibly until Gasquet’s monograph appeared in 1893 where it is made clear that vacancies were due not only to death but also to “exchange, or resignation” and that such cases must be deducted.205 Twigg’s statement is followed by a reference to Thompson’s work of 1947 on the organization of the English clergy in the Late Middle Ages. However, the point that vacancies were due also to resignations, exchanges of livings, pluralities206 and absenteeism is strongly emphasized by Thompson in his

201

Benedictow 2004: 360–7. Benedictow 2004: 362–77. 203 Russell 1948: 221–2, 230. 204 Twigg 1984: 59. 205 Gasquet 1908: 86. 206 The concept of plurality refers to the quite frequent occurrence that the incumbent also held (an)other benefice(s) and was represented in the parish by his vicar. 202

twigg’s alternative theory

603

pioneering studies of 1911 and 1914 of the registers of institutions of the dioceses of Lincoln and York.207 This has since been generally taken into account by scholars; Hatcher for example states that “one has to be especially careful to eliminate all vacancies excepting those arising from death.”208 However, if Twigg had mentioned Thompson’s two excellent studies, it would be difficult for him to avoid mentioning that after having taken these problems of resignations of vacancies into account and deducted them from the material, Thompson still found mortality rates of 40.2 and 44.2 per cent respectively, without taking into account institutions in vacancies caused by the Black Death performed in the following couple of years, which would have added substantially to the mortality rates (see above). Lunn’s study of the diocese of Coventry and Lichfield’s bishop’s register where also all resignations are noted have produced a mortality rate of 40.1 per cent, likewise without taking into account Black Death-related institutions in vacancies which were filled in the following couple of years. Pickard found a mortality rate among parish priests in the diocese of Exeter of 51.5 per cent in the period of the Black Death, but when surplus institutions after deduction of normal mortality in the following years are taken into account, the real mortality rate appears to have been about ten percentage points higher. Resignations have been found in the diocese of Ely’s bishop’s register and the two studies performed on them have reached mortality rates of 57 and 60 per cent respectively, which should make mortality at around at least the same level certain whatever the possible inaccuracy of the registration of resignations and other causes of vacancies.209 In sharp contrast to Twigg’s account, Hatcher concluded in 1977 that “great weight must be attached to a revised average death-rate of around 35–40 per cent for beneficed clergy.”210 None of these mortality figures for the beneficed clergy in various dioceses is below 40 per cent and the average must be something like 45 per cent. Thorough source-critical and epidemiological discussion of the mortality among the beneficed clergy in my monograph on the Black Death led me to conclude that the available data summarized in Table 31211 should be considered “minima or more likely

207 208 209 210 211

Thompson 1911: 303–4, 315–6; Thompson 1914: 97–102. Hatcher 1977: 25. Benedictow 2004: 354–7. Hatcher 1977: 25. Benedictow 2004: 356.

604

chapter fourteen

underestimations,”212 with the implied suggestion that the real mortality rate was on the order of 50 per cent. After having gone thoroughly over the studies and evidence cited above a second time, above I conclude that the mortality rate probably was even higher when BlackDeath-related vacancies which were filled in the following years are consistently taken into account. The discrepancy between these estimates and Hatcher’s is not the important point here, which is what Twigg should have known and taken into serious consideration at the time he was writing his monograph, and the fact that the available estimates of mortality among the parish clergy would have had damaging consequences for his theory. How could it be that the mortality of tenants-in-chief in the Black Death should be under half of the average mortality among the regular clergy of a dozen monastic houses built of stone like the castles of the lay lords, namely 45 per cent?213 Twigg mentions Hatcher’s population mortality estimate of 1977 of 30–45 per cent, especially his central estimate of 35–40 per cent but neglects to take it into account.214 The way this is justified should be considered: Twigg asserts that “Hatcher considered that the estimate produced by the E.A. Kosminsky (1955) of a national death rate of 30–45 per cent is the most reasonable one.” This is not correct, the estimate is entirely Hatcher’s own based on an independent, cogent and thorough discussion of sources, studies, data and problems.215 Kosminsky, the Soviet historian of the Academy of Sciences in Moscow, does not make any population estimate for any time in the High Middle Ages or in the Late Middle Ages. On the contrary, Kosminsky rejects the notion that there was a long-term late medieval sharp population reduction. He acknowledges that there was a “decrease in population in the 14th and 15th centuries,” however, he maintains that it was not “directly related to the Black Death of 1348–9 and the epidemics of the 1360s” since “the decline in population began earlier than the Black Death, and that it continued longer than could be accounted for by the results of the plague.” Instead, Kosminsky launches his own doctrinaire Marxist explanation of a population decline based on the evolution of feudal rent, class struggle, a crisis of feudalism, the development of

212 213 214 215

Benedictow 2004: 343–58. Hatcher 1977: 22. Twigg 1984: 72; Hatcher 1977: 25. Hatcher 1977: 21–5.

twigg’s alternative theory

605

“the labour service system,” and “especially burdensome forms of exploitation,” “a further intensification of serfdom,” “the most intense feudal exploitation of the English peasantry” and, finally, the conclusion: “The growth of feudal exploitation began to exhaust peasant agriculture and at the same time to whittle down the productive forces of feudal society, destroying the conditions for reproduction of the labour force.”216 Thus, according to Kosminsky, the real reason for the late medieval population decline, in the modest form which he accepts, was caused by the intense exploitation of the peasantry within the framework of feudal society and its detrimental effects on reproduction among the peasant classes. Does Twigg cite this misleading assertion about the source of Hatcher’s mortality estimate because he needs to discredit Hatcher’s estimate, since it is incompatible with his anthrax theory? Why does he associate Hatcher’s estimate with Kosminsky’s dogmatic Marxist analysis which Hatcher, in fact, dismisses out of hand?217 Only four years after Twigg’s monograph was published, Smith increased the estimate of mortality in the Black Death to around 50 per cent on the basis of much the same data that were available to Twigg.218 It was just a question of taking a serious and unprejudiced interest in the subject. Without going into the matter in further detail, we can be certain that the available data at the time Twigg wrote his monograph had made it clear that the level of mortality, the generalized mortality rate in the Black Death, was very much higher than Russell had claimed. This explains Twigg’s curious emergency landing in Russell’s untenable and obsolete mortality figures: all other current and reliable data and discussions of the subject at the time he was writing his monograph showed such high mortality rates in the Black Death that they would directly invalidate his anthrax theory. Only this can explain Twigg’s statement that Earlier estimates of a death rate of one- to two-thirds of the population through plague (Seebohm, 1865; Gasquet 1908) have been reviewed and modern work shows that the population had begun to decline before

216 Kosminsky 1955: 14, 22, 32. He repeats this analysis a few years later, see Kosminsky 1957. 217 Hatcher 1977: 12–3. 218 Smith 1988: 208–9. Cf. Benedictow 2004: 342–77.

606

chapter fourteen 1348 and that the plague losses in 1348–50 were perhaps nearer 20 per cent of the population (Russell, 1948).219

In order to save his theory, Twigg must compare Russell’s figures, which at the time he wrote his book were more than a generation old, and throughout this period had been generally rejected, with studies published in 1865 and 1908, passing by all relevant later scholarly works, and all scholarly work on the topic between 1948 and 1984. Instead, it should have been clear to Twigg for quite a number of years that Seebohm’s and Gasquet’s estimates were still respectable, even had gained in respectability, especially if it is taken into account that they both tended to give priority to a mortality rate of around 50 per cent, the magnitude of the population loss in the Black Death which Smith arrived at in 1988.220 The pre-plague population estimate of five million used by Gasquet is also much closer to modern population estimates than Russell’s and the post-plague estimate of something like 2.5 million corresponds quite closely to modern estimates. However, Russell’s untenable and generally rejected estimate was still too high for Twigg and could still serve as grounds for falsification of his theory or at least for rendering it highly improbable. Taking into account the normal lethality rate of anthrax, a population mortality rate of 20 per cent would imply quite unrealistically that every person in England of whatever social class, gender or age, had eaten anthraxcontaminated meat. This is the reason Twigg needs arguments for further reductions of the estimate of the specific mortality caused by the Black Death. He argues that one must also take into account “the presence of a variety of infectious and other diseases, the twenty per cent reduction of the population must include these and cannot be attributed to plague alone.”221 Twigg wisely does not attempt to indicate how many percentage points he would like to deduct on the basis of this argument but leaves it to the reader to make a substantial further deduction on the impression of a plethora of serious infectious diseases and other diseases that affected population mortality. According to demographic science, Twigg’s argument here really concerns normal mortality in the period which should be deducted in order to produce an estimate of the net mortality effect of plague in the period of the

219 220 221

Twigg 1984: 70–1. Hollingsworth 1969: 264; Gasquet 1908: 225–7, 237–8. Twigg 1984: 72.

twigg’s alternative theory

607

Black Death. However, Russell has already deducted normal mortality! Assuming (erroneously) that the Black Death lasted for three years, 1348–50222 he states: “The reduction of the initial loss to 20 per cent proceeds from better calculation of plague losses, which could take into account age specific mortality […], discounting of ordinary mortality of the three years and avoidance of other statistical difficulties.”223 Thus, in order to produce as low a mortality rate as possible, Twigg deducts twice the normal mortality in the period of the Black Death. The mortality rate of 20 per cent and the information on deductions stand on the same page and in direct connection as qualifying explanations of the concluding mortality rate. Correcting for age-related bias in his original material, Russell reduced his original estimate of mortality among tenants-in chief from 27.3 per cent to 23.6, which shows that Russell made a deduction for ordinary mortality in the three plague years of 3.6 per cent.224 Russell reduced this mortality estimate further, as mentioned, to 20 per cent by using the Poll-Tax registers of 1377 for retrospective analysis. This means that Twigg would like to arrive at a net plague mortality figure of 16.4 per cent. However, fearing that this is not a sufficiently low mortality rate to be suitable for making a convincing case for anthrax, Twigg presents the following speculative argument: “It is not beyond the bounds of possibility that more than one new and exceptionally virulent disease organism invaded Europe during this period.”225 One may legitimately wonder what Twigg thinks he can gain for the defence

222 In England, the Black Death broke out shortly before 24 June 1348 and lasted into the late autumn of 1349 that is, somewhat less than a year and a half. 223 Russell 1948: 367. 224 Russell 1948: 216. Distributed on three years, Russell’s deduction for normal mortality implies a notion of normal yearly mortality at the time of c. 1.2 per cent, a figure I find difficult to understand, although it presumably relates to the untenably low normal mortality rates, also according to Russell’s own reactions, emerging from his material on tenants-in-chief. Russell 1948: 210–1. A normal annual mortality rate of 3.6 per cent is quite usual for the early modern period, especially the eighteenth century, in Western and Northern Europe. In an epoch-making paper for medieval demographic research, Hatcher has shown beyond any doubt that late-medieval normal or average mortality rates were much higher than corresponding early-modern mortality rates. Hatcher 2003. His views correspond closely to my own views, Benedictow 1996b: 29–91, 189–91. Benedictow 1996c: 156–74; Benedictow 2003: 238–44; Benedictow 2004: 250–6. Russell’s deduction for normal yearly mortality and Twigg’s should have been significantly higher. 225 Twigg 1984: 72.

608

chapter fourteen

of his theory by forwarding this arbitrary idea without any empirical or evidentiary support. Concluding Remarks In a paper published in 1996, Scott and Duncan supported or were at least attracted to Twigg’s anthrax theory with respect to their discussion of an epidemic in Penrith and the surrounding region in the 1590s which contemporaries called plague. In their discussion of this theory, the difficulties remain unresolved in incompatible statements on the characteristic or defining features of anthrax. They start by asserting that anthrax “can be spread easily from person to person”226 and make on this basis a number of quite strange speculative efforts in order to produce an epidemiological theory to this effect. However, on the next page they point out that “human infection is almost invariably from animal sources.”227 Clearly, Scott and Duncan eventually reconsidered their support for Twigg’s anthrax theory and invented their own theory. All the other advocates of alternative theories reject Twigg’s theory (as they all reject each other’s theories). Karlsson rejects it on the ground that “no mortality of any kind of animals is ever mentioned in the [Icelandic] annals.”228 This is not correct: serious epizootics causing great mortality among the cattle and the sheep respectively in the island are mentioned in the annals, in fact they were so serious that they caused widespread starvation and also considerable mortality among the human population since “many farmsteads were deserted.” As it is said that this occurred when “no ship arrived from Norway,” the source of the infections must have been internal in the island.229 Twigg has presented an alternative theory of the microbiological nature of historical plague with such significant epidemiological and historical flaws that it has been generally rejected as an obviously untenable theory. Nonetheless, Karlsson, Scott and Duncan, and Cohn credit him with the great epidemiological erudition and insight to have shown in a definite way that the Black Death could not have been

226 227 228 229

Scott and Duncan 1996: 18. Scott and Duncan 1996: 19. Karlsson 1996: 281. See, for instance, Islandske Annaler 1888: 324, 383.

twigg’s alternative theory

609

rat-borne bubonic plague. The reason is that Twigg’s rejection of historical plagues as being bubonic plague functions as a justification for the construction of their alternative theories.230

230 Cohn asserts that I, like some other named scholars, “cite Twigg in their bibliographies but in their texts give his arguments no hearing at all.” Cohn 2002: 53. This is not true, as all other of his comments on my thesis. At the time I wrote my thesis, Twigg’s theory had not received any favourable comments from other scholars, which constituted a case for not focusing on it in a thesis aimed at clarifying the microbiological identity of medieval plague in the Nordic countries. In this situation, it appeared appropriate to focus on what disease medieval plague could have been and not on what was agreed that it could not have been. However, I have not passed Twigg’s theory by in silence as Cohn asserts. I point out that the “suggestion of anthrax has not attracted any support for obvious reasons” and assume in good faith that it is a good argument that, “according to the standard works on microbiology, ‘the mortality rate is low and the great majority recover in a few days’ .”230 At the time, I could not foresee the necessity or potential usefulness of detailing my views on Twigg’s monograph. Nunc factum est.

CHAPTER FIFTEEN

THE ALTERNATIVE THEORY OF SCOTT AND DUNCAN Introduction Scott and Duncan are an historian (historical demographer) and biologist respectively. They present their alternative theory in two works with the character of monographs published in 2001 and 2004. The first monograph must be considered the principal work; the second is mainly an abridged and popularized version of the first. However, it also contains new developments and changes of opinion on important points which remain empirically unsubstantiated and unexplained. These works have an academically unsatisfactory form. In the first monograph they do not provide the usual apparatus of footnotes, but like Twigg, refer to works in parentheses in the running text without indication of pages, which makes the task of checking the correctness of the references extremely difficult and time-consuming. It is also a form that is poorly suited to multiple references and for enlarging or deepening comments. It is not possible within a reasonable time frame to read whole monographs or papers in order to hunt down purported passages of support or objects of criticism. It might be argued that scholars who know the relevant studies intimately after decades of diligent work in this field of research will have great advantages, but this should not be the case. According to the standards of scholarly work, every point or assertion should be easily testable by students as well as by scholars, by every reader irrespective of background. This problem is aggravated because many assertions or pieces of purported information are not accompanied by any reference. The first book contains a bibliography, but many of the works entered in it are not referred to in the text and quite a number have no direct bearing on their alternative theory. In their second monograph, Scott and Duncan have dispensed completely with references and bibliography. It is implied that one should start by reading their first monograph on this topic, but this makes the idea of writing a popularized version for amateur historians and enthusiastic readers of history a bit pointless, and so this monograph also has an unsatisfactory form as popularization. This contrasts

the alternative theory of scott and duncan

611

sharply with the pervasive effort made by Ziegler to make his popular history of the Black Death in England readily testable (although he was not an historian by profession). In the prefaces to their monographs, Scott and Duncan refer to Twigg as a “stalwart friend,” “salute” his “pioneering work and acknowledge gratefully his generous help in the early stages of this project.”1 They also state that he “was the first to recognize that the Black Death was not an outbreak of bubonic plague,” presenting this conclusion as a point not open to doubt, as would be the ordinary scholarly attitude for good methodological reasons. Inevitably, this attitude means that they accept unquestioningly his arguments against the bubonic plague theory and base this part of their case on his monograph instead of reading the primary research studies and the standard works on plague and acquiring independent knowledge (see below). These arguments are meticulously discussed above both in Part 2, “Basic Conditions for Bubonic Plague in Medieval Europe” and in relation to Twigg’s work and theory in the preceding chapter, and have been shown to be generally untenable or invalid. Here the focus will therefore be on Scott and Duncan’s theory. However, one should note that, according to their information, the alternative theory of filoviridal disease was suggested by Twigg.2 Since this category of disease is as different from anthrax as well-nigh possible, this implies that Twigg not only has rejected his own theory of anthrax but also openly admits that this idea must have been as far intellectually astray in the academic “woods so wild” as well-nigh possible. It is not clear why his rejection of the bubonicplague theory should be any more trustworthy than his sudden radically different suggestion of an alternative theory. Disparaging Views of Historians and Physicians: Motive and Objective Like other scholars who wish to introduce a revolutionary new theory in a field of research that has been developed by large numbers of dedicated scholars over several generations, Scott and Duncan have a lot of rejecting to do. They make a number of sweeping negative assertions about the work of unnamed plague scholars in general. All or at least 1 2

Scott and Duncan 2001: xiii; Scott and Duncan 2004: viii. Scott and Duncan 2004: viii.

612

chapter fifteen

the great majority of scholars who have been engaged in primary plague research and who have written the outstanding standard text books on plague and their historical perspectives are inevitably implicated. All these assertions are untrue, for instance: Nobody compared the two diseases [historical and modern plague: my insertion] objectively and for the whole of the twentieth century this view, based solely on the appearance of one symptom [buboes: my insertion], was written on tablets of stone and universally accepted without question. […] No scientist should base conclusions or develop a hypothesis on the basis of a single observation or experiment. No doctor would make a diagnosis on the basis of a single symptom: instead he would examine his patient carefully […].3

The need to present such untenable accusations is revealing. All the authors of the standard works on plague, Simpson, Sticker, Wu LienTeh, Hirst, Pollitzer and Butler, present a wide range of clinical manifestations of plague and also acknowledge that this was the case with historical plague epidemics. See, for instance, Hirst’s discussion of this subject in his monograph. Even Hirst’s citation of the contemporary Irish Friar John Clyn’s description of plague cases in the Black Death contains five important clinical features (my numbering): “[…] many died of [1] boils and abscesses, and [2] pustules on their shins and [3] under their armpits; [4] others frantic with pain in their head, and [5] others spitting blood […].” When medieval chroniclers comment on the Black Death’s physical manifestations they quite often give several clinical features. When Hirst concludes his discussion of this topic, he does not refer to one clinical feature, but states: “There can be no doubt, however, judging from the detailed descriptions that have come down to us, of the clinical identity of the plagues of ancient and modern times.” Hirst also mentions other distinguishing features, comparing the plague pandemics of the Early Middle Ages, the Late Middle Ages and Early Modern Ages, and the modern pandemic that started in 1894: “All three pandemics spread along the main lines of communication in a similar way at a similar rate; it seems improbable, therefore, that their epidemiology can really be very different.”4 To my knowledge, no scholar has focused on buboes alone, although, as shown above, the normal occurrence of buboes in diseased persons constitutes a defining feature of bubonic plague and, despite Scott and 3 4

Scott and Duncan 2004: 167. Hirst 1953: 13, 121–2.

the alternative theory of scott and duncan

613

Duncan’s disparaging remarks, would suffice as a clinical criterion allowing certain identification of bubonic plague. This is confirmed by their own source on bubonic plague, a chapter in a general textbook on infectious diseases by A.B. Christie5 (see below). Scott and Duncan go on to make generalized assertions of intellectual incompetence and dishonesty against all scholars who have supported the bubonic plague theory: Their universal and unquestioning acceptance of the view that […] plague was no more than a series of epidemics of bubonic plague […]. This universal and unquestioning acceptance in about 1900 of the view that haemorrhagic plague [their own theory presented as indisputable and uncontroversial truth] was no more than a series of epidemics of bubonic plague was a complete reversal of the opinion that had previously been held for over 500 years [completely untrue], and the history books had to be rewritten. Various tales about the plagues had to be embroidered or even adapted to fit with the new story of bubonic plague.6 Once blind acceptance of bubonic plague has been abandoned […].7

Not only are medical scholars the subject of such sweeping denigrating assertions, historians are also collectively belittled for their massive incompetence and/or intellectual dishonesty, in this case on the basis of two arguments (my numbering): Unfortunately, historians of Europe in the 20th century, almost universally, have concluded that all plagues in the Middle Ages were bubonic, in spite of the fact that [1] the people at that time saw clearly that it spread person-to person and [2], even in the 14th century, had already instituted specific quarantine periods. A major objective of this book is to examine the historical facts dispassionately, eschewing any preconceived notion […].8

The subject of contemporary views of epidemic disease has been discussed above on several occasions.9 In relation to this quotation, it must be said that one of the conspicuous features of Scott and Duncan’s monographs is their negligence of historical epidemiology, how people in the past attempted to understand the mass occurrence of disease and 5 6 7 8 9

Christie 1980: 762. Scott and Duncan 2004: 167–8. Scott and Duncan 2001: 269. Scott and Duncan 2001: 7. Above: 78–82, 342–5.

614

chapter fifteen

mortality in an area. However, small glimpses of this subject slip out, inadvertently as it may seem, a few times in their works, implying that they actually have some real knowledge of it. This occurs first in their paper of 1996, before their alternative theory was developed, and again in their first monograph when they cite this paragraph verbatim: […] it was believed that ‘miasma’ or noxious vapours in the atmosphere were responsible for the disease, and that miasma could be retained in clothes or bedding for long periods and transported, possibly by domestic animals, from house to house (Slack 1985).10

In 2001, they remembered what they had known in 1996 on the basis of Slack’s fine presentation of contemporary miasmatic views and their behavioural consequences. Seventy-five pages later in the same monograph, there is another sudden corroborative glimpse, and this time in an original phrase: The general populace believed that they caught the plague because the infection was in the air of the place.11

This glimpse of historical epidemiology is prompted by their wish to explain away contemporary notions of the short time elapsing between the infection of a person by plague and the outbreak of the disease, which is inherent in miasmatic theory, but runs contrary to their arbitrary assertion of a very long time of incubation (see below). Then, another sixty pages later, they describe the anti-epidemic measures taken by the rector of Eyam: When the plague was over, Mompesson ordered that all woollen clothing and bedding should be burnt and he set an example by burning his own effects so that, as he said in a letter to his uncle, he had scarcely enough to clothe himself. Presumably they believed that the infection might be contained in the clothing because the symptoms of the pestilence could reappear 3 weeks after a person had died.12

These words make no impression on Scott and Duncan, and on the next page they reiterate their mantra: “It is clear from the foregoing that at the time of the epidemic the people of Eyam believed that it was caused by person-to-person contact.” These glimpses reveal the highly problematic character of their repeated assertions that people of the

10 11 12

Scott, Duncan and Duncan 1996: 19; Scott and Duncan 2001: 145. Scott and Duncan 2001: 220. Scott and Duncan 2001: 281.

the alternative theory of scott and duncan

615

Middle Ages or the Early Modern Period “saw clearly” that plague spread by interhuman cross-infection. Instead, when medieval and early modern people did not believe that epidemic disease was God’s punishment for their sins, they would alternatively or concurrently believe or think that it was caused by miasma. According to miasmatic theory, miasma was composed of poisonous vapours from rotting matter which rose from the ground and were spread by the wind. Miasma could stick to clothing, bedding, and other objects used by sick people that were called fomites: people could contract disease from touching such fomites. In contrast to Scott’s and Duncan’s repeated assertions, contemporary people’s impressions of what they actually observed contain close reflections of what modern research on bubonic plague has clarified, namely that bubonic plague is spread by clothing, bedding, luggage and merchandise (see above). What is new is the modern knowledge that the normal vehicle of spread is infected rat fleas concealed there. This explains also early notions of the usefulness of quarantines, of isolation of diseased persons and objects used by them, including merchandise, and prohibition of trade with areas where epidemics were raging. As now can clearly be seen, their assertions that historians have not observed the obvious are unjustified and untenable. Scott and Duncan refer to Slack’s magisterial monograph on plague in Tudor and Stuart England. This monograph contains a broad presentation of contemporary people’s opinions on the causation of epidemic disease, vast material on the empirical reflections of bubonic plague, and many citations of primary studies and standard works on plague which permit the intensive use of comparative methodology for identification of the disease, and should have shown that Slack and other historians are competent and intellectually honest persons who have come to support the bubonic-plague theory for good reasons. The Material Scholarly Basis of Scott and Duncan’s Alternative Theory Like Twigg, Scott and Duncan have a strong predilection for outdated works and signally ignore works representing current research. This is the case with their prolific and enthusiastic use of Creighton’s monograph on the History of Epidemics in Britain (to the Extinction of Plague) of 1891. Scott and Duncan praise this work, not from the perspective of

616

chapter fifteen

the history of medicine, but uncritically as an outstanding work of undiminished value, and in the same passage, anoint him as the “doyen of epidemiologists”: His approach in his classic work, which was to provide a chronicle of death and disease in the life and people of England, was that of a professional historian and he worked with great care on his sources. We have relied heavily on his data series in our earlier work.13

No modern medievalist would suggest that Creighton was fond of source-criticism and his use of medieval chroniclers is characterized by gross naivety; but it is only fair to add that Creighton was not an historian, as Scott and Duncan maintain, but a physician and anatomist, a fact clearly stated on the front page of his monograph. Creighton has an agenda: among British medical scholars he was the last unflinching champion of miasmatic theory of epidemic disease and spent much of his academic life in the defence of this theory.14 His relation to medical science is characterized by proto-scientific attitudes and an incomplete scientific methodology. Inevitably, his scholarly beliefs and agenda caused to include in his work much material, discussions and views that today would be unceremoniously rejected as unscientific and untenable. Carmichael sums up this problem thus: “Scott and Duncan borrow heavily from Charles Creighton’s History of Epidemics in the British Isles (1891–4), a famous compendium made by a relatively unknown medical practitioner who was bent on gathering evidence against the germ theory of disease.”15 Even the IPRC, who were fully occupied with their battle against plague, felt obliged to carry out specific experiments to disprove Creighton’s views, since he still enjoyed some authority in some quarters at the time: The belief that the infection of plague resides in the soil has been entertained and advocated by Creighton (1905) who adopted it in his History of Epidemics in Britain (1891) and reaffirmed it in 1905 after having paid a visit of investigation to India. He thought the infection rose to the interior of dwellings with he ground air and was commonly taken in by man with the breath.16

13

Scott and Duncan 2001: 15. See, for instance, Hirst 1953: 57, 74, 93. This point is made also by Carmichael 2003: 255. 15 Carmichael 2003: 255. 16 IPRC 1907f: 711. 14

the alternative theory of scott and duncan

617

The fact that rats or guinea pigs contracted plague only in the presence of rat fleas was demonstrated definitely and indisputably in the Commission’s first paper.17 Scott and Duncan refer to or cite Creighton’s monograph a total of fifty-six times,18 not once so much as intimating a word about its problematic nature. This puts in perspective also Scott and Duncan’s assertion that Creighton “probably knew something about the biology of bubonic plague when he was writing in 1891, because this was being elucidated at the time.”19 In fact the first breakthrough on plague biology was Yersin’s identification of the plague bacterium in 1894, three years after the first publication of Creighton’s monograph,20 and concomitantly with the reprint in 1894 (with the second volume taking the history of epidemics in England to Creighton’s own time). It would take two decades before the blocking mechanism that makes fleas infective was discovered and this crucial biological aspect of the transmission of bubonic plague was clarified. Scott and Duncan maintain that Creighton should “probably” have known something about the biology of plague before anything was known about it, and the evidence on which the high level of tenability of “probable” is based, remains inexplicable. Indeed, at the time Creighton wrote his monograph(s) he rejected the germ theory of epidemic disease, and since he continued to do so his whole life, and did so specifically in the case of bubonic plague, the scholarly elucidation of the biology of bubonic plague was of no consequence to his views. The theory of miasmatic epidemiology is the underpinning of all his work.21 With this background, Scott and Duncan’s comment on W. Furness’s book on The History of Penrith which was published in 1894, three years after Creighton’s monograph, becomes interesting: “it was written at a time before the true biology of bubonic plague had been

17

IPRC 1906a: 425–82. Scott and Duncan 2001: 15, 80, 86, 110–1, 149–50, 152, 159–60, 163, 165–6, 170, 173, 183, 189, 193–5, 197–9, 201, 204–6, 209, 212, 216, 218–20, 228, 243, 245, 257, 261, 362. 19 Scott and Duncan 2001: 15. 20 Yersin 1894: 664–7. Cf., for instance, Simpson 1905: 64; Sticker 1910: 5; Lien-Teh 1936a: 21–3; Hirst 1953: 106–9; Butler 1983: 15–22, Butler has, in fact, written a short biography of Yersin on pages 10–25. 21 This can be seen also from the subsequent reprint of the first volume in 1894 together with the new second volume which takes Britain’s epidemic history “to the present time.” See the bibliography here. 18

618

chapter fifteen

elucidated.”22 They are in such urgent need of arguments that this repeatedly overshadows their better judgement. Scott and Duncan argue as if they do not know anything about Creighton, his scholarly position and ambitions. The point is that they wish to argue that Creighton’s monograph can be taken in support of their own theory of the nature of historical plague epidemics which likewise is not based on any role for black rats and their fleas, because it is based on miasmatic theory. In other words, they wish to make a case for why they can base their alternative theory on much material that is structured and interpreted according to miasmatic epidemiological theory.23 Since Creighton knew only one type of contagion, namely miasma, he “did not believe in the specificity of epidemic disease”: any disease could be plague or develop into plague, which makes his monograph very special and fraught with dangers. Thus, for Creighton “plague was a kind of typhus of the soil, typhus being due to poison generated in unhealthy air”; typhus could, for instance, easily develop into bubonic plague, and bubonic plague was also “due to a poison emanating from putrescent corpses.” “Not only could typhus be transmuted into plague, but he wrote in 1894 of ‘the breeding of typhus from the effluvia of dysentery. ’”24 Creighton comments on the second plague epidemic of 1361–2 by speaking of a “recrudescence, then, of the seeds of plague in English soil […],” which shows that he considered both the Black Death and the subsequent wave of plague was caused by miasmatic gases emanating from the soil.25 Scott and Duncan have read and used this passage in Creighton’s work and therefore know this well, but will not share this information with their readers. They present his assertion that this second plague, at least in some places, among them Florence, was as destructive as the Black Death, disregarding or overlooking the fact that Creighton’s references are to the contemporary Florentine authors Petrarch and Boccaccio,26 and that neither of them have the second plague in mind, but the first, the Black Death.27 The assertion about mortality in the second plague in Florence is at variance with

22

Scott and Duncan 2001: 117. Scott and Duncan 2001: 15. 24 Hirst 1953: 74–5. 25 Creigthon 1891: 203. 26 Scott and Duncan 2001: 110. 27 Boccaccio wrote Il Decamerone around 1350; Petrarch never lived in Florence because his father had been exiled from the city, but mostly in Avignon, although he visited Florence briefly in 1350 when he also befriended Boccaccio. 23

the alternative theory of scott and duncan

619

Herlihy and Klapisch-Zuber’s modern standard work on late medieval Florentine demography.28 The assertion regarding levels of mortality in the two first plague epidemics in Florence is also incompatible with E. Fiumi’s classic studies on late medieval Florentine demography.29 Since Herlihy and Klapisch-Zuber’s monograph was published in 1978 and Fiumi’s studies in the 1950s, they were readily available to Scott and Duncan. Creighton accuses bacteriologists of “disdaining any discussion of the possibility of a tertium quid, such as Pettenkofer’s soil activation factor or Sydenham’s mysterious atmospheric influence.”30 This puts in perspective the very problematic nature of Scott and Duncan’s repeated assertions that people in the sixteenth century were fully aware that disease spread by “person-to-person contact.” Their monograph’s index contains a wide array of words like “measles,” “malaria,” and “household contact rate,” but the most important term of the historical medicine and epidemiology on which they rely, “miasma,” does not appear. When Scott and Duncan inform their readers that they “have relied heavily on his [Creighton’s: my insertion] data series in our earlier work,” this shows that they base their work on unscientific and obsolete data which inevitably imbue their work with protoscientific miasmatic analyses and historical material with dire consequences for tenability and validity. This also puts in perspective the fact that there is hardly any concrete reflection in Scott and Duncan’s monographs of acquaintance with modern research literature on bubonic plague. This pertains not only to the primary medical research literature but also to the fine standard medical works on bubonic plague written by outstanding scholars with great first-hand experience of plague in the field and in the laboratories and unrivalled knowledge of the research literature on this disease. This is also the case with the standard works cited in their bibliography, namely Pollitzer 1954, Wu Lien-Teh 1926, and Wu Lien-Teh, Chun, Pollitzer et al. 1936. Hirst’s and Sticker’s central standard works and E.-R. Brygoo’s small monograph summarizing French medical plague researchers’ comprehensive and important work in Madagascar are not even mentioned in their bibliography. Only one work of the IPRC’s huge production of pioneering plague studies is mentioned with a 28 29 30

Herlihy and Klapisch-Zuber 1978: 195–6. Fiumi 1950: 89–94, 110–1, 119–58; Fiumi 1958: 480–1. Hirst 1953: 93.

620

chapter fifteen

specific reference, but in a way that makes it (almost) certain that they have not read it (see below), and by implication anything else from this important corpus of primary research on bubonic plague. When standard works on plague are mentioned, for instance, “Wu, 1926” = Wu Lien-Teh’s standard work on primary pneumonic plague, or “Wu et al., 1936” the standard work co-authored by Wu Lien-Teh, J.W.C. Chun, R. Pollitzer and C.Y. Wu in 1936,31 their assertions as to what they contain are erroneous, which may be taken to indicate that they have not read them. “Wu et al., 1936” is a confused reference to two different authors named Wu, namely Wu Lien-Teh and C.Y. Wu, who wrote four of the chapters or sections, an indication that they have not held the monograph in their hands. In this reference, the opinion is attributed to the author that the high mortality of 50 per cent in the epidemic of bubonic plague in Marseilles 1720–2 could be due to the fact “that pneumonic plague was responsible for a high proportion of the deaths.”32 In these chapters, nothing to this effect is stated in any of the three instances where this epidemic in Marseilles is mentioned.33 It is a fictitious reference serving the purpose of defending Scott and Duncan’s assertion that mortality rates in bubonic plague are generally small in order to hide the inadequacy of their own alternative theory for explaining high mortality rates (see below). Other references, for instance, to Chinese and Indian plague history, are similarly erroneous.34

31

Scott and Duncan 2001: 7. Cf. ibid. 47. Scott and Duncan 2001: 341. 33 Wu Lien-Teh 1936a: 5; Wu Lien-Teh 1936b: 226; C.Y. Wu 1936b: 511. 34 “[…] the disease [bubonic plague] has been identified (presumably correctly) and recorded in detail from China since ad 37 (Wu, 1926, Wu et al., 1936) […],” “there are said to have been 233 outbreaks [of bubonic plague: my insertion] in China between ad 37 and 1718. However, nothing to this effect is stated in Wu Lien-Teh 1926. This makes it clear that Scott and Duncan do not know this standard work and its brief historical introduction on this mode of plague, but have taken the reference from elsewhere for second-hand or third-hand use. The second monograph they refer to, Wu Lien-Teh, Chun, Pollitzer and Wu 1936, is an outstanding standard work on plague written by a team of prominent plague researchers. The historical introduction on plague is not written by Wu et al., but by Wu Lien-Teh alone. In the historical introduction, Wu Lien-Teh 1936a, he makes it clear that among the epidemics mentioned in Chinese historical sources between 224 b.c. and a.d. 1718 none is referred to by words or terms that imply plague, only by unspecific general terms meaning pestilence or epidemic. This register of epidemics is taken from the Imperial encyclopaedia that was produced under the orders of Emperor Kang-Hsi in 1726 and is cited by Wu Lien-Teh at the end of the chapter. However, Wu Lien-Teh also took upon himself the task of reading through the old Chinese medical literature where he found at long last (after 32

the alternative theory of scott and duncan

621

Scott and Duncan inform their readers that, for their medical and epidemiological knowledge of bubonic plague, they rely on a textbook by A.B. Christie providing a general introduction to infectious diseases, more precisely on “the first edition of his book Infectious Diseases: Epidemiology and Clinical Practice, published in 1969.” They maintain that he “has provided an admirable account of the epidemiology of modern bubonic plague and the following pages are very much based on his overview.”35 Their praise reflects their need to lead attention away from the fact that they base their knowledge of bubonic plague on a chapter in a general textbook on infectious diseases which has serious weaknesses. Despite their numerous and consistent references to the first edition of this textbook of 1969, this edition does not contain any chapter on plague, neither does the second edition of 1974. A chapter on plague is first introduced in the third edition of 1980, which could suggest that most of their references were produced by someone else.36 This shows that Scott and Duncan did not have any ambition to acquire good knowledge of bubonic plague through earnest, independent reading of the primary medical research literature or the standard medical works on bubonic plague that summarize the research literature and the vast personal experience of their authors. Instead, they

“years of patient search among such books”) evidence of bubonic plague in a.d. 610, a.d. 652 and next, not until 1642 and in 1644, when there is a reference to bubonic plague with secondary pneumonic manifestations. Why do Scott and Duncan start in a.d. 37, when Wu Lien-Teh starts in 224 b.c.? They cannot have read Wu Lien-Teh’s text, as they pretend. They may possibly have been influenced by some flawed comments by Twigg to the same effect, Twigg 1984: 23. These are only a few illustrations of their pervasive negligence of the primary works on the history of bubonic plague which characterizes their monographs and which makes them dependent on second-hand or third-hand accounts from which they select the elements that may support their alternative theory. This serves a function; in this case it permits them to seemingly underpin an assertion to the effect that bubonic plague was a disease that was “predominantly” rampant far away from Europe, in India and Central and Eastern Asia, but did not come from these parts of the world to Europe until the third pandemic, 250–300 years after historical plague epidemics ended. Scott and Duncan 2001: 7–8, 171, 389. Instead, there are interesting reasons to assume that bubonic plague came to China from Europe, as the first epidemics in China correspond in time to the Justinianic pandemic, and the seventeenth-century epidemics correspond to the early modern plague epidemics in Europe and appear to have established at least one plague reservoir, namely in Yunnan province. Plague in India is mentioned only in 1031 and 1615, and then again not until the nineteenth century. Benedictow 2004: 42–3. 35 Scott and Duncan 2001: 15–6. 36 The reference to Christie’s textbook may have been found in Twigg’s monograph, although Twigg uses it only for information on other contagious diseases and refers to the edition of 1980. Twigg 1984: 209, 213, 215, 245.

622

chapter fifteen

base their work on a chapter of twenty-four pages37 in a general textbook on infectious diseases, written primarily for medical students or as a manual for general practitioners by an author with a tiny research background on plague. However, only three of these twenty-four pages relate directly to plague among human beings which is of primary relevance to their work.38 Most of the pages are used for formal bacteriological and medical information and epidemiological descriptions of the types of rodents and fleas that entertain enzootic and epizootic plague in nature today and how they could come into contact with peridomestic rodents and, thus, produce the potential for endemic or epidemic plague developments. Obviously, and for easily understandable and acceptable reasons, Christie is mainly concerned with plague cases or in more general terms plague-related situations which physicians may encounter in plague areas today, mostly in developing countries. Also for obvious reasons, in a textbook aimed mainly at medical students or general practitioners who need concrete practical information on diseases that they are likely to meet in their practice, plague is considered a peripheral disease of low priority in relation to much more usual and therefore important contemporary diseases. This is the reason that plague was left out of the two first editions and, when a chapter on plague was eventually inserted into the textbook, it was written with hardly any interest in historical plague epidemics. In contrast to, for instance, Hirst’s or Sticker’s standard works, information on plague in this textbook is not selected or organized for the purpose of facilitating comparison between modern bubonic plague and historical plague epidemics, but for very different and respectable purposes. It does not provide the information really required by Scott and Duncan and leaves, therefore, much leeway for unfounded assertions on characteristic features of bubonic plague. In comparison, Pollitzer’s monograph Plague of 1954 has 698 pages and 1478 footnotes with full bibliographical references included; Wu Lien-Teh’s monograph A Treatise on Pneumonic Plague of 1926 has 464 pages with 1329 footnotes with full bibliographical references included. The important standard work by Wu Lien-Teh, Chun, Pollitzer and Wu of 1936 which Scott and Duncan refer to without having read comprises 547 heavily annotated pages containing 910 references to plague 37 38

When four pages on tularaemia are deducted. Christie 1980: 760–2.

the alternative theory of scott and duncan

623

studies. Hirst’s monograph on historical plague epidemics of 1953, which is not even mentioned by Scott and Duncan, is constructed entirely on historical lines and systematically compares modern studies with the various reflections and manifestations of historical plague epidemics, has 481 footnotes based on 407 works according to Author Index. Scott and Duncan can legitimately disagree with these excellent scholars, but the requirements of good scholarly work and rules of academic engagement are very different from those they follow. It is disappointing that they do not have the confidence in the quality of their own work to make their premises, objections and assertions easily testable according to the ordinary standards of scholarly and scientific work. This stands out in contrast to the vast amount of scholarly studies which are meticulously presented and discussed according to ordinary scientific requirements by all those fine scholars they denigrate with their misleading and disparaging assertions (see above). Christie’s chapter on plague exhibits serious weaknesses both in the knowledge of plague and in familiarity with primary plague studies and the standard works on this disease. He actually believes, for instance, that the fact that rats eat the carcasses of rats which had died from plague is an important factor in the spread of plague among rats: “A rat might get plague from eating a rat or other rodent dead of the plague, though rats are not always easy to infect in feeding experiments. In Bombay only 38 per cent of wild rats could be infected when fed on dead infected rats, though 70 per cent of Punjab rats were infected in this way.”39 In support of this assertion he refers to the very first report of the IPRC published in 1906 in The Journal of Hygiene, albeit only to the first page, leaving it to the critical reader to plough through the following 115 pages in the hunt for the basis of his assertion, which proves to be non-existent, as any scholar acquainted with the IPRC’s works would instantly know. Instead, the IPRC published their first study of this topic in their Report no. XIII the following year. Although it is pointed out in this Report that rats caught in Mumbai or the Punjab can be infected by feeding them “with the viscera of dead plague rats,” that is “with grossly infected material” (Lamb), the Commission’s conclusions are clear: “It would appear that in nature intestinal infection rarely or never takes place, and that in consequence rats do not become

39

Christie 1980: 756.

624

chapter fifteen

infected by eating the carcasses of their comrades.”40 Thus, the Commission’s conclusion is the opposite of that which Christie attributes to them. This conclusion is also reiterated in Lamb’s summary of the Commission’s studies until May 1907.41 Later, the IPRC carried out further experiments on rat epizootics in special godowns where many rats were eaten but “that there is no reason for thinking that alimentary infection played any part in the production of these epidemics.”42 The “Advisory Committee for Plague Investigation in India,” who supervised the IPRC’s work, concluded very clearly: Rats may be infected by feeding them upon the bodies of other rats dead of plague. The distribution of the lesions in the bodies of naturally infected rats correspond with that in rats experimentally infected by means of fleas and not with that in rats infected by feeding. The Committee, therefore, conclude that in nature plague is spread among rats by the agency of rat fleas.43

This makes Christie’s assertion, which is supported by Scott and Duncan, to the effect that human beings can contract bubonic plague from the eating of undercooked camel flesh most unlikely, and it is not supported by the papers referred to. It is a fact that camels can contract and die from plague, but as to the epidemiological significance, interest should focus on the role of fleas. One is entitled to wonder how the fictitious reference to the IPRC’s work came about. For his description of the main forms of plague Christie appears to base his presentation unduly on a paper by Choksy44 of 1909 which exhibits an incomplete terminology and insight into the basic forms of plague (see the presentation above on the basis of subsequent primary research and the standard works on plague). Choksy has, for example, an incomplete or deficient understanding of the difference between primary septicaemic plague and secondary septicaemic plague. Probably, this is the reason that Christie appears to believe that “if an infected flea injects pathogens into a healthy host, these go straight into its bloodstream,”45 which is an assertion to the effect that primary septicaemic plague is the normal form of plague infection, 40

IPRC 1907a: 381. Lamb 1908: iii–iv, 34–5, 41. Several studies appeared in later issues of Journal of Hygiene but had been used by Lamb. See also IPRC 1907c: 421–35; 1907d: 436–56. 42 IPRC 1910a: 332. 43 IPRC 1910e: 566. The author’s italics. 44 Not a member of IPRC. 45 Christie 1969: 753. 41

the alternative theory of scott and duncan

625

a form which arises when a flea discharges contagion directly into a blood vessel. In reality, it is normally a peripheral phenomenon comprising a few per cent of plague cases. Philip and Hirst, who have made the best study of this form of plague, underline “the comparative rarity of the primary septicaemic variety of plague.”46 This is important because primary septicaemic plague is so fulminant that it rarely causes the development of secondary pneumonia which gives rise to primary pneumonic plague, and the average duration of the course of illness of a statistically valid number of such cases was 14.5–15 hours,47 which is at variance with the normally observed duration of the course of illness of bubonic plague of 3–5 days. When plague contagion is discharged directly into a blood vessel, the mode of infection will not affect the lymph nodes, which is associated with subcutaneous introduction of infection through abrasions or cuts in the skin, as will normally be the case with the bites of infective fleas, and will therefore not lead to the formation of buboes. Or to put it more succinctly, infective rat fleas will normally discharge plague contagion at a subcutaneous level where it will be in the catchment area of the lymphatic system and will, accordingly, be drained through a lymph vessel to a lymph node which consequent upon the infection will begin to swell and develop into a bubo. Another related point is that primary septicaemic plague is so fulminant that there will not even be time for the development of buboes and other typical clinical features of plague.48 Christie’s misunderstandings make the term “bubonic plague” and the dominant mode of bubonic plague difficult to explain. However, he is not consistent. Christie correctly describes the first phase of the development of secondary septicaemic plague, that is, when plague contagion “begins its course via the regional lymphatics [after a bite of a blocked flea],” but goes on to maintain that in these cases “the infection travels on through the lymphatic vessels and nodes and invades the blood stream,”49 which is another erroneous assertion of general bacteraemia and primary septicaemia in plague cases. In fact, in almost half of plague cases the infection is confined wholly or predominantly to the lymph nodes,

46 47 48 49

Philip and Hirst 1917: 534. Philip and Hirst 1917: 530, 535, see also above: 7–8. Philip and Hirst 1917: 530–8. Christie 1980: 751–2, 762.

