Exotic Small Mammal Care and Husbandry

Exotic Small Mammal Care and Husbandry

Exotic Small Mammal Care and Husbandry

Ron E. Banks, DVM, DACLAM, DACVPM, CPIA Julie M. Sharp, DVM Sonia D. Doss, M.Ed., RLATG Deborah A. Vanderford, DVM

All authors are staff at the Office of Animal Welfare Assurance, Duke University, Durham, North Carolina

A John Wiley & Sons, Inc., Publication

Edition first published 2010 © 2010 Ron E. Banks, Julie M. Sharp, Sonia D. Doss, Deborah A. Vanderford Blackwell Publishing was acquired by John Wiley & Sons in February 2007. Blackwell’s publishing program has been merged with Wiley’s global Scientific, Technical, and Medical business to form Wiley-Blackwell. Editorial Office 2121 State Avenue, Ames, Iowa 50014-8300, USA For details of our global editorial offices, for customer services, and for information about how to apply for permission to reuse the copyright material in this book, please see our website at www.wiley.com/wiley-blackwell. Authorization to photocopy items for internal or personal use, or the internal or personal use of specific clients, is granted by Blackwell Publishing, provided that the base fee is paid directly to the Copyright Clearance Center, 222 Rosewood Drive, Danvers, MA 01923. For those organizations that have been granted a photocopy license by CCC, a separate system of payments has been arranged. The fee codes for users of the Transactional Reporting Service are ISBN-13: 978-0-8138-1022-5/2010. Designations used by companies to distinguish their products are often claimed as trademarks. All brand names and product names used in this book are trade names, service marks, trademarks or registered trademarks of their respective owners. The publisher is not associated with any product or vendor mentioned in this book. This publication is designed to provide accurate and authoritative information in regard to the subject matter covered. It is sold on the understanding that the publisher is not engaged in rendering professional services. If professional advice or other expert assistance is required, the services of a competent professional should be sought. Disclaimer The contents of this work are intended to further general scientific research, understanding, and discussion only and are not intended and should not be relied upon as recommending or promoting a specific method, diagnosis, or treatment by practitioners for any particular patient. The publisher and the author make no representations or warranties with respect to the accuracy or completeness of the contents of this work and specifically disclaim all warranties, including without limitation any implied warranties of fitness for a particular purpose. In view of ongoing research, equipment modifications, changes in governmental regulations, and the constant flow of information relating to the use of medicines, equipment, and devices, the reader is urged to review and evaluate the information provided in the package insert or instructions for each medicine, equipment, or device for, among other things, any changes in the instructions or indication of usage and for added warnings and precautions. Readers should consult with a specialist where appropriate. The fact that an organization or Website is referred to in this work as a citation and/or a potential source of further information does not mean that the author or the publisher endorses the information the organization or Website may provide or recommendations it may make. Further, readers should be aware that Internet Websites listed in this work may have changed or disappeared between when this work was written and when it is read. No warranty may be created or extended by any promotional statements for this work. Neither the publisher nor the author shall be liable for any damages arising herefrom. Library of Congress Cataloging-in-Publication Data Exotic small mammal care and husbandry / Ron E. Banks . . . [et al.]. p. ; cm. Includes bibliographical references and index. ISBN 978-0-8138-1022-5 (pbk. : alk. paper) 1. Exotic animals. 2. Pets. I. Banks, Ron E. [DNLM: 1. Animal Welfare. 2. Veterinary Medicine. 3. Animal Husbandry. Animals, Domestic. SF 745 E96 2010] SF413.E96 2010 636–dc22 2009041421 A catalog record for this book is available from the U.S. Library of Congress. Set in 9.5 on 11.5 pt Sabon by Toppan Best-set Premedia Limited Printed in Singapore 1 2010

4.

Contents

Acknowledgments

vii

1

Introduction

3

2

Enrichment

11

3

Preventive Medicine

21

4

Rabbits

49

5

Ferrets

61

6

Mice

73

7

Rats

81

8

Gerbils

93

9

Hamsters

103

10 Guinea pigs

115

11 Chinchillas

125

12 Degus

137

13 Hedgehogs

143

14 Sugar Gliders

157

15

169

Opossums

Index

175

Color plate appears between pages 80 and 81

v

Acknowledgments

The authors acknowledge the many unnamed and on occasion unknown contributors to our education and training in the field of husbandry and veterinary medicine. No accomplishment is a singular achievement, and without the assistance of many this book would not have been possible. Thank you. It is the desire and hope of the authors that this text will be used for the betterment of the animals with which we share this globe and for improvement of the condition and environment in which they live. Our commitment to

strong and effective stewardship of the conditions in which we and animals live is the highest ideal one can assign to a human-and-animal relationship; the engaged manner of our compassionate care and our progressive husbandry is the best reflection of our humaneness. The authors wish to acknowledge Mr. Ian Thomas for all line drawing illustrations as well as the following individuals for assistance with photographs: Amy M. McArdle, CVT, LATG; Dan Johnson, DVM; Judi Fox, Cynthia Prevost, and Dorcas O’Rourke, DVM.

vii

Exotic Small Mammal Care and Husbandry

1

Introduction

The role of the veterinary technician continues to develop and mature. Although historically the duties allotted to the veterinary technician have been supportive and responsive—that is, do what you are told when you are told to do it—the current, progressive veterinary climate offers increasing levels of responsibility for engagement. Principal to the modern veterinary technician is the ability to have a dramatic impact on the well-being of the pet by educating the pet owner and assisting with building and maintaining a strong relationship of stewardship and compassion of the pet owner with the pet. To best accomplish this task, the veterinary technician must clearly understand the impact of a variety of factors, both intrinsic and extrinsic, and the role each factor may play in the health and well-being of the small mammal pet. Any list of factors that affect the well-being of a pet would be incomplete, but to provide an outline for this discussion we should consider those in the following list as having the potential to affect the pet’s well-being: • • • • • • • • • • •

Genetics Age Gender Immune status Circadian rhythms Endocrine system Cage design Bedding choices Cage accessories Enrichment strategies Watering options

• • • • • • • • • • • • • • • • •

Feeding options Temperature Humidity Thermal neutral zones Ventilation Illumination Noise Transportation Overcrowding Isolation Social ranking Handling Chemicals used in sanitation Air quality Water intake Feeds and diets Adventitial diseases

The take-home questions for any discussion such as this are: • What is the pet owner doing that may impact the well-being of the pet? • Is the impact of those actions improving or detracting from the well-being of the pet? We will discuss the factors affecting the pet’s well-being by considering those which are intrinsic and those which are extrinsic.

INTRINSIC FACTORS AFFECTING WELL-BEING

Intrinsic factors are those that are inherent to the animal, including genetics, age, sex, health, 3

4

nutritional status, immune status, circadian rhythms, and endocrine factors.

Genetics Although genetic factors generally are not a concern for small mammal species, excessive inbreeding may present a spectrum of disease states which interfere with the well-being of the pet. For example, malocclusion in a rabbit is highly heritable, especially in selected lines, and will interfere with normal nutrition and regular animal-initiated activities. Malocclusion may interfere with grooming, and it will interfere with selecting and chewing preferred foodstuffs. Pet owners should be discouraged from breeding their own pets because they generally do not have sufficient numbers of animals to provide a varied genetic stock and because additional animals may also add to the abundance of unwanted pets. Breeders must have genetic diversity if they are to maximize a strong and healthy population of pet animals. Even in the best of circumstances, mismating, spontaneous mutations, chromosomal aberrations, and residual heterozygosity may result in undesirable offspring. Afflicted offspring should be neutered; if not, at least they should be prevented from mating.

Age Neonatal animals have an immature immune system. That may oversimplify the situation, but it is important to note that the very young are susceptible to conditions or circumstances which would not be important to older animals. Rodents less than 1 week of age are exothermic, which means they cannot control their body temperature. Neonatal pups or kittens, when removed from the nest, will become hypothermic relatively quickly. As a general statement, these young animals begin to develop their “internal furnace” around 1 week of age, and by 6–8 weeks of age are fully capable of maintaining a steady core body temperature. Age becomes critically important when considering placement of the cage in a room where the windows allow sunlight and there is variable air flow. A stable, and even warm, place is important for the well-being of neonatal animals. Although not as pronounced, the same kinds of concerns exist for the very old animal too. In both cases the status of

Exotic Small Mammal Care and Husbandry

immune function is important as neither the very young nor the very old can successfully mount a strong immune challenge to infection. The geriatric animal is prone to increased disease states as the organ systems begin to fail; the young animal is prone to similar concerns, but because of physiologic systems that are not fully functional at the time of birth. This is often species dependent: a guinea pig is “precocious” and ready for all that life can throw at it, whereas a ferret requires weeks of nurturing and care to survive to healthy adulthood.

Gender Gender may also mark an important consideration for animal well-being. For example, 80% of New Zealand White female rabbits will have uterine adenocarcinoma by 4 years of age; males are not affected (as they obviously lack a uterus). Biomedical research has shown a clear distinction between the susceptibility of mammary tumors to certain chemicals and gender. In the Wistar-Furth rat, 100% of females, but only 19% of males, will develop mammary tumors to DMBA (a carcinogenic chemical used in breast tumor research).

Immune system Immunologic dysfunction (including hypersensitivity and allergy, autoimmunity, and immunodeficiency) may influence experimental outcome. A litany of agents or situations can alter immune function, such as age, nutritional status, a host of chemicals, various drugs, select food additives, many metals, and specific microbes. In certain circumstances, the immune response may be decreased (most common) or increased in response to the interference of outside agents.

Circadian rhythms Many behavioral, biochemical, and physiologic parameters (daily, rhythmic, minima and maxima) occur at specific times. For example, blood counts and coagulation times, plasma steroid, body temperature, sensitivity to audiogenic seizure induction (in gerbils), drug metabolism and toxicity (e.g., anesthesia and analgesia), and susceptibility to neoplasia are influenced by circadian rhythms. Although the veterinary technician may not be able to impact most of these items by modulating circadian

Introduction

rhythms, it is worthwhile to recognize that circadian rhythms may impact therapies, enrichment strategies, and outcomes of the pet patient.

5

approach is generally desirable (e.g., rodents’ preference for solid floors over wire floors), it must be managed for its effectiveness (e.g., a preference for sunflower seeds may interfere with generalized nutrition and well-being).

Endocrine factors Sex hormones are important determinants of hepatic cytochrome P450 enzyme activity. Castrating male rats decreases the ability to biotransform xenobiotics and, by extension, can affect the required amount of anesthetic for subsequent events (i.e., castration may extend the effectiveness and duration of anesthesia). Neonatal gonadectomy of select strains of mice leads to high incidence of estrogen-secreting adrenal tumors; so if small mammals are to be neutered, awaiting puberty in the species may be worthwhile. EXTRINSIC FACTORS AFFECTING WELL-BEING

Extrinsic factors are those that are external to the animal and include physical factors (macroenvironment vs. microenvironment, cage design, caging accessories), chemical factors (air, water, diet, and drugs), microbial agents, stressors, and environmental factors (temperature, humidity, ventilation, illumination, and noise).

Physical factors The single most important thing a veterinary technician can do is to stop thinking of small mammals as small humans. Just because humans would like something does not mean it is a good choice for the small pet. The focus of consideration for the pet’s well-being is the animal’s environment: The microenvironment is the environment immediately surrounding the animal. It may be the cage, the pen, the box, or the room. The microenvironment is where the animal lives. By extension, the macroenvironment is where the animal’s container is maintained—the macroenvironment is where the humans live. Although the macroenvironment contributes extensively to the microenvironment, one must be principally focused on the “nose of the beast” to achieve a preferred, healthful, supportive, and enriching microenvironment. One way to state it is “what is the animal’s preference?” Even though this

Cage design The style or design of the cage used for housing the animal affects its well-being. All other factors being the same, cage design can determine the amount of air, light, and sound the animal receives. Cage design can also impact the amount of heat, humidity, and gaseous waste dissipated into the macroenvironment. Again, all items being equal, plastics or polycarbonate caging materials tend to be an acceptable compromise for most situations. Plastics filter the light, diminish the sound, and foster a stable microenvironment (heat or cool). However, if not properly ventilated, plastics may also limit the amount of fresh air available and thus increase ammonia level, humidity, and the risk of airborne infection. Studies generally indicate that static (plasticwalled) caging is preferable to slatted wirewalled caging for most small mammals. Many pet owners choose slatted wire-walled cages because it allows for increased “communication and interaction” with their pet, but such caging can have significant disadvantages. For example, a slatted wire-walled cage will allow free exchange of air, but air flow through an accumulation of fecal matter is not a good idea. The preferred caging design is one that provides for normal physiologic and behavioral needs, allows conspecific social interaction, facilitates development of hierarchies within or between enclosures, remains clean and dry, has adequate ventilation, assures access to food and water, serves as a secure environment, is free of sharp edges, and allows an animal to be observed with minimal disturbance. Cage accessories should receive the same general consideration as caging materials. Items that come in direct contact with the pet should be nonreactive, nonpalatable, smooth and impervious, durable, corrosion resistant, and sturdy. In certain specific situations natural materials such as wood may be used, although the wood should be in the form of branches from pesticide-free trees, without signs of tree disease or damage, and replaced frequently to

6

prevent ingestion or allow for it to become unsanitary. Wood of certain trees may have undesirable products (e.g., tannins in oak, aromatic hydrocarbons in pine and cedar) that could negatively impact the pet animals, and therefore such wood should not be used. Galvanized metal and rubber stoppers may be used, but only if the animal shows no interest in chewing or licking the metal or rubber. Both the zinc in galvanized metal and the rubber of the stopper may have a negative impact on the animal’s well-being.

Water Too little water is not good and too much water is not good either. Water should be checked daily, as lack of water can kill in as little as 24 hours! Many small animals will not eat if they are not able to drink; considering that most animal feeds are dry kibble, an absence of water may also result in feed intake concerns. In species with a large cecum or appendix (e.g., guinea pigs and rabbits), where the microbes are dependent upon a fluid environment, lack of sufficient water may also result in gut dysbiosis and could result in disease from microbial toxin production or dieoff of desirable microorganisms.

Feeders The style of feeder used for a species is dependent upon the needs of the species, but all feeders have common criteria for selection. A feeder should allow access to food, minimize contamination with feces and urine, and accommodate group housing considerations, which may require multiple feeding and watering points, while also optimizing the diet consumption.

Temperature and humidity Species-specific temperature and humidity preferences are reviewed in the species chapters, but certain generalized concepts and issues remain. Management of a stable environment is the most critical aspect of temperature and humidity. Constantly changing temperature and humidity is more harmful to the well-being of the animal than any specific temperature (within reason of course). A general recommendation for all species is 30% to 70% relative humidity. Although there is little evidence for strict control of relative humidity, it is also

Exotic Small Mammal Care and Husbandry

true that variations in relative humidity are better tolerated at lower temperatures, due to heat loss mechanisms of most animals. Low relative humidity may be more associated with pollution- (e.g., ozone and dust) associated respiratory disease while high relative humidity may be more closely linked to infectious disease (e.g., fungi and bacteria) transmission. Temperature extremes also have an effect on other aspects of animal care and support. Lactating rats exposed to 95 °F (35 °C) for 6 hours daily produced less milk than rats housed at 72 °F (22 °C) Reproduction in rats also decreases markedly at 90 °F (32 °C) (e.g., retarded testicular development).

Thermo-neutral zone The thermo-neutral zone (TNZ) is that range of temperatures where no energy is expended by an animal to either cool or heat itself. The TNZ differs by species and does not necessarily relate to the comfort of the animal. As a general rule, animals are most comfortable at a temperature toward the low end or just outside of the low TNZ temperature. Exposure of unadapted animals to temperature higher than 85 °F or lower than 40 °F without access to shelter may produce clinical effects that could be life threatening. If the temperature change is of short duration and low magnitude, then few signs are expected and even fewer will be observed. However, if the temperature deviation continues (duration and magnitude), animals will exhibit huddling, curling up, nest building, and increased general activity (all are signs indicating a desire to remove itself or protect itself from the environment). If the deviation continues further (duration and magnitude), animals will alter their metabolism rate and will consume more water and more (or less) food; the growth rate will also be affected. In cases where the temperature changes are colder, animals will enter into hibernation, torpor, or aestivation, will begin nonshivering thermogenesis (brown fat utilization), will have peripheral vascular changes shunting more blood to the core of the body and away from the appendages (the tail of rodents is used for thermoregulation to eliminate excess heat), and will exhibit piloerection (hair standing up).

Introduction

If the temperature deviation (duration and magnitude) lasts for 14–21 days, then the body increases its fat stores, thickens the fur coat, and significantly restricts heat radiation.

Ventilation The purpose of ventilation in most circumstances is to remove thermal loads, dilute gaseous and particulate contaminants, and adjust moisture content. Few, if any, pet cages are so secure that oxygen needs of the animal are ever in doubt. The macroenvironment of most homes provides a fresh air exchange of one to two air changes per hour. Adequate room ventilation does not necessarily ensure adequate ventilation of the microenvironment! Although not generally a concern, if ammonia in the cage is high or the bedding remains moist for extended periods, then the cage’s location should be considered and perhaps changed or a supplemental fan should be provided to assure a sufficiently dry cage. Because small mammals may also cause an allergic response, a response that can be cumulative, it is generally preferable to maintain the cage as close to an exhaust air duct as possible, but not immediately adjacent to the exhaust vent to prevent strong drafts that can stress the animal.

Illumination Small mammals are generally crepuscular (more active at dusk or dawn). They do not require light as intense as humans and in fact will tend to withdraw from intense light levels. They will adjust to the light schedules we use in our homes, but left alone small mammals prefer 14 : 10 (light/dark) to 10 : 14 (light/dark). Increasing or decreasing light levels can affect breeding receptivity in some species, but less so in others. Albino animals have pink eyes and are relatively more susceptible to phototoxic retinopathy than pigmented species. Albino animals, if maintained in continuous light, can develop blindness within 18 months. Illumination can also affect medicinal treatment through hepatic enzyme activation. During the light cycle, rodents given a barbiturate will sleep longer than rodents given the same dose during their dark cycle. It is important to ask the pet

7

owner whether the animal is kept exclusively indoors (where light and dark are generally the same year round) or whether the animal is principally an outdoor animal (where light and dark cycles may vary significantly over the year). As a general guideline, small animals require only 325 lux (approximately 30 footcandles) of light for normal function and development.

Noise Noise is a significant factor for the well-being of small animals, but it is rarely considered. Small animals tend to hear at a higher frequency compared with humans, but most also hear well at the human upper end (yes, heavy rock music is heard by the pet rat). Noise levels around animals should never exceed 85 dB as auditory effects of noise can occur at >85 dB. The effects are dependent upon the intensity of the noise and the duration (either point or cumulative) of the noise event. Destruction of sensory hairs and supporting cells can start at 90 dB, mechanical damage in rats occurs at 160 dB, and pain has been reported in rats at 140 dB. Rats have developed inner ear damage after prolonged exposure to 100 dB. Noise also produces direct physiologic effects. Increases in serum cholesterol and in adrenal weights occur in rats exposed to 83 dB and intermittent sound of 114 dB. Audiogenic stress due to pulsed noise exceeding 83 dB may cause reduced fertility in rodents, and audiogenic seizures occur in gerbils and select strains of mice. Radios, alarms, and timers should not be placed close to small animals. Computer video screens, large fans, and other household motors frequently have ultrasounds that can be highly distressful to small animals. These devices should not be used near small animals unless they have been checked for ultrasonic frequencies. In some cases, artificial background noise may be useful in masking sudden unexpected noise.

Transportation Any time the animal leaves its home cage, it is being transported—usually just for a trip to the backyard but sometimes much further. Transportation can be a significant stressor for these species, requiring an acclimation period after

8

transportation before “normal” signs are once again observed. Adolescent rats require 1–5 days for complete physiologic recovery after being transported. The use of a similar cage, with familiar accessories, the same food, and some of the same water can lessen the effect of the transport. During transport, animals should be protected from sunlight or wind by placing an opaque cover over the cage. The vision system of animals sees things differently from humans, and the rapid and repeated movement that occurs during transit can be highly stressful. If transport occurs in a vehicle the cage should be secured on the floor or seat of the car using a bungee cord or similar device to prevent tumbling in the event of a quick stop. Care should be taken to secure the top and bottom of the cage to prevent dislodgement and escape of the animal during transit.

Overcrowding and isolation Animals are generally social creatures (certain exceptions occur during breeding season or due to reproductive processes). Animals may experience adverse conditions from being either overcrowded or isolated. Overcrowding can be mitigated to some degree by effective utilization of enrichment paradigms (e.g., hiding boxes, red film). In many cases, aggressive behavior will be strain- or even sex-specific. Group-housed mice show marked adrenal response that is directly proportional to the animal density. In these conditions, the subordinate animal has the higher adrenal weight and plasma cortisone level due to its stress associated with being subordinate. Once social groups have been established, fighting may occur if the groups are reassorted or if a new member joins the group. Breeding and reproduction can also be influenced by group housing. Grouped-housed rodents frequently become anestrous and will synchronize the estrous cycles in the presence of a male (Whitten and Bruce effect).

Handling Regular and gentle handling reduces animal stress and decreases the risk of fear-provoked biting. Correct handling and restraint techniques are critical. Failure to handle gently and correctly may result in injury to the animals and to the handler. The ears of the rabbit are

Exotic Small Mammal Care and Husbandry

not genetically placed handholds, and the tail of a mouse was not placed there so you could safely pick it up. Veterinary technicians have a special duty to teach and train pet owners on proper methods of restraint and handling.

Chemicals The potential list of chemicals that could negatively impact animals would be an entire study in toxicology, but we shall concentrate on general concepts and issues related to chemical exposure. Air, feed, water, bedding, and caging materials may all present potential chemical concerns. Chemicals may enter via damaged skin, the intestinal tract, or the respiratory tract. While the list of potential effects of chemical insult is long, the more common outcomes are changes in the hepatic microsomal enzymes, the biotransformation of medications, and the regulation of oxygen radical removal (associated with cancer development). Chemicals may serve as local irritants, produce generalized disease, alter immune functions, provide allergen exposure, be a source of mutagen, or even function as a teratogen.

Air quality Air quality is not simply an argument for clean air or sufficient air, but rather for appropriate air. Air can become a disadvantage for these small mammal species. At 68 °F (20 °C), air moving at 60 linear feet per minute has a cooling effect of 45 °F (7 °C). Air this cold, no matter how clean, can significantly stress the animals, especially the neonate or the geriatric animal. High airflow also has a “wash-out effect” upon pheromones. Clean air is not necessarily a good concept either. Because animals communicate by pheromone, in some cases even to the exclusion of verbal communication, elimination of pheromones prevents the creation of a “home sweet home” for the pet and never allows its complete integration into the cage environment. Air can also be excessively dirty. Humans can sense airborne ammonia at around 25 ppm (parts per million). Animals begin to show respiratory impact of elevated ammonia at 10 ppm. In some cases, low-level ammonia enhances the potential disease impact. Mycoplasma pulmonis, in the presence of low-level ammonia, will

Introduction

have an increased severity of lung lesions, enhanced growth of the organism, and greater adherence (decreased clearance) of secondary bacteria in the lungs.

Water quality Most pet animals are provided drinking water from the home tap. In some cases, it is wonderful water, but in other cases, it may be a concern for the pets and their owners. Although most municipal water is treated with chloramines to discourage bacterial growth, high levels of chloramines may affect the immune system. Stressed or injured animals may benefit from filtered water until their return to a healthy state.

Diets Dietary requirements are addressed in the species chapters of this text, but they deserve a general mention in our review of external factors that may affect the well-being of the pet. Likely the most common cause of dietary modification is provision of treats. Many pet owners will use treats to encourage specific behavior to get the pet to eat. Treats should be limited and never exceed 5% of the total required dietary intake of the animal. Variations in quantity or quality of essential vita-

9

mins or minerals may alter drug metabolizing systems, affect membrane integrity, or predispose to the effects of carcinogens. In certain cases, selection of specific treats may serve to benefit the animal’s well-being, as in the case of vitamin C requirements and guinea pigs, or roughage requirement and rabbits. In all cases, diet milling date and storage conditions should be monitored because fat-soluble vitamins will be leached when stored at high temperatures and other vitamins may lose potency if stored for excessive periods of time. Just because it looks like a pelleted pet ration doesn’t mean it is worth feeding to the pet. The most important concern for a dietary discussion is to avoid abrupt diet changes; when changes are required, do so over a period of 2–3 weeks if possible. Although not as habitual as other animals, these small mammals can benefit from changing the feed from time to time and familiarizing them with alternate feedstuffs. Such planning has on occasion facilitated the medical management of a sick patient when presented with diets different from those served at home.

Adventitial diseases Diseases common to particular species will be addressed in each of the species chapters.

Enrichment

The strong and interactive relationship between a pet and its human companion serves to benefit both. If we begin with the premise that “animals are what make us humane” (another way to say it is “animals are the basis for our compassionate relationships to other creatures, including humans”), then our desire to maximize their environment and make their lives as comfortable as possible becomes a logical reason for considering enrichment of the pets’ environment. Recognizing the bond that exists between humans and animals, as well as the value animals bring to the human existence, makes the desire to enhance the environment of animals an easy discussion. Enrichment in many contexts simply means creating an environment that both allows and encourages species-specific activities. For example, rodents like to burrow and aquatic species like to hide behind or within structures. If we provide a deep layer of soft sand for the aquatic creatures and a box for the rodent pet, we haven’t caused any harm, but we have missed an opportunity to make their environments as “normal” as possible. “Normal” is quite difficult to truly assess in animals, especially those that have never seen the out-of-doors. Our perceptions of normal must be guided by the animal’s interest in and motivation to use the enrichment item. Even though many captive animals have never lived in the “wild,” enrichment strategies can be guided by the natural habitats and behaviors of their wild counterparts. A clear recognition of normal is critical to a complete patient assessment as well as selection of enrichment

2 strategies for the patient under consideration. If you are unaware of normal, how will you be able to assess a change, either positive or negative, in the animal you are observing? Knowing normal is the key to quality enrichment of the animal’s life! Development of an ethogram is one way to determine normal. An ethogram compares the time budgeted by the animal for a given task or activity. By observing the actions or activities from a range of options, one can deduce that this animal finds greater satisfaction with activity A over activity B. The more the observations, the more confidence one has in the outcomes of animal ethograms. A word of caution is necessary at this point: each of us would rather eat candy than swim four lengths of the pool, but we would all agree that the pool exercise would be more beneficial, especially if performed daily. Consideration of animal “preferences” using educated judgments can guide the technician in selecting beneficial activities or devices for the environmental enrichment. The goal of an enrichment strategy is to improve (or maintain) the health of the animal. Animals that are active and engaged in their environment are also generally more healthy than those that sit quietly for hours and hours with little to do and nothing to explore. “Doing” is a part of being healthy. Enrichment can also be used as a tool for assessing the health and well-being of animals. Animals that lack exploratory behavior may be in discomfort from osteoarthritis or other disease states. Providing enrichment through exploratory 11

12

behavior (e.g., hiding treats in grass, in hay, or inside boxes), especially when provided just prior to the dark cycle, will decrease stereotypic behaviors common of poorly enriched animals. Keen observation of an animal during enrichment activities will provide several useful clinical tools for assessing the condition of the patient. Observation of an animal’s activity level is one method the veterinary technician may use to “hear” what the animal is saying. Enrichment falls into two general categories: social enrichment and nonsocial enrichment. Social enrichment requires interaction of the animal with other animals or with humans. Social enrichment may include time spent holding, petting, walking, or playing with the pet. Social enrichment is important to decrease the pet’s anxiety or “reactiveness” to humans. Generally speaking, an animal that has spent significant quantities of time with humans, and has been handled gently during those interactions, is less likely to bite or scratch than one that has had limited human contact or rough handling. However, having human social interaction is not the only way to provide enrichment to the animal. Often, conspecific interactions (e.g., interaction with one’s own kind) are the most advantageous. Conspecifics already understand the language of the species; they recognize common odors, see common visuals, and react in a similar manner to other stimuli. In other words, conspecifics already know how to read moods, respond appropriately, and communicate readily. For social species, whenever possible, animals should be housed with members of their own species. In certain cases, there are restrictions on how conspecific housing should occur. For example, hamsters raised alone and then grouped as adults will often attack and severely injure each other. Rats, however, are highly social animals and, given the option, will curl together when sleeping and will be in close contact when awake. These are examples of direct social enrichment. Social enrichment may also be indirect. Animals may be placed nearby, but without the ability to touch. Since most small animals communicate in a hearing range above human hearing (ultrasound), proximity of location may provide good social enrichment while pro-

Exotic Small Mammal Care and Husbandry

tecting the individual animals. Although not the same as direct contact, being able to hear each other and see each other may provide sufficient interaction to decrease stress and improve well-being. Mirrors may be used for animals that have well-developed sight, but shiny surfaces can also be a detriment, especially if the animal is frightened by reflections or is an individual that is aggressive toward other members of its species. Seeing a reflection in a mirror can stimulate social behavior, encourage activity, and even provide for a sense of companionship. Exercise can be either social or nonsocial. Small mammals may be transferred from their home cage to an exercise pen for various periods of time. The novelty of the exercise pen will stimulate the pet and encourage exploration. The use of an exercise pen also requires that we consider the advantages and disadvantages of such an arrangement, especially if there are multiple species using the same area. The exercise pen should be sanitized effectively between uses. Most of the small mammal species are either prey or predator, depending upon the context of the moment. A rat is generally considered a predator to a mouse, but if a ferret were introduced, then the rat could be considered the prey species. Placing a ferret in an exercise pen, then removing it and placing a rat in the same pen without sanitation, would not be a pleasant experience for the rat: it would sense the predator animal and would be more concerned with escaping and evading the predator than with the novelty of curious exploration. Small rodents, especially gerbils, mice, and rats, are thigmotactic, meaning they prefer to be near a wall than in an open space. Knowing this, one should consider maximizing wall surfaces as an enrichment strategy and, to the extent possible, minimizing the wide-open spaces in the home cage or the enrichment pen. This can be accomplished by use of tunnels, boxes, or other devices that provide wall surfaces. Small mammals (e.g., rodents, rabbits) are crepuscular, a term used to describe animals that are primarily active during twilight (either or both dawn and dusk). There are two behavioral relationships of such animals that can facilitate selection of an appropriate environment and care strategy.