626

chapter fifteen

which is their primary function.50 Christie soon forgets, it seems, his erroneous description of secondary septicaemia altogether and reserves the term septicaemic for primary septicaemic plague. It is cases of normal bubonic plague that develop into secondary septicaemic plague when bacteria filter into the blood stream from the bubo after plague toxin have broken down the surrounding lymphatic tissue. Such cases of secondary septicaemic plague tend to develop sufficiently slowly to allow the development of secondary pneumonia so often mentioned in the sources in the form of “spitting of blood.” This is the clinical form of plague that can give rise to primary pneumonic plague. According to the plague research literature, secondary pneumonic plague develops in 10–25 per cent of all plague cases (see above). Unfortunately, Christie erroneously maintains that only 5 per cent of plague cases develop secondary pneumonic plague51 which is a misunderstanding probably arising from a rapid and superficial reading of Choksy’s text where he refers to the distribution of plague types in an epidemic in Hong Kong in 1904.52 This is a piece of information from the very infancy of plague research, and a good illustration of the problems arising from ignoring most of the primary research studies and the standard works on plague. Unfortunately, due to Scott’s and Duncan’s failure to read these works, they rely on Christie’s brief and flawed presentation of these important aspects of plague disease.53 Christie’s comments on primary pneumonic plague are written on the basis of a few peripheral studies without use of the central works on this mode of plague disease.54 For this reason, he cannot benefit from the great quantity of knowledge available on this disease that was obtained in connection with the only two known large or largish epidemics of this disease, namely the Manchurian epidemics of 1910–1 and 1920–1. He does not even know that the Manchurian epidemics were primary pneumonic plague and not bubonic plague as demonstrated by his assertion that “60,000 hunters caught plague from marmots which they sought for their skins between 1910 and 1911 in Manchuria,”55 which demonstrates ignorance of the factual 50 Benedictow 1993/1996a: 242–64, where available data on septicaemia are summarized. 51 Christie 1980: 762. 52 Choksy 1909: 352. 53 Scott and Duncan 2000: 58. 54 Christie 1980, references nos. 11, 33, 97, 112, 116. 55 Christie 1980: 760.

the alternative theory of scott and duncan

627

circumstances and also of the main scholarly works on primary pneumonic plague. This is confirmed by the accompanying reference which shows that Christie has picked up this piece of misinformation in a general introductory work on human parasitology written by two parasitologists, Chandler and Read 1961, which contains about 3.5 pages on plague where the focus is legitimately on the role of fleas as parasites. The fact that primary pneumonic plague is spread by cross-infection through the agency of droplets is not mentioned and the reference to the events in Manchuria shows that the parasitologists know nothing about this modality of plague which is not spread by insects.56 Unfortunately, Christie’s account is uncritically picked up and used by Scott and Duncan, since they have not acquired enough independent knowledge to enable them to recognize such misinformation.57 However, Scott and Duncan do not refer to Christie on this point, but refer instead incorrectly to “Wu et al. 1936.” Of course, Wu Lien-Teh, who was director of the North Manchurian Plague Prevention Service, has not written this, neither in his report on the epidemic in Manchuria in 1910–1, “First Report of the North Manchurian Plague Prevention Service,” The Journal of Hygiene 13 (1913–4): 237–99, nor in his report on “The Second Pneumonic Plague Epidemic in Manchuria,” The Journal of Hygiene 21 (1922–3): 262–88, nor in his monograph on primary pneumonic plague of 1926, nor in his three chapters in the standard work of 1936. It is simply a fictitious reference. Scott and Duncan also refer to Chandler and Read 1961, Christie’s reference, so the origin of their citation is obvious. Since they do not provide information on the relevant pages in the works to which they refer, this practice can be easily concealed and is difficult to reveal. Although the erroneous character of the untenable reference to Chandler and Read is uncovered in this case and in other cases above and below, the unpleasant question of the extent of this practise remains unresolved. Christie provides also untenable (really obsolete) information on extrinsic incubation time of Xenopsylla cheopis, i.e., the amount of time from which a flea becomes infected until it becomes blocked and infective, also called the infection-infectivity interval. The average cannot be “about 21 days”58 because this is incompatible with the rhythm or pace

56 57 58

Chandler and Read 1961: 653. Scott and Duncan 2001: 66; Scott and Duncan 2004: 179. Christie 1980: 754. Cf. Eskey 1938: 52–3; Eskey and Haas 1939: 1473.

628

chapter fifteen

of development of plague from when contagion is introduced into a rat colony to the transition into an outbreak among human beings, i.e. the latency period of 19–27 days, for which it is now possible to provide a fully satisfactory explanation. The scholarly consensus on the extrinsic incubation time of Xenopsylla cheopis is 3–9 days (under normal circumstances), with the emphasis on the lower reaches of this range.59 These remarks on Christie’s chapter on plague will serve to underline that Scott’s and Duncan’s uncritical and unstinting praise of it is not warranted, although it certainly has some strengths in the form of correct information. One should also take into account the comprehensive critical remarks on this text book and Scott and Duncan’s use of it given above.60 However, most importantly it does not provide the information needed to construct a comparative model between the epidemiological and clinical manifestations, the defining features of bubonic plague, and historical plague epidemics. But neither do Scott and Duncan construct a real typology of the clinical and epidemiological manifestations of filoviridal diseases which can serve as the basis for the other part of the comparative model. This is the reason that Scott and Duncan do not produce a valid and tenable comparison of bubonic plague and Ebola or Marburg disease that can serve as a valid basis for their conclusion or alternative theory. Conspicuously, Christie’s chapter contains significant elements that are strongly at variance with their theory, but which remain ignored and unmentioned. The Demography of Historical Plague It has been demonstrated above in the discussion of Twigg’s demographic arguments that they are deficient and outdated. Scott and Duncan express their indebtedness to Twigg “for his overview of the available [demographic] information and for drawing attention to the shortcomings of the data.”61 This demographic overview is, as shown, based on J.C. Russell’s obsolete and highly problematic study of mortality among the baronial class based on inquisitions post mortem and on Shrewsbury’s discussion of mortality among the beneficed clergy on data mostly produced by Lunn in a lost thesis.62 This means that all the 59 60 61 62

See Appendix 3: 682–7. Above: 87–91, 338–9. Scott and Duncan 2001: 106. Benedictow 2004: 344–5, 353–4, 356–7, 411.

the alternative theory of scott and duncan

629

excellent work that has been carried out on English medieval and early modern demography after 1948 is ignored, that is, most of the available research in these fields of study. Their ignorance of English demographic history of the period is demonstrated by their assertion that “these are the only statistics available to us.”63 Uniquely in the European historiography of the Black Death, there are in fact available to them seventy-nine manorial studies of the mortality among rural populations which constituted around 85 per cent of the English population at the time, and these studies are distributed over large parts of England’s territory, thus, the number of studies and their distribution provide a good level of social and demographic representativeness. They show a general level of mortality in the Black Death of 60 per cent or slightly higher.64 Scott and Duncan ignore also a number of mortality studies based on another type of manorial registers, tithing lists relating to frankpledge jurisdiction that are not quite so good sources, but good enough to allow estimates that independently reveal the unsustainability of their conclusion on the mortality level caused by the Black Death (see below).65 Their ignorance of English demographic history is so pervasive that they, like Twigg (or rather following Twigg), assert that “the population of England did not fully recover for 150 years,”66 i.e., that it only regained its pre-plague demographic strength around 1500. Instead, around 1500, the size of the English post-Black-Death population was at its minimum, “and there are few signs of sustained recovery before the second quarter of the sixteenth century.”67 However, Scott and Duncan insist erroneously and, as is so often the case, without a supporting footnote or reference, that Historians have long been puzzled by the paradoxical rapid recovery of the population of England after the undoubted heavy mortality of the Black Death […].68

Who are these historians? So far as I know, the objective fact is that at least since Postan’s important paper of 1950 on the late medieval demographic crisis69 historians have not been puzzled by any rapid recovery, 63 64 65 66 67 68 69

Scott and Duncan 2001: 106. Benedictow 2004: 362–8, 375. Benedictow 2004: 368–74. Scott and Duncan 2001: 6, 20, 98. Hatcher and Bailey 2001: 31; Hatcher 2003: 93–101, 105. Scott and Duncan 2001: 20. Postan 1950: 328–44.

630

chapter fifteen

because they have, on the contrary, been puzzled by the duration and the magnitude of the decline and the late start of sustained recovery. In fact, the English population had not regained its pre-plague strength on the eve of the Industrial Revolution about 200 years after the beginning of the recovery, almost 400 years after the Black Death.70 Around 1500, the English population was “scarcely more than 2 million people in the country,” still very much lower than Russell’s preplague estimate of 3.7 million, in fact almost a half. So, what can be the basis of Twigg’s and Scott’s and Duncan’s assertion on this point? They do not refer to any other study for support. English historians have generally dismissed out of hand Russell’s estimate of 3.7 million as far too low. Most English scholars agree now that the population numbered about six million inhabitants on the eve of the Black Death and this is, then, the current scholarly consensus (see above). Thus in 1500, the English population was around or only slightly above one-third of its pre-plague size and it had not fully recovered its pre-plague size 400 years later. Scott and Duncan pay a high price for relying on a zoologist for their historical demographic data, instead of taking on the ordinary scholarly task of acquiring satisfactory knowledge of this central piece of data for their subject. Scott and Duncan’s special relationship to English demographic history serves a purpose, namely, to keep estimates of mortality and the reduction of the population in the Black Death down to levels that would not be obviously incompatible with their alternative theory, that historical plague was caused by a filoviridal virus. Filoviridal diseases are characterized by very inefficient methods of transmission with correspondingly limited powers of dissemination and mortality, so inefficient that high population mortality rates must be excluded (see below). Thus, in a monograph in which they discuss the possible microbiological nature of the most devastating epidemic in history, they present an alternative contagion which is characterized by small or tiny outbreaks (see below) which would not be observable in medieval sources. On the other hand, they proclaim that bubonic plague cannot cause high mortality rates, although this is documented71 and they admit that this was the case with the epidemic in southern France 1720–2.72 In addition to the studies on the inquisitions post mortem and on the beneficed clergy, Scott and Duncan base their assessment of the 70 71 72

Benedictow 1993/1996: 105–8. See, for instance, Hirst 1953: 103. See also above: 201–2. Scott and Duncan 2001: 340–1.

the alternative theory of scott and duncan

631

mortality caused by the Black Death in England on studies of much later plague epidemics, namely on the mortality rate estimated for the plague epidemic in Penrith in 1597–8, and on a reference to unsubstantiated assertions of mortality in Italian cities at the level of 40–50 per cent based on data relating to the period 1476–657.73 This must be fallacious: what occurred in Italy 135 years later at the time of the Renaissance and the transition to the Early Modern Period, or 250 years later in Scotland in the established phase of early modern society cannot have evidentiary bearing on the assessment of the mortality effects of the Black Death. Scott and Duncan should instead have based their discussion of this topic on the available estimates of the mortality rates for Italian cities and rural districts in the Black Death. They show much higher mortality rates, in the range of 50–60 per cent.74 Scott and Duncan maintain that mortality in the city of York in the Black Death was 32 per cent and that the city, thus, “was relatively lightly affected.”75 M. Sellers states in The Victoria History of the County of York that seventeen of the twenty-one beneficed parish priests in the city died, representing a mortality rate of 81 per cent, which is the only demographic data on mortality in the Black Death available for the city.76 This piece of information is also cited by Shrewsbury.77 On this fictitious basis, Scott and Duncan “conclude that the mortality in the more populous parts of England during the Great Pestilence may well have been at least 30%.”78 This assertion implies that when less populous areas are taken into consideration, which have a significantly lower level of total mortality, one may perhaps arrive at something like 25–30 per cent. Thus, they produce a mortality estimate in the Black Death based on a fictitious assertion as to the mortality in York and an arbitrary assertion that mortality rates would have to be lower in rural England. Since not a single population mortality rate is available for an English urban centre in the Black Death, how can they know that mortality rates would be lower in rural England? This mortality estimate is obviously methodologically as well as factually seriously flawed and

73

Scott and Duncan 2001: 103, 303–4, 312–4. Benedictow 2004: 285–307. 75 Scott and Duncan 2001: 94. 76 Sellers 1913/1974: 440. For available data on urban mortality among the English beneficed clergy, see Benedictow 2004: 359. 77 Shrewsbury 1971: 110. 78 Scott and Duncan 2001: 103. 74

632

chapter fifteen

must be rejected. The estimates of medievalist demographers like Hatcher or R. Smith should have been used. Since about 85 per cent of the English population lived in the countryside,79 the crucial point must be that the manorial studies, seventy-nine manorial studies with a wide geographical distribution, show an average mortality rate among the customary tenants of about 55 per cent, corresponding to a generalized population mortality rate of at least 60 per cent.80 This estimate must be close to the mortality rate of the English population, which is incompatible with Scott and Duncan’s need for a low mortality level which could possibly save their alternative theory. The reference to the “more populous parts” appears intended to convey the opinion that the level of mortality generally was higher in the more populous parts of England than in the less densely or sparsely populated parts of England, Northumberland and County Durham being specifically mentioned.81 This is contrary to the well established fact that the mortality rates among the rural populations at twenty-six manors in County Durham and at two manors in Northumberland show the same level as in the more populous parts of southern England.82 The point is that this usual density-dependent structure of increasing mortality rates with increasing density of population serves Scott and Duncan’s alternative theory, because it is based on a type of disease spread by cross-infection, and this is an inherent feature of all diseases spread by this method. Instead, the absence of correlation between population density and level of mortality (or inverse correlation) implies a disease that is spread by different mechanism(s), in this case by rat fleas. In a specific chapter above on this subject, it has been shown that inverse correlation between population density and mortality is a consistent and unique feature of bubonic plague which is also exhibited by historical plague epidemics, and that this unique feature reflects the fact that this disease is transmitted and disseminated by rat fleas. This feature therefore constitutes a defining feature of bubonic plague and a means of identification of the microbiological nature of historical plague as bubonic plague. It was also shown that Scott and Duncan’s discussion of this subject was untenable.83 79 80 81 82 83

Hatcher and Bailey 2001: 140, cf. 50. Benedictow 2004: 362–7, 375–6. Scott and Duncan 2001: 98. Benedictow 2004: 344, 347–8, 364–7. See above: chapter 8, especially pp. 301–11. Cf. above: 34–8.

the alternative theory of scott and duncan

633

The Reed-Frost Theory of Epidemiology After this presentation of some central or characteristic features of Scott and Duncan’s monograph, it is the paramount task to construct a comparative model that can serve as a real basis for identification of the microbiological nature of historical plague epidemics. Scott and Duncan base their epidemiological analysis leading to the establishment of their own alternative theory on an unpublished epidemiological model by L.J. Reed and W.H. Frost. This model was presented by J. Maia, a Portuguese scholar at the University of Porto, in a paper of 196884 and has subsequently generally attracted little interest. An important reason for this is probably that it is of such limited use. As Maia strongly emphasizes on the first page: “As presented, the theory applies only to simple situations as illustrated by an outbreak of measles in a closed group.”85 Obviously, this means that the Reed-Frost theory is of very limited usefulness and of peripheral interest for the study of epidemic diseases spread by cross-infection, particularly viral diseases disseminated by droplets. It also means that it is not usable for the analysis of diseases transmitted by other means or mechanisms, for example by insects, and in relation to populations under circumstances which cannot be considered to approximate a closed group. Obviously, the Reed-Frost model is unusable and invalid for the study of bubonic plague in medieval society on both counts. As underlined by Maia, at the time this model had only been “utilized in the teaching” of epidemiology at the Johns Hopkins University. Consequently, knowledge of it was limited at the time and today it is almost unknown by epidemiologists and more generally oriented reviewers. This situation will therefore introduce an element of caution in the way reviewers relate to their theory, since they might otherwise tend to assume that Scott and Duncan had respectable intentions and made this choice because it provides useful insights not provided by established epidemiological theories. The Reed-Frost model completely dominates Scott and Duncan’s various epidemiological discussions and analyses, it is mentioned by name thirty-six times throughout their monograph and many more times indirectly; this prolific use provides

84

Maia 1968: 167–200. A closed demographic group is one not affected by immigration or emigration so that, for instance, all changes of size will be due to the net outcome of births and deaths among the persons constituting the population. 85

634

chapter fifteen

the false impression of fresh new insights and great importance.86 However, in the same journal in which Maia’s paper appeared, in the immediately following paper serious objections to the Reed-Frost model are raised by another scholar, Helen Abbey, who was working at the Johns Hopkins University.87 This shows that the editors of Human Biology must have had serious objections or reservations which required immediate comments, and which explains why the Reed-Frost model and the theory on which it was based never was published by the authors and is known only indirectly through Maia’s paper. Scott and Duncan have, as it seems, chosen to ignore all this and also to keep their readers in ignorance of it. On page 355, at the end of Scott and Duncan’s monograph of 2001, a terrible truth inadvertently slips out: “Furthermore, typhus epidemics do not follow Reed and Frost dynamics because it is a disease with an arthropod vector.” Typhus is transmitted by lice which are insects, one of the four classes of animals which constitute the phylum of arthropods. Bubonic plague is transmitted and disseminated by another type of arthropods, namely fleas, mainly rat fleas, usually of the species Xenopsylla cheopis associated with black rats. Consequently, the corollary must also be true, namely that the Reed-Frost model is not usable for the study of bubonic plague, because it is “a disease with an arthropod vector.” Throughout their monograph Scott and Duncan never even hint that the Reed-Frost model is, according to its own underlying premises, unusable for the analysis of epidemics of bubonic plague, and that it is potentially usable only for the analysis of epidemic diseases spread by interhuman cross-infection and as such mainly restricted to viral diseases transmitted by droplets in closed populations. It is in this perspective that one should consider Abbey’s severe objections: The Reed-Frost Theory of the spread of epidemics has been tested on two series of observations derived from disease and population conditions which approximate the assumptions of the theory [closed population: my insertion]. The first series is composed of epidemics of measles, chickenpox and German measles in boarding school populations […]. The second series consists of epidemics of measles in families each of which is a

86 Scott and Duncan 2000: 28, 32, 45, 70, 79, 80, 85, 89, 90, 107, 121, 123, 148, 151, 159, 165, 170, 173, 190, 229, 236, 247–8, 249, 250, 263, 328, 263, 355–6, 359, 362, 364, 366, 368, 372. 87 Abbey 1968: 201–33.

the alternative theory of scott and duncan

635

universe having four (reported) susceptible members. The model was fitted to the reported cases by generation of the disease and reported number of susceptibles at the beginning of the epidemic. The theory fails to fit either series of observations.88

This explains why the Reed-Frost theory and the model of the spread of epidemics based on it have never attracted significant interest even in the case of viral diseases spread by cross-infection, not even at the university where it was conceived. It must to a large extent be considered a failed epidemiological theory. Thus, at the heart of Scott and Duncan’s monograph is a sinister secret. In a monograph designed to show that historical plague cannot have been bubonic plague and to provide an alternative theory, they have deliberately and in complete secrecy chosen to use an epidemiological model that, according to the methodology of social and medical science, cannot be used to test historical evidence produced by epidemics of bubonic plague. In principle, the Reed-Frost model is not appropriate for probing or examining the pivotal and crucial question at the heart of the discussion of whether or not historical plague epidemics could have been bubonic plague transmitted by rat fleas or could or must have been another disease. As such the whole monograph is based on a fallacy of methodology. Inevitably, this must be obvious also to Scott and Duncan. In the first presentation of the Reed-Frost model, they introduce, for instance, the concept of “serial generation time” which “has been defined as the period between the appearance of symptoms in successive cases in a chain of infection that is spread person-to-person.” They state also that it “seems that the causative agent of plague was most infectious, and droplet transmission person-to-person was most efficacious under warm conditions.”89 Here it is explicitly stated that the Reed-Frost model by definition can only be used for analysis of epidemics spreading by interhuman cross-infection, and by implication is unusable for the study of diseases spread by insects. Unfortunately, nothing is said about the further limitations and weaknesses of the model as being restricted to viral diseases, and thus also for this reason unusable for the study of bubonic plague. Only diseases disseminated by droplets are being specifically mentioned (measles, chickenpox, and

88 89

Abbey 1968: 231. Scott and Duncan 2002: 28, 365–6.

636

chapter fifteen

rubella/German measles). This must also be the reason that Scott and Duncan spuriously claim that filoviridal haemorrhagic disease spread by “droplet transmission person-to-person”90 (see below). It is a general characteristic of medical or social-science models that the interaction of the input of premises and the structure of correlates constituting them will tend to reproduce their underlying suppositions or presumptions, and also that incorrect inputs will tend to produce obviously unreasonable or untenable outcomes. The Reed-Frost model is constructed in a way that will tend to make all inputs of historical evidence produce confirmation of Scott’s and Duncan’s pre-conceived view that historical plague was a viral disease spread by cross-infection. When such a model is applied to evidence pertaining to an epidemic of bubonic plague, a type of disease which it is not constructed to handle, it will tend to produce the features of a phantom disease with an unknown set of characteristics or manifestations. This is also the case, as will be seen below, when Scott and Duncan have to admit that their alternative disease is completely unknown or an unknown strongly mutated variant of filoviridal disease. Every time Scott and Duncan conclude that the epidemiological analysis of a plague epidemic according to the Reed-Frost model proves that it cannot have been bubonic plague, it represents a fallacy of methodology, for instance, also on page 355: “In conclusion, all the major plague epidemics exhibited Reed and Frost dynamics typical of an infectious disease with a long incubation period.” The Filoviridal Theory of Historical Plague: A Study in Academic Fiction Scott and Duncan’s alternative theory of historical plague is that it was caused by filoviridal disease, some form of Ebola or Marburg haemorrhagic disease. These epidemic diseases occur in some parts of Western sub-Saharan Africa and in Sudan; they are caused by two closely related viral pathogens constituting the family of RNA viruses called the Filoviridae.91 Outbreaks of these diseases have never been registered

90

Scott and Duncan 2002: 365. Registered in the two Congolese states, and in Gabon, Sudan, and the Ivory Coast, according to www.cdc.gov/ndicod/dvrd/spd/mnpages/dispages/ebola.htm 2003: 1–4; and www.cdc.gov/ndicod/dvrd/spd/mnpages/dispages/ebotabl.htm 2003: 1–3 91

the alternative theory of scott and duncan

637

outside sub-Saharan Africa, and it appears mostly in Western Africa, a fact which from the outset gives Scott and Duncan’s alternative theory quite a problematic character, since this fact indicates very strongly the necessity of specific local condition(s). The scholarly mode of working is to endeavour to disprove one’s own hypothesis, which means that a scholarly discussion of a hypothesis will be imbued with the crucial scholarly values of source-criticism, doubt and counter-arguments about the validity or tenability of the various points made and the level of quality of supporting material. If earnest endeavours to disprove a hypothesis do not succeed, then something of value and a level of tenability for the hypothesis have been achieved. The selection of whatever arguments or evidence fit a hypothesis or theory is a way of working that will inevitably lead to the seeming corroboration of any hypothesis, but is obviously without scientific or scholarly value. Nothing is more valuable in scholarly work than doubt, source-criticism, counter-arguments and counterevidence. Scott and Duncan claim that they will examine the “historical facts dispassionately, eschewing any preconceived notion.”92 This is hard to reconcile with the fact that they declare that historical plague epidemics were “haemorrhagic plague” and not bubonic plague in the introduction of their monograph,93 before any evidence has been presented and discussed, and is, then, monotonously reiterated as an established fact throughout the monograph. This is rather an example of the triumph of pre-conceived notions and “passion.” It means that their principal monograph does not have an academic form in the fundamental sense that it is not structured according to its inherent nature as a thesis, i.e., introducing a problem, a possible solution or explanatory hypothesis and at least a strategy and likely relevant material for resolving the problem. This will structure the further process of researching the thesis: the scholar will go on to collect, collate, and examine the evidence in order to test the possible validity and tenability of the hypothesis or to seek out a solution, and form a conclusion at the end of the thesis. Since Scott and Duncan start by proclaiming their theory to be true, they pretend that they can legitimately conclude that any characteristic

92 93

Scott and Duncan 2001: 7, cf. 1. Scott and Duncan 2001: 1, 7–10.

638

chapter fifteen

feature of historical plague epidemics must be reflections or manifestations of their phantom haemorrhagic disease. (1) When historical sources state that plague victims in historical epidemics presented with buboes and at exactly the same corporal locations as modern bubonic plague, this simply proves that the normal occurrence of buboes and their normal locations are characteristic features of haemorrhagic plague.94 And the corollary (1B): if contemporary physicians or barbersurgeons incised mature buboes, this proves that such simple surgery was a suitable treatment for haemorrhagic buboes.95 (2) When the “symptoms were violet and black spots and blotches […] or small red spots” this is “indicative of a haemorrhagic disease,” as was “the bubo and pustules.”96 (3) “The signs, symptoms and autopsy reports of victims of bubonic plague are entirely different from these: they do not display God’s tokens. Nor is there widespread necrosis of the internal organs.”97 (4) When the duration of the disease is 3–5 days, this proves that this is the duration of the course of illness of haemorrhaghic plague.98 (5) When the epidemics at Penrith and Eyam and other epidemics have a long duration of 14–5 months, this shows that haemorrhagic disease is characterized by this duration. (6) When these epidemics are most dynamic in warm summer and autumn weather, and last so long because they are suppressed by cold winter weather and recrudesce in spring with the warmer weather, this seasonal pattern proves that filo-viridal disease, which according to their assertions are spread by droplets, thrives in warm weather, not in cold weather, and so on.99 Obviously, this is a clear instance of the fallacy of methodology called circular inference. Scott and Duncan have turned this into a systematic approach on which they base their alternative theory. The absolute condition or principle of falsifiability for scholarly and scientific assertions and subsequent merciless empirical testing are thrown out of the court of methodology at the cost of making their assertions invalid and untenable. This makes it essential to perform further testing or checking of their assertions by comparing them to the known clinical and epidemiological manifestations of filoviridal diseases and

94 95 96 97 98 99

Scott and Duncan 2001: 306, 362, 380–1, 388. Scott and Duncan 2001: 388. Scott and Duncan 2001: 306. Scott and Duncan 2004: 224. Scott and Duncan 2001: 85, 107–8, 144, 207–9, 380–1. Scott and Duncan 2001: 119–37, 148, 152–3, 190, 193, 364–6.

the alternative theory of scott and duncan

639

bubonic plague in order to identify possible correspondences. The six topics just listed and the question of incubation period, which in this case is closely associated with the question of latency periods commented on above and with their theory of dissemination, will be the focus of the discussion. According to Scott and Duncan, the point of departure for their work leading to the principal monograph of 2001 and their alternative theory to the effect that historical plague was caused by filoviridal disease is a paper Scott, Duncan and S.R. Duncan published in 1996: “The Plague in Penrith, Cumbria, 1597/8: Its Causes, Biology and Consequences.”100 A useful beginning for the further discussion of their work is the opening statement in the preface of the principal monograph referring to this study of plague epidemics in north-western England 1597–8: “A plague struck this part of England and spread rapidly in 1597–8 and it was obvious from a basic training in zoology that this was not an outbreak of bubonic plague.”101 This assertion refers to the untenable notion, thoroughly discussed above, that bubonic plague spreads only very slowly between conterminous rat colonies. There is nothing about the spread of the epidemic at Penrith that is incompatible with the ordinary pattern and spread rates of bubonic plague. With this background, one should note that, in the discussion of the nature of the disease in their paper, they consider that it exhibited features compatible with bubonic plague and also anthrax, undisturbed by elementary zoological knowledge. In their monograph, this is ignored, which clears the way for an entirely new and revolutionary theory. The crucial observations are: (1) Twenty-two or twenty-three days elapsed from the first plague death in Penrith, that of a stranger called Andrew Hogson, and the next plague death (depending on the time of the day he died);102 “Wasn’t this a very long interval for a normal infection? Surely this was remarkable.”103 (2) The duration of the epidemic, which lasted fifteen months, “a remarkably long time for an infectious “epidemic.”

100 101 102 103

Scott and Duncan 1996: 1–21; 2001: 115–48; 2004: 153–63. Scott and Duncan 2001: xiii. Scott and Ducan and Duncan 1996: 3; Scott and Duncan 2001: 116, 128. Scott and Duncan 2004: 7, 9.

640

chapter fifteen

(3) The development rhythm of the epidemic in three phases: (i) the epidemic began with a single death in late September 1597 and rose to a small autumnal peak in November–December, (ii) during the winter (January–February) there was only one plague death, (iii) the pestilence appeared again in spring 1598 and rose to a peak in June–July before slowly subsiding in the autumn. (4) The seasonality of the epidemic. (5) The duration of the course of illness, namely 3–5 days.104 Scott and Duncan analyse these main features of the epidemic at Penrith with the Reed-Frost model and conclude that: The third phase clearly follows the typical Reed and Frost dynamics of an infectious disease spread person-to-person (see section 2.5). This phase lasted about 8 months and, in this respect, the outbreak is comparable with the epidemics in the dioceses during the Black Death (see Fig. 4.2) and with plagues in other rural towns, examples of which are shown in Fig. 5.2. The duration of the main part of the epidemic in each of these populations was always long, usually between 7 and 10 months, and this is indicative of a long serial generation time, as shown in Fig. 2.5 This conclusion is supported by the initial events at Penrith, where 22 days elapsed after the death of Andrew Hogson before the next victim was buried, giving a minimum serial generation time of 22 days. A feature of Fig 5.1 is the slow build-up of the epidemic in early spring, which is also indicative of a long serial generation time and a low mean contact rate (see Fig, 2.5). Figure 5.3A shows Reed and Frost modelling […]. All Read and Frost models predict that over 90% of the population would be infected, which was not the case with [bubonic] plague […] the modelling is instructive and it demonstrates how the shape of the mortality curve (see Figs. 5.1 and 5.2) is determined by the long serial generation time and the low effective contact rate […].105

This is excellent material for a study of the fallacious use of a model: all of the various elements produced and explained according to the premises and predictions of the Reed-Frost model are formed by the internal suppositions and structures of this model. This is the case, for instance, with the purported long serial generation time which will lead them to a fallacious and untenable assertion on incubation time and further to their theory of historical plague as filoviridal disease. 104 105

Scott and Duncan 2001: 117, 128. Scott and Duncan 2001: 121.

the alternative theory of scott and duncan

641

All of the epidemiological features mentioned are instead entirely compatible with bubonic plague as has been shown in various chapters above: on the pace and rhythm of development of plague epidemics, latency periods, seasonality, duration of time from infection to death and the sequence of initial deaths, and the duration of the course of illness. Another obviously very important epidemiological feature is the duration and pattern of development of historical plague epidemics. Scott and Duncan simply declare that the duration of the epidemic at Penrith was “a remarkably long time for an infectious epidemic. Once again, the villain has left his mark.”106 On this basis, they maintain that the duration of an epidemic of fifteen months was a defining feature of epidemics caused by filoviridal virus infection (“the villain”), which they identify also with the duration of the epidemic at Eyam of fourteen months. However, they conspicuously fail to provide any comparative information on epidemics caused by a filoviridal virus in order to substantiate the claim that this duration is a (defining) property of this disease. The reason is, presumably, that a single instance of an epidemic caused by a filoviridal virus of anywhere near this duration has never been observed; epidemics of these diseases typically last a few months.107 The epidemiological point is clear and concrete: filoviridal viruses are transmitted by inefficient mechanisms requiring transmission of living cells and therefore direct physical contact between two persons in circumstances where mutual cuts or abrasions in the skin permit transmission of contaminated cells. This means that the chain of transmission is tenuous and tends to be rapidly broken, making for episodic and small or tiny outbreaks. By 2003, “approximately 1500 cases with slightly over 1,000 deaths had been recorded since the virus was discovered” in 1976.108 The long duration of the epidemics at Penrith and Eyam is due to the same peculiar seasonal pattern. In both cases, the epidemics break out in the autumn and after quite a short period of increasing activity they suddenly begin to falter, subside and eventually almost completely disappear in the coldest winter months, before the advent of spring brings warmer weather when the epidemic again breaks out and reaches its 106

Scott and Duncan 2004: 154. www.who.int/inf-fs/en/fact103.html 2003: 2; www.who.int/inf-fs/en/fact103 .html 2003: 1–3. 108 www.who.int/inf-fs/en/fact103.html 2003: 2. 107

642

chapter fifteen

pinnacle in late summer and early autumn and, then, again begins to falter, subside and eventually disappear completely with the second advent of cold weather.109 This seasonality of the plague epidemics at Penrith and Eyam is representative, it has been observed all over Europe from the time of the Black Death to the end of the plague period over three hundred years later. In the chapter on plague seasonality, it was shown that this pattern is a unique and therefore defining feature of bubonic plague.110 No theory of the microbiological nature of historical plague and its means of transmission can be accepted which does not readily provide a well-founded explanation of this particular seasonal pattern and demonstrate that this is not a defining feature of bubonic plague, but is associated with an alternative microbiological theory. It is a central and self-evidently true tenet of epidemiology that all diseases spread by cross-infection, whether by droplets or other means of direct interhuman dissemination and transmission, flourish in cold weather for the simple reason that people tend to stay or huddle closer together and stay more indoors in more crowded rooms to keep warm, a behavioural strategy that reduces interpersonal distance and obviously facilitates the direct spread of microbiological agents by crossinfection. This means that the seasonal pattern of plague epidemics is incompatible with all diseases spread by cross-infection, also the filoviridal viruses of Ebola and Marburg haemorrhagic diseases which are spread by “direct contact with the blood and/or secretions of an infected person” or “direct contact with the blood, secretions, organs or semen of infected persons.”111 Thus, also Ebola and Marburg haemorrhagic diseases or possible variants of filoviridal diseases would tend to exhibit stronger powers of spread in cold weather than in warm weather, a pattern which is at complete variance with that of historical plague epidemics. In sharp contrast, the peculiar seasonal pattern of historical plague epidemics can be easily explained according to the epidemiological mechanisms of dissemination and transmission of bubonic plague. There are two main factors which provide explanatory powers. Firstly, cold weather will prevent or impede the reproductive process of fleas,

109

Scott, Duncan and Duncan 1996: 17; Scott and Duncan 2004: 154; Shrewsbury 1971: 523; Bradley 1977a: 87; Coleman 1986: 383. 110 See above: 396–484. 111 www.cdc.gov/ncidod/dvrd/spb/mnpages/dispages/ebola.htm 2003: 2; www.who .int/inf-fs/en/fact103.html 2003: 1.

the alternative theory of scott and duncan

643

because the development of eggs and the survival and development of larvae and cocoons are temperature-dependent and significantly or seriously negatively affected by chilly or cold weather. The number of adult rat fleas which enjoy a pleasant life in the fur of the rat with a good microclimate and easy opportunity of feeding, will diminish as some of them are scratched off or simply fall off, while their number will not be replenished from the reproductive process.112 A diminishing number of rat fleas will reduce correspondingly the potential intensity of epidemic developments. Secondly, plague septicaemia in rats falls sharply in temperatures below 10 °C, so that feeding rat fleas will be much less infected and, consequently, will develop blockage at much lower rates.113 Thus, the strong tendency of historical plague epidemics in Europe to disappear or, especially in Southern Europe, continue in a more or less sporadic endemic form in wintry weather, and correspondingly the pronounced tendency of transseasonal epidemics can be easily explained in relation to the epidemiological mechanisms of bubonic plague and be established as a defining property of this disease. In contrast, it remains inexplicable in terms of epidemics caused by filoviridal viruses (and by all other diseases spread by crossinfection). Shrewsbury, Bradley and Coleman correctly point out that the seasonal pattern and time-course of the epidemic at Eyam exhibit the characteristic features of bubonic plague epidemics.114 In the words of Coleman, for instance: The timing of the outbreak in autumn, the transient decline during the winter months and the peak in summer is also typical, and largely reflects the influence of the weather, since the activity and survival of rat-fleas is temperature-dependent.

The next stage in the process leading to Scott and Duncan’s alternative theory of historical plague as filoviridal disease is the invention of a purported long incubation time: Three factors point to a long incubation period for the disease. (i) The duration of the summer epidemic in phase three, as explained above. (ii) In both Penrith and Eyam (Chapter 10) the epidemic began with the death of a stranger or visitor who had taken up lodgings and was living, albeit temporarily, in the town. He must have been infected elsewhere,

112 113 114

For a detailed discussion of these matters see Benedictow 1993/1996: 160–70. Lamb 1908: 88–90; Hirst 1953: 271–82, 340–5; Seal 1969: 288–9. Above: 397. Shrewsbury 1971: 524–7, 529; Bradley 1977a: 70–1; Coleman 1986: 382.

644

chapter fifteen perhaps some considerable distance away, and brought the disease into the community whilst still not showing any symptoms […]. The death of the first victim, the incoming stranger, was followed by an interval of 15 (Eyam; see Chapter 10) or 22 (Penrith) days […]. The early stages of these outbreaks, whilst the epidemic was being established, that we have studied in detail, are much more informative than are the confusing events in mid-summer when the infection spread with devastating rapidity. We have analysed a number of these outbreaks (see following chapters) and have determined from a number of sources the following epidemiological parameters: Latent period: 10–2 days. Infectious period before symptoms: 20–2 days. Period of symptoms: 5 days. Total infectious period: 25–7 days. Total time from point of infection to death: 37 days, a very long time […].115

The first part of the citation relating to the first epidemic events in Eyam and Penrith is obviously central to the argument, and this part will therefore be discussed first. As shown above, the course of the summer epidemic and the whole course of the epidemic are entirely compatible with the seasonality of a bubonic plague epidemic which arrives in the autumn, is arrested by chilly and cold weather and forced to retreat into a smouldering existence in the rat colonies, revealing its presence with the occasional plague death (one in February), and then recrudesces with the advent of warmer spring weather, finally to explode with summer warmth. Viral diseases spreading by crossinfection have in common that they spread more efficiently in cold weather when people keep closer together, whether the disease is spread by aerial transmission with droplets or by direct physical contact and transmission of living cells (if we exclude transmission via contaminated hypodermic needles). Also, droplets drift longer in chilly, cold and moist air which increases their probability of reaching other persons. Scott and Duncan attempt to get around this problem by seeking arguments to the effect that for this specific filoviridal disease this was not the case, without presenting the general problem and informing their readers why the mechanism of interhuman transmission or diffusion should be different in this case and not follow the general pattern.116 115 116

Scott and Duncan 2001: 128. Scott and Duncan 2001: 365–6.

the alternative theory of scott and duncan

645

The first plague victim in Eyam died 6 September 1665, on the third or fourth day of his illness,117 and was buried the next day. Presuming that the disease was bubonic plague, the time of incubation would be three to five days, which indicates that he was infected in the period 30 August–1 September. According to the oral tradition among the inhabitants of Eyam conveyed by W. Wood, the local historian who lived there and published a history of the epidemic in 1842, he was a tailor who had received a box with cloth from London where the last plague epidemic was raging. This story reflects the fact that people in the Early Modern Period recognized the dangers in times of plague of shipments of cloth or of second hand clothing left by plague victims, which have also been confirmed by modern plague research on more concrete grounds, incriminating rat fleas as the great “villain” hiding in such matter.118 In this respect, this account is quite similar to how plague was shipped from Mumbai to London in a case of clothes early in the plague epidemic in India.119 As pointed out by Bradley, after 176 years the oral tradition was no longer entirely reliable,120 for instance, that the tailor fell immediately ill after having opened the box. Source-criticism will indicate that this part of the account must be presumed to be a reflection of the typical feature of folkloristic oral dramatization by compression of the sequence of events. At the time, it would also have been inspired by miasmatic epidemiology that does not draw on notions of microbiological agents and has at best only hazy ideas about incubation, much like Boccaccio’s hogs which rooted with their snouts in the ragged clothing of a pauper diseased from plague and almost immediately fell dead to the ground. Thus, the process of oral (and literary) dramatization has led to a compression of the time between the time of arrival of the box of cloth and the time the tailor fell dramatically ill (a few days later) so that the connection between the events would be obvious and dramatic. The details of local oral tradition can be left out here; it suffices to point out that this account of how plague reached Eyam from London is easily compatible with the usual mechanism of spread of bubonic plague over a distance, namely of metastatic spread (spread per saltum) by rat fleas, and that heavily infected rat fleas in a relatively 117 118 119 120

Bradley 1977a: 64–5, 68–9. Hirst 1953: 310–1, 314–20. Hirst 1953: 311. Cf. Simpson 2005: 201. Bradley 1977a: 64, 68–9.

646

chapter fifteen

humid climate can survive for many weeks under favourable conditions of transportation as, for instance, in cloth, for at least fifty days in temperatures under 15 °C.121 In this case, the traditional account relates that the cloth was damp and the tailor therefore took it out of the box to hang it out to dry in front of the fire, a detail which increases the realism and trustworthiness of the history. The subsequent rhythm of epidemic events is also compatible with the pattern of bubonic plague. After having fed on the tailor, an infected flea (or fleas) concealed in the cloth would seek out their normal host, house rats. The second victim was interred 22 September, not fifteen but sixteen or seventeen days after the death of the tailor and twentytwo or twenty-three days after the beginning of the process of infective transmission. As can be seen, this is a very fine match for the general time structure of the two first cases of an epidemic of bubonic plague comprising the epidemiological developments from infection of the house rats and the course of the epizootic (ten to fourteen days), the release of rat fleas and the period of starvation until they attack people (three days) and the course of incubation and illness (six to ten days), in all nineteen to twenty-seven days, as documented above.122 This is also an excellent match with the subsequent epidemics events at Penrith where the second plague burial followed twenty-two or twenty-three days after the first. The difference is probably due to the fact that Andrew Hogson was infected at the time he arrived at Penrith which compresses the time horizon of the developments leading to the next case, and variation in the time that the rat fleas they brought with them took to find a rat host. In the case of the beginning of the epidemic at Eyam, the process of spread in the rat colonies would begin whilst the tailor was incubating the disease or was ill. As pointed out in the chapter on latency, the observation of this peculiar delay in the opening sequel of the two first deaths was made by the early plague researchers, by Simond, Hankin, Sticker and the IPRC, and was later underlined in all standard works of bubonic plague as being a characteristic or distinguishing feature of this disease,123 what here is called a defining feature or property. It is difficult to understand

121

Bacot and Martin 1914: 437; Hirst 1953: 322; C.Y. Wu 1936a: 260–1, 287. See for instance Hirst 1953: 324, 330–1. See also above: 178–82. 122 See above: 279–80. 123 IPRC 1907g: 764–5; Lamb 1908: 21, 51–2; Sticker 1910: 220; Wu Lien-Teh 1936c: 387. See above: 281–3.

the alternative theory of scott and duncan

647

how Scott and Duncan can have missed this information. In their paper of 1996 they refer to the excellent standard work on plague by Pollitzer of 1954124 where this information is given in the opening pages of the chapter on the epidemiology of bubonic plague.125 In Shrewsbury’s monograph the concept of latent period is presented under the term “lag interval” on pages 3–4; Scott and Duncan have used Shrewsbury’s monograph extensively, referring to Shrewsbury by name 116 times.126 The plague epidemic at Eyam has been the subject of considerable scholarly interest. In 1977, L. Bradley published an outstanding paper on the epidemic at Eyam based on family-reconstitution of the parish registers; M.P. Coleman’s fine paper of 1986 is at least partly also based on this technique; and Shrewsbury discusses the epidemic quite thoroughly, over quite a number of pages. Cohn and Alfani maintain that Scott and Duncan performed a family-reconstitution study of the plague at Eyam, but this is not correct: only Bradley has done that, and Coleman at least partially, but Scott and Duncan only use wording or phrasing that could easily produce such an impression.127 They also insert their assumption of the very long incubation period. Bradley, Coleman, and Shrewsbury point out that the duration of the time lag between the first and second plague victim is characteristic of the early development phase of bubonic plague, and represents a defining property and an important factor for the identification of the disease as bubonic plague.128 This point has been comprehensively documented above in the chapter on latency.129 One should note that Scott and Duncan refer to Shrewsbury’s and Bradley’s works, but do not argue why Bradley and Shrewsbury were erroneous on this point. The second part of the citation can now be usefully discussed. Crucially for their argument, Scott and Duncan assert that the normal or average duration of the disease from infection to death was thirtyseven days and that infected persons were infective throughout the whole of this period. The incubation period can be estimated by subtraction of five days for the course of illness and lasted, consequently,

124

Scott, Duncan and Duncan 1996: 16. Pollitzer 1954: 485. 126 See above: 285 and fn. 21. 127 Cohn and Alfani 2007: 181–4. However, Scott has performed a familyreconstitution study of the plague in Penrith 1597–8, which is cited in Scott, Duncan and Duncan 1996. 128 Shrewsbury 1971: 524; Bradley 1977a: 70–2; Coleman 1986: 382. 129 See above, chapter 8: 279–88. 125

648

chapter fifteen

normally or on average thirty-two days. More specifically, they also maintain that they used a computer model130 and the Reed-Frost model131 to calculate that this disease had an incubation time of thirtytwo days132 and that “a person once infected had over a month in which he could travel a considerable distance before the dreaded symptoms appeared.” This crucial point can usefully be amplified and enlarged upon by some passages from their monograph: The key to understanding the epidemiology of the plague lies in the lengthy incubation period and, because of this, apparently healthy infectives could move around the country on foot or horseback covering considerable distances before they were struck down.133 In contrast [to bubonic plague: my insertion], infectious diseases with very long latent and pre-symptomatic infectious periods (as we suggest for haemorrhagic plague) would allow widespread progressive, wave-like dissemination (see the Black Death, Chapter 4) when movement through the metapopulation was mainly on foot, or, in later centuries, more rapidly along the established communication corridors when travellers and carriers [of the disease: my insertion] had time to move long distances across Europe by horse.134 […] the lengthy incubation period provided a long time during which each victim could achieve onward transmission […].135 A symptomless infective could spread the infection widely.136 By parasitising healthy travellers, it crossed alpine passes into northern Italy; it travelled enormous distances inland by the river systems; it crossed the Mediterranean to Italy and Spain and the Atlantic to Portugal and the northern Spanish coast; it crossed the Channel and North Sea to England, Scotland and Iceland and the Baltic to Norway.137

Ignoring the evidence and the fact that all other scholars and the Icelandic chroniclers agree that the Black Death did not reach Iceland and that it is geographically impossible to cross the Baltic to Norway, these citations contain important information on their theory. Clearly, Scott and Duncan assert that the disease was haemorrhagic plague,

130 131 132 133 134 135 136 137

Scott and Duncan 2004: 162. Scott and Duncan 2001: 28, 355. Scott and Duncan 2001: 128. Cf. above: 285, 288. Scott and Duncan 2001: 134. Scott and Duncan 2001: 46. Scott and Duncan 2001: 364. Scott and Duncan 2001: 366. Scott and Duncan 2001: 376.

the alternative theory of scott and duncan

649

that haemorrhagic plague was characterized by a very long incubation period of thirty-two days and that persons infected by this disease were highly contagious during this period and could travel about without symptoms, contaminating towns and villages on their way. Such mysterious highly contagious persons, “infectives” in Scott’s and Duncan’s terminology, play a crucial role in their outline of the mechanisms and dynamics of the spread of historical plague.138 In their view, this constitutes decisive evidence that historical plague really was some variant of Ebola or Marburg haemorrhagic disease. However, Scott and Duncan are conspicuously loath to test their assertions with relevant and adequate information on the manifestations of filoviridal disease according to the accumulated knowledge of modern medical science. One should note that, according to updated modern medical science on these dise ases as cited by the leading medical experts at the CDC (Centers of Disease Control, Special Pathogens Branch) and WHO (World Health Organization), the “incubation period for Ebola haemorrhagic fever ranges from 2 to 21 days, i.e., on average, 9.5 days, not 32 days.139 According to the twentieth edition of Manson’s Tropical Diseases, the incubation period is, on average, seven to fourteen days,140 normally presumably around ten days. The medical scientific knowledge of the incubation period of Ebola disease and Marburg disease is incompatible with the result of their purported computation and this cornerstone and necessary condition of their alternative theory is therefore false. On the basis of ordinary scholarly considerations this would constitute decisive proof that historical plague was not caused by a filoviridal disease. The CDC also indicates that “infections with Ebola virus are acute, there is no carrier state,”141 which shows that Scott’s and Duncan’s numerous assertions to the contrary are not based on medical evidence. This is not accidental: Scott and Duncan portray the two types of haemorrhagic diseases as highly or rather extremely infectious, while, according to the CDC and WHO, these diseases spread only by “direct contact with the blood and/or secretions of an infected person”/or “direct contact with the blood, secretions, organs or semen of infected 138

Scott and Duncan 2001: 108, 134, 361, 366, 371. www.cdc.gov/ncidod/dvrd/spb/mnpages/dispages/ebola.htm 2003: 3; www.who .int/inf-fs/en/fact103.html 2003: 1. 140 Manson’s Tropical Diseases 1996: 653. 141 www.cdc.gov/ncidod/dvrd/spb/mnpages/dispages/ebola.htm 2003: 3; www.who .int/inf-fs/en/fact103.html 2003: 1. 139

650

chapter fifteen

persons”142 and this transmission occurs only by contact with a patient “in the acute stage of the disease,” and only if the person becoming infected has abrasions or cuts in the skin at the point of physical contact permitting contagion to enter (before the time of syringes).143 An outbreak of Ebola haemorrhagic fever in a locality in the Democratic Republic of Congo was subjected to an intensive study comprising twenty-seven households in which someone had been infected with the Ebola virus. It transpired that none of “the 78 household members who had no physical contact with a case during the clinical illness were infected. Ebola Haemorrhagic Fever is transmitted principally by direct physical contact with an ill person or their body fluids during the later stages of illness.”144 Clearly, this is a highly restrictive condition for the transmission of infection (compared, for instance, with air-borne cross-infection by infectious droplets) which makes for weak, even very weak powers of spread. This is the reason that filoviridal diseases appear “in sporadic, small or mostly even tiny outbreaks” and explains why there is “no carrier state.” Thus, all known and medically studied outbreaks of this type of diseases are characteristically sporadic and small even in their core areas in Western Africa. Contrary to Scott and Duncan’s assertions throughout their monograph,145 filoviridal diseases do not have the infectious properties necessary to explain the huge mortalities caused by historical plague epidemics. The reason that the references in this discussion are mainly to Ebola haemorrhagic disease is that the overwhelming proportion of cases of fioloviridal disease belongs to this category. Marburg disease is a rarity among the cases of a quite rare type of disease, which means that the constellation of necessary conditions allowing infection of human beings are even more specific, rare and local. Scott’s and Duncan’s dramatic accounts of extremely infective carriers of the disease walking or travelling through the late medieval and early modern countryside or towns disseminating the disease with tremendous efficiency are imaginary and fictitious. However, these accounts of mysterious “infectives” play a crucial role, for they are called upon in order to explain the spread of historical plague epidemics. 142 www.cdc.gov/ncidod/dvrd/spb/mnpages/dispages/ebola.htm 2003: 2; www.who .int/inf-fs/en/fact103.html 2003: 1. 143 Manson’s Tropical Diseases 1996: 653. 144 Dowell, Mukunu, Ksiazek et al. 1999: S87–S91. 145 See for instance Scott and Duncan 2001: 363, 376.

the alternative theory of scott and duncan

651

According to Scott and Duncan, the duration of the course of illness of historical plague disease normally is three to five days, and this proves that this is the duration of the course of illness of haemorrhaghic plague.146 However, they do not provide evidentiary support for this view. This does not mean that there is not interesting evidence available. In the study of twenty-seven households in a locality in the Democratic Republic of Congo where at least one member had contracted Ebola haemorrhagic fever (see above), it was discovered that: the median duration of the early phase of illness at home was 4 days (range 0–9). The median duration of the late (hospital) phase of illness, from admission to death or discharge, was 6 days (range 2–13) […]. The median duration of illness, defined as the time from onset of fever to death, was 10 days.147

This shows that the median duration of the course of filoviridal illness, the duration which occurs most often, is 2.5 times longer than observed in historical plague. The outcome of this particular study corresponds closely to the generalized information on this point given in the latest edition of Manson’s Tropical diseases 1996 that “Death occurs most commonly on the ninth day, but between the second and twenty-first day.”148 Again, Scott and Duncan’s assertion on the characteristic or defining features of haemorrhagic filoviridal disesase can be shown to be fictitious or spurious. According to the general standard works on bubonic plague, the normal or average duration of the course of illness in bubonic plague is three to five days, which corresponds to the observations made in historical plague epidemics and therefore constitutes evidence to the effect that these epidemics were bubonic plague. As mentioned above, Scott and Duncan assert with respect to important clinical manifestations that the “symptoms [of historical haemorrhagic plague] were violet and black spots and blotches […] or small red spots, indicative of a haemorrhagic disease, the bubo and pustules.”149 “Thus, when all the characteristic clinical features of bubonic plague are observed by contemporaries,150 Scott and Duncan simply declare that this is evidence of haemorrhagic plague without providing any research-based support to the effect that this is the case. This does

146 147 148 149 150

Scott and Duncan 2001: 85, 107–8, 144, 207–9, 380–1. Dowell, Mukunu, Kalazek et al. 1999: S88–9. Manson’s Tropical Diseases 1996: 653. Scott and Duncan 2001: 306. See above: 639–45.

652

chapter fifteen

not mean that relevant information is not available: according to Manson’s Tropical Diseases 1996, filoviridal disease does not display any such clinical features but “on the fifth to seventh day a morbilliform [measle-like] rash (never haemorrhagic) is visible on white but not African skins.”151 Neither are any of these clinical cutaneous manifestations mentioned in the presentations of the CDC or WHO on filoviridal haemorrhagic diseases, only the rash.152 Thus, haemorrhagic disease is not characterized by cutaneous haemorrhagic manifestations, i.e., by black, violet or red spots or blotches on the skin, contrary to what Scott and Duncan arbitrarily maintain. Neither are pustules mentioned in association with filoviridal diseases. Instead, all these features are, as shown above, usual manifestations in cases of bubonic plague. Scott and Duncan also assert, as mentioned previously, that the ordinary clinical occurrence of buboes does not at all prove that a disease is bubonic plague, but that buboes are also a characteristic feature of of haemorrhagic plague and other infectious diseases and, consequently, do not constitute a defining feature for a single specific disease.153 Centrally, they argue that it is a fact that the victims of both diseases [bubonic plague and haemorrhagic filoviridal diseases: my insertion] presented with enlarged glands and subcutaneous swellings […] The characteristic (but not specific symptom) of bubonic plague is the appearance of the bubo […] victims of haemorrhagic plague also sometimes presented with swollen lymph glands.154

These two assertions are obviously at variance with each other, since in the first citation buboes are presented as a general clinical feature of filoviridal disease, while in the second citation it is presented as an incidental or episodic type of occurrence. It has been demonstrated above as an indisputable fact that buboes as an ordinary clinical manifestation of an epidemic disease are a characteristic feature only of bubonic

151

Manson’s Tropical Diseases 1996: 653. Centers for Disease Control and Prevention, Special Pathogens Branch, www .cdc.gov./ncidod/dvrd/spb/mnpages/dispages/marburg.htm; Centers for Disease Control and Prevention, Special Pathogens Branch, www.cdc.gov./ncidod/dvrd/spb/ mnpages/dispages/ebola.htm, and same but ebotabl.htm. 2003. “Ebola Hemorrhagic Fever and Table Showing Known Cases and Outbreaks, In Chronological Order,” pp. 1–4 and 1–3; WHO Information: 2003. www.who.int/inf-fs/en,fact. “Ebola Haemorrhagic Fever,” Fact Sheet No. 103. 153 Scott and Duncan 2001: 6–7, 306, 362, 380–1, 388. 154 Scott and Duncan 2001: 362; Scott and Duncan 2004: 167. 152

the alternative theory of scott and duncan

653

plague and as such a defining feature of bubonic plague. Scott and Duncan’s crucial assertions to the effect that buboes are also an ordinary and characteristic clinical feature of other infectious diseases and of any or some form of Ebola or Marburg haemorrhagic disease are not supported by any reference(s) in a footnote or in the text to studies providing such clinical evidence, not in this context or anywhere else in their monographs. When Scott and Duncan at the very end of their monograph finally provide some systematic but deficient clinical and epidemiological information on filoviridal types of disease, their presentation does not contain a word about buboes.155 In the research literature published in the three decades following the discovery of Filoviridae in 1976, not a single patient has been registered who presented with a bubo or “swollen lymph glands.” This is the reason Scott and Duncan are unable to present a single case in support of their assertions on this crucial point, despite the fact that presumably most serious infectious diseases may occasionally infect a lymph node and cause the development of a bubo when infection enters through cuts or abrasions in the skin. In their monographs Scott and Duncan regularly claim identity between the incidence of buboes in cases of bubonic plague and in “haemorrhagic plague,” but the formulation “sometimes presented with swollen lymph glands” indicates episodic individual occurrence, which they also are unable to document. However, even if incidental or episodic occurrence had been registered, this would not have significance for the present discussion, since incidental occurrence is quite an ordinary feature of infectious diseases. The pivotal point is that bubonic plague is the only epidemic disease that presents with buboes as a regular and ordinary feature of the clinical panorama and this is therefore a defining feature of bubonic plague. It was shown above that this is stated in Scott and Duncan’s main source of medical information on bubonic plague, Christie’s textbook, where it is specified that buboes are a “distinguishing feature” of this disease.156 The Significance of Autopsies Finally, Scott and Duncan turn to autopsies of plague victims, comparing and discussing one modern autopsy of 1900 and three historical 155 156

Scott and Duncan 2001: 384–9. See above: 339.

654

chapter fifteen

autopsies from around 1660. Inexplicably, they have succeeded in finding just one modern report of an autopsy of a plague victim. This is a description of an autopsy of a sailor who had been aboard a ship sailing from Rosario in Argentina via Buenos Aires to King’s Lynn and died from plague near Cardiff in 1900.157 This autopsy was performed by two physicians, W.G. Savage and D.A. Fitzgerald, who had no prior experience with plague patients or plague autopsies and who had no background for deductive inference. It was also performed under difficult circumstances putting considerable restraints on their work: “The post-mortem examination of the patient W.G. was made at the mortuary attached to the crematorium […] owing to unavoidable conditions a more complete examination could not be made.”158 This is the only case of a modern autopsy of a plague corpse mentioned by Scott and Duncan, although thousands have been performed and numerous cases are described or reported in the standard works on plague. This paper is not mentioned in any of the standard works on plague. This calls for some methodological comments: a single specimen or individual occurrence, or, in this case, an isolated autopsy cannot be used for drawing generalized inference to fact or reality, it can only be used for establishing working hypotheses. Only a broader and more composite set of data including independent cases can constitute material for deduction and inference to reality or fact. As such, it is fallacious to use the autopsy of the sailor for inference to reality or fact and also introduce it as part of a comparison with historical autopsies for the purpose of making possible empirical differentiation between modern and historical plague. However, Scott and Duncan state undeterred and unreservedly: The important point to note here is that there are only limited signs of necrosis in this autopsy report, in stark contrast with the post-mortem examinations of those who died from haemorrhagic plague.159

The concluding reference is to the three historical autopsies which will be discussed immediately below; first some preliminary comments on the modern autopsy are needed. Since Scott and Duncan have named their alternative disease “haemorrhagic plague” and have identified it as a filoviridal disease, one must be permitted to presume that

157 158 159

Savage and Fitzgerald 1900: 1232–6. Cf. Walford 1900: 1232. Savage and Fitzgerald 1900: 1235. Scott and Duncan 2001: 71.

the alternative theory of scott and duncan

655

haemorrhages would be the characteristic feature. Yet here suddenly necrosis, not haemorrhages, is the crucial or decisive point, and this sudden new crucial point and turn of argument is based on a single autopsy by a couple of physicians who have never before seen a plague corpse. However, although Scott and Duncan seem to describe the autopsy report in some detail, central points are not mentioned. Savage and Fitzgerald emphasize that “All the cultivations made from the blood remained quite sterile.”160 This signifies that this plague patient, in contrast to over half of bubonic plague patients, did not develop significant secondary septicaemia.161 Consequently, “the solvent action of plague bacillus and its glutinous toxins”162 had not broken down the walls of veins or tissues of buboes to a degree permitting microbes to enter directly into the blood circulation.163 Since there is often an initial transient septicaemia in plague cases, this indicates that the infection dose (ID) in this case was small and the immune apparatus succeeded in eliminating the plague bacteria circulating in the blood stream.164 In septicaemic cases, the blood stream becomes the agent for the distribution of the plague bacilli to the organs of the body, and the plague toxins will damage the walls of veins and produce haemorrhages and necrosis in the internal organs and tissues, cutaneous haemorrhages and petechial or ecchymotic manifestations reflecting the bursting of damaged capillaries. This lack of (significant) septicaemia and, as it seems, small ID in the patient, are shown also by the unusual duration of the course of illness which began, according to the sailor’s wife, on 21 September and ended, according to the medical statement, with his death 4 October, after fourteen days of illness,165 in sharp contrast to the usual duration of three to five days. This is a strong indication of an atypical case of bubonic plague, information which Scott and Duncan neglect to pass on to their readers. It may seem that Scott and Duncan endeavoured to find an autopsy of an atypical case without significant septicaemia in order to be able to formulate a view on internal necrosis as a pivotal differential feature of haemorrhagic filoviridal plague in contrast to bubonic plague. 160 161 162 163 164 165

Savage and Fitzgerald 1900: 1235. Benedictow 19993/1996: 243–58. Simpson 1905: 235. Simpson 1905: 227–34. Pollitzer 1954: 204–5, 414. Savage and Fitzgerald 1900: 1234.

656

chapter fifteen

The question must now be asked: Why do Scott and Duncan believe that the standard works on plague do not describe autopsies? In fact, several of them do, and on the basis of thousands of autopsies produced by and presented by outstanding scholars who have had overwhelming opportunities to perform autopsies on plague cases in India, China and elsewhere. In his chapter “Morbid Anatomy and Pathology,” Simpson provides over twenty-three pages of both generalized information from a great mass of autopsies and detailed descriptions of thirteen individual autopsies of plague cases. These thirteen autopsies could constitute an acceptable basis for generalized inference to the manifestations of plague disease as observed in post-mortem examinations at a significant level of tenability but represent in this case a representative sample of a much greater number of autopsies. Scott and Duncan’s approach to this question is so extraordinary that I found it worthwhile to count the number of times Simpson uses the terms “haemorrhage” and “necrosis” in the twenty-three pages. The tally was that the term “haemorrhagic” or “haemorrhages” are used a total of seventy-two times, and the term “necrosis” or “necrotic” sixteen times. Summarizing the significance of these clinical manifestations, Simpson states: Haemorrhages are, in fact, one of the characteristics of the disease [bubonic plague: my insertion]. There are haemorrhages in nearly every organ of the body, on the serous and mucous coats of the cavities, and in and around the specially affected lymphatic glands. The plague bacilli and their toxins appear to have a peculiar coagulative and necrotic effect on the wall of the smaller veins and minute capillaries, leading to exudations.166 Bubonic plague, judged by the pathological changes observed in the dead body, is a disease both of the lymphatic and vascular system, on which the plague bacilli and its toxins when brought in contact with them in large numbers and quantity exercise an inflammatory, coagulative and necrotic effect. The microbic agent and its toxins thus acting lead to enlargement of the external and internal lymph glands, necrosis of their substance and often haemorrhage or infiltration into the surrounding tissues, to dilatation of the veins and capillaries, to destruction of their walls, to haemorrhagic extravasations into nearly every part of the body.167

166 167

Simpson 1905: 235. Simpson 1905: 239.

the alternative theory of scott and duncan

657

This summary of observations made in post-mortem examinations or autopsies of plague victims is in full accordance with the shorter accounts in other later standard works on plague.168 It is bubonic plague which is the true haemorrhagic plague, and this is manifested externally by petechiae and ecchymoses on the skin and occasional bleeding from the nose and mouth,169 and internally by comprehensive haemorrhages in the internal parts of the body.170 There is often comprehensive necrosis of the internal organs and the vascular system in cases of bubonic plague. Scott and Duncan use the isolated single modern autopsy for comparison with descriptions of three historical autopsies, again without taking into account questions of historicity and source-criticism. First, they cite a description of a single post-mortem examination made clandestinely by George Thompson, the physician, during the last plague in London in 1665,171 “in his time greatly daring.”172 This is the only post-mortem which is known to have been performed in connection with English plague epidemics. Thus, Thompson was not only without prior experience in performing an autopsy on a plague victim, he had no formal anatomical training in post-mortem examinations of dead persons on which he could base his examination and understanding of what he observed. Consequently, his interpretations of what he saw were dependent on and affected by his highly deficient knowledge of human anatomy and its tremendous complexity. Scott and Duncan also repeat Cipolla’s citations of two brief contemporary reports on autopsies performed in Naples and Rome respectively in 1656–7173 which were originally published by P. Savio.174 These three historical autopsies represent the neonatal phase of the development of European anatomy by post-mortem examinations, and they are performed by physicians without formal training in anatomical dissection and with highly limited understanding of the functions of the various parts of 168

Pollitzer 1936: 158–62; Chun 1936: 311–2; Pollitzer 1954: 203–17. Simpson 1905: 247, 265; Manson’s Tropical Diseases 1921: 268. 170 Cf. Manson’s Tropical Diseases 1982: 339: “The characteristic appearance of plague in a necropsy is that of engorgement and haemorrhage, nearly every organ of the body participating more or less.” 171 Scott and Duncan 2001: 219. 172 Bell 1951: 128–9. The complete description of the autopsy is cited by Bell 1951: 335–8. 173 Scott and Duncan 2001: 306; Scott and Duncan 2004: 224. 174 Savio 1972: 139–40; Cipolla 1981: 95–6. 169

658

chapter fifteen

human anatomy and what caused changes in the appearance of various internal organs and tissues.175 Cipolla states the point tersely: it must be conceded that the rudimentary technology and the inability to distinguish between pathological and cadaveric conditions made the post-mortem reports of the period in question practically useless.176

The second part of Scott’s and Duncan’s comparison disappears here into thin air as useless, a victim of the poor level of development of medicine at the time. However, in addition Thompson’s autopsy performed on a body still lying in its coffin can only be used as evidence on the beginning of the history of medical autopsies in early modern Europe. In his account, Thompson is frank about his purpose: he did the autopsy for his “own instruction, and the satisfaction of all inquisitive persons.”177 Thus, both parts of the comparison are useless for the application of comparative methodology. It is a fallacious circular assertion when Scott and Duncan summarily conclude that these are “post-mortem examinations of those who died from haemorrhagic plague” as if this identification of the disease is self-evidently correct and not the central problem to be resolved. In their monograph, Scott and Duncan cite part of one of the Italian autopsies and conclude: “The similarities between the foregoing and the case reports, description of symptoms and autopsy reports of plagues in England, particularly in London, are striking.”178 The use of the plural form indicating that more than one autopsy was performed in England at the time is confusing and must be a slip of the pen, as there is only one. Clearly, the fact that there are similarities between the English autopsy and the two Italian autopsies does not warrant any specific conclusion as to the identity of the disease and does not affect the identification with bubonic plague. When Scott and Duncan later revert to the topic of autopsies, they refer first to Thompson’s autopsy and maintain that it shows conclusively that, in patients who died, these outward signs [petechiae: my insertion] were accompanied by extensive internal necrosis in which “no organ was found to be free from changes” […] comparable degradative and necrotic changes were found in the autopsies in

175 176 177 178

Scott and Duncan 2001: 71, 381. Cipolla 1981: 96. See fn. 172. Scott and Duncan 2001: 306.

the alternative theory of scott and duncan

659

Rome and Naples in 1656–7 (section 11.3.2). These signs are all indicative of a severe haemorrhagic illness.179

This crucial assertion that extensive internal necrosis proves the identity of the disease to be filoviridal haemorrhagic disease is based on two erroneous assumptions: (1) Scott and Duncan imply on the basis of the single modern British autopsy of 1900 that bubonic plague cases do not present with external comprehensive cutaneous haemorrhages and with comprehensive internal haemorrhages and necrosis, which has been shown above not to be correct, on the contrary, exactly the opposite is the case. The choice of the British autopsy of 1900 serves the objective of allowing them to maintain that the three historical autopsies with their probable descriptions of necrosis cannot be bubonic plague and therefore must be cases of filoviridal haemorrhagic disease. This is, then, an instructive example of the fallacious use of comparative methodology because the modern part is not representative and the historical part of the comparison is based on only three cases imbued with serious evidential weaknesses of quality, competence, and anatomical knowledge. Crucially, it is fallacious because the identity of the disease studied in the historical autopsies has not been clarified by comparison with representative modern autopsies of bubonic plague cases and representative autopsies of victims of filoviridal disease.180 In their popularized monograph, Scott and Duncan cite and comment on Thompson’s autopsy and the two Italian autopsies in purported comparative perspective with modern autopsies of bubonic plague and state this even more clearly: The signs, symptoms and autopsy reports of victims of bubonic plague are entirely different from these: they do not display God’s tokens, nor is there widespread necrosis of the internal organs.181

Here Scott and Duncan erroneously assert that they have presented a sufficient number of modern autopsies of bubonic plague cases to permit generalized conclusions and also erroneously assert that autopsies of cases of bubonic plague did not display petechiae or widespread internal necrosis. On both of these points, Scott’s and Duncan’s argument must be considered misleading. 179 180 181

Scott and Duncan 2001: 381. See also Cipolla’s valuable remarks on these problems in 1981: 94. Scott and Duncan 2004: 223–4.

660

chapter fifteen

(2) The other assumption which allows them to produce this autopsybased argument is their claim that comprehensive necrosis is characteristic of cases of Ebola or Marburg haemorrhagic diseases without presenting any evidence in support based on necropsies of victims, despite the fact that some relevant evidence is available: the CDC make a few relevant comments to the effect that a “rash, red eyes, hiccups, internal and external bleeding may be seen in some patients.”182 The WHO’s statement on the matter is quite similar: “rash, limited kidney and liver functions, and both internal and external bleeding.” As can be seen, in these works nothing is said about necrosis. However, in the last edition of Manson’s Tropical Diseases it is stated that The virus is pantropic183 and invades cells producing necrotic lesions in all organs. The liver shows necrosis of single hepatocytes184 with fatty degeneration and necrosis at the periphery of the lobules […] Bleeding occurs in the majority of cases, appearing towards the end of the fifth day with haematemesis185 and bloody diarrhoea. On the fifth to seventh day a morbilliform186 rash (never haemorrhagic) is visible on white but not African skins.187

According to Manson’s Tropical Diseases, the clinical features of the Marburg form of filoviridal disease “are almost identical to Ebola virus disease.”188 Thus, although Scott and Duncan have neglected to document the main clinical features of filoviridal diseases, it can be confirmed on their behalf that such cases are, indeed, characterized by internal and external bleeding and by widespread necrosis of internal organs. However, since this is also the case with bubonic plague, these features cannot serve as a base for differential identification of the infection by reports of post mortems produced around 1660. It is probable that there are differences which can serve the differential 182

www.cdc.gov/ndicod/dvrd/spd/mnpages/dispages/ebola.htm 2003: 3. “Pantropic” means having an affinity for or indiscriminately affecting many kinds of tissues. 184 Hepatocytes make up 70–80 per cent of the cytoplasmic (gelatinous mass that “fills” most cells) mass of the liver. These cells are involved in protein synthesis, protein storage and transformation of carbohydrates, synthesis of cholesterol, bile salts and phospholipids, and detoxification, modification and excretion of exogenous and endogenous substances. The hepatocyte also initiates the formation and secretion of bile. 185 “Haematemesis” means vomiting of blood. 186 “Morbilliform” means resembling measles. 187 Manson’s Tropical Diseases 1996: 653. 188 Manson’s Tropical Diseases 1996: 654. 183

the alternative theory of scott and duncan

661

identification exist and establishment of another defining feature, but they can only be ascertained by modern pathologists or anatomists as part of a project aimed at this objective. The African Confinement Importantly, with respect to Filoviridae “researchers believe that the virus is zoonotic189 and is normally maintained in an animal host that is native to the African continent.” A special study on the possible host animal emphasizes that “Marburg and virulent Ebola viruses are maintained in hosts that are rare and have little contact with humans or do not readily transmit the virus.”190 This point makes it rather impossible to envisage outbreaks and spread in Europe or Asia of these diseases where this (these?) animal host(s?) and microbiological zootic reservoir(s) do(es?) not live. Instead of facing this problem, Scott and Duncan start their discussion of the spread of the Black Death in Europe with Sicily and must reject the possibility that the Genoese galleys returning from the Crimea were the source of infection. They support or borrow an untenable view of Twigg191 to the effect that the Black Death could have been shipped to European Mediterranean ports out of Syria or the Levant.192 In reality and long established fact, the disease arrived about the same time in Syria and the Levant as in England, long after it had arrived and spread in large parts of Mediterranean Europe and spread from Marseilles all the way to Bordeaux on the Atlantic coast of France, whence the contagion was shipped to Rouen, Melcombe Regis and north-western Spain (A Coruña?).193 In an effort to strengthen their effort to avoid having to address the origin of the Black Death in the south-eastern Russian plague reservoir and transportation by ship out of the Crimea and via Constantinople to the European Mediterranean cities, and move closer instead to the homeland of filoviridal viruses, Scott and Duncan arbitrarily add North Africa:

189 Any infectious disease that is able to be transmitted (vectored) from animals, both wild and domestic, to humans. 190 Monath 1999: S127. 191 Above: 581, 585–6. Benedictow 2004. 57–67, and map pages 1–2. 192 Scott and Duncan 2001: 317, 318, 328, 332, 370, 384. 193 Benedictow 2004: 62–5, 68–104, 126–30.

662

chapter fifteen The Great Pestilence most probably originated in the Levant or from the ports of North Africa.194

This is simply impossible and is easily corrected.195 “Most probably” is an assessment of tenability at the highest possible level which requires maximum empirical documentation. Scott and Duncan have not consulted the only and fine monograph on the spread of the Black Death in the Middle East and North Africa by M.W. Dols, which would have clarified the matter. Scott and Duncan maintain also that the plague epidemics which came from overseas in the fourteenth and fifteenth centuries probably originated from the Levant and North Africa and entered via the ports at Venice and Sicily, or from France via Genoa and Leghorn [Constantinople: my insertion].196

Here the level of tenability is lowered to “probably,” which is much higher than hypothetical or possible and requires a good empirical documentation. However, they again offer no evidence. Summary and Conclusion It has been shown in the preceding discussion and analysis of the alternative theory of Scott and Duncan that it is not based on modern medical research on Ebola or Marburg haemorraghic diseases and therefore has an arbitrary character. This has led to their arbitrary assertions of a strongly mutated variant of one these pathogens which should have equipped it with greatly different properties from the genetic origin and that miraculously were tailor-made to the needs of their alternative theory. As noted above, to introduce the concept of evolutionary developments by mutation without presenting a functional principle of selection is a fallacy of methodology. This mutated variant is arbitrarily assumed to have disappeared at the cost of making it impossible to satisfy the central requirement for all scientific work, namely testability. However, the theory is too flawed to be rescued by such means. In the popularized version of their monograph, they do not reject the filoviridal theory altogether but they also launch a theory of an unknown

194 195 196

Scott and Duncan 2001: 370, 317, 318, 328. Benedictow 2004. 65–7. Scott and Duncan 2001: 317.

the alternative theory of scott and duncan

663

type of disease that also since has disappeared. This may suggest that medical scholars have pointed out to them that the filoviridal basis of their theory is at great variance with present knowledge on filoviridal diseases. Scott and Duncan have invented a phantom disease that suits their case for an alternative theory but does not fit the facts on the ground.

CHAPTER SIXTEEN

COHN’S ALTERNATIVE THEORY Cohn concludes with absolute certainty that the Black Death was not bubonic plague caused by Yersinia pestis but he is completely unable to identify any known disease that could have been the cause of the Black Death or later historical plague epidemics.1 Since he argues strongly both in his introduction and in his concluding chapter that survivors of the disease acquired good and lasting immunity, and that plague therefore soon took on the character of a child disease, he has clearly a viral disease in mind: after several strikes, it became domesticated as a disease largely of children. By contrast, to repeat, modern Yersinia pestis is unusual: humans have no natural immunity to it and cannot acquire it.2

He also has in mind a disease spread by cross-infection with high spread rates as emphasized on the first page and repeatedly later.3 Considering that we are discussing an epidemic disease operating with great formative powers on European society over several centuries which wreaked havoc in over thirty large-scale waves across the Continent and in innumerable local outbreaks between these waves, and which therefore left much evidence of various kinds to posterity, much more evidence than any other disease, this may seem a rather puzzling outcome. The bubonic plague theory represents a consensus based on ample material evidence and studies by numerous fine and outstanding scholars and researchers. It has been shown in Part 3 and elsewhere that rejection of this huge corpus of fine scholarly work requires comprehensive breaches of the ordinary methodological and source-critical principles of scholarly work and comprehensive negligence of the 1

Cohn 2002: 1, 247. Cohn 2002: 2–3, 249, 212, 238, 249. As shown above, Yersinia pestis produces, as usual for bacterial pathogens, only relatively weak and transient immunity in survivors, and re-infection of survivors in the same epidemic is quite usual. See chapter 6: 212–7. 3 Cohn 2002: 1–3, 138–9, 209; Cohn 2005: 1354–5. Cohn and Alfani 2005: 203, where the spread rates of historical plague is said to be similar to those of influenza. 2

cohn’s alternative theory

665

primary research and standard works on bubonic and primary pneumonic plague. In order to clear the way for his own alternative theory, Cohn shows himself willing in his Part I to employ extraordinary means to disparage the work of all scholars in the field of historical and medical bubonic-plague research who have made valuable contributions and confirmed the bubonic-plague theory, which means almost every scholar in the field. The revealing character of these endeavours is reflected in the titles of the chapters “Scientists Square the Circle” and “Historians Square the Circle,” an accusation of prevailing incompetence and intellectual dishonesty which cannot be credible to anyone as characteristics of the dedicated work of historians and physicians on the subject. In fact it is only revealing of the sort of means his alternative theory requires. In Part 2, “How S.K. Cohn Makes Physicians and Historians Square the Circle” it is shown that his assertions and purported material points are untenable and invalid. Cohn’s monograph is therefore primarily characterized by a furious attack on the bubonic plague theory of historical plague and only marginally by the development of an alternative theory, since he is unable to identify and present in a testable form an alternative disease known to modern microbiology or medicine. In this construction, his monograph differs sharply from the monographs of Twigg and Scott and Duncan and from Karlsson’s paper where the construction and establishment of an alternative theory stand squarely in focus. In these cases, the attacks on the bubonic-plague theory serve the legitimate purpose of being attempts at clearing the way for the alternative theories, although in the practical implementation they have been shown to be untenable and exhibit little respect for the limitations of the methodology of historical, medical, and social science. The various central aspects of Cohn’s frontal attack on the bubonic plague theory have also been thoroughly discussed in various chapters of this monograph and have been shown to be untenable for various methodological and material reasons.4 Cohn concludes that historical plague must have been a viral disease spread by cross-infection that since has disappeared, and that is all he will say about the central matter of his monograph.5 This reveals that

4 Above: 26–69, 74–7, 84, 86, 93–7, 136, 144–5, 151–273, 289–301, 314–20, 324–5, 340–80, 386 fn. 20, 387, 411–5, 487–8, 562, 647. 5 Cohn 2002: 247–50.

666

chapter sixteen

his monograph is an unsuccessful attempt to construct an alternative theory without being willing to admit defeat. Against the broad background of the preceding discussions of Cohn’s principal arguments, it can therefore be dealt with briefly. It should suffice to refer to part 4, chapter 10, “Defining Feature 4: DNA of Yersinia pestis Reclaimed from Skeletal Remains in Historical Plague Graves” which presents the by now quite considerable material on DNA and proteins of Yersinia pestis recovered in plague graves from the first pandemic of plague, the so-called Justinianic pandemic of 541–766, and the second pandemic of 1346–722. The systematic identification of the DNA of Yersinia pestis in quite numerous studies of dental pulp and also proteins of DNA in bone material taken from skeletal remains in plague graves of these periods situated in highly varied locations and parts of Europe, represent a decisive breakthrough. These by now quite numerous and geographically varied studies exclude accidental findings and also exclude the possibility that there could have been a concomitant incidence of some other disease that should have been overlooked in all these studies. Also, each of the other defining features presented and discussed in Part 4 excludes Cohn’s at best rudimentary alternative theory, and the collective impact is devastating. Bubonic plague is the only known epidemic disease that presents with buboes as an ordinary clinical feature: it is a defining feature of bubonic plague. The only other disease which normally presents with buboes is tularaemia, also a bacterial disease which is also normally transmitted by insects. And this is not, as underlined above, a coincidence, but associated with how ectoparasites transmitting contagion will often or normally deposit it subcutaneously in a position suitable for drainage through lymphatic tracts to lymph nodes. Epidemic occurrence of buboes is, nonetheless, a defining feature of bubonic plague, since tularaemia has only an episodic or endemic type of occurrence and only outside human cultivated areas, principally in forests and other types of wilderness, and is highly associated with hunters who in these environments will be at risk of being exposed to specific ectoparasites (see above). No epidemic viral disease is known that is clinically characterized by the normal occurrence of buboes. In principle, this represents an exception-free rule which also for all practical purposes excludes chance. There must be a systematic massive reason producing systematic clinical reflections or lack of reflections in the form of an exception-free rule. One could start by asking how contagion conveyed

cohn’s alternative theory

667

by droplets in cross-infection and inhaled into the lungs would spread from there to lymph nodes with anything approaching normal or frequent incidence? The lymph nodes are part of the body’s first line of defence against invasion through the skin, which explains the exclusive role played by ectoparasites in disseminating disease characterized by buboes as a normal or ordinary clinical feature. Cohn’s assertion about the microbiological viral nature of historical plague contagion contains therefore also an unformulated assertion to the effect that the only viral disease that ever presented with buboes as a normal clinical feature in patients, has since disappeared. This unique feature could on scholarly premises possibly be discussed in terms of the usefulness of speculative ideas or, perhaps, of microprobabilities. Since Cohn does not even attempt to explain how inhaled viral contagion could be spread (frequently) to the lymph nodes, these suggestions should also rather be excluded from consideration. Viral diseases imply good and durable immunity in survivors and Cohn argues energetically that this was the case in historical plague epidemics. However, it has been shown above that his material is much too deficient to be usable for such an evidentiary purpose. It has also been shown that there are, in fact, quite numerous references in contemporary sources to re-infections of the same person, also in the same epidemic, and even cases of persons who had been infected three times in the same epidemic. It has also been shown that the mortality rates caused by historical plague epidemics and the long-term development of population size depend on the absence of immunity so that the whole population is susceptible to plague infection the next time an epidemic appears, including survivors. One important aspect of mortality in the case of a disease that does not provide lasting immunity in survivors and which therefore affects the whole population next time it appears, including the adult population, is that parents fall ill and cannot provide nursing care for their children or each other, which causes considerable supermortality in the form of secondary catastrophic mortality, especially among children, the most vulnerable part of the population. When the adult population is also affected, economic work grinds to a halt; in the case of historical plague epidemics this is often in late summer and early autumn before the start of the harvest. Plague epidemics are therefore often accompanied by and followed by malnutrition or starvation that cause further supermortality and also may unleash hungerrelated diseases in weakened and vulnerable populations.

668

chapter sixteen

These are important arguments and perspectives for the understanding of the huge mortality rates in historical plague epidemics and their long-term demographic effects. This means that while a disease which confers immunity in survivors in principle may have as serious an impact as other types of infectious diseases in the first original onslaught on a naïve population, it must be very unlikely that a disease which confers long-term immunity and therefore mostly hits children when it reappears could cause the dramatic long-term decline of the European population which was observed in the Late Middle Ages. Arguably, it is not possible according to quite mechanical demographic considerations. In this perspective, it becomes highly unlikely that historical plague could have been a disease conferring lasting and good immunity in survivors. Cohn is unable to explain why a viral disease spreading efficiently by cross-infection should have a seasonality strongly associated with the warmer seasons, a feature so easily explicable by a theory based on a disease transmitted and spread by insects. The powers of spread of this type of viral disease tend to increase with cold wintry weather when people tend to crowd or huddle closer together in small(er) rooms which can more easily and affordably be heated and is, therefore, the best time for colds and influenza, for instance. Cohn does not attempt to identify any argument that can serve to explain this seasonal feature of historical plague as a reflection of a viral disease spreading by crossinfection, which represents an independent reason for falsification of this theory. The unique feature of latency periods is also inexplicable in terms of Cohn’s alternative theory or any other alternative theory based on interhuman cross-infection. Scott and Duncan at least try to address and resolve this particular and conspicuous feature of historical plague instead of ignoring it. The pattern of latency periods in modern and historical plague, which is easily explicable on the basis of the known properties and developments of bubonic plague infection by rat fleas, remains unexplained by all advocates of alternative theories, and therefore retains its status as a unique and consequently defining feature of this disease. Cohn does address the extraordinary and unique feature of bubonic plague called the inverse correlation between population density and mortality/ morbidity rates. His ferocious and unfair attacks on Hankin’s pioneering observation of this phenomenon not only in contemporary India but also in historical plague epidemics is a sad chapter in the

cohn’s alternative theory

669

historiography of plague, as is his willingness to ignore all later research corroborating and enlarging upon Hankin’s original observation. This feature is incompatible with the theory of a virus spreading by crossinfection, which would enjoy increasing powers of spread with increasing population density of susceptible populations. Cohn appears to believe that no legitimate scholarly demand can be made on him for explanation of the disappearance of his alternative viral contagion. It is just presented as a magic act for naïve believers, which on methodological grounds makes it legitimate to presume that it disappeared into the thin air from which it was taken. One should consider the fact that Cohn has invented a virus with great powers of transmission and dissemination within the enormous variation of social milieus and circumstances and societal structures in the broad European experience over three centuries and two historical periods, or if the Justinianic pandemic is included, two more centuries and another historical period must be added. One should also consider the fact that a pathogen with great powers of transmission and dissemination in such enormously varied social milieus and circumstances and societies would have dynamic properties that would make it most unlikely that it would simply disappear. As a minimum, the demand must be made on Cohn, or rather he should have made this demand on himself, to illustrate or demonstrate how such diseases historically have disappeared in order to identify the social or physical conditions in which this would occur and provide this part of his theory a deductive basis, however slight. When Cohn does not fulfil this minimal demand on his theory, it shows that his theory is just arbitrary. This is a point in the discussion where a helpful hand could be useful. It is not accidental that historically important or significant epidemic diseases have displayed strong dynamic properties and therefore generally seem, as far as can be ascertained, to be around still today. Only quite recently has it been possible to witness how historically important epidemic diseases, through the efforts of modern medical science and huge vaccination programs implemented by national governments and in a global perspective by the UN, have been eradicated or appear to be in the process of eradication, such as smallpox and poliomyelitis, respectively. The extreme rarity of the disappearance of a historically significant epidemic disease in the pre-scientific past can be ascertained by a look at E.H. Ackerknecht’s monograph on the history and geography of the most important diseases: he does not present a single case.

670

chapter sixteen

However, there is actually one instance available for study. The only historically known disease of some significance to have disappeared by itself is the sweating sickness (Sudor Anglicus) which appeared in England in the years 1485, 1506–8, 1517, 1528, and 1551,6 but spread also abroad in 1529 reaching, for instance, Denmark, south-eastern Norway and the Duchies of Schleswig and Holstein in northern Germany.7 The long intermissions of this disease could be taken to indicate some special problems or requirements of transmission or dissemination which made it susceptible to extinction and also indicate a zootic reservoir. It can hardly have been a viral disease disseminated by cross-infection since it primarily spread in the late summer and early autumn,8 which may indicate an insect-borne or water-borne disease.9 The demographic effects of the epidemics of this disease appears to have been quite small,10 “it had only minor effects on mortality in larger communities,”11 which can also be taken to indicate an inefficient mode of transmission. An important aspect of this point is that the course of disease appears to have been extraordinary severe and brief, death often occurring within twenty-four hours according to contemporaries.12 According to the Norwegian and Danish Councillor of the Realm Henrik Krummedike in a private letter to his daughter, people “die very

6

Shrewsbury 1971: 154–68, 180–5; Slack 1985: 70–1. Christiansen 2005: 80–96; Benedictow 2002: 148–50. Ibs 1996: 126–7. Christiansen 2005: 88–9, has not found Henrik Krummedike’s letter from Norway to his daughter in 1529, mentioned by C.F. Allen 1870. It is published in Diplomatarium Norvegicum, vol. IX, no. 644, 16 September 1529, and cited in Benedictow 1977: 132, and 2nd ed. 1987, and is more comprehensively and better discussed in my Norwegian plague history of 2002: 150–2. Allen is mistaken in assuming that it was written in Oslo; it was written in the Danish port town of Varberg in the county of Halland on the eastern side of Kattegat north of the Sound after Henrik Krummedike had returned from Oslo where he was a leading member of Duke Christian’s entourage as a leading member of the Council of the Realm and expert on Norwegian affairs. In this letter Henrik Krummedike is thus referring to the sweating sickness in Halland, the northeastern Danish border province with Sweden which was not conterminous with the Norwegian border province Båhuslen in the north, since a narrow band of land along the estuary of R. Göta Älv was Swedish and separated Båhuslen from Halland. Other sources associated with Henrik Krummedike (whose private archive is preserved) show that the sweating sickness spread in a serious way also into Båhuslen where it caused some desertion of tenancies. Benedictow 2002: 152. 8 Christensen 2005. 83; Slack 1985: 83–4. See also date of letter mentioned in previous footnote. 9 See above: 311. 10 Slack 1985: 70–1; Benedictow 2002: 152; Christensen 2005: 82–3. 11 Slack 1985: 71. 12 Slack 1985: 70. 7

cohn’s alternative theory

671

fast, so that when they get it, they could hardly stand it for half a day or one day at the most.”13 This feature provides an explanation for its disappearance, namely that it killed its victims too fast to allow sufficient incidence of transmission to occur and assure its survival by infection, so the probability of transmission of the infection from one diseased person to a healthy person fell under one and the epidemic faded away, and soon also the disease itself for ever.14 This is the pattern or model of primary pneumonic plague which cannot sustain an independent existence in continuous form because it is contagious on average only in 0.8 day (see above), much the same as in the case of the sweating sickness, but can arise anew from cases of bubonic plague who develop septicaemia (note also the development of noncontagious forms, see above). Not a single case of an important epidemic disease with great powers of spread in a great variety of social circumstances over centuries is known to the history of medicine to have disappeared by itself as presumed by Cohn’s theory, which emphasizes its arbitrary character and why it is very improbable. At the heart of Cohn’s alternative theory is therefore an assertion of the unique occurrence of such a phenomenon, so superbly unique that he is not able to exemplify its factual occurrence in history and its social premises. Methodology is turned on its head when this serves the defence of his theory by providing a quasiexplanation of why his theory is not testable and, as he seems to believe, therefore not falsifiable. However, it must again be emphasized that testability and falsifiability are indispensable properties of all scholarly hypotheses compatible with the methodology of science, untestability means falsification ipso facto as a tenable and valid assertion of any aspect of (human) reality. Cohn’s alternative theory of the microbiological nature of historical plague can be rejected or invalidated on a number of independent grounds, since it is incompatible with methodological, medical, epidemiological, microbiological and other types of ordinary empirical premises. Some of his assertions or the central implications of his theory must be deemed extraordinarily improbable or speculative. One should consider that all margins of uncertainty relate to each other

13 Diplomatarium Norvegicum, vol. IX, no. 644, 16 September 1529, see also footnote 203. My translation from the original source. 14 See also above: fn. 5.

672

chapter sixteen

multiplicatively, and the multiplicative effects of highly improbable or speculative assertions are only observable in an intellectual electronic microscope. This reflects also the fact that Cohn’s monograph is primarily a fierce attack on the bubonic-plague theory of historical plague, since he is unable to identify and present an alternative disease known to modern microbiology or medicine or, as it seems, identifiable by paleomicrobiological analysis. Instead, his inability to identify an alternative disease and the extraordinary means he employs to do away with the bubonic-plague theory reflects the fact that the bubonic plague theory is solidly founded in good scholarly work.

EPILOGUE In this monograph, the alternative theories of the microbiological nature of historical plague presented by the so-called revisionists against the bubonic plague theory have been thoroughly discussed. The central arguments against the bubonic plague theory have been discussed in comprehensive separate chapters in Part 3 and shown to be based on ignorance of the primary studies and standard works on bubonic plague. On the basis of the scholarly literature, it has been demonstrated that their central assertions are untenable; these tenets include: (1) the assertion that bubonic plague spreads only contiguously between conterminous rat colonies, (2) the assertion that the black rat was not widespread and usual all over Europe, (3) the belief that the relatively small mortality rates in India around 1900 compared with historical plague epidemics were due to differences between the diseases (rather than the availability of modern anti-plague techniques in India), and (4) the assertion that survivors acquired persistent immunity for which there is no evidence (instead there is much evidence to the contrary which indicates a bacterial disease). All basic conditions for the spread of bubonic-plague epidemics were present in Europe at the time of the Black Death and bubonic plague has the properties needed for spreading efficiently all over pre-Industrial Europe. Next, in Part 4 it was shown on the basis of the medical and epidemiological literature that bubonic plague is characterized by a number of defining features which are common to modern bubonic plague and historical plague epidemics, among them (1) latency periods, (2) inverse correlation between mortality rate and population density, (3) seasonality, (4) buboes as a normal clinical feature in epidemics, and (5) the reclamation of the DNA and proteins of Yersinis pestis in biological material taken from historical plague graves associated with the Justinianic pandemic 541–766 and the late medieval and early modern epidemic in the period 1346–1722. The correspondence between defining features of modern bubonic plague and historical plague constitutes definite proof, with several instances of independent sufficient proof, that historical plague epidemics were bubonic plague. In Part 5, it was demonstrated that all of the alternative theories are impossible, are argued in methodologically and source-critically

674

epilogue

seriously flawed ways and on epidemiologically, medically, and materially untenable grounds. On these grounds, the tenability of the bubonic-plague theory of historical plague epidemics is confirmed. Criticism, objections and the ambition to construct new explanatory models or new theories are at the heart of all good scholarly work. It has been a central objective of this monograph to improve the standards of possible alternative theories of the nature of bubonic plague in the future by a comprehensive presentation of the methodological and material prerequisites or conditions which must be satisfied in order to form serious academic propositions deserving of serious discussion in this field of scholarly work and research.