Enrichment

First, crepuscular animals have decreased bright light vision and enhanced dim light vision. The best overall enrichment strategy for these animals includes protection from direct or intense sunlight. Crepuscular animals will be most active when the lights are low. Light in most homes is at the high end of the preferred intensity for small mammals, so decreasing light levels by turning off a light or two may increase the pet’s activity level. Using a night light in the pet’s room may simulate a moonlit night and, for crepuscular species, may keep the animal active most of the night. Second, crepuscular animals lack the ability to sense red or yellow light. We can take advantage of this knowledge by surrounding a sleeping box with red or yellow color (e.g., a film or a plastic sheet). The animal will believe it is dark, but humans can view the animal inside. Using a red or yellow film may allow good observation of the patient without the patient being aware it is being observed. As an aside, the definition of crepuscular includes the terms matutinal (or matinal, indicating activity at dawn) and vespertine (indicating activity at dusk). Most small mammals prefer one or the other, but will have activity during both time periods. In addition to exercise, proper caging selection can be considered a nonsocial enrichment. Sanitizable products (e.g., metal, plastics) are generally preferable to nonsanitizable products (e.g., wood). Certain metals should be avoided (e.g., zinc–coated metals, copper, and iron) as these products can be ingested or absorbed into the animal’s system and cause disease. From a sanitary standpoint, the use of hard plastic or metal provides an easily sanitizable surface. However, from the perspective of an animal’s well-being, such materials can be highly disruptive to the animal’s comfort. Metal is cold and hard, and plastic can be too. Both products are nonabsorbent, preventing the segregation of waste products in the environment. Some have suggested the use of wire mesh or screening for animals. In theory it allows waste products to migrate from the animal’s environment and keep the animals dry. However, studies have shown that animals prefer hard surfaces to wire surfaces. When considering that a geriatric animal may have difficultly moving on wire or that a heavy animal may have ulcers or feet

13

sores from the wire surface, the use of wire flooring in most applications is not recommended. A modification of the wire flooring concept is the slatted floor, where the surface is composed of flat bars approximately ¼ inch wide or larger. These floors are preferred to wire and do assist in keeping the animal dry and clean, but they do not allow for bedding products and, depending upon the caging type, may be drafty for the animal. In most applications, the preferred outcome is a compromise between the most easily sanitizable environment and the most enriched environment. For burrowing animals, providing clean, absorbent, and soft material on a solid nonporous surface (e.g., plastic) to dig and construct nests and passageways allows the animal an opportunity to explore, to follow its curiosity, and to build its “home.” At times, the compromise between providing soft and absorbent materials and providing materials that can be effectively sanitized becomes troublesome. Selection of an appropriate substrate for the comfort of the animal while assuring effective sanitation often requires the use of different materials (e.g., a hard easily sanitizable surface for the exterior and a soft absorbent material for the interior). For most species, cage placement is a critical item. For example, the placement of the cage near a window could offer some species an enriching atmosphere with novel stimuli during the course of the day; for others, especially guinea pigs, placement near a drafty window would provide short-term enrichment but increase the infectious disease potential (e.g., guinea pigs are highly stressed by drafty conditions). Placement near a window also requires close monitoring of the cage temperature. Sunlight streaming through on a sunny day can increase the cage temperature above the optimal range in a very short period of time, even to dangerous levels. Small mammals are more tolerant of cold than of heat, and they can rapidly develop hyperthermia when in direct sunlight. When we remember the crepuscular nature of many of these species, most will sleep during the day; thus the placement near a window for novel stimuli becomes more of a health concern than an enrichment advantage. The cage environment is another variation of nonsocial enrichment. Cages may have

14

hiding places and foraging opportunities (hiding feed in burrows, burying feed in Astroturf, mixing a desirable feed into the fibers of a sheet of synthetic fleece, or other similar devices that encourage the animal to “work” for the feed reward). The cage environment may also include balls, mobile toys, oddly shaped items to chew, natural wood products, or even small sections of fabric that were used by the human companion (a small square of old bedding used by the human companion will have residual human scents that can facilitate a familiarity between the animal and the human). Natural products, such as branches or leaves, should be removed and replaced when they become excessively soiled with excrement. Bedding can serve an enormous role in the well-being and enriched environment of these animals. The amount of bedding used should be sufficient to keep the animal dry between cage changes, without coming into contact with watering devices. Bedding selection is also an important variable affecting the well-being of the pet. Bedding made of softwood products such as pine or cedar may affect the animal’s metabolism and may in some cases actually interfere with recovery from anesthesia or even disease states. For example, red cedar shavings are commonly used for pet bedding because the red cedar smells fresh. That fresh smell is principally two aromatic hydrocarbons (cedrene and cedrol) that induce specific liver enzymes, which can alter rates of anesthesia and interfere with metabolism of certain medications. Likewise, spruce and pine shavings contain alphapinene, another volatile hydrocarbon that also induces hepatic enzymes. Heat treatments (such as autoclaving) can reduce the concentration of aromatic hydrocarbons and might prevent induction of hepatic microsomal enzymes. Hardwood shavings (beech and aspen) or corncob chips are generally preferred over the softwood beddings. Hardwood products do not have the volatile compounds found in softwood products. Hardwood is absorbent and can serve as effective bedding material. Hardwood bedding is available in a variety of chip sizes (to be discussed later). Hardwood may also cause injury to the neonate or the infirm

Exotic Small Mammal Care and Husbandry

from the sharp edges commonly found on the chips. Paper products, depending upon the source and processing of the paper, may be useful to consider, but there may also be disadvantages with these products. Paper may have residual ink or bleaching agents that may affect their use. Fibrous products can be very useful for small mammal bedding. The long fiber length facilitates nest building, encourages manipulation, and provides enhanced opportunity for foraging. Disadvantages may include the source of fibrous products. Corn or beet husks may have residual fungal contamination if not properly treated (generally autoclaved) and managed (kept cool and dry). These concerns with fungal interference intensify when the fibrous products become wet. Bedding type also affects thermoregulatory stability, core temperature, and motor activity. Mice housed on deep bedding maintain significantly higher core temperatures during the day. During the night, however, core temperatures and motor activity show no difference, probably more related to activity on the bedding rather than burrowing into the bedding. Although deeper bedding has a positive impact upon core body temperatures, deep bedding can also present a risk of touching the water bottle sipper and draining the bottle of water, wetting the bedding, and causing hypothermia in the caged animals. In this case, the deep bedding presents the opportunity to injure the animal rather than to support its well-being. Animals do have preferences for certain types of bedding. Beddings consisting of relatively small particles (1.2 mm × 1.6 mm) are generally avoided by rodents, whereas large fibrous bedding materials are preferred by mice and rats. Size and manipulability are among the main determinants of the appreciation of bedding particles by mice and rats. Lastly, when considering the air in the cage, ammonia is the single most common and most important airborne pollutant in the pet cage. Certain beddings have a higher ammonia generation potential than do other bedding materials. The following bedding materials are ranked from highest to lowest in ammonia generation potential: aspen shavings; pine shavings; reclaimed wood pulp; loose virgin pulp; hard-

Enrichment

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wood chips; recycled paper; pelleted virgin cellulose; and corncobs. We must note, however, that routine and regular cage cleaning can overcome concerns with ammonia generation in any of the bedding products. How then should a bedding product be assessed for supporting the well-being of the pet? An ideal bedding material should be dust free, nonpalatable, absorbent, and free of microbial and toxic contaminants. No bedding is ideal for all species. No bedding is ideal for all care conditions. However, bedding is a controllable environmental factor—one that may enrich or detract from the environment! A good place to start is with hardwood bedding. Feed products may also be used as a means of enrichment, though overfeeding of supplements can have deleterious effects. All pets require a nutritious ration. Small pets consume small quantities of feed, and provision of too much enrichment feed can interfere with the required basic nutrition of the pet. As a general rule, supplements and food enrichments should not exceed 10% of the standard diet. Feed supplements must also be selected based upon the species. Rabbits enjoy carrot tops, but should not be given too many carrots (excessive amounts of carrots can cause gastritis and

subsequent gastrointestinal distress). Guinea pigs enjoy green leafy vegetables such as kale, but should not be given iceberg lettuce since it has almost no nutritional value and may cause GI distress in large volumes. Hamsters and gerbils are hoarders and prefer to hide feed for eating at a later time; providing at least some of the ration on the floor of the cage and mixed into clean bedding is a more natural situation for these species and will foster positive behaviors (as opposed to feeding in a food bowl, or especially feeding with a wire-bar hanging lid). Rodents enjoy oil seeds (e.g., sunflower seeds), but the quantity should be restricted since given the choice rodents will consume only sunflower seeds and develop nutritional deficits by failing to consume sufficient balanced ration. At other times, the use of supplementation can have medicinal value. Although most animals internally manufacture the components of vitamin C and therefore do not require vitamin C in the diet, guinea pigs are one species that cannot, and therefore must consume sufficient quantities of vitamin C or they will develop scurvy. Providing guinea pigs a small enrichment of a citrus fruit (e.g., orange, lemon), especially if the ration being fed is not

Table 2.1 Rodents (mice, rats, hamsters, gerbils, degus): These normal behaviors should be considered in the development of an overall strategy of enrichment. Gnawing

The teeth of many rodents grow continually and, without gnawing, will overgrow and cause pain or disease. Gnawing is a critical life behavior for rodents.

Burrowing, hiding, daylight sleeping

Rodent eyes are sensitive to intense light, such as occurs during the day. Burrowing is one method of escaping from intense sunlight.

Exploring, climbing, seeking feed

Rodents are “explorers”; they prefer to search for their food as a means of “normal” food acquisition. Hiding feed encourages exploration, increases exercise, and provides normal behavior.

Grooming

Grooming of one’s cage mates is a strong social activity that builds bonds of trust and relationship. Grooming also serves as basic sanitation for the coat, removing excess debris and dander while combing and smoothing the fur.

Nesting

Nesting is a behavior that consolidates the “family,” provides social contact, facilitates grooming, and gives a sense of a thigmotactic environment.

Thigmotactic

Rodents do not have good vision; therefore they depend upon their whiskers and sensory fibers around the head and shoulders. Rodents prefer being next to a wall and will choose a close and confined space rather than an expanse of floor.

Neophobia

Although novel stimuli are useful, presentation of new-tasting food enrichments will generally be met by a small nibble, then restraint from further consumption until time has passed. This evolutionary survival mechanism prevents the ingestion of poisonous foodstuffs. Novel foodstuffs may initially be rejected but subsequently preferred to another novel introduction.

Table 2.2 Guinea pig: These normal behaviors should be should be considered in the development of an overall strategy of enrichment. Scatter, freeze

When sensing “danger,” the guinea pig will do one of two things: either run quickly to a less dense location or freeze in place and hope the danger passes.

Linear hierarchies

Guinea pigs form strong relationships to other guinea pigs in the area. Separating or regrouping animals may engender unnecessary distress.

Territorial

Guinea pigs are strongly territorial. They do not readily accept newcomers and will chase or corner new inhabitants.

Vocalizations

Guinea pigs have a large repertoire of sounds and inflections to communicate their intentions. This is one species where vision is less important than indirect communication such as vocalization.

Cover

Being a burrow-dwelling rodent, guinea pigs prefer some form of cover to be “safe.” Enrichment strategies should always include opportunities to hide.

Table 2.3 Rabbit: These normal behaviors should be considered in the development of an overall strategy of enrichment. Chewing

Rabbits require regular chewing to maintain proper apposition of the front teeth.

Thumping

Rabbits do not vocalize very well or very frequently, but rather use thumping as a means to communicate their message. Often associated with an aggressive posture, thumping can be the harbinger of an aggressive action to follow.

Locomote (hop or roll)

Rabbits use these maneuvers to escape or evade. Rabbits in a playful mood may also exhibit these behaviors.

Nudging, nose

Rabbits use nudging as a softer means of communicating (softer than thumping). The rabbit will press its nose in the direction it desires the opponent to move.

Fur pulling

Does will pull their fur immediately prior to kindling to provide soft down for their kits.

Grooming

Rabbits groom constantly, never satisfied with the present status of things. Rabbits that are prevented from grooming may appear depressed.

Table 2.4 Ferret: These normal behaviors should be considered in the development of an overall strategy of enrichment. Alligator roll

This is a behavior important for establishing dominance between two animals. Single animals may grab the socks, feet, or loose skin of their human companions in an attempt to “alligator roll” them.

Backing into a corner

This is a behavior seen for urinating and defecating, but it may also be a sign of fear. If the animal hisses, the fear response is likely. Picking up these animals can result in serious injury.

Bottle brush, “puffy” tail

A “puffy” tail, or “bottle brush tail,” is an indication of fright or excitement. Other signs should also be noted (hissing would be fear) to determine the actual meaning of this sign.

Chasing or lunging

This is a playful behavior.

“Dancing”

Jumping from side to side in a playful series of antics, “dancing” is generally a sign of excitement, but it may also be an indication of aggression.

Dooking or chirping

This is the sound made while excited.

Food, water, litter-pan digging

This is a normal behavior where the animal digs for its feed or for a place to defecate. This can occur at any time and, while not harmful, can be a mess to clean up.

Food or water bowl tipping

This is a behavior probably related to the curious and digging nature of the animal.

Hissing

Hissing is a behavioral sign of fear or anger or a show of intimidation.

Running into things

This is not necessarily a behavior of its own; ferrets have poor eyesight and, when in a hurry, can run directly into things—or off a balcony or stairs.

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Enrichment

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Table 2.5 Sugar glider: These normal behaviors should be considered in the development of an overall strategy of enrichment.

Table 2.7 Chinchilla: These normal behaviors should be considered in the development of an overall strategy of enrichment.

Nocturnal

Social

Chinchillas are highly social and active animals that like companionship. In their natural habitat, they live in herds ranging up to 100 or more animals.

Nocturnal

They are most active at night and sleep during the day. Eating occurs at night.

Fur dropping

Frightened animals will “drop fur” rapidly.

Chirps or squeaks; barks

These are common communication sounds indicating any number of expressions from play to fear.

Sugar gliders have acute night vision, but limited day (bright-light) vision.

Vocalization They often vocalize for no apparent reason, but likely for simple communication. Social

In nature they may be found in groups of 30–50.

Territorial

Sugar gliders use urine and scent glands to identify territory (even humans).

Table 2.6 Hedgehog: These normal behaviors should be included in an overall strategy of enrichment. Curling

This is a behavior to indicate “enough,” or simply a need to escape for a time.

Anointing, or anting

Production of a large amount of foamy saliva when they encounter an unfamiliar smell—they will lick at the novel item until frothy saliva develops, then rub the saliva on their quills. This is the process of anointing, also called anting.

Chirping, whistling, purring

These are sounds indicating comfort and contentment—a happy hedgehog.

Snorting, hissing, clicking

These are sounds indicting discomfort, fear, or aggression—an unhappy hedgehog.

Foraging for food

Digging and climbing are beneficial hedgehog behaviors.

Solitary

These are not social animals and should be housed separately.

Diurnal

They are most active at dawn and dusk, although some remain on the move until 3 a.m. Frequent handling during the day can help change the hedgehog’s habits and help reduce the nighttime activities.

fresh, will prevent the development of this disease while also providing a pleasing enhancement to the regular diet. Enrichment strategies should always be developed in the context of the natural behavior of the animal. For example, rodents generally have limited vision but a well-developed sense of smell and hearing. Providing visual stimulation to the pet rat or gerbil will likely not provide an enriching activity. However, providing items that stimulate the sense of smell or the sense of hearing may be far more engaging and satisfying to the animals. All animals have certain behaviors, sometimes based upon physiological needs (e.g., gnawing in rodents to keep the teeth trimmed). Examples of behaviors include those given in Tables 2.1–2.7.

ENRICHMENT STRATEGIES

Enrichment strategies must be considered species by species. The types and styles of enrichment for one species can be inappropriate for another species. Enrichment strategies should be formulated according to the normal behaviors of the pet; therefore it is key to clearly recognize normal behavior in a species prior to recommending any enrichment strategy.

Rodents Almost any item that is nontoxic and safe can be used as part of a rodent enrichment strategy. These may include the following: • Bedding (burrowing and exploring for rodents)

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• • • • • • • • • • • • • • • • • • • •

Burrows (generally a plastic product) Cage dividers (increasing wall surfaces) Climbing accessories Exercise devices (running wheels) Film canisters Foraging devices Tunnel (provides closeness and wall surface) Gnaw blocks or sticks Group or social housing (not hamsters, adult male mice, or female rats) Hide boxes Ladders Mazes Soft music Nest boxes or nest-building material (hay, tissues, or wood-wool) Platforms PVC pipe (½- to 1-inch diameter is best) Ramps Shelves Shuttle box (also called transport box) Tubes (such as those from rolls of toilet tissue or paper towels)

Rabbits Almost any item that is nontoxic and safe can be used as part of a rabbit enrichment strategy. These include the following: • • • • • • • • • • • • • • • • •

Balls (hard plastic) Bedding (straw, wood chips) Burrows (oatmeal cans, boxes) Free range (e.g., a clean and pesticide-free backyard) Fresh fruits or vegetables (limit sugary fruits; use more vegetables) Gnawing objects (aspen wood or apple wood) Group housing Soft music Nest boxes Nesting material (tissues, straw, dust-free hay) Pair housing (except adult males) PVC pipe Resting shelf Roughage or forage (limit alfalfa; prefer grass hay) Varied diet Suspended shiny objects Brass “canning rings” (tough enough to chew, soft enough to bend)

Exotic Small Mammal Care and Husbandry

Ferrets Almost any item that is nontoxic and safe can be used as part of a ferret enrichment strategy. These include the following: • • • • • • • • • • • • • • •

Balls Bite cups Crickets Foraging devices Fur-covered movable toys Hammocks Hide-and-seek tunnels Mazes Moving preymodels Music Nest boxes Plastic burrows PVC tubes Shelters Swimming pans

Sugar glider Almost any item that is nontoxic and safe can be used as part of a sugar glider enrichment strategy. These include the following: • • • • • • • • • • • • • • • • •

Bedding Burrows Cage dividers Climbing accessories Climbing frame Foraging devices Group or social housing Hide boxes Mazes Soft music Nest boxes or nest-building material (hay, tissues, or wood-wool) Platforms in cages PVC pipe (2- to 3-inch diameter is best) Ramps Shelves Shuttle box (also called transport box) Tubes (such as those from rolls of toilet tissue or paper towels)

Hedgehog Almost any item that is nontoxic and safe can be used as part of a hedgehog enrichment strategy. These include the following:

Enrichment

• • • • • • • • • • • • • • • •

Bedding Burrows Cage dividers Foraging devices Group or social housing Hide boxes Ladders Mazes Soft music Nest boxes or nest-building material (hay, tissues, or wood-wool) Platforms PVC pipe (2- to 3-inch diameter is best) Ramps Shelves Shuttle box (also called transport box) Tubes (such as those from rolls of toilet tissue or paper towels)

Chinchilla Almost any item that is nontoxic and safe can be used as part of a chinchilla enrichment strategy. These include the following:

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• • • • • • • • • • • • • • • • • •

Bedding Burrows Cage dividers Dust baths Foraging devices Group or social housing Hide boxes Ladders Mazes Soft music Nest boxes or nest-building material (hay, tissues, or wood-wool) Platforms PVC pipe (2- to 3-inch diameter is best) Ramps Sand bath Shelves Shuttle box (also called transport box) Tubes (such as those from rolls of toilet tissue or paper towels)

Preventive Medicine

Veterinary technicians are often required to consult and advise clients concerning the health of their pets and the potential diseases that may be transmitted to the client’s family. Even more frequently, veterinary technicians work alongside the veterinarian in diagnosing and treating communicable diseases. A clear understanding of the potential diseases that our pets, or our patients, may share is crucial for the veterinary technician to achieve maximum impact. Let’s begin, therefore, with the recognition that we have a closely intertwined relationship with our pets and our animal charges. We live with animals and we work with animals. Diseases that we may pick up at work can affect our pets at home, and diseases at home can affect the health of our patients at work. Animals can carry a number of diseases that are important to our pets—and our family members. The term for diseases transmitted between animals and humans is “zoonoses.” The World Health Organization defines zoonoses (zoonosis, sing.) as “Those diseases and infections which are naturally transmitted between vertebrate animals and man.” The effects of zoonotic disease may be direct illness, negative feelings of family members about the pet, monetary cost of treating the disease, potential legal implications if the animal infects or injures a neighbor child, and the loss of the friendship and companionship of the animal due to unmitigated disease. Recognizing zoonotic disease and the potential for zoonoses is an important aspect of quality medical service. However, before discussing specific zoonoses,

3 we must understand a few basic concepts about zoonotic disease. There are five primary modes of zoonotic disease transmission: fecal material, urine, blood, saliva, and milk. Certain of these modes of transmission are easy to envision. For example, fecal contamination has and will make people ill; parasites and other diseasecausing agents are often transmitted in fecal material. Other methods of transmission may not be as obvious; for example, saliva is not something we think we are sharing with our patients, but as they groom themselves they are spreading their saliva on their fur coat. We then pet them or brush them, and in addition to removing loose fur we are also removing dried saliva proteins or potentially infectious particles. Recognizing the mode of disease transmission is important to understanding how to limit the spread of disease. Each of these primary modes of transmission may be further subdivided according to the specific route by which a contagion gains admittance to the body: aerosolization (breathing in airborne contaminants), mucous membrane (touching our mouth, eyes, or nose with contaminants on our hands), or contact with the bedding or animals (this route may include direct contact with the skin). Considering these routes of infection, and adding the modes of transmission, we can see that washing our hands to protect ourselves from fecal or urinary output may not be sufficient. Fecal material may dry out, releasing small particulate matter that becomes airborne and is subsequently inhaled. 21

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Knowing the mode and route of infection is not sufficient alone to clearly understand the probability of disease transmission from animals to humans. The probability of developing a disease is influenced by several factors, including the following: A. Length of time the animal is infective: Animals with parasitic diseases often are infective for years. Animals with viral diseases often are infective for days to weeks. B. Length of the incubation period in animals: For diseases with long incubation periods, infected animals may be observed as “normal” for long periods of time, because the animals may move housing locations or even die before becoming infective for humans. C. Stability of the agent in the environment: Enveloped viruses (e.g., canine coronavirus, murine hepatitis virus) are less hardy and can be more easily destroyed by common disinfectants than nonenveloped viruses (e.g., feline leukemia, parvovirus, rabies), which are very hardy and may persist for long periods of time. This factor is most important in direct transmission, where the virus may be exposed to environmental changes. D. Population density of the animals in the home or clinic: Large concentrations of animals spread disease more rapidly than few animals in a common location. E. Husbandry practices: Daily sanitation, especially when tied to an appropriate disinfecting chemical, can disrupt or break the infectious cycle and prevent transmission of disease. F. Control of wild rodents and insects: Generally, wild animals have a variety of infectious agents, some of which may be significant to the pet or the client. G. Virulence of the agent: Another way to think of virulence is how “hot” is the agent, or how “aggressive” is it, or how “rapidly will it spread?” For example, Coxiella burnetti requires only 10 organisms to cause disease, whereas Pasteurella generally requires thousands of organisms to cause disease.

Exotic Small Mammal Care and Husbandry

H. Route of transmission: Viral infections more readily result from mucous membrane contact than “palm of the hand” contact. Zoonoses may also be classified in a number of ways. A useful system of classification is based on the type of life cycle of the infective organism. This system is most practical and seems the most useful in planning a preventive medicine program. The following categories are recommended by the World Health Organization Expert Committee on Zoonoses: A. Direct zoonoses: Agent is transmitted from infected vertebrate host to a susceptible vertebrate host by direct contact, fomite, or a mechanical vector. No developmental change or propagation of the organism occurs during the transmission. Examples are rabies, trichinosis, and brucellosis. B. Cyclozoonoses: Agent requires more than one vertebrate host, but no invertebrate host. Examples are human taeniasis, echinococcosis, and pentastome infections. C. Metazoonoses: Agent multiplies, develops, or both in an invertebrate host before transmission to a vertebrate host is possible. (This means that a definite prepatent or incubation period must be completed before transmission.) Examples are arboviruses, plague, and schistosomiasis. D. Saprozoonoses: Transmission of these infections requires a nonanimal development site or reservoir, such as food plants, soil, or other organic material. Examples are larva migrans and some of the mycotic diseases. The direction of disease transmission is also worthwhile knowing. For example, if a disease is common in animals and easily transmitted among animals but only rarely infects humans, then the control and prevention measures are very different from a disease that is shared readily and equally between humans and animals. The manners of describing the direction of transmission are as follows: Anthropozoonoses: Infections transmitted to humans from lower vertebrates. Zooanthropozoonoses: Infections transmitted from humans to animals.

Preventive Medicine

Amphixenoses: Infections maintained in both humans and lower vertebrates; may be naturally transmitted in either direction. Zoonoses may also be organized by etiologic (causative) agent. This is the structure we will follow for our continuing review: A. Bacterial 1. Bacteria 2. Spirochetes 3. Chlamydia 4. Rickettsia 5. Mycoplasmas B. Fungal C. Viral D. Parasitic 1. Protozoan 2. Helminth a. Nematode b. Cestode

BACTERIAL DISEASES

Systemic infections Brucellosis Agent: Brucellosis is caused by the following organisms: Brucella Brucella Brucella Brucella

abortus—cattle, sheep canis—dogs melitensis—sheep, goats suis—swine

Reservoir and incidence: Of the preceding species, we will only casually recognize the significance of the agricultural impact of B. abortus. Instead we will focus our attention on B. canis, once considered the most likely zoonotic agent, due to extensive numbers of roaming animals. Even today, the prevalence of Brucella may be as high as 10% in dogs in the US and the UK, and substantially higher in other parts of the world (e.g., Mediterranean and Arabian Gulf regions, Latin America, Africa, and Asia). Brucella canis is well adapted to dogs and is not the subject of any large-scale eradication program in the general dog population, as Brucella has been in agricultural animals. Humans appear to be quite resistant to B. canis infection, although occa-

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sionally it has been transmitted to humans. Veterinarians and veterinary technicians exposed to the blood of infected animals are the primary risk populations; pet owners are generally considered not at risk of this disease, except in the cases where there are immunecompromised people (e.g., cancer patients, HIV-infected individuals, transplantation patients). These groups should not handle infected dogs. Transmission: There are two recognized modes of transmission of B. canis: 1. Most likely cause for technicians—contact with infected animals, especially aborted fetuses, fluids or membranes, or urine 2. More likely cause for pet owners—airborne Disease in animals: In animals, the disease may cause the following: 1. Abortions 2. Infertility, testicular abnormalities, poor semen quality in dogs 3. Inapparent infection, which may also be common, as indicated by seropositivity (presence of antigen or antibody) Disease in humans: In the few human cases recorded, bacteremia was a fairly common finding, along with lymphadenopathy, splenomegaly, fever, headache, chills, orchitis, weakness, nausea, and weight loss. However, many of these same symptoms could be caused by the annual flu outbreak or any number of other minor diseases. Diagnosis: A rapid slide agglutination test is available. Standard tube agglutination has been used, and a 2-mercaptoethanol test can distinguish an active disease from a recovery from earlier illness. In certain cases, blood cultures and additional serologic tests may be used to confirm slide test results. Treatment: The therapy varies by geography. Generally, tetracycline/streptomycin combination has been used in the United States, whereas doxycycline/rifampin combination has been the preferred option in Europe.

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Prevention and control: Although the risk is low, individuals working with suspect positive animals should use disposable gloves and protective eyewear. Chlorine, oxidizers, organic iodine, and quaternary ammonium compounds are rapid bactericidal agents.

Exotic Small Mammal Care and Husbandry

reservoir is swine (pharynx may be heavily colonized), so veterinary care of swine— whether farm-reared or pet pigs—should include consideration of this agent. There have also been cases of this disease associated with caring for sick puppies and kittens but without a clear connection to swine.

Yersiniosis Agent: Animals are susceptible to three Yersinia species that are potentially zoonotic, all of which are gram-negative, rod-shaped bacteria: (1) Y. pseudotuberculosis; (2) Y. enterocolitica; (3) Y. pestis.

Yersiniosis—Y. pseudotuberculosis Agent: Yersinia pseudotuberculosis are gramnegative, non-spore-forming rods. Reservoir and incidence: This organism is ubiquitous in nature and can be isolated from dust, soil, water, and milk. Natural infections occur in humans, birds, rodents, rabbits, guinea pigs, mice, cats, nonhuman primates, sheep, swine, and goats. Direct zoonotic transmission has been documented from rabbits to humans, although other species may potentially transmit the disease as well. Transmission: Yersinia is generally transmitted by fecal contamination in food or water. Good feed and water sanitation will disrupt most transmission from animals to humans. Disease in animals: Guinea pigs, rabbits, and hamsters exhibit poor condition and enlarged lymph nodes. Nonhuman primates exhibit ulcerative colitis. Disease in humans: Humans exhibit mesenteric lymphadenitis, which can be confused with appendicitis and septicemia. Diagnosis: Isolation using cold enrichment technique (difficult to isolate).

Yersiniosis—Y. enterocolitica Yersinia enterocolitica (sometimes called Pasteurella X disease) causes a form of yersiniosis that may produce gastroenteritis in humans, with an acute watery diarrhea. On rare occasions, it may produce a mesenteric lymphadenitis that mimics appendicitis. The primary

Yersiniosis—Y. pestis Agent: Yersinia pestis is a gram-negative rodshaped bacteria and is the causative agent of plague. Reservoir and incidence: This disease is endemic in certain wild rodent populations in southwestern United States as well as in Africa and Asia. Plague surveys have also found evidence of this agent widespread in wild animal populations all across the western Great Plains region of the United States. Whereas prairie dogs and select peromyscus (deer mouse) and related species are reservoirs in the United States, the more important reservoirs worldwide are the roof rat, Rattus rattus, and the urban rat (sometimes also called the Norwegian rat), R. norvegicus. In the United States, from 1970 to 1995, a total of 341 cases of human plague (average, 13 cases per year) were reported (CDC, 1996). The disease is also associated with cats, goats, camels, rabbits, dogs, coyotes, prairie dogs, and fox squirrels. Cats have been the source of infection in several human cases. Domestic cats are a principal cause of human pneumonic plague in the United States. Persons working in veterinary practices should be especially aware of the risks involved in handling Y. pestis–infected cats. Dogs and cats may serve as passive transporters of infected rodent fleas into the home. Transmission: The primary method of transmission involves contact with infected rodent fleas (over three-quarters of human cases) or direct rodent contact. Fleas may remain infected for months, so the disease may be apparent, go into “hiding,” and recur at a later time. A protein secreted by Yersinia serves as a coagulase that causes blood ingested by the flea to clot in the proventriculus. The bacillus proliferates in the proventriculus, and thousands of organisms are subsequently produced. The flea regurgitates to clear its obstruction after biting

Preventive Medicine

an animal or person. The material is injected intradermally or subdermally, and a new infection is born. This coagulase produced by the organism is inactivated by high environmental temperatures and this is believed to explain the disruption of plague transmission during very hot weather—the blood fails to coagulate and the organisms cannot reproduce in the flea’s proventriculus. Human infections from nonrodent species usually result from direct contact with infected tissues, by scratch or bite injuries, and handling of infected animals. The pulmonary form of this disease is often rapid in onset and dramatic in its incapacitation of the patient; the disease results from airborne or droplet infection from infected animals. Disease in animals: In dogs, this is generally a brief self-limiting illness. In cats, the disease is often severe and a fatal infection, with fever, lymphadenopathy, hemorrhagic pneumonia, and encephalitis. Cats may also develop a long-term infection resulting in the development of abscesses containing thick, creamy pus. Rodents may carry the disease asymptomatically (the method of the disease surviving a “hot environmental spell”) or develop fatal disease and die. Disease in humans: Incubation of the plague agent is 2–6 days; it may be called bubonic, septicemic, or pneumonic plague depending on the pattern of distribution of the infection. Bubonic is the most common form, causing fever and swollen, tender lymph nodes (called buboes). Pneumonic plague is systemic plague with lung involvement. Mortality may exceed 50%.

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5. Radiographic examination of the thorax will help determine whether the animal has pneumonic plague and, thus, whether aerosol transmission is a danger. Treatment: Streptomycin with tetracycline or chloramphenicol is commonly used to treat the infection. Prevention and control: The easiest and most effective recommendation for prevention of this disease is the elimination of wild rodents in and around the home and fleas on the family pet. In some areas of the world where endemicity is present, public health departments provide a sentinel animal program. There are vaccines available for high-risk personnel, but these are not often required. If you suspect an infected animal, isolate the animal, use appropriate gloves and protective clothing, and treat with an effective parasiticide (if eliminating the fleas) or an appropriate antibiotic.

Tuberculosis Agent, reservoir and incidence: Tuberculosis (TB) is caused by the gram-positive, acid-fast, aerobic bacillus of the Mycobacterium genus. The three most common species of mycobacteria and their susceptible hosts are the following:

Diagnosis: This disease is diagnosed by:

1. M. bovis (susceptible hosts include most warm-blooded vertebrates) 2. M. avium–intracellulare complex (susceptible hosts are birds, swine, sheep, cattle, mink, dogs, cats, humans, and cold-blooded animals) 3. M. tuberculosis (susceptible hosts are humans, nonhuman primates, dogs, and swine)

1. Impression smears of aspirates or blood stained with Gram’s or Giemsa’s stain. Organisms have a typical “safety pin” appearance. 2. Culture of the organisms can be performed by reference laboratories. 3. Fluorescent antibody (FA) assay of smear is confirmatory. 4. Serology via complement fixation, passive hemagglutination, and immunofluorescence [indirect fluorescent antibody (IFA) assay].