APPENDIX ONE

BLACK DEATH MORTALITY IN SIENA: THE MATERIAL PROVIDED BY THE NECROLOGY OF THE MONASTERY OF SAN DOMENICO IN CAMPOREGIO AND SUMMARIZED IN TABLE 5 This appendix contains the demographic material used and systematized in Chapter 6: 245–68 and serves the purposes of full documentation and testability and supplementary presentation of source-critical principles. The Necrology is written in Latin by scribes who were not trained in keeping demographic records. They have no standard form in which they record the information, and thus they provide varying types or pieces of information. Scribes often give only very brief and incomplete information on social status, occupation or profession, marital status (for women), and so on. They also have varying personal knowledge of the persons they record as buried in the cemetery. One scribe takes a strong interest, probably because he thought it was responsibility to do so, in giving accurate descriptions of the location of the place of interment within the cemetery or buildings. One should note that the Necrology’s editor has numbered the burials, but because more than one person was laid to rest in the same grave on a number of occasions, the number of interred is somewhat higher than the number of burials. In some cases, the bones of persons buried elsewhere are transferred to a grave in the cemetery, and so on, burials that must be deleted from the material. On two occasions in the Black Death, a number of unknown persons, three and four to six persons respectively, are laid in the same grave without specification of name or gender, namely 796–3, 839–4/6, which means that the number of registered males and females are smaller than the number of interred. All human beings are either sons or daughters, whatever their age. The Latin terms filius and filia are used to designate patronymics for identification of fathers independent of age; one must, therefore, keep in mind that use of these terms do not specifically denote a child, though they are also used to designate children. The terms filius and filia are inaccurate terms for indications of age. The only certain identifications of non-adult age, i.e., below the age fifteen, are the terms puer = boy (Nos. 843, 881, 896, 976, 996, 1176, 1212/1229, 1227, 1231, 1233, 1425, 1909), puella = girl, (Nos. 466, 913, 1189, 1224, 1234, 1427, 1450, 1839), and parvulis = boy (1116–2, 1550). The term juvenis = youth (1054, 1070–2, 1071, 1667) denotes persons around age fifteen. For practical reasons, here the age category of child, ages 0–14, includes all that are called filius or filia or iuvenis without indication of marital status or other indication of adult age (for instance, no. 113; Lippa, bighina nostra, filia domine angele), or no. 1138 (Iohanna filia Antonii et uxor […]), which may produce a slight exaggeration in the number of children. In the years 1338–46

676

appendix one

there are sixteen cases where the scribe(s) indicate(s) that the father is dead by adding olim = “deceased,” to the father’s name; this happens in the cases of seven males and nine females (551, 582, 597, 608, 611, 667, 892; 279, 294, 312, 633, 658, 1021). Since this practice is discontinued by subsequent scribes (except for one case in 1351, no. 892, and one in 1360, no. 1021), and since the father had died, at least some and quite likely most of these recorded as filii or filiae presumably were adults, and for practical reasons all of these persons are considered adults; the other option would be to delete these entries from the material. In the presentation of the basic material of children, males are mentioned first under each period or year (M) and females next (F). Children 1337–39: Nos. M (1337) 236; M (1339) 304; F (1337) 255. Children 1340: Nos. M 333, 412, 417, 473, 492; F 378, 393, 413, 463, 465, 466, 472, 485. Children 1341–47: Nos. M (1341) 515; M (1343) 577; M (1344) 609, 621; M (1345) 638; M (1346) 664; M (1347) 703, 706, 720; F (1341) 508, 519, 530; F (1342) 546, 553; F (1345) 651; F (1747) 705. Children 1348: Nos. M 779, 783, 792, 813, 837, 838, 840, 843; F 747, 782, 785, 791, 800–2, 807, 834. Children 1349–62: Nos. M (1349) 873, 881; M (1351) 896; M (1359) 976, 996; 1008; M (1361) 1038, 1054, M (1362) 1070–2, 1072. F (1349) 871, 878; F (1353) 913; F (1358) 953; F (1360) 1032; F (1362) 1071. Children 1363: Nos. M 1078, 1083, 1084, 1086, 1089, 1094, 1099, 1100, 1115, 1116–2, 1117, 1119, 1131, 1143, 1152, 1154, 1161, 1164, 1167, 1174, 1176, 1178, 1179, 1196, 1206, 1207, 1211, 1212(/1229), 1215, 1217, 1218, 1220, 1223, 1227, 1231, 1232, 1233, 1235, 1238, 1239, 1245, 1250, 1261, 1268, 1273, 1282, 1287, 1289, 1290, 1296, 1297, 1300, 1302, 1309, 1310, 1328, 1329, 1334, 1337, 1339, 1340, 1342, 1344, 1346, 1347, 1350, 1356, 1359, 1360, 1365, 1371, 1379, 1380, 1383, 1389, 1393, 1394; F 1081, 1087–2, 1093, 1094, 1102, 1103, 1106, 1107, 1112, 1118, 1121, 1123, 1126, 1128, 1130, 1134, 1136, 1142, 1145, 1147, 1153, 1157, 1158, 1159, 1162, 1165, 1166, 1170, 1177, 1183, 1184, 1188, 1189, 1192, 1200, 1201, 1204, 1205, 1214, 1219, 1222, 1224, 1234, 1241, 1242, 1249, 1252, 1259, 1265, 1266, 1269, 1270, 1277, 1280, 1295, 1311, 1315, 1321, 1323, 1324, 1330, 1343, 1345, 1353, 1358, 1363, 1374, 1375, 1376, 1378, 1386, 1390, 1391, 1396. Children 1364–73: Nos. M (1364) 1402; M (1365) 1425; M (1368), 1456, 1463; M (1369) 1470; M (1370) 1491; M (1371) 1509, 1511, 1528; M (1372) 1537; M (1373) 1550; F (1365) 1427; F (1367) 1450; F (1369) 1487; F (1371) 1522. Children 1374: Nos. M 1563, 1568, 1571, 1585, 1587, 1593, 1596, 1597, 1601, 1606, 1609, 1615, 1617, 1624, 1625, 1632, 1633, 1636, 1638, 1639, 1640, 1642, 1643, 1644, 1648, 1650, 1651, 1654, 1656, 1665, 1670, 1673, 1677, 1679, 1689, 1696, 1697, 1699, 1700, 1704, 1705, 1708, 1710, 1711, 1713, 1716, 1718, 1720, 1722, 1723, 1724, 1725, 1726, 1728, 1730, 1731, 1732, 1735, 1736, 1737, 1741, 1744, 1746, 1755, 1756, 1757, 1758, 1761, 1764, 1766, 1767, 1771, 1777; F 1572, 1573, 1576, 1591, 1592, 1594, 1600, 1605, 1608, 1610, 1611, 1612, 1613, 1614, 1616, 1618, 1619, 1621, 1622, 1623,

black death mortality in siena

677

1627, 1628, 1629, 1635, 1637, 1646, 1647, 1649, 1652, 1653, 1658, 1664, 1666, 1669, 1671, 1680, 1682, 1684, 1685, 1686, 1687, 1692, 1701, 1703–2, 1706, 1712, 1704, 1721, 1738, 1739, 1752, 1763, 1775, 1778, 1779, 1781, 1782, 1783, 1784, 1785, 1786. Children 1375–78: Nos. M (1376) 1809; F (1375) 1791, 1792, 1793; F (1376) 1810; F (1378) 1839. Adults 1337–39: Nos. M (1337) 212, 214, 217, 220, 223, 224, 226, 227, 228, 232, 233, 238, 239, 240, 246, 247, 248, 252, 253, 256, 257, 258, 260; M (1338) 262, 263, 264, 265, 266, 267, 268, 270, 273, 274, 275, 276, 281, 286, 287; M (1339) 295, 297, 298, 299, 300, 302, 306, 311, 313, 314, 316, 317, 318, 320, 323, 325, 326, 327, 329; F (1337) 213, 215, 216, 218, 219, 222, 221, 225, 229, 230, 231, 234, 235, 237, 241, 242, 243, 244, 245, 249, 250, 251, 254, 259, 261; F (1338) 269, 271, 272, 277, 278, 279, 280, 282, 283, 284, 285, 288, 289, 290, 291, 292; F (1339) 293, 294, 296, 301, 303, 305, 307, 308, 309, 310, 312, 315, 319, 321, 322, 324, 328, 330. Adults 1340: Nos. M 331, 334, 335, 336, 337, 340, 341, 343, 346, 347, 348, 354, 355, 356, 357, 360, 361, 362, 363, 364, 366, 368, 370, 371, 375, 379, 380, 382, 384, 385, 386, 387, 388, 392, 396, 397, 398, 400, 401, 404, 408, 414, 418, 423, 424, 426, 428, 431, 435, 436, 441, 443, 444, 445, 450, 451, 452, 454, 460, 461, 468, 470, 471, 480, 484, 488, 489, 494, 497, 499, 503, 504; F 332, 338, 339, 342, 344, 345, 349, 350, 351, 352, 353, 358, 359, 365, 367, 369, 372, 373, 374, 376, 377, 381, 383, 389, 390, 391, 394, 395, 399, 402, 403, 405, 406, 407, 409, 410, 411, 415, 416, 419, 420, 421, 422, 425, 427, 429, 430, 432, 433, 434, 437, 438, 439, 440, 442, 446, 447, 448, 449, 453, 455, 456, 457, 458, 459, 462, 464, 467, 469, 474, 475, 476, 477, 478, 479, 481, 482, 483, 486, 487, 490, 491, 493, 495, 496, 489, 500, 501, 502, 505, 506. Adults 1341–47: M (1341) 509, 510, 511, 512, 514, 517, 518, 520, 521, 523, 526, 527, 529, 533, 536, 537; M (1342) 538, 539, 540, 541, 542, 547, 551, 555, 559, 563, 566; M (1343) 569, 570, 571, 573, 574, 575, 576, 578, 582, 584, 585, 586, 588; M (1344) 595, 596, 597, 598, 600, 601, 602, 604, 605, 607, 608, 610, 611, 612, 613, 617, 618; M (1345) 622, 624, 625, 627, 629, 630, 632, 637, 639, 640, 641, 644, 647, 650; M (1346) 653, 654, 655, 657, 667, 669, 670, 672, 674; M (1347) 679, 681, 685, 686, 687, 689, 694, 698, 699, 701, 702, 704, 707, 708, 714, 716, 717, 718, 719, 722, 723, 725, 726, 728, 729; F (1341) 507, 513, 516, 522, 524, 525, 528, 531, 532, 534, 535; F (1342) 543, 544, 545, 548, 549, 550, 552, 554, 556, 557, 558, 560, 561, 562, 564, 565, 567, 568; F (1343) 572, 579, 580, 581, 583, 587; F (1344) 589, 590, 591, 592, 593, 594, 599, 603, 606, 614, 615, 616, 619, 620; F (1345) 623, 626, 628, 631, 633, 634, 635, 636, 638, 642, 643, 645, 646, 648, 649, 652; F (1346) 656, 658, 659, 660, 661, 662, 663, 665, 666, 668, 671, 673, 675, 676, 677, 678; F (1347) 680, 682, 683, 684, 688, 690, 691, 692, 693, 695, 696, 697, 700, 709, 710, 711, 712, 713, 715, 721, 724, 727. Adults 1348: Nos. M 730, 731, 732, 734, 735, 737, 738, 739, 740, 743, 750, 752, 745, 755, 763, 765, 766, 767, 772, 781, 784, 787, 788, 790, 801, 803, 805, 808, 809, 812, 814, 815, 816, 820, 822, 823, 824, 825, 826, 827, 829, 833, 835, 836, 841, 842, 844, 845, 846, 848, 850, 852, 853, 854, 859, 860, 861; F 733, 736, 741, 742, 744, 745, 746, 748, 749, 751, 753, 756, 757, 758, 759, 760, 761, 762,

678

appendix one

764, 768, 769, 770, 771, 773, 774, 776, 777, 778, 775, 780, 783, 786, 789, 793, 794, 795, 797, 798, 799, 802, 804, 806, 810, 811, 816, 817, 818, 819, 821, 828, 830, 831, 832, 847, 849, 851, 855, 856, 857, 858, 862, 863, 864, 865. Burials of unknown persons, three and 4–6 respectively, without indication also of gender: 796–3, 839–4/6. Adults 1349–62: Nos. M (1349) 866, 868, 872, 876, 877, 879, 880, 882; M (1350) 884, 886, 888, 890; M (1351) 892, 893, 898; M (1352) 899, 900, 901, 901, 902, 903, 905; M (1353) 908, 909, 911, 916; M (1354) 917, 918, 919, 920, 922; M (1355) 927, 928, 929, 931; M (1356) 934, 935; M (1357) 939, 940; M (1358) 942, 943, 944, 945, 946, 948, 952, 954, 955, 956, 957, 958; M (1359) 960, 961, 965, 966, 967, 968, 970, 971, 974, 975, 977, 978, 982, 983, 984, 986, 988, 989, 990, 991, 992–2, 993, 995, 997, 998, 999, 1000, 1001, 1002, 1003, 1004, 1005, 1010, 1011; M (1360) 1012, 1013, 1014, 1016, 1017, 1019, 1020, 1022, 1024, 1025, 1026, 1028, 1029, 1031, 1033, 1036; M (1361) 1037, 1039, 1041, 1042, 1044, 1047, 1048, 1049, 1050, 1051, 1053, 1055; M (1362) 1058, 1060, 1063, 1064, 1066, 1067, 1068; F (1349) 867, 869, 870, 874, 875; F (1350) 885, 889, 891; F (1351) 894, 895, 897; F (1352) 904, 906, 907; F (1353) 910, 912, 914, 915; (1354) 921, 923, 924, 925; F (1355) 926, 930; F (1356) 932, 933, 936, 937; F (1357) 938; F (1358) 941, 947, 949, 950, 951; F (1359) 959, 962, 963, 964, 919, 972, 973, 979, 980, 981, 985, 987, 994, 1006, 1007, 1009; F (1360) 1015, 1018, 1021, 1028, 1027, 1030,1031; F (1361) 1040, 1043, 1045, 1046, 1052, 1056, 1057; F (1362) 1059, 1061, 1062, 1065, 1069. Adults 1363: Nos. M (1363) 1073, 1075, 1082, 1085, 1090, 1101, 1105, 1108, 1111, 1114, 1120, 1122, 1124, 1127, 1129, 1132, 1133, 1135, 1139, 1141, 1144, 1146, 1148, 1149, 1150, 1156, 1160, 1168, 1172, 1173, 1175, 1181, 1186, 1187, 1193, 1194, 1195, 1197, 1199, 1202, 1203, 1209, 1213, 1216, 1221, 1225, 1226, 1236, 1240, 1243, 1246, 1247, 1248, 1251, 1253, 1254, 1255, 1256, 1258, 1260, 1262, 1263, 1271, 1274, 1275, 1276, 1278, 1279, 1281, 1286, 1291, 1292, 1293, 1294, 1299, 1304, 1305, 1307, 1312, 1314, 1317, 1318, 1319, 1320, 1325, 1326, 1327, 1333, 1335, 1349, 1354, 1355, 1357, 1364, 1366, 1367, 1369, 1370, 1372, 1373, 1377, 1381, 1382, 1385, 1387, 1392, 1397, 1398, 1399; F (1363) 1074, 1076, 1077, 1079, 1080, 1088, 1091, 1092, 1095, 1097, 1096, 1098, 1104, 1109, 1113, 1125, 1137, 1138, 1140, 1151, 1155, 1163, 1169, 1171, 1180, 1182, 1185, 1190, 1191, 1198, 1200, 1208, 1210, 1232, 1237, 1244, 1257, 1264, 1267, 1272, 1283, 1284, 1285, 1288, 1298, 1301, 1303, 1306, 1308, 1313, 1316, 1327, 1331, 1332, 1336, 1338, 1341, 1348, 1351, 1352, 1361, 1362, 1368, 1384, 1388, 1400. Adults 1364–73: M (1364) 1401, 1405, 1406, 1407, 1409,1410, 1411; M (1365) 1414, 1419, 1421, 1423,1426, 1428; M (1366) 1431, 1432, 1435, 1436; M (1367) 1439, 1440, 1442, 1443, 1446, 1451; M (1368) 1458, 1459, 1460, 1461, 1462, 1464, 1468, 1469; M (1369) 1474, 1475, 1476, 1477, 1478, 1479, 1483, 1485, 1488; M (1370) 1489, 1490, 1492, 1498, 1499, 1500, 1501, 1503, 1504, 1505; M (1371) 1507, 1508, 1513, 1518, 1519, 1520, 1523, 1524, 1526; M (1372) 1530, 1534, 1535, 1539, 1542, 1543, 1546; M (1373) 1548, 1549, 1552, 1553, 1555, 1556; F (1364) 1403, 1404, 1408, 1412; F (1365) 1413, 1415, 1416, 1417, 1418, 1420, 1422, 1424; F (1366) 1429, 1430, 1433, 1434,

black death mortality in siena

679

1437; F (1367) 1438, 1441, 1444, 1445, 1447, 1448, 1449, 1452, 1453, 1454, 1455; F (1368) 1457, 1465, 1466, 1467; F (1369) 1471, 1472, 1473, 1480, 1481, 1482, 1484, 1486; F (1370) 1493, 1494, 1495, 1496, 1497, 1502, 1506; F (1371) 1510, 1512, 1514, 1515, 1516, 1517, 1521, 1525; F (1372) 1529, 1531, 1532, 1533, 1536, 1538, 1540, 1541, 1544, 1545; F (1373) 1547, 1551, 1554, 1557, 1558, 1559. Adults 1374: Nos. M 1560, 1562, 1565, 1566, 1575, 1579, 1580, 1581, 1583, 1584, 1586, 1589, 1599, 1604, 1620, 1626, 1631, 1645, 1660, 1661, 1662, 1668, 1672, 1675, 1676, 1681, 1683, 1693, 1694, 1695, 1698, 1709, 1715, 1717, 1727, 1729, 1733, 1734, 1740, 1742, 1745, 1747, 1749, 1750, 1754, 1759, 1760, 1762, 1770, 1772, 1773, 1774, 1787, 1789; F 1561, 1564, 1567, 1569, 1570,1574, 1578, 1582, 1588, 1590, 1595, 1598, 1602, 1603, 1607, 1630, 1634, 1641, 1655, 1657, 1659, 1663, 1674, 1678, 1688, 1690, 1691, 1702, 1707, 1719, 1743, 1748, 1751, 1752, 1765, 1768, 1769, 1776, 1780, 1788. Adults 1375–78: M (1375) 1794, 1798, 1799, 1800, 1802, 1804; M (1376) 1805, 1806, 1807, 1808, 1811, 1813, 1815, 1817; M (1377) 1820, 1821, 1822, 1823, 1824, 1825; M (1378) 1830, 1831, 1835, 1836, 1840, 1841, 1843; F (1375) 1790, 1795, 1796, 1797, 1801, 1803; F (1376) 1812, 1814, 1818, 1819; F (1377) 1826, 1827, 1828, 1829; F (1378) 1832, 1833, 1834, 1837, 1838, 1842.

APPENDIX TWO

THE ACCOUNTS OF THE ICELANDIC EPIDEMICS OF 1402–4 AND 1494–5 GIVEN IN ICELANDIC ANNALS1 These Icelandic accounts are important in the discussion of Gunnar Karlsson’s views in Chapter 13 above. The most informative accounts of the first epidemic are provided by the New Annal (Nyi Annáll)2 and the Lawman’s Annal (Lögmanns-annáll); I translate here the account in the first version: [1402] Came out there [to Iceland] such a great virulent pestilence [‘bráðasótt’] that men died within the third night, until a vow was made to celebrate three votive masses with prayers and burning candles. It was also vowed to practise dry fast [i.e. only eat vegetable foods] until Candlemas [2 February] and, forever, water-fast before Christmas. After this, most people had time to confess before they died. In the autumn, the pestilence ravaged the southern regions so terribly that holdings were left completely deserted widely around. In many places, those who survived were unable to take care of themselves. Dominus Ali Svarthöfdason was the first priest to die in autumn, and next Brother Grimus, priest in the church of Skálholt, then one after another of the resident priests, Councillor Dominus Höskuldar on Christmas Day itself. Then died in this place [Skálholt] all the learned men and lay men, except the bishop himself and two lay men. [1403] The year of great mortality in Iceland. Died Abbot Pal in Videy and Dominus Thorstein from Helgafell. Died Dominus Runolf from Thykkvabær and six brethren, but six others survived. Died Abbess Halldora in Kirkjubær and seven sisters, but six survived. Domina Gudrun Halldorsdottir was consecrated abbess. Three times all servants there died, so that in the end, the remaining sisters themselves had to milk the cows. And most of them were very unskilled, as should be expected, because they had never before done such work. To the church were brought, according to the count, 675 dead persons. After that, the count was given up, because of the multitude who died. Likewise, the same year, all the servants at Thykkvabær also died three times, so that only two brethren remained there and one male servant of the court. [Here follow the names of six well-known dead persons, presumably victims of the epidemic.]3 [1404] Second winter of mortality. In Skálholt [the cathedral centre of one of the two Icelandic dioceses] all the servants died three times. Three priests died and most of the clerics. Two priests survived. 1

My translations from Icelandic Norse. Cf. Steffensen 1974: 45. 3 Annales islandici posteriorum sæcolorum 1922–7: 9–11. Also the Icelandic Vatnsfjarðarannáll hinn elzti relates to this epidemic but it is written so long after the event and is so infested with source-critical problems that it is not mentioned by Gunnar Karlsson (or Jón Stephenson) who in other works shows good knowledge of these important types of sources to Icelandic medieval and early modern history. Annales islandici postseriorum sæcolorum, 1933–8: 22. 2

the accounts of the icelandic epidemics

681

The most informative account of the later plague of 1494–5 is found in the Bishops’ Annals of Jón Egilsson (Biskupa-annálar Jóns Egilssonar), translated below in the somewhat compressed version of the Fitjaannáll (Fit.), but it should be noted that the Skarðsárannáll (Skar.) also contains some interesting information. [Fit. 1494] At that time, pestilence and a great plague visited all Iceland, except in the [area of the] Vestfjords, from Holt in Saurbær. Then, local communities widely around were deserted. That plague is said to have come out of blue cloth which had come out to Hvalf jord [from abroad] (but some say to Hafnarfjord at Fornubudir). And when it first came out of the cloth, it was like a bird to look at, and from it smoke went up in the air. It reached all places in this country, except, as has been said above, in the Vestfjords. Four farmsteads in the east are also mentioned as not having been visited, those are […]. Where there were nine siblings on a holding, only two or three survived. From Botnsa southwards to Hvitskeggshvammi (that is the whole [district of the] moot of Kjalarness) there were no more than two boys, eleven winters of age, alive, and none others of the same age in the whole bailiwick. That was Björn Olafsson, who later was priest in Krysuvik, and Jón Oddsson who lived in Njardvik. Both became old men […]. That mortality was in the summer [i.e., of 1494], and almost all local communities were desolated. And at most of the farmsteads not more than two or three survived, in some places one, and in some places none, and in some places children lying at the breast of their dead mothers. In Skálholt, one child remained. Every day, three or four and sometimes more were brought to the church at the same time, and when six, seven or eight brought the dead to the church, then did not return more than three, at the most four. They died while bringing others to the grave, and ended in it themselves. Women sat dead beside their buckets in the stalls and in the sheep sheds, so that three or four ended in many graves. Much property then came in the hands of many, almost everybody received inheritance from relatives, third cousins or closer relations […].4 [Skar. 1495–96] Great pestilence and plague over the whole of Iceland except in the Vestfjords, from Holt in Saurbær: wide areas were desolated. Abbot Asgrimur and all the prominent men in the North died except twenty with the bishop. Every priest had to have seven churches. Then poor, common people came from the Vestf jords, married men with wives and children, because they knew that there were abandoned holdings in the north of the country. They could choose the land on which they would settle, and many northerners are descended from them.5

4 Annales islandici posteriorum sæculorum 1927–32: 27–8. Cf. Safn til sögu Islands 1856: 43–4. 5 Annales islandici posteriorum sæculorum 1922–7: 74–5.

APPENDIX THREE

THE EXTRINSIC INCUBATION PERIOD AND THE STRUCTURE AND COMPOSITION OF THE LATENCY PERIOD In order to understand and explain the defining feature of bubonic plague designated the latency period, some technical aspects of the epizootic process among rats and the functions of their fleas must be identified and clarified. A.B. Christie states that the time that passes between when a species of fleas becomes infected and when it becomes blocked and infective is twenty-one days.1 Technically, this period is called the extrinsic incubation period or the infection-infectivity interval and represents a highly variable property between various species of fleas. Christie’s number of days cannot be correct since it is at variance with the established duration of the (first) latency period of nineteen to twenty-seven days. Christie is here referring to the early research on this subject carried out by C.R. Eskey and V.H. Haas seventy years ago. They found that the extrinsic incubation in X. cheopis varied from 5 to 31 days, with an average of 21 days, at a mean temperature of 66° F., while in the case of N. fasciatus [the flea of the brown rat] this period varied from 6 to 116 days, with an average of 41 days […] the average length of the extrinsic incubation period of plague in X. cheopis which were kept in an incubator at 72° to 80° F. was 15 days, or 6 days less than in the case of this species kept at a mean temperature of 66° F. Therefore, it would seem that an increase in temperature may reduce the length of the extrinsic incubation period of plague in these fleas.2

The importance of the observation of the effect of temperature on the extrinsic incubation period for X. cheopis is obvious, since it is a typical fur flea which enjoys in rat fur a stable and favourable microclimate, a condition that would not be well simulated under laboratory conditions. Since the temperature in rat fur will be higher than in rat burrows, this indicates that X. cheopis would tend to become blocked in one-third or less of the time required by N. fasciatus. These results were part of a large-scale study of fleas involved in plague in the south-western U.S.A. which was published in complete form the following year. Eskey and Haas make the following comments in relation to their findings on extrinsic incubation period cited above: In the case of fleas found capable of transmitting plague the length of time required for the extrinsic incubation of the infection is believed to be the most important of all factors in determining the efficiency with which the different species acted as vectors. For instance, if one species transmits in half the time required for another, then the first species will spread the infection twice as

1 2

Above: 626. Eskey and Haas 1939: 1473.

the extrinsic incubation period

683

rapidly as the second, provided infected hosts give rise to an average of one vector each. But, if the flea infestation of the infected hosts is sufficient for them to continue to produce 2 or 3 transmitting fleas per animal or if each infected flea infects more than one host, the dissemination will be by geometrical progression, and the fleas with the short incubation will be many times more active vectors than the fleas requiring twice as long before their bites become infectious […] the bites of rat fleas, X. cheopis, were infectious in a shorter time after their infection than any other species of fleas that transmitted plague in sufficient numbers for judging the average extrinsic incubation for the species. The ability of infected X. cheopis to transmit plague after a shorter extrinsic incubation than all other species undoubtedly accounts for their superiority as vectors.3

Clearly, Eskey and Haas emphasize the properties of Xenopsylla cheopis which make it a superior vector of plague disease. A few years later, A.L. Burroughs, the entomologist, published a special study of “the vector efficiency” of nine species of fleas, among them Xenopsylla cheopis, Nosopsyllus fasciatus, and Pulex irritans, the term “vector efficiency” including all of the relevant factors affecting the capability and frequency with which they would transmit plague, and concluded: X. cheopis, in these experiments, proved to be the vector par excellence that it has long been claimed to be. Of the species studied under comparable conditions, Xenopsylla cheopis was much the best vector. Nosopsyllus fasciatus was better than the others […].4

This shows that Burroughs mainly confirmed the consistent findings of previous studies of the ability of various species of fleas to function as vectors of plague from the beginning of such studies. This does not mean that Nosopsyllus fasciatus did not have significant ability to develop blockage and transmit plague according to this study, since eleven out of forty-eight fleas blocked, but only six of them transmitted plague. However, its ability to transmit plague was much weaker than that of Xenopsylla cheopis, in fact only about a third: “ratio of transmission to fleas used” was 0.660 in the case of X. cheopis but only 0.213 in the case of N. fasciatus, which, nonetheless, compares well with 0 in the case of P. irritans.5 The different blockage rates relate to differences in the physiology and anatomy of the different types of fleas, making the rat flea the plague flea “par excellence,” a characteristic noted by several prominent plague scholars.6 Or in the words of Perry and Fetherston, X. cheopis “is considered the classic vector and is the standard against which all other fleas are measured.” This point is highlighted in Pollitzer and Meyer’s conclusive comment: “these findings confirm the paramount importance of highly efficient vector species in the transmission of plague.”7

3

Eskey and Haas 1940: 43–4. Burroughs 1947: 381. 5 Burroughs 1947: 384, 394. 6 C.Y. Wu 1936: 250; Girard 1943: 32; Burroughs 1947: 381; Brygoo 1966: 39, Perry and Fetherston 1997: 51, 53. 7 Pollitzer and Meyer 1961: 467. 4

684

appendix three

One should note Burroughs’s use of the phrase “under comparable conditions,” since it contains the potentially fallacious notion that formal equality of conditions for various species of fleas in the laboratory, in incubators or test tubes, means real equality of living conditions whatever the ordinary conditions in the biotopes or ecological niches to which they were evolutionarily adapted. In the context of the present discussion, this implies the unformulated and untested hypothesis that this also means real equality with respect to the conditions effecting the pace and relative incidence with which these species of fleas would tend to become blocked in nature. This may not appear obviously likely in relation to the difference between fur fleas and nest fleas, for example. In this connection, one may usefully note Burroughs’s observation that Nosopsyllus fasciatus “apparently feeds better than Xenopsylla cheopis under the conditions of individual feeding described.”8 At this point of the discussion it is appropriate to cite Hirst’s warning: “Experience has shown that deductions from laboratory experiments and observations are by no means always applicable to natural conditions in the field.”9 Or as formulated by Christie in his textbook on infectious diseases: “Experiment may imitate but it cannot reproduce nature, and laboratory findings often do not tally with what happens in the field.”10 This is clearly relevant in this case, as empirical testing will show, as we will see. In all fairness, it must be added that Burroughs too was aware of this problem in more general terms: “A knowledge of the vector efficiency of a species of flea acquired experimentally in the laboratory is probably, at best, only an approximation of its natural vector efficiency. This is inevitable because of ignorance of the ecology of most species of fleas precludes the duplication of natural conditions.”11 The gradually decreasing duration of the extrinsic incubation period of X. cheopis in scholarly studies may be taken to suggest that researchers have gradually succeeded in reducing the effects of laboratory conditions in this respect, which is not to suggest that those conditions do not still affect the outcome significantly. The IPRC showed the basis of the latency period, specifically that from the time of the introduction of an infective rat flea into a rat colony it took about 10–14 days before the colony was so severely reduced that rat fleas leaving dead rats had difficulties in finding a new rat host and after a few days began to attack human beings in their proximity. This means that the extrinsic incubation time must be considerably shorter, since one must also take into account the time needed for the subsequent periods of incubation and illness of infected rats and the extrinsic incubation time of their fleas that would make them infective. This has been confirmed and accepted by the authors of the other standard works on plague.12 In this connection, several factors must

8

Burroughs 1947: 384. Hirst 1953: 165. 10 Christie 1980: 755. 11 Burroughs 1947: 389. 12 Wu 1936c: 387; Hirst 1953: 140–1; Pollitzer 1954: 485; Pollitzer and Meyer 1961: 452. 9

the extrinsic incubation period

685

be taken into account: the extrinsic incubation time or the infection-infectivity interval varies strongly with temperature and the degree of septicaemia in the blood the fleas ingest, and also with the species of flea because there are large differences in the propensity of fleas to develop blockage. Xenopsylla cheopis, the flea of the black rat, develops this condition more easily and rapidly than any other type of flea: “X. cheopis, in these experiments, proved to the be the vector par excellence that it has long been claimed to be.”13 These factors affect also the proportion of fleas that becomes infective, which is crucial for the intensity of epidemic developments. These are variables that make the relationship between laboratory conditions and conditions in nature or in the field of plague disease quite tenuous in this case.14 In the words of Pollitzer: “Little doubt can exist that, under the climatic conditions prevailing during the plague seasons, the extrinsic incubation time is short.” More attention should therefore be paid to the finding that Xenopsylla cheopis could block in only five days,15 and to the fact that Christie wisely repeats: “laboratory findings often do not tally with what happens in the field.”16 These points are important because they relate to the pace and rhythm of development of plague epidemics which represent central defining features of bubonic plague. Subsequent research has tended to reduce further the extrinsic incubation time in X. cheopis and therefore to increase its vector efficiency. In 1997, Perry and Fetherston indicated the normal time from infection to blockage in the range of three to nine days and, since I have not noted any objections,17 this must be considered the present scholarly consensus on the matter. However, the periods of extrinsic incubation time established by the entomologists are clearly very much too long not only for Nosopsyllus fasciatus to produce such a temporal pattern of development characterizing the latency period, it is also too long for the species of fleas which exhibited much the shortest extrinsic incubation time, namely Xenopsylla cheopis, and clearly this must be our focus. The extrinsic incubation period recorded for this species of flea has now, as mentioned, been established at three to nine days, presumably with increasing proportions of fleas blocking in the higher reaches of this range. This is problematic as the outline of a standard scenario of spread of

13

Burroughs 1947: 381. Pollitzer 1954: 351–5; Hirst 1953: 323. 15 Hirst 1953: 323. 16 Christie 1980: 754–5. 17 Perry and Fetherston 1997: 51. “Two days after an infected blood meal, the stomach exhibits clusters of brown specks containing Y. pestis. These develop into cohesive dark brown masses, containing bacilli, a fibrinoid-like material, and probably hemin […]. Between days 3 and 9 after the infected blood meal, the bacterial masses may completely block the proventriculus [= “fore stomach”], extend into the esophagus [= gullet], and prevent ingested blood from reaching the stomach […] as the hungry flea repeatedly attempts to feed, the blood sucked from the mammalian host distends the esophagus, mixes with bacilli and is regurgitated into the mammalian host when the feeding attempt is terminated.” 14

686

appendix three

plague contagion based on standard assumptions will readily show. The point of departure is the introduction into a rat colony of a blocked X. cheopis which after having ridden in clothing or luggage will soon after arrival at a new human habitation infect a rat. It would normally take at least four to five days before the rat developed sufficiently severe septicaemia18 to cause the heavy infection of the fleas feeding on it necessary to produce blockage of their ventricular systems. According to the average duration of the course of plague illness for this species, the rat would die 7.2 days after infection.19 The substantial majority of the about seven fleas leaving this dead rat would normally tend to become blocked and infective about two days later when they could infect two or more rats on which they had settled and then a new period of incubation and disease of 7.2 days would follow before these fleas were released from their dead hosts and possibly or probably would have difficulties in finding new rat hosts. After about three days of fasting they would be blocked and would begin attacking human beings in their proximity, producing the first fatality among them after a period of eight days on average. Summarizing the time elements of this process, the most favourable assumptions for the most efficient vector of plague would produce a latency period of 27.4 days, corresponding quite accurately to the maximum duration of the standard latency period. There would among the great numbers of such cases in a plague epidemic be a significant number of cases where the earlier reaches of the range of extrinsic incubation time would tend to occur, however, for the epidemic process as a whole this rather long latency period would appear to be perhaps incompatible with the rapid pace of the epidemic developments. There are two factors which can function independently at least as partial explanations for this finding and together can provide a full explanation. The first factor or explanation relates to the adverse circumstances for this species of fleas under laboratory conditions, which was pointed out above; these adverse circumstances tend to delay the process of blockage formation and the relative incidence with which it will occur. Since the objective of this estimate is to establish the normal rhythm of the process from the introduction of a blocked rat flea in a rat colony to the first human fatality, it is quite likely that in nature, in real life under normal circumstances in rat fur, X. cheopis would tend to block quite often in the shortest time or in lowest reaches of the recorded time of the blockage-developing process, namely in three or four days. An extrinsic incubation period of three to five days would have to be quite usual in order to bring the process within the perimeter of the empirically well established ordinary duration of the latency period of nineteen to twenty-seven days when this flea is involved, albeit mostly in the higher reaches of this range. Still it would be difficult to explain the lower reaches of this range. The second factor may resolve this problem. In a research project on the sensitivity of fleas to temperature, it was shown that X. cheopis infected with

18 19

IPRC 1906c: 521. IPRC 1907g: 759.

the extrinsic incubation period

687

Yersinia pestis after feeding on infected rats preferred an ambient temperature up to 1.6 °C cooler than did non-infected fleas. Further observations indicated that this change in thermal preference is important in the transmission of plague from rat to human by X. cheopis for two main reasons: (1) rats have core temperatures approximately 1.5 °C higher than human beings. (2) infected rats would react with fever to the plague infection which would produce a further increase in temperature.20 “In view of the preference for cooler temperatures in plague-infected rat fleas, it is possible that the fleas would actually prefer the human host. This being the case, temperature becomes an important factor in the transfer of Y. pestis from rat to man.”21 In short, infected rat fleas of the species X. cheopis would tend to leave the host in an early phase of the febrile process which sets in after the end of the incubation period of about three days and would leave the rat two to four days before it normally will have died. With this background, it appears possible to conclude that recent research has enabled construction of a fully tenable explanation of the duration of nineteen to twenty-seven days of the first latency period in plague epidemics, the period from the introduction of a blocked flea in a colony of black rats until the first human fatality. This latency period is only compatible with the normal flea (Xenopsylla cheopis) of the black rat acting as the vector of transmission of bubonic plague between rats and man. Clearly, this flea satisfies the conditions of empirical testing.

20 21

Thomas, Karstens, and Schwann 1993: 209–13. Brown 1995: 931; Perry and Fetherston 1997: 55.

GLOSSARY Abscess

Bacteraemia Blain Boil Carbuncle

Case mortality rate Case fatality rate Cutaneous Ecchymosis Endemic

Entomology Enzootic Epidemic Epidemiology Epitaxis Epizootic Eschar

Local inflammation of body tissue with deep suppuration [secretion of pus] caused by bacteria which destroy the cells in the centre of the area and leave a cavity filled with pus. Presence of bacteria in the blood stream. See sepsis, primary and secondary septicaemic plague. Pustule or vesicle, see below, historical word. Hard inflamed lymph node which may suppurate, often used in the past to indicate plague bubo. Localized dead body tissue (gangrene) caused by plague bacteria (or staphylococci), usually by bacteria left in the site of a flea’s bite, in which case it is called a primary carbuncle. See lethality rate. See lethality rate. Affecting the skin (Latin cutis=skin) see also subcutaneous The passage of blood from ruptured blood vessels into subcutaneous (see below) tissue, marked by a purple discoloration of the skin. See petechiae. Sporadic cases of an infectious disease in a human population, too few to be considered usefully designated an epidemic, but which show that a particular type of contagion occurs in a population, is called an endemic phase or situation. The discipline of natural science which studies insects. Sporadic incidence of contagious disease among animals, cf. endemic. Disease that spreads rapidly through a population or community for a period. Science of epidemics, especially how epidemics are spread and transmitted. Bleeding from the nose (in plague caused by weakening of local blood vessels by the action of plague toxins). Disease spreading among animals, i.e., a term corresponding to the term epidemic among human beings. A scab, the crustlike surface of a healing skin lesion, or a slough, resulting from injury by gangrene, burn, or caustics.

glossary Expectoration

Fatality rate Haemorrhage/ haemorrhaging Incubation period Infection dose

Lethality rate Lethal dose

Life table

Mixed epidemic

Morbidity Morbidity rate Mortality Mortality rate

Naïve population

689

Eject from lung airways thrown up by coughing. In the case of plague, this bloody expectoration may contain plague bacteria from consolidated ulcers formed in the lungs by plague bacteria transported there in the blood stream (see secondary pneumonic plague), which can be inhaled by other persons and give rise to primary pneumonic plage (see below). See lethality rate. Bleeding. See also Ecchymosis and Petchiae. The period from infection to the outbreak of disease. A measure of virulence usually expressed as ID50, i.e., the number of microorganisms or micrograms of their toxin (see this term) with which human beings (or animals) must be infected in order to cause a morbidity rate of 50 per cent. See Lethal dose. The proportion of those who contract a disease which dies from it. A measure of virulence usually expressed as LD50, i.e., the number of microorganisms or micrograms of their toxin (see this term) with which human beings (or animals) must be infected in order to cause a mortality rate of 50 per cent. See Infection dose. Life tables are based on series of age-specific death rates for each gender and, shows, thus, the probabilities of dying within particular age intervals according to various life expectancies at birth. Or, if focusing on the probabilities of surviving, life tables show life expectancies at each age level in societies with various life expectancies at birth. Epidemic of bubonic plague comprising substantial proportions of cases of primary pneumonic plague, occasionally also of primary septicaemic plague. (1) The quality of being ill/morbid; (2) incidence of an infectious disease. Proportion of a population which contracts a specific disease. The number of people who die within a particular period of time or on a particular occasion. The proportion of a population which die no matter the causal factors. Plague mortality is the proportion of a population which dies from this disease in an epidemic. Population without experience with a disease or diseases, all members being equally susceptible.

690 Paleomicrobiology Pandemic

Pathogen Pathogenicity Petechiae/ plague spots

Plague focus/ plague reservoir Plague pox/ plague variola Primary pneumonic plague

Primary septicaemic plague

glossary Study of DNA or specific proteins reclaimed from biological material of the past taken from remains of human beings or animals. (1) Disease spreading in a serious way over large parts of the world; (2) series of waves of epidemics. In European history, plague has ravaged populations in three protracted series of waves of epidemics which are called pandemics. The first plague pandemic occurred in the period a.d. 541–767; the second plague pandemic occurred in the period 1346–1722 in most of Europe, longer in Turkish Balkans and Russia. The Black Death is the first gigantic, particularly disastrous and notorious wave of plague epidemics of the second plague pandemic. A third plague pandemic broke out in 1894, but was stopped by countermeasures based on modern medicine and epidemiology around 1940. Microorganism than can cause disease. The ability of microorganisms to cause disease, cf. virulence. Dark coloured spots in the skin due to invasion by plague bacteria of the capillary vessels of the skin, i.e., consequent upon the development of septicaemia in the blood stream. Plague toxin weakens the walls of the blood vessels which tend to break and leak drops of blood, haemorrhages, which presents through the skin as dark coloured spots, also called plague spots, by contemporary Englishmen often designated (God’s) token, since their appearance heralded imminent and certain death. See Ecchymosis. In many areas of the world where wild rodents live in great density, in colonies or otherwise, plague circulates continuously in the rodent population. Such a rodent population is called a plague focus. Patients who presents with so numerous pustules or vesicles that the clinical picture resembles smallpox. Patients with primary lung infections have been infected by way of the respiratory system. Droplets containing plague bacteria coughed up by persons that have plague infection in the lungs (pulmonary plague) are the source of infection (rarely also animals). (Cf. secondary pneumonic plague, and expectoration). This form of plague occurs when a flea disposits plague infection directly into a blood vessel or it is passed directly on into the bloodstream without

glossary

Pulmonary plague

Pure epidemics of primary pneumonic plague

Pustules

Secondary pneumonic plague

691

stoppage in a lymphatic gland (and development of a bubo). Characterized by dramatic and rapid course of illness leading to certain death without development of bubo(es). Fulminant type of primary pneumonic plague, i.e., caused by plague infection through the respiratory tract. Dissection of lungs of such cases do not show pneumonic foci of plague bacteria which produce the cough with bloody sputum but present with only hyperaemic (an excess of blood) and oedematous (accumulation of excessive fluid) changes in the lungs as well as marked septicaemic (see Sepsis) features. These cases are designated pulmonary plague because, though they are anatomically similar to the septicaemic cases encountered in bubonic plague, they were etiologically different from them, the infection having entered through the respiratory tract. Concept referring to the hypothetical notion that epidemics of primary pneumonic plague can arise directly from droplet contamination, for instance from the skinning of a plague infected animal or from cats who have contracted primary pneumonic plague from the killing of plague infected rodents. This has never been observed in the field or reality. All known epidemics of primary pneumonic plague have originated in cases of bubonic plague who have developed secondary pneumonic plague (see below). This form is, nonetheless, the notional basis of two alternative epidemiological theories of plague in the past maintained by C. Morris and G. Karlsson and discussed extensively in this monograph, see also Index of Subjects and Index of Names. Resemble vesicles and are due to invasion of the skin by plague bacteria through the blood-stream, i.e., consequent upon the development of septicaemia. See also Blain and Petechiae/plague spots. In cases of bubonic plague in which plague bacteria pass on into the bloodstream plague bacteria are transported also to the lungs where they quite often consolidate and develop ulcers that cause a frequent cough with bloody expectoration. This condition is called secondary pneumonic plague, i.e., a pneumonic condition that is secondary to the primary infection of buboes. These cases are almost invariably mortal. Such cases are the origin of primary pneumonic plague.

692 Secondary septicaemic plague

Sepsis, septicaemic

Subcutaneous Toxin

Vector Virulence

glossary In about half of all cases of bubonic plague, bacteria at some point manage to overwhelm the lymphatic system and pass on into the blood stream, causing a bacteraemia which is secondary to the primary bubonic condition, cf. primary bacteraemic plague. These cases are almost invariably mortal. The majority of cases of sepsis are due to bacterial infections, infecting agents or toxins, which invade the blood stream. This allows them to spread to almost every organ of the body. In this book, the terms bacteraemia and bacteramic are used in the same meaning. Lying or situated under the skin. See also cutaneous A poison produced by microorganisms. Each specific type of pathogenic microorganism produces its own toxin which causes a particular disease when present in the system of a human or animal body. Carrier of disease, especially insect that conveys pathogenic organisms from one person or animal to another. This term is closely related to the term pathogenicity, i.e., the ability of microorganisms to cause disease, but introduces in addition the concept of degree in order to make it possible to differentiate between the disparate abilities of various pathogenic microorganisms to produce disease and cause death in infected persons. Virulence is measured in terms of the number of microorganisms or the micrograms of toxin needed to kill a given host when administered by a certain route. This is called the lethal dose (see this term).

BIBLIOGRAPHY German, Nordic and Norse personal names and place names may include letters not used in English. In the bibliography and the index these letters are entered alphabetically according to the following rules: Å/å = AA/aa (pronounced “aw” as in “saw” in English); Ä/ä, Æ/æ = AE/ae; ü = y; Ö/ö, Ø/Ø = OE, oe; ð (pronounced “th” as in “the” in English) = d. Þ/þ (pronounced “th” as in “think” in English) are, in the Icelandic alphabet, placed after the letter y, an arrangement which is followed here, according to their custom (for lack of any logical alternative), although Icelandic person names are not placed according to their Christian names, but according to their surnames in accordance with normal international standards. Abbey H. 1968. “An Examination of the Reed-Frost Theory of Epidemics.” Human Biology. 24: 201–33. Cf. J. de Oliveira Costa Maia 1968. Aboudharam G., Drancourt M., Dutour O., Martin H. et al. 2005. “Validation de la saisonnalité des décés et authenticité biologique de la nature de l’épidémie.” In: B. Bizot, D. Castex, P. Reynaud, M. Signoli (eds.). La saison d’une peste (avril-septembre 1590). Le Cimetière des Fédons à Lambesc (Bouches-du-Rhône). Paris: CNRS Éditions. 63–7. Absalon Pederssøn (Beyer). 1963. Dagbok og Oration om Mester Geble. [Diary and Oration on Master Geble.] R. Iversen (ed.) Vol. 2, Kommentarbind [Commentary] by H. Nilsen. Oslo: Universitetsforlaget. Ackerkncht E.H. 1963. Geschichte und Geographie der wichtigsten Krankheiten. Stuttgart: Ferdinand Enke Verlag. Achtman M., Morelli G., Zhu P. et al. 2004. “Microevolution and History of the Plague Bacillus, Yersinia pestis.” Proceedings of the National Academy of Sciences of the United States of America. 101: 17837–42. The Agrarian History of England and Wales. 1988. Vol. 2. H.E. Hallam (ed.). Cambridge: Cambridge University Press. Akiander M. 1849. Utdrag ur Ryska Annaler. Helsinki: Simelii arfvingar. Alexander J.T. 1980. Bubonic Plague in Early Modern Russia. Baltimore: The Johns Hopkins University Press. Allen P. 1997. “The ‘Justinianic’ plague.” Byzantion. 49: 5–20. Anderson R.M. 1982. “Directly Transmitted Viral and Bacterial Infections of Man.” In: The Population Dynamics of Infectious Diseases. 1–37. Anglada C. 1869. Études su les maladies éteintes. Paris. Annales islandici posteriorum sæculorum. Annáles 1400–800. 1922–7. Vol. 1, and 1933–8. Vol. 3. Hið íslenzk bókmentafélag: Reykjavik. Appleby A.B. 1980. “The Disappearance of Plague: A Continuing Puzzle.” The Economic History Review. 2nd Series. 33: 161–73. Archaeozoological Studies. 1975. A.T. Clason (ed.). North-Holland Publishing Company: Amsterdam, Oxford, 1975. (See Lepiksaar) Archiv für Geschichte der Medizin. 1910–25. K. Sudhoff (ed.). Vols. 4–9, 11, 14, 16. Leipzig: Verlag von Johann Ambrosius Barth. Armit H.W. 1907. “The Toxicology of Nickel Carbonyl.” The Journal of Hygiene. 7: 525–51. Armitage P., West B., and Steedman K. 1984. “New Evidence of Black Rat in Roman London.” London Archaeologist. 4: 375–83.