In addition to the “common” forms of TB, there are also uncommon forms that occur in certain situations. “Atypical Mycobacterium,” M. scrofulaceum, M. kansasii, and M. intracellulare, have been reported in monkeys and may be present in soil and water. People who keep primates as pets, especially if these individuals or members of their family are immunocompromised (due to other diseases such as HIV), should be alert for pulmonary disease that can be resistant to treatment. The incidence of

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human TB has decreased dramatically in the past several decades due to the Bovine Test and Eradication Program and the availability of effective therapy. Tuberculosis does still occur in humans in the United States and other countries. Although all three types are capable of causing disease, M. tuberculosis (var hominis) is by far the most common. Currently, the incidence of human tuberculosis is increasing as a result of the AIDS epidemic. The late 1990s saw an increase in the number of human cases, reversing a declining trend from the middle of the century up until the mid-1980s. The rise in human tuberculosis is also complicated by a rise in drug-resistant cases. Nonhuman primates may carry all three forms of the disease, but most infections found in pet animals are caused by M. tuberculosis var hominis; this is an example of an anthropozoonosis. In close confinement the disease can spread rapidly. Transmission: Mycobacterium bacilli are transmitted from infected animals or infected tissue primarily via the aerosol route, but the disease may also be contracted via ingestion or cutaneous inoculation of the bacilli. Personnel caring for infected animals as well as those performing necropsies on infected animals are at higher risk for contracting the disease. Exposure to dusty bedding of infected animals, coughing of infected animals, and aerosolization of the organism during sanitation procedures may also be sources of the disease in the veterinary hospital environment. Once within the body the organism may spread throughout the lungs, lymphatics, blood vascular system, and many visceral organs. Disease in nonhuman primates: Signs of TB may be insidious with only slight behavioral changes noticed, followed by anorexia and lethargy. Often animals die suddenly while appearing, up to the point of death, as being in good condition. Other signs that might be seen include diarrhea, suppuration of lymph nodes, ulceration of the skin, and palpable splenomegaly and hepatomegaly. The organ of predilection is the lung, but lesions may also be seen in the pleura, intestines, lymph nodes, liver, kidney, spleen, and peritoneum. Under the surface of these tissues are yellowish-white to

Exotic Small Mammal Care and Husbandry

gray nodules filled with caseous material that may rupture and produce cavitation. Although skeletal involvement is rare, tuberculosis of the spine may cause paralysis of the hind limbs, commonly called Potts disease. Disease in humans: In humans the clinical signs depend on the organ system involved. The most familiar signs related to pulmonary TB are cough, sputum production, and hemoptysis. The human patient may be asymptomatic for years. General signs may include anorexia, weight loss, lassitude, fatigue, fever, chills and cachexia. Tuberculosis may affect virtually every other organ system, with signs or symptoms relating to the individual system. Miliary TB may be more often associated with the very young or old people. Cutaneous TB is also called pathologist’s wart. Mycobacterium avium ssp. paratuberculosis (formerly M. paratuberculosis) has been implicated as a possible cause of Crohn’s disease in people. Diagnosis: The diagnosis of TB is often difficult. Three tests are commonly used for presumptive diagnosis: Animals are generally diagnosed by an intradermal TB test, radiography, or an acid-fast stained smear. In cases where the animal has died, histopathology may also be used. Prevention and control: The best measures of prevention include a multifaceted approach of pet owner education (especially if the owner has immunocompromised individuals in their lifestyle and there are primate pets involved). A regular health surveillance program for humans and monkeys is critical to catching the disease during the early phases, and it offers the best surveillance tool for this disease. Although a vaccine is available in Europe, it is not used in North America because it results in a positive TB test, which requires additional assessment tools to rule out active infection. The vaccine, BCG (Bacille Calmette-Guerin) is a modified strain of M. Bovis and is effective when used in high risk groups. Isoniazid therapy is currently effective in treating nonresistant mycobacterial strains, but the survival of this disease for thousands of years would suggest prevention is the better option than attempting to cure the disease.

Preventive Medicine

Listeriosis Agent: There are seven recognized species of Listeria, with L. monocytogenes and L. ivanovii considered pathogenic—presumably related to the presence of a hemolytic enzyme, listeriolysin O. Listeria are gram-positive, small pleomorphic rods. Reservoir and incidence: This agent is isolated from fish, birds, swine, horses, ruminants, guinea pigs, ferrets, gerbils, rabbits, and chinchillas. Transmission: Oral and conjunctival routes are most common but other means of transmission can occur. Cutaneous listeriosis appears to be the occupation-related form most likely acquired by animal care and technical staff. In one case, reported in a dairy farmer who assisted in delivering a calf, the organism was subsequently isolated from vaginal pustules on the cow. Disease in animals: The signs observed with this disease depend in some part upon the species infected. For example, in rabbits, vaginal discharge, abortion, and metritis in pregnant does is common; in rodents and birds it is more likely to find generalized septicemia; in ruminants, encephalitis or mastitis may be seen. Disease in humans: Cutaneous involvement, coryza, conjunctivitis, metritis with abortion, sepsis, and meningitis all have been reported in humans. Most cases of listeriosis develop in people who are immunocompromised, elderly, or pregnant or who have handled fetal or newborn tissues from infected animals while not using adequate personal protective measures. Diagnosis: This is not an easy organism to culture and will require special media and laboratory equipment. Prevention and control: Caution and protective clothing when handling infected tissues are the best measures to prevent an infection from this agent.

Leptospirosis Agent: The agent is a spirochete, Leptospira (130 serotypes).

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Reservoir and incidence: Most animal species have one or more serotypes of Leptospira that may infect them. Rats, mice, field moles, guinea pigs, gerbils, squirrels, rabbits, hamsters, reptiles, nonhuman primates, livestock, and dogs have all been reported to host leptospira organisms. Up to 40% of stray dogs have been found to be seropositive to one or more serotypes of Leptospira. Rodents (especially rats and mice) can host and shed L. ballum throughout their entire life and during shedding may not exhibit any clinical manifestations. This is a unique feature of rodent infection with leptospires. On occasion the first indication of an infected animal will be reports of human infections with this agent. Transmission: Infection generally occurs from handling affected animals or tissues, contaminating hands or abrasions with rodent urine, or aerosol exposure during cage cleaning. There is a single case of a mother transmitting the disease to her breast-fed infant, presumptively through the breast milk, although fomite contamination from the environment could not be ruled out. Disease in animals: In animals, the disease is generally inapparent but conjunctivitis, pneumonia, jaundice, and hemorrhage have been reported. Pet monkeys have exhibited hepatic necrosis and interstitial nephritis. Abortion and persistent renal infections have also been reported in some animals. Generally speaking, host-adapted strains produce mild illness in the host animals, with nonadapted strains causing more severe disease in the new species. Disease in humans: The disease in humans ranges from inapparent infection to severe infection and including death. There is generally a biphasic illness that consists of weakness, headache, myalgia, malaise, chills, and fever, followed by leukocytosis, painful orchitis (testes not usually enlarged), conjunctival effusion, and rash. Diagnosis: This agent has a characteristic presentation under a silver stain such as Warthin–Starry, but serological diagnosis and isolation of organisms and culture are necessary for definitive diagnosis. Culturing leptospires is

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difficult and requires several weeks. Serology is accomplished by indirect hemagglutination, agglutination, complement fixation (CF), microagglutination, and FA techniques. The “preferred test” is the Modified Microtiter Agglutination Test. A 1 : 100 or greater titer is of diagnostic importance. Leptospires can be recovered only from mature mice even though antibodies can be detected from infected mice of all ages. Treatment: Chlortetracycline, dihydrostreptomycin, penicillin G, and amoxicillin have all been used effectively to treat this disease. Leptospira ballum was eliminated from a rodent breeding colony (mice) by using 1,000 g chlortetracycline HCL/ton of feed for 10 days. Prevention and control: The best prevention in this case is vaccination of cattle, swine, and dogs. There are no vaccines for rodents or other pets.

Lyme disease (borreliosis) Agent: This agent varies around the world. Borrelia burgdorferi is found in the United States and Canada; B. garinii and B. afzelii are found in Europe; B. japonica is found in Japan and Asia. Incidence: Borreliosis was first implicated in 1982 as the causative agent in a 1975 epidemic of juvenile inflammatory arthropathy in Old Lyme, Connecticut, and named after the town where the disease occurred. Lyme disease is now considered endemic in more than 23 states and southeastern Ontario, Canada. It is the most frequently reported tick-associated disease in North America. With over 15,000 cases reported annually, eight states accounted for 91% of the nationally reported cases (Connecticut, Rhode Island, New York, New Jersey, Delaware, Pennsylvania, Maryland, and Wisconsin, from most to fewest cases reported). Reservoir and incidence: Lyme disease is transmitted principally by Ixodes spp. ticks. Ixodes are three-host ticks with a 2- to 3-year life cycle. Larvae feed primarily on rodents, especially mice. Nymphs feed on all hosts and are primarily responsible for transmission of the disease to people. Infected ticks must be

Exotic Small Mammal Care and Husbandry

attached to the host for approximately 48 hours before spirochetes are transmitted. Ixodid ticks have a broad range of hosts. Ixodes scapularis is the primary vector in the eastern and midwestern United States, I. pacificus on the Pacific Coast of the United States, I. ricinus in Europe, and I. persulcatus in eastern Russia and Eurasia. Peromyscus leucopus, the white-footed mouse, is the primary reservoir in the northeastern United States. The deer mouse (P. maniculatus), chipmunks (Tamias striatus), voles (Microtus pennsylvanicus), house mice (Mus musculus), Norway rats (Rattus norvegicus), and rabbits (Oryctolagus cuniculus) can also transfer infection to ticks, but with less efficiency than the white-footed mouse. In northern California the dusky-footed woodrat (Neotoma fuscipes) is the primary reservoir, and I. pacificus serves as a vector for transmitting the disease to humans. In northern Colorado borreliosis transmission is maintained by the Mexican woodrat (N. mexicana) and I. spinipalpis. Cotton rats (Sigmodon hispidus) and rice rats (Oryzomys palustris) are potential reservoirs. Reptiles and birds can be infected with spirochetes, but their role as reservoirs remains poorly defined. White-tailed deer (Odocoileus virginianus) and roe deer can serve as primary hosts of adult ticks, but they do not appear to serve as reservoirs for the spirochete. Recent studies have suggested that arthropod vectors may not be necessary for transmission; in these cases it appears the organism was transmitted by direct contact with mice and dogs. Assuming direct transmission is possible, it is most likely via infected urine; the agent has been found in the kidney and urine of feral hosts. It has also been isolated from blood, cerebrospinal fluid (CSF), tissues, and joints. Transplacental infection has occurred in humans. Spirochetes can penetrate skin, but the public health risk from this mode of transmission is not known. Disease in animals: Clinical signs of infection are not seen in the primary reservoirs. In dogs, diagnosis is usually clinical due to sensitivity and specificity problems with serologic test kits. Signs include transient, recurrent, brief episodes of gait abnormality associated with swollen joints, anorexia, lethargy, and response to antibiotic treatment.

Preventive Medicine

Disease in humans: Multisystemic disease that may have chronic sequelae is the more common finding. An annular rash known as erythema chronicum migrans (ECM) develops in the area of the tick bite. The outer edge of the ECM lesion expands and develops a ringlike appearance as the center of the lesion clears. Human patients may also experience flulike symptoms, which resolve in about 3 weeks. Eight percent of people develop mild cardiac involvement several weeks after infection, which is generally transient. Fifteen percent of affected humans develop neurologic disorders such as facial nerve palsies that usually resolve without treatment. Sixty percent of human cases develop the most common sequelae, arthritis. Disease may remain latent with symptoms developing 4 years after seroconversion. Diagnosis: The recommended test is detection of antibody titers. Evaluation for CSF antibody can be used to diagnose Lyme neuro-borreliosis. Culture of the expanding border of an ECM lesion is definitive but is difficult and requires special media such as Barbour–Stoener–Kelly media. Diagnosis may be made histologically with Dieterle silver stain or immunoperoxidase stains but is often unrewarding. Treatment: Antibiotics such as doxycycline for adults, amoxicillin for children, and intravenous ceftriaxone for active neuro-borreliosis have been successfully used. Prevention and control: Tick control is the best method of preventing the spread of this disease. Technical staff should be careful when removing ticks or when handling potentially infective materials. There are two vaccines currently marketed for dogs, both of which are reasonably effective. For humans, a proposed vaccine containing two “outer surface proteins” (A and B) provides dual protection by protecting the host as well as eliminating the spirochete in the intestinal tract of the attached ticks.

Enteric infections Campylobacteriosis Agent: Campylobacter (Vibrio) fetus ssp. jejuni is a gram-negative, microaerophilic,

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curved, motile rod that is worldwide in distribution. Reservoir and incidence: This agent is commonly found as a commensal in the gastrointestinal tract of ruminants, swine, dogs, cats, fowl, rodents, and monkeys. Of 218 human cases of C. jejuni infection in the northwest United States, 6.3% were attributed to exposure to animals with diarrhea (principally dogs). Many of these cases were diarrhetic puppies from pounds or shelters. Prevalence surveys showed that Campylobacter can be isolated from an average of 25%–30% of all dogs and 10%–15% of all cats tested. Pet birds, chickens, and kittens have also been implicated as reservoirs of this disease. Veterinary technicians have occasionally contracted this disease but usually from cleaning excretions of infected animals. The organism was first isolated in 1979, so it is a relativly “new” disease. Transmission: Transmission is generally via a fecal–oral route, through contamination of food or water, or by direct contact with infected fecal material. The organism has also been isolated from house flies, so good insect control is valuable when sick or diarrhetic animals are present. At 4 °C, the organism is viable for 3 weeks in feces and milk, 4 weeks in water, and 5 weeks in urine. Winter temperatures may preserve the organism rather than eliminate it. Campylobacter may be shed in the feces for at least 6 weeks after infection. Commercial animal feeds have been considered as potential sources of the organism. Disease in animals: Affected animals are generally presented with a history of diarrhea, which may range from excessive soft stool to watery and fetid. Campylobacter may be shed for extremely long periods of time in stool. Carrier animals may not show any signs of disease (they may have “normal” stool). Younger animals seem more likely to acquire the infection, but it is unclear whether the increased infection rate is related more to their generally more curious behavior or to their immature immune system. In either case, young animals have been implicated as more commonly being the cause of the disease. Ferrets appear to be especially susceptible, having

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signs ranging from asymptomatic to proliferative colitis. Ferrets have been shown to shed organisms for up to 16 weeks. Campylobacter has also been shown to cause hepatitis in poultry and abortion in ruminants. Disease in humans: Humans will experience acute gastrointestinal illness, diarrhea with or without blood, abdominal pain, and general constitutional symptoms, without fever. Usually, campylobacter is a brief, albeit painful, self-limiting disease. The asymptomatic carrier state in humans is rare. Reinfection is possible in both animals and humans. Diagnosis: Campylobacter may be identified using dark field or phase contrast microscopy of fecal material. This should be confirmed by stool culture, which requires a special selective growth medium (CAMPY-BAP) and incubation at 43 °C with 10% CO2, 5% O2, and 85% nitrogen. A Warthin–Starry silver stain and histology sections may also be employed. Various seroconversion techniques may also be considered. Treatment: Animals may be treated based on culture and sensitivity. Currently erythromycin is the drug of choice, but it does not eliminate the carrier state. Prevention and control: In select circumstances, vaccines provide partial protection of short duration; however, routine use is not recommended. Control should be aimed at isolation of affected individuals and improvement of personal hygiene. An increased awareness of the potential of infection due to Campylobacter is of primary importance to preventing a common animal pathogen from affecting humans in the area. Related organisms, Arcobacter cryaerophilus and A. butzleri, formerly called Campylobacter-like, also cause diarrhea and enterocolitis in humans. In farm animals they have been shown to cause abortion, stillbirths, and diarrhea. Many consider Arcobacter as a new and emerging human and animal pathogen.

Salmonella Agent: Salmonella is a gram-negative bacteria. It is suggested that all salmonellae belong

Exotic Small Mammal Care and Husbandry

to a single species, S. enterica, with multiple serotypes. Out of 2,296 recognized serotypes of Salmonella, S. typhimurium and S. enteritidis have been associated most commonly with lab animal colony infections. The most frequently isolated serotypes from nonhuman sources in the United States are S. typhimurium, S. enteritidis, S. heidelberg, S. hadar, and S. choleraesuis. A multiple-drug-resistant strain of S. enterica serotype typhimurium known as Definitive Type 104 (DT104) has emerged as an increasing cause of Salmonella infections. DT104 isolates are highly resistant to antimicrobial agents, frequently demonstrating a pattern of resistance to ampicillin, chloramphenicol, streptomycin, sulfonamides, and tetracyclines. All Salmonella infections, except for S. typhi, S. paratyphi A, and S. paratyphi C, are considered zoonoses. Reservoir and incidence: Salmonella occurs worldwide. Salmonella inhabits the intestinal tract of many animals, including birds, rodents (rats, mice, hamsters, guinea pigs), monkeys, and humans. Salmonella DT104 has been isolated from cats, wild birds, rodents, foxes, and badgers, and it has been transmitted from cattle and sheep to people. The house mouse may also be a reservoir of the infection and may play a role in human and animal salmonellosis. Humans or animals may serve as asymptomatic carriers of Salmonella. Salmonella prevalence in the US canine population has been reported to range from 5% to 10%. In another study, 11% of humane society cats were found to carry Salmonella. Birds, reptiles, and turtles are especially dangerous sources of salmonellosis; over 90% of all reptiles harbor Salmonella. In 1970, turtles alone caused 280,000 human cases of salmonellosis. Responding to the public health crisis, the Food and Drug Administration (FDA), in a 1975 ruling, issued a prohibition against the selling of viable turtle eggs or live turtles with a carapace length <10.2 cm (4 inches). The small “box turtle” was a common pet at that time and the cause of almost all cases of zoonotic salmonellosis in children. After the FDA ruling, there was a 77% decrease in turtleassociated salmonellosis. As a side note, marine (ocean) turtles have not been shown to be a reservoir of Salmonella.

Preventive Medicine

Transmission: This infection occurs via indirect transmission through contaminated food and water. It is possible, but less likely, that transmission may also be by direct contact and inhalation. Salmonella DT104 is associated with contact with sick farm animals and eating contaminated meats. Salmonella is a common contaminant of sewage and is found in many environmental water sources. Environmental contamination (low-lying wet areas, swampy areas) continues to be a potential source of infection for animals and secondarily for personnel handling those animals. Animal feed containing animal by-products may be a source of Salmonella contamination, especially if the diets consist of raw meal and have not undergone the pelleting process. Neonates, old animals, animals with concurrent infections, and stressed animals are most susceptible to disease. Disease in animals: There are five basic patterns of infection in animals: 1. Primary salmonellosis—septicemia, acute enteritis, or chronic enteritis. 2. Concurrent disease or stress—another disease creates conditions making the individual more susceptible to a secondary disease such as salmonellosis. 3. Chronic carrier—shows no signs of the disease, appears healthy yet continues to seed the environment with the disease agent. 4. Temporary carrier—is generally quite ill, but provides large quantities of disease agent to the environment. 5. Latent infection—does not express the disease, appears healthy. Disease in humans: This disease manifests itself as acute gastroenteritis with sudden onset of abdominal pain, diarrhea, nausea, and fever. It may lead to septicemia, or it could show as a long-term inapparent infection. Diagnosis: The preferred manner of diagnosis is fecal culture with selective media. Caution: False negatives do occur because organisms may be shed intermittently. In certain animals, the carrier state bacterium has been localized to the gall bladder (monkeys).

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Prevention and control: Obtain pets from a “clean” source. Treatment should be based on culture and sensitivity, rather than prophylactic therapy that may cause bacterial resistance. Use good sanitation, protective clothing, and gloves when working with suspect animals. Rodent, bird, and wild animal control is important, and cleanup of contamination may be helpful in preventing infection in pets. The best measure of prevention is strong personal hygiene.

Helicobacter Agent: Although there are numerous helicobacters known to science, only Helicobacter heilmannii (H. bizzozeronii) and H. felis have been implicated in zoonotic transmission at this time. Reservoir and incidence: Currently reports are sparse, but because these agents colonize in a small percentage of humans with gastritis (primary species in humans with gastritis is H. pyloris), and no environmental source for these bacteria has been recognized, pets have been implicated as a possible source of infection. Three reports of human gastritis caused by these two species implicate cats and dogs as the probable sources of infection. Helicobacter pylori has recently been isolated from commercially reared cats and it has been shown to experimentally colonize in both dogs and cats. It has also been shown experimentally that the specific (human) strain of H. pylori also infects and induces persistent gastritis in cats. Transmission: This is principally a fecal–oral transmission, although one case suggested a child was infected by repeated exposure to infected dog vomitus. Disease in animals: This disease may range from inapparent infection to active chronic gastritis. Disease in humans: Clinically, the same range of expression observed in animals may also be observed in humans. Diagnosis: Culture, biopsy, and histopathology are the most frequent methods of diagnosis. A urease tissue assay, urea breath test,

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serology, or polymerase chain reaction (PCR) may also prove worthwhile in select cases. Treatment and prevention: Treatment consists of a triple therapy regimen with amoxicillin or tetracycline; metronidazole; and bismuth subsalicylate. Other regimens with reported success include ranitidine or omeprazole.

Respiratory or cutaneous infections Erysipeloid Agent: The agent is Erysipelothrix rhusiopathiae (insidiosa). It was discovered by Robert Koch, who called it the Bacillus of Mouse Septicemia. Reservoir and incidence: A saprophyte of soil, water, and decaying organic matter, erysipelothrix may be a pathogen in pigs, lambs, calves, poultry, aquatic species, and wild and pet rodents. Although many pet species may be affected, pigs probably represent the most likely source of exposure. Zoonotic transmission from pet rodents has not been reported. Transmission: The potential for zoonotic transmission is contamination of wounds by handling infected tissues. Disease in animals: Called Diamond Skin Disease in pigs due to the characteristic lesions. The organism causes clotting in the small arteries of the skin, resulting in a diamond-like appearance due to the affected branching vessels not having blood supply and the surrounding tissue dying. The same organism causes arthritis in many species, and has been reported to manifest as “bluing” of the redskinned areas of poultry. It is generally a septicemic disease, and the sequelae associated with systemic disease should be considered. Disease in humans: Disease in humans is called erysipeloid and is primarily occupationrelated to owners of pigs, or those who work or care for sick or injured pigs. Inflammatory lesions of the skin, with elevated erythematous edge that spreads circumferentially, are the most common findings. Septicemia is an infrequent complication. Diagnosis: The organism can be cultured from the lesion or blood.

Exotic Small Mammal Care and Husbandry

Prevention and control: Although personal protective measures (gloves, hand washing, etc.) may prevent zoonotic potential, treatment of infected animals can be accomplished with penicillins. A vaccine is available for swine and turkeys, but it should not be used in pets.

Meliodosis Agent: Burkholderia pseudomallei (Pseudomonas pseudomallei) is a motile, gram-negative rod. Reservoir and incidence: This agent is a normal inhabitant of surface soil and water in many tropical areas, especially Southeast Asia. It occurs in wild rodents, goats, pigs, and sheep, and it has been identified in numerous nonhuman primate species. Transmission: Transmission occurs via the bite of an infected rodent, or by inhalation from moist soil or a stagnant water reservoir, or by ingestion of contaminated feeds. Disease in animals: Skin lesions appear with chronic draining, fistulous tracks. Emaciation and multiple abscesses in lung, bone, and viscera also occur. A chronic draining purulent skin lesion should be suspect. Incubation period in a host can be 6 months to 3 years, making identification of the source of transmission extremely difficult. Disease in humans: Clinical disease is not common in humans, but subclinical disease in endemic areas (based on serology) is common. There is a high case fatality rate (80%) for people who do develop clinical signs of multiple abscesses or draining fistulas. Diagnosis: This disease is diagnosed by culture and isolation from lesions.

Tularemia (rabbit fever) Agent: Two strains of Francisella tularensis are agents: Type A strain (F. tularensis var. tularensis) is only seen in North America and causes the disease in humans and rabbits. Type B strain (F. tularensis var. palaearctica) is found worldwide except for Australia and Antarctica (marine animals) and has lower virulence.

Preventive Medicine

Reservoir and incidence: This is a common and often fatal septicemic disease of rabbits, squirrels, muskrats, deer, bull snakes, sheep, wild rodents, cats, and dogs. The major reservoirs in North America include rabbits, ticks, and muskrats. It has also been reported in monkeys at city zoos, most probably infected by wandering rabbits or rodents. Recent reports suggest that tularemia should be considered in cats with a history of ingesting wild prey that manifest signs of malaise, lymphadenopathy, and oral ulcers. Transmission: The handling of tissue from infected animals is the primary means of transmission. Direct contact with skin (it doesn’t have to be a skin lesion) is sufficient for human infection to occur. There have been reported human infections also due to a cat bite, a cat scratch, or a pet monkey bite. The disease may also be transmitted by biting insects, such as ticks or deerflies. Less commonly, it has been transmitted by inhalation, ingestion, and exposure of mucous membranes. Disease in animals: The most typical gross lesions are white-gray foci of necrosis found on surfaces of the spleen, liver, and lymph nodes. Generalized illness and cutaneous hemorrhage has also been reported. Disease in humans: Two forms of this disease exist: the ulceroglandular form (75%–85% of cases), and the typhoidal form (5%–15% of cases). Pleuropulmonary complications develop in 30%–80% of typhoidal cases and 10%– 15% of ulceroglandular cases. Diagnosis: The agents may be cultured, but this requires specialized laboratory equipment and agar (glucose cysteine agar with thiamine or cystine heart agar). Immunofluorescent techniques may be used for agent identification in tissues, and an agglutination titer (must see fourfold rise in titer between acute and convalescent serum) can also serve as a diagnostic tool. Prevention and control: As with many diseases, strong personal protective measures are always worthwhile. Technicians should at a minimum wear gloves while handling poten-

33

tially infected animals or tissues. Controlling ticks is an important aspect of disease management. An experimental vaccine for high-risk personnel does exist in specialized research settings (this agent has been suggested as a potential biological warfare agent; the vaccine is available just in case). Treatment is fairly simple; caught in the early stages, streptomycin or gentamicin is effective at eliminating the agent.

Streptococci There is an overlap of disease-producing streptococci of animals and humans, but generally speaking zoonotic transmission appears rare. Agent:

There are three agents:

1. Gram-positive cocci, many pathogenic species of Streptococcus, including S. pneumoniae, S. pyogenes (Group A), S. suis, and S. (Enterococcus) faecalis. 2. Lancefield serologic Group C organisms produce most disease in pet animals. Only occasionally are Groups A, B, D, and G implicated in animal infections. 3. Most human infection is caused by Lancefield Group A. Groups B, C, D, F, and G can also be pathogenic in humans. Reservoir and incidence: Streptococcus occurs in many species, including calves, monkeys, guinea pigs, rats, and humans. Pet cats and dogs have been implicated in recurrent strep sore throat infections in members of the household. However, if a Group A Streptococcus is found (which is the more common finding), it is highly unlikely that an animal reservoir was involved. Streptococcus suis has been isolated from swine, cattle, cats, and horses; human infections have been reported mostly in western Europe with two cases reported in Canada. Transmission: Fomite transmission may occur, but inhalation is also a common means of transmitting the disease. Disease in animals: Often this disease is inapparent, but it may range from mild respiratory disease to severe pneumonia. Meningoencephalitis has been reported in monkeys (S. pneu-

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moniae). Streptococcus suis causes meningitis, pericarditis, and pneumonia in pigs. Disease in humans: As with animals, this disease is highly variable and may be observed as a sore throat, pneumonia, or other systemic condition such as mastitis or abscessation. When S. suis becomes systemic, generalized septicemia, joint pain, and meningitis may occur. Streptococcus pyogenes (Group A) has resulted in a toxic-shock-like syndrome and necrotizing fasciitis. Diagnosis: Isolation and culture. Prevention and control: The key to preventing this disease is wearing of protective clothing and proper safety equipment when working with animals having the disease. Hand washing after working with any animal is considered a minimum, and this is a case where hand washing is highly effective at preventing incidental transmission.

Pseudomonas Agent: Pseudomonas aeruginosa is a small, motile, gram-negative rod. Reservoir and incidence: Normally, pseudomonas is a saprophytic (not dangerous) organism that is ubiquitous (found many places) in the environment.

Exotic Small Mammal Care and Husbandry

where the abscess has grown to a remarkable size and the animal continues to be “normal.” The medical concern begins when the abscess occurs in a physiologically important area of the body where it may be life threatening— nervous system, liver, kidney—rather than a subcutaneous location (rarely are significant signs observed). Disease in humans: This disease is rare in an immunologically “normal” individual, but immunosuppression or other ongoing diseases may provide the “open door” for a serious, even fatal, infection with pseudomonas. Client education is critical when there are immunosuppressed humans living near or with animals that may have pseudomonas. Diagnosis: Culture and treatment of the affected animal is generally successful. In advanced cases, draining the abscess and treatment of secondary sequelae may be necessary. Prevention and control: Due to the ubiquitous nature of this agent, it is difficult to truly prevent the agent from being in or near animals. The best measure of prevention is a strong program of good animal husbandry and rapid treatment of affected animals with properly selected antibiotics.

Staphylococci Agent:

Transmission: Pets and their human companions may both serve as the disease host. Two outbreaks of Pseudomonas infection within a small mouse colony were linked to the infected human companions. What is curious is that while we clearly recognize pseudomonas in animals and humans, and the same subtypes of the agent are found in both human and animal disease conditions, there has yet to be a single case of documented animal-to-human transmission. It is likely that animal-to-human transmission has occurred, but the ubiquitous nature of this agent makes it difficult to be certain of the incident source. Disease in animals: Often animals carry this agent with no evidence of disease. There are, however, plenty of cases of pseudomonas abscessation, especially of rodents and rabbits,

Staphylococcus spp.

Reservoir and incidence: Normally a saprophytic (not dangerous) organism that is ubiquitous (found many places) in the environment, this agent can be found on all mammals, from the skin to the gastrointestinal tract. Transmission: Because this agent is a commensal for mammals, discussion of transmission is not necessary. It becomes more of a review of the stress factors on the individual that allowed for the development of disease from the individual’s own staphylococcus colonies. As with pseudomonas, while we clearly recognize staphylococcus in animals and humans, there had yet to be a single case of documented animal-to-human transmission. It is likely that animal-to-human transmission has occurred, but the ubiquitous nature of this

Preventive Medicine

agent makes it difficult to be certain of the incident source. Supporting an argument of potential zoonotic transmission, human phage types of S. aureus have caused disease with immune-compromised research rodent colonies. In these same research rodent colonies, human care providers have been found to have seroconverted to the same phage type, thereby supporting an argument for zoonotic transmission of this agent. However, the real potential of zoonotic transmission remains poorly understood. Disease in animals: Often animals carry this agent with no evidence of disease. There are, however, numerous examples of staphylococcus abscessation in rodents and rabbits. The majority of these cases present simply as a “normal” animal with a very large abscess. As with pseudomonas, the medical concern occurs when the abscessation occurs in a physiologically important area of the body where it may be life threatening—nervous system, liver, kidney—rather than a subcutaneous location (rarely are significant signs observed). Disease in humans: This disease is rare in an immunologically “normal” individual, but immunosuppression or other ongoing diseases may provide the “open door” for a serious, even fatal infection. Client education is critical when there are immunosuppressed humans living near or with animals that may have staphylococcus. Diagnosis: Culture and treatment of the affected animal is generally successful. In advanced cases, draining the abscess and treatment of secondary sequellae may be necessary. Prevention and control: Due to the ubiquitous nature of this agent, it is difficult to truly prevent the agent from being in or near animals. The best measure of prevention is a strong program of good animal husbandry and rapid treatment of affected animals with properly selected antibiotics.