694

bibliography

Arthur P. 2005. The Impact of the Black Death on Seventeen Units of Account of the Bishopric of Wincester. Thesis for Doctor of Philosophy, University of Southampton at University College of Winchester. Vols. 1–2. Astill G. and Grant A. 1988. “The Medieval Countryside: Efficiency, Progress and Change.” In The Countryside of Medieval England 1988: 213–34. Audoin-Rouzeau F. 1999. “Le rat noir (Rattus rattus) et la peste dans l’occident antique et médiéval.” Bulletin de la Société de Pathologie Exotique. 92: 422–6. ——. 2003. Les chemins de la peste. Le rat, la puce et l’homme. Rennes: Presses Universitaires de Rennes. Audoin-Rouzeau F. and Vigne J.-F. 1994. “La colonisation de l’Europe par le Rat noir (Rattus rattus).” Revue de Paléobiologie. 13: 125–45. Bacot A., see Indian Plague Research Commission. Bailey M. 1996. “Demographic Decline in Late Medieval England: Some Thoughts on Recent Research.” The Economic History Review. 49: 1–19. Balfour A. 1922. “Observations on Wild Rats in England, with an Account of their Ecto- and Endoparasites.” Parasitology. 14: 282–99. Baltazard M. 1959. “Nouvelles données sur la transmission interhumaine.” Bulletin de l’Académie nationale de médecine. 13 October 1959: 517–25. ——. 1960. “Déclin et destin d’une maladie infectieuse: la peste.” Bulletin of WHO: Geneva, 23: 247–62. Baltazard M., Bahmanyar P., Mostachfi P. et al. 1960. “Recherches sur la peste en Iran.” Bulletin of WHO: Geneva, 23: 141–54. Bannerman W.B. 1906. “The Spread of Plague in India.” The Journal of Hygiene. 6; 179–211. Baratier E. 1961. La démographie provençale du XIIIe au XVIe siècle. Paris: S.E.V.P.E.N. Bartsocas C.S. 1966. “Two Fourteenth-century Descriptions of the ‘Black Death’.” Journal of the History of Medicine and Allied Sciences. 21: 394–400. Baulant M. 1968. “Le prix des grains à Paris de 1431 à 1788.” Annales Économies Société Civilisations. 23: 520–40. Bell W.G. 1951. The Great Plague in London in 1665. 2nd ed. London: the Bodley Head. Bellamy J.G. 1989. Bastard Feudalism and the Law. London: Longman. Belletini A. 1973. “La popolazione italiana dall’inizio dell’era volgare ai giorni nostri. Valutazioni e tendenze.” In: Storia d’Italia. Vol. 5: 489–532. Benedictow, O.J. 1985. “Walløe, Juhasz og pestens sosiologi” [= Walløe, Juhasz and the Sociology of Plague]. Historisk tidsskrift: 84–93. [No volume number]. ——. 1987. “Morbidity in Historical Plague Epidemics.” Population Studies. 41: 401–31. ——. 1989. “Review” [of P. Slack. The Impact of Plague in Tudor and Stuart England]. Bulletin of the History of Medicine. 63: 655–9. ——. 1993, repr. 1996a. Plague in the Late Medieval Nordic Countries. Epidemiologcal Studies. Oslo: Middelalderforlaget. ——. 1996b. The Medieval Demographic System of the Nordic Countries. Oslo: Middelalderforlaget. ——. 1996c. “The Demography of the Viking Age and the High Middle Ages in the Nordic Countries.” Scandinavian Journal of History. 21: 151–82. ——. 2002. Svartedauen og senere pestepidemier i Norge. Pestepidemienes historie i Norge 1348–654 [= The Black Death and later Plague Epidemics in Norway. The History of Plague Epidemics in Norway, 1348–654]. Oslo: Unipub. ——. 2003. “Demographic Conditions.” In The Cambridge History of Scandinavia. Vol. 1: 237–49. ——. 2004. The Black Death. A Complete History. Woodbridge, UK: Boydell & Brewer. ——. 2005. “The Black Death.” History Today. 55: 42–9. ——. 2006. “Svartedauen i Norge: Ankomst, spredning, dødelighet” [= The Black Death in Norway: Arrival, Spread, Mortality]. Collegium Medievale. 19: 83–163.

bibliography

695

Benediktsson J. 1970. “Skálholtsannáll.” Kulturhistorisk leksikon for nordisk middelalder. Vol. 15. Oslo: Gyldendal Norsk Forlag. Berg G. 1969. “Råttfälla.” Kulturhistorisk leksikon for nordisk middelalder. 14: 576–7. Berglund J. 1986. “The Decline of the Norse Settlements in Greenland.” Arctic Anthropology. 23: 113–34. Bergquist H. 1957. “Skeletal Finds of Black Rat from the Early Middle Ages.” Archaeology of Lund. Lund: 1: 11–84. Berqquist H. and Lepiksaar J. 1957. “Medieval Bones Found in Lund.” Archaeology of Lund. Lund: 1: 98–103. Bernström J. 1969. “Råttor och möss.” Kulturhistorisk leksikon for nordisk middelalder. Vol. 14: 577–83. ——. 1971. “Spindeldjur och insekter.” Kulturhistorisk leksikon for nordisk middelalder. Vol. 16: 488–99. Berthe M. 1984. Famines et épidémies dans les campagne navarraises à la fin du moyen âge. Vols. 1–2. Paris: S.F.I.E.D. Bertrand J.B. 1805/1973. A Historical Relation of the Plague at Marseilles in the Year 1720… [Relation historique de la peste de Marseille en 1720]. Translated from the French manuscript of Mons. Bertrand, physician at Marseilles who attended during the whole time of the malady, by Anne Plumptre. With an introduction, and a variety of notes by the translator. London: Printed for Joseph Mawnan by R. Taylor and Co. 1805. Brookefield, VT: Gregg International Publishers Limited. Bianucci R., Rahalison L., Ferroglio E. et al. 2007. “Détection de l’antigène F1 de Yersinia pestis dans les restes humains anciens à l’aide d’un test de diagnostic rapide.” Comptes Rendues Biologies. 330, no. 10: 747–54. Bianucci R., Rahalison L., Massa E. et al. March 2008. “Technical Note: A Rapid Diagnostic Test Detects Plague in Ancient Human Remains: An Example of the Interaction Between Archeological and Biological Approaches (Southeastern France, 16th–18th Centuries).” American Journal of Physical Anthropology, 136: 361–7. Bibikova V.A. 1977. “Contemporary Views on the Interrelationships between Fleas and the Pathogens of Human and Animal Diseases.” Annual Review of Entomology. 22: 23–32. Bibikova V.A. and Alekseyev A.N. 1969. “Zarazhennost’ i blokoobrazovanie v zavisimosti ot kolichestva popavshikh v blokh mikrobov chumy” [= Contagiousness and formation of blockage as variables of the number of plague microbes ingested by fleas]. Parazitologiya. 8: 196–202. Bibikova V.A. and Klassovskiy L.N. 1974. Peredacha chumy blokhami [= Transmission of plague by fleas]. Moscow: “Meditsina.” Bickel W. 1956. “Über die Pest in der Schweiz.” Studium Generale. 9: 513–5. Biraben J.-N. 1975. Les hommes et la peste en France et dans les pays européens et méditerranéens. Vols. 1–2. Paris: Mouton. ——. April 1979. “La peste Noire en terre d’islam.” L’histoire. 11: 30–40. ——. 1988. “L’hygiène, la maladie, la mort.” In Histoire de la population française: 421–62. Biraben J.-N. and Le Goff J. 1969. “La Peste dans le Haut Moyen Age.” Annales Économies Sociétés Civilisations. 24: 1484–510. The Black Death. A Turning Point in History? 1971. W.M. Bowsky (ed.) New York: Holt, Rinehart and Winston. Blanc G. 1956. “Une opinion nonconformiste sur le mode de transmission de la peste.” Revue d’Hygiene et de Médecine Sociale. 4; 536–62. ——. 1961. “La disparition de la peste et ses causes épidémiologiques.” La Semaine des hôpitaux. 37: 105–10. Blanc G. and Baltazard M. 1941. “Recherches expérimentales sur la peste. L’infection de la Puce de l’Homme, Pulex irritans L.” Comptes rendus hebdomadaires de séances de l’Académie des sciences. 213: 813–6. ——. 1942. “Rôle de ectoparasites humains dans la transmission de la peste.” Bulletin de l’Académie Nationale de Medecine. 126: 446–8.

696

bibliography

——. 1943. “Quelque remarques à propos du mémoire de G. Girard sur les ‘ectoparasites humains dans l’épidémiologie de la peste’.” Bulletin de la Société de pathologie exotique. 36: 208–16. Discussions. Ibidem: 216–7. ——. 1945 “Recherches sur le mode de transmission naturelle de la peste bubonique et septicémique.” Archives de l’Institut Pasteur du Maroc. 3, cahier 5: 173–354. Block M.G. 1711. Atskillige Anmaerkningar Oefwer naerwarande Pestilentias Beskaffenhet, Motande, Botande Och Utrotande Uti Östergoetland. Linköping: Published by the author. Blockmans W.P. 1980. “The Social and Economic Effects of Plague in the Low Countries 1349–1500.” Revue Belge de Philologie et d’Histoire (Belgisch Tijdschift voor Philologie en Geschiedenis). 58: 833–63. Boccaccio G. 1976. Tutte le opere di Giovanni Boccaccio. V. Branca (ed.). Vol. 4. Milan: Mondadori. ——. 1982 (around 1350). Decameron. The John Payne Translation, Revised and Annotated by C. S. Singleton. Vols. 1–3. Berkely and Los Angeles, California: University of California Press. ——. 1906. Decameron, prima giornata. Strassburg: Bibliotheca romanica. See also Stories of Boccaccio. Boessneck J. and Von den Driesch A. 1979. “Die Tierknochenfunde mit Ausnahme der Fischknochen.” In: Eketorp. Befestigung auf Öland/Schweden. Die Fauna. Vol. 3: 24–421. Boucher C.E. 1938. “The Black Death in Bristol.” Transactions of the Bristol and Gloucestershire Archaeological Society. 60: 31–46. Bowsky W.M. 1964. “The Impact of the Black Death upon Sienese Government and Society.” Speculum. 39: 1–34. Brachman P.S. 1980. “Inhalation Anthrax.” Annals of the New York Academy of Science. 353: 83–93. ——. 1990. “Anthrax.” In: Tropical and Geographical Medicine: 877–81. Bradley L. 1977a. “The Most Famous of All English Plagues: A Detailed Analysis of the Plague at Eyam 1665–6.” In The Plague Reconsidered: 63–94. ——. 1977b. “The Geographical Spread of Plague.” In The Plague Reconsidered: 127–32. ——. 1977c. “Some Medical Aspects of Plague.” In The Plague Reconsidered: 11–23. Bratianu G.I. 1929. Recherches sur le commerce génois dans la mer Noire au XIIIe siècle. Paris: Librairie Orientaliste Paul Geuthner. Bridbury A. 1973. “The Black Death.” The Economic History Review. 2nd Series, 26: 577–92. Brown R. 1995. “Is Behavioural Thermoregulation a Factor in Flea-to-Human Transmission of Yersinia pestis?” The Lancet. 345, April 8: 930. Browne J. 1720. A Practical Treatise of the Plague, and all Pestilential Infections that have happen’d in this Island for the Last Century. Laying down the Rules and Methods then used by the most Learned Physicians of those Times … as well as what are now Proper to be used, in order to prevent the Spreading of that Contagion. With a Prefatory Epistle address’d to Dr. Mead, on account of his Short Discourse concerning Pestilential Contagion. London: Printed for J. Wilcox, and sold by J. Roberts. ——. 1917–8. “Certain Aspects of the Theory of Epidemiology in Special Relation to Plague.” Proceedings of the Royal Society of Medicine. 11: 85–131. Brygoo E.-R. 1966. “Épidémiologie de la peste à Madagascar.” Archives de l’Institut Pasteur de Madagascar. 35: 7–147. Burkle F. 1973. “Plague as Seen in South Vietnamese Children. A Chronicle of Observations and Treatment under Adverse Conditions.” Clinical Pediatrics. 12: 291–8. Burnet F.M. and White D.O. 1972. Natural History of Infectious Disease. 4th ed. Cambridge: Cambridge University Press.

bibliography

697

Burroughs A.L. 1947. “Sylvatic Plague Studies. The Vector Efficiency of Nine Species of Fleas compared with Xenopsylla cheopis.” Journal of Hygiene. 45: 371–96. Busvine J.R. 1975. Arthropod Vectors of Disease. London: Edward Arnold. ——. 1976. Insects, Hygiene and History. London: The Athlone Press. Butler T. 1972. “A Clinical Study of Bubonic Plague. Observations of the 1970 Vietnam Epidemic with Emphasis on Coagulation Studies, Skin Histology and Electrocardiograms. The American Journal of Medicine. 53: 268–76. ——. 1979. “Plague and Tularemia.” Pediatric Clinics of North America. 26: 355–66. ——. 1983. Plague and Other Yersinia Infections. New York: Plenum Medical Book Company. ——. 1993. “Plague.” In Tropical and Geographical Medicine: 884–9. Butler T., Bell W.R., Linh N.N. et al. 1974. “Yersinia pestis Infection in Vietnam. I. Clinical and Hematologic Aspects.” The Journal of Infectious Diseases. 129 (Suppl.): S78–S84. Byrne E.H. 1930/1970. Genoese Shipping in the Twelfth and Thirteenth Centuries. Cambridge, Massachussetts: The Mediaeval Academy of America. New York: Kraus Reprint Co. The Cambridge History of Scandinavia. 2003. Vol. 1. Prehistory to 1520. K. Helle (ed.). Cambridge: Cambridge University Press. The Cambridge Economic History of Europe. 1966. Vol. 1. The Agrarian Life of the Middle Ages. 2nd edn. Cambridge: Cambridge University Press. Campbell A.M. 1931. The Black Death and Men of Learning. New York: History of Science Society Publications. Campbell B.M.S. 1985. “Review of G. Twigg, ‘The Black Death: a Biological Reappraisal.’ ” Journal of Historical Geography. 48: 313–4. Cantey J.R. 11974. “Clinical Observations and Treatment with Kanamycin.” Archives of Internal Medicine. 133: 280–3. Carmichael A.G. 1978. Epidemic Diseases in Early Renaissance Florence. PhD dissertation, Duke University. ——. 1983. “Plague Legislation in the Italian Renaissance.” Bulletin of the History of Medicine 57: 508–25. ——. 1986. Plague and the Poor in Renaissance Florence. Cambridge: Cambridge University Press. ——. 1998. “The Last Plague. The Uses of Memory in the Renaissance Epidemics.” Journal of Medicine and Allied Sciences. 53: 132–60. ——. 2003. “Plague and More Plagues.” Early Science and Medicine. 8: 253–66. Carpentier É. 1962a. Une ville devant la peste. Orvieto et la Peste Noire de 1348. Paris: Université de Paris, Faculté de lettres et sciences humaines. ——. 1962b. “Autour de la Peste Noire: Famines et épidémies dans l’histoire du XIVe siècle.” Annales ESC. 17: 1062–92. Cartwright F.F. 1977. A Social History of Medicine. London and New York: Longman. Carus-Wilson E.M. 1966. “The Iceland Trade.” In Studies in English Trade in the Fifteenth Century: 155–82. Castex D. 2008. “Identification and Interpretation of Historical Cemeteries Linked to Epidemics,” In Paleomicrobiology. Past Human Infections: 23–48. Castiglioni A. 1927. Storia della medicina. Milan: Società editrice “Unitas.” ——. 1931. Histoire de la médecine. (Bibliotèque Médicale.) J. Bertrand (transl. and ed.). Paris: Payot. ——. 1947, repr. 1975. A History of Medicine. E.B. Krumbhaar (transl. and ed.). New York: Knopf. Repr. 1975, New York: J. Aronson, Inc. Cayla P. 1906. L’épidémie de peste de 1348 à Narbonne. Montpellier. Cazelles M.R. 1962/1965. “La peste de 1348–9 en langue d’oïl. Épidémie prolétarienne et enfantine.” Bulletin philologique et historique du Comité des travaux historiques et scientifiques (jusqu’en 1610): 293–305.

698

bibliography

Centers for Disease Control and Prevention, Special Pathogens Branch, www.cdc.gov./ ncidod/dvrd/spb/mnpages/dispages/marburg.htm Centers for Disease Control and Prevention, Special Pathogens Branch, www.cdc.gov./ ncidod/dvrd/spb/mnpages/dispages/ebola.htm, and same address ending ebotabl .htm. 2003. “Ebola Hemorrhagic Fever and Table Showing Known Cases and Outbreaks, In Chronological Order.” pp. 1–4 and 1–3. Centers for Disease Control and Prevention. February 2006 (day of consultation). “FAQ’s – Medical Facts About Anthrax” 1–2. www.cdc.gov./ncidod/dbend/ diseaseinfo/anthrax Chandler A.C. and Read C.P. 1961. Introduction to Parasitology with Special Reference to the Parasites of Man. 10th ed. New York: John Wiley & Sons, Inc. Cheng T.C. 1986.General Parasitology. 2nd ed. Orlando, etc.: Academic Press College Division, Harcourt Brace Jovanovich, Publishers. Chick H. and Martin C.J. 1911. “The Fleas Common on Rats in Different Parts of the World and the Readiness with Which They Bite Man.” The Journal of Hygiene. 11: 122–36. Choksy K.B.N.H. 1909. “The Various Types of Plague and their Clinical Manifestations.” American Journal of the Medical Science. 138: 351–66. Christiansen J. 2005. “Den engelske svedesyge. En analyse af epidemien i Danmark i 1529.” Historisk tidsskrift [Denmark]. 105: 80–96. Christensen P. 2003. “ ‘In these Perilous Times’: Plague and Plague Policies in Early Modern Denmark.” Medical History. 47: 413–50. Christie A.B. 1980. Infectious Diseases: Epidemiology and Clinical Practice. 3rd ed. Edinburgh: Churchill Livingstone. 1st ed. 1969, 2nd ed. 1974, 4th ed. 1987. The Chronicle of Jean de Venette. 1953. R.A. Newhall (ed.). New York: Columbia University Press. Chun J.W.T. 1936. “Clinical Features.” In Wu, Chun, Pollitzer, et al. Plague. A Manual for Medical and Public Health Workers: 309–33. CIA. 2005. www.cia.gov. World Fact Book. “Plague.” Ciano C. 1976. La sanità marittima nell’età medicea. (“Biblioteca del Bolletino Storico Pisano”.) Pisa: Pacini Editore. Cipolla C.M. 1973. Cristofano and the Plague. A Study in the History of Public Health in the Age of Galileo. Berkely: University of California Press. ——. 1974. “The Plague and the Pre-Malthus Malthusians.” The Journal of European Economic History. 3: 277–84. ——. 1976a. Public Health and the Medical Profession in the Renaissance. Cambridge: Cambridge University Press. ——. 1976b. Before the Industrial Revolution. European Society and Economy, 1000–700. London: Methuen & Co. Ltd. ——. 1977. Chi ruppe i rastelli a Monte Lupo? Bologna: Il Mulino. ——. 1978. “Peste del 1630–1 nell’Empolese.” Archivio Storico Italiano. 136: 469–81. ——. 1979. Faith, Reason, and the Plague in Seventeenth-Century Tuscany. Ithaca, New York: Cornell University Press. Public Health and the Medical Profession in the Renaissance. ——. 1981. Fighting the Plague in Seventeenth-Century Italy. Wisconsin. The University of Wisconsin Press. ——. 1986. Contro un nemico invisibile. Epidemie e strutture sanitarie nell’Italia del Rinascimento. Bologna: Il Mulino. ——. 1992. Miasmas and Disease. Public Health and the Environment in the Preinudstrial Age. New Haven and London: Yale University Press. Cipolla C.M. and Zanetti D.E. 1972. “Peste et mortalité différentielle.” Annales de démographie historique. 1972: 197–202. Clark P. and Slack P. 1976. English Towns in Transition, 1500–700. London: Oxford University Press.

bibliography

699

Cliff A.D. and Haggett P. 1985. The Spread of Measles in Fiji and the Pacific: Spatial Components in the Transmission of Epidemic Waves through Island Communities. Canberra: Research School of Pacific Studies, Australian National University. Clot-Bey A.B. 1851a. Leçon sur la peste d’Égypte. Paris: Chez Victor Masson, Libraire. ——. 1851b. Coup d’oeil sur la peste et les quarantaines. Paris: Chez Victor Masson, Libraire. Coale A.J. and Demeny P. with Vaughan B. 1983. Regional Model Life Tables and Stable Populations. 2nd edn. New York: Academic Press. Cohn S.K., Jr. 1992. The Cult of Remembrance and the Black Death. Six Renaissance Cities in Central Italy. Baltimore: the Johns Hopkins University Press. ——. 2002. The Black Death Transformed: Disease and Culture in Early Renaissance Europe. London: Hodder Headline Group. ——. 2005. [Review of O.J. Benedictow, The Black Death. The Complete History 2004]. The New England Journal of Medicine, 352; March 10: 1354–5. ——. 2008. “Epidemiology of the Black Death and Successive Waves of Plague.” Medical History. Suppl. (27): 74–100. ——. and Alfani G. 2007. “Households and Plague in Early Modern Italy.” The Journal of Interdisciplinary History. 38: 177–205. Coleman M.P. 1986. “A Plague Epidemic in Voluntary Quarantine.” International Journal of Epidemiolgoy. 15: 379–85. Colonna d’Istria M. 1968. Étude épidémiologique de la peste de 1720 à Marseille. Thèse de médecine. Marseilles: Faculté mixte de médecine et de pharmacie de Marseille. Cooper A. and Poinar H. 2000. “Ancient DNA: Do it Right or Not at All.” Science. 289: 1139. Copeman W.S.C. 1960. Doctors and Disease in Tudor Times. London: Dawson’s of Pall Mall. Cosmacini G. 1994. Storia della medicina e della sanità in Italia dalla peste Europea alla Guerra mondiale 1348–918. Bari: Editori Laterza. 1st ed. 1987–6th edn. 1994. Coulton G.G. 1947. Medieval Panorama. The English Scene from Conquest to Reformation. Cambridge: Cambridge University Press. The Countryside of Medieval England. 1988. G. Astill and A. Grant (eds.). Oxford: Basil Blackwell. Cox J.C. 1907. “Ecclesiastical History.” In The Victoria History of the County of Berkshire. Vol. 2: 1–49. ——. 1910. The Parish Registers of England. London: Methuen & Co. Ltd. Creighton C. 1891. A History of Epidemics in Britain from a.d. 664 to the Extinction of Plague. Cambridge: At the University Press. ——. 1894. 1965 A History of Epidemics in Britain. Vol. 1. From a.d. 664 to the Extinction of Plague. Vol. 2. From the Extinction of the Plague to the Present Time. Cambridge: At the University Press. Repr. 1965. London: Frank Cass & Co. Ltd. Croix A. 1967. “La démographie du pays nantais au XVIe siècle.” Annales de démographie historique: 63–90. ——. 1981. La Bretagne au 16e et 17e siècles. La vie, la mort, la foi. Paris: Maloine S.A. Crook L.D. and Tempest B. 1992. “Plague. A Clinical Review of 27 Cases.” Archives of Internal Medicine. 152: 1253–56. Davis D.E. 1986. “The Scarcity of Rats and the Black Death: an Ecological History.” Journal of Interdisciplinary History. 16: 455–70. Davis R.A. 1989. “The Effect of the Black Death on the Parish Priests of the Medieval Diocese of Coventry and Lichfield.” Historical Research. 62: 85–90. Del Panta L. 1980. Le epidemie nella storia demografica italiana (secoli XIV–XIX). Turin: Lescher editore. Delille G. 1974. “Un problème de démographie historique: Hommes et femmes face à la mort.” Mélanges de l’Ecole française de Rome. Moyen-Age, Temps modernes 86: 419–43.

700

bibliography

Deportes P. 1977. Reims et les Remois aux XIIIème et XIVème siècles. Vols. 1–2. (Thèse présentée devant l’Université de Paris.) Lille: Service de reproduction des théses, Université de Lille. Develin Sergeant-Major. 1896. Views in Chitral: Taken During the Advance of the 3rd Brigade of the Chitral Relief Force under the Command of W.F. Gatacre. London. Devignat R. 1951. “Variétés de l’espece Pasteurella pestis.” Bulletin of WHO. 4: 247–63. ——. 1953. “Répartition géographique des trois variétés de Pasteurella pestis.” Experimental Cell Biology. 16: 509–14. Diemerbroeck Ijsbrand van. 1646. De peste libri quatuor, truculentissimi morbi historiam ratione & experientia? confirmatam exhibentes. Arnhem: Ex officina Joannis Iacobi bibliopolae. Diemerbroeck Ysbrand van. 1722. Treatise Concerning the Pestilence: Describing its Particular Causes, Various Symptoms, and Method of Cure. Written originally in Latin, by Isbrand de Diemerbroeck, M.D. And abridg’d, and translated into English, by Thomas Stanton, surgeon. London: Printed for J. Downing. Dieudonné A. and Otto R. 1928. “Die Pest.” In: Handbuch der Pathogenen Mikroorganismen. 1928: 179–412. Plates and map. Dijkstra J.G. 1921. Een epidemiologische beschouwing van de nederlandsche pest-epidemieën der XVIIde eeuw. Doctoral thesis, University of Amsterdam. Amsterdam. Diplomatarium Norvegicum. 1851–2. Vol. 2; Diplomatarium Norvegicum. 1860–1. Vol. 4; Diplomatarium Norvegicum. 1871–4. Vol. 8; Diplomatarium Norvegicum. 1878. Vol. 9. C.C. Lange and C.R. Unger (eds.). Christiania [Oslo]: Mallings Forlagsbokhandel. D’Irsay S. 1926. “Notes to the Origin of the Expression: Atra Mors.” Isis. 8: 328–32. Dohar W.J. 1994. The Black Death and Pastoral Leadership. The Diocese of Hereford in the Fourteenth Century. Philadelphia: University of Pennsylvania Press. Dols M.W. 1977. The Black Death in the Middle East. Princeton: Princeton University Press. Dongsheng Z., Yanping H., Yajun S., et al. 2004. “Comparative and Evolutionary Genomics of Yersinia pestis.” Microbes and Infection. 6: 1226–34. Donowitz L.G. 2003. “Pediatric Infection Control.” In Principles and Practice of Pediatric Infectious Diseases: 17–27. Dowell F.S., Mukunu R., Ksiazek T.-G., Khan A.S., Rollin P.E., and Peters C.J. 1999. “Transmission of Ebola Hemorrhagic Fever: A Study of Risk Factors in Family Members, Kikwit, Democratic Republic of Congo, 1995.” The Journal of Infectious Diseases. 179 (Suppl 1): S87–S91. Drancourt M., Aboudharam G., Signoli M., Dutour O., Raoult D. 1998. “Detection of 400-year old Yersinia pestis DNA in Human Dental Pulp: An Approach to the Diagnosis of Ancient Septicemia.” Proceedings of the National Academy of Sciences of the United States of America (online): 95: 12637–40. Drancourt M. and Raoult D. 2002. “Molecular Insights into the History of Plague.” Microbes and Infection. 4: 105–9. ——. 2004. “Molecular Detection of Yersinia pestis in Dental Pulp.” Microbiology. 150: 263–4. ——. 2008a. “Molecular Detection of Past Pathogens.” In: Paleomicrobiology: Past Human Infections: 55–68. ——. 2008b. “Past Plague.” In: Paleomicrobiology: Past Human Infections: 145–60. Drancourt M., Roux V., La V.D. et al. 2004. “Genotyping, Orientalis-like Yersinia pestis, and Plague Pandemics.” Emerging Infectious Diseases. www.cdc.gov/eid. Vol. 10: 1585–92. Drancourt M., Houhamdi L., Raoult D. 2006. “Yersinia pestis as a Telluric, Human Ectoparasite-born Organism.” Lancet Infectious Diseases. 6: 234–41.

bibliography

701

Drancourt M., Signoli M., La V.D. et al. 2007. “Yersinia pestis Orientalis in Remains of Ancient Plague Patients.” Emerging Infectious Diseases. 3, No. 2: 332–3. (pdf available from www.cdc.gov/EID/content/13/2/332.htm.) Dubois H. 1988. “La dépression (XIVe et XVe siècles).” In Histoire de la population Française: 313–66. Dujardin-Beaumetz E. 1933. “Communication. Remarque à propos de la communication de Marcel Leger sur les cas de Pestis levissima.” Bulletin de la Société de Pathologie exotique. 23: 892–4. Dupacqier J. 1972. “De l’animal à l’homme: le mécanisme autorégulateur des populations traditionelles.” Revue de l’Institut de sociologie: 177–98. Dyer C. 1988. “Documentary Evidence: Problems and Enquiries.” In The Countryside of Medieval England: 12–35. Dyer A.D. 1978. “The Influence of Bubonic Plague in England, 1500–1667.” Medical History. 22: 308–26. Ecclestone M. 1999. “Mortality of Rural Landless Men before the Black Death: the Glastonbury Head-tax Lists.” Local Population Studies. 63: 6–29. Eckert E.A. 1996. The Structure of Plagues and Pestilences in Early Modern Europe. Central Europe, 1560–1640. Basel: Karger AG. Eketorp. Befestigung auf Öland/Schweden. Die Fauna. 1979. Vol. 3. J. Boessneck et al. (eds.). Stockholm: Royal Academy of Letters, History and Antiquities. Eldevik T. 2006. “En ny istid truer?” Dagbladet. 13 January: 48 Eskey C.R. 1930. “Chief Etiological Factors of Plague in Ecuador and the Antiplague Campaign.” Public Health Reports. 45: 2077–115. ——. 1938. “Recent Devlopments in our Knowledge of Plague Transmission.” Public Health Reports. 53: 49–58. Eskey C.R. and Haas V.H. 1939. “Plague in the Western Part of the United States. Infection in Rodents, Experimental Transmission by Fleas, and Inoculation Tests for Infection.” Public Health Reports. 54: 1467–81. ——. 1940. “Plague in the Western Part of the United States.” Public Health Bulletin. No. 254: 1–82. Essays in Quantitative Economic History. 1974. R. Floud (ed.) for the Economic History Society. Oxford: Clarendon Press. Cf. Ohlin 1966, below. Estrade F. 1935. “Observations relative à la biologie de Xenopsylla cheopis en Emyrne.” Bulletin de la Société de pathologie exotique. 28: 293–8. Faire de l’histoire. Noveaux objets. 1974. J. Le Goff and P. Nora (eds.). Paris: Gallimard. Favreau R. 1967. “Épidémies à Poitiers et dans le centre ouest à la fin du moyen âge.” Bibliothèque de l’École des Chartes. 125: 349–98. Festschrift für Hermann Heimpel zum70. Geburtstag am 19. September 1971. 1972. Mitarbeitern des Max-Planck-Instituts für Geschichte (eds.). Vol. 2. Göttingen: Vandehoeck & Ruprecht. Ficino M(arsilio). 1983. Consilio contro la pestilenzia. E. Musacchio (ed.). Bologna: Capelli editore. Original written c. 1480. Fiumi E. 1950. “La demografia fiorentina nelle pagine di Giovanni Villani.” Archivio Storico Italiano. 108: 78–158. ——. 1958. “Fioritura e decadenza dell’economia fiorentina.” Archivio Storico Italiano. 116: 443–510. Fletcher J.M.J. 1922. “The Black Death in Dorset, 1348–9.” Proceedings of the Dorset Natural History and Antiquarian Field Club. 43: 1–14. Fourastié J. 1972. “From the Traditional to the ‘Tertiary’ Life Cycle.” In Readings in Population: 29–38. Fritzner J. 1954. Ordbog over Det gamle norske Sprog. 2nd ed. Vol. 2. Oslo: Trygve Juul Møllers Forlag. Gasquet F.A. 1908. The Black Death of 1348 and 1349. 2nd edn. London: George Bell and Sons.

702

bibliography

Gatacre B. 1910. General Gatacre. The Story of the Life and Services of Sir William Forbes Gatacre, 1843–906. London: John Murray. Gatacre W.F. 1897. Report on the Bubonic Plague in Bombay, 1896–7. Vols. 1–2. Bombay: Times of India. Genicôt L. 1966. “Crisis: From the Middle Ages to Modern Times.” In The Cambridge Economic History of Europe. Vol. 1. The Agrarian Life of the Middle Ages: 660–741. Gilbert T.P., Cuccui J., White W., et al. 2004a. “Absence of Yersinia pestis-specific DNA in Human Teeth from Five European Excavations of Putative Plague Victims.” Microbiology. 150: 341–54. ——. 2004b. “Response to Drancourt and Raoult.” Microbiology. 150: 264–5. Gilliam J.F 1961. “The Plague under Marcus Aurelius.” American Journal of Philology. 82: 225–51. Girard G. 1943. “Les ectoparasites de l’homme dans l’épidémiologie de la peste.” Bulletin de la Société de pathologie exotique et de ses filiales. 36: 4–43. ——. 1955. “Plague.” Annual Reviews of Microbiology. 9: 253–76. ——. 1959. “Considerations sur l’épidémiologie de la peste. Caractéristiques des centres endémiques asiatiques et africains.” Revue de médécine et d’hygiène d’outre-mer. No. 281; Oct. 1959: 114–20. Glénisson J. 1968–9. “La seconde peste: L’épidémie de 1360–2 en France et en Europe.” Annuaire-Bulletin de la Société de l’histoire de France. Années 1968–9. [Paris, 1971]: 27–38. Gomez H.F. and Clearly T.G. 2003 “Yersinia Species.” In Principles and Practice of Pediatric Infectious diseases: 839–43. Gottfried R.S. 1978. Epidemic Disease in Fifteenth Century England. The Medieval Response and the Demographic Consequences. Leicester: Leicester University Press. Grandsen A. 1957. “A Fourteenth Century Chronicle from the Grey Friars at Lynn.” The English Historical Review. 72: 270–8. Grant A. 1988. “Animal Resources.” In The Countryside of Medieval England 1988: 149–87. Gras P. 1939. “Le registre paroissial de Givry (1334–57) et la peste noire en Bourgogne.” Bibliothèque de l’École des chartes. 100: 295–308. Greenwood M. See IPRC, Reports nos. XLIV, XLV. ——. 1935. Epidemics and Crowd-Diseases. An Introduction to the Study of Epidemiology. London: Williams & Norgate LTD. Hårding B. 1992. “Osteological Report – the Quarter Trädgårdsmestaren [= the Gardener] – Sigtuna.” Sten Tesch, the Director of Sigtuna Museum, has most kindly sent me copies of relevant pages of Hårding’s unpublished report, namely pages 0–1 [sic], 3–4, 27. ——. 1993. “Risikabelt å være katt i det medeltida Sigtuna.” Populär Arkeologi. 23–6. Hallam E.H. 1988. “Population Movements in England, 1086–1350.” In The Agrarian History of England and Wales. Vol. 2: 508–93. Handbuch der Pathogenen Mikroorganismen. 1928. W. Kolle, R. Kraus und P. Uhlenhuth (eds.). Vol. 4. 3rd ed. Jena: G. Fischer Verlag. Hankin E.H. 1905. “On the Epidemiology of Plague.” The Journal of Hygiene. 5: 48–83. Hannes Þorsteinnsson. 1922–7. “Annáll Björns lögréttumanns Jónssonar á Skarðsá eða Skarðsárannáll 1400–1640.” In Annales islandici posteriorum sæculorum. Annáles 1400–800. Vol. 1: 28–45. ——. 1933–8. “Annáll séra Jóns prófasts Arasonar í Vatnsfirði eða Vatnsfajrðarannáll hinn elzti 1395–654.” In Annales islandici posteriorum sæculorum. Annáles 1400– 800. Vol. 3: 1–20. Harvey B. 1993. Living and Dying in England, 1100–1540. Oxford: Clarendon Press. Hatcher J. 1977/1987 (several reprints). Plague, Population and the English Economy 1348–530. Houndmills, Basingstoke, Hampshire: Macmillan Education Ltd.

bibliography

703

——. 1986. “Mortality in the Fifteenth Century: Some New Evidence.” The Economic History Review. 2nd series, 39: 19–38. ——. 2003. “Understanding the Population History of England.” Past & Present. No. 180: 83–130. Hatcher J. and Bailey M. 2001. Modelling the Middle Ages. The History and Theory of England’s Economic Development. Oxford: Oxford University Press. Hatcher J., Piper A.J., and Stone D. 2006. “Monastic Mortality: Durham Priory, 1395– 1529.” The Economic History Review. 59: 667–87. Health, Medicine and Mortality in the Sixteenth Century. 1979. C. Webster (ed.). Cambridge: Cambridge University Press. Helgeandsholmen. 1000 år i Stockholms ström. 1983. G. Dahlbeck (ed.). Stockholm: Liber Förlag. Helle K. 1982. Bergen Bys historie. Bergen: Universitetsforlaget. Herlihy D. and Klapisch-Zuber C. 1978. Les toscans et leurs familles. Paris: Edition de l’école des hautes études en sciences sociales. Hicks M.A. 1995. Bastard Feudalism. London: Routledge. Hinnebusch B.T., Perry R.D. and Schwan T.G. 1996. “Role of the Yersinia pestis hemin storage (hms) locus in the transmission of plague by fleas.” Science. 273: 367–70. Hirsch A. 1860–4. Handbuch der historisch-geographischen Pathologie. Vols. 1–2. Erlangen: Enke. Hirst L.F. 1927. “Rat-flea Surveys and their Use as a Guide to Plague Preventive Measures.” Transactions fo the Royal Society of Tropical Medicine and Hygiene. 21: No. 2: 87–108. ——. 1953. The Conquest of Plague. Oxford: Clarendon Press. Histoire de la population française. 1988. Vol. 1. Paris: Presses Universitaires de France. Hollingsworth T.H. 1969. Historical Demography. London: The Sources of History Limited. Holmes, T.S. 1911. “Ecclesiastical History.” In W. Page (ed.). The Victoria History of the County of Somerset. Vol. 2. Hufthammer A.K. 2006. Personal communications by e-mail 10 January 2006 on findings of rat bones in medieval and early modern sites in Norway after sieving for them started in recent years. Høvsgaard T. 2008. “Den svarte Pestilentze—på Grønland? En vandring ad historieskrivningens vildveje.” Historisk Tidsskrift [Denmark]. 108: 188–96. Ibs J.H. 1994. Die Pest in Schleswig-Holstein von 1350 bis 1547–8. (Kieler Werkstücke, Reihe A: Beiträge zur schleswig-holsteinischen und skandinavischen Geschichte, 12.) Frankfurt am Main: Peter Lang. An Icelandic-English Dictionary. 1975. 2nd edn. Oxford: Clarendon Press. I Congrés Hispano-Luso-Italià de Demografia Històrica. Asociación de Demografía Histórica y Società Italiana di Demografia Storica. 1987. Barcelona. Vol. 1. Indian Plague Commission 1898–9. “Minutes of Evidence.” British Parliamentary Papers. Vol. 30–2. Mumbai: At the Secretariat. Indian Plague Research Commission. 1906a. Reports on Plague Investigations in India, I. “Experiments upon the Transmission of Plague by Fleas.” The Journal of Hygiene. 6: 425–82. ——. 1906b. Reports on Plague Investigations in India, II. N.C. Rothschild, “Note on the Species of Fleas Found upon Rats, Mus rattus and Mus decumanus, in Different Parts of the World, and on Some Variations in the Proportion of Each Species in Different Localities.” The Journal of Hygiene. 6: 483–5. ——. 1906c. Reports on Plague Investigations in India, VIII. “On the Number of Plague Bacilli in the Blood, Urine, and Faeces Respectively of Rats which had Died of Plague.” The Journal of Hygiene. 6: 519–23. ——. 1906d. Reports on Plague Investigations in India, IX. “On the Quantitative Estimation of the Septicaemia in Human Plague.” The Journal of Hygiene. 6d: 524–9.

704

bibliography

——. 1907a. Reports on Plague Investigations in India, XIII. “Transmission of Plague by Feeding Rats with Infected Material.” The Journal of Hygiene. 7: 373–81. ——. 1907b. Reports on Plague Investigations in India, XV. “Further Observations on the Transmission of Plague by Fleas, with Special Reference to the Fate of the Plague Bacillus in the Body of the Rat Flea (P. cheopis).” The Journal of Hygiene. 7: 395–420. ——. 1907c. Reports on Plague Investigations in India, XVI. “Experimental Production of Plague Epidemics among Animals.” The Journal of Hygiene. 7: 421–35. ——. 1907d. Reports on Plague Investigations in India, XVII. “Experiments in Plague Houses in Bombay.” The Journal of Hygiene. 7: 436–56. ——. 1907e. Reports on Plague Investigations in India, XX. “A Note on Man as a Host of the Indian Rat Flea (P. Cheopis).” The Journal of Hygiene. 7: 472–6. ——. 1907f. Reports on Plague Investigations in India, XXI. “Digest of Recent Observations of the Epidemiology of Plague.” The Journal of Hygiene. 7: 694–723. ——. 1907g. Reports on Plague Investigations in India, XXII. “The Epidemiological Observations Made by the Commission in Bombay City.” The Journal of Hygiene. 7: 724–98. ——. 1907h. Reports on Plague Investigations in India, XXIII. “Observations made in Four Villages in the Neigbourhood of Bombay.” The Journal of Hygiene. 7: 799–873. ——. 1907i. Reports on Plague Investigations in India, XXIV. “General Considerations Regarding the Spread of Infection, Infectivity of Houses, etc., in Bombay City and Island.” The Journal of Hygiene, 7: 874–94. ——. 1907j. Reports on Plague Investigations in India, XXV. “Observations in the Punjab Villages of Dhand and Kasel.” The Journal of Hygiene. 7: 895–985. ——. 1908a. Reports on Plague Investigations in India, XXVI. D. T. Verzhbitskiy,1 “The Part Played by Insects in the Epidemiology of Plague.” The Journal of Hygiene. 8: 162–208. ——. 1908b. Reports on Plague Investigations in India, XXIX. “Observations on the Bionomics of Fleas with Special Reference to Pulex cheopis [= Xenopsylla cheopis].” The Journal of Hygiene. 8: 236–59. ——. 1908c. Reports on Plague Investigations in India, XXXI. “On the Seasonal Prevalence of Plague in India.” The Journal of Hygiene. 8: 266–301. ——. 1910a. Reports on Plague Investigations in India, XXXIII. “The Experimental Production of Plague Epidemics among Animals (Third Communication).” The Journal of Hygiene. 10: 315–34. ——. 1910b. Reports on Plague Investigations in India, XXXV. M. Greenwood and G. Lamb, “On the Spread of Epidemic Plague through Districts with Scattered Villages.” The Journal of Hygiene. 10: 349–443, plus Maps I–XLVIII. For authors, see Report no. XLV, footnote 1. ——. 1910c. Reports on Plague Investigations in India, XXXVI. “Observations on Rat and Human Plague in Belgaum 1908–9.” The Journal of Hygiene. 10: 446–82, plus Maps I–XVII. ——. 1910d. Reports on Plague Investigations in India, XXXVII. “Observations on Plague in Poona.” The Journal of Hygiene. 10: 483–535, plus Maps I–V. ——. 1910e. Reports on Plague Investigations in India, XXXIX. “Interim Report of the Advisory Committee for Plague Investigation in India.” The Journal of Hygiene. 10: 566–8. ——. 1911a. Reports on Plague Investigations in India. XLIV. M. Greenwood, “Statistical Investigation of Plague in the Punjab. Second Report: On the Connection between

1 In the original translation, the author’s name is transcribed as Verjbitski, I endevour consistently to use modern transcription from Russian to English.

bibliography

705

Proximity to Railways and Frequency of Epidemics.” The Journal of Hygiene. Plague Supplement I. 11: 47–61. ——. 1911b. Reports on Plague Investigations in India. XLV. M. Greenwood, “Statistical Investigation of Plague in the Punjab. Third Report: On Some of the Factors which Influence the Prevalence of Plague.” Journal of Hygiene. Plague Supplement I. 11: 62–156. Appendix I. “A Note on English Plague Experience with Reference to Relative Mortality in Towns and Villages.” Ibid: 93–6, 150–1. ——. 1911c. Reports on Plague Investigations in India, XLVI. “Observations on Plague in Eastern Bengal and Assam.” The Journal of Hygiene. Plague Supplement I. 12: 157–93. ——. 1912. Reports on Plague Investigations in India, XLVIII. “Plague in Madras City.” The Journal of Hygiene. Plague Supplement II. 12: 207–20. ——. 1914a. Reports on Plague Investigations in India, LXVII. A. Bacot and C.J. Martin, 1914. “Observations on the Mechanism of the Transmission of Plague by Fleas.” The Journal of Hygiene. 14: 423–39. ——. 1914b. Reports on Plague Investigations in India, LXIX. W. Bacot, “A Study of the Bionomics of the Common Rat Fleas and othe Species Associated with Human Habitations, with Special Reference to the Influence of Temperature and Humidity at Various Periods of the Life History of the Insect.” The Journal of Hygiene. 14: 447–655. Industrialization in Two Systems: Essays in Honor of Alexander Gerschenkron. 1966. H. Rosovsky (ed.). New York: John Wiley & Sons, Inc. I Necrologi di San Domenico in Camporegio. (Epoca Cateriniana.) 1937. (Fontes Vitae S. Catharinae Senensis Historici. Vol. XX) M. Hyacinthi Laurent (ed.). Florence: G.C. Sansoni. Innsikt og Utsyn. Festskrift til Jørn Sandnes. 1996. Trondheim: Department of History, The Norwegian University of Science and Technology (NTNU)/ (Historisk institutt, Norges Teknisk-Naturvitenskapelige Universitet). IPRC = The Indian Plague Research Commission Islandske Annaler indtil 1578. 1888, repr. 1997. G. Storm (ed.). Christiania [=Oslo]: Det norske historiske Kildeskriftfond. James T.B. 1998. “The Black Death in Berkshire and Wiltshire.” The Hatcher Review. 5: 11–20. ——. 1999. “The Black Death in Hampshire.” Hampshire Papers. No. 18, December: 1–28. ——. 2001. “Years of Pestilence.” British Archaeology. October. No. 61: 8–13. Jawetz E., Melnick J.L., Adelberg E.A. 1982. Review of Medical Microbiology. 15th ed. Los Altos, California: Lange Medical Publications. JNMA, Journal of the Norwegian Medical Association = Tidsskrift for Den norske legeforening. Kahn A.S. 2003. “Ebola and Marburg Viruses.” In Principles and Practice of Pediatric Infectious Diseases: 1166–8. Karlsson G. 1996. “Plague Without Rats: The Case of Fifteenth-century Iceland,” Journal of Medieval History, 22: 263–84. Karlsson G. and Kjartansson H.S. 1994. “Plágurnar miklu á Islandi,” 32: 11–74. Key G., Fielding A.H., Goulding M.J., et al. 1998. “Ship Rats Rattus rattus on the Shiant Islands, Hebrides, Scotland.” Journal of Zoology. 245: 228–33. Keys D. 1999. Catastrophe: An Investigation into the Origins of the Modern World. London: Century. Klein I. 1988. “Plague, Policy and Popular Unrest in British India.” Modern Asia Studies. 43: 723–55. Klimenko V.C. 1910. “O chumnykh epidemiyakh v Rossii.” Voyenno-medicinskiy Zhurnal. 229: 657–63. Knudsen L.G. 2005. Pesten grasserer! En undersøgelse av pesten I Danmark i 1650’erne. [Kerteminde]: Landbohistorisk Selskab.