Rat bite fever Agent: Gram-negative, pleomorphic bacillus. Two different agents can cause disease:

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1. Streptobacillus moniliformis (Haverhill fever—named after a 1926 outbreak in Haverhill, Massachusetts, attributed to contaminated milk). 2. Spirillum minus (Sodoku). Reservoir and incidence: The agent is present in the oral and respiratory passages of a large number of asymptomatic rodents, especially rats and mice. Incidence of disease, however, appears to be low. Transmission: Generally, human infection comes from close association with infected rodents, usually the bite of an infected rodent. Historically, or in parts of the world where dairy or food sanitation is lacking, infection may also occur via ingestion of contaminated milk or food. Disease in animals: In rats and mice, the infection of an immune-competent animal is inapparent. For conditions where the rodent is diseased, acute, systemic and fatal conditions occur, exhibiting suppurative polyarthritis, swelling, and loss of digits or limbs (for survivors of the disease). Disease in humans: In humans, an acute febrile disease may result following a bite from a rodent. Clinical symptoms include inflammation, lymphadenopathy, and nonspecific signs such as a rash on the extremities (often just the soles and palms). Arthritis has occurred with S. moniliformis. Because the two agents have vastly different incubation periods, the time from potential infection to onset of disease may offer insight into which agent is at fault. Streptobacillus moniliformis only requires hours to 1–3 days for clinical disease. Spirillum minus incubates in the body for 1–6 weeks prior to erupting with clinical disease. In both cases, and in immune-competent individuals, symptoms usually resolve spontaneously, assisted by the appropriate antibiotic. If left untreated, complications may lead to pneumonia, hepatitis, enteritis, and endocarditis. Diagnosis: Culture is the primary method of confirming the disease. Streptobacillus moniliformis requires 10%–20% horse or rabbit serum and reduced oxygen tension. Spirillum

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minus cannot be grown under laboratory conditions; culture may require tissue samples from the infected individual or inoculation into a test rodent with subsequent identification by histology and dark field microscopy. Prevention and control: Proper post-bite treatment of a rodent bite is the best prevention. Extensive washing or scrubbing of the bitten area and application of a topical antibiotic are generally considered effective.

Pasteurellosis Agent: Pasteurella multocida Reservoir and incidence: This agent inhabits the oral cavity and upper respiratory tract of many animals (rabbits, dogs, cats, mice, birds, pigs). Transmission: Infection may occur from an infected animal or via inhalation. One such report noted that a pet owner kissing her dog on the mouth cultured positive for the disease. A subsequent assessment considered the numerous dental caries as being the entry point into her body. Disease in animals: This agent can cause acute pneumonia or septicemic disease in many species. Especially in the rabbit, one may see chronic infection of the upper respiratory tract and the middle ear. Disease in humans: The symptoms and clinical presentation depend upon the development of the disease. Humans may develop septicemia after being bitten by an infected or carrier animal.

Exotic Small Mammal Care and Husbandry

Reservoir and incidence: Bordetella is a common cause of acute respiratory disease in dogs, cats, guinea pigs, rats, rabbits, pigs, horses, monkeys, and sometimes humans. Sometimes called kennel cough, this agent may reside at kennels or animal lodging locations and be spread to new boarders. Transmission: This agent is spread by shedding of respiratory droplets to susceptible animals in close contact or at least near enough for inhalation. Transmission from animals to man has not been reported. Most rabbits and many humans are carriers for bordetella and are the species where bordetella is of greatest significance; one should never house or maintain rabbits and guinea pigs in the same space. In rabbits, the disease is generally inconsequential. In guinea pigs this can be a fatal and rapidly spreading (to other guinea pigs) disease. Disease in animals: Bordetella in animals is an acute respiratory disease, with a hacking cough as the most common presentation. Many of these animals will become carriers of the disease. It is generally not an important disease from the standpoint of being life threatening, but the damage to the client’s “good-will” when retrieving their boarded animal may be significant. In the very young, the aged, ill, or immune-compromised animals, this disease may be life threatening. Disease in humans: Rarely an important disease in humans, it can cause lung abscesses or a whooping-cough-like syndrome.

Prevention and control: The best prevention involves proper treatment of bite wounds with washing and rinsing and the use of effective antibiotics (penicillins, tetracycline, others). When working with potentially infected animals, technicians should wear protective clothing: at a minimum a mask, clothes cover, and gloves.

Prevention and control: A bacterin is available for this agent, but the nasal vaccine is generally considered adequate. In either case, immunity, while strong, is short lived and should be repeated every 6–8 months if animals will be group-housed or if reinfection becomes a potential. Because there have been no zoonotic cases reported, the potential for human infection is low; however, the possibility of transmission by humans to other animals is high. Protective clothing, a face mask, and gloves are recommended.

Bordetellosis

DF-2 and DF-2-like

Agent: Bordetella bronchiseptica, a gramnegative bacillus

Agent: Historically known as Dysgonic Fermenter 2 (DF-2) or DF-2-like organisms, this

Preventive Medicine

group of agents has been renamed Capnocytophaga canimorsus and C. cynodegni, respectively. Reservoir and incidence: Both are found as part of oral flora of normal dogs and cats. The C. cynodegni is closely related to C. canimorsus and causes localized infections following bite wounds but is incapable of causing septicemia like C. canimorsus. Serious C. canimorsus infections in humans are most commonly reported in splenectomized or immunocompromised people, following a bite from dog or cat. More than 40 cases have been reported, many fatal, since first reported in 1976. Transmission: This agent generally requires close contact, a bite, or a scratch from dog (most common), cat, sheep, or cattle. Disease in humans: Capnocytophaga canimorsus infection can lead to cellulitis and overwhelming bacteremia, meningitis, endocarditis, and disseminated intravascular coagulation (DIC). Most serious disease and fatalities have occurred in splenectomized people; however, Capnocytophaga spp. have been associated with infections in both immunocompromised and immunocompetent people. Diagnosis: The diagnosis often occurs through a combination of history, clinical signs, and culture. This organism is very slow growing and may require 8 days or longer of incubation to be visualized. The microscopic examination of the blood smear or buffy coat with Gram’s stain is necessary to detect gramnegative bacilli in neutrophils. Prevention and control: This disease is yet another case in which the technician should be aware of the risk to immune-compromised family members or friends. High-risk individuals may wish to avoid petting or playing with dogs and cats; at a minimum, good hand washing after the interaction has occurred is important. All bite wounds should be treated, but simple antibiotics, even penicillin, are generally effective against this agent. In high-risk individuals, treatment even without signs of infection is recommended.

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Chlamydial diseases Bartonellosis (previously cat scratch disease) Agent: There are four agents: Bartonella henselae [historically associated with cat scratch disease (CSD)], B. quintana (trench fever), B. vinsonii, and B. elizabethae. An indirect fluorescent-antibody (IFA) test for the detection of humoral response to Rochalimaea henselae was developed; its relatively high sensitivity (88%) and specificity (94%) for CSD suggested that R. henselae or a closely related organism may have had an etiologic role. Although a polymerase chain reaction (PCR) assay for Afipia felis showed positive results against specimens from patients with CSD, most investigators believed that R. henselae was the primary etiological agent, with A. felis playing only a minor role. In 1993, convincing evidence was provided to justify reclassification of the four species in the genus Rochalimaea. These four species were united with the genus and named B. henselae, B. quintana, B. vinsonii, and B. elizabethae. This reclassification resulted in the transfer of these organisms from the family Rickettsiaceae to the family Bartonellaceae and removed the family Bartonellaceae from the order Rickettsiales (JAVMA, 1995, p.16). Historically CSD produced a nonfatal and usually mild disease that was also called benign inoculation lymphoreticulosis or nonbacterial regional lymphadenitis. Bartonella spp. are also associated with bacillary angiomatosis, a vasoproliferative tissue reaction seen mainly in immunocompromised individuals, such as AIDS patients or individuals undergoing cancer therapy. Bartonella spp. have also been associated with several other distinct clinical syndromes in people, including bacillary peliosis hepatitis, relapsing fever, endocarditis, retinitis, and pulmonary granulomas. Reservoir and incidence: Bartonella henselae bacteremia has been documented in 25%–41% of healthy cats. Serologic surveys show an overall prevalence of 28% in the United States, lower in the Midwest and Great Plains and higher in the Southeast. High seroprevalence correlated with warm, humid climates. The Centers for Disease Control and Prevention estimates 22,000 cases of CSD

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annually in the United States [(MMWR, 1995 (43:49, p. 915)). Transmission: Human cases of CSD have been strongly associated with cats less than 1 year old, a history of a bite or scratch, contact with fleas. Bartonella henselae has been isolated from fleas obtaining blood meals from naturally infected cats, but vector competence has not been reported. Disease in humans: A primary lesion, most common on the neck or extremities, will develop in 50% of cases and appears approximately 10 days after a bite or scratch. A pustule persists for 1–2 weeks; 10–14 days after the lesion appears, lymphadenopathy develops and usually regresses within 6 weeks. Thirty to fifty percent of the enlarged nodes become suppurative. Of the approximately 65% who develop systemic illness, fever and malaise are the symptoms most often noted. Approximately 10% of previously recognized CSD cases were accompanied by tonsillitis, encephalitis, cerebral arteritis, myelitis, granulomatous hepatitis, splenitis, osteolysis, pneumonia, pleural effusion, and thrombocytopenic purpura. The disease is usually benign and most patients recover spontaneously without sequelae within 2 months. Many unrecognized cases probably occur. Disease appears to confer lifelong immunity. Diagnosis: 1. Isolation of organism 2. PCR 3. Seroconversion [IFA or enzyme-linked immunosorbent assay (ELISA)] with acute disease Prevention and control: 1. Education 2. Wash hands after handling cat 3. Wash cuts and scratches promptly and do not allow cat to lick an open wound

Rickettsial diseases Ehrlichiosis Agent: Ehrlichia chaffeensis.

Exotic Small Mammal Care and Husbandry

Reservoir and incidence: The existence of a reservoir other than the tick is unknown. Because of the similarity between the clinical presentation of E. canis infection in dogs and E. chaffeensis infection in people, and the serologic cross-reaction between the two species, E. canis was considered the etiologic agent of human ehrlichiosis in North America until E. chaffeensis was isolated and characterized in the early 1990s. Ehrlichia canis is not a human pathogen. Transmission: Transmission is via tick bite— the Lone Star tick, Amblyomma americanum, which has a geographic and seasonal distribution compatible with the epidemiology of monocytic ehrlichiosis. Disease in humans: human pathogen.

Ehrlichia canis is not a

Diagnosis: The nonspecific signs and symptoms compatible with ehrlichiosis, added to a history of tick bite or tick contact, may provide strong suspicion. Indirect IFA showing fourfold rise in antibody titer or PCR can be used to confirm the infection. Prevention and control: This disease is best prevented by control of the tick vectors.

Rocky Mountain spotted fever (RMSF) Agent:

Rickettsia rickettsii

Reservoir and incidence: Dogs, wild rodents, and rabbits may each serve as a reservoir host for this disease, which is reported most commonly from the continental United States. The name for this disease comes from its index reports of tick fever in the Rocky Mountain region; however, less than 1% of the cases of the disease occur in this area. Most cases of Rocky Mountain spotted fever (RMSF) occur in the south Atlantic, south central, and southeast states. Twothirds of all human cases are reported in children. Transmission: Distribution of RMSF centers around three vector ticks: Dermacentor andersoni (American wood tick), D. variabilis (American dog tick), and Amblyomma ameri-

Preventive Medicine

canum (Lone Star tick). Ticks are both reservoir and vector, transmitting the organism transovarially. Direct transmission from dogs to humans does not occur, and dogs are unlikely reservoirs as they develop a low rickettsemia. Disease in animals: The signs are highly variable, but they include fever, vomiting, diarrhea, depression, and dependent edema. Ocular lesions are common in dogs and include subconjunctival hemorrhage, hyphema, anterior uveitis, retinal petechiae, and focal retinal edema. Disease in humans: Symptoms are multisystemic with fever, headache, myalgia, maculopapular rash (12%), shock, coma, and death (5%–10%). Diagnosis: Serology is accurate. However, it takes several days using the Weil–Felix testing (agglutination of sera with Proteus spp. antigens), and it is only accurate after the second week of illness. Complement fixation and microimmunofluorescent tests are also used. Direct FA of infected tissues appears a promising modality for the future. Treatment, prevention, and control: Treatment of the active disease consists of tetracycline or chloramphenicol. Chloramphenicol may thwart the increase in antibody concentration in dogs and interferes with serodiagnosis. The most effective measure is the control of ticks on newly arrived animals. Technicians should note that after removal from the animal, the ticks remain infected. Proper removal and disposal with appropriate precautions is required.

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Transmission: The rodent mite, Allodermanyssus sanguineus, transmits the infectious agent to mice and humans. Disease in animals: General malaise and signs of “not feeling well.” Animals may die, but often it is from secondary infections or other causes. Disease in humans: The disease causes chills, fever, and rashes. Usually it is self-limiting, lasting about 1 week. Prevention and control: The key for this disease is to prevent wild mice from accessing the home or the areas where pets are held. Although mites are the vector for the disease, a good mite control program for pet animals is also worthwhile, especially in areas where urban vermin infestation is a potential.

Murine typhus Agent:

Rickettsia typhi (R. mooseri)

Reservoir and incidence: This is a natural pathogen of rats and mice. Other mammals that may serve as a reservoir include cats and their ectoparasites. Outbreaks continue to occur in the United States, and more commonly along the southwest border states. Transmission: The organism is transmitted by fleas (Xenopsylla cheopis, Nasopsyllus fasciatus). Infected flea bites will transmit the disease to either rodents or humans. Disease in animals: Signs would be expected to be similar to humans, but recording chills is difficult, and capturing a fever is dependent upon the time of assessment. Rashes may be the only indication of a problem.

Rickettsial pox Agent: Rickettsia akari Reservoir and incidence: The house mouse is the reservoir host. The disease is most commonly seen in rodent-infested urban dwellings (e.g., New York City and other eastern US cities). Rats and moles can also harbor the organism. Pet rodents may also become infected, but usually through association with vermin-infested dwellings.

Disease in humans: In humans, symptoms include chills, fever, and rash. These are usually self-limiting, lasting only a few days to weeks. Prevention and control: Similar to other conditions, the key is controlling the reservoir and the vectors. In endemic areas, eliminating fleas and preventing access of rats into the house or areas where pets are maintained is necessary to prevent infection.

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Typhuslike (unnamed) disease Agent: Rickettsia felis Reservoir and incidence: This is a “new” rickettsial disease identified by comparison of 16S rRNA and 17-kDa protein gene segment comparisons. In select areas such as southern California and Texas, the classic rat–flea–rat cycle of R. typhi has been replaced by a peridomestic animal cycle involving free-ranging cats, dogs, and opossums and their fleas. Rickettsia felis was identified from the blood of a hospitalized febrile patient and from the patient’s fleas in the course of epidemiologic investigations. Rickettsia felis has also been isolated from cat fleas.

Exotic Small Mammal Care and Husbandry

M. canis (pathogen for dogs) has been isolated from the throat of a pet dog and from each human member of the household. M. fermitans (incognitus) (human pathogen), commonly associated with genital disease, has been suggested to be a cofactor for HIV infections but certainly is a common “opportunistic pathogen” in HIV patients. It remains unclear whether actual infection with clinical disease can result from such colonization. On rare occasions, veterinarians or veterinary technicians may contract mycoplasma while treating infected pets (e.g., cat abscess).

FUNGAL INFECTIONS

Transmission: This disease may be transmitted by fleas (Xenopsylla cheopis, Nasopsyllus fasciatus) to other animals or humans.

Dermatomycosis (ringworm)

Disease in animals: Signs would be expected to be similar to humans, but recording chills is difficult, and capturing a fever is dependent upon the time of assessment. Rashes may be the only indication of a problem.

1. Geophilic—inhabit soil 2. Zoophilic—parasitic on animals 3. Anthropophilic—primarily infect humans

Disease in humans: The symptoms in humans are the typical typhuslike symptoms of chills, fever, and rash. Prevention and control: Similar to other conditions, the key is controlling the reservoir and the vectors. In endemic areas, eliminating fleas from pet cats and preventing access of infested cats into the house or areas where pets or humans live is necessary to prevent infection.

Mycoplasma infections Mycoplasma Agent: Mycoplasmas lack a cell wall and are the smallest known organisms capable of freeliving existence. They are believed to be relatively host specific, but mycoplasmas that cause disease in lower animals have been isolated from man, for example: Mycoplasma arthritidis (rodent pathogen) has been isolated from the human genital tract, synovial fluid, bone marrow, and lymph nodes.

Agent: Ringworm agents are classified as follows:

All of these can produce disease in humans and animals. Ringworm agents are also grouped in three genera: 1. Microsporum 2. Trichophyton 3. Epidermophyton Reservoir and incidence: Exposure to reservoir hosts harboring different dermatophytes determines the type and incidence of infection in humans. Trichophyton mentagrophytes is most commonly transmitted to humans from rodents (dogs are frequent carriers); M. canis from cats (dogs are also frequent carriers); T. verrucosum from cattle; and M. gypseum from dogs and rodents (occasionally cats). Transmission: Direct or indirect contact with asymptomatic animals or with skin lesions of infected animals is the primary mode of transmission. Contaminated bedding and diagnostic or care equipment may also serve as fomites for disease transmission. Fungi in air, in dust, or on surfaces of a room provide long-term con-

Preventive Medicine

cerns for reintroduction of the disease (spores persist on contaminated surfaces). Disease in animals: In rodents and cats, the disease is often asymptomatic and not recognized until people are affected. Dogs often show classic skin lesions. Disease in humans: While usually self-limiting, the human may have mild scaling, redness, and occasionally vesicles or fissures. There will be thickening and discoloring of nails, and there may develop circular lesions that clear in the center forming a ring. Fungal infections in humans are categorized as to the location on the body: 1. Tinea capitis—scalp and hair 2. Tinea corporis—body [extremities (arms and hands) are most often affected in infections acquired from animals]. 3. Tinea pedis—foot 4. Tinea unguim—nails Diagnosis: KOH mount of skin scrapings remains a tried and true method. Fungal cultures may serve as definitive diagnosis. Treatment: A variety of antifungals, even dilute sodium hypochlorite (Clorox) or 2% iodide wash, may be effective in eliminating the disease. Prevention and control: All newly received pets should be screened by closely inspecting all body surfaces for hair loss, patchiness, or rashes. Routine sanitation of the environment and caging should serve to prevent contamination. Technicians should wear gloves and protective clothing when treating affected animals. VIRAL DISEASE

Hemorrhagic fever with renal syndrome (HFRS) Agent: The Bunyaviridae family, Hantavirus genus, includes four distinct groups of Hantaan-related viruses. Reservoir and incidence: Recognized originally in troops serving in the Korean War,

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this virus was named Hantaan after a river in the endemic area of Korea where it was found. There are five hosts (all rodents) of this virus: Apodemus sp.—striped field mouse Rattus norvegicus and R. rattus—rats (both may be pets) Microtus pennsylvanicus—meadow vole Peromyscus leucopus—white-footed mouse Clethriomys glareolus—bank vole Disease in animals: This is a chronic, asymptomatic infection. The virus is shed for extended periods in body fluids. Disease in humans: In the “renal form” of the disease, after a 13- to 22-day incubation period, clinical symptoms of high fever, myalgia, headache, lumbar pain, diarrhea, nausea, vomiting, nephritis, hemorrhage, and shock occur. Mortality may reach 10%. Transmission: This disease is aerosolized from urine, feces, or respiratory secretions of infected rodents. There have been unconfirmed reports of transmission by rodent bite. It is spread horizontally between rodents by saliva. Vertical transmission is thought not to occur. Person-to-person transmission is thought not to occur. Arthropods do not serve as important vectors. Diagnosis: Diagnosis can be based upon serology using indirect immunofluoresence, HI to further determine type of hantavirus, and virus isolation. Prevention and control: Unless wild-caught rodents are being held as pets, there is little risk of this disease. Education and general sanitation that discourages rodent harborage and removes buildup of dust and debris are effective control measures.

Lymphocytic choriomeningitis (LCM) Agent:

Arenavirus

Reservoir and incidence: Wild mice (Mus musculus) of the United States, Asia, Africa, and Europe. The virus has not been isolated from mice in Australia. Wild mice will usually be the index case that may infect pets or

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humans. Of many latent viruses present in mice, only the lymphocytic choriomeningitis (LCM) virus naturally infects humans. The LCM virus can easily be transmitted from animals to humans. This virus was first isolated by Armstrong and Lillie during investigation of a St. Louis encephalitis outbreak in 1933. Mice and hamsters are the only species in which long-term, asymptomatic infection is known to exist. There have been over 200 documented cases associated with pet hamsters in the United States.

Exotic Small Mammal Care and Husbandry

Prevention and control: Infection can be prevented by keeping wild mice out of homes and areas where animals are kept and by controlling ectoparasites and roaches. Technicians should use protective clothing and proper care when handling infected animals or tissues. Basic hand washing is an important step to prevent personal infection.

BITES AND SCRATCHES

Bites Transmission: Humans can be infected with LCM virus directly from feces or urine of mice or hamsters, or indirectly by inhaling the dried excreta carried on aerosolized dust originating from the animal cages or rooms. Technicians may become infected by improper handling of infected murine tissues or being bitten by infected mice. Disease in animals: Acute disease and death, runting, nonspecific signs, or asymptomatic mice all occur. Most mice will recover but become persistent tolerant infection (PTI) spreaders. These animals have no antibody response, making it very difficult to diagnose by common methods. Mice that are congenitally infected are normal at birth and appear normal for most of their life span, and they consistently shed virus in the blood, tissues, and urine. A rudimentary but accurate assessment tool is the production of characteristic convulsive seizures that can be produced in LCM mice by picking them up by the base of the tail and twirling them. This assessment should be performed carefully so as to not injure the animal. Disease in humans: The signs and symptoms can vary dramatically, from a mild flulike syndrome with or without involvement of the CNS, up to a fatal meningioencephalitis. A small number of patients will be hospitalized for prolonged periods and may experience debilitating, chronic sequelae, including fatigue, headache, and depression. Diagnosis: A variety of tests may be used for diagnosis, including IFA, rising antibody titers, and virus isolation.

Health authorities report that more than 1 million people are bitten by dogs each year; however, it is estimated that only half of all bites are reported: Dogs—84% Cats—10% Rodents—4% Skunks and foxes—1% Other (small mammal pets)—1% It is estimated that more than 43,000 people are bitten by rats and mice in the United States each year. Bites cause pain, anxiety, wound disfigurement, and wound infections. Many organisms are capable of infecting animal bite wounds, including Pasteurella spp., V-hemolytic Streptococcus, Staphylococcus aureus, Bacteroides, Fusobacterium, Capnocytophaga canimorsus (previously DF-2), Clostridium tetani, Streptobacillus moniliformis, and Spirillum minus and have been previously discussed. Pasteurella multocida may be responsible for up to 50% and 90% of infections from dog and cat bite wounds, respectively. Treatment: There are specific steps technicians should follow for treatment of bite wounds: 1. Maintain records of all bites and scratches in the animal facility. 2. Notify a physician. The veterinary hospital should have an occupational medicine physician who understands the problems associated with animal handling and is informed about zoonotic diseases. 3. Clean the wound properly, using lots of water, soaps, and disinfecting agents.

Preventive Medicine

Allergic sensitivities Allergic skin and respiratory reactions are quite common in people who have rodent pets and personnel who work closely with rodents. Hypersensitivity reactions in response to animals include the following: a. b. c. d. e. f. g.

Nasal congestion Runny nose Sneezing Itching of eyes Angioedema Asthma A variety of skin manifestations (localized urticaria and eczema)

43

use exhaust hoods (for treatment or surgical procedures), filter tops or closed bags for dirty bedding, and facility clothing, masks, and respirators. An important concept of protecting one’s self and family is to remove all clothing worn while working at the veterinary hospital and launder that clothing at the hospital rather than taking it home to be laundered (and thereby exposing one’s family and pets to potential disease agents).

PARASITIC INFECTIONS AND INFESTATIONS

Toxoplasmosis Almost any animal can cause an allergic sensitivity. Maximal allergenic activity in humans resulted from the albumin fraction of pelt extracts from rats, mice, and rabbits. The fraction of guinea pig extract with maximum allergic activity seems to be a prealbumin. Two major allergens in mouse serum, skin, and urine have been identified. The major urinary protein complex in rodents (especially rat and mouse) is an extremely high allergenic agent. The mechanism of transport involves drying of the rodent urine and adherence of the urine protein to dust or bedding particles, which become airborne and are then inhaled. Diagnosis: Diagnosis of acquired allergies may require a history of animal relationship (pets at home plus animals worked with in the veterinary hospital), a physical exam, pulmonary function tests, skin testing, and laboratory tests [CBC, immunoglobulins and IgE antibody specific to one allergen as measured by the RAST (radio-allergosorbent test) as well as nasal smears for eosinophilia and serum precipitants to specific allergens]. Treatment, prevention, and control: In some cases, pharmacologic treatment is the best approach, but allergen immunotherapy, complete avoidance of the antigen, and reducing exposure to the offending antigen are critically important. Steps veterinary technicians may take to improve their ability to work with animals include the following: reduce the direct animal contact time, increase room ventilation,

Agent: The Toxoplasma gondii organism is 4–7 microns long and 2–4 microns wide. It belongs to the subphylum Apicocomplexa, family Eimeriidae. Reservoir and incidence: Infection in humans and lower animals is widespread. An estimated 500 million humans have been infected with the organism, and close to 40% of adults in the United States have antibodies to T. gondii. Serologic surveys in the United States using the Sabin–Feldman dye test have demonstrated T. gondii infection in 30%–80% of cats. The significance of this finding is that, presumably, all serologically positive cats have shed Toxoplasma oocysts and could re-shed organisms during reinfection or reactivation. Although this text does not include cats as a discussed species, this is a disease that involves cats but causes disease in rodents and humans. The life cycle of this organism begins with a definitive host (sexual reproduction and shedding of oocysts). The domestic cat predominates as the reservoir for zoonotic transmission in the home. Intermediate hosts include mice, rats, hamsters, guinea pigs, other rodents, rabbits, and many other species. Transmission: For pets, dried cat fecal matter is sufficient to result in an infection. For humans, consuming meat containing cysts or tachyzoites, or contamination of the hands while cleaning litter pans and subsequent ingestion of oocysts results in human infestation. Because oocysts become infective only after 2–3 days of sporulation, cleaning of the litter

44

pan daily will prevent the development of infective oocysts. Disease in animals: Most postnatally acquired infections in cats are asymptomatic. When infected, cats shed for 1–2 weeks, during which time this becomes a public health hazard, especially to pregnant women. Oocyst shedding is reactivated by induction of hypercorticism or superinfection with other feline microorganisms. Disease in humans: Although the disease is very common in humans, clinical disease is of low incidence and occurs only sporadically. Postnatal infection is less severe and commonly presents as a generalized lymphadenopathy that may resolve without treatment in a few weeks. Congenital infection (infection of the infant during pregnancy) may result in systemic disease with severe neuropathological changes. Rarely, serious ocular or systemic toxoplasmosis can be acquired by older individuals or reactivated in immunocompromised individuals. At any age, clinical symptoms may include fever, skin eruption, malaise, myalgia, arthralgia, cervical lymphadenopathy, pneumonia, myocarditis, meningoencephalitis, and chorioretinitis. Diagnosis: Serology, isolation, microscopic demonstration of organisms in smear or section, and demonstration of oocyst are the most common methods to diagnose the disease. Paired serum samples taken one or more weeks apart may also be evaluated by the following: a. IFA—serial titers of suspected infections b. Sabin-Feldman dye test—most sensitive test, but not readily available c. IHA—for screening, but not definitive because can be negative early in disease d. ELISA While serology of humans is useful, serology in cats is not useful because either a seropositive or seronegative cat could potentially shed oocysts at a later time. Prevention and control: Technicians are key for assuring effective prevention. The answer? Education, education, education. Recognizing

Exotic Small Mammal Care and Husbandry

the significant impact of disease upon the unborn, the immunocompromised, and the aged may require particular protections or procedures to assure their health and safety. Pet owners should carefully control their cat’s diet, feeding only known items and preventing the consumption dead rodents. Rigorous sanitation of the cat’s living space is effective, especially if litter pans are cleaned daily (because oocysts are not infective for 2–3 days after the fecal matter is dropped in the litter pan). Veterinary technicians and others should wear gloves when cleaning sick or injured animals (because subsequent stress such as another disease can cause a recurrence of oocyst excretion in cats). By all means, be sure to wash your hands vigorously prior to eating, and avoid rare (or raw) meat, especially pork or mutton. Cooking to greater than 65 °C, or until color changes to light tan, is sufficient to kill oocysts. Lastly, pregnant women should avoid contact with cat feces and should avoid working in soil or gardens that could be contaminated by cats, etc.

Pneumocystis carinii Agent: Pneumocystis carinii is a protozoan parasite that occurs worldwide and causes Pneumocystic pneumonia. It is an extracellular organism that some scientists believe is a distinct organism from animals to humans. The taxonomy is uncertain. Reservoir and incidence: All rodents, rabbits, and numerous other animals may harbor this agent. The incidence is unknown due to the high variability of the agent in species and location. Transmission: Although the contagious pattern suggests patient-to-patient transmission in humans and acquisition from the environment are the primary routes of infection, recognizing the high degree of similarity in the agents found in animals and humans, zoonotic transmission cannot be ruled out. Disease in animals: Respiratory disease has been reported that clinically is similar to that reported in humans. Disease in humans: This disease is more often observed in infants or debilitated individuals

Preventive Medicine

45

with neoplasia, poor nutrition, or immunodeficiency. It is frequently fatal in humans, resulting in a diffuse desquamative alveolitis as the parenchyma fills with edematous and foamy fluid containing numerous parasites.

Disease in animals: In animals, severe watery diarrhea occurs; however, the disease is often inapparent in guinea pigs. Two strains of Cryptosporidium with different host ranges parasitize the intestinal tract of guinea pigs.

Treatment: Trimethoprim and sulfamethoxazole appear to be effective at controlling the disease (it is not possible to fully eliminate the organisms).

Disease in humans: Most recorded cases in humans have occurred in immunodeficient individuals, but the organism is capable of causing disease by itself. Prognosis for immunologically compromised individuals is grave because effective chemotherapeutic means of eliminating the parasite are not available. Usually the signs present after a 4- to 12-day incubation period with flulike disease including fever, malaise, nausea, and protracted watery diarrhea. It is usually self-limiting, with complications in those with impaired immune response.

Cryptosporidiosis Agent: Extracellular protozoal organisms, similar to coccidia, in the genus Cryptosporidium with 19 species, suborder Eimeriorina are the agent for cryptosporidiosis. The taxonomy of species is somewhat controversial but is considered to be infective across species lines. Reservoir and incidence: This agent may be found in guinea pigs, mice, rats, rabbits, and many other species. Among animals, dogs appear to be resistant to infection, although they have been found to be serologically positive. Transmission: No intermediate host is required, thus infection can occur by ingestion of infective sporulated oocysts. In contrast to other coccidians, these oocysts are sporulated and infectious at the time of excretion. In fact, the organism can exist within the host, causing immediate reinfection. Most commonly, the oocyst localizes in the small and large intestines but it may also be associated with invasion of the stomach, bile ducts, pancreatic ducts, and gallbladder. Cryptosporidium parvum commonly parasitizes the intestinal tract of humans. Cryptosporidium muris infects the stomach of mice and is thought to be more host- and tissue-specific than C. parvum, although it has been found in the gastric glands of adult cattle as well. Although strains of Cryptosporidium that are predominant in calves and humans are cross transmissible and can infect various other host species, isolates from guinea pigs and calves probably have different host ranges. The isolate of Cryptosporidium sp. from chickens is not infectious for mice. There is no evidence that C. muris can infect human beings.

Diagnosis: The organism may be identified by H&E staining of intestinal specimens taken within 1–2 hours of death of the animals. The small size of the organisms, 4–6 microns, and low excretion rates in infected individuals make detection difficult. Centrifugation of fecal flotation in a high-gravity salt or sugar solution, and smears of the supernate stained with Giemsa, PAS, Kinyouns, or Ziehl–Nielsen aid in identification of oocysts and maximizes detecting the organism. Phase contrast aids detection with coverslip flotations. Formalin fixation is recommended due to the potential of fecal–oral transmission. Prevention and control: A 5% ammonia or 10% formalin solution will kill oocysts after 18 hours, or heating of contaminated materials to 65 °C for 30 minutes. Freezing will also kill oocysts. No treatment is known to eliminate it in the host. Treatment consists of supportive therapy. The organism is refractory to antibiotic therapy. Cages or pens should be thoroughly cleaned with ammonia solution and allowed to dry for several days between animals. Immunosuppressed individuals should not work with or have as pets infected animals.

Helminth infections Many of the helminth parasites common to both animals and humans have an indirect life cycle that can be easily interrupted, but if left

46

unchecked will become zoonotic. Parasites with a direct life cycle do not require an intermediate host and therefore may cause infection more readily. Proper quarantine, surveillance, and treatment to decrease endoparasitic burden, routine sanitation to eliminate parasitic ova before they can become infective, and education of pet owners on standard hygiene practices are measures that can be taken to prevent transmission of these diseases.

Nematodes Capillariasis Agent: Capillaria hepatica (capillary liver worm). Reservoir and incidence: These parasites have a worldwide distribution with selected locations having a high prevalence. They are primarily a parasite of rodents, but other rodent and mammalian species may be affected. Peromyscus maniculatus and Clethrionomys gapperi are the major hosts in North America. Transmission: In nature, rats and mice are usually infected by eating meat containing the parasite. They then seed the environment with eggs passed in their feces, which are ingested by other animals or humans. When eggs are ingested by another animal or human host, the parasite penetrates the intestinal wall and migrates to the liver via portal circulation. Disease in animals: With heavy infections the animal may become emaciated, jaundiced, and show ascites. Parasites mature and deposit eggs in liver tissue. Disease in humans: Subclinical infection is suspected in humans, as in rodents. When not treated, the infection may lead to death. More commonly, fever, hepatomegaly, eosinophilia, leukocytosis, and hypergammaglobulinemia occur.

Exotic Small Mammal Care and Husbandry

cooking of foods and water when living in nature, preventing pica, and other sanitary practices.

Hymenolepis diminuta Agent: Hymenolepis diminuta is the common tapeworm of rats. Size varies from 100 to 600 mm. Hosts: This parasite is found in the small intestine of rats, mice, humans, and hamsters. Insects that serve as obligatory intermediate hosts include beetles, cockroaches, earwigs, fleas, and mealworms. Occurrence: Historically a common parasite, its occurrence is rare due to improved sanitation and vermin control. Distribution: It is found in Africa, South America, the Caribbean, Italy, Japan, the United States, and the countries of the former USSR. Transmission: The transmission is simple: rat—insect—rat or rat—insect—human. Rats ingest various arthropod intermediate hosts. Humans become infected by accidental ingestion of the cysticercoid larvae that are present in infected intermediate arthropod hosts in contaminated grain. This parasite is rare in the mouse due to faster intestinal emptying time in mice. Disease in animals: This disease produces no symptoms or pathological lesion. Disease in humans: There is no known serious pathology in humans. Diagnosis: Diagnosis examination.

is

made

by

stool

Prevention and control: Elimination of insects will prevent the continuation of the life cycle and development of the infective cysts.

Diagnosis: A liver biopsy, history of living in nature or unsanitary conditions, and clinical symptoms collectively offer the diagnosis.

Hymenolepis nana

Prevention and control: The key to preventing this disease is health education, boiling or

Hosts: Mice, rats, and occasionally humans may serve as host for this parasite. The parasite

Agent:

Hymenolepis nana (dwarf tapeworm)

Preventive Medicine

measures 5–90 mm long, with its size inversely proportional to the number of worms in the host. A distinguishing feature of the mature segment is the “three testes,” one on the left and two on the right side of the median line. Reservoir and incidence: This parasite is cosmopolitan in distribution, just as common in cold as in warm climates. Infection rates are higher in children than in adults, and more common in institutions such as children’s homes and orphanages, than in children who live in single-family homes. Transmission: The parasite uses either a direct fecal–oral cycle or indirect ingestion from accidental ingestion of infected insects. Human infection is caused by ingestion of H. nana eggs, or by ingestion of infected intermediate hosts such as fleas, mealworms, beetles, or cockroaches. Although the more common life cycle is direct, insects that may serve as intermediate hosts include Ctenocephalides canis, X. cheops, P. irritans, and B. germanica. The eggs are infective when passed from the body of the host but do not survive long outside the body. Autoinfection can occur from eggs hatching within the intestine. Disease in animals: There is no serious pathology or symptoms associated with this parasite in animals. The parasite does consume carbohydrate from the intestine of the host and therefore may compete for nutrition, including vitamins and amino acids. Young rodents are more resistant than older rodents, due to the short length of the intestine in young mice. Autoinfection is responsible for persistent infection in murine and human hosts. Disease in humans: Symptoms depend on the number of worms in the body. Metabolic wastes from the parasite can be absorbed and

47

may cause toxemia in humans. Considerable irritation of the small intestinal mucosa may also occur with large numbers of worms. Some human patients may experience headaches, diarrhea, anal itching, anorexia, and convulsions. Autoinfection may occur and the disease may last for as long as 22 months. Diagnosis: This parasite is easily observed in a fecal flotation (segments are not passed in feces, look for eggs only). Prevention and control: A variety of treatments are available for this parasite, but to prevent autoinfection, treatments should be repeated or extended. Treatment intervals should not exceed 7 days. Additional supportive measures include good personal hygiene, effective use of protective clothing and gloves, strong vermin control, and protection of feed grain from grain beetles.

REFERENCES Centers for Disease Control and Prevention (CDC). 1994. Summary of Notifiable Diseases, United States, 1994. MMWR 1995 43(49). Centers for Disease Control and Prevention (CDC). 1996. Summary of Notifiable Diseases, United States, 1996. MMWR 1997 45(53). Available at www.cdc.gov/ncphi/disss/nndss/ annsum (accessed September 9, 2009). JAVMA. 1995. Zoonosis Updates. J. American Veterinary Medical Association 207. Margileth, A.M., and Hayden, G.F. 1993. Cat scratch disease – From feline affection to human infection. New England Journal of Medicine 329:53–54. Small Animal Compendium. 1993. Small Animal Compendium for Continuing Education 15:3, March 1993.

Rabbits

4

Rabbits are generally docile and engaging animals. Their quiet nature and relatively simple housing and husbandry requirements have contributed to their increasing popularity as pets. COMMON BREEDS

Currently more than 45 breeds are recognized by the American Rabbit Breeders Association, all derived from the domestic rabbit, Oryctolagus cuniculus. Many rabbit breeds have been developed for physical traits such as body conformation and fur characteristics. A complete index of recognized breeds is available on the website of the American Rabbit Breeders Association, Inc., at www.arba.net. BASIC ANATOMY AND PHYSIOLOGY

Rabbits have a large muscle mass compared to their skeleton. The muscle mass comprises greater than 50% of the body weight and the skeleton only 7%–8% (Donnelly, 2004). This feature makes them predisposed to fractures of the limbs or vertebrae if not properly restrained during handling. Rabbits can be removed from a cage by grasping the loose skin over the shoulders with one hand to lift the rabbit from the cage while supporting the hindquarters by placing a hand under the rump. They can be carried by tucking the head into one arm while supporting the rear in the other (Fig. 4.1). This will prevent the rabbit from kicking its powerful legs and causing injury to its back.

Fig. 4.1 Proper rabbit manual restraint. For color detail, please see color plate section.

Rabbits’ fur is very fine and their skin very delicate. Extreme care should be taken, using fine clipper blades, when clipping hair for surgery to avoid tearing the skin. Their feet are covered with coarse fur instead of footpads. Ulcerative pododermatitis, commonly called sore hocks, is frequently encountered in overweight rabbits housed on wire cage flooring. Male and female rabbits have well-developed scent glands, including the chin glands, the anal glands, and the inguinal glands. Male rabbits mark their territory more aggressively than females, and dominant animals of both sexes mark more than submissive animals. Rabbits have a very well-developed sense of smell. Breathing is characterized by twitching the nostrils to direct the flow of air over the turbinates where olfactory cells are located. 49

50

Exotic Small Mammal Care and Husbandry

Table 4.1 Basic biological parameters. Body weight

Adult male: 2–5 kg Adult female: 2–6 kg Birth weight: 30–60 g

Body temperature

37.8 °C–39.4 °C (100 °F–103 °F)

Reproductive data

Sexual maturity Female: 4–9 months Male: 6–10 months Estrous cycle: 15–17 days Ovulation: induced Gestation length: 29–35 days Litter size: 4–10 Weaning age: 4–6 weeks

Life span (captivity)

5–7 years

Heart rate

130–325 beats per minute

Respiratory rate

32–60 breaths per minute

Food intake

50 g/kg/day

Water intake

50–100 mL/kg/day

From: Bradley (2001); Carpenter (2005); Donnelly (2004); Suckow and Douglas (1997).

Because rabbits are obligate nasal breathers, open-mouthed breathing is generally considered a poor prognostic indicator (Donnelly, 2004). The teeth of rabbits grow continuously throughout their lives. The dental formula is 2(2/1 incisors, 0/0 canines, 3/2 premolars, 3/3 molars) = 28. The two lower incisors rest between the four large upper incisors and peg teeth. Incisor malocclusion is seen commonly in pet rabbits, particularly with mandibular prognathism (Fig. 4.2). The relatively small mouth opening makes endotracheal intubation in rabbits challenging. The gastrointestinal tract of rabbits is very large and contains a coiled cecum that can hold up to 40% of the ingesta. The colon regulates the formation of hard and soft fecal pellets. Rabbits consume soft pellets, or cecotrophs, directly from the anus for nutritional benefit, primarily protein and B vitamins (Suckow et al., 2002). Table 4.1 gives the basic biological parameters of rabbits. Urine is a major route of calcium excretion in rabbits, with normal urine having a cloudy appearance ranging to a thick and creamy con-

Fig. 4.2 Mandibular prognathism and malocclusion. (Photo courtesy of Dan H. Johnson, DVM, Avian and Exotic Animal Care, Raleigh, NC.) For color detail, please see color plate section.

sistency due to the high concentration of ammonium magnesium phosphate and calcium carbonate monohydrate precipitates. The color can vary from yellow to reddish, often mistaken for blood, and is somewhat dependent upon the diet. (See section “Clinical techniques,” Table 4.3.) REPRODUCTION AND SEXING

Sex determination is performed by gently applying pressure above the genitalia. In males, the penis will evert and appears like a rounded protrusion with a circular opening (urethra) at the distal tip. The vulva has a more slit-like appearance (Bradley, 2001) (Fig. 4.3a). Males have two scrotal sacs cranial to the penis (Fig. 4.3b). Male rabbits have open inguinal rings and can retract their testes. Puberty generally occurs between 5 and 8 months of age in larger breeds and between 4 and 5 months in smaller breeds. The reproductive life of a doe generally lasts up to 3 years, though bucks will remain useful as breeders for 5–6 years. Spaying and neutering pet rabbits has many benefits. Neutered males and spayed females tend to mark their territory less and be less aggressive. Spaying females can prevent reproductive neoplasia. Uterine adenocarcinoma is reported to have a high incidence of up to 80% in certain breeds (Antinoff, 1999).

Rabbits

a

51

b

Fig. 4.3a External genitalia of a female rabbit. For color detail, please see color plate section.

Fig. 4.3b External genitalia of a male rabbit. For color detail, please see color plate section.

The breeding cycle in rabbits is influenced by day length and environmental temperature, with the highest conception rates in the spring. Receptive does exhibit lordosis (flattening of the back, raising of the pelvis) in response to attempts by a buck to mount. The gestation period is approximately 30–32 days. In the last days of gestation, mammary gland development occurs and does can be observed pulling hair from the abdomen to make a nest. Kits are usually born in the early morning. Litter sizes vary with breed, with smaller breeds producing 4–5 kits, and large breeds producing 8–12 kits. Kits typically nurse only once a day for 3–5 minutes, in which time they can drink up to 20% of their body weight. Solid food can be consumed by 3 weeks of age, and kits can be weaned at 5–8 weeks of age. There are several published formulas available for hand-rearing rabbits if needed in cases of orphaned kits or poor maternal care. Combinations of KMR Kitten Milk Replacer and Multi-Milk powder (PetAg, Hampshire, IL, www.petag.com) will provide appropriate

nutritional support for neonates. Neonates should be fed three times a day until they establish a regular feeding pattern. To stimulate urination and defecation, the anogenital area should be gently stroked with a warm, wet cotton-tipped applicator. HUSBANDRY

Rabbits can be housed indoors or outdoors. Wire cages are preferable to aquariums as they provide better ventilation and allow feces and urine to fall through the floor. Cages should be three times the length of the rabbit when fully stretched out (Bradley, 2001). A portion of the cage can be bedded with straw, shavings, or cardboard to provide a resting place off the wire. Aromatic wood shavings, such as pine and cedar, can cause respiratory and dermatological problems and have been associated with elevated liver enzymes (Bradley, 2001). Rabbits can be easily trained to use a litter box, as they commonly urinate and defecate in the same place repeatedly.

52

Outdoor housing should provide shade and shelter from wind and temperatures below 39.2 °F (4 °C). Rabbits are more tolerant of cold temperatures than heat and are generally intolerant of temperatures above 82.4 °F (28 °C) as they are unable to sweat and they pant ineffectively (Donnelly, 2004). NUTRITION

Rabbits are strict herbivores. The ideal diet for maintenance is comprised of a good quality pelleted feed with a protein content of 16% and a fiber content of 16% (Brooks, 2004). Unlimited amounts of grass hay should be offered daily. Timothy hay is preferred over legume hays such as alfalfa. A minimum of 1 cup of fresh leafy vegetables per each 4 lb of body weight should be offered daily. Vegetables high in oxalates, such as spinach, kale, and cabbage should be fed sparingly. Free-choice feeding of pelleted food alone can result in overeating, obesity, and diarrhea. ENRICHMENT

Toys and other distractions are beneficial to promote activity and prevent boredom in caged rabbits. Sturdy plastic, nontoxic toys are appropriate. A tunnel or hidebox can simulate a burrow in the wild. HANDLING AND RESTRAINT

As mentioned previously, proper restraint is imperative for rabbits to prevent skeletal injuries. One hand should lift and support the rear end, with the other grasping the forelegs. Rabbits should not be lifted by the ears or scruff. With proper restraint, rabbits can be safely carried and restrained for physical examinations. PHYSICAL EXAMINATION

The examination table should be covered with a towel to prevent slipping. To facilitate abdominal palpation, roll the rabbit on its back and cradle it against your abdomen. This posi-

Exotic Small Mammal Care and Husbandry

tion is also helpful for examining the perineal region and taking a rectal temperature. Oral examination is very challenging in rabbits due to the small size of their oral cavity. An otoscope cone with a light source can be used to visualize the caudal aspects of the oral cavity. Many specialized products are now available to assist in oral examination in rabbits. For more detailed oral examination, chemical restraint is often required.

CLINICAL TECHNIQUES

Blood samples can be obtained from multiple readily accessible sites in rabbits: the marginal ear vein, central ear artery, lateral saphenous vein, and the jugular vein (under anesthesia). For smaller rabbits, it is preferable to puncture the vein with a 25- or 27-gauge needle and allow blood to drip from the needle hub into a collection tube, as the use of a syringe generally causes collapse of small vessels. Annual blood work is recommended for rabbits older than 4 years to screen for common geriatric conditions. Reference ranges for hematological and biochemical values are presented in Table 4.2. Cystocentesis can be performed in rabbits by a technique similar to that used in cats. Rabbits should be scruffed with one hand, with feet restrained by the other, on their backs. Samples should be analyzed using standard methods. Interpretation of results should take into consideration that pigment and mineralization is normally found in rabbit urine. Normal urinalysis values in rabbits can be found in Table 4.3. Fecal examination should be performed in juvenile rabbits and in any rabbit presenting for diarrhea. A direct smear should be performed to evaluate for coccidea and to check for the presence of intestinal parasites. Rabbit feces normally contain a moderate amount of yeast organisms. Indwelling catheters are indicated in hospitalized rabbits that are critically ill, to deliver intravenous (IV) medications and fluid therapy. The preferred sites for intravenous catheter placement are the saphenous and cephalic veins. Complications associated with phlebitis have been reported with indwelling catheters in the ear veins (Mader, 2004).

Rabbits

53

Table 4.2 Reference ranges for hematology and serum biochemical values for rabbits.

Table 4.3 urinalysis.

Value

Specific gravity

1.003–1.036

pH

8.2

Crystals

Calcium carbonate monohydrate, anhydrous calcium carbonate, ammonium magnesium phosphate

Casts, cells, bacteria

Rare

Reference Interval

RBC (×10 cells/μL)

4.9–7.8

Hemoglobin (g/dL)

10.0–17.4

6

Hematocrit (%) WBC (×103 cells/μL)

31–50 5.2–12.5

Reference

Neutrohphils (%)

20–75

WBC

Occasional

Lymphocytes (%)

30–85

RBC

Occasional

ranges

Monocytes (%)

2–10

Albumin

Occasional in young

Eosinophils (%)

0–5

130 mL/kg/day

Basophils (%)

0–8

Average urine production

Platelets (×103 cells/μL) Total blood volume (mL/kg)

250–650 55–70

Total protein (g/dL)

5.4–8.3

Albumin (g/dL)

2.4–4.6

Globulin (g/dL)

1.5–2.8

Glucose (mg/dL)

75–155

Cholesterol (mg/dL)

10–80

Blood urea nitrogen (mg/dL) Creatinine (mg/dL)

13–30 0.5–2.5

Aspartate aminotransferase (U/L)

14–113

Alaline aminotransferase (U/L)

14–80

Alkaline phosphatase (U/L) Total bilirubin (mg/dL) Sodium (mmol/L) Potassium (mmol/L) Chloride (mmol/L)

4–16 0.0–0.75 131–155 3.6–6.9 92–112

Phosphorus (mg/dL)

2.3–6.9

Calcium (mg/dL)

5.6–14

From: Carpenter (2005); Mader (2004); Vennen and Mitchell (2008).

for

rabbit

From: Carpenter (2005); Mader (2004); Vennen and Mitchell (2009).

Oral medications are best delivered in a suspension form. Alternatively, tablets can be crushed and mixed with a palatable nutritional supplement and offered by mouth (PO). Nasogastric intubation can be performed in patients that require delivery of nutritional support [Critical Care for Herbivores, Oxbow pet products (www.oxbowanimalhealth.com), Murdock, NE]. PREVENTIVE HEALTH

There are no routine vaccinations recommended for pet rabbits. COMMON DISEASES

The rabbit formulary is presented in Table 4.4.

Gastrointestinal diseases Preferred sites for intramuscular (IM) injection are the large epaxial muscles on either side of the spine or the quadriceps. Volumes from 0.25 to 1.5 mL can be safely administered depending on the size of the rabbit. Subcutaneous (SC) injections and fluids can be delivered in the loose skin over the shoulders. Up to 100 mL volume of replacement fluids can be administered to mildly dehydrated rabbits. Intravenous injections can be administered in the lateral saphenous or cephalic veins.

Many gastrointestinal problems in rabbits are induced by feeding inappropriate diets that alter the intestinal microflora and affect pH and motility. Gastric stasis syndrome is common in rabbits and is associated with a low-fiber high-carbohydrate diet, stress, decreased exercise, and hair ingestion (Jenkins, 2004). Rabbits present with prolonged anorexia and decreased stool production. Radiographs may not be helpful in differentiating between this condition and gastric trichobezoar (hair

Table 4.4 Rabbit formulary. Agents

Dosage (mg/kg)

Route

SC, IM, IV

Antimicrobial Agents Amikacin

5–10 divided q8–24h

Amoxicillin

Do not use

Amoxicillin/clavulanic acid

Do not use

Ampicillin

Do not use

Cephalexin

11–22 q8h

PO

Ciprofloxacin

10–22 q12–24h

PO

Clindamycin

Do not use

Doxycycline

2.5 q12h

PO

Enrofloxacin

5–15 q12h

PO, SC, IM

Gentamicin

4 q24h

SC, IM

Metronidazole

20 q12h

PO

Penicillin G

40–60,000 IU/kg q48h

SC

Trimethoprim-sulfa

30 q12h

PO, SC

Griseofulvin

12.5 q12h

PO

Lime sulfur dip (2.5%)

Dip q7d for 4 treatments

Topical

Fenbendazole

10–20 repeat in 14 days

PO

Imidacloprid

1 cat dose q30d

Topical

Ivermectin

0.2–0.4 q10–14d

SC

Lufenuron

30 q30d

PO

Antifungal Agents

Antiparasitic Agents

Praziquantel

5–10 repeat in 10 days

PO, SC, IM

Pyrantel pamoate

5–10 repeat in 14 days

PO

Sulfadimethoxine

50 once, then 25 mg/kg q24h for 10–20 days

PO

Selamectin

6–10

Topical

Sulfmerazine

100

PO

Sulfaquinoxaline

1 mg/mL

Drinking water

Chemical Restraint, Anesthesia, Analgesia Acepromazine

0.25–1.0

IM

Atipamazole

0.001 for medetomidine reversal

SC

Atropine

0.1–0.5

IM, SC

Buprenorphine

0.01–0.05 q6–12h

SC, IM, IV

Butorphanol

0.1–0.5 q4–6h

SC, IM, IV

Carprofen

1–2.2 q12h

PO

Diazepam

1–3

IM, IV

Flunixin meglumine

0.3–2.0 q12–24h

SC, IM

Glycopyrrolate

0.01–0.02

SC

Isoflurane

3%–5% for induction, 2%–3% for maintenance

Inhalation

Ketamine

20–50

IM

Ketamine + acepromazine

25–40(K)/0.25–1.0 (A)

IM

54

Rabbits

55

Table 4.4 Continued Agents

Dosage (mg/kg)

Route

Ketamine + diazepam

10–15(K)/0.3–0.5 (D)

IM, IV

Ketamine + medetomidine

0.35 mg/kg(M) IM, 5–20 mg/kg(K) IV 15 minutes later

IM + IV

Ketamine + midazolam

25(K)/2–5(M)

IM

Ketoprofen

1 q 12–24h

SC, IM

Medetomidine

0.25

SC, IM

Meloxicam

0.1–0.2 q24h

PO

Midazolam

1–2

IM

Morphine

2–5 q4h

IM

Naloxone

0.01–0.1

SC, IP

Oxymorphone

0.05–0.20 q8–12h

SC, IM

Pentobarbital

20–45

IP

Propofol

2–3 mg/kg for induction, maintain with 1 mg/kg

IV

Yohimbine

0.5–1.0

IM, IV

Miscellaneous Agents Calcium gluconate

100

IM

Cimetadine

5–10 q8–12h

PO, SC, IM, IV

Cisipride

0.5 q8–12h

PO

Dexamethasone

0.5–2.0

IM, SC, IV

Diphenhydramine

2

SC

Epinephrine

0.2

IV

Furosemide

2–5 q12h

PO, SC

Metoclopramide

0.5 q8–24h

PO, SC, IM

Oxytocin

0.1–3.0 IU/kg

SC, IM, IV

Papain enzyme

1–2 tablets q24h for 3–5 days

PO

Pineapple juice

10 mL/animal q24h for 3–5 days

PO

Prednisone

0.5–2.0 q12h

PO

From: Carpenter (2005); Morrisey and Carpenter (2004).

ball), which will have a similar radiographic appearance and presentation. Rabbits are often treated symptomatically with oral lubricants, protein-digesting agents (e.g., papain, pineapple juice), rehydration, and force-feeding (fruit or vegetable baby food) to stimulate gastric motility. Antibiotics and motility-enhancing agents are sometimes indicated. Rabbits requiring surgical treatment for this condition have a poor prognosis. Enteritis caused by bacterial agents is a common clinical disease in pet rabbits. Symptoms range from mild diarrhea with soft or pasty stools to acute, severe enterotoxemia progressing to death. Clostridium spiroforme is the primary causative agent of enterotoxemia

in rabbits. Recently weaned animals are at risk because they have an undeveloped population of gut microflora, which allows the etiologic agent to proliferate. Affected animals exhibit clinical signs including watery brown diarrhea, anorexia, dehydration, polydipsia, pyrexia or hypothermia, bloat, and grinding of teeth (Suckow et al., 2002). Infection is generally fatal within 48 hours. Colibacillosis is caused by a pathogenic strain of Escherichia coli. This disease most commonly affects post-weaning rabbits. Morbidity and mortality rates vary depending on the serotype, but they can range from mild diarrhea to 50% mortality. Affected rabbits should be treated with supportive care and

56

appropriate antibiotics based on culture results. Tyzzer’s disease, caused by Clostridium piliforme, occurs in many species, including rabbits. Affected rabbits develop profuse, watery diarrhea, anorexia, and dehydration and typically die within 1–2 days. Treatment is often unsuccessful, but proper sanitation can prevent the disease. Proliferative enteropathy, caused by Lawsonia intracellularis, has been reported in rabbits. Weanlings are most commonly affected. They develop diarrhea, depression, and dehydration. The disease is rarely fatal and runs its course in 1–2 weeks. Dysbiosis is a common cause of enteritis in rabbits and is caused by the administration of antibiotics that disrupt the normal bacterial flora of the gastrointestinal tract resulting in proliferation of pathogenic bacteria. Clindamycin, lincomycin, ampicillin, amoxicillin, amoxicillin–clavulanic acid, cephalosporins, many penicillins, and erythromycin can induce this condition in rabbits (Jenkins, 2004). Several enteric viruses can affect rabbits and cause gastrointestinal disease. Rotavirus is mildly pathogenic, but can result in serious clinical disease when rabbits are co-infected with E. coli. Coronavirus outbreaks have been reported. Clinical signs include diarrhea, abdominal swelling, and death. Rabbit caliciviral disease (RCD), formerly rabbit hemorrhagic disease, was first reported in the United States in 2000. Rabbits older than 2 months are typically affected. Clinical signs include abdominal distension, constipation, diarrhea, tachypnea, and cyanosis. Morbidity is high with mortality approaching 100%. Coccideosis is a common cause of enteric disease in rabbits. At least 12 species of Eimeria spp. are reported to infect rabbits, with varying pathogenicity. Symptoms range from mild to severe, generally depending on the parasite burden and immune status of the rabbit. Diagnosis is made by identification of the oocysts in feces. Prevention of the disease can be accomplished by strict sanitation and avoiding infected feces and contaminated drinking water. Sulfa drugs have been found to be safe and effective as treatments in rabbits. Pinworm infections are common in rabbits. Two species are commonly reported, Passal-

Exotic Small Mammal Care and Husbandry

urus ambiguus and P. nonanulatus. Treatment with fenbendazole 10–20 mg/kg PO repeated in 10–14 days has been successful at eliminating the infection. Piperazine added to drinking water at a dose of 200 mg/kg PO repeated in 10 days has also been effective (Jenkins, 2004).

Respiratory disease Respiratory disease in rabbits is caused primarily by bacterial agents. Pasturellosis is a common disease in pet rabbits and is caused by the gram-negative coccobacillus Pasturella multocida. Upper respiratory signs (rhinitis, sinusitis, conjunctivitis), are commonly referred to as “snuffles.” The infection can extend to the middle ear canal and result in otitis. Signs of inner ear involvement include torticollis, nystagmus, and ataxia. Radiographs can assist in a diagnosis of otitis media by illustrating soft tissue opacity within the bulla and thickening of the normally thin-walled bullae. Hematogenous spread of the disease can result in septicemia, pneumonia, pleuritis, pericarditis, and generalized abscessation. Pasturellosis is less common in pet rabbits than in past years with the establishment of Pasturella-free rabbitries. Treatment should include supportive care and antibiotic therapy based on culture and sensitivity. No vaccine is currently available for prevention. Bordatella bronchiseptica is a respiratory pathogen in rabbits, guinea pigs, dogs, cats, and pigs. Clinical signs include serous nasal discharge, bronchopneumonia, and pleuritis in weanling rabbits. It is suspected as a co-pathogen and predisposing factor for P. multocida infections (Deeb, 2004).

Reproductive and urogenital disease Uterine adenocarcinoma is the most common neoplasia in rabbits. Certain breeds report an incidence of 50%–80% in rabbits older than 4 years (Pare and Paul-Murphy, 2004). Early clinical signs may be hematuria or serosanguinous vaginal discharge. Tumors typically metastasize to lung, liver, and other organs. Radiography and ultrasound can assist in establishing a diagnosis. Pulmonary metastasis carries a grave prognosis. Ovariohysterectomy

Rabbits

should be recommended for pet rabbits prior to 2 years of age to prevent this disease. Pyometra and endometritis can occur in breeding rabbits. Clinical signs include abdominal enlargement, vaginal discharge, anorexia, and lethargy. Abdominal ultrasound and cytological assessment of vaginal discharge can be performed to support the diagnosis. Pregnancy toxemia is a metabolic disease that occurs in the last week of gestation. Predisposing factors include obesity, stress, and anorexia. Anorexia, weakness, ataxia, dyspnea, and coma progressing to death are common clinical presentations. Treatment is usually unrewarding. Prevention hinges on providing adequate nutrition and husbandry in late gestation. Treponematosis, commonly known as rabbit syphilis or vent disease, is caused by the spirochete Treponema paraluiscuniculi. Typical lesions occur on the vulvar or preputial region, though autoinfection can lead to facial lesions. Lesions begin as vesicles and papules and progress to crusts and scales. Diagnosis is based on serological testing or skin biopsy. Rabbits can be successfully treated with parenteral penicillin (Penicillin G benzathine–penicillin G procaine at 42,000 to 84,000 IU/kg SC at 7-day intervals for three injections) (Pare and PaulMurphy, 2004). Rabbits with hypercalcuria are predisposed to the formation of uroliths. This condition is more common in obese rabbits that are fed a free-choice pelleted diet and/or alfalfa hay. Clinical signs include anorexia, lethargy, hematuria, stranguria, grinding of teeth, and urine scald of the perineum. Treatment depends on the location of the lesion and ranges from urohydropropulsion to cystotomy. Dietary modification is critical for prevention and treatment.

Neurological and musculoskeletal disease Encephalitozoonosis is caused by infection with the protozoan parasite Encephalitozoon cuniculi. Clinical signs include head tilt, behavioral changes, ataxia, nystagmus, or seizures. Diagnosis is based on serology in rabbits exhibiting clinical signs. Elimination of the parasites is accomplished by treatment with anthelmintics (albendazole, oxibendazole, fendabazole).

57

Pasturellosis should be considered as a differential diagnosis for head tilt. Splay leg is a common musculoskeletal condition that occurs in young rabbits, several days to months old. Affected animals cannot adduct their limbs and have difficulty ambulating to food and water. Euthanasia is usually indicated. This condition is an inherited disease and, as such, breeding of affected individuals and parents should be discouraged (Suckow et al., 2002). Traumatic vertebral fracture is the most common cause of posterior paresis and paralysis in rabbits, with lumbar vertebra 7 (L7) most often affected. The history typically includes a traumatic incident involving struggling or restraint. Clinical signs include paresis and urinary or fecal incontinence. Radiographs are diagnostic. In most cases, euthanasia is indicated. In less severe cases, conservative medical management includes administration of nonsteroidal anti-inflammatory drugs, manual bladder expression, and, in some cases, use of a wheelchair (Deeb and Carpenter, 2004).