706

bibliography

Knudsen L.G. 2009. “The Course of a Mid-17th Century Plague Epidemic in Denmark.” In: Living with the Black Death: 113–34. Kohn G.C. 1995. The Wordsworth Encyclopedia of Plague and Pestilence. New York: Facts on File. Kongespeilet. 1947. Trans. A.W. Brøgger. Oslo: H. Ashehoug & Co. Kowal A.O. 1972. “Danilo Samoilowitz: An Eighteenth-Century Epidemiologis and his Role in the Moscow Plague (1770–2).” Journal of the History orf Medicine and Allied Sciences. 27: 434–46. Kosminsky E.A. 1955. “The Evolution of Feudal Rent in England from the XIth to the XVth Centuries.” Past & Present. 7: 12–36. ——. 1957. “Peut-on considererer le XIV et le XV siècles comme l’époque de la décadence de l’économie européenne?” In Studi in onore di Armando Sapori: 551–69. Krüger S. 1972. “Krise der Zeit als Ursache der Pest?” In Festschrift für Hermann Heimpel: 839–83. Kulturhistorisk leksikon for nordisk middelalder. 1956–78. Vols. 1–22. Oslo: Gyldendal Norsk Forlag. La V.D. Aboudharam G., Drancourt M. and Raoult D. 2008. “Dental Pulp as a Tool for the Retrospective Diagnosis of Infectious Diseases.” In Paleomicrobiology: Past Human Infections 175–96. Lamb G. 1908. The Etiology and Epidemiology of Plague. A Summary of the Work of the Plague Commission. Calcutta: Superintendet of Government Printing, India. Lamb H.H. 1995. Climate, History and the Modern World. 2nd ed. London and New York: Routledge. Land, Kinship and Life-Cycle. 1984. R.M. Smith (ed.). Cambridge: Cambridge University Press. Langen de C.D. and Lichtenstein A. 1936. A Clinical Text-Book of Tropical Medicine. 1st English ed. From the Rev. 3rd Dutch ed. Batavia, Surabaya, Amsterdam: G. Kolff & Co. Legters L.J., Cottingham A.J., Jr., Hunter D.H. 1970. “Clinical and Epidemiologic Notes on a Defined Outbreak of Plague in Vietnam.” The American Journal of Tropical Medicine and Hygiene. 19: 639–52. Le Méné M. 1964. “La population nantaise à la fin du XVe siècle.” Annales de Bretagne. 71: 189–220. Lepiksaar J. 1965. “Djurrester från det medeltida Ny Varberg.” Varbergs Museum. Årsbok. 16: 73–102. ——. 1969. “Nytt om djur från det medeltida Ny Varberg.” Varbergs Museum. Årsbok. 20: 37–68. ——. 1975. “Über die Tierknochenfunde aus den mittelalterlichen Siedlungen Südschwedens.” In Archaeozoological Studies: 230–9. Le Roy Ladurie E. 1965. “Le climat des XIe et XVIe siècles: séries comparées.” Annales ESC. 20: 899–922. ——. 1967. Histoire du climat depuis l’an mil. Paris: Flammarion. —— 1974. “Le climat. L’histoire de la pluie et du beau temps.” In Faire de l’histoire: 3–30. Lettré E. 1840–1. “Opuscule relatif à la peste de 1348.” Bibliothèque de l’École des Chartes. 2: 201–43. Lie R. 1988. “Animal Bones.” In: De arkeologiske utgravninger i Gamlebyen, Oslo. Vol. 5. E. Schia (ed.). Øvre Ervik: Alvheim & Eide: 153–96. Liston W.G. 1924. “The Milroy Lectures on The Plague.” The British Medical Journal. 1924: 900–3, 950–4, 997–1001. Little L.K. 2007. “Life and Afterlife of the First Plague Pandemic.” In Plague and the End of Anitquity: 3–32. Livi Bacchi M. 1978. La société italienne devant les crises de mortalité. Florence: Dipartimento statistico, Facultá di economia e commercio, Università di Firenze.

bibliography

707

Living with the Black Death. L. Bisgaard and L. Søndergaard (eds.). Odense: University Press of Southern Denmark. Loghem van J.J. 1918. “The Plague of the 17th Century Compared with the Plague of Our Days.” Janus. Revue internationale de l’histoire des sciences de la méedecine. 5: 95–107. ——. 1925. “Le rat domestique et la lutte contre la peste au XVIIe siècle.” Revue d’hygiène (et de police sanitaire), 47: 521–7. Loghem van J.J. and Swellengrebel N.H. 1914. “Kontinuerliche und metastatische Pestverbreitung.” Medical Microbiology and Immunology. 77: 460–81. Lomas T. 1984. “South–East Durham: Late Fourteenth and Fifteenth Centuries.” In The Peasant Land Market: 253–327. Lopez R.S. 1971, repr. 1976. The Commercial Revolution of the Middle Ages, 950–1350. Cambridge: Cambridge University Press. Loschky D. and Childers B.D. 1993. “Early English Mortality.” The Journal of Interdisciplinary History. 24: 85–97. Lunn J. 1937. The Black Death in the Bishop’s Registers. Ph.D. thesis, Cambridge University. (No known copy exists, and I have not been able to consult the work.) McArthur N. 1968. Island Populations of the Pacific. Canberra: Australian National University Press. MacArthur W.P. 1925–6. “Old-Time Plague in Britain.” Transactions of the Royal Society of Tropical Medicine and Hygiene. 19: 355–72. ——. 1949. “The Identification of Some Pestilences Recorded in the Irish Annals.” Irish Historical Studies. 6: 169–88. ——. 1952. “The Occurrence of the Rat in Early Europe. The Plague of the Philistines (1 Sam., 5, 6).” Transactions of the Royal Society of Tropical Medicine and Hygiene, 46: 209–12, 464. McCormick M. 2003. “Rats, Communications, and Plague: Toward and Ecological History.” Journal of Interdisciplinary History. 34: 1–25. ——. 2007. “Toward a Molecular History of the Justinianic Pandemic.” In: Plague and the End of Antiquity: 290–312. McFarlane K.B. 1973. The Nobility of Later Medieval England. Oxford: Clarendon Press. McKeough A. and Loy T. 2002. “Ring-a-Ring-a-Rosy: DNA Analysis of the Plague Bacillus from Late Medieval London.” Ancient Biomolecules. 4: 145. McNeill W.H. 1979. Plagues and Peoples. Harmondsworth: Penguin Books. Maddicot J. 2007. “Plague in Seventh-Century England.” In Plague and the End of Antiquity: 171–214. Maia J. de Oliveira Costa. 1968. Human Biology. 24: 167–200. See H. Abbey 1968. Manchurian Plague Prevention Service. Memorial Volume. 1934. Ed. Wu Lien-Teh. Shanghai, China: National Quarantine Service. Mansa F.V. 1873. Bidrag til Folkesygdommenes og Sundhedspleiens Historie I Danmark fra de ældste Tider til Begyndelsen avf det attende Aarhundrede, Copenhagen: Gyldendalske Boghandel. Manson’s Tropical Diseases. 1921. 7th edn. P.H. Manson-Bahr (ed.). London: Baillière Tindall. ——. 1936. 10th edn. P.H. Manson-Bahr (ed.). Baltimore: W. Wood and Co. (American edn. of the English edn. of 1935). ——. 1982. 18th edn. London: Baillière Tindall. ——. 1987. 19th edn. London: Baillière Tindall ——. 1996. 20th edn. G.C. Cook (ed.). London: WB Saunders Company Ltd. Marshall J.D., J.R., Joy R.J.T., Ai N.V. et al. 1967. “Plague in Vietnam 1965–6.” American Journal of Epidemiology. 86: 603–16. Marthinsen L. “Maksimum og minimum. Norsk busetnadshistorie etter DNØ.” In Innsikt og Utsyn. Festskrift til Jørn Sandnes 1996: 144–82.

708

bibliography

Marthinsen L. 1997. “Halvard Bjørkvik: Folketap og sammenbrudd 1350–520.” Heimen. 34: 193–202. Martin J. 1859. Essai sur la topographie physique et médicale de la ville de Narbonne. Montpellier. Mate M. 1984. “Agrarian Economy after the Black Death: The Manors of Canterbury Cathedral Priory, 1348–91.” The Economic History Review. 37: 341–54. Mead R. 1720. A Short Discourse concerning Pestilential Contagion, and the Methods to be Used to Prevent It. London: S. Buckley [etc.]. Menneske og maktene – når gamle sanningar ikkje gjeld lenger. 2004. Seminarrapport Utstein Kloster. Haugaland Akademi. Meyer K.F. 1946–7. “The Prevention of Plague in the Light of Newer Knowledge.” Annals of The New York Academy of Sciences. 48: 429–65. ——. 1950. “Immunity in Plague: A Critical Consideration of some Recent Studies.” Journal of Immunology. 64: 139–63. ——. 1957. “The Natural History of Plague and Psittacosis.” Public Health Reports. 72: 705–79. Mielke J.H., Jorde L.B., Gene P. et al. 1984. “Historical Epidemiologoy of Smallpox in Åland, Finland: 1751–1890.” Demography. 21: 271–95. Miller E. and Hatcher J. 1978. Medieval England. Rural Society and Economic Change, 1086–348. London and New York: Longman. ——. 1995. Medieval England: Towns, Commerce and Crafts, 1086–348. London: Longman. Mocquette H.C.H. 1925. “Pestepidemieën in Rotterdam.” Rotterdaamsch jaarboekje. 3d Series, 3: 10–52. Mogren M. 2000. Faxeholm i maktens landskap: en historisk arkeologi. Stockholm: Almqvist & Wiksell International. Monath P.T. 1999. “Ecology of Marburg and Ebola Viruses: Speculations and Directions for Future Research.” The Journal of Infections Diseases. 179 (Suppl. 1): S127–S138. Morony M.G. 2007. “ ‘For Whom Does the Writer Write?’: The First Bubonic Plague Pandemic According to Syriac Sources.” In Plague and the End of Antiquity: 59–86. Morris C. 1971. “Review Article: ‘The Plague in Britain,’ ” The Historical Journal. 14: 205–15. Motolinía T. de. 1951. Motolinia’s History of the Indians of New Spain. F. Borgia Steck (ed.) Washington, D.C.: Academy of American Franciscan History. Mullett C.F. 1956. The Bubonic Plague and Engand. An Essay in the History of Preventive Medicine. Lexington: University of Kentucky Press. Myhre B. 2004. “Byllepest, systemkollaps eller samfunnsendring på 500-tallet?.” In Menneske og maktene 2004: 62–73. Narkevich M.I., Onishchenko G.G., Naumov A.V. et al. 1991. “Kharakteristika epidemicheskikh proiavleniy chumy v SSSR za period s 1920 po 1989 g.”. Zhurnal mikrobiologii, epidemiologii i immunobiologii. 12: 31–3. Nash A.E. 1980. “The Mortality Pattern of the Wiltshire Lords of the Manor.” Southern History. 2: 31–43. Naso I. 1982. Medici e strutture sanitarie nella società tardo-medievale. Il Piemonte dei secoli XIV e XV. Milan: Franco Angeli Editore. Naturens liv i ord och bild. 1928. Vol. 2. L.A. Jägerskiöld och T. Pehrson (eds.). Stockholm: Bokförlaget Natur och Kultur. Nohl J. 1961. The Black Death. A Chronicle of the Plague Compiled from Contemporary Sources. London: Unwin Books. Originally published in German 1926. Noordegraaf L. and Valk G. 1996. De Gave Gods. De pest in Holland van af de late middeleeuwen. 2nd ed. Amsterdam: Uitgeverij Bert Bakker. Nordisk Kultur. 1934. Vol. 16B. Oslo: Aschehoug & Co. Norske Regnskaber og Jordebøger fra det 16de Aarhundrede. 1887–983. H.J. HuitfeldtKaas (ed.). Vols. 1–5. Christiania [= Oslo]: Det Norske historiske Kildeskriftfond.

bibliography

709

Nybelin O. 1928. “Den svarta råttan och den bruna.” In Naturens liv i ord och bild. Vol. 2: 850–7. Oeding P. 1988. “Sykdom og død i de islandske annaler frem til år 1500.” Tidsskrift for den Norske Lægeforening (Journal of the Norwegian Medical Association). 108: 3202–7. Ohlin G. 1966. “No Safety in Numbers: Some Pitfalls of Historical Statistics.” In Industrialization in Two Systems: 68–90. Reprinted in Essays in Quantitative Economic History, 1974. Orrman E. 2003. “Church and Society.” In The Cambridge History of Scandinavia. Vol. 1: 421–62. Oswald N.C. 1977. “Epidemics in Devon, 1538–837.” The Devonshire Association for the Advancement of Science, Literature and Art. Reports and Transactions. 109: 73–116. Owens C. 1990. “Plague in New Mexico.” Journal of Community Health Nursing. 7: 153–8. Oxford Advanced Learner’s Dictionary of Current English. 1989. Fourth ed. Oxford: Oxford University Press. Paleomicrobiology. Past Human Infections. 2008. Raoult and M. Drancourt (eds.). Berlin and Heidelberg: Springer. A Parisian Journal 1405–49. 1968. Transl. From the Anonymous Journal d’un Bourgeois de Paris. Ed. J. Shirley. Oxford: Clarendon Press. The Peasant Land Market in Medieval England. 1984. P.D.A. Harvey (ed.). Oxford: Clarendon Press. Pelc A. Ceny v Krakowie [The Prices in Krakow]. Krakow 1938. Perrenoud A. 1978. “Les mécanismes de récuperation d’une population frappée par la peste. L’épidémie de 1636–40 à Genève.” Revue suisse d’histoire. 28: 265–88. Perroy E. 1949. “A l’origine d’une économie contractée: les crises du XIVe siècle.” Annales. Économies société civilizations = Annales. Histoire, sciences sociales = Annales (Paris). 4: 167–82. Perry D.P. and Fetherston J. 1997. “Yersinia pestis—Etiologic Agent of Plague.” Clinical Microbiological Reviews. 10, No. 1: 35–66. Persson B.E.B. 1994. “Att studera historiska farsoter.” Sydsvenska medicinhistoriska sällskapets årsskrift. 31: 91–117. ——. 2001. Pestens gåta. Farsoter i det tidiga 1700-talets Skåne. Lund: Historiska institutionen. Petrie G.F., Todd R.E., Skander R. et al. 1924–5. “A Report on Plague Investigations in Egypt.” The Journal of Hygiene. 23: 117–50. Philip W.M. and Hirst L.F. 1917. “A Report on the Outbreak of the Plague in Colombo, 1914–16.” The Journal of Hygiene. 15: 527–64. Pickard R. 1947. The Population and Epidemics of Exeter in Pre-Census Times. Exeter: The Author. Plague and the End of Antiquity. The Pandemic of 541–750. 2007. L.K. Little (ed.) Cambridge: Cambridge University Press. Plague Manual: Epidemiology, Distribtution, Surveillance and Control. 1999. Geneva: WHO. The Plague Reconsidered. A New Look at its Origins and Effects in 16th and 17th Century England. 1977. Matlock: Published by “Local Population Studies”. Pollitzer R. 1936. “Pathology.” In Wu, Chun, Pollitzer et al. Plague. A Manual for Medical and Public Health Workers: 139–66. ——. 1954. Plague. Geneva: WHO. ——. 1960. “A Review of Recent Literature on Plague.” Bulletin of the WHO. 23: 313–400. Pollitzer R. and Li C.C. 1943. “Some Observations on the Decline of Pneumonic Plague Epidemics.” Chinese Medical Journal. 61: 212–6.

710

bibliography

——. 1943. Journal of Infectious Diseases. 72: 160–2. Pollitzer R. and Meyer K.F. 1961. “The Ecology of Plague.” In Studies in Disease Ecology. 433–590. Poos L.R. and Smith R.M. 1984. “ ‘Legal Windows Onto Historical Populations?’ Recent Research on Demography and the Manor Court in Medieval England.” Law and History Review. 2: 128–52. (Cf. Razi 1985, 1987.) ——. 1985. “ ‘Shades Still on the Window’: A Reply to Zvi Razi.” Law and History Review. 3: 409–29. (Cf. Razi 1985, 1987.) The Population Dynamics of Infectious Diseases. Theory and Applications. 1982. R.M Anderson (ed.). London and New York: Chapman and Hall. Postan M.M. 1950. “Some Economic Evidence of Declining Population in the Later Middle Ages.” The Economic History Review. 2nd Series. 2: 328–44. ——. 1966. “Medieval Agrarian History in its Prime: England.” In Cambridge Economic History of Europe. Vol. 1. 549–632. Pounds N.J.G. 1974. An Economic History of Medieval Europe. London: Longman Group LTD. Prat G. 1952. “Albi et la Peste Noire.” Annales du Midi. 64: 15–25. Prentice M.B., Gilbert T.P., and Cooper A. 2004. “Was the Black Death Caused by Yersinia pestis?” Lancet Infectious Diseases. 4: 72. Principles and Practice of Pediatric Infectious Diseases. 2003. S.S. Long, L.K. Pickering, C.G. Prober (eds.). New York: Churchill Livingstore/Imprint of Elsevier Science. Pusch C.M., Rahalison L., Blin N. et al. 2004. “Yersinial F1 Antigen and the Cause of Black Death.” The Lancet Infectious Diseases. 4: 484–5. Rackham J. 1979. “Rattus rattus: the Introduction of the Black Rat into Britain.” Antiquity. 53: 112–20. Raoult D., Aboudharam G., Crubézy E., Larrouy G., Ludes B., Drancourt M. 2000. “Molecular Identification by ‘Suicide PCR’ of Yersinia pestis as the Agent of Medieval Black Death.” Proceedings of the National Academy of Sciences of the United States of America (online) 97: 12800–3. Raoult D. and Drancourt M. “Cause of Black Death.” 2002. The Lancet Infectious Diseases. 2: 459. Ravensdale J. 1984. “Population Changes and the Transfer of Customary Land on a Cambridgeshire Manor in the Fourteenth Century.” In Land, Kinship and Life-Cycle: 197–225. Razi Z. 1980. Life, Marriage and Death in a Medieval Parish. Economy, Society and Demography in Halesowen 1270–1400. Cambridge: Cambridge University Press. ——. 1985. “The Use of Manorial Court Rolls in Demographic Analysis. A Reconsideration.” Law and History Review: 191–200. (Cf. Poos and Smith.) ——. 1987. “The Demographic Transparency of Manorial Court Rolls.” Law and History Review. 5: 523–35. (Cf. Poos and Smith.) Readings in Population. 1972. W. Petersen (ed.). New York: Macmillan. Reed W.P., Palmer D.L., Williams R.C. et al. 1970. “Bubonic Plague in the Southwestern United States.” Medicine. 49: 465–86. Rees W. 1923. “The Black Death in England and Wales, as Exhibited in Manorial Documents.” Proceedings of the Royal Society of Medicine (Section of the History of Medicine), 16: 27–45. Reichstein H. 1974. “Bemerkungen zur Verbreitungsgeschichte der Hausratte (Rattus rattus Linné, 1758) an Hand jüngeren Knochenfunde aus Haithabu.” Die Heimat. 81: 113–4. ——. 1987. “Archözoologie und die prähistorische Verbreitung von Kleinsäugern.” Sitzungsberichte der Gesellschaft Naturforschender Freunde zu Berlin. 27: 9–21. Renardy C. 1974. “Un témoin de la grande peste: maître Simon de Couvin, Chanoine de Saint-Jean l’Évangeliste à Liège († 1367).” Revue Belge de Philologie et d’Histoire. 52: 273–92.

bibliography

711

Roberts L.R. and Janovy J. Jr. 2000. Gerald D. Schmidt & Larry S. Roberts’ Foundations of Parasitology. 6th ed. Boston: McGraw-Hill Higher Education. Roccatagliata A. 1976. “Varazioni climatiche, pestilenze e vita sociale nel territorio alessandrino nei secc. XIII–XVII.” Rivista di storia arte e archeologia per le province di Alessandria e Asti. 85: 185–216. Rothschild 1906, see Indian Plague Research Commission. Russell J.C. 1948. British Medieval Population. Albuquerque: The University of New Mexico Press. ——. 1958. Late Ancient and Medieval Population. (Transactions of the American Philosophical Society, New Series, Vol. 48, Part 3, 1958). Philadelphia: The American Philosophical Society. ——. 1968. “That Earlier Plague.” Demography. 5: 174–84. Russell P. 1791. A Treatise of the Plague: Containing and Historical Journal, and Medical Account, of the Plague, at Aleppo, in the years 1760, 1761, and 1762. Also, remarks on Quarantines, Lazarettos, and the Administration of Police in Times of Pestilence. To which is added, an Appendix, containing Cases of the Plague; and an Account of the Weather, during the Pestilential Season. London: G.G.J. and J. Robinson. Russell W.M.S. and Russell C. 1983. “Evolutionary and Social Aspects of Disease.” Ecology of Disease. 2: 95–106. Sagnir. Tímarit um söguleg efni. 1997. 18: 73–113. Les saison d’une peste (avril–septembre 1590): Le cimetière des Fédons à Lambesc. 2005. B. Bizot (ed.). Rouen: CNRS Editions. Sallares R. 2007. “Ecology, Evolution, and Epidemiology of Plague.” In Plague and the End of Antiquity: 231–89. Sandnes J. 1968. “Garder, bruk og folketall i Norge i høgmiddelalderen.” Historisk tidsskrift [Norway]. 47: 261–92. Sarris P. 2002. “The Justinian Plague: Origin and Effects.” Continuity and Change. 17, 169–82. Savage W.G. and Fitzgerald D.A. 1900. “A Case of Plague from a Clinical and Pathological Point of View.” The British Medical Journal. Oct. 27: 1232–6. Savio P. 1972. “Ricerche sulla peste di Roma degli anni 1656–7.” Archivio della Deputazione Romana de Storia Patria. 95: 113–42. Sawyer P. 2003. “The Viking Expansion.” In The Cambridge History of Scandinavia, Vol. 1: 105–20. Schofield R. 1977. “An Anatomy of an Epidemic: Colyton, November 1645 to November 1646.” In The Plague Reconsidered: 95–132. Scott S., Duncan C.J. and Duncan S.R. 1996. “The Plague in Penrith, Cumbria, 1597/8: Its Causes, Biology and Consequences.” Annals of Human Biology. 23: 1–21. Scott S. and Duncan C.J. 2001. Biology of Plagues: Evidence from Historical Populations. Cambridge: University Press. ——. 2004. Return of the Black Death. The World’s Greatest Serial Killer. Chichester, UK: Wiley. Seal S.C. 1969. “Epidemiological Studies of Plague in India.” Bulletin of the World Health Organization. 23. 283–92. Seebohm F. 1865. “The Black Death and its Place in History.” Fortnightly Review. 2: 149–60, 268–79. Sellers M. 1913/1974. “Social and Economic History.” In W. Page (ed.). The Victoria History of the County of York. Vol. 3: 435–85. Shrewsbury J.F.D. 1971. A History of Bubonic Plague in the British Isles. Cambridge: The University Press. Shirk M.V. 1981. “The Black Death in Aragon, 1348–51.” Journal of Medieval History. 7: 357–68. Signoli M., Séguy I., Biraben J.-N. et al. 2002a. “Paléodemographie et démographie historique en contexte épidémique: la peste en Provence au XVIIIe siècle.” Population. 57: 821–47.

712

bibliography

——. 2002b. “Paleodemography and Historical Demograpy in the Context of an Epidemic: Plague in Provence in the Eighteenth Century.” Population (English ed.). 57: 829–54. Simond P.L. 1898. “La propagation de la peste.” Annales de l’Institut Pasteur. 12: 625–87. Simpson W.J. 1905. A Treatise on Plague Dealing with the Historical, Epidemiological, Clinical, Therapeutic and Preventive Aspects of the Disease. Cambridge: At the University Press. Slack P. 1977. “The Local Incidence of Epidemic Disease. The Case of Bristol 1540– 1650.” In The Plague Reconsidered: 49–62. ——. 1979. “Mortality Crises and Epidemic Disease in England 1485–610.” In Health, Medicine and Mortality in the Sixteenth Century: 9–59. ——. 1981. “The Disappearance of Plague: An Alternative View.” The Economic History Review. 2nd Series. 34: 469–76. ——. 1985. The Impact of Plague in Tudor and Stuart England. Routledge & Kegan Paul: London. Smith M.D. and Than N.D. 1996. “Plague.” Manson’s Tropical Diseases. 20th ed. G.C. Cook (ed.). London: WB Saunders Company Ltd. Smith R.S. 1988. “Human Resources.” In The Countryside of Medieval England: 189–212. Snorre Sturlason. 1899, repr. 2003. Kongesagaer. Kristiania [= Oslo]: J.M. Stenersens & Co’s Forlag. Snyder J.C. 1965. “Typhus Fever Rickettsiae.” In Viral and Rickettsial Infections of Man: 1094–5 Stampfli H.R. 1965–6. “Die Tierreste aus der römischen Villa ‘Ersigen–Murain’ in Gegenüberstellung zu anderen Zeitgleichen Funden aus der Schweiz und dem Ausland.” Jahrbuch des Bernischen Historischen Museums in Bern. 45–6: 449–69. Steen S. 1934. “Veiene og leden I Norge”, in Nordisk Kultur. Vol. 16B: 217–28. ——. 1942. Ferd og Fest. Reiseliv i norsk sagatid og middelalder. 2nd edn. Oslo: Aschehoug & Co. Steffensen J. 1974. “Plague in Iceland.” Nordisk medicinhistorisk Årsbok. 40–55. Sternbach G. 2003. “The History of Anthrax.” Journal of Emergency Medicine. 24: 463–7. Sticker G. 1908, 1910. Abhandlungen aus der Seuchengeschichte und Seuchenlenhre. Vol. 1, Part 1 and Part 2. Die Pest. Giessen: Alfred Tölpermann. Storia d’Italia. 1973. Vol. 5. Turin: Einaudi. Stories of Boccaccio (The Decameron). N. d. (c. 1350). John Payne (transl.). London. Studi in onore di Armando Sapori. 1957. Milano: Istituto Editoriale Cisalpino. Studies in Disease Ecology. 1961. J.M. May (ed.). New York: Hafner Publishing Co. Studies in English Trade in the Fifteenth Century. 1966. 2nd repr. London: Routledge & Kegan Paul Ltd. Taylor J. 1625, repr. 1636. The Fearefull Summer or Londons Calamitie, The Countries Discourtesie, And both their Miserie. Printed by Authorities in Oxford, in the last great Infection of the Plague, 1625. Oxford: Authorities in Oxford. Teichert M. 1985. “Beitrag zur Faunengeschichte der Hausratte. Rattus rattus L.” Zeitschrift für Archäologie. 19: 263–9. Thomas R.E., Karstens R.H., and Schwann T.G. 1993. “Effect of Yersinia pestis Infection on Temperature Preference and Movement of the Oriental Rat Flea (Xenopsylla cheopis) (Siphonaptera: Pulicidae).” Journal of Entomology. 30: 209–13. Thompson A.H. 1911. “Registers of John Gynewell, Bishop of Lincoln, for the Years 1347–50.” The Archaeological Journal. 68: 301–60. ——. 1914. “The Pestilences of the Fourteenth Century in the Diocese of York.” The Archaeological Journal. 71: 97–154.

bibliography

713

Thompson J.A. 1906. “On the Epidemiology of Plague.” The Journal of Hygiene. 6: 537–69. Tieh T.H., Landauer E., Miyagawa F. et al. 1948. “Primary Pneumonic Plague in Mukden, 1946, and Report of 39 Cases with 3 Recoveries.” Journal of Infectious Diseases. 82: 52–8. Tiflov V.E. 1964. “Sud’ba bakterial’nykh kul’tur v organizme blokhi” [= The Fate of Bacterial Cultures in the Flea’s Organism]. Ektoparazity. Fauna, biologiya i prakticheskoye znachenie. 4: 181–98. Tikhomirov E. 1999. “Epidemiology and Distribution of Plague.” In Plague Manual: 11–41. Titow J.Z. 1969. English Rural Society, 1200–350. London: George Allen & Unwin. ——. 1978. [Review of J. Hatcher, Plague, Population and the English Economy]. The Economic History Review. 31: 466–7. Tollefsen S. “Overdriver rotteproblem.” Vestkanten. 8 December 2005: 7. Tropical and Geographical Medicine. 1993. K.S. Warren and A.A.F. Mahmoud (eds.) 2nd ed. New York, etc.: McGraw-Hill Information Services Company. Trow-Smith R. 1957. A History of British Livestock Husbandry to 1700. London: Routledge and Kegan Paul. Twigg G. 1984. The Black Death: A Biological Reappraisal. London: Batsford Academic and Educational. Tzortzis S. and Signoli M. 2009. “Les tranchées des Capucins de Ferriéres (Martigues, Bouches-du-Rhône, France). Un charnier de l’épidémie de peste de 1720 à 1722 en Provence.” Comptes Rendus Palevol. 8: 749–60. Ulsig E. 1991. “Pest og befolkningsnedgang i Danmark i det 14. århundrede.” Historisk tidsskrift (Denmark). 91: 21–43. ——. 1994. [Review of O.J. Benedictow, Plague in the Late Medieval Nordic Countries]. Historisk tidsskrift (Norway). 73: 94–104. Vahtola J. 2003. “Population and Settlement.” In The Cambridge History of Scandinavia. 559–80. Vaquer Bennassar O. 1987. “La peste de 1652 en Mallorca.” In I Congrés Hispano Luso Italià de Demografia Històrica: 128–36. Veale E.M. 1966. The English Fur Trade in the Later Middle Ages. Oxford: Clarendon Press. Venezia e la peste 1348–1797. 1979. Venice: Comune di Venezia, Marsilio Editori. The Victoria History of the County of Berkshire. 1907. Vol. 2. P.H. Ditchfield and W. Page (eds.). London: Archibald Constable and Company Ltd. The Victoria History of the County of Somerset. 1911. Vol. 2. W. Page (ed.). London: The University of London Institute of Historical Research. The Victoria History of the County of York. 1913, 1974. Vol. 3. W. Page (ed.). London: The University of London Institute of Historical Research. Reprint 1974. Vilar P. 1962. La Catalogne dans l’Espagne moderne. Vol. 1. Paris: S.E.V.P.E.N. Vilkuna K. 1969. “Råttor och möss. Finland.” Kulturhistorisk leksikon for nordisk middelalder. Vol. 14: 583–4. Villani M. 1995. Cronica con la continuazione di Filippo Villani. G. Porta (ed.). Vol. 2. Parma: Fondazione P. Bembo/U. Guanda. Viral and Rickettsial Infections of Man. 1965. F.L. Horsfall, Jr. and I. Tamm (eds.). London and Philadelphia: Pitman Medical Publishing Co., LTD, and J.B. Lippincott Company. Vretemark M. 1983. “Svartråttan—snyltgäst och pestspridare.” In Helgeandsholmen. 1000 år i Stockholms ström: 294, 467. Walford E. 1900. “Notes on the Introduction of a Case of Plague into the Neighbourhood of Cardiff.” The Biritish Medical Journal. Oct. 27: 1232. Walløe, L. 1982. “Pest og folketall 1350–750.” [Plague and Population Size 1350–750] Historisk tidsskrift/Journal of the Norwegian Historical Association: 1–45. English

714

bibliography

translation 1995. “Plague and Population: Norway 1350–750.” Avhandlinger (Norske videnskaps-akademi), New Series 17: 1–48. ——. 2007. “Var Yersinia pestis årsak til svartedauden?” [Was Yersinia pestis the Cause of the Black Death?] Tidsskrift for Den norske legeforening/ Journal of the Norwegian Medical Association. 127: 3193. ——. 2008. “Medieval and Modern Bubonic Plague: Some Clinical Continuities.” Medical History. Suppl. 27: 59–73. Watts D.G. 1998. “The Black Death in Dorset and Hampshire.” The Hatcher Review. 5: 21–31. Wayne K.R., Leonard J.A., Cooper A. 1999. “Full of Sound and Fury: The Recent History of Ancient DNA.” Annual Review of Ecology and Systematics. 30: 457–77. Weber M. 1966. The City. New York: Free Press. Welty T.K., Grabman J., Kompare E. et al. 1985. “Nineteen Cases of Plague in Arizona.” Clinical Medicine. 142: 641–6. Weiner G.M. 1970. “The Demographic Effects of the Venetian Plagues of 1575–77 and 1630–31.” Genus. 26: 41–55. Wiechman I. and Grupe G. 2005. “Detection of Yersinia pestis DNA in Two Early Medieval Skeletal Finds from Aschheim (Upper Bavaria, 6th Century a.d.).” American Journal of Physical Anthropology. 126: 48–55. Wigh B. 2001. Animal Husbandry in the Viking Age Town of Birka and Its Hinterland. Excavations in the Black Earth, 1990–5. Stockholm: Birka Studies. Williams N.J. 1988. The Maritime Trade of the East Anglian Ports, 1550–1590. Oxford: Clarendon Press. Woehlkens E. 1954. Pest und Ruhr im 16. und 17. Jahrhundert. Uelzen: Becker Verlag Uelzen. WHO Information: 2003. “Ebola Haemorrhagic Fever.” Fact Sheet No. 103. www.who .int/inf-fs/en,fact. WHO, Media centre. October 2001. “Anthrax Overview,” Fact sheet no. 264, 1–2. www .who.int/inf-fs/en Wood W. 1842. The History and Antiquities of Eyam, with a Minute Account of the Great Plague which Desolated that Village, AD 1666. London: Tiller. Wood J. and DeWitte-Aviña S. 2003. “Was the Black Death Yersinial Plague?” The Lancet Infectious Diseases. 3: 327–8. ——. 2004. “Was the Black Death Yersinial Plague?” The Lancet Infectious Diseases. 4: 485. Wood J.W., Ferrel R.J., and DeWitte-Aviña S.N. 2003. “The Temporal Dynamics of the Fourteenth-Century Black Death: New Evidence from English Ecclesiastical Records.” Human Biology. 75: 427–48. Wright J., Jr. 1641. Londons Lamentation. Or a fit admonishment for City and Countrey, wherein is described certaine causes of this affliction and visitation of the Plague, yeare 1641, which the Lord hath been pleased to inflict upon us, and withal what meanes must be used to the Lord, to gaine his mercy and favor, with an excellent sprirituall medicine to be used for the preservative both of Body and Soule. London: Printed by E.P. Wrigley E.A. and Schofield R. 1981, 1989. The Population History of England, 1541– 1871: A Reconstruction. London: Edward Arnold. 2nd ed. 1989. Wu C.Y. 1936a. “Insect Vectors.” In: Wu, Chun, Pollitzer et al. Plague. A Manual for Medical and Public Health Workers. 248–308. ——. 1936b. “The Problem of Ship-borne Plague.” In: Wu, Chun, Pollitzer et al. Plague. A Manual for Medical and Public Health Workers: 485–511. Wu Lien-Teh. 1913–4. “First Report of the North Manchurian Plague Prevention Service.” The Journal of Hygiene. 13: 237–99 and 15 photographic plates. ——. 1922–3. “The Second Pneumonic Plague Epidemic in Manchuria.” The Journal of Hygiene. 21: 262–88.

bibliography

715

——. 1926. A Treatise on Pneumonic Plague. Geneva: League of Nations, Health Organisation. ——. 1927–8. “Recent Knowledge on Pneumonic Plague.” North Manchurian Plague Prevention Service. Reports. 6: 55–92 ——. 1934a. “A Short History of the Manchurian Plague Prevention Service.” In Manchurian Plague Prevention Service. Memorial Volume: 1–12. ——. 1934b. “Inaugural Address delivered at the International Plague Conference in Mukden, 1911.” In Manchurian Plague Prevention Service. Memorial Volume: 13–9. ——. 1936a. “Historical Aspects.” In Wu, Chun, Pollitzer et al. Plague. A Manual for Medical and Public Health Workers: 1–55. ——. 1936b. “Hosts and Carriers.” In Wu, Chun, Pollitzer et al. Plague. A Manual for Medical and Public Health Workers: 195–248. ——. 1936c. “Epidemiological Factors.” In Wu, Chun, Pollitzer et al. Plague. A Manual for Medical and Publich Health Workers: 383–423. Wu Lien-Teh, Chun J.W.H., Pollitzer R. 1934. “Clinical Observations upon the Second Manchurian Plague Epidemic, 1920–1.” In Manchurian Plague Prevention Service. Memorial Volume: 79–99. Wu Lien-Teh, Chun J.W.H., Pollitzer R., Wu C.Y. 1936. Plague. A Manual for Medical and Public Health Workers. Shanghai: National Quarantine Service. www.skansen-akvariet.se/vara_djur/html/svartratta.html www.cdc.gov www.cdc.gov./ncidod, Centers of Disease Control, FAQ’s – Medical Facts About Anthrax 1–2. www.who.int/inf, WHO. www.who.int/inf-fs/en, WHO, Media centre, Fact Sheet no. 264, October 2001: 1–2. Yersin A. 1894. “La peste bubonique à Hong-Kong.” Annales de l’Institut de Pasteur, Paris. 8: 662–7. Ziegler P. 1969. The Black Death. London: Collins. I have used the identical text in my personal copy of the paperback edition published in 1970. Harmondsworth, Middlesex: Pelican Books. Zinsser H. 1934, 1985. Rats, Lice & History. The Biography of a Bacillus. London: Papermac. Zitelli A. and Palmer R.J. 1979. “Le teorie mediche sulla peste e il contesto veneziano.” In Venezia e la peste 1348–1797: 21–8.

INDEX OF SUBJECTS1 Alternative microbiological theories of plague in the past Anthrax, Twigg’s alternative theory 17–9, 82 fn. 33, 284, 327, 331 and fn. 82, 411, 424, 464, 470, 487–8, 495, 553–609 and fn. 230, 611, 639 Airborne anthrax, see miasmatictelluric theory Cutaneous anthrax 556–9, 563, 571–3, 578, 590 fn. 145 Epizootics among domestic animals in the past 566, 574–81, 608 Gastro-intestinal anthrax 318, 556–9, 572 Interhuman transmission, never observed 558, 563 Miasmatic-telluric theory, see also Epidemiological theories 562–6 Mortality rate of gastro-intestinal anthrax 557 Murrain, see Epizootics Pulmonary or inhalational anthrax (occasional incidence) 556–7, 563, 572, 578, 591 fn. 144 Visceral anthrax, see gastrointestinal anthrax Woolsorters disease, see Cutaneous anthrax Zoonoses of domestic animals, see Murrain

Cohn’s disease, (see fn. 1, point 5) 16–7, 205–73, 289–90, 340–1, 411, 415, 664–72 Viral disease spread by droplets 1, 6–7, 28, 43, 66, 200, 205–73, 340, 379–80, 411, 415, 664–70 Immunity, see also Viral disease 205–273 Child disease, see also Viral disease, Black Death, Child diseases below 218– 273 Buboes 340–80 Ebola and Marburg haemorrhagic diseases 18, 207, 284–90, 334–40, 464, 487, 610–663 Afrian Confinement 581, 586, 636, 650, 661–2 Bubo? 334–40, 638 Carrier state? 288, 649–50 Clinical and epidemiological features: fiction and facts 284–90, 305–8, 632, 636–661 Density dependence, see also the Inverse correlation 290, 305–8, 632 Incubation period 285, 288, 648–9 Latency period 284–8, 639–41 Reed-Frost theory and model, see also Epidemiological theories 633–6, 640, 648

1 (1) The Index consists of an Index of Subjects, Index of Geographical Names and People and Index of Names. (2) For medical and epidemiological terms see also the Glossary, pp. 688–692. (3) German and Nordic personal names and geographical names may include letters not used in English that are entered alphabetically in the Index according to the following phonetic rules: Å, å = AA, aa; Ä, ä, Æ, æ = AE, ae; ü = y; Ø, ø, Ö, ö = OE, oe; ǫ = oe; ð = D, d; Þ, Þ = Th, th. (4) In order to make titles of annals and chronicles and similar types of sources more immediately and generally comprehensible, many of them have been translated into English in the text and are entered according to the English translation in the Index. (5) S.K. Cohn, Jr. claims to have identified historical plague as an unknown disease which he does not name, it is therefore entered in the Index of Subjects under Cohn’s disease.

718

index of subjects

Symptomless (travelling) infectives?, construed, see also Carrier state? 648–50 Transmission 649–50 Unknown mutated variant, see also Evolutionary theory 17–18, 487, 636, 662 Alternative epidemiological theories of the Black Death and plague in the past2 Human-flea theory (Blanc, Baltazard, Walløe) 5, 9–16 and fns. 28 and 35, 28–9, 67, 110–2, 395 fn. 42 Low-intensity theory of bubonic plague (Shrewsbury) 16–7, 489–91 Primary pneumonic plague in Iceland (Steffensen) 16, 493, 500–22, 526–32, 535–8, 540–2, 550–552 Pure primary pneumonic plague (Morris and Karlsson) 320–1, 332, 410, 487–8, 490–1, 493–552 American physicians (Vietnam War), see also Butler 44–6 Anglo-Saxon England 127–8, 130, 134 Annals, see Chronicles under Sources Anthrax, see Alternative microbiological theories Astrological-miasmatic theory, see Epidemiological theories Autopsies, see Plague, autopsies Barber surgeons 334, 638 Bastard feudalism 255, 349 Bastard statistics, see also Quasistatistics (Cohn) 255–7, 346–9, 354–6, 359 Black Death (1346–1353) Map of spread, p. 2, 14–8, 20, 27–32, 34–7, 39–43, 56–7, 59–62, 74, 76, 79–80, 82, 84, 86, 91, 98–9, 106–10, 113–6, 122, 126, 135, 137, 139, 147–8, 151–2, 169–70, 173, 177, 180, 185, 187–8, 191–2, 194, 201, 207, 218–23, 226, 231–3, 235–73, 289–90, 292, 294, 269–9, 314–6, 308, 311–2, 321, 323–7, 329–32, 340–80, 382–4, 386 fn. 20, 390–4 fn. 39, 398, 400–1, 403–6, 407, 410–1, 413, 415–6, 418 and fn. 61, 420–5, 432, 436–84, 489–91, 493, 496, 498, 500 fn. 17, 519, 521–2, 527, 530–1 and fn. 108, 534 fn.