Dermatological diseases Ulcerative pododermatitis, commonly called sore hocks, is a chronic ulcerative dermatitis of the plantar metatarsal and metacarpal regions of the feet. Animals confined in small cages with wire floors are predisposed to this condition. Obesity, stress, and poor sanitation are also contributing factors. Treatment involves cleaning and debriding necrotic tissue, bandaging, and using topical and systemic antibiotics. Dermatophytosis, commonly called ringworm, is a zoonotic disease that is usually selflimiting and often asymptomatic in rabbits (Hess, 2004). Trichophyton mentagrophytes is most commonly isolated. Diagnosis is based on fungal culture or on identification of fungal forms on KOH prep. Treatment consists of the application of topical and administration of systemic antifungal agents for 3–4 months. Disinfection of the environment is essential to prevent reinfection. Rabbits are susceptible to mite infestation with the ear mite, Psoroptes cuniculi (Fig. 4.4). Clinical signs of mite infestation include crusting of the external ear canal, pruritis, and head shaking. Recommended treatment is with iver-

58

Fig. 4.4 Mite infestation with Psoroptes cuniculi. (Photo courtesy of Dan H. Johnson, DVM, Avian and Exotic Animal Care, Raleigh, NC.)

mectin (Ivomec, Merck, AgVet Division, Rahway, NJ) 0.4 mg/kg SC q12–14 days for three treatments. Cheyletiella spp. are nonpruritic mites that infest the area over the scapulae. Lesions are typically mild and nonpruritic. Diagnosis is based on skin scraping. Sarcoptes scabiei and Notoedres cati are burrowing mites that cause intense pruritis, alopecia, and abrasions. Skin scrapings are diagnostic and treatment with ivermectin is recommended. Myiasis is a condition encountered by rabbits housed outdoors in warm environments. The larvae of Cuterebra species, or bot flies, infest the subcutaneous tissue, especially the dorsum, inguinal, and ventral cervical regions. A breathing hole on the surface is usually visible. Surgical excision of the larvae and debridement of necrotic tissue is indicated. REFERENCES American Rabbit Breeders Association. www. arba.net/Breeds.htm (accessed November 4, 2009). Antinoff, N. 1999. Physical Examination and Preventive Care of Rabbits. Veterinary Clinics of North America: Exotic Animal Practice 2(2):405–427. Bradley, T.A. 2001. What Every Veterinarian Needs to Know About Rabbits. Exotic DVM 3(1):42–46.

Exotic Small Mammal Care and Husbandry

Brooks, D.L. 2004. Nutrition and Gastrointestinal Physiology. In Quesenberry, K.E., and Carpenter, J.W. (eds.). Ferrets, Rabbits, and Rodents: Clinical Medicine and Surgery. Second edition. Saunders, St. Louis, MO, pp. 155–160. Carpenter, J.W. 2005. Exotic Animal Formulary. Third edition. Elsevier Saunders, St. Louis, MO, 440–441. Deeb, B.J. 2004. Respiratory Disease and Pasturellosis. In Quesenberry, K.E., and Carpenter, J.W. (eds.). Ferrets, Rabbits, and Rodents: Clinical Medicine and Surgery. Second edition. Saunders, St. Louis, MO, pp. 172–182. Deeb, B.J., and Carpenter, J.W. 2004. Neurologic and Musculoskeletal Diseases. In Quesenberry, K.E., and Carpenter, J.W. (eds.). Ferrets, Rabbits, and Rodents: Clinical Medicine and Surgery. Second edition. Saunders, St. Louis, MO, pp. 203–210. Donnelly, T.M. 2004. Basic Anatomy, Physiology, and Husbandry. In Quesenberry, K.E., and Carpenter, J.W. (eds.). Ferrets, Rabbits, and Rodents: Clinical Medicine and Surgery. Second edition. Saunders, St. Louis, MO, pp. 136–146. Hess, L. 2004. Dermatologic Diseases. In Quesenberry, K.E., and Carpenter, J.W. (eds.). Ferrets, Rabbits, and Rodents: Clinical Medicine and Surgery. Second edition. Saunders, St. Louis, MO, pp. 194–202. Jenkins, J.R. 2004. Gastrointestinal Diseases. In Quesenberry, K.E., and Carpenter, J.W. (eds.). Ferrets, Rabbits, and Rodents: Clinical Medicine and Surgery. Second edition. Saunders, St. Louis, MO, pp. 161–171. Mader, D.R. 2004. Basic Approach to Veterinary Care. In Quesenberry, K.E., and Carpenter, J.W. (eds.). Ferrets, Rabbits, and Rodents: Clinical Medicine and Surgery. Second edition. Saunders, St. Louis, MO, pp. 147–154. Morrisey, J. K., and Carpenter, J.W. 2004. Formulary. In Quesenberry, K.E., and Carpenter, J.W. (eds.). Ferrets, Rabbits, and Rodents: Clinical Medicine and Surgery. Second edition. Saunders, St. Louis, MO, pp. 436–444. Pare, J.A., and Paul-Murphy, J. 2004. Disorders of the Reproductive and Urinary Systems. In Quesenberry, K.E., and Carpenter, J.W. (eds.). Ferrets, Rabbits, and Rodents: Clinical Medicine and Surgery. Second edition. Saunders, St. Louis, MO, pp. 183–193. Suckow, M.A., Brammer, D.W., Rush, H.G., and Chrisp, C.E. 2002. Biology and Diseases of

Rabbits

Rabbits. In Fox, J.G., Anderson, L.C., Loew, F.M., and Quimby, F.W. (eds.). Laboratory Animal Medicine. Second edition. Academic Press, San Francisco, CA, pp. 329–364. Suckow, M.A., and Douglas, F.A. 1997. The Laboratory Rabbit. CRC Press, Boca Raton, FL.

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Vennen, K.M., and Mitchell, M.A. 2009. Rabbits. In Mitchell, M.A., and Tully, T.N., Jr. (eds.). Manual of Exotic Pet Practice. Saunders, St. Louis, MO, pp. 375–405.

Ferrets

COMMON BREEDS

The domestic ferret—Mustela putorius furo, which loosely translates as “mouse-eating smelly thief”—is a descendent of the European polecat (Fig. 5.1). The North American blackfooted ferret, Mustela putorius nigripes, is another popular breed acquired as a pet. In general, ferrets make good pets because they are playful and friendly. They can be trained to use a litter box and to come when called, and they are most active during the early morning and evening hours. Ferrets were initially maintained for vermin control because they are small and can fit into tight spaces. They are expert predators and are naturally curious of their surroundings, making them suitable for rabbit hunting as well. Ferrets

5 are used in biomedical research to investigate areas of virology, toxicology, endocrinology, and reproductive physiology (Marini et al., 2002). BASIC ANATOMY AND PHYSIOLOGY

The long tubular body of the ferret allows them to get into small spaces, such as holes in the ground, during hunting. Their coat color can be categorized as sable/wild, albino, cinnamon/ sandy, silver, black-eyed white, chocolate, Siamese, panda, or shetland sable. They molt in the spring and fall routinely accompanied by some color changes in the coat. Females will lose their hair after ovulation, with regrowth after each successful mating. Neutered ferrets do not have as dramatic changes in molting or color changing as intact ferrets. A ferret’s coat color may change considerably over time, making it not as useful a form of identification as microchips or tattoos. REPRODUCTION AND SEXING

Fig. 5.1 Normal ferret (copyright Eric Isselée, Dreamstime.com). For color detail, please see color plate section.

Male ferrets are referred to as hobs, females are jills, and they are easy to differentiate. Hobs have a preputial opening midabdomen, the os penis can be easily palpated under the skin, and testicles are located cranioventral to the anus if neutering has not yet been performed. Jills have a small, distinct vulva and a shorter anogenital distance. Males are usually larger in size than females, particularly if they have not been castrated (Fig. 5.2). 61

62

Exotic Small Mammal Care and Husbandry

Table 5.1 Biological profile and normal physiologic values.

Fig. 5.2 Male ferret (left) and female ferret (right) size differentiation. (Photo courtesy of Dan H. Johnson, DVM, Avian and Exotic Animal Care, Raleigh, NC.)

Most ferrets sold as pets in the United States are neutered and de-scented by 5–6 weeks in an effort to reduce aggression and minimize their odor. Breeders will usually delay neutering until puberty. Some elect delayed neutering in an attempt to minimize the development of adrenal disease later in life. It is thought the neutering removes the natural hormonal negative feedback, resulting in adrenal hyperplasia or neoplasia from persistently elevated levels of gonadotropic luteinizing hormone (LH) (Kiefer and Johnson, 2006). Jills are induced ovulators and experience a prolonged estrus. Aplastic anemia develops if they do not ovulate; therefore they should be spayed if they are not going to be bred. Jills reach sexual maturity by 9–12 months of age and are sexually active from March to August unless the photoperiod is adjusted, which can change the onset of estrus and prolong the breeding period. During this time both jills and hobs have an increased odor from their scent glands, oil secretion in the coat, and urine. White fur will become yellow as a result of the increased oil production (Brown, 2004). The onset of estrus is noted by vulvar swelling and changes in vaginal cytology. Mating can appear quite violent, but if the female is receptive she will become limp when the male grasps her by the neck. If mating is not successful, the jill may experience pseudopregnancy. (The biological profile of ferrets is presented in Table 5.1.)

Body weight

Adult male: 800–3,000 g Adult female: 700–1,200 g

Rectal temperature

100 °F–104 °F (37.7 °C–40 °C)

Reproductive data

Gestation length: 42 days Weaning age: 6–8 weeks Seasonally polyestrous Induced ovulators Litter size: 1–18 (average 8) Birth weight: 6–12 g Sexual maturity: 6–12 months

Life span

5–8 years

Heart rate

200–255 beats per minute

Respiratory rate

33–36 breaths per minute

Food consumption

43 g/kg/day

Water consumption

75–100 mL/day

Dental formula

2(I 3/3, C 1/1, P 4/3, M 1/2)

Urine volume

26–28 mL/day

From: Brown (2004); Kiefer and Johnson (2006).

Jills can have 1–2 litters per year under natural lighting, but 3–4 litters may be possible with manipulation of the photoperiod. An average litter size is 8 kits, but can range from 1 to 18 kits. Gestation normally lasts 42 days, and it is best to single-house pregnant jills for the last 2–3 weeks of gestation. A nesting box or similar materials should be available, and there should be minimal stress to prevent cannibalization of the newborn kits. Kits are born with a thin white hair coat and are blind and deaf. Their eyes and ears open at 32–34 days of age after they have become active and are eating soft food, which can occur as early as 21 days of age. Kits are usually weaned by 6–8 weeks of age or 300–450 g body weight (Brown, 2004). UNIQUE FEATURES OF IMPORTANCE

There are many characteristics unique to ferrets that owners should be aware of. For instance, male ferrets will typically become twice the size of female ferrets if allowed to become sexually mature prior to being neutered. Also, ferrets do

Ferrets

not have sweat glands and therefore are prone to overheating. They also have very good night vision and sense of smell, which aid them in hunting. Ferrets have a pair of anal glands or “scent glands” that contribute to their musky odor and are routinely removed or “de-scented” by 5–6 weeks of age when they are neutered. Sebaceous secretions of the skin also contribute to their musky odor, and they can be bathed frequently as well as have their cages cleaned routinely to manage the odor. There are some unique features of the ferret that should be taken into account both before and after surgery. Because the gastrointestinal transit time is 3–3.5 hours, ferrets should not be fasted more than 3–6 hours or their blood glucose levels will be significantly affected. Ferrets are also very susceptible to acetaminophen toxicity like cats. Caution should be taken when using any nonsteroidal anti-inflammatory drug (NSAID), and the cyclooxygenase 2 (COX-2) drugs may be better choices for pain management (Quesenberry and Orcutt, 2004).

HOUSING

Ferrets can be housed both indoors and outdoors, depending upon the climate. Open wire cages with solid or wire floors are designed for ferrets in many sizes and designs with multiple levels. These are ideal for adequate ventilation and ease of sanitation. If wooden cages are handmade, care should be taken to eliminate sharp edges and corners as well as to make them easy to sanitize. Outdoor enclosures need to have a shaded area for protection from the sun and heat. Nest boxes should also be provided to allow for a safe, dark area for sleeping. They often prefer to sleep in a hammock, towel, or t-shirt, although rips, holes, or unraveled edges should be avoided to prevent strangulation (Fig. 5.3). These items can also be washed frequently to minimize their musky odor. Enrichment is essential for ferrets, in addition to roaming time outside the cage. Ferrets are escape artists, so all cages should be secure and checked frequently for possible escape routes. If a ferret can fit its head through an opening, its body will likely follow.

63

Fig. 5.3 Ferret in loose towel used for burrowing and sleeping in cage.

HUSBANDRY

Ferrets are very social and should be pair- or group-housed, as long as they have been neutered or are all females to prevent aggression or unintended breeding. Ferrets are very playful, which can sometimes be confused with aggression because they will often bite each other on the nape of the neck. Ferrets should be monitored as play can sometimes lead to aggressive actions. Hissing, screaming, and jaw snapping are defensive behaviors to watch for. They will elicit a loud high-pitched scream when they are afraid, which is not a sign of pain. One way to prevent play biting at the nape of the neck or nipping at people’s ankles, hands, and feet is to put a bitter-tasting substance on the area. There are many commercially available products for this purpose (Brown, 2004). Cages should be cleaned as needed based upon the number of ferrets kept together and the mess that they create, but weekly cleaning is typically sufficient. They can be litter box trained, making cage cleaning and changing much easier. Ferrets tend to back up in the corner of the box to urinate and defecate, so the sides of the litter box should be tall enough to contain the waste. Aspen shavings, recycled paper products, or commercial pelleted litter should be used for bedding and litter instead of cedar or pine shavings or clay/clumping cat litter. Ferrets should have access to a litter box in play areas as well because they are not

64

Exotic Small Mammal Care and Husbandry

always able to reach the cage in time to use the box due to their short gastrointestinal tract. Food can be provided in dishes while water bottles are typically placed on the sides of the cage. Galvanized materials should be avoided to prevent zinc toxicity, which can occur if they chew on the devices. Ferrets will usually eat about 43 grams of food per kilogram of body weight per day (g/kg/day) and drink 75–100 mL of water each day. Food and water should be provided ad libitum as long as they do not become obese, in which case slight food restriction becomes necessary.

colic valve such as other animals have (Willard, 2002). Because of this, they need to eat frequently and be provided a highly digestible formulation. Ferrets can usually be given free access to food, as they rarely overeat and become obese. Nutrition is critical to the reproductive success of jills as well. Inadequate diet can cause decreased conception rates and small litter sizes, and it may contribute to the development of pregnancy toxemia. They should be fed a high-calorie diet with meat products between litters if they are bred routinely (Bell, 2004b).

NUTRITION

Ferrets are obligate carnivores that require diets high in fat (15%–20%) and protein (30%–35%) and very low in fiber because it is not digestible (Kiefer and Johnson, 2006). Commercial diets are now available that are specially formulated for ferrets to be nutritionally complete and balanced. Historically, owners would provide a mixture of ferret chow, cat or kitten foods, and supplements that now are not necessary. Dairy products, sugary treats such as fruits, and high-fiber foods such as vegetables should be avoided. The transit time of the digestive tract of ferrets is about 3 hours. Ferrets have limited absorptive capacity because of their short gastrointestinal tract, minimal epithelial folding of the colon, low concentrations of some brush boarder enzymes, and lack of a cecum or ileo-

a Fig. 5.4

ENRICHMENT

Ferrets should have a few hours of play outside the cage each day. Also, the more time a ferret spends inside a cage, the more enrichment it needs (Fig. 5.4a,b). Because of their curious nature and ability to fit into small spaces, the outdoor play area should be “ferret-proofed” to block off any holes or openings to other areas from which it would be difficult to retrieve the ferret. The area should be checked each time to be sure new defects have not formed that would allow the ferrets to escape and investigate new territory. When left out of their cages to roam and play, ferrets should be carefully supervised to prevent ingestion of harmful substances or objects. Furniture should be covered on the bottom with wood or some sort of material to prevent chewing and burrowing into foam

b (a and b) Enrichment devices within cage or play area.

Ferrets

rubber or furniture and mattresses. Any items in the area such as shoes, rubber bands, electric cords, and dog or cat toys should be removed as well. These items can pose significant health risks if ingested and could cause an obstruction of the intestines. Toys that are provided both

65

inside and outside the cage should not be made of rubber or latex, but instead should be items such as paper bags, hard plastic toys, and tunnels of dryer exhaust tubing to allow for safe burrowing activity and entertainment (Kiefer and Johnson, 2006). HANDLING, RESTRAINT, AND PHYSICAL EXAM

Fig. 5.5 Manual restraint of a ferret while distracting with Nutri-Cal. For color detail, please see color plate section.

a

Most ferrets are docile and can easily be handled, but they will bite without warning so it is best to ask the owner if the ferret has a history of biting. Younger ferrets will have more a tendency to nip, as well as nursing females or ferrets that have not been handled much. It is important to know the laws in your area for unvaccinated and vaccinated ferrets in case someone is bitten during the course of the exam. Animals that are well socialized can typically be handled on the table with light restraint

b

Fig. 5.6 (a and b) Manual restraint options for physical exam or manipulations. Note the “yawn” reaction in Fig. 5.6b. (Photos courtesy of Dan H. Johnson, DVM, Avian and Exotic Animal Care, Raleigh, NC.)

66

Exotic Small Mammal Care and Husbandry

for most of the exam. Ferrets can also be distracted with Nutri-Cal or canned food while a simple examination is performed or in conjunction with restraint during a procedure (Fig. 5.5). The ferret can picked up and supported while the abdomen is palpated and the thorax auscultated. They should be scruffed at the base of the neck for vaccinations or any procedure that may cause the animal to attempt to escape or bite. For animals that have a history of biting or are stressed, they can be scruffed at the nape of the neck and suspended above the table. This method will usually calm the ferret to the point of yawning (Fig. 5.6a,b).

CLINICAL TECHNIQUES

Sample collection—venipuncture Blood can be collected from a variety of locations, depending on the amount of blood that is needed. Ferrets can usually be manually restrained and distracted with food while obtaining a sample, minimizing the need for anesthesia or sedation. If blood is being collected for blood glucose measurement, food should not be used as a distraction. Most laboratories can perform routine complete blood cell counts (CBC) and serum chemistries with about 1.5 mL of blood. Larger volumes of

blood can be collected from either the jugular vein or the cranial vena cava, but the lateral saphenous vein or cephalic vein can be used to collect smaller amounts of blood for tests such as packed cell volume (PCV) or a blood glucose reading. A 27- or 28-gauge needle or tuberculin syringe can be used in these locations. (Reference ranges for hematological and biochemical values are presented in Tables 5.2 and 5.3.) For jugular vein collection, the ferret can be restrained in a similar manner as the cat, with the head extended and the forelegs pulled toward the chest. The vein is held off by applying pressure in the sternal area with the thumb of the person collecting the sample. Visibility can be improved by shaving the neck and swabbing the site with alcohol. Depending on the size of the ferret, a 25- or 22-gauge needle and a 3 mL syringe can be used to collect between 1 and 3 mL to be placed in heparinized microtubules for the best blood-to-plasma ratio (Taylor, 2001). Once the jugular is accessed, the head can be manipulated up and down to aid in pumping blood into the syringe more quickly.

Table 5.3 Laboratory normal values—complete serum biochemical values. Biochemical Parameter

Reference Interval

Total protein (g/dL)

5.9–6.0

Table 5.2 Laboratory normal values—complete blood cell count.

Albumin (g/dL)

3.4–3.5

Globulin (g/dL)

2.4–2.6

Hematologic Parameter

Glucose (mg/dL)

Reference Interval

RBC (×106 cells/μL)

9.3–9.69

Hemoglobin (g/dL)

16.2–16.8

Hematocrit (%)

48.4–49.8

WBC (×10 cells/μL) 3

7.0–9.2

Neutrohphils (%)

47–50

Lymphocytes (%)

45–48

Cholesterol (mg/dL)

93–134 158–183

Blood urea nitrogen (mg/dL)

10–45

Creatinine (mg/dL)

0.4–0.9

Total Bilirubin (mg/dL)

0.2

Aspartate aminotransferase (IU/L)

76–97

Alaline aminotransferase (IU/L) 138–210 Alkaline phosphatase (IU/L)

31–84

Monocytes (%)

1.0–1.19

Eosinophils (%)

3–3.5

Potassium (mEq/L)

4.2–7.7

Basophils (%)

0–0.49

Chloride (mEq/L)

102–125

Sodium (mEq/L)

137–162

Platelets (×103 cells/μL)

730–766

Phosphorus (mg/dL)

8.0–11.8

Total blood volume (mL)

50–60 mL/kg

Calcium (mg/dL)

4.0–9.1

From: Kiefer and Johnson (2006); Lichtenberger (2005).

From: Kiefer and Johnson (2006).

Ferrets

Restraint for collection from the cranial vena cava is similar except that the ferret is in dorsal recumbency with the head, neck, and front legs positioned as described for jugular vein access. Anesthesia is recommended for fractious ferrets, but if the ferret is not anesthetized a second assistant should restrain the pelvis and rear legs. The notch between the manubrium and the first rib is located, and a 25-gauge needle is inserted at a 25- to 45-degree angle to the body directed toward the opposite rear leg (Quesenberry and Orcutt, 2004). The vein is very superficial and the heart is not threatened by this technique because it is located more caudally in the chest when compared with other animals (Taylor, 2001).

Drug administration Medications can be administered subcutaneously (SC), intravenously (IV), and intramuscularly (IM) as with most other species. Subcutaneous injections should be administered over the shoulders or in the flank regions where there is the most loose skin. This is a preferred route of administration over intramuscular injections due to the limited muscle mass of the ferret. The quadriceps and biceps femoris muscle groups are the most common sites for intramuscular injections. Both the cephalic and saphenous veins can be used for intravenous administration of drugs as well. Medications can also be administered orally (PO) in a liquid form and by oral gavage if necessary.

Sample collection—cystocentesis The techniques for collecting urine in ferrets are similar to those used for dogs and cats. A voided sample can be collected during natural micturition or as a result of manual expression of the bladder. A cystocentesis can be performed as well using a 25-gauge needle, though the ferret may need to be briefly anesthetized to prevent trauma to the thin bladder wall if the animal struggles. Ferrets can also be catheterized if necessary, though it can be difficult depending on the clinical presentation of the ferret. Male ferrets with adrenal disease can become “blocked” because the prostate gland enlarges such that it constricts the urethra,

67

making catheterization difficult (Quesenberry and Orcutt, 2004).

Sample collection—fecal samples Fecal samples can be collected for analysis or culture if necessary. A fresh sample can be taken from the cage for most routine screenings. Sometimes a fecal swab is needed and can be collected from the rectum after being moistened with sterile saline.

PREVENTIVE HEALTH

Vaccinations New ferrets should be quarantined for a minimum of 2 weeks before being introduced to other ferrets, followed by a physical examination, fecal examination, and administration of any vaccinations that are due. Ferrets should have a routine physical exam every 6–12 months and be vaccinated annually for rabies and canine distemper viruses. Care should be taken when vaccinating ferrets because they are prone to experience anaphylactic reactions to vaccinations, requiring veterinary treatment. Typically only a single vaccine will be given on a visit, with a 2- to 4-week interval between vaccinations. Animals should be closely monitored for a few hours following administration of a vaccine, and a premedication of antihistamine should be given to any ferret with a history of vaccine reactions. A ferret-approved rabies virus vaccine should be administered at 3 months of age and then annually. Due to the variation in state and local government requirements, veterinarians should contact the local governmental agencies to determine the requirements for their city and state. There are two canine distemper killed virus vaccines that are commercially available, Fervac-D and PureVax. Vaccination for canine distemper should follow a series of boosters in young ferrets at 6, 10, and 14 weeks of age followed by annual boosters (Kiefer and Johnson, 2006).

Endoparasites and ectoparasites Even though it is uncommon for ferrets to have endoparasites, they should be routinely evaluated for both ecto- and endoparasites during the physical exam. Endoparasites that may be

68

Exotic Small Mammal Care and Husbandry

detected during a fecal examination include coccidia (Isospora species), Giardia, and Cryptosporidium. Otodectes cynotis is the species of ear mites that is common to the ferret. An external exam of the ear can determine if an ear swab to check for ear mites is needed. Ferrets should also receive heartworm and flea and tick preventive year round. A dental prophylaxis may be needed annually as well, and routine blood work should be performed when ferrets are over 2–3 years of age. A fasting glucose level should be taken as part of the screening as well.

Neutering Ferrets are routinely spayed or castrated. The surgery can be performed as early as 4–6 weeks of age and should be done before 6 months of age in an effort to minimize odor. Their anal glands can be removed at the time of neutering; removal is recommended to minimize their musky odor. Owners should be warned that despite these procedures ferrets will still have a musky odor, though it will be less than that of an intact animal with intact anal glands.

COMMON DISEASES

Pancreatic tumors Ferrets between 3 and 8 years of age can develop a tumor of the pancreatic beta cells that will cause an overproduction of insulin. Both male and female ferrets are affected equally. This overproduction of insulin creates a state of hypoglycemia that can affect both the neurologic and adrenergic systems. Neurologic signs of hypoglycemia include mental dullness, lack of coordination, seizures, and coma. The adrenergic symptoms include increased heart rate, hypothermia, tremors, and irritability (Marini et al., 2002). Once diagnosed, the disease can be managed either medically or surgically depending on the severity of the disease and the health of the ferret. Medical management includes drug therapy with prednisone and diazoxide with dietary changes. Surgical excision of the affected portion of the pancreas is the treatment of choice in ferrets under 6 years of age or those that also have adrenal disease. Surgical

Fig. 5.7 Typical alopecia pattern associated with adrenal disease in ferrets. (Photo courtesy of Dan H. Johnson, DVM, Avian and Exotic Animal Care, Raleigh, NC.) For color detail, please see color plate section.

therapy will not necessarily cure the disease but will slow its progression considerably (Quesenberry and Rosenthal, 2004).

Adrenal disease Adrenal disease can occur when one or both of the adrenal glands becomes enlarged and overproduces steroid hormones. The adrenal enlargement is often due to the presence of adrenocortical tumors in ferrets between 3 and 6 years of age and may be closely linked to early spay and castration procedures (JohnsonDelaney, 2006). Bilaterally symmetrical hair loss in a very distinct pattern over the tail head, sacrum, flank, and lateral trunk is the most common clinical sign of the disease (Fig. 5.7). They may also be itchy or have a “pear-shaped” abdomen. Females will have an enlarged vulva and males may have difficulty urinating due to an enlarged prostate, both as a result of elevated hormone levels secreted by the overactive adrenal gland(s) (Fig. 5.8). Adrenal disease can be treated surgically or medically. Surgical excision of the affected gland is performed. It is not uncommon to have bilateral involvement, in which case one adrenal is completely removed and a partial adrenalectomy is performed on the contralateral gland (Antinoff et al., 2000). Medical management with drugs, such as leuprolide acetate or melatonin, will work to decrease sex steroid production from the overactive adrenal gland.

Ferrets

69

Therapy may consist of any combination of surgery, radiation, or chemotherapy. Animals may go into remission for 3 months to 5 years (Marini et al., 2002).

Skin tumors The most common epithelial tumors are basal cell tumors and mast cell tumors. They can occur anywhere on the body and are benign. Once they are surgically removed, they generally will not recur if all of the tissue was removed. Histological evaluation is necessary to distinguish these tumors from the malignant and metastatic squamous cell carcinomas and apocrine gland adenocarcinomas that have a guarded prognosis (Marini et al., 2002).

Gastrointestinal disease

Fig. 5.8 Typical vulvar swelling associated with adrenal disease in ferrets. (Photo courtesy of Dan H. Johnson, DVM, Avian and Exotic Animal Care, Raleigh, NC.)

Medical management alone is an option if the owners are not able to afford surgery or the animal is not a good candidate for surgery. Ferrets that undergo surgical therapy alone do not appear to live as long as ferrets treated medically, and there appears to be a slight advantage to performing surgical debulking in conjunction with leuprolide acetate therapy (Johnson-Delany, 2006).

Lymphosarcoma Lymphosarcoma can affect ferrets of any age, but young ferrets less than 2 years of age most often develop leukemia and/or mediastinal lymphoma, and ferrets over 3 years of age will present with multicentric solid tumors. Clinically ferrets may have difficulty breathing, have enlarged peripheral lymph nodes on palpation, or have vague signs of lethargy, inappetence, and weight loss. A diagnosis may be made from a CBC or fine needle aspirates of affected lymph nodes or other organs involved such as the liver, spleen, or gastrointestinal tract.

Ferrets with gastrointestinal disease may have a range of clinical symptoms from vomiting, diarrhea, weight loss, inappetence, and lethargy to various degrees. There are several diseases that should be considered when evaluating a ferret for gastrointestinal problems. These include Helicobacter mustalae infection, proliferative bowel disease (PBD), epizootic catarrhal enteritis (ECE), inflammatory bowel disease (IBD), eosinophilic gastroenteritis, and foreign bodies. Helicobacter infection is common across many species and can cause severe ulceration of the stomach in ferrets. It can be diagnosed by culture of gastric biopsy samples. The disease can become apparent when animals are under stress from surgery, unrelated illness, changes in diet, and rapid growth. Ferrets may also have black, tarry stools or staining of the perianal region as a result of a bleeding gastric ulcer. Treatment for H. mustalae requires multidrug therapy and may be lifelong (Bell, 2004a). Lawsonia intracellularis is the causative organism of PBD. Proliferative bowel disease usually affects juvenile ferrets from 10 to 16 weeks of age that are rapidly growing and may be under environmental or nutritional stress. Transmission is likely fecal–oral but is on the decline, probably as a result of improved quality of care and nutrition. Ferrets with PBD may be more susceptible to other diseases because they are significantly debilitated by the disease.

70

Adult ferrets are most susceptible to ECE because it is highly transmissible and usually is associated with a recent exposure to a new, younger ferret that is an asymptomatic carrier of the disease. It is thought that a coronavirus is responsible for the disease. Though many ferrets can be affected, ECE has a low mortality rate when appropriate therapy is provided. Treatment involves supportive therapy with fluids, antibiotics, and isolation from other ferrets. Therapy may be long term and include steroids and diet change. The causative agent of IBD has not been identified but may be associated with a food allergy or any type of inflammatory process. Elevated serum chemistry values such as lipase and globulin levels help in predicting IBD. Inflammatory bowel disease usually has a gradual onset; it can be confirmed with surgical biopsies of various segments of the intestine as well as any enlarged lymph nodes, which may be an indication of progression to lymphoma when IBD is left untreated. Treatment is usually lifelong and aimed at dietary changes to novel proteins or to specially formulated diets for hypersensitivity in conjunction with immunosuppressive therapy with various immune modulator medications (Burgess and Garner, 2002). Eosinophilic gastroenteritis is a generalized inflammatory process similar to IBD but with the presence of elevated numbers of eosinophils. There is no specific agent identified as the cause of this disease, but a dietary allergy component and parasitism are suspected. Granuloma formation within the intestinal tract can be identified during surgery while obtaining biopsies. Therapy with parasite elimination, diet changes, and immunosuppression can be long term (Bell, 2004a). A foreign body should be considered when a ferret is having gastrointestinal signs. Due to their curious nature and habit of chewing on items in their environment, it is not uncommon for ferrets to ingest foreign objects that can cause a blockage or obstruction of the gastrointestinal tract. Surgical therapy to remove the object is needed and careful supervision of items available in their environment will be essential to prevent a recurrence.