2

115, 536–52, 553–5, 558–65, 567–74, 576–608, 611–2, 618, 629–31, 640, 642, 648, 661–2, 664, 673, 675–9, 690 Mortality rates, inegalitarian according to social class, age and gender 218–73, 299 Children 42–3, 218–35, 240–1, 254–73, 598 Youth 222–4, 236–7 Women/females 257–8, 262–3, 348, 602 Mortality according to social class Customary tenantry 241, 299, 466, 480–2, 602, 632 Poor and destitute 224, 229, 239, 241–3 Rural proletarians: cottagers, sub-tenants, garciones 241–3 and fn. 136, 299, 602 Tenants-in-chief 421–5, 596–7, 600, 604, 607 and fn. 224 Mortality of English parish priests in the Black Death according to first institutions 436, 453–8 and fns. 161, 163, 462–3, 470–1, 475, 479, 603, 631 Origin of name Black Death 571–4 Seasonality of spread of the Black Death, see also Plague seasonality an Winter epidemics 108, 330, 398, 400–7, 413–6, 418, 420–5, 432–9, 445–6, 463–83, 521, 642 According to institutions of parish priests (England) 463–83, 521, 642 Winter epidemics? 108–9, 113, 252, 330, 397–426, 428, 433, 435–7, 460, 463, 471, 474–6, 479, 482–4, 521 Spread rates of the Black Death, see also Plague, Spread rates 27–32, 113–5, 151–2, 172–3, 464–5, 467– 77, 585, 589–93, 595 Territorial origin of the Black Death 499–500 and fn. 17, 571, 580–1, 585–6, 620–1 and fn. 34, 661 Boil, see Plague, Bubo and Glossary 324, 331–2 and fn. 82, 347, 353–4, 356, 358, 363–4, 368–9 and fn. 180, 372–3, 491, 511, 540–1, 548, 612, 688

See also Blanc and Baltazard, Shrewsbury, Morris, Karlsson, Walløe.

index of subjects Organization of anti-plague measures In India 194–205 In Hong Kong 202 Bronze Age 121 Cardinal feature, see Plague, Defining feature Camels and plague 624 Cats 124, 137, 513, 691 Cattle, see also Anthrax 81, 555–7, 566–7, 575–7, 579, 590, 592, 594, 608 CDC, see Centers of Disease Control Censuses, see Demographic sources Centers of Disease Control and Prevention (CDC), see Index of Names Child diseases 207, 212, 248–35, 240, 252, 267–8, 664 Concept of (infectious) child disease 222, 224, 227–8, 231, 233, 235 Fulminant development of plague disease 233, 268 Mortality of parents, effects on mortality of children 233–4, 268, 667 Supermortality of children in bubonic plague 222–3, 233–7, 240, 271, 667 Chinese Imperial Encyclopaedia 620 Chroniclers, see Sources Civilizations (and concept), 47, 49–50 and fn. 61, 254, 568–9 Cohn’s disease, see fn. 1, point 5 and Alternative microbiological theories Commensal rats, see Plague, black rats Corrody/corrodians 427 and fn. 84 Defining feature, see Plague Distinguishing feature, see Plague, Defining feature Demography, see also Population Demographic sources, see also Black Death and Sources of religious institutions Bills of mortality 304, 434 Censuses, Icelandic of 1703, Indian of 1911, Chinese of 1912 52, 221, 238, 515, 532 Parish registers, see Sources relating to religious institutions Poll Tax 1377–1378 600 Cemetery populations 232, 254, 261–3

719

Demographic techniques and structures Family reconstitution 62, 66, 68, 202, 234, 647 Household size 65, 67, 202, 517 fn. 68, 601 Life expectancy 52, 148, 229 and fn. 92, 230–1, 424, 428, 595, 600 Life tables 229–32, 424, 597–8, 689 Mortality according to size of family 62, 65, 68, 146, 202–4, 268 Mortality rates (pre-plague), see also Plague, mortality Density dependence, see Plague, Inverse correlation Diseases, see specific entries on Anthrax, Cohn’s disease, Ebola disease, and Plague Dysentery 65, 327, 489, 509, 618 Exanthematic typhus 64–5, 67, 145, 311, 322, 339, 489–91, 498, 509–10, 618, 634 Foot-and-mouth disease, see also Alternative theories, Anthrax 562–3, 575, 580 German measles/Rubella 634, 636 Influenza 17, 19, 64, 67, 145–6, 489, 590, 664fn. 3, 668 Leprosy 322 and fn. 30 Measles 205, 308, 489, 619, 633–5, 660, 698 Poliomyelitis 669 Small pox 205, 214, 317–8, 322, 327, 373–4, 376 Sweating sickness 311, 670–1 and fn. 7 Syphilis 322 Tuberculosis 322, 540 Tularaemia, see also Diseases 319–20, 361, 379, 622 fn. 37, 666 Disparaging views of historians and physicians Cohn 21–2, 25–69, 136, 172, 179–80, 211, 353, 359 Cohn, disparaging views of Benedictow’s work 29–30, 56–60, 62–3, 67–8, 74–5, 148–50, 169–80, 290–301 Scott&Duncan 83, 87–8, 287, 611–5 DNA, see Genetic aspects, Plague pathogen, Paleomicrobiology Early Modern Europe 3, 26–7, 35, 56, 66, 74–5, 80–1, 84, 86, 100, 103, 109, 122, 124, 130, 194, 199–201, 203–4 and fn. 35, 220, 226, 228, 277, 281,

720

index of subjects

301, 323, 350, 369, 416, 421, 502 fn. 23, 521, 569, 592, 607 fn. 24, 612, 615, 621 fn. 34, 629, 631, 645, 650, 658, 673, 680 Ebola and Marburg haemorrhagic diseases, see Alternative microbiological theories of historical plague Ectoparasites (bloodsucking insects), see Fleas, lice, ticks 5, 11–5 and fn. 28, 112, 320, 379, 666–7 Emunctoria, see also Galenic universalism 356, 359, 366 Enzootic, episodic spread among animals, see also Epizootic 4, 191, 203, 399, 622, 688 Epidemiological theories of contagion and dissemination Astrological theory see Miasmatictelluric theory Evil eye, infection by (evil) look 84, 362 Fomites, infection by contaminated objects 54–5, 81, 358–9, 615 Hippocratic-Galenic epidemiology, see Miasmatic theory Miasmatic-telluric theory/miasmaticastrological theory 39, 79, 560, 562, 564–6 Miasmatic and miasmaticcontagionistic theories, airborne and contagious miasma 54–5, 64, 81–4, 91, 111–2, 220, 326, 337, 350, 352–3, 355, 358, 361–2, 509, 547, 560–5 and fn. 32, 589–90, 614–9, 645, 681 Microbiological epidemiological theory 4, 7–8, 18, 21, 80, 318, 380, 395, 553, 642 Reed-Frost theory and model 63–6 Religious theory of epidemic disease 79, 81, 356, 615 Epizootic, see Glossary, also under Rats and Alternative microbiological theories Epizootics among domestic animals in England, see Murrain Epizootics among domestic animals in medieval Iceland 608 Murrain (including zoonoses in sheep) 83, 555, 562, 573, 576–7, 579–80 Evil eye, see Epidemiological theories 119–20, 140, 399

Evolutionary theory, evolution of species by selection of properties 18, 116–122 Adaptation and change of fleas 119–20, 141, 399 Adaptation of horses by change of size and rougher coat 118–19 Adaptation of rats by change of size and rougher coat 117–22, 131, 135, 137–41, 399, 440–1 Selection of plague strains by blockage in fleas 210–1 Fallacious mutational theories (not based on evolution by selection), see Methodology Theory of Karlsson 16, 18, 77, 487, 494–6, 535 Theory of Scott and Duncan 17–8, 636, 662 Filoviridae, see Ebola and Marburg Fleas, development from egg to imago 112, 396–7, 642–3 Natural mortality rate 396 Fleas, Evolutionary adaptation, see Evolutionary theory Fur fleas and nest fleas 108, 397, 406, 682, 684 Species in the text. See also Plague, Flea vector, Types of spread Nosopsyllus fasciatus (flea of the brown rat) 12, 683–5 Pulex cheopis, see Xenopsylla cheopis Pulex irritans (human flea) 10–1, 13 and fn. 35, 28–9, 683 Xenopsylla cheopis (flea of the black rat), see also Plague, Flea vector 5–6, 10, 12–3, 28–9, 89, 103, 119, 141, 156, 166–7, 180, 279, 398, 582, 627–8, 634, 682–7 Vector capacity/efficiency 5, 9–14, 28–9, 46, 66–7, 180, 203, 375, 393, 395, 407, 555, 582, 634, 682–7, 692 Fomites, see Epidemiological theories Galenic universalism 54, 359 Genetic aspects, see Evolutionary theory, Mutation and Paleomicrobiology God’s token, see also Petechiae 286, 369 and fn. 180, 374, 638, 659, 690 Great Plague (in London), 1664–66, 83, 210, 286, 304, 373–4, 413, 549, 554, 567–8

index of subjects Haemorrhagic disease/plague, see Alternative microbiological theories, Ebola and Marburg Hanseatic cities/league 332, 403, 405, 418, 506–7, 569 Hanseatic congregations in Bergen 332 House rats, see Rats, Black rats Heriots 241, 466, 481–2 Hippocratic-Galenic medicine, see Epidemiological theories and Miasma Hospitals 48, 147–8, 162, 168, 198, 216, 279–80 fn. 3, 312, 316, 322, 364, 370, 372, 414, 515, 518, 545, 651 Humanists 322, 343–4, 350, 361, 401 Hunters 319, 513, 626, 666 Ice Age, see also Little Ice Age 120 Icelandic epidemics of 1402–04 and 1494–95, see Chapter 13: 493–552, Alternative epidemiological theories under Gunnar Karlsson, and Appendix 2 Climatic specificity 528–30, 536 Clinical descriptions 536–42 Provenance? 501–7, 511 Mortality rate 530–3 Mutation?, see Evolutionary theory Painfulness of buboes 542–50 Pleuritic pain in cases of primary pneumonic plague? 537–42, 546, 550 Pure primary pneumonic plague in Iceland? 533–5 Immunity, see Plague Immunity, viral diseases 17, 145, 147–8, 205–46, 249–50, 252–3, 264, 267–8, 272–3, 313 fn. 1, 393, 664, 667–8, 673 Incubation, see Plague, clinical features, and Ebola disease Indian Plague Commission 33, 38, 51, 175–6, 203 fn. 35, 213, 703 Indian Plague Research Commission 3, 33–5, 41, 47–50, 53, 56–9, 66, 74–6, 92–4, 102–3, 105, 108, 111, 118, 140, 148–204, 277, 279–80 and fn. 3, 284, 291–3, 296, 301, 373–4, 396, 416, 419, 567, 599, 616, 619, 623–4, 646, 684, 703–5 Inheritance, see also Wills 262 fn. 168, 267, 269–70, 424, 443, 681 Institutions of parish priests, see Black Death, Mortality, Seasonality and Sources of religious institutions

721

IPRC, see Indian Plague Research Commission Justinianic (first) pandemic (541–766 ce) 3, 27, 214, 283, 327–9, 388–91 and fns. 29–31, 574, 621 fn. 34, 666, 669, 673 Latency periods, see Plague, Defining feature, Epidemiology, see Appendix 3 Lethal dose (LD) 73, 689, 692 Lethality, see Demography and Plague Lice (human) 9, 12 and fn. 28, 64, 67, 395 fn. 42, 634 License to marry, see Merchets Little Ice Age 416–7 Lymph nodes and Lymph tracts/vessels, see Plague, buboes Malthusian theory and analysis 269 and fn. 178, 517 Manchurian epidemics of primary pneumonic plague, see Primary pneumonic plague, Wu Lien-Teh and Bibliography 31, 511–27, 534 fn. 115, 535, 539, 626–7 Marburg disease, see Ebola disease Marriage 195 and fn. 5, 268–74 Marriage register, parish (Givry) 270 Merchets (feudal license to marriage) 271 Sterility 269 Marxism, see also Kosminskiy 604–5 Medieval and early modern medicine, see also Source criticism 81–2, 215, 220, 233, 326, 346–59, 361–3, 366–7 Clinical observation and examination of patients, contemporary 346, 348, 351–6, 358, 361–3, 365–7 Medication, examples 353, 358 Medieval mind 78–84, 219–21, 344, 346, 348–51, 353–4, 358–9, 361–7, 589–92 Metastatic spread, see Plague, types of spread Methodology, principles and fallacies Anachronisms 82 and fn. 33, 83, 100–1, 103, 120, 130, 357 Anachronisms and the functions of historical periodization 99–102, 120, 130, 192, 228, 631, 669 Analogies, use, see also Fallacious use 100, 521, 563–4

722

index of subjects

Argumentum or inference ex silentio, see Fallacy of Bastard statistics, see Quasi-material and Quasi-statistics Comparative methodology, see also In pari materia 31, 44, 86, 192–3, 194–6, 201, 304, 362, 537, 570, 615, 657–9 Contemporaneity of events, methodological implications 439, 462, 575, 592 Explanation, character and function of 39, 116, 164, 207, 209–10, 219, 263, 269, 310, 319–20, 339, 359, 469, 497, 529, 565, 569, 590, 604, 628, 669, 671, 686 Fallacious use of analogy 100–1, 563–6 Fallacious use of comparative methodology 31, 86, 172, 192–4, 201, 262, 304, 362, 365, 399, 537, 570, 659, 684 Fallacious use of evolutionary theory and selection 8, 399, 494, 496, 535, 575, 662 Fallacious use of models 633–6, 640 Fallacious use of wills (Cohn) 36–7, 225–6, 260–2 and fn. 168 Fallacy of abduction (inference from single case to fact/ generalizing) 355, 528–9, 654, 657 Fallacy of argumentum or inference ex silentio, inference from silence 78, 85–91, 97, 342–4 Fallacy of circular inference 30, 232, 334–5, 563, 576, 638, 658 Fallacy of distribution 347 Fallacy of invalidability (infalsifiability), see Testability 13, 17, 58, 123, 183, 218, 221, 245, 247, 247, 293, 341, 357, 364, 439, 484, 553–4, 564, 638, 662, 671, 675 Fallibility, see Invalidability, Testability Hypotheses, uses of 63–4, 100–1, 105–6, 111, 117–8, 121, 145, 162–3, 235, 243, 267, 291, 296, 340, 355, 364, 500, 528, 556, 563, 575, 612, 637, 654, 671, 684

Idée fixe (Cohn) 33, 61–2 In pari materia, see also Fallacious use of Comparative methodology 31, 86, 192–3, 304, 362, 537, 570 Necessary and sufficient conditions 7, 19–20, 30–4, 37, 74, 76, 89, 103, 105, 112, 152, 180, 222, 262, 265–6, 289, 301, 308, 339, 379, 416, 459, 490, 501, 511, 514, 522, 524, 530, 535–6, 554, 558, 613, 626, 649–50, 686 Quasi-explanation (Cohn) 67 Random distribution and randomness 64–5, 307, 365, 368, 377 Representativeness 31, 126, 222, 263, 280 fn. 3, 315, 345, 348, 352, 421–2 and fn. 68, 424–5, 427, 440, 442, 445, 455, 517 fn. 68, 542, 571, 580, 597, 600–1, 629, 642, 656, 659 Rule of regularity 307, 387 fn. 20 Selective reading 25, 57–9, 273, 294, 567, 571 Speculation 106, 174, 207, 529, 564, 578, 593 Tenability, level of 37, 57, 106–7, 117, 158, 244, 293, 299, 340–1, 362, 364, 426, 511, 564, 617, 637, 656, 662 Testability, see Fallacy of invalidability Valid samples 346, 348, 356, 362, 365 Working hypotheses, see hypotheses Miasma, miasmatic theory, see Epidemiological theories Mutation, see Evolutionary theory Nestorian graveyeard at Issyk-Kul (see Index of Geographical Names and People) 571 Naïve populations, see Glossary 206, 212, 235, 305 fn. 40, 668, 689 Necrology, see under Sources, religious Norse3 and Norse populations 99, 134, 537, 540, 693 Obituary, see under Sources, religious Paleomicrobiology of plague, the study of DNA and proteins of plague

3 Language of the Scandinavian populations and in Iceland and Greenland in the Viking Age and the High Middle Ages, hence Norse(-speaking) people and populations.

index of subjects pathogen of the past 18, 115, 381–95, 472, 487, 690 Microbiological identity of plague pathogen Yersinia pestis 381–95 Yersinia pestis, Biovars Orientalis, Antiquae, Medievalis 387–8, 392–5, 487 (494) Yersinia pestis Orientalis (in all three pandemics) 387–8, 392–4, 487–9 DNA and proteins, specific of bubonic plague 218, 278, 329, 381–5, 387–9 and fn. 28 no. 6, 391–3 and fn. 36, 535, 666, 673 Pali plague epidemic (India), see also Pali 43 Pandemics of plague, 541–766, 1346–1722, 1894–c. 1940 CE, see also Justinianic (first) pandemic 27–8, 40, 110, 387–8, 394–5, 487, 612, 690 Pathognomonic feature, see Defining feature 277–8 Physicians, contemporary, see also Plague tracts, Medieval Medicine Chalin de Vinario 233, 357 Giovanni da Santa Sofia 353–4 Guy de Chauliac 109, 534 fn. 115 Plague, bubonic rat-borne Historical terminology for bubonic plague epidemics 40, 322–34, 342 Forms of bubonic plague. See also Buboes, Clinical features and Glossary Bubonic plague, main subject of monograph but see 3–9, and Part Four 277–395 Mixed epidemics 109, 420, 520–1, 534 fn. 115, 689 Plague pox/Plague variola 376–7, 690 Primary septicaemic plague 7–8, 313, 524, 624–6, 689–90 Secondary pneumonic plague 8, 107 and fn. 120, 313 fn. 5, 330 fn. 77, 332, 491–3, 513, 528, 534 fn. 115, 549–50, 552, 621, 625–6, 689–91 Secondary septicaemic plague 7–8, 313, 449, 548 fn. 144, 624–6, 655, 688, 692 Anti-plague measures Anti-plague measures in contemporary Europe 48–52, 55, 92, 95–6, 194–5, 203–4 and fn. 35, 209–11, 306, 310–1, 352–3, 362, 510, 519, 613–5

723

Evacuation 20 Isolation by local rejection of strangers or travellers 310 Isolation 195, 510, 615 Quarantine and trade embargo 55, 195, 209, 613–5 Anti-plague measures in Australia 47–52, 175 Anti-plague measures by colonial authorities in Hong Kong 1894–: 90–1, 202, 277, 373–4, 519, 570 Anti-plague measures in India 1896–c. 1920 48–52, 95–6, 175, 194–205, 372, 673 Anti-plague measures in Manchuria 1910–22 497, 499, 517–9, 525–6 Autopsies, post-mortem examinations of bubonic plague cases Contemporary autopsies 653–4, 657–9 Modern autopsies 373, 525–6, 539, 654–6 Buboes, normal clinical feature in plague, defining feature 312–80 Contemporary notions and observations of buboes 322–334 Buboes: Cohn’s problems 340–59 Buboes: Boccaccio and Cohn 359–80 Buboes and Tularaemia Intense painfulness, sharp pangs of pain 40, 324, 331, 333–4, 537–51 Suppuration 549, 688 Buboes, anatomical sites, associated with lymph nodes or (infrequently) glands All over the body (Cohn) 366 Axillas/arm pits 314, 319, 323, 326, 328–30, 332–3, 354–5, 347, 356, 359, 363, 366–7, 369 fn. 190, 491, 542–5, 547–9, 612 Breasts, under (Cohn) 364 Femoral 314, 316–7, 328, 332, 356, 366, 545, 548 Groin/inguinal-femoral 40, 153, 286, 314–16, 323–33, 342, 347, 354–5, 359, 363–4, 366–9, and fn. 180, 542–5, 547–9 Neck 286, 314, 319, 328–9, 333, 347, 356, 359, 364–7, 542, 545–6, 550, 648 Nose (Cohn) 364

724

index of subjects

Other (infrequent) locations 313, 328, 351, 364, 366, Thigh, see Femoral Buboes, causation and function Infective flea bite 313, 625 Lymphatic nodes and glands 313 and fns. 1–2, 314, 317–8, 320–1, 326, 328, 330, 335, 337–8, 366–8, 540, 542, 544–5, 548–9, 652–3, 656, 666–7, 691, 699 Lymphatic system 5, 7, 313, 317, 545, 625, 656, 692 Lymphatic tissue broken down by plague toxin 626 Lymph tracts/vessels 5, 313, 317–8, 320, 379, 540, 625 Buboes, proportions of locations 312, 314–6 Case mortality rates, see Lethality Clinical features of plague, see also Glossary and Defining features Blains, see Pustules Bleeding from the nose (epitaxis)367, 657, 688 Blisters, see Cuticles, Pustules Bloody expectoration/sputum and cough (from secondary pneumonia) 8, 330–2 and fn. 77, 334, 491–2, 534 fn. 115, 547–9 and fn. 144, 552, 612, 626, 689 Buboes, see above Carbuncles 326, 330–6 and fn. 82, 353, 373, 375, 491 Cuticles, see Pustules Duration of illness 279–80 and fn. 83, 288, 331, 534 fn. 115, 549 Ecchymosis, ecchymotic spots or patches 373 and fn. 188, 375, 378, 655, 688 Eschar 377, 688 Extreme brevity of illness (primary septicaemia) 7–8, 84, 313, 524, 625, 690 Fever, sudden and high 157, 328–30, 334, 351, 544–5, 548–9 Haemorrhages, cutaneous, see Petechiae Haemorrhages, internal 655–7, 659 Headache, extreme 330–4 and fn. 84, 491, 545, 548–9, 612 Incubation period 279–80, 281–2, 286, 288, 645–6, 689 Necrosis 18, 375, 638, 654–9 Papules, see also Pustules 374, 377

Petechiae, cutaneous haemorrhages, see also God’s token 333–4, 346, 359, 368–70 and fn. 180, 373–8, 638, 651–2, 655, 657–9, 690 Plague pox/Plague variola 376–7, 690 Plague spots, see Petechiae Pustules 331–3, 359, 364, 368–78, 491, 559, 571–3, 612, 638, 651–2, 690–1 Secondary septicaemia 499, 626, 655 Vesicles 373–8, 690 Clustering of cases 64–5, 67–8, 145–6, 199–204, 268 Defining clinical and epidemiological features 277–484 Concept of defining feature 277–8 Buboes as unique normal clinical feature 312–80 Development of bubonic plague epidemic, temporal rhythm 277–81, (682–7) Inverse correlation between mortality and population density 16, 20, 34–8, 273, 289–311, 632, 668, 673 Latency periods, see also Epidemiology 6, 16, 43, 75, 279–88, 402, 431, 433, 466, 628, 639, 641, 644–8, 668, 673, 682–7 DNA or proteins of plague from historical plague graves, see Paleomicrobiology Epidemiology, see also spread of the Black Death, and for the initial epizootic phases see Latency period under Defining features and Epizootic under Rats Endemic phase 6, 85, 247, 280, 304, 452, 524, 688 Epidemic phase 6, 247–8, 280, 282, 401, 431 Duration of disease in human beings (incubation + illness) 279–80 and fn. 3, 282, 286, 313, 331, 534 and fn. 115, 549, 625 Duration of plague disease in rats 686 Duration of epidemics 398–420 Flea vector of human plague par excellence, X. cheopis (see also

index of subjects Evolutionary theory) 4–5, 12, 119–20, 141, 151–93, 683 Attracted to man 6, 156–7, 160–1, 166 Blockage, development of 5, 627–8, 682–5 Blockage, selection of virulent strains 210–1 Extrinsic incubation period, see also Appendix 3 and Evolutionary theory 627–8, 682–7 Fur flea 108, 397–8, 406, 682, 684, 686 Infection-infectivity interval, see Extrinsic incubation period Sensitivity to temperature in surroundings and in the host 682, 686–7 Septicaemia in human beings and rats 5, 14 Septicaemia, level required for blockage 10–1 Survival period of infected, unfed fleas 167, 180, 582, 645–6 Vector capacity/efficiency 11, 682–7 Forms of spread by infected rat fleas Contiguous spread between conterminous rat colonies 6, 113, 146, 151, 155, 165, 167, 179, 175, 178, 182, 189, 191, 193, 280, 567 Human-flea theory, see Interhuman transmission Interhuman transmission by Pulex irritans (human flea) 9–16 Metastatic spread over various distances 6, 27, 104, 116, 144, 151–93, 202, 280, 286–7, 293, 401, 433, 465, 472, 488, 492, 553, 568, 582, 585–6, 593, 595, 645 Saltatory spread, spread per saltum, see Metastatic spread Medium of transportation of infected rat fleas Bedding 55, 154, 159, 174, 181–4, 187, 528, 614–5 Clothing, clothes actively worn 6, 9, 13, 27, 55–6, 104, 116, 145, 151 fn. 3, 153–4, 158–62, 166–8, 171, 173–6, 178–80, 182–4, 187, 195, 283, 286, 314, 317, 358, 361, 363, 427, 472, 476, 492, 528, 568, 593, 595, 614–5, 645, 686 Cotton 27, 56, 166–7, 178–9, 183–4

725

Grain/farina/bran, see also rice 27, 56, 101–2, 105, 115, 129–30, 151 fn. 3, 159–62, 166–7, 171, 178–9, 183–4, 193, 393, 401, 418–9, 492, 582 Gunny bags 162, 178, 183–4 Hides 178, 183–4 Luggage/Baggage 6, 27, 56, 104, 116, 158 fn. 24, 162, 165–8, 171, 173–4, 176, 178–9, 181–4, 187, 412, 472, 476, 568, 593, 595, 615, 686 Merchandise, commodities 6, 55, 104, 153, 159–61, 164–8, 171, 173–4, 178–9, 183, 187, 419, 472, 492, 590, 593, 615 Rags 118, 183–4, 361 Rice 113, 166, 168, 179, Stockfish 418–9, 502, 506 Textiles 27, 151, 159, 174, 286, 645–6, 681 Woolens, wool packs 27, 179, 331, 502, 555, 614 Means of communication transporting infective rat fleas Horse, packhorse, horseback, cart 105, 132, 165, 172, 174, 444, 447, 472, 476, 648 Human beings/travellers, see also Clothing and Luggage 104, 163–5, 173–181 and fn. 85, 183–5, 189–9, 196, 202, 310, 580 Lorry 165 Railway 41, 58–9, 162, 164–5, 168, 170–2, 174, 176, 178, 196, 517, 519 Roads, main 114, 116, 173, 191 Sailing ships, boats, and barges 55, 132, 153, 165, 168, 180, 185–7, 191, 398, 405, 419, 472–3, 477, 501–5 and fn. 26, 569, 582, 586–7, 589–90, 594 Steamships 170, 176, 185, 196 Fatality rates, see Lethality Immunity, see also Re-infection Lethality rates, see also Virulence 9 and fn. 14, 142, 205, 208, 210–1, 218, 220–1 and fn. 69, 233, 268, 296, 302, 512, 520 fn. 78, 557–9, 572, 578, 591, 606, 689 Mass graves 256, 266, 381, 383, 385, 388, 391 fns. 32 and 34 Morbidity rates 296–7, 300, 302, 468, 689

726

index of subjects

Mortality rates according to occupation 39–40, 143–5, 264 and fn. 171, 558, 572 Plague pneumonic, secondary, see Bubonic plague, Forms Plague reservoirs (foci) 203, 513, 580–1, 621 fn. 34, 661, 690 Plague seasonality, see also Black Death and Winter epidemics 75, 141, 247–53, 335, 396–436, 474, 528–9, 640–2, 644, 668 Seasonality of plague in England 1340–1666 420–83 Transseasonal or multiseasonal type 398–420 Re-infection, see also Immunity 212–17 Sociology of rat-based plague 142–50 Spread rates of bubonic plague, see also Black Death, Koliwada and India 17, 19–20, 27–32, 57, 113, 151–94, 170–6, 590, 639, 664 and fn. 3 Koliwada 94, 170, 173, 176, 178, 189, 198 India 151–94 Vaccine, Haffkine’s anti-plague of 1896 196 Virulence 43, 209, 360, 525, 527, 529, 689, 692 Historical stability by selection of virulent strains by blockage 210–1 Plague pneumonic (spread by cross-infection) Primary pneumonic plague 8 and fn. 13, 12, 27, 31–2, 107–9 and fn. 120, 113, 167, 213, 313 fn. 5, 321, 332, 376 fn. 200, 416, 420 fn. 66, 491–552, 625 Communicability/diffusibility (low) 499, 518–28, 535 Duration of epidemics, see also spontaneous decline 505, 518–27, 639–42 Duration of illness 523–4, 533–4 and fn. 115, 548–9 and fn. 144, 552, 571 Mortality rates 519, (530–3), 535 Pulmonary plague 525, 527, 563, 690–1 Pure epidemics of primary pneumonic plague? 8, 16, 77, 394, 492–9, 511–4, 521–2, 527, 533, 691

Rise from secondary septicaemic plague, see also Glossary 8, 499, 516, 523–4, 626, 691 Size of epidemics 8, 518–22 Spontaneous decline 518–27 Plague tracts, see also Medieval and early modern medicine 350–9 Specific medical works mentioned in the text 350, 354–5, 357 Pleistocene 121 Population developments, see also Demography and Malthusian theory 209, 489, 558, 595–608, 629–30, 668 Population size 600–6 Price history 178, 269 fn. 178, 421 Quasi-empirical material (Cohn) 218–24, 230–2, 237–45, 246–61, 267–8, 341–59, 364–5, 367–79 Quasi-statistics and bastard statistics (Cohn), see also Quasi-empirical material 245, 255–7, 341–9, 354–6, 359, 365, 367, 370 Racism, accusation of, see also Ashburton Thompson and Hirst 46–54, 174–5 Rats, see also Plague, Forms of spread, Evolutionary theory Terminology on rats Commensal rats, domestic rats, peridomestic rats, see Black rat Mus decumanus, Rattus norvegicus see Brown rat 134 Rattus rattus, Mus rattus, see Black rat 134 Vǫlsk mus, see Black rat 134–5, 137 History and role in plague of rats Black rats in Europe, Prehistoric times 120–1 Black rats in Europe, finds of bones from Roman to early modern periods 122–42 Black rat (Rattus rattus), history in Europe 53–4, 73–150, 180–1, 286–8, 301, 395, 406, 417, 419, 488, 495, 618, 634 Black rat, role in plague epidemics, its rat flea X. cheopis, see under Fleas, Plague-Flea Vector 3–4, 6–7, 20, 29–30, 73–5, 158, 160, 168, 170–3 and fn. 55, 180–1, 191, 197–201, 281,

index of subjects 286–7, 300–1, 396–8, 406, 419, 488, 495, 634, 646 Black rat, relevant elements of modern history in Europe 1700–1950 138–40 Brown/grey rat (Rattus norvegicus), history in Europe and role in plague epidemics, rat flea Nosopsyllus fasciatus, see under Fleas 53, 73–5, 99–100, 119–20, 125, 129–30, 133–4, 138–40, 147, 417 Rats, behaviour of black rats Black rats, burrowing 92–6, 101–2, 123–5, 140, 149, 172, 180, 682 Cannibalism 93–4, 623 Colonies, defending territories 102, 185–6, 200, 279–80, 287, 301, 582–3, 628, 684–7 Dying rats, hiding in inaccessible places 92–6 Environments/biotopes/ecological niches, habitats 53–4, 92, 119, 124–5, 140, 172, 301 Fertility 118–9 Houses and house rats 74, 76, 92, 96, 120, 131, 168, 197, 301 Mortality, natural rate 92 Rat falls 78, 80, 85, 92, 96–7, 112 Ship rats 92, 131, 135, 301, 705 Size, variation, see Evolutionary theory Epizootic, course of developments 6–7, 66, 185, 200–1, 279–81, 582–3, 627–8, 646, 682–7 Septicaemia in rats, level and temperature dependency 5, 10–1, 14, 397, 643 Reed-Frost theory and model, see Epidemiological theories Regular clergy, see Sources, religious Renaissance 68, 80–1, 146, 209, 262, 322, 343, 350–1, 353, 531 fn. 108, 631 Revisionists, see Alternative theories Selective reading, see Methodology Sheep 555, 562, 573, 575–6, 579, 590, 592, 594, 608, 681 Ship rat, see Rats Small pox 205, 214, 317–8, 322, 327, 373–4, 376 Sources (written), non-religious Chronicles and annals

727

Annal of Fitja (Fitjaannáll) 681 Annal of Skálholt (Skálholtsannáll) 531, 536–7, 551, 680–1 Annal of Skarðsa (Skarðsárannáll) 681 Bishop’s Annals of Jón Egilsson 681 The Brut 223 Cronica (by the Villani brothers) 243 fn. 136, 258, 323–5 and fns. 34 and 43–4, 344, 347, 360, 413, 531 fn. 108 Fragment of an Annal of Skálholt 536–7 and fn. 120, 551 Grey Friars’ Chronicle 472 Lawman’s Annal (Lögmannsannáll) 99 fn. 91, 401, 536–7 and fn. 118, 547, 551, 680 New Annal (Nýi Annáll) 502, 680 The Oldest Annal of Vatnsfjörðr (Vatnsfjarðarannáll hinn elzti) 502, 680 fn. 3 Official registrations Calendar of the Close Rolls 223 Compoix d’Albi 239 Florentine Books of Dead 235, 264 Wills (non-religious) 36–7, 225–6, 260, 262 and fn. 168, 401, 413–4, 430–2 Wills, Court of Hustings 36–7 Literary and proto-scientific sources Book of Nature, by Konrad von Megenberg 355 La Divina Comedia, by Dante Alighieri 343 Il Decamerone, by G. Boccaccio 201, 344, 359–60, 379, 618 fn. 27 Libellus de judicio Solis in conviviis Saturni, seu de horrenda illa peste, by Simon Couvin 39 fn. 37 Sources relating to religious institutions Bishop’s registers 440–1 and fn. 137, 443, 445–6, 449–51, 455–6, 460–1, 463, 468–9, 484, 603 Bishops’ administrations and co-travelling staffs 444–5, 447–8, 460, 462, 468 Bishops’ circulation of dioceses 444, 447–8 Bishop’s registers and institutions of parish priests, see also Black Death, Mortality and Seasonality according to institutions 192, 434 fn. 111, 436–84, 379, 618 fn. 27

728

index of subjects Duration of vacancies in parish benefices 436–63, 467, 470–1, 475, 483, 602–4 Institution of parish benefices in the hands of the king 440–5 Lapses of parish benefices to the bishop 455, 461, 483 Mortality according to first institutions, see Black Death Patronage and advowsons 443–4, 451 Pluralism and absenteeism 443, 447, 602 Vacancies by exchange, resignation, retirement 438, 443, 445–6, 450–1, 456–7, 470, 602 Diocese of Bath and Wells (Sommerset to the R. Avon) 449–50, 459, 463, 475–8 Diocese of Coventry and Lichfield (Shropshire, Staffordshire, Derbyshire) 192, 445, 449, 454–5, 460–1, 603 Diocese of Ely (Cambridgshire) 449–50, 455–6, 465, 603 Diocese of Exeter (Cornwall and Devon) 449–50, 453, 455, 463, 470–4, 603 Diocese of Hereford (Herefordshire, Shropshire to the R. Severn) 449, 456–8 Diocese of Lincoln (Oxfordhsire, Buckinghamshire, Hertfordshire, Bedfordshire, Huntingdon, Rutland) 439–40, 449, 451–2, 603 Diocese of Norwich 449 Diocese of Salisbury (Dorset, Wiltshire, Berkshire) 437, 461, 463, 465, 467–70, 474 Diocese of Winchester (Hampshire, Surrey) 241, 449, 463, 479–82 Diocese of Worcester (Worcestershire, Gloucestershire, Warwickshire) 449, 458, 460, 475 Diocese of York (Nottinghamshire, Yorkshire to the R. Tees and R. Humber, Lancashire (from the R. Ribble) 439–42 and fn. 137, 446, 449, 603, 631

Books registrating endowments for religious services Calendars 238, 341–2 Necrologies, see also below 341–2 Necrology of the Monastery of San Domenico in Camporegio 218, 231–2, 245–68, 273, 325 and fn. 45, 675–9 Obituaries, see also below 426, 429 Obituary of the Cathedral of Lund 59–60 Obituary of Christ Church Priory, Canterbury 426 Obituary of Santa Maria Novella in Florence 261 Parish registers Parish registers of Central Europe 521 Parish registers of Colyton 62, 66, 202, 234 Parish registers of Devonshire 295, 433–4, 474 Parish registers of Eyam 68, 410, 647 Parish registers of Givry 108, 114, 270 Parish registers of Penrith 284, 647 fn. 127 Registers of monks 60, 224–5, 229 fn. 89, 426–30 and fns. 87 and 93, 453 Saints’ lives 364 Source criticism Cohn, deficient or lacking source criticism, see also Quasi-statistics and Quasi-empirical material 36–7, 39–40, 42–3, 55, 59–60, 67–8, 86, 144–5, 200–1, 218–24, 230–2, 236–40, 242–5, 247–68, 341–58, 359–70, 372, 380 Source criticism and the Medieval mind 78–84, 85–91, 219–24, 235, 254–5, 259–67, 324–58, 359–70, 380 Soviet plague research(ers) 3, 10, 58, 210 Spread per saltum/by leaps, see Plague, spread Stalinist biological theory xv Statistics, see also Quasi-statistics Bimodal pattern 296 Binomial expansion 64 Comparative statistical inference 345

index of subjects Extrapolation 247, 251 Random distribution 64–5, 307 Sweating sickness, see Diseases Ticks 319 Trading stations on the Black Sea and the Mediterranean 588 Tudor and Stuart England 179, 294, 432, 615

729

Tularaemia, see Diseases Vietnam War, plague research 3, 44–6, 193, 233–4, 315, 377, 520–1 and fn. 82, 524, 545, 566 Viking Period 125–6, 132–4, 140, 395 Viral diseases, see immunity Zoogeography 104–5

INDEX OF GEOGRAPHICAL NAMES AND PEOPLE1 A Coruña 661 Adriatic Sea 588 Africa(n), see also South Africa 9, 29, 87–9, 98, 188, 191, 386–7 fn. 20, 581, 585–6, 637, 650, 660–2 Aix-en-Provence (southern France) 190 Akershus castle (Norway, Oslo) 404 Akkerman, see Mauro Castro Albi (southern France) 239 Aleppo (Syria) 214 Alessandria (Italy northern, Piedmont) 190 Alexandria 569, 581, 585–7 Almería (Spain southern) 55 Alps, Alpine113, 404, 411, 415–6, 648 Alverdiscott, parish of (England, North Devon) 472–3 Ambala, district (India, province of Punjab) 154 Americas 92, 167, 186 North America(ns) 44–6 and fn. 52, 58, 92, 120, 193, 513, 523, 541, 545 South America(ns) 92, 167, 182, 376–7 Amsterdam, see also Jordan 127, 146, 226 Amur R. (Manchuria) 515 Andenes, bailiwick of (northern Norway) 419 Anglo-Saxon (England) 127–8, 130, 134 Ansford, village (England, Somerset) 476 Antarctic Continent, see Macqarie I. Apt (France southern) 190 Arctic Circle 418–9 and fn. 61 Arctic regions, see also Polar regions and sub-Arctic 417–9 and fn. 61 Argentina 654 Arthur Road (India, Mumbai), hospital 372 Ascheim (Bavaria, Germany) 329, 389–90 Asia 166, 193, 520, 621 fn. 34, 661 Asia Minor, see also Turkey 586

1

Assam, province (India) 148–9 Astrakhan Guberniya (Russia, at Caspian Sea) 520 Atlantic Ocean, see also North Atlantic 404, 648, 661 Atmour Mistigid, hamlet (Egypt, north of Aswan) 166 Aubagne (southern France) 190, 383, 390 Augst (Switzerland), see Augusta Raurica Australia(ns) 51–2, 91, 93, 155, 174–5, 186, 383 Augusta Raurica (Roman precursor of Augst) 127 Austria(n)(s) 127, 213, 371, 389–90, 404–5, 507 Avignon (Papal city, Provence) 109, 147, 220–1 and fn. 68, 357, 521, 534 fn. 115, 593, 618 fn. 27 Avon R. (England south-western) 459, 475, 477 Aylesbury, parish (England, Buckinghamshire south east), see Walton 127–8 Båhuslen (medieval Norway) 670 fn. 7 Baden-Würtemberg (Germany southwestern) 404 Balkan 195, 690 Baltic Sea 99, 131, 133, 139, 394, 403, 405, 407 and fn. 45, 569, 648 Baltimore (U.S.A.) 103 Bangladesh, Bengal Barnstaple (England, North Devon) 472–3, 478 Barcelona 585 Basle (Switzerland) 405 Batcombe, manor (England, Somerset) 478 Bath and Wells, diocese of (England, Somerset) 449–50, 459, 463, 475 Bavaria (Germany) 329, 389–90, 507 Beddingham, Roman villa (England, Sussex) 127

Regarding special letters, see introduction to the Index of Subjects, fn. 1, no. 3.

index of geographical names and people Bay of Barnstaple (England, North Devon) 472 Belgaum (India) 94, 102–3, 118 fn. 150, 140 fn. 224, 161–2, 198 Belgorod(-Dnestrovskyi), see Mauro Castro Bengal East (Bangladesh) 148–9 Bergen (Norway) 113, 115, 136, 140, 332 fn. 84, 385, 393, 400–3, 406–8, 418–9, 435, 502, 504–6 and fn. 41, 530, 536–7, 541–2, 546–7, 550–2 Bergen, King’s Mansion [= Kongsgården] 502 and fn. 22, 506 Bergenhus castle (in Bergen) 506 Bern (Switzerland) 10 Berkshire (England) 140, 465, 469 Bethesda (U.S.A., Maryland) 371 Bihar (India) 379 Birka (Sweden, west of Stockholm) 132 Bishop’s Waltham, manor (England, Hampshire) 482 Black Sea 586, 588 Bodmin (England, Cornwall) 475 and fn. 218 Bohemia 121 Bohuslän, see Båhuslen Bombay, see Mumbai Bombay City and Island, see Mumbai Bombay Presidency, see Mumbai Bordeaux (France south-western) 114, 393, 477, 584, 593–4, 661 Botnsa (Iceland) 681 Brabant (Netherlands) 325 Brazil 120, 141 Brenner Pass (Switzerland eastern) 404 Bridford, parish of (England, Devonshire) 295 Bridgewater (England, Somerset) 477 Bridport, parish (England Dorset) 468 Bristol (England) 14, 146–7, 185, 415, 459–60, 465, 472–3, 475, 477–8 Bristol Channel 478 Britain, British, see also Britain Roman and England 36, 85, 101, 185, 210, 222, 243, 257, 336, 341, 371, 489, 491, 502–4 and fn. 26, 507–8, 553, 571, 584, 615–7 and fn. 21 Britain Roman 128 Brough of Birsay, island north west of Orkney’s Mainland 129 Bruges (Low Countries) 104, 569 Brunswick (Germany) 216 Buckinghamshire (England) 127, 465 Buenos Aires 654

731

Burgundy (France) 114, 270, 593 Burma = Myan Mar 98, 185 Cadbury North and South, manors (England, Somerset) 467 Caffa, see Kaffa California 172 Cairo (Egypt) 571, 575, 585 Calais (France north-western) 594 Calcutta (India), see Kolkata Cambridge, University of 35, 449, 517, 566 Cambridgeshire, county of (England south-eastern) 271, 430, 455, 465 Camporegio, monastery and cemetery (Siena, Italy), see also Necrology 218, 231, 245–68, 325 fn. 45, 675–9 Canterbury (England southeastern) 224, 229 fn. 89, 426–9, 465 fn. 192, 479 Canton (Guangzhou, China) 90–1, 153, 202, 568 Carcassone, (France south-western Mediterranean) 593 Cardiff (Wales) 185, 654 Cassis (France southern) 383, 390 Castlecary, village (England, Somerset) 476 Catalonia (Spain) 294, 298 Catania (Italy, Sicily) 548 Cathedral’s parish (Norway, Bergen) 406–8, 435 Central Provinces (colonial India) 35, 397 Cetatea Alba, see Trebizond Ceylon, see Sri Lanka Chambery (County of Savoy/ France) 241 Channel Islands, see also English Channel 594 Charybdis (mythological whirlpool) 363 Cheshire, county (England central-east) 188, 287 fn. 28 Chester (Chestershire, England) 287 China, Chinese 3, 13–4, 90, 94, 153, 166, 182, 234, 291 fn. 4, 316, 334, 375, 497–500 and fn. 17, 515, 517–8 and fn. 69, 520, 523, 526, 534, 543, 566, 568, 620–1 and fn. 34, 656 Chios I. (Greek, on the coast of Asia Minor/Turkey) 588 Christ Church, parish in Bristol 147 Christ Church Priory (England, Canterbury) 224, 229 fn. 89, 426, 429, 465 fn. 192, 479

732

index of geographical names and people

Church of Friars Minor at Bodmin (England) 475 Clevedon (England, Somerset) 477 Colchester (England) 407 Cologne (Germany) 127, 324, 326, 330 Colombo (Sri Lanka) 95–6, 185–6 Colyton (England, Devonshire) 65, 67–8, 142, 145, 202, 234, 295, 406 Comtat Venaissin (France, region ar. Avignon) 190 Congo, Democratic Republic 650–1 Constance (Switzerland) 404 Constantinople 82, 185, 323, 328, 331, 393, 500 fn. 17, 562, 569, 577, 581, 585–8, 661–2 Continent (Europe) 73, 181, 306, 319, 562, 579, 661, 664 Copenhagen (Denmark) 59, 386, 409 Corfu (Greece, Kerkyra) 588 Corhampton, manor (England, Hampshire) 482 Cornwall (England) 453–4, 471, 474–5 Coron, see Koroni Corsica I. (Genoa, to France 1768) 119, 140 Corone, see Koroni Cottenham, manor (England, Cambridgeshire) 271 Couvin (Belgium) 39 and fn. 38 Coventry and Lichfield, diocese (England) 192, 445, 454–5, 460, 603 Crete I. 121 Crimea 323, 331, 393, 500 fn. 17, 569, 581, 583–6, 661 Dalinor mines (Manchuria) 523 Dalmatia(n) (c. present-day Croatia+Albania) 346 Damerham, manor (England, Hampshire) 482 Danube R. 128 Dean Prior, parish (England, Devon) 295 Dee R. (England) Denmark 60, 125, 133, 135, 322, 394, 403, 504, 507 and fn. 45, 550, 572, 670 Derbyshire (England), see also Eyam 77, 188 fn. 101, 561 Developing countries 210, 396, 622 Devon(shire), county (England) 67, 119, 287, 295, 433, 453, 466, 471–6, 478–9 Dhund/Dhand, village (India, Punjab) 94 Ditcheat, manor (England, Somerset) 478

Dnestr R., estuary of (Russia) 588 Dorset, county (England) 453, 465–71, 478–9, 483 Dreux (France) 390–1 Dubrovnik, (Croatia), see Ragusa Durham, county (England) 271, 632 Durham priory 229 fn. 89, 428, 430 fn. 93 East Anglia (England) 151, 405, 430 fn. 93 Ecuador (South America) 376 Edinburgh (Scotland) 508, 510 Egypt(ian) 58, 92, 94–5, 166, 182–4, 214, 397, 520 and fn. 82, 585–6 Eisenach (Germany) 326 Ely, diocese (England, Cambridgeshire) 449–50, 455–6 England, English 16, 34, 36, 48, 77, 81, 85–6, 99, 111, 113–6, 119, 125, 127–31, 134–5, 147–8, 155, 169, 179, 185, 188, 195 fn. 5, 209–10, 214, 216, 223, 225–6, 234, 243, 255, 257, 269, 271, 289–90, 293–6, 299, 303–6, 309–11, 322 fn. 30, 325, 327, 331–3, 341–2, 346, 349, 352, 369, 372, 393, 401, 403–5, 407, 415–17 and fn. 59, 420–84, 489–90, 500, 502–4 and fn. 26, 506–11, 513, 518–9, 530–1, 535, 540–1, 554, 557, 560, 562, 565–6, 571–2, 574–9 and fn. 69, 582–3, 585–7, 589, 593–6, 599–602, 605–7 and fn. 222, 611, 615–8, 629–32 and fn. 76, 639, 648, 657–8, 661, 670, 690 English Channel 596, 648 Essex (England) 405, 480 Europe(an) 14, 17, 20, 26, 30, 35, 40, 42, 48–50, 52–3, 56, 73, 75, 77, 87–9, 97–8, 100, 104, 106–8, 111, 113, 120–2, 126, 136, 140–1, 143, 148, 173, 179–81, 194–6, 199, 201–4 and fn. 35, 207, 214, 221–2, 258, 269, 277, 291–3, 296, 299, 301, 305 fn. 40, 319, 323, 325, 327, 331, 340, 344–5, 383–4, 392, 395, 397, 399, 415, 417, 420, 432, 434, 464, 488, 490, 492, 495, 501, 505, 507, 510–7, 527, 540, 554, 559, 562, 565, 568–70, 576–8 and fn. 86, 580, 583–5, 592–3, 600, 607, 611, 613, 621 fn. 34, 642–3, 648, 657–8, 661, 664, 666, 668–9, 673, 690

index of geographical names and people Europe Central 191, 392, 394, 521 Europe Eastern 195, 296, 331 Europe Northern 12, 73, 77, 98, 105–7, 116–22, 126–8, 131, 140, 181, 188, 191, 269, 290, 394–5, 398, 400, 406, 416, 506–7, 530, 535, 565–6, 607 fn. 224 Europe North-western 107, 128, 131, 391, 393, 399, 507 and fn. 45 Europe Roman 106, 128 Europe Southern 73, 121–2, 124, 209, 269, 398–9, 412–3, 581, 584–6, 643, 661 Europe Western 77, 86, 106–7, 117, 128, 131, 195 fn. 5, 269 and fn. 178, 399, 432, 607 fn. 224 Evercreech, village (England, Somerset) 476 Exe R. (England) 473 Exeter (England) 295, 473 Exeter, diocese of (England) 449–50, 453, 455, 463, 470–1, 603 Eyam (England, Derbyshire) 68, 77, 188 fn. 101, 285–7, 410, 561–2, 614, 638, 641–7 Faccombe Netherton (England) 140 Faxeholm (Sweden) 133 and fn. 194 Fingrith, manor (England, Essex) 405 Finland 138–9 Finnmark (Norway) 418 fn. 61 Flanders (Low Countries) 216, 569 Florence, Florentine (Italy) 62, 68, 104, 146, 201, 209, 215 and fn. 47, 221, 232, 235, 251, 261, 264–5, 271, 273, 323–6 and fns. 33 and 45, 330, 344, 347–8, 353, 359–61, 413, 531 and fn. 108, 558, 591, 618–9 and fn. 27 Fosen (Norway) 418 France, French, see also Provence and Languedoc 9, 12 fn. 28, 29, 31, 39, 43, 58, 86, 92, 101, 107–8, 134, 147–8 and fn. 244, 181, 188, 214, 217, 223–4, 226, 236–7 and fn. 109, 239, 241–2, 269, 281, 295–8 and fn. 19, 303, 305–6, 308, 324–5, 327, 329–30, 341, 352, 371, 381–6, 388, 390–5 and fn. 29, 400, 405, 566, 573–4, 585, 593–4, 619, 630, 661–2 Frankfurt on the Oder (Germany) 326 Fremington, village (England, Devon) 473 Freston (England, Suffolk) 186 Frome Braunch, manor (England, Somerset) 114, 459, 476–7