Exotic Small Mammal Care and Husbandry

Canine distemper Canine distemper virus (CDV) is one of the most common respiratory diseases of ferrets. It is spread by aerosol exposure as well as direct contact with infected feces, urine, and skin. Once an unvaccinated ferret is exposed it will start to exhibit signs in 7–10 days. Ferrets will develop pneumonia resulting in trouble breathing, nasal discharge, fever, lethargy, inappetence, cyanotic mucus membranes, and abnormal lung sounds. Mortality rates associated with CDV infection in ferrets is near 100% because there is no specific treatment for the disease. However, CDV can be prevented with vaccination.

Heart disease Heart disease in ferrets usually results in congestive heart failure and can be due to a variety of causes. The same diagnostic techniques are used to diagnose the cause as with other species, including chest radiographs, echocardiograms, and electrocardiograms. The heart will be enlarged, but the reason for the enlargement depends upon the condition identified from these tests. The enlarged heart may be due to the following: dilated cardiomyopathy, where the heart walls are thin and the chambers are dilated; hypertrophic cardiomyopathy, where the heart walls are very thickened and the chambers are small as a result; valvular disease, where one or more of the heart valves is not functioning properly causing the heart to work harder; myocarditis, where the heart muscle is inflamed, preventing the heart from functioning properly; and heartworm disease, where the presence of worms within the chambers of the heart causes disruption of the blood flow and function of the heart. The cause of most of these conditions is not known, and the only one that can be prevented is heartworm disease (Antinoff et al., 2000).

TREATMENTS

Table 5.4 presents the formulary and drug dosages for ferrets.

Table 5.4

Formulary.

Agent

Dosage (mg/kg)

Route

Acepromazine

0.1–0.5

SC, IM

Amikacin

8–16 divided q8–24h

IM, SC, IV

Amitraz

0.3% q7d

Topical

Amoxicillin

10–30 q8–12h

PO

Amoxicillin/clavulanic acid

12.5–25 q8–12h

PO

Ampicillin

5–30 q8–12h

SC, IM, IV

Atropine

0.04

IM, SC, IV

Buprenorphine

0.01–0.03 q8–12h

SC, IM, IV

Carprofen

1 q12–24h

PO

Cephalexin

15–30 q8–12h

PO

Ciprofloxacin

10–30 q24h

PO

Clindamycin

5–10 q12h

PO

Cimetidine

10 q8h

PO, SC, IM, IV

Dexamethasone

0.5–2.0

IM, IV, SC

Diazepam

1–2

IM

Diphenhydramine

0.5–2.0 q8–12h

PO, SC, IM

Enrofloxacin

5–15 q12h

PO, SC, IM

Fenbendazole

20 q24h × 5 days

PO

Furosamide

2 q8–12h

PO, SC, IM, IV

Glycopyrrolate

0.01

IM

Griseofulvin

25 q12h

PO

Isoflurane

To effect

IH

Ivermectin

0.2–0.4 repeat in 14 days 0.05 q30d for heartworm prevention

PO, SC PO, SC

Ketaconazole

10–30 q12–24h

PO

Ketamine

10–50

IM

Ketamine + acepromazine

20–35(K) +0.2–0.35(A)

SC, IM

Ketamine + diazepam

10–20(K) + 1–2(D)

IM

Ketamine + medetomidine

5–8(K) + 0.08–0.1(M)

IM

Ketoprofen

1 q24h

PO, SC, IM

Medetomidine

0.1

IM, SC

Metoclopramide

0.2–1.0 q6–8h

PO, SC, IM

Metronidazole

15–20 q12h

PO

Morphine

0.5–5.0 q2–6h

SC, IM

Neomycin

10 q6–8h

PO

Oxymorphone

0.05–0.2 q8–12h

SC, IM, IV

Oxytocin

0.2–3.0 IU/kg

SC, IM

Prednisone

0.5–2.0 q12–24h

PO

Procaine penicillin G

40,000 IU/kg q24h

SC

Tetracycline

20–25 q8–12h

PO PO in drinking water

Trimethoprim sulfamethoxazole

15–30 q12h

PO, SC

Yohimbine

0.5

IM

From: Morrisey and Carpenter (2004). 71

72

Fluid administration Fluids can be administered subcutaneously, intraosseously in the proximal femur, or intravenously, preferably intravenously if the animal is ill. An indwelling intravenous catheter can be most easily placed in either the cephalic or lateral saphenous vein. Jugular vein catheters are more difficult to place and usually require anesthesia. Ferrets in hypovolemic shock can be treated with IV administration of crystalloids and colloids while being warmed. Initially an isotonic crystalloid such as Plasma-Lyte A is infused at 10–15 mL/kg. A 6% Hetastarch solution can then be administered at 5 mL/kg over 5–10 minutes. Maintenance crystalloids can be administered at 2 mL/kg per hour (mL/ kg/h) once the heart rate is stable and systolic blood pressure is >90 mmHg. Ferrets can be predisposed to pulmonary edema from volume overload, so they should be monitored carefully (Lichtenberger, 2005).

Nutritional support When most ferrets get sick, they usually require some form of nutritional support because they do not have much body fat. Depending on the severity of the disease, various methods can be used to provide nutritional support. Ferrets can be force-fed liquid diets by syringe in 5–10 mL increments 3–4 times a day. Meat-based soft foods for hospitalized cats and dogs can be used in addition to baby foods, liquid soy-based products, and high-energy pastes. These should only be given for a few days as they are not nutritionally complete for ferrets, but they can be used until the ferret will eat a more complete diet. If force-feeding does not work, an esophagostomy tube can be placed or total parenteral nutrition (TPN) can be provided as well (Quesenberry and Orcutt, 2004).

REFERENCES Antinoff, Natalie, Garner, Michael, and Burgess, Mark. 2000. A Review of Diseases of the Ferret. Exotic DVM 2(2): 33–40. Bell, Judith A. 2004a. Gastrointestinal Diseases: Part II. In Quesenberry, K.E., and Carpenter, J.W. (eds.). Ferrets, Rabbits, and Rodents:

Exotic Small Mammal Care and Husbandry

Clinical Medicine and Surgery. Second edition. Saunders, St. Louis, MO, pp. 33–38. Bell, Judith A. 2004b. Periparturient and Neonatal Diseases. In Quesenberry, K.E., and Carpenter, J.W. (eds.). Ferrets, Rabbits, and Rodents: Clinical Medicine and Surgery. Second edition. Saunders, St. Louis, MO, pp. 50–56. Brown, Susan A. 2004. Basic Anatomy, Physiology, and Husbandry. In Quesenberry, K.E., and Carpenter, J.W. (eds.). Ferrets, Rabbits, and Rodents: Clinical Medicine and Surgery. Second edition. Saunders, St. Louis, MO, pp. 2–11. Burgess, Mark, and Garner, Michael. 2002. Clinical Aspects of Inflammatory Bowel Disease in Ferrets. Exotic DVM 4(2):29–34. Johnson-Delaney, Cathy. 2006. Ferret Adrenal Disease: 2006 Perspective. Exotic DVM 8(3):31–34. Kiefer, Kristina M., and Johnson, Dan. 2006. What Veterinarians Need to Know about Ferrets. Exotic DVM 8(2):38–43. Lichtenberger, Marla. 2005. Shock, Fluid Therapy, Anesthesia and Analgesia in the Ferret. Exotic DVM 7(2):24–30. Marini, Robert P., Otto, Glen, Erdman, Susan, Palley, Lori, and Fox, James G. 2002. Biology and Diseases of Ferrets. In Fox, J.G., Anderson, L.C., Loew, F.M., and Quimby, F.W. (eds.). Laboratory Animal Medicine. Second edition. Academic Press, San Diego, pp. 483–513. Morrisey, James K., and Carpenter, James W. 2004. Formulary. In Quesenberry, K.E., and Carpenter, J.W. (eds.). Ferrets, Rabbits, and Rodents: Clinical Medicine and Surgery. Second edition. Saunders, St. Louis, MO, pp. 436–444. Quesenberry, Katherine E., and Orcutt, Connie. 2004. Basic Approach to Veterinary Care. In Quesenberry, K.E., and Carpenter, J.W. (eds.). Ferrets, Rabbits, and Rodents: Clinical Medicine and Surgery. Second edition. Saunders, St. Louis, MO, pp. 13–23. Quesenberry, Katherine E., and Rosenthal, Karen L. 2004. Endocrine Diseases. In Quesenberry, K.E., and Carpenter, J.W. (eds.). Ferrets, Rabbits, and Rodents: Clinical Medicine and Surgery. Second edition. Saunders, St. Louis, MO, pp. 79–89. Taylor, Bobbi. 2001. Alternate Technique for Venipuncture in Ferrets. Exotic DVM 2(6):37–39. Willard, Thomas R. 2002. Exotic Animal Nutrition: Ferrets. Exotic DVM 4(4):36–37.

6

Mice

Mice have been used in scientific research since the 1600s. The ability to create genetically engineered mice, as well as their small size, short generation time, and ease of breeding, have made mice the most widely used experimental animal (Suckow et al., 2001). Standard laboratory mice, Mus musculus, are usually white, but “fancy mice” or pet varieties are available in a multitude of varieties, including satin, long-haired, pied, and various solid colors (Bihun and Bauck, 2004). Mice can be good pets for older children, but may be too skittish for younger children to handle. They require little space and are relatively inexpensive to maintain. BASIC ANATOMY AND PHYSIOLOGY

Mice have physical characteristics typical of members of the order Rodentia. Typical body weight for an adult is 30 g, with males being larger than females. Mice are nocturnal and most often eat and engage in nesting and burrowing behaviors at night. Table 6.1 lists the basic biological parameters for mice. The dental formula of the mouse is 2(1/1 incisors, 0/0 canines, 0/0 premolars, and 3/3 molars). Their incisors continually erupt and will overgrow if malocclusion occurs. Mice have exophthalmic eyes. The Harderian gland is found within the orbit and produces secretions for ocular lubrication. The secretions contain porphyrins, which give the tears a red appearance. In stressed or diseased animals, increased tear production can be mis-

Table 6.1 Basic biologic parameters. Body weight

Adult male: 20–40 g Adult female: 18–35 g Birth weight: 1–1.5 g

Body temperature

36.5–38.0 °C (97.5–100.4 °F)

Reproductive data

Sexual maturity Female: 6 weeks Male: 6 weeks Estrous cycle: 4–5 days Gestation length: 19–21 days Litter size: 7–11 Weaning age: 18–21 days

Life span (captivity)

12–36 months

Heart rate

427–697 beats per minute

Respiratory rate

91–216 breaths per minute

Food intake

3–5 g/adult

Water intake

5–8 mL/adult

From: Bihun and Bauck (2004); Suckow et al. (2001).

taken for bleeding from the eyes (Bihun and Bauck, 2004). REPRODUCTION AND SEXING

Males are typically twice the size of females. Adult males can be distinguished from females by the presence of a scrotal sac containing the testes (Fig. 6.1). Rodents have open inguinal rings and can retract their testes into the abdomen. In young mice, sexing can be accomplished by comparing the anogenital distance, 73

74

Exotic Small Mammal Care and Husbandry

Fig. 6.2 Increased anogenital distance in male (left) than female (right) mouse.

Fig. 6.1 Differentiation of female (left) from male (right) external genitalia. For color detail, please see color plate section.

which is greater in males than in females (Fig. 6.2). Mice become sexually mature by 7–8 weeks of age. Females are polyestrous and cycle every 4–5 days. Mating is usually detected by the formation of a vaginal plug, which is a white mass that fills the vagina formed from secretions of the coagulating and vesicular glands of the male mouse. Gestation is typically 19–21 days, with an average litter size of 10–12 pups. The optimal weaning age in mice is 21 days. HOUSING AND HUSBANDRY

The choice of caging system should take into consideration ease of cleaning, ability to contain mice without escape, and ventilation. Although wire cages offer the benefit of good ventilation and climbing as enrichment, a small-gauge wire will be necessary to prevent escape. Aquarium-type cages are more secure

and allow for provision of deep bedding and nesting. Cage tops should be screened to secure mice. The optimal temperature range for mice is 64 °F to 79 °F (18 °C to 26 °C). Water bottles should be mounted and should be checked daily. Rodent food pellets can be provided in dishes kept on the floor to minimize contamination with feces and urine. There are many different types of bedding available, ranging from recycled paper to wood shavings. Cedar shavings have been shown to affect microsomal oxidative liver enzymes in rats and mice and potentially cause dermatological and respiratory effects (Bihun and Bauck, 2004). Environmental enrichment and exercise are important in captive mice. Exercise wheels, tunnels, nesting material, and exercise balls improve the quality of life for the pets and can promote human interaction and bonding. Most rodents have similar nutritional requirements. Formulated diets (pellets or blocks) are more nutritionally complete than seed diets, which are high in fat. A minimum protein requirement of 16% and fat content of 4%–5% is appropriate for a maintenance diet in mice. Breeding animals may require a protein content of up to 20%. Adult mice drink 6–7 mL of water per day. Decreased water consumption will decrease food consumption (Jacoby et al., 2002).

Mice

75

HANDLING AND RESTRAINT

Mice are very active and will run away when you try to capture them. The easiest way to immobilize them is to grasp them initially at the base of the tail. While still holding them by the tail, use the forefinger and thumb to gently pin down the head and grasp the “scruff” (loose tissue at the back of the neck). The rest of the body then can be cradled in the palm of your hand. Commercial restraint devices are available that allow for hands-free restraint (Fig. 6.3). Ideally, mice should be acclimated

Fig. 6.3 Commercial restraint device for mice.

to these devices over a period of time to minimize stress. PHYSICAL EXAM

Many diseases in small rodents are the result of improper husbandry or nutrition. Rodents should be examined in their home cages to evaluate water provision, food, bedding, and sanitation. General behavior and activity level in the cage should be observed. Findings such as ruffled fur or a hunched position can indicate illness. A thorough medical history is crucial to making a correct diagnosis. The information should include the source of the animal, primary caregiver, food preferences, duration of illness, and what other types of animals are in the household. Rodents should be weighed on a gram scale for accuracy. Gentle abdominal palpation can be performed to assess for masses and body condition. A small otoscope is helpful to evaluate the eyes, ears, and oral cavity. Incisor problems are common in small rodents. Respiratory and heart rates are difficult to measure in rodents. Normal physiologic parameters are listed in Table 6.1 (see section “Basic anatomy and physiology”). The coat should be evalu-

Table 6.2 Reference ranges for hematology and serum biochemical values for mice. Value

Reference Interval

RBC (×10 cells/μL)

7.9–10.1

Hemoglobin (g/dL)

11.0–14.5

6

Hematocrit (%) WBC (×103 cells/μL)

37–46 5.0–13.7

Neutrohphils (%)

10–40

Lymphocytes (%)

55–95

Monocytes (%)

0.1–3.5

Value Glucose (mg/dL)

73–183

Cholesterol (mg/dL)

59–103

Blood urea nitrogen (mg/dL)

18–31

Creatinine (mg/dL)

0.48–1.1

Aspartate aminotransferase (U/L)

101–214

Alaline aminotransferase (U/L)

Eosinophils (%)

0–4

Alkaline phosphatase (U/L)

Basophils (%)

0–0.3

Total bilirubin (mg/dL)

Platelets (×103 cells/μL) Total blood volume (mL/kg) Total protein (g/dL)

600–1,200 70–80 59–103

Reference Interval

Sodium (mmol/L)

44–87 43–71 0.3–0.8 143–164

Potassium (mmol/L)

6.3–8.0

Chloride (mmol/L)

105–118

Albumin (g/dL)

2.5–4.8

Phosphorus (mg/dL)

5.2–9.4

Globulin (g/dL)

0.6

Calcium (mg/dL)

4.6–9.6

From: Bihun and Bauck (2004); Suckow et al. (2001).

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Exotic Small Mammal Care and Husbandry

ated for hair loss, skin lesions, masses, or evidence of parasites. Special attention should be paid to the condition of the footpads and nails (Daviau, 1999). SAMPLE COLLECTION

Urine and fecal samples are easy to obtain in mice. It is a normal reflex for mice to urinate when picked up. The quantity is often sufficient for a dipstick analysis. Fecal samples can be evaluated by flotation and direct smear for evidence of intestinal parasites. Blood collection sites include the lateral saphenous vein, lateral tail vein, and maxillary “facial” vein. Retro-orbital blood collection is not recommended because of the potential to injure the eye. Cardiocentesis is reserved for terminal patients under anesthesia. As a general rule, 10% of the total blood volume can be withdrawn without adverse effects every 3–4 weeks. The blood volume of the average adult mouse is 2–2.75 mL. Reference ranges for hematological and biochemical values are presented in Table 6.2.

Fig. 6.4

Oral gavage technique in mice.

common endoparasites and ectoparasites, if detected, can be routinely treated with ivermectin, although this agent is not approved for use in these species.

DRUG ADMINISTRATION

Drug administration can be challenging in small rodents. Most therapeutic agents must be diluted with 0.9% NaCl prior to administration. In a hospital setting, medication can be administered by injection or oral gavage (PO). Because mice have a small muscle mass, subcutaneous (SC) or intraperitoneal (IP) injection is used most commonly. Therapeutic agents can be administered at home in food or drinking water. If not eating, oral medications can be administered by oral gavage using a bulb-ended metal feeding tube or flexible feeding tube (Fig. 6.4). PREVENTIVE HEALTH

Preventing disease in small rodents is usually more effective than treatment. Acquiring animals from reliable sources and providing optimal husbandry and nutrition will prevent most common diseases. No vaccines are routinely recommended for rodents. Many

COMMON DISEASES

Pet rodents may present with nonspecific clinical signs such as ruffled fur, a hunched appearance, reluctance to move, and anorexia. The most common diseases in mice are dermatopathies, enteropathies, and pneumonia (Donnelly, 2004). Table 6.3 presents the mouse formulary.

Gastronintestinal disease Diarrhea is uncommonly seen in pet mice, although it is sometimes associated with overfeeding green vegetables. Endoparasitic infections are common, but not clearly associated with clinical disease. Giardia muris and Spironucleus muris are pear-shaped, flagellated protozoan parasites found in the duodenum of young mice or immunocompromised adult mice. Infected animals may be asymptomatic or show signs of weight loss, rough haircoat, or abdominal distension. Diagnosis is based on the demonstration of trophozoites in fecal wet

Table 6.3 Mouse formulary. Agents

Dosage (mg/kg)

Route

Amikacin

10 q12h

SC, IM

Ampicillin

20–50 q12h

PO, SC, IM

Ciprofloxacin

10 q12h

PO

Doxycycline

5 q12h

PO

Enrofloxacin

5–10 q12h

PO, SC, IM

Gentamicin

5–10 q12h

SC, IM

Metronidazole

10–40 q24h

PO

Penicillin G

22,000 IU/kg q24h

SC, IM

Trimethoprim-sulfa

15–30 q12h

PO, SC

Griseofulvin

25 q24h

PO

Lime sulfur dip (2.5%)

Dip q7d for 4–6 treatments

Topical

Antimicrobial Agents

Antifungal Agents

Antiparasitic Agents Amitraz

1.4 mL/L q7d

Topical

Fenbendazole

20 q24h for 5 days

PO

Ivermectin

0.2–0.4 q10–14d

SC

Praziquantel

6–10 repeat in 10 days

PO, SC, IM

Sulfadimethoxine

10–15 q12h

PO

Sulfmerazine

1 mg/mL

Drinking water

Sulfaquinoxaline

1 mg/mL

Drinking water

Chemical Restraint, Anesthesia, Analgesia Acepromazine

0.5–1.0

IM

Atipamazole

1–2.5

SC

Atropine

0.1–0.4

IM, SC

Buprenorphine

0.05–2.5 q6–12h

SC, IP, IM

Butorphanol

1–5 q4h

SC

Carprofen

5–10

PO

Diazepam

3–5

IM

Flunixin meglumine

2.5 q12–24h

SC

Glycopyrrolate

0.01–0.02

SC

Ibuprofen

7–15 q4h

PO

Isoflurane

0.25%-4.0% to effect

Inhalation

Ketamine

22–44

IM

Ketamine + medetomidine

50–75 (K)/10 (M)

IP

Ketamine + xylazine

50 (K)/5 (X)

IP

Ketoprofen

5 q24h

SC, IM

Medetomidine

0.1

SC, IM

77

78

Exotic Small Mammal Care and Husbandry

Table 6.3 Continued Agents

Dosage (mg/kg)

Route

Midazolam

1–2

IM

Morphine

2–5 q2–4h

SC, IM

Naloxone

0.01–0.1

SC, IP

Oxymorphone

0.2–0.5 q6–12h

SC, IM

Pentobarbital

50–90

IP

Cimetadine

5–10 q6–12h

PO, SC, IM, IV

Dexamethasone

0.5–2.0

IM, SC, IV

Diphenhydramine

1–2 q12h

PO, SC

Furosemide

2–10 q12h

PO, SC

Metoclopramide

0.2–1.0 q12h

PO, SC, IM

Oxytocin

0.2–3.0 IU/kg

SC, IM, IV

Prednisone

0.5–2.2

SC, IM

Miscellaneous Agents

From: Carpenter (2005); Morrisey and Carpenter (2004).

mounts. Metronidazole (0.04%-0.10% for 14 days) delivered in drinking water is usually effective at treating intestinal protozoal infections (Donnelly, 2004). Pinworm infection is common and considered nonpathogenic. The two species commonly diagnosed are Syphacia obvelata and Aspicularis tetraptera. Diagnosis of S. obvelata is made by evaluation of a Scotch tape prep of the perianal region to demonstrate ova, as adult worms deposit eggs around the anus. Aspicularis tetraptera ova can be found on a fecal float or direct smear. Mice are typically asymptomatic, but some animals will exhibit rectal prolapse. Treatment with ivermectin 2 mg/kg PO given twice at 10-day intervals has been shown to be effective at eliminating pinworm infection in mice. Tyzzer’s disease, caused by the gram-negative bacterium Clostridium piliforme, can infect mice resulting in clinical signs of lethargy, diarrhea, and death. Although not common in pet mice, this agent can affect many species, including rats, hamsters, and rabbits. Diagnosis is based on demonstration of the typical intracellular organisms in tissue sections of liver and intestine.

Helicobacteriosis is a common infection of laboratory mice. Helicobacter is a gram-negative spiral-shaped organism that has been isolated from the gastrointestinal tract of many mammals, including humans. Although mice are usually asymptomatic, infection can result in intestinal inflammation, diarrhea, and rectal prolapse. Effective treatment has been achieved with triple therapy with amoxicillin, metronidazole, and bismuth administered for 2 weeks. Salmonellosis can be spread by asymptomatic carriers. Infection is more common in young mice and can result in septicemia and death. Clinical signs include lethargy, weight loss, abdominal distension, and death. Salmonella has the potential for zoonotic infection and it is recommended that affected animals be euthanized.

Respiratory disease Respiratory disease is common in mice and rats. Mycoplasmosis pulmonis is a gram-negative bacterium that is responsible for murine respiratory mycoplasmosis (MRM). Clinical signs include suppurative rhinitis, otitis media, and chronic pneumonia. “Chattering” and

Mice

79

dyspnea can be observed in affected mice. Animals that survive typically develop chronic infections. Sendai virus is a paramyxovirus related to human parainfluenza virus 1 (Jacoby et al., 2002). Infected mice exhibit weight loss, dyspnea, “chattering,” and crusting of the eyes. Sendai virus is transmitted by aerosol and is highly infectious. Neonates typically do not survive. Adult mice may develop secondary opportunistic infections.

Neurological diseases Lymphocytic choriomeningitis virus (LCMV) is widely distributed in North and South America. Wild mice are the reservoir for infection. Infected mice can exhibit neurological forms of disease (head tremors, seizures, death) or visceral forms of disease (glomerulonephritis). Although uncommon in pet mice, this agent is important because it can infect people and cause mild to serious or fatal disease (Suckow et al., 2001).

Dermatological disease Diseases of the skin are commonly seen in pet mice. Mice establish a social hierarchy when housed in groups and engage in fighting and barbering. The dominant mouse will nibble the whiskers and hair around the face from the submissive cage mates (Fig. 6.5). Fur mites typically infest the head, neck, and shoulder area, causing pruritis, patchy alopecia, and ulceration. The following three species are most common: Myobia musculi, Myocoptes musculinus, and Radfordia affinis. Identification of mites or eggs on skin scrapings is diagnostic. Mites are spread by direct contact with infected mice or bedding. Treatment with ivermectin (0.2 mg/kg SC or PO) twice at 10day intervals is effective. Skin swellings may be caused by abscesses or neoplasia. In group-housed animals, bite wounds can become secondarily infected with various opportunistic pathogens, including Staphylococcus aureus, Pasteurella pneumotropica, and Streptococcus pyogenes. Fine needle aspirate will demonstrate a mucopuru-

Fig. 6.5 Barbering in mice. For color detail, please see color plate section.

lent exudate. The most common subcutaneous tumor in mice is mammary adenocarcinomas. In some strains of mice, the incidence is as high as 70% (Donnelly, 2004). REFERENCES Bihun, C., and Bauck, L. 2004. Basic Anatomy, Physiology, Husbandry, and Clinical Techniques. In Quesenberry, K.E., and Carpenter, J.W. (eds.). Ferrets, Rabbits, and Rodents: Clinical Medicine and Surgery. Second edition. Saunders, St. Louis, MO, pp. 286–298. Carpenter, J.W. 2005. Exotic Animal Formulary. Third edition. Elsevier Saunders, St. Louis, MO, pp. 377–408. Daviau, J. 1999. Clinical Evaluation of Rodents. Veterinary Clinics of North America: Exotic Animal Practice 2(2): pp. 429–445. Donnelly, T.M. 2004. Disease Problems of Small Rodents. In Quesenberry, K.E., and Carpenter, J.W. (eds.). Ferrets, Rabbits, and Rodents: Clinical Medicine and Surgery. Second edition. Saunders, St. Louis, MO, pp. 299–315.

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Jacoby, R.O., Fox, J.G., and Davisson, M. 2002. Biology and Diseases of Mice. In Fox, J.G., Anderson, L.C., Loew, F.M., and Quimby, F.W. (eds.). Laboratory Animal Medicine. Second edition. Academic Press, San Diego, CA, pp. 35–120. Morrisey, J.K., and Carpenter, J.W. 2004. Formulary. In Quesenberry, K.E., and Carpenter,

Exotic Small Mammal Care and Husbandry

J.W. (eds.). Ferrets, Rabbits, and Rodents: Clinical Medicine and Surgery. Second edition. Saunders, St. Louis, MO, pp. 436–444. Suckow, M.A., Danneman, P., and Brayton, C. 2001. The Laboratory Mouse. CRC Press, Boca Raton, FL.

Fig. 4.1 Proper rabbit manual restraint.

a Fig. 4.3

Fig. 4.2 Mandibular prognathism and malocclusion. (Photo courtesy of Dan H. Johnson, DVM, Avian and Exotic Animal Care, Raleigh, NC.)

b a External genitalia of a female rabbit.

Fig. 4.3 b External genitalia of a male rabbit.

Fig. 5.1 Normal ferret (copyright Eric Isselée, Dreamstime.com).

Fig. 5.5 Manual restraint of a ferret while distracting with Nutri-Cal. CP-1

Fig. 5.7 Typical alopecia pattern associated with adrenal disease in ferrets. (Photo courtesy of Dan H. Johnson, DVM, Avian and Exotic Animal Care, Raleigh, NC.)

Fig. 6.1 Differentiation of female (left) from male (right) external genitalia.

Fig. 6.5

Barbering in mice.

Fig. 7.2

Fig. 7.11 stress. CP-2

Albino rat.

Rat with porphyrin staining due to

Fig. 7.6 Rat housed on corncob bedding with paper towel added for enrichment. Notice how the paper towel has been shredded into small pieces.

Fig. 7.9 Blood collection from the saphenous vein.

Fig. 8.1 Pofile of a normal gerbil. (Copyright Eric Isselée, Dreamstime.com.)

Fig. 8.2 Gerbil abdomen with ventral gland located centrally. (Photo courtesy of Dan H. Johnson, DVM, Avian and Exotic Animal Care, Raleigh, NC.)

Fig. 8.4 Degloved tail tip of gerbil. (Photo courtesy of Dan H. Johnson, DVM, Avian and Exotic Animal Care, Raleigh, NC.)

CP-3

Fig. 9.1 Normal hamster in cage. (Photo courtesy of Dan H. Johnson, DVM, Avian and Exotic Animal Care, Raleigh, NC.)

Fig. 9.3 Isolated hamster cheek pouch. (Photo courtesy of Dan H. Johnson, DVM, Avian and Exotic Animal Care, Raleigh, NC.)

Fig. 9.7 Female gerbil with a litter of pups. (Photo courtesy of Dan H. Johnson, DVM, Avian and Exotic Animal Care, Raleigh, NC.)

Fig. 9.9 Hamster in tubing enrichment device. (Copyright Alina Cardiae, Dreamstime.com.)

b Fig. 10.1 b Abyssinian guinea pigs. (Copyright Stefan Andronache, Dreamstime.com.) a Fig. 10.1 a Coat color variation in guinea pigs. CP-4

Fig. 10.5 Ulcerative pododermatitis in a guinea pig. (Photo courtesy of Dan H. Johnson, DVM, Avian and Exotic Animal Care, Raleigh, NC.)

Fig. 10.6 Trixacarus caviae infection. (Photo courtesy of Dan H. Johnson, DVM, Avian and Exotic Animal Care, Raleigh, NC.)

Fig. 11.1 The most common pet species, Chinchilla laniger. (Photo courtesy of Dan H. Johnson, DVM, Avian and Exotic Animal Care, Raleigh, NC.)

Fig. 11.8 Fur ring removed from a male chinchilla. (Photo courtesy of Dan H. Johnson, DVM, Avian and Exotic Animal Care, Raleigh, NC.)

Fig. 12.1 Profile of a normal degu. (Copyright Daniel Rajszczak, Dreamstime.com.)

Fig. 11.9 Fur slip in a chinchilla. (Photo courtesy of Dan H. Johnson, DVM, Avian and Exotic Animal Care, Raleigh, NC.) CP-5

Fig. 12.2 Ventral abdomen of female (left) and male (right) degu genitalia. (Photo courtesy of Dan H. Johnson, DVM, Avian and Exotic Animal Care, Raleigh, NC.)

Fig. 12.5 Degloved tail of a degu requiring surgical correction. (Photo courtesy of Dan H. Johnson, DVM, Avian and Exotic Animal Care, Raleigh, NC.)

Fig. 13.2 Balled-up hedgehog. (Photo courtesy of Dan H. Johnson, DVM, Avian and Exotic Animal Care, Raleigh, NC.)

Fig. 13.4 Self-anting (anointing). (Photo courtesy of Dan H. Johnson, DVM, Avian and Exotic Animal Care, Raleigh, NC.)

CP-6

Fig. 14.1 Sugar glider. (Photo courtesy of Dan H. Johnson, DVM, Avian and Exotic Animal Care, Raleigh, NC.)

Fig. 13.8 Obese hedgehog. (Photo courtesy of Dan H. Johnson, DVM, Avian and Exotic Animal Care, Raleigh, NC.)

Fig. 14.3 Sugar glider grasping plant. (Photo courtesy of Judi Fox.)

Fig. 14.9 Sugar glider enrichment. (Photo courtesy of Judi Fox.)

CP-7

Fig. 14.10 Sugar glider in nest box. (Photo courtesy of Dan H. Johnson, DVM, Avian and exotic Animal Care, Raleigh, NC.)

Fig. 15.1 Adult Didelphis virginiana. (Copyright Teekaygee, Dreamstime.com.)

Fig. 15.2

CP-8

Juvenile Didelphis virginiana.

Fig. 15.4 Abdominal pouch with litter. (Photo courtesy of Dan H. Johnson, DVM, Avian and Exotic Animal Care, Raleigh, NC.)