733

Friuli (Italy) 330 Gabon (Africa West) 636 fn. 91 Gallia, see Gaul Garhwali (India) 112 Gascony (France south-western, region) 472, 477, 593 Gaul (Roman province, Gallia) 128, 327 Gaza (Middle East, area) 586 Geneva (Switzerland) 121, 127 Genoa, Genoese (Italy) 104, 191, 413, 569, 586–91 and fn. 145, 594, 661–2 Germania, Germanic (Roman province, “Germany”) 127–8, 131 Germany, German 113, 121, 131, 134–5, 143, 216, 225, 322, 325–6, 330–1, 342, 344, 346, 354–5, 371, 389–90 and fn. 28 no. 6, 392, 394, 404–5, 411, 415, 503–4 and fn. 27, 506–7, 569, 573, 670 Ghent (Low Countries) 558 Gignac (France) 190 Gillingham (England) 466–7 Givry (France, Burgundy) 108, 114, 270 Glasgow, Glaswegians (Scotland) 185, 364, 367 Glastonbury Abbey (England) 241, 299 Gloucester, (England) 114, 460 Gloucestershire (England) 475 Godthåb (Greenland) 418 Göta Älv (Sweden) 670 fn. 7 Golden Horde (Mongol Khanate, south-eastern Russia) 580, 588 Gorhambury (England) 127 Gotland I. (Sweden) 133 Gouda (Netherlands) 506–7 Greece, Greek 82, 346, 563, 571, 588 and fn. 132 Greenland 98–9, 411, 415–6, 418 Grimsby (England) 465 Guangzhou (China), see Canton Gudbrandsdalen, principal valley (Norway) 137 Gudhem, monastery (Sweden) 133 Guelders (Netherlands) 503 fn. 27, 506–7 Gulf of Gdansk (Poland) 131 Gulf Stream 139, 399, 404, 418 Hälsingland (Sweden) 133 and fn. 193, 138 Hafnarfjord at Fornubudir (Iceland) 681 Haithabu (Germany) 131, 135

734

index of geographical names and people

Halesowen, manor (England, Worcestershire) 241, 271, 478, 598 Halland, Denmark2 135, 138, 403, 670 fn. 7 Halmstad, port town (see Halland and fn. 2) 403 Hampshire (England) 140, 463, 479–80, 482 Harbin (Manchuria) 515, 517–8, 523 Hardanger (Norway) 557 Harnai (India) 153 Harwich (England) 465 Heacham, manor (England, Norfolk) 575 Hebrides Is. (Scotland, north-west of), see Shiant Is. 119 Helgafell (Iceland) 680 Helgeland, bailiwick (Norway) 419 Hereford, diocese (England) 449, 456, 458 Hertfordshire (England) 430 Hesse (Germany, region) 326 High Ham, manor (England, Somerset) 478 Holt in Saurbær (Iceland) 681 Hong Kong (China) 90–2, 185–6, 192, 202, 213, 314, 316, 373–4, 626 Honiton (England, Devon) 472 Hubli (India, Deccan) 284 Hull (England) 185, 465 Hunan, province (China) 526, 528 Hvalfjord (Iceland) 681 Hvitskeggshvammi (Iceland) 681 Iceland(ers, -ic) 30, 77, 99, 118–9 and fn. 153, 401, 416, 418, 493–552, 518, 608, 648, 680–1 Icelandic waters 502–3, 506 India(n) 3, 13–4, 20, 33–8, 40–5, 47–53, 58, 66, 74–5, 91–4, 98, 108–12, 121–2, 149, 153–5, 158, 168, 174–5, 177, 179, 182–3, 185, 188, 194–204, 213, 217, 234, 277, 279–81 and fn. 3, 284, 289–91, 293, 295–6, 301, 303–7, 316, 322, 334, 364, 366–8, 370–5, 396–7, 399, 464, 488, 519–20, 543, 553, 566–8, 570–1, 581, 599–600,

616, 620–1 and fn. 34, 624, 645, 656, 668, 673 Indonesia, see also Java I. 3, 58, 91, 167, 520, 543 Innsbruck (Austria) 404 Ireland 114, 128, 134, 306, 325–6, 465, 477, 503 Issyk-Kul L. (Ysyk-Köl) (Central Asia, Kirghizistan) 571 Istria (Italy)3 330 Italy 55, 185, 188, 191, 200, 209–10, 215 fn. 47, 226, 229, 234, 246–7, 293, 295–8, 302, 322–5, 330, 341–6, 350, 352–3, 391 fn. 33, 393, 411–4, 548, 569, 581, 585, 588, 591, 631, 648, 658–9 Ivory Coast (Africa West) 636 fn. 91 Japan(ese) 25, 518 Jemtland (medieval Norway)4 418 Jordan (quarter in Amsterdam) 67, 146 Jutland (Denmark) 403 Kaffa (the Crimea) 331, 393, 577, 581, 585–90 and fn. 144 Kilkenny, monastery (Ireland) 332, 491 King’s Lynn (England) 115, 393, 401, 654 Kirghizistan, see Issyk-Kul Kirkjubær (Iceland) 680 Kjalarness, meeting place of moot (Iceland) 681 Koliwada, northerly part of Sion 94, 170, 173, 176, 189, 198 Kolkata, formerly Calcutta (India) 185, 192, 194, 196, 373 Koroni (Coron, Greece, Pelopponese) 588 Krakow (Poland) 269 fn. 178 Kronstadt Fortress (Russia, by St Petersburg) 214 Krysuvik (Iceland) 681 Lambesc (France) 381 and fn. 3, 390–2 and fn. 35 Landshut (Germany, Bavaria) 507

2 Halland is a region situated north of the Sound on the eastern side of Kattegat. Halland was a Danish province until mid-seventeenth century, when it was conquered by Sweden; see also Scania. 3 Now part of Croatia. 4 Present-day Sweden, Jämtland.

index of geographical names and people Languedoc (France) 190, 236 and fn. 109, 390 Les Pennes-les Septèmes (France) 190 Levant (Middle East, region) 586, 588, 661–2 Liège (Netherlands) 326 Lincoln, diocese (England) 439–40, 449, 452, 603 Liverpool (England) 185 Lofoten, bailiwick (Norway) 419 Lombardy (Italy) 121 London(er) 36–7, 79 fn. 21, 83, 104, 127, 144, 147, 186, 204, 215–6, 223, 286, 302, 304, 306, 308–10, 333, 335–6, 373–5, 378, 383–4, 390–1, 393, 405, 409, 429, 432–5, 465 fn. 192, 479–80, 490, 531, 549, 554, 558, 567–8, 577–9, 645, 657–8 Low Countries, see the Netherlands Lübeck (Germany) 104 Lund (Sweden), see also Scania5 59–60, 132–3, 135, 403 Lundegaard L. (Bergen, Norway) 332 fn. 34 Lynn, see King’s Lynn Madagascar 3, 13–4, 58, 92, 180, 182, 334, 520–1 and fn. 82, 566, 582, 619 Mälaren L. (Sweden) 132 Mahlgahla (India, Punjab) 282 Mainz (Germany) 216 Málaga (Spain) 588 Malang (Indonesia, Java) 168, 182 Malpas (England, Chesire) Manchester (England) 385 Manchouli (Manchuria) 517 Manchuria 8, 31, 120, 141, 234, 497, 512, 514–20, 523, 534 fn. 115, 535, 539, 626–7 Mantua (Italy) 413 Macqarie I. (sub-antarctic, between Tasmania and Antarctica) 119, 140 Marnhull, manor (England, Dorset) 478 Marseilles 12 fn. 28, 114, 188, 191, 220–1, 283, 305, 307–8, 381–3, 388–93 and fns. 28 no. 4 and 35, 577, 587, 591–3, 620, 661

5

735

Martigues (France) 383, 388–91 and fns. 28 no. 4 and 34 Mauro Castro, trading station (Russia)6 588 Mayrargue (France) 190 Mecklenburg (Germany) 121 Mediterranean littoral 73, 98, 101, 105–6, 117, 119, 128, 397, 415, 562, 565, 577, 581, 583, 586–7, 594, 648, 661 Melcombe Regis7 (medieval England) 114, 116, 437, 462, 465–6, 468–9, 471–2 and fn. 209, 474, 476–7, 479, 483, 586–7, 593–4 and fn. 162, 661 Mells, manor (England, Somerset) 478 Mende (France) 307 Meon R. (England southern) 480 Messina (Italy, Sicily) 393, 548, 581, 587–8, 590 Middle East 581, 583–5, 587–8, 590 Milan (Italy), see also Nonantola 66, 147, 200 Milan, stalli, poor quarters 147 Mirabeau (France) 190 Modena (Italy) 324 Modon, harbour (Greece, Pelopponese) 588 Monemvasia, port town (Greece) 588 Montpellier (France southern) 39 and fn. 39, 236, 326, 382, 390–3 Morocco 9–10, 13, 28–31, 58 Moscow (Russia) xv, 148, 214, 604 Mumbai (Bombay in citations, India) 74–5, 92, 94, 102, 140 fn. 224, 153, 156–9, 161–3, 171, 176, 188–9 and fn. 103, 192, 194, 196, 198, 203, 213, 284, 291, 316, 364–5, 370, 372, 399, 567, 599, 623 Munich (Germany, Bavaria) 329, 389–91, and fn. 30 Myanmar, see Burma Namdalen (Norway) 418 Naples (Italy) 302, 574, 588, 657, 659 Nauplion (port town Greece, Pelopponese) 588

Lund used to be the cathedral city of the Danish archbishop. See Scania and fn. 8. The ancient Greek colony of Tyras, later called Akkerman, from 1946 with the slavic name of Belgorod(-Dnestrovskyi), in Romanian Cetatea Alba. 7 Melcombe Regis was situated within the area of present-day Weymouth. 6

736

index of geographical names and people

Narbonne (France) 324 and fn. 38, 326 and fn. 52, 330 Navarre (medieval kingdom in Spain) 294, 298 Neston (England) 287 and fn. 28 Netherlands 127–8, 135, 225–6, 403, 503–4 and fn. 27, 506 Newark (England) 452 Newenham, Cistertian house of (England, Honiton) 472 Nidaros, see Trondheim Nile Delta (Egypt) 397 Njardvik (Iceland) 681 Nonantola (Italy northern) 66, 200 Nordic countries, see also Scandinavia 10, 30, 46, 57, 59–60, 63, 98–9, 102, 115, 124–6, 131–2, 134–9, 141, 216–7, 232, 301, 319, 322 fn. 30, 371, 395, 400, 406–7, 416–7, 512, 569, 609 fn. 230 Nordland (Norway) 472–3 Norfolk, county of (England southeastern) 430, 432, 579 Norrköping (Sweden) 217, 313 fn. 4, 549 Norrland (Sweden) 138 Northam 472–3 North Devon, see Devonshire North Sea 405, 407, 507, 648 North America, see America North Atlantic 119, 404, 494, 506 Northumberland (England) 632 North-West Passage 98, 112 Norton, manor (County Durham, England) 271 Norway, Norwegian(s) xv, 13–4, 16, 30, 59–60, 99, 102–3, 113, 115 and fn. 145, 119, 131, 136–40 and fn. 213, 143, 195 fn. 5, 225, 269–70, 304, 322, 327, 332 fn. 84, 385, 393–5, 399–403, 416–20 and fn. 61, 449, 464, 493, 501–7 and fns. 22, 40–1 and 45, 510–1, 527–31, 536, 538, 551–2, 576, 608, 648, 670 and fn. 7 Norwich (England) 304 Norwich, diocese (England) 449 Nottinghamshire (England) 452 Novgorod (Russia) 364, 521 Nuremberg (Germany) 507 Ny-Varberg, convent (medieval Denmark, Halland), see also Varberg 133, 135

Örebro, county (Sweden) 133 Öland I. (Sweden, in the Baltic) 133 Orient(al) 98 Orkney I. (Scotland) 129 Oslo (Norway) 10, 103, 111, 115, 124, 186, 225, 371, 393–4, 400, 403–4, 670 fn. 7 Otter R. (England) 453, 466, 472 Ottery St Mary, collegiate church (England, Devon) 453, 466, 472 Oxford, town (England) 435, 508–9 Oxford, University of 29, 385, 566 Oxfordshire, county of (England) 465 Padua (Italy) 351, 353–4 Palatinate, Upper (Germany, region) 330 Pale (medieval eastern Ireland) 114, 465, 477 Pali (India) 43 Parel, village (India, near Mumbai) 102–3, 153, 157, 159 Paris 9, 39 and fn. 39, 113–4, 134, 221, 237, 242, 324, 326, 355, 371, 389–92, 586, 593 and fn. 158 Parma (Italy) 326 Patiala State and city (India, the Punjab) 154 Penrith (England) 284, 287, 410 and fn. 37, 608, 617, 631, 638–44, 646 and fn. 127 Persian Gulf 328 Peru 397 Pfäfers (Switzerland) 404 Piacenza (Italy northern) 548, 589 Piedmont (Italy, region) 201, 298, 352 Pilton, manor (England, Somerset) 478 Pisa (Italy) 413 Pithay, parish, (Bristol, England) 147 Plymouth (England) 295 Poitiers (France) 201 Poland 7, 131, 269 and fn. 178, 331, 394 Polar regions 41–7 Pompeii 124 Poona, see Pune Portishead (England, Somerset) 477 Portugal 648 Prato (Tuscany, Italy) 298 Provence (France) 190, 220–1, 298, 381, 383, 390–1 and fn. 32, 592 Pune (India) 140 fn. 224, 162–3, 198–9, 399

index of geographical names and people Punjab (India) 40, 58, 92, 94, 102, 118 fn. 150, 154, 163–4, 171, 200, 282, 291–3, 297, 399, 520, 623 Puy-Sainte-Réparade (France) 383, 390–1 Ragusa (present-day Dubrovnik) 588 Ramundeboda (Sweden) 133 Rangoon (Myanmar), see Yangôn Ratnagiri Collectorate, colonial term, (India, Maharashtra), see Harnai 153 Regensburg (Germany) 355 Reims, see Rheims Rheims (France) 324, 329–30, 400 Rhenish region (Germany) 521 Rhine R. 128 Rhône R. (France) 190 Ribe (Denmark) 403 Riez (France) 190 Rødøy, parish (Norway) 419 Rome 413–4, 574, 567, 659 Roman Empire (Western) 106, 127–8, 343 Rosario, port (Argentina) 654 Roskilde (Zealand I., Denmark) 409 Rostock, University of (Germany) 322 Rouen (France) 86, 114, 585, 593–4 and fn. 162, 661 Russia(n)/Soviet Union xv, 3, 10, 58, 134, 195, 210, 325–6, 394, 514, 518, 520, 523, 576, 580–1, 585, 604, 661, 690 Sahara(n) (Africa) 566 St Albans, town (England) 127 St Germanus Church (Stuttgart, Germany) 389 fn. 28, no. 6 St Giles’ Church (London) 554 St Martin’s monastery (Tournai) 237 St Olaves Church (London) 567 fn. 39 Sainte-Tulle (France) 190 Santa Maria Novella monastery and cemetery (Italy, Florence) 261

737

Salisbury, diocese (England) 437, 461, 463, 465, 467 Salon (France) 383, 390 Salten, bailiwick (Norway) 419 San Gimignano city (Tuscany, Italy) 298 Santo Spirito, quarter in Florence 68, 146 Saurbær (Iceland), see also Holt 681 Savoy, County of (now France) 241, 298 Scania (medieval Denmark)8 59–60, 133 Schleswig and Holstein, Duchies9 670 Scotland, Scottish 119, 201, 306, 310, 416, 503 and fn. 26, 510, 530, 631, 648 Seine R. (France) 114 Sens (France) 329, 389–91 and fn. 29 Sheffield (England) 307–8 Shetland Is. (Scotland) 118 Shiant Is. (Scotland, Hebrides) 119 Shropshire, county (England) 127 Siberia(n) 517 Sicily I. (Italy) 364, 548, 574, 581, 586–7, 590, 661–2 Siena (Italy), see also Camporegio and Necrology 218, 231, 245–68, 270, 273, 324–5, 675–79 Sigtuna (Sweden) 126, 132 Singapore 168 Sion, village (India, near Mumbai), see also Koliwada 94, 157–8, 170–1, 173, 176, 178, 189, 198 and fn. 13, 567 Skagen, part of Stavanger 136 Skálholt (Iceland, cathedral city) 531, 536–7 and fn. 120, 551, 680–1 Slavic territories 131 Smuszewo (Poland) 131 Solent strait of (England) 480 Småland (Sweden)10 Söderhamn (Sweden northern), see Hälsingland Somerset, county (England), see also Bath and Wells 114, 450, 459, 466, 474–80 Sound (between Denmark and Sweden) 59, 132–3, 135, 670 fn. 7

8 Scania was a Danish province until mid-seventeenth century when it was conquered by Sweden together with Halland and Blekinge and the Norwegian areas Båhuslen and Jemtland. 9 The Duchies of Schleswig and Holstein were under the Danish Crown at the time. 10 Småland was Sweden’s southernmost province until the conquests of the midseventeenth century.

738

index of geographical names and people

South America, see America South Africa(n) 87–9, 88, 191 Southampton (England) 309, 480 South Wales (Australia, region) 46 Soviet Union, see Russia/Soviet Union Spain, Spanish 269, 294, 198, 303, 576, 648, 661 Spalato (present day Split, Croatia) 588 Split, see Spalato Sri Lanka (Ceylon) 52–3, 95–6, 185–6 Stad (Norway) 505 Stavanger (Norway), see also Skagen 136, 403 Stepney (in London) 554, 562 Stettin (Szczecin present-day Poland) 131 Stockholm (Sweden) 126, 132–3, 507 fn. 45 Stour R. (England) 405, 465, 432, 480 Stuttgart (Germany) 389–90 and fn. 28, no. 6, 392–3 sub-Arctic regions, see also Arctic 416–8 and fn. 61 sub-Saharan Africa 636–7 Sudan 636 and fn. 91 Sudbury (England) 465, 480 Suffolk, county (England) 405, 430, 432, 480 Sungari R. (Manchuria) 515 Surabaya (Indonesia, Java) 168 Surrey, county (England) 479 Sussex, county (England) 127, 479 Swanick, manor (England, Hampshire) 481 Sweden, Swedish 11, 59–60, 99, 119, 126, 133, 138–40, 216–7, 313 fn. 4, 327, 394–5, 403, 407, 507 and fn. 45, 531, 549–50, 572, 670 fn. 7 Switzerland, Swiss 127, 371, 404–5 Sydney (Australia) 48, 51, 93 Syria(c) 328, 581, 585–6, 661 Tavastland, county (Finland), in Finnish Hämeen lään 139 Taw R. (England, Devon) 473 Thuringia (Germany, region) 326 Thykkvabær (Iceland) Titchfield, manor (England, Hampshire) 480, 482 Tiveden, district (Sweden) 133

Tiverton (England, Devon) 295, 473 Tolkmicko (Poland) 131 Tønsberg (Norway) 136–7 Torridge R. (England, Devon) 472 Toulon (France) 382 Tournai (Low Countries) 237, 242 Trebizond (Asia Minor/Turkey) 588 Trøndelag (Norway) 428 Trondheim (medieval name Nidaros, Norway) 113, 115, 136, 400–2, 419, 505 Tropical zones 120, 141, 396, 416 Tunis(ia) (Africa North) 569, 588 Turkey, see also Asia Minor 328 Tuscany (region, Italy) 302, 353, 412–3 Tyras, ancient Greek settlement 588 fn. 132 Tyrol(ese), see also Alps 404 Uelzen (Germany) 143 Ugborough (England, Devon) 295 United Provinces (colonial India) 163 Uppsala (Sweden) 133 U.S.A., see America Uzbekistan 364 Vadstena, convent (Sweden) 507 Värmland (Sweden) 138 Västergötland (Sweden) 133, 403 Valkenburg, village (Netherlands) 127 Valle Susa (Piedmont, Italy) 298 Varberg (medieval Denmark, Halland),11 see also Ny-Varberg 133, 670 fn. 7 Venice, Venetian 8, 104, 191, 216, 302, 349, 357 fn. 143, 404, 569, 587–9, 594, 662 Venice and Terrafirma (Italy) 302 Verdun (France) 386 Vestfjords, area of (Iceland) 510, 681 Videy (Iceland) 680 Vienna (Austria) 329, 388–391 and fn. 31 Vietnam(ese) 3, 44–5, 193, 233–4, 315–6, 377, 520–1 and fn. 82, 524, 545, 566 Vikings 118, 131, 134 Viking Period/Age 125–6, 132–4, 140, 395 Visby (Sweden, Gotland I.) 133, 140, 403

11 Varberg was Danish until the mid-seventeenth century when conquered by Sweden.

index of geographical names and people Vitrolle (France) 190, 383, 390 Vladivastok (Russia) 514 Wadhala, village (India, near Mumbai) 157–8 Wales 364, 518 Waltersdorf (Germany) 131 Walton, manor (England, Somerset) 478 Walton, hamlet (England, Buckinghamshire), see also Aylebury 127–8 Westminster (England, city of London) 567 Westminster Abbey (England, London) 229 fn. 89, 428–9 Weston-super-mare (England, Somerset) 477 Westphalia (Germany, region) 326 West Chickerell, parish (England, Dorset) 468 Weymouth, see Melcombe Regis Widworthy, parish of (Devon, England) 295 Wiltshire, county (England) 465–7, 469–70, 474

739

Winchester, diocese (England) 241, 449, 463, 479, 482 Wittenberg (Germany) 327 Worcester, diocese (England) 449, 458, 460, 475 Worcestershire, county (England) 241, 271 Worli, village (India, near Mumbai) 157–8 Wroxeter (England, Shropshire) 127 Yangôn, formerly Rangoon (Myanmar) 166, 168, 185–6 York, city (England) 127, 151, 631 York, diocese (England) 152, 439–42 and fn. 137, 446–7, 449, 603 Yunnan (China) 621 fn. 34 Zadar (Croatia, Dalmatian coast), see Zara Zara, Venetian port (present-day Zadar, Dalmatian coast) 588 Zealand I. (Denmark) 409

INDEX OF NAMES1 Aboudharam M. 381, 392 fns. 35–6 Aberth J. 56, 179, 450 Abbey H. 634 Absalon Pederssøn Beyer, Norwegian humanist 332 fn. 84, 401–2, 407 Ackerknecht E.H. 669 Adam of Murimuth, chronicler 223 Adelberg E.A., see Jawetz, Melnick and Adelberg Advisory Committee for Plague Investigation in India 108, 624 Agnolo di Tura, chronicler 247–8, 250, 265, 276 Alfani G., see Cohn Alfred the Great, King 131 Ali(Oli) Svarthöfdason, Icelandic priest 680 Al-Maqrizi, Arab chronicler 586 Allen C.F., Danish historian 670 Andrew Hogson, plague victim in Penrith 284, 639–40, 646 Arthur P. 482 Asgrimur, Abbot (Icelander) 681 Audoin-Rouzeau F. 11–2 Audoin-Rouzeau F and Vigne F.-J. 126, 129 fn. 178, 136 Axon W.E.A. 287 Bacot A. 119 Bailey M. 601 Baltazard M., see Blanc and Baltazard Bannerman W.B. 153–4, 159 fn. 28, 203 fn. 35, 291 Baratier E. 220, 592 Barnes J. 560, 577 Bath and Wells, diocese of, bishop, see Ralph of Shrewsbury

Bell W.G. 216, 310, 333, 374–5, 549, 569, 657 fn. 172 Belletini A. 229 Benedetti Alessandro, physician 350 Benedictow O.J. xv–xvi, 5 fn. 5, 8 fn. 13, 9–12 and fns. 14, 28–9, 16–7 and fn. 40, 19, 30–1, 37–8, 44–6 and fn. 52, 50–2, 56–60, 62–3, 67–9, 74–5, 91, 96–9 and fn. 74, 103, 107–9, 111, 113–5 and fns. 142 and 145, 119 fn. 153, 124 fn. 164, 126–8 and fn. 167, 130, 135–7, 140 fn. 224, 146, 148, 152, 169, 171–3, 176–7, 186–7 and fn. 98, 191–2, 195, 199–201, 203 fn. 35, 210 and fns. 18–9, 213, 215, 217, 219–20 and fn. 69, 225, 229 and fn. 89, 232, 238, 240–1, 243, 246, 252, 259, 261, 264 and fn. 171, 267, 269 fn. 178, 273, 279–80 and fn. 3, 287 fn. 28, 290, 294– 8, 300–2, 307–8, 314–5, 322, 324 and fn. 38, 330 fn. 77, 332 fn. 84, 334, 336, 341, 349, 352 fn. 129, 358–9, 368 fn. 176, 370, 377 and fn. 205, 385, 390 fn. 28, 393–4 and fn. 39, 396, 398, 400–2, 416, 418 fn. 61, 420 fn. 66, 432 fn. 104, 436, 438 and fn. 129, 441, 445 fn. 144, 450 and fn. 150, 463–5 and fn. 192, 471 fn. 206, 478, 487, 490, 492–3, 495–501 and fns. 8, 11, 503–4 and fns. 30–1, 506, 511–2, 516–21 and fn. 68, 527, 529, 531–2, 534 fn. 115, 536–8 and fn. 118, 540–3, 545–7, 550, 554–5, 558 and fn. 14, 564, 567 and fn. 39, 569, 578 and fn. 86, 584–5, 590 fn. 143, 593–4 and fns. 157, 160, 598–9 and fn. 188, 602–4, 607 fn. 224, 609 fn. 230, 612, 629, 631 fn. 74, 656, 670 fn. 7, 680, 685

1 (1) The Index of Names registers personal names and names of institutions in the running text, also supplementary information and comments in fns. but not authors of works referred to in the fns. (2) Medieval and classical persons are entered according to Christian name, except in the cases of persons who are normally or systematically known by surnames; modern persons are entered according to surname. (3) Regarding special letters, see introduction to the Index of Subjects, fn. 1, no. 3.

index of names Berglund J. 99 Bertrand J.B. 214, 217 Berthe M. 294 Beverwijk van J., Dutch physician 333 Bibikova V.A. and Klassovskij L.N. 58 Biraben J.-N. 333, 586 Biraben J.-N. and Le Goff J. 390 fn. 29, 514 Björn Olafsson, Icelander, later priest at Krysuvik 681 Blanc G. and Baltazard M. 9–15 and fn. 28, 29–31, 58, 110 Block G., Swedish physician 216–7, 313 fn. 4, 549 Boccaccio G., Italian author (1313– 1375) 201, 344, 359–80 and fn. 180, 618 and fn. 27, 645 Brachman P.S. 556 Bradley L. 62–3, 67–9, 410, 561–2, 643, 645, 647 Bridbury A. 273 Brossollet J., see Mollaret Brygoo E.-R. 58, 619 Burnet E.M. (and White D.O.) 289–90 and fn. 410–1, 414 Burroughs A.L. 683–4 Butler T. 10–1 and fn. 18, 25, 44–6 and fn. 52, 193, 315–7 and fn. 20, 319, 377–8, 545, 612 Byrne E.H. 588 Campbell B.M.S. 577, 579 Cantey J.R. 545 Cantor N. 56, 179 Carmichael A. 54–5, 68, 84, 146, 231, 235, 264, 325 fn. 44, 359, 370–2, 400, 584–5, 616 and fn. 14 Carpentier É. 237, 239–40, 584 Castiglioni A. 352 Cazelles M.R. 147, 236–7 and fn. 109, 240, 242–4, 268 CDC, see Centers for Disease Control (and Protection) Centers for Disease Control and Protection 3, 11–2, 649, 652, 660 Chalin de Vinario 233, 357 Chandler A.C. and Read C.P. 627 Charlemagne 574 Chenot A. 214 Christian, Prince of Denmark 670 fn. 7 Choksy K.B.N.H. 366, 624, 626 Christie A.B. 88–90, 388–9, 613, 621–8, 653, 682, 684–5 Ch’uan, physician 516

741

Chun J.W.T 90, 316, 375–6, 539, 543, 567, 571, 619–20 and fn. 34, 622 Ciano C. 209 Cipolla C.M. 60–1, 209, 226, 293–4, 352–3, 658 Clark Ronaldson W. 154 Clot-Bey A.B. 214–5 Cohn S.K., Jr. 16–9, 21–2, 25–69, 74–7, 85–6, 93, 96, 98, 135–6, 144–5, 148–52 and fn. 3, 154, 156, 164, 169–80, 182, 184, 186, 194, 196 and fn. 7, 200–1, 204–5, 207–8, 211–68 and fns. 47, 136 and 168, 273, 283, 289–94 and fn. 17, 297, 299, 314–7, 321, 323–6 and fns. 33, 44–5, 333–4 and fn. 88, 340–80, 386–7 and fn. 20, 389 fn. 28 no. 6, 392–3 and fn. 35–6, 400–2, 410–5, 464, 487–8, 490, 495, 541, 562, 608–9 and fn. 230, 647, 664–72 Cohn S.K. and Alfani G. 66, 200, 647, 664 fn. 2 Coleman M.P. 410, 643, 647 Collie, Major 153 Commander of Akerhus Castle (Oslo), see Peder Hansen (Litle) Commodus, Roman Emperor (180—192 ce) 343 Cooper A. 384–5, 387 Cosmacini G. 215 fn. 46 Coulton G.G. 449, 472 Court of Hustings (London), see Wills Cox J.C. 467, 567 fn. 39 Creighton C. 36–7, 81, 242–3, 257 fn. 156, 309–10, 333, 335–6 and fn. 100, 475 fn. 218, 507–10, 560 and fn. 21, 589–90, 615–9 Dang L.V. 387–8 Dante Alighieri (1265–1321) 343 Davis D.E. 73–4, 76, 98–121 and fn. 47, 226, 234–5, 246–7, 250–1, 413–4 Davis R.A. 454 and fns. 162–3, 461 Defoe D. 83 Devignat R. 387 de Langen C.D. and Lichtenstein A. 58, 96, 212, 543–4 Del Panta L. 209, 215 fn. 47, 226, 234–5, 246–7, 250–1, 413–4 Diocletianus, Roman Emperor (284–305) 343 Dijkstra J.G. 67–8, 146 Diemerbroeck I. 216–7 D’Irsay S. 572–3 Dörbeck F. 58

742

index of names

Dohar W.J. 456–7 Dols M.W. 56, 583, 585–7, 662 Drancourt M. 12 fn. 28, 192, 381, 385–7, 392 fn. 35–6, 395 fn. 42 Dubois H. 226, 236, 330 and fn. 17, 400, 405, 514 Duncan C.J., see Scott and Duncan Duncan S.R., see Scott, Duncan and Duncan Dutour O. 381, 292 fn. 35 Ecclestone M. 241 Eckert E.A. 521 Eldevik T. 139 fn. 213 Engelsen R. 143 Eske Bille, Chancellor of the Realm, Denmark 404, 409 Eskey C.R. 376 Eskey C.R. and Haas V.H. 682–3 Estrade F. 58, 180 Evagrius 214, 217 Fenyuk B.K. 58 Fetherston J., see Perry Ficino Marsilio, physician (1433–1499) 215 and fns. 46–7, 350, 352, 357 Fitzgerald D.A. 654–5, see also Savage Fiumi E. 226, 619 Fletcher J.M.J. 467–8, 470 Fracastoro G., Italian physician (1484–1553) 322 Frost W.H., see Reed Furness W. 617 Gabriele de Mussis 548–9, 589–90 Galen(os), Greek physician (c.130–c. 200 ce) 356 see also Index of Subjects: Galenic Galfrid le Baker, chronicler 332, 557 Gallienus, Roman Emperor (253–268) 543 Gasquet F.A. 108–9, 438–9 and fn. 129, 450, 454–60 and fns. 161 and 170, 466–7, 470–2, 477, 479, 553, 560–1, 565, 572, 583, 587, 589–90, 592–3 and fn. 158, 602, 605–6 Gatacre W.F., Brigadier-General 371–4 Gatari, Galeazzo, Bartolomeo, Andrea, brothers and chroniclers of Padua 351–2 Genicôt L. 273 Geoffrey le Baker, chronicler 242–4, 332–3, 557

George Leene, plague victim, son of William Leene 287–8 Gilbert M.T.P. 384–7 and fn. 20, 392 Gillaume de Machet, poet 329 Gille, see le Muisit Gillingham, Squire of 466 Giovanni (di Pagnolo) Morelli, chronicler 347, 413 Giovanni da Parma, chronicler 346 Giovanni da Santa Sofia, professor of medicine (d. 1389) 353–4 Girard G. 9–10, 58 Giseler G.O. 216 Glénisson J. 240, 268 Gottfried R.S. 56, 225, 293–4, 296, 430–2 and fn. 104 Grandisson, Bishop, diocese of Exeter 455 Gras P. 108 Greenwood M., member of IPRC 3, 33–4, 41, 58, 163–4, 227, 291–4 and fn. 17, 296, 567 Gregory of Tours, Bishop 283, 327, 329 Grimus, Friar, priest in the church of Skálholt, Iceland 680 Guaineri Antonio, physician 357 Guy de Chauliac, papal physician in Avignon 109, 534 fn. 115 Gudrun Halldordsdottir, Abbess consecrated at Thykkvabær, Iceland 680 Hårding B. 126 Haas V.H., see Eskey Håkon V, King of Norway 531 Haffkine W., see also Haffkine’s antiplague vaccine 196 Hallam E.H. 601 Halldora, Abbess at Kirkjubær, Iceland 680 Hankin E.H. 34–44, 59, 112, 158, 236, 281–2, 289–96, 303, 646, 668–9 Harrod H. 561, 579 Harvey B. 229 fn. 89, 429, 432 Hatcher J. 221, 224, 226, 229 and fn. 89, 417 fn. 59, 422–3, 425–30 and fns. 87 and 93, 432, 474, 500 fn. 17, 508, 510, 531, 561, 595–8, 600–1, 603–5, 607 fn. 224, 632 Hatcher J., Piper A.J., and Stone D 229 fn. 89, 428 fn. 87, 430 fn. 93 Hatcher J., see Miller Hecker J.F.K. 560 and fn. 21, 572, 577, 583 and fn. 104, 585–6

index of names Henry Knigton, chronicler 223, 272–3, 480 Henry of Hervordia, chronicler 242 Herlihy D. and Klapisch-Zuber C. 232 and fn. 97, 264 fn. 171, 273, 412–4, 619 Hingeston- Randolph, Rev. Prebendary 450, 471 Hirsch A. 109, 111–2 and fn. 132 Hirst F.L., see also Philip 3, 9–10, 25–32, 35, 45–6, 50–5, 73, 75–6, 81, 95–6, 98, 109–10, 112–3, 120–1, 166, 178–80, 183–7, 193, 196 fn. 7, 203 fn. 35, 234, 282, 286, 321, 375, 432 fn. 104, 491 fn. 8, 523, 540, 544, 564 fn. 32, 567, 571– 2, 582, 612, 616, 619, 622–3, 625, 643 fn. 113, 684 Hodges N. 216 Hörnick von L. 216 Höskuldar, Councillor at Skálholt, Iceland 680 Hollingsworth T.H. 596 Hufthammer A.K. 73 fn. 1, 136 Ibn Khatimah, chronicler 55 James T.B. 119 fn. 154 Jankibai, Indian 157 Jawetz E., see Jawetz, Melnick and Adelberg Jawetz, Melnick and Adelberg 558, 562–3 Jean de Venette, chronicler 80, 223, 236, 268–9 Jehan de Blanzy, burgher of Rheims 329 Joakim Beck, Chancellor of the Exchequer, Denmark 409 John Clyn, Friar of Kilkenny, chronicler 332, 491–2, 557, 612 John of Reading, chronicler 223 Jón Oddsson 681 Kang-Hsi, Emperor (China) 620 fn. 34 Karlsson G. 16–9, 76–7, 194, 283, 290, 299, 312, 321, 394, 480, 487–8, 490– 552, 608, 665, 680 and fn. 3, 691 Karlsson G. and Kjartansson H.S. 493, 495 fn. 6, 501 Kinch J. 60 Kirchoff G. 213, 217 Kitasato S. 25 Kjartansson H.S., see Karlsson Klapisch-Zuber C., see Herlihy D. Klassovskiy L.N., see Bibikova

743

Klein I. 49 and fn. 60, 179 Klimenko V.C. 58, 520 Konrad von Megenberg, natural scientist 355–6 Kosminsky E.A. 604–5 Krummedike Henrik, Norwegian and Danish Councillor of the Realm 670–1 and fn. 7 Krummedike Sofie, daughter, 670–1 Krüger S. 355–6 and fn. 137 Lamb G., Senior Member of IPRC 33 and fn. 24, 41, 48–9, 75, 94, 109, 158–9 and fn. 28, 161, 195, 203 and fn. 35, 396–7, 623–4 Langen de C.D. and Lichtenstein A.A. 58, 96, 212, 543–4 Langer W.L. 584 Leclainche E. 573–4 Leeuwenhoek von A. 80 Le Goff, see Biraben Lepiskaar J. 133 Le Roy Ladurie E. 56, 179, 417 Li C.C, see Pollitzer and Li Lichtenstein A.A., see Langen de Liston W.G., member of IPRC 3, 33, 41, 88, 90, 153, 156, 164–5, 567 Livi-Bacchi M. 226, 246–7, 261 Loghem van J.J., see also next entry 75, 78, 97 Loghem van J.J. and Swellengrebel N.H. 3, 58, 75, 78, 96, 111, 167–9, 176–7, 179, 182–3 Lomas T. 271 London, diocese of, bishop, see Ralph Stratfort Lopez R.S. 104, 107, 588 Lunn J. 439, 449–52, 474 fn. 163, 457, 461, 463, 467–8, 470–2, 479, 483–4, 603, 628 Lysenko T.D. xv Machiavello A. 180 fn. 78, 376 McArthur W.J. 3 McCormick M. 119, 126–9 and fn. 178, 140 McNeill W.H. 500 and fn. 17 Magnus Eriksson, king of Norway and Sweden 327 Maia J. 633–4 Malmborg G. 133 and fn. 192, 140 fn. 233 Mansa F.V 504

744

index of names

Marchionne (di Coppo) Stefani, chronicler 265, 326 Marcus Aurelius, Roman Emperor (161–180 ce) 343 Martin C.J. 109–10 Martinez Dr. 376 Massaria A. 215 Matheson C. 128 Mead R. 561 and fn. 24 Melnick J.L., see Jawetz, Melnick and Adelberg Meyer K., see also Pollitzer 212 and fn. 26, 512 Michele da Piazza/Michael of Piazza, Franciscan friar 333 fn. 88, 360 fn. 155, 548–9 Miller E. and Hatcher M. 601 Mollaret H.H. and Brossolet J. 56 Mompesson W., Rector of Eyam 614 Morony M.G. 328 Morris C. 16–7, 19, 312, 321, 332, 410, 487–93, 496–9, 512–4, 518–9, 533–5 and fn. 115, 691 Muisit le G. 236–7, 242

Petrarch Francesco (1304–1374) 618 and fn. 27 Petrie G.F. 58, 95, 166, 182 Pettenkofer M. von 619 Philip W.M. and Hirst L.F. 625 Pickard R. 438 fn. 129, 450, 453–4 and fn. 161, 471, 475, 603 Piper A.J., see Hatcher, Piper and Stone Planck? 112 Pollitzer R. 3, 7 and fn. 8, 9–10, 13 and fn. 35, 31–2, 45, 75, 90, 101–3, 113, 118–20, 142, 181–7 and fn. 85, 193, 207–8, 212–3, 280 fn. 3, 314–6, 321, 375–6 and fn. 200, 378, 525, 539, 544–5, 554, 567, 571, 612, 619–20 and fn. 34, 622, 647, 685 Pollitzer R. and Li C.C. 526, 528 Pollitzer R. and Meyer K. 177–80, 184, 529, 683 Postan M.M. 226, 596, 588 Pounds N.J.G. 220 fn. 68, 588 Prat G. 237, 239–40, 242, 244 Procopius, Byzantine physician 328 Pusch C.M. 389 fn. 28 no. 6, 392

Narajan Laxuman, Indian, 157 Nash A.E. 147 and fn. 243 Naso I. 352 Nikephoros Gregoras, historian/ chronicler 82 Nohl J. 321, 333 fn. 88, 369 fn. 180 Noordegraaf L. and Valk G. 226 Nybelin O. 138

Ralph Shrewsbury, bishop of Bath and Wells (1329–1363) 459 Ralph Stratford, bishop, diocese of London (1340–1354) 465 fn. 192, 479–80 Ramji Motiram, Indian 157 Raoult D. 12 fn. 28, 192, 381, 38–7, 392 fn. 35 Ravensdale J. 27 Razi Z. 241, 271, 478, 598 Read C.P., see Chandler Reed L.J. and Frost W.H. 633–6, 640, 648 Rees W. 577–8 Roux V. 387–8 Runolf, Friar of Thykkvabær 680 Russell J.C. 226, 421–6, 429–30, 432, 435–6, 438, 460, 475, 479, 596–602, 605–7 and fn. 224, 630 Russell P. 214

Odysseus (Ulysses) 363 Ohlin G. 596, 599 Orosius, Roman historian 131 Orraeus von G. 214 and fn. 37 Orrman E. 516–7 and fn. 68 Ottar, Norwegian Viking merchant and explorer 131 Pál, Abbot in Videy, Iceland 680 Palmer R.J., see also Zitelli 43, 349–51 and fn. 124 Peder Hansen (Litle), Commander of Akerhus Castle (Oslo) (1536–1551) 404 Perroy E. 237, 239–40, 244 Persson B.E.B. 11 Perry D.P. and Fetherston J. 11, 683, 685 and fn. 17

Sabine E.L. 579 Samoilowitz D. 214 St Germanus 389 St Remi 329 Savage W.G. and Fitzgerald D.A. 654–5 Savio P. 657

index of names Schofield R. 62–9, 45–6, 202–3, 226, 234, 406–7, 415 Scott S. 207, 610 Scott S. and Duncan C.J. 16–9, 66, 76–7, 82–4 and fn. 33, 87–91, 98–9, 127–30, 151, 156–8, 164, 172, 178–91, 194, 199–200, 205–14, 217–8, 221, 284–5, 287–8 and fn. 28, 290, 293, 298–9, 301–11, 321, 334–40, 385–6 and fn. 20, 398, 407, 410–1, 415–7, 419–20, 436–7, 439, 442, 445–6, 462–5, 468, 470–2, 474, 482–4, 487–8, 490, 495, 499, 503, 554, 562, 581, 584–6, 590–1, 595, 600, 608, 610–63, 665, 668 Seebohm F. 438, 602, 605–6 Segal A.E., see Vasil’ev Sellers M. 631 Shirk M.V. 294 Shrewsbury J.F.D. 16–7, 19, 30, 54, 128, 151, 223, 226, 278, 283, 285 and fn. 21, 287 fn. 28, 333, 398, 407, 420, 433, 437–9, 449–51, 453–4, 457, 461–4, 467–8, 470–1, 475, 479, 483–4, 487, 489–92, 496, 498, 501, 503–4 and fn. 26, 507–10, 512–3, 552–3, 560, 562, 572, 628, 631, 643, 647 Sigurðsson J.V. 516–7 fn. 68 Simon of Couvin 39–40 and fns. 38–9, 42, 236 Simond P.L. 43, 281–2, 646 Simpson W.J. 3, 40–1, 108–9, 153, 196, 202–3 and fn. 35, 366–7, 373–6, 378, 542–3, 545, 554, 567–8 and fn. 39, 570, 612, 656 Singleton C.S. 395 fn. 153 Slack P. 56, 62, 68, 146–7, 179, 209–10 and fn. 18, 226, 287, 294–6, 304, 306, 309–11, 322, 333, 415, 432–3, 435, 508, 510, 614–5 Smith R.M. 601, 605–6, 632 Snorri Sturluson 137 Steffensen J. 493, 500, 502 fn.23, 504, 506–12, 514–5, 519, 522, 526–30, 532, 535–8, 540–2, 550, 552 Sticker G. 3, 143, 213–5, 221, 282, 284, 314, 322, 324 fn. 38, 326, 330 fn. 78,

745

331, 363 fn. 159, 369 fn. 180, 504, 507, 520, 548, 554, 567, 570–1 and fn. 50, 574–5, 612, 619, 622, 646 Stone D, see Hatcher, Piper and Stone Sudhoff K. 341 Sutherland I. 356–7 Swellengrebel N.H., see also Loghem van 58, 96, 111, 167–9, 176–7, 179, 182–3 Swinnas W., Dutch physician 333 Sydenham T. 619 Taylor J. 435 Thomson G.M 98 Thompson Ashburton J. 46–53, 93–5, 111, 155–6, 174–5 Thompson A.H. 151–2, 439–42 and fn. 137, 446, 449, 452, 602–3 Thorlak, ship owner, Icelander 536 fn. 128 Thorstein, priest at Helgafell, Iceland 680 Titow J. 596 Twigg G. 16–7, 19, 76, 78, 85, 87, 96, 98–9, 103, 117, 119–23, 128–30, 138, 140, 151, 153–4, 156, 164, 170, 172, 177–8 and fn. 67, 180–6, 188, 191, 194, 205, 220–1, 283–4, 290, 292–3, 317–8, 327–8, 405, 407, 411, 415–6, 419–20, 422–3, 425, 435–9, 442, 445–6, 449, 461–5, 468, 470–1, 474, 482–4, 487–8, 490, 495, 553–611, 615, 621 fns. 34 and 36, 628–30, 661, 665 Ulsig E. Danish historian 60 Vahtola J., Finnish historian 99 Valk G., see Noordegraaf Vasil’jev2 K.G. and Segal A.E. 58 Valerianus, Roman Emperor (253–260) 343 Veale E.M. 578 and fn. 86 Vigne F.-J., see Audoin-Rouzeau Vilar R. 294 Villani Filippo, chronicler 324

2 The phonetical symbol l’ refers to the phonem palatalized l, phonetically written lj.

746

index of names

Villani Giovanni, chronicler 344, 347, 531 fn. 108 Villani Matteo, chronicler 243 fn. 136, 258, 323–5 and fns. 34, 43–4, 360, 413 Villani brothers 344 Viverius Jacobus, Dutch physician 333 Vogel de, Dr 168, 182–3 Wakil A.W. 58 Walløe L. 12–15 and fn. 29, 400–2 and fn. 18 Weber M. 104 White D.O., see Burnet WHO, see World Health Organization Wigh B. 132 and fn. 186 World Health Organization 3, 11–3, 556 fn. 6, 558 fn. 15, 649–50, 652 and fn. 152, 660 William Dene, chronicler, monk of Rochester 448 William Leene, plague victim, see also George Leene 287–8 Woehlkens E. 68, 143–4, 146

Wood W. 561–2, 654 Wrigley E.A. 226 Woodall J. 216 Wood-Legh K.L. 450 Wu C.Y. 166–7, 179, 539, 567, 620, 622 Wu Lien-Teh 3, 31–2, 45, 75, 90, 97, 113 and fn. 137, 142, 172 fn. 55, 208, 213, 321, 498–500 and fn. 17, 512–26 and fns. 66 and 70, 529, 534 fn. 115, 538–9, 554, 567, 612, 619–22 and fn. 34, 627 Yersin A. 25, 92, 314, 316, 337, 617 and fn. 20 Ziegler P 439, 441, 450 and fn. 150, 472, 553–4, 572, 578, 584, 591–3 and fn. 158, 611 Zinsser H. 490 Zitelli A. and Palmer R. 54, 449–51 and fn. 124 Zouche William 452