7

Rats

The rat (Rattus norvegicus) is a common pet belonging to the order Rodentia and the family Muridae. Rats are thought to have originated in the areas now known as southern Russia and Northern China. There are over 130 species in the genus Rattus, although the two most prominent are the black rat and the brown rat (Kohn and Clifford, 2002). The black rat (R. rattus) was well-known in Europe by 1100 AD and the brown rat (R. norvegicus) was a common occurrence in Europe by the 1700s. Rats are good pets for children because they are large enough to be easily handled, are non-aggressive, are social, are easily trainable, and rarely bite. Rats are also intelligent and affectionate, thus adding to their desirability as a pet species.

Fig. 7.1

Hooded rat.

COMMON BREEDS

Orr (2002) describes five types of fancy rats bred in the United Kingdom: self (one solid color), marked (Irish, Berkshire, Hooded, Capped), silver (recognized self-color containing equal numbers of nonsilver and silver guard hairs), any other variety (Siamese, Agouti), and rex (coat is evenly curled and there are as few guard hairs as possible). In the United States the most common pet rat species is R. norvegicus, with the hooded (Fig. 7.1) and white (Fig. 7.2) rat being the most frequent color variations (Tully, 2008). Albino rats tend to be calmer than hooded rats, which are more likely to be aggressive (Leck, 1999).

Fig. 7.2 Albino rat. For color detail, please see color plate section. 81

82

Exotic Small Mammal Care and Husbandry

BASIC ANATOMY AND PHYSIOLOGY

Rats are nocturnal and are characterized by elongated body shape, small eyes and ears, short fur, and hairless tails. Their long tail may comprise up to 85% of the total body length. The tail is generally longer in the female than in the male and is useful in maintaining balance and thermoregulation. The body is covered with hair except on the nose, lips, palms of forelimbs, and soles of hind limbs. There are two types of hair: guard hairs, which have a long shaft, and under hairs, which do not have a long shaft. The hair grows in a cyclical pattern with hair growing in length for 17 days then resting for 17 days (Kohn and Clifford, 2002). Rats also have specialized tactile hairs called vibrissae that are used in sensory input. As rats get older the white hair coat can turn a yellowish color. Rat eyes are bulging, the eyelids are well developed, and the only visible structure is the cornea (Kohn and Clifford, 2002). Albino rats, as are other albino animals, are inclined toward poor eyesight. Rats have a lacrimal gland located behind the eyeball, called the Harde-

Fig. 7.4

Male rat.

rian gland (Leck, 1999). This gland produces a porphyrin secretion that is red in color. These secretions tend to be produced when the rat is stressed or ill. Each limb has five digits with a nail. Rats have open inguinal canals, a divided stomach, a large cecum, a diffuse pancreas, and an os penis.

Fig. 7.3

Rat teeth. (Courtesy of Ian Thomas.)

Fig. 7.5

Female rat.

Rats

Rats are omnivores and have one permanent set of teeth. The teeth grow continuously (Fig. 7.3) and must be worn down by chewing and gnawing. The dental formula is 2(1/1 incisors, 0/0 canines, 0/0 premolars, 3/3 molars). Malocclusion may occur if the incisors are misaligned and cannot be sufficiently worn down by normal gnawing activities. REPRODUCTION AND SEXING

It is fairly easy to distinguish gender in rats as the distance between the anus and the genital opening, called the anogenital distance, is about twice as long in the male as in the female (Figs. 7.4 and 7.5). Males have a distinct scrotum located between the anus and the prepucial opening, although the testicles can be retracted into the abdomen. Only female rats possess nipples. The presence of a copulatory plug formed by semen coagulation indicates mating has occurred. The estrous cycle lasts 4–5 days and contains distinct components: proestrus (∼12 hours duration), estrus (∼12 hours duration), metestrus (∼21 hours duration), and diestrus (∼57 hours duration) (Sharp and LaRegina, 1998). Parturition lasts about 90 minutes and a post-partum estrus occurs with about 50% fertility. Breeding system can be either a monogamous pair or a polygamous group consisting of one male housed with up to six females. Litter size is from 3 to 18 pups depending on species. Rats are generally weaned at 20–21 days of age. (Table 7.1 gives the basic biological parameters of rats.) UNIQUE FEATURES OF IMPORTANCE

Rats have brown fat, which plays a role in thermogenesis during exposure to the cold. This fat is distributed throughout the ventral, lateral, and dorsal aspects of the neck but is primarily found between the scapulae. Brown fat is often confused with salivary glands or lymph nodes. The rat does not have a gall bladder nor does it have the ability to vomit, due to the presence of a limiting ridge at the junction of the stomach and the esophagus. Rats, like other rodents, do not have sweat glands, cannot

83

Table 7.1 Basic biologic parameters. Body weight

Adult male: 450–520 g Adult female: 250–400 g Birth weight: 5–6 g

Length

Body: 23–28 cm (9–11 inches) Tail: 18–23 cm (7–9 inches)

Body temperature

35.9 °C–37.5 °C (96.6 °F–99.5 °F)

Reproductive data

Sexual maturity Female: 40–65 days Male: 40–65 days Estrous cycle: 4–5 days Duration of estrus: 13–15 hours Female continuously polyestrous Postpartum estrus Gestation length: 20–23 days Litter size: 3–18 Weaning age: 21 days Breeding life: 14 months

Life span (captivity)

2–4 years

Heart rate

250–600 beats per minute

Respiratory rate

66–150 breaths per minute

Food intake

20–60 g/day

Water intake

15–30 mL/day

From: Bistner et al. (2000); Kahn (2007); Lawson (2001); Sharp and LaRegina (1998).

pant, and are poor regulators of core body temperature although they can dissipate heat through their ears and tails (Bihun and Bauck, 2004). The tail vessels can vasoconstrict when heat conservation is necessary and can vasodilate to dissipate heat. Rats adapt more readily to cold temperatures than to heat. Rats have poor vision and cannot detect color. Rats, as other rodent species, are coprophagic. HOUSING AND HUSBANDRY

Rats tend to be social but can do well when housed in small groups or singly. Unlike mice, adult males can be housed together with few problems. Cages should be large enough to allow the rats to nest, burrow, and exercise. Cages should be easy to clean as poor husbandry practices can lead to disease conditions.

84

Rat cages should be escape-proof and constructed of a material that is not easily chewed. Cage sides could be constructed of wire or metal mesh, Plexiglas, or plastic. An open screen top is suggested for solid-walled enclosures to help aid in ventilation and to prevent escape. If the household contains other pets such as cats, dogs, or ferrets, the enclosure may require a sturdier top to ensure the rats’ safety. Leck (1999) recommends housing for each adult rat should be at least 24″W × 24″L × 12″H. Because rats like to climb, a cage that is taller than the recommended height and fitted with ramps and ropes would be preferred. Bedding can consist of recycled paper products, hardwood chips or shavings, or shredded paper (Fig. 7.6). Pine and cedar bedding should not be used as it can affect liver enzymes. Bedding should be approximately ¼″ to 1” deep and should be changed several times a week. Ideal room temperatures should be between 65 °F and 80 °F (18–26 °C) and relative humidity should be maintained between 40% and 70%. Cages should be located away from windows and drafts to avoid extreme temperature fluctuations. NUTRITION

Exotic Small Mammal Care and Husbandry

diet is that the rat can select the palatable seeds and ignore the less desirable seeds; therefore, a balanced diet is not achieved and obesity is likely to occur. Rodent diets that are in the form of pellets or blocks are recommended because they provide a more uniform diet. Commercial diets are readily available that meet the rat’s nutritional requirements. Fresh vegetables and fruits can be added to the diet in small amounts. Adult rats need 5–10 g of pellets per 100 g of body weight daily. Water should be provided ad libitum via drinking bottle with sipper tube, although rats generally only drink 10 mL of water per 100 g of body weight daily.

ENRICHMENT

Rats, like other rodents, can benefit from having objects in their environment they can manipulate. Objects that provide for the normal activities of burrowing and gnawing are ideal. These objects include wooden blocks, balls, shredded paper, plastic PVC pipes, nylon bones, nesting material, and social housing. Enrichment can also include frequent handling as well as supervised time outside of the cage in a contained environment.

Pet rodents are often fed a seed diet (Bihun and Bauck, 2004). The problem with this type of HANDLING, RESTRAINT, AND PHYSICAL EXAM

Fig. 7.6 Rat housed on corncob bedding with paper towel added for enrichment. Notice how the paper towel has been shredded into small pieces. For color detail, please see color plate section.

Frequent handling of rats will accustom them to humans and will help ease the stress associated with manipulation and restraint. Rats can be picked up by the base of the tail but should not be held in that position for more than a few seconds. Rats can be carried by picking them up and placing them on the opposite forearm of the handler in order to support the rat’s body weight. Proper restraint can avoid injury to the rat and to the handler. Smaller rats can be restrained by grasping the loose skin over the neck and back. Larger rats can be restrained by grasping the rat around the thorax with the handler’s thumb or index finger under the mandible (Figs. 7.7 and 7.8). Most rats can be

Table 7.2 Preanesthetic agents used in rats. Agent

Dosage

Route

Effects

Acepromazine

2.5 mg/kg

IM, IP

Sedation

Atropine

0.05 mg/kg

IP, SQ

Parasympatholytic

Diazepam

2.5–5.0 mg/kg

IM, IP

Sedation

Fentanyl/droperidol (Innovar-vet)

0.5 mg/kg

IM

Immobilization and analgesia

Fentanyl/fluanisone (Hypnorm)

0.2–0.5 mL/kg 0.3–0.6 mL/kg

IM IP

Sedation with some analgesia

Glycopyrrolate

0.5 mg/kg

IM

Parasympatholytic

Ketamine

50–100 mg/kg

IP, IM

Sedation, immobilization

Medetomidine

0.03–0.1 mg/kg

IP, SQ

Sedation, some analgesia

Midazolam

5 mg/kg

IP

Sedation

Xylazine

1–5 mg/kg

IM, IP

Sedation, some analgesia

From: Hawk and Leary (1999); Sharp and LaRegina (1998).

Table 7.3 Anesthetic agents used in rats. Agent

Dosage

Route

Alphaxalone/alphadolone (Saffan)

10–12 mg/kg

IV

Azaperone + ketamine

(A) 50 mg/kg + (K) 87 mg/kg give ¼ to 1½ times dose depending on length of anesthesia

IM

Chloral hydrate (10% solution)

200–400 mg/kg

IP

Fentanyl + medetomidine

(F) 300 μg/kg + (M) 300 μg/kg

IP

Fentanyl/droperidol (Innovar-vet)

0.02–0.06 mL/100 g 0.13–0.5 mL/kg

IP IM IM

Fentanyl/fluanisone (Hypnorm)

0.5 mL/kg

Fentanyl/fluanisone + diazepam

(F)0.6 mL/kg + (D)2.5 mg/kg

IP

Inactin

80–110 mg/kg

IP

Ketamine

44–100 mg/kg 75 mg/kg

IM IP

Ketamine + acepromazine

(K) 30–75 mg/kg + (A) 2.5–3 mg/kg

IP

Ketamine + detomidine

(K) 40–60 mg/kg + (D) 5–10 mg/kg

IM

Ketamine + diazepam

(K) 40–80 mg/kg + (D) 5–10 kg/kg

IP

Ketamine + medetomidine

(K) 75 mg/kg + (M) 0.5 mg/kg

IP

Ketamine + midazolam

(K) 75 mg/kg + (M) 5 mg/kg

IP

Ketamine + xylazine

(K) 40–80 mg/kg + (X) 5–10 mg/kg (K) 90 mg/kg + (X) 10 mg/kg

IP IM

Methohexital

7–15 mg/kg

IV

Pentobarbital

30–50 mg/kg

IP

Propofol

10–12 mg/kg

IV

Thiopental

30 mg/kg

IV

Tiletamine/zolazepam (Telazol)

20–40 mg/kg

IP

Tribromoethanol

300 mg/kg

IP

Urethane

1,000 mg/kg

IP

From: Carpenter (2005); Hawk and Leary (1999); Hawk et al. (2005); Sharp and LaRegina (1998).

85

Table 7.4 Analgesics used in rats. Agent

Dosage

Route

Acepromazine

1–2 mg/kg

IM

Acetaminophen

110–300 mg/kg 100–300 mg/kg 6 mg/mL in drinking water

PO PO

Alphaxalone/alphadolone

9–12 mg/kg

IP

Aminopyrine

200 mg/kg 650 mg total

SC PO

Antipyrine

220–600 mg/kg

SC

Aspirin

100 mg/kg 400 mg/kg

PO SC, PO

Buprenorphine

0.1–0.5 mg/kg 0.006 mg/mL in drinking water 0.01–0.05 mg/kg q8–12h 0.1–0.25 mg/kg q8–12h

SC, IV

Butorphanol

0.05–2.0 mg/kg q4h

SC

Carprofen

2–5 mg/kg

SC

Chlorpromazine

3–5 mg/kg 3–35 mg/kg

IV IM

Codeine

25–90 mg/kg q4h

SC

Diazepam

2 mg/kg 2.5–4 mg/kg

IV IM, IP

Diclofenac

10 mg/kg

PO

Fentanyl/droperidol (Innovar-Vet)

0.13–.5 mg/kg

IM

Fentanyl/fluanisone

0.3–0.6 mg/kg 0.2–0.5 mg/kg

IP IM

IV, SC PO

Flunixin

1.1–2.5 mg/kg

SC, IM

Ibuprofen

10–30 mg/kg

PO

Indomethacin

2 mg/kg

PO

Ketoprofen

33 mg/kg

PO

Medetomidine

30–100 μg/kg

IP, SC

Meperidine

10–20 mg/kg

SC, IM

Midazolam

2 mg/kg 4–5 mg/kg

IV IM, IP

Morphine

2–5 mg/kg hourly 10 mg/kg q2–4h

SC SC

Nalbuphine

1–5 mg/kg q3–4h 0.1 mg/kg 1 mg/kg

IM IV IP, SC PO

Naproxen

14.5 mg/kg

Oxymorphone

0.15 mg/kg

IM

Pentazocine

10 mg/kg q1–4h

SC

Pethidine

20 mg/kg q2–3h

SC, IM

Phenacetin

100 mg/kg q4h

PO

Phenylbutazone

20 mg/kg

PO

Piroxicam

3 mg/kg

PO

Xylazine

1–8 mg/kg 10 mg/kg

IM IP

From: Carpenter (2005); Hawk and Leary (1999); Hawk et al. (2005); Sharp and LaRegina (1998).

86

Rats

87

Fig. 7.8

Manual rat restraint.

Fig. 7.7 Manual rat restraint method referred to as the “claw.”

handled without injury to the rat or the handlers, but occasionally the use of protective leather or wire-mesh gloves may be warranted to avoid injury to the handler. Mechanical and chemical restraint can also be used with uncooperative rats (Tables 7.2–7.4, analgesic and anesthetic agents used in rats). The physical exam should include recording body temperature, checking body weight, and listening to the heart and lungs. The overall general body condition should be assessed during the exam. Swollen areas can indicate the presence of an abscess or tumor. The hair coat of a healthy rat should be smooth and groomed. A poor hair coat can indicate the presence of ectoparasites, poor nutrition and other husbandry practices, or stress. Ears should be thoroughly checked for abnormalities, and the teeth should be observed for malocclusion. Teeth can be trimmed to allow for proper alignment. The teeth can overgrow if the rat cannot gnaw to wear down the new tooth growth. This is an instance where the availability of enrichment objects on which

the rat can chew will greatly benefit the rat’s dental health. CLINICAL TECHNIQUES

Sample collection—venipuncture Since rats are relatively small in size it is important to keep the volume of blood collected to a minimum. A general guideline is to remove no more than 10% of the blood volume at a time and no more often than 3 to 4 weeks. Blood collection from the lateral saphenous vein (Fig. 7.9) is minimally invasive and can be repeated as needed. The lateral tail veins can also be used, although these vessels require more restraint as well as skill at blood collection. For ease of blood collection, the tail veins may be dilated by placing the tail under a heat lamp or in warm water. Blood collection from the orbital venous plexus or sinus is not recommended due to potential risk of injury to the eye and surrounding tissue. Cardiac puncture can be used to obtain large amounts of blood but should only be used in animals that will be subsequently euthanized.

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Exotic Small Mammal Care and Husbandry

Table 7.5 Rat clinical chemistry and hematologic reference ranges.

Fig. 7.9 Blood collection from the saphenous vein. For color detail, please see color plate section.

Sample collection—cystocentesis A small amount of urine can be obtained by restraining the rat over a clean solid surface. The restraint generally causes urination and a free-catch or table-top sample can be easily collected. Manual expression of the bladder can be used to collect a larger quantity. Catheterization of the female can be easily performed; however, this procedure is virtually impossible to perform in males due to the structure of the urethra.

Value

Normal Range

Packed cell volume (PCV)

35%–57%

Red blood cell count (RBC)

5–10 × 106/μL

White blood cell count (WBC)

3–17 × 103/μL

Hemoglobin (Hb)

11–19 g/dL

Mean corpuscular volume (MCV)

46–65 fL

Reticulocytes

0%–25%

Platelets

200–1,500 × 103/μL

Neutrophils

13%–26%

Lymphocytes

65%–83%

Monocytes

0%–4%

Eosinophils

0%–4%

Basophils

0%–1%

Glucose

80–300 mg/dL

Alanine aminotransferase (ALT) 20–224 IU/L Calcium

9.6–15 mg/dL

Phosphorus

6.0–8.0 mg/dL

Sodium

129–150 mEq/L

Potassium

4.6–6.0 mEq/L

Chloride

97–110 mEq/L

Blood urea nitrogen (BUN)

15–21 mg/dL

Creatinine

0.2–0.8 mg/dL

Total protein

5.6–7.6 g/dL

Albumin

3.8–4.8 g/dL

Drug administration

Total bilirubin

0.20–0.55 mg/dL

Drug administration in rats, as well as other rodents, can be challenging as most drugs are formulated for larger species; thus, dilution of these concentrated drugs is generally required for administration to rodents. Small volumes (0.2–0.3 mL) can be injected via 21-gauge needle intramuscularly (IM) into the quadriceps, triceps, or gluteal muscles. Intraperitoneal (IP) injections of up to 10 mL can be given in the lower right quadrant of the abdomen with a 22- to 26-gauge needle. As with blood collection, the saphenous or tail vein may be used to inject via the intravenous (IV) route using a 23-gauge needle. Only a small amount (0.5 mL) should be injected into the tail vein. Intragastric administration of drugs can be accomplished by using a feeding needle or a flexible catheter. The most common and desirable method of drug administration in the rat is the subcutaneous (SC) route. A large volume

Plasma volume

36–45 mg/kg

Blood volume

58–70 mg/kg

From: Carpenter (2005); Hawk and Leary (1999); Sharp and LaRegina (1998).

(5–10 mL) can be injected into the loose skin over the neck or back with minimal discomfort to the rat. Reference ranges for hematologic and biochemical values are presented in Table 7.5. PREVENTIVE HEALTH

There are no currently required or recommended vaccinations for rats; however, they may benefit from an annual veterinary visit. This visit should include a physical exam and

Rats

89

a thorough review of the husbandry practices, including diet and nutrition. Blood work and fecal exams may be recommended by the veterinarian as well as biannual visits to evaluate weight, trim nails, and assess general health and well-being, including dental health. Since rats are prey species they do not typically show overt signs of pain; therefore, it can be difficult for owners to determine if their rat is in pain or ill. Common signs of illness include rough hair coat (piloerection), hunched posture, anorexia, increase in aggression, and avoidance behaviors (Evans, 2006). If the owner observes any subtle changes in the behavior or aggression level of their rat a visit to the veterinarian is suggested. Endoparasites that have been identified in rats include pinworms (Syphacia muris, S. obvelata, and Aspicularis tetraptera), nema-

todes (Trichosomoides crassicauda), a protozoan parasite (Giardia muris), the rat tapeworm (Hymenolepsis diminuta), and the dwarf tapeworm (H. nana). Pinworms are very difficult to eradicate but treatment includes ivermectin, piperazine, and fenbendazole. Effective tapeworm treatments include thiabendazole and praziquantel. Giardia muris can be effectively treated with metronidazole or oxytetracycline. Table 7.6 presents parasiticides used in rats. Identified ectoparasites include Demodex nanus, the tropical rat mite (Ornithonyssus bacotic), the rat fur mite (Radfordia ensifera), fleas, and the spined rat louse (Polyplax spinulosa) (Tully and Mitchell, 2001). The rat fur mite can cause hair loss and pruritis. Mite infestations can be successfully treated with ivermectin, permethrin dusts, and other miticides.

Table 7.6 Parasiticides used in rats. Agent

Dosage

Carbaryl

Dust with 5% powder or dilute 1 : 1 with talc

Fenbendazole

8–12 mg/kg BW/day in feed daily on alternating weeks 20 mg/kg for 5 days 150 ppm in feed for five 7-day periods with treatments separated by 7 days

Route

PO

Ivermectin

200 μg/kg 3 mg/kg 2 mg/kg for 3 treatments at 7–9 day intervals 2 mg/kg topical as a spot method every 14 days for three treatments

SC PO PO

Ketoconazole

10–40 mg/kg for 14 days

PO

Malathion

5 mL in 1% suspension in bedding

Methyridine

125 mg/kg

SC, IP

Mebendazole

10 mg/kg for 5 days

PO

Metronidazole

20–60 mg/kg q8–12h

PO

Niclosamide

100 mg/kg 10 mg/100 g as a drench, repeat in 2 weeks 1 mg/g feed for 2 weeks separated by 1 week

PO

Nitrofurantoin

0.2% in feed for 6–8 weeks

Piperazine

2 mg/mL drinking water

Praziquantel

5 mg/kg 10 mg/kg

Pyrivinium palmoate

0.003% in drinking water for 30 days 0.012% in feed for 30 days

Quinacrine hydrochloride

75 mg/kg q8h

PO

Thiabendazole

200 mg/kg for 5 days 0.1% in feed

PO

From: Carpenter (2005); Hawk and Leary (1999); Hawk et al. (2005).

SC PO

90

Fig. 7.10 Rat prepared for surgical removal of mammary tumor. (Photo courtesy of Dan H. Johnson, DVM, Avian and Exotic Animal Care, Raleigh, NC.)

COMMON DISEASES

Ulcerative dermatitis The most common cause of ulcerative dermatitis in rats is Staphylococcus aureus. Trimming the toenails may be effective in reducing the level of self-mutilation associated with scratching. Good sanitation procedures can help control S. aureus.

Neoplasia Rats are susceptible to tumors, and the most common subcutaneous tumor is fibroadenoma of the mammary tissue (Fig. 7.10). Ovariohysterectomy at an early age can reduce the incidence level in female rats. These tumors are generally well encapsulated, do not metastasize, and can be surgically removed.

Porphyrin staining The presence of porphyrins, secreted from the Harderian glands located behind the eyes, indicates a response to stress and/or disease (Fig. 7.11). The underlying cause should be investigated and addressed as the presence of these “red tears” may be due to stress related to housing or husbandry or may be associated with a disease.

Enteritis Diarrhea and enteritis are common signs of illness in rats and can be caused by a variety of

Exotic Small Mammal Care and Husbandry

Fig. 7.11 Rat with porphyrin staining due to stress. For color detail, please see color plate section.

agents. Diarrhea may be caused by a sudden change in diet; thus any changes to the feeding regimen should be introduced over a period of time. Salmonella typhimurium or S. enteritidis can also cause chronic or acute diarrhea. Orr (2002) recommends euthanasia of pet rats with Salmonella due to its zoonotic potential.

Tyzzer’s disease Tyzzer’s disease is caused by Clostridium piliforme, formerly known as Bacillus piliformis. The disease manifests as anorexia, diarrhea, generalized illness, dehydration, and death. Poor husbandry practices, such as high environmental temperature or overcrowded housing conditions, may trigger the disease.

Respiratory disease Respiratory disease is common in many rodent species, and rats are no exception. The most common agents in rats are identified as Mycoplasma pulmonis alone or in conjunction with Streptococcus pneumoniae, Corynebacterium kutscheri, Sendai virus, and cilia-associated respiratory (CAR) bacillus (Orr, 2002). Clinical signs include dyspnea, sneezing, rhinitis, and labored respiratory sounds accompanied by red tears, weight loss, hunched posture, and labored breathing. Treatment for respiratory diseases includes enrofloxacin, tetracyclines, tylosin, sulphonamides, and cephalosporins. Table 7.7 presents anti-infectives used in rats.

Table 7.7 Anti-infectives used in rats. Agent

Dosage

Route

Amikacin Amoxicillin Ampicillin Cephalexin

2–5 mg/kg q8–12h 150 mg/kg q12h 50–150 mg/kg q12h 60 mg/kg 15 mg/kg 30 mg/kg 20 mg/100 g q8h 50 mg/kg q12h 10–50 mg/kg 2.5–5 mg/kg q12h 10 mg/kg q12h 0.5 mg/100 g 5–8 mg/kg 25 mg/100 g every 10 days 50 mg/kg q12h 2 mg/mL drinking water 0.2% in feed for 6–8 weeks 60 mg/kg q72h of long-acting drug 100,000 IU/kg 15,000 IU/20 mL drinking water 0.02% in drinking water 665–950 mg/L drinking water 450–643 mg/L drinking water 20 mg/kg q12h 100 mg/kg 30–50 mg/kg q12h 0.5 mg/kg of 240 mg/mL solution 10 mg/kg q24h 10 mg/100 g for 21 days

SC, IM SC, IM SC PO SC IM PO PO IM, SC PO, SC, IM SC IM SC PO IM

Cephaloridine Chloramphenicol palmitate Chloramphenicol succinate Enrofloxacin Gentamicin Griseofulvin Neomycin Nitrofurantoin Oxytetracycline Penicillin (potassium) Penicillin (oral) Sulfamerizine Sulfamethazine Tetracycline

Trimethoprim-sulfa Tylosin

SC IM

PO SC PO, SC SC SC PO

From: Hawk and Leary (1999); Hawk et al. (2005); Sharp and LaRegina (1998).

Table 7.8 Miscellaneous drugs used in rats. Agent

Dosage

Route

Agent

Dosage

Route

Acetylcysteine Alloxan

400 mg/kg 40 mg/kg 200 mg/kg 10 mg/kg 20 mg/kg 30 mg/kg 1 mg/kg 0.02–0.05 mg/kg 5 mg/kg 400 mg/kg 3–5 mg/kg 3–35 mg/kg 0.25–1.25 mg/day 15–100 mg/kg/day 25 mg/kg/day 10 mg/kg 5–10 mg/kg 0.01–1 mg/kg

IP IV IP, SC SC IP PO IP, SC SC, IM, IV IV PO IV IM SC, IM, PO SC IP SC IV IV

Glycopyrrolate

0.01–0.5 mg/kg 0.01–0.02 mg/kg 10 mg/kg 3 mg/kg 240 mg/kg in feed 150 mg/kg 0.009 mg/kg 0.1 mg/kg 1 mg/kg 2 mg/kg 0.01–0.1 mg/kg 1U 2 mg/kg 55 mg/kg 50–60 mg/kg 22 mg/kg 0.04–0.4 mg/kg 0.45 mg/kg 2.1 mg/kg

IM SC IV IP

Amitriptyline

Atipamezole Atropine Bretylium Chlorpromazine Cortisone Cyclosporine Diphenhydramine Doxapram Gallamine

From: Hawk and Leary (1999); Hawk et al. (2005).

Heparin Indapamide Iron Meprobamate Metocurine Nalbuphine Nalorphine Naloxone Oxytocin Pancuronium Streptozotocin

Tubocurarine Vecuronium Yohimbine

IM IV IV IP, SC IV IP, IV SC, IM IV IV IP IM IV IV IP 91

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TREATMENTS

Medications can be administered orally via drinking water, but accurate dosing may not be achieved as rats may not drink distasteful liquids. Medications can be mixed with small amounts of a highly palatable food; however, the most accurate delivery of oral medications is oral gavage via a catheter or gavage needle. To increase food consumption highly palatable foods such as baby food or fruit can be offered. Regular diet can be ground and soaked with water to aid in water intake and ease of consumption. Warmed fluids can be administered intraperitoneally for quick absorption or subcutaneously if slower absorption is desired. Table 7.8 presents miscellaneous agents used in rats. REFERENCES Bihun, C., and Bauck, L. 2004. Basic Anatomy, Physiology, Husbandry, and Clinical Techniques. In Quesenberry, K.E., and Carpenter, J. (eds.). Ferrets, Rabbits, and Rodents: Clinical Medicine and Surgery. Second edition. Saunders, St. Louis, MO, pp. 286–298. Bistner, S.I., Ford, R.B., and Ruffe, M.R. 2000. Kirk and Bistner’s Handbook of Veterinary Procedures and Emergency Treatment. Seventh edition. W.B. Saunders, Philadelphia, PA. Carpenter, James W. 2005. Exotic Animal Formulary. Third edition. Elsevier Saunders, St. Louis, MO, pp. 377–408. Evans, E.I. 2006. Small Rodent Behavior: Mice,

Exotic Small Mammal Care and Husbandry

Rats, Gerbils, and Hamsters. In Bays, T.B., Lightfoot, T., and Mayer, J. (eds.). Exotic Pet Behavior: Birds, Reptiles, and Small Mammals. Elsevier Saunders, St. Louis, MO, pp. 239–261. Hawk, C.T., and Leary, S.L. 1999. Formulary for Laboratory Animals. Second edition. Iowa State University Press, Ames, IA. Hawk, C.T., Leary, S.L., and Morris, T.H. 2005. Formulary for Laboratory Animals. Third edition. Blackwell Publishing, Ames, IA. Kahn, C.M. 2007. The Merck/Merial Manual for Pet Health. Home Edition. Merck & Co., Whitehouse Station, NJ. Kohn, D.F., and Clifford, C.B. 2002. Biology and Diseases of Rats. In Fox, J.G., Anderson, L.C., Loew, F.M., and Quimby, F.W. (eds.). Laboratory Animal Medicine. Second edition. Elsevier Science, San Diego, CA, pp. 121–165. Lawson, P.T. 2001. ALAT Training Manual. Sheridan Books, Chelsea, MI. Leck, S. 1999. Rats: What Veterinarians Need to Know. Exotic DVM 1(5):42–44. Orr, H.E. 2002. Rats and Mice. In Meredith, A., and Redrobe, S. (eds.). BSAVA Manual of Exotic Pets. Fourth edition. BSAVA, Quedgeley, Gloucester, UK, pp. 13–25. Sharp, P.E., and LaRegina, M.C. 1998. The Laboratory Rat. CRC Press, Boca Raton, FL. Tully, T.N., Jr. 2008. Mice and Rats. In Mitchell, M.A., and Tully, T.N., Jr. (eds.). Manual of Exotic Pet Practice. Saunders, St. Louis, MO, pp. 326–344. Tully, T.N., Jr., and Mitchell, M.A. 2001. A Technician’s Guide to Exotic Animal Care. AAHA Press, Lakewood, CO.

Gerbils

COMMON BREEDS

There are many breeds of gerbils that range in size considerably. The most common pet gerbil is the Mongolian gerbil, Meriones unguiculatus (Fig. 8.1). Mongolian gerbils that are sold as pets and used in research in the United States come from a colony of 11 pairs that were imported to the United States in 1954, originating from eastern Mongolia (Donnelly and Quimby, 2002). Other names for the gerbil include jird, desert rat, and sand rat. “Jird” typically refers to gerbils that belong to the genus Meriones. They can have a variety of coat colors, including agouti (the normal freeranging type), cinnamon, black, albino, blue, lilac, white, cream, sable, and silver. The most popular are those that have multiple colors and

Fig. 8.1 Profile of a normal gerbil. (Copyright Eric Isselée, Dreamstime.com.) For color detail, please see color plate section.

8 are referred to as spotted (Leck and JohnsonDelaney, 2004). Gerbils make good pets for children because of their gentle nature when handled properly. They are more active during the day, climbing and playing with items in their environment, and are more disease resistant than hamsters. Gerbils can be pair-housed after weaning but should be placed together before puberty (which typically occurs at 6–7 weeks of age) to prevent severe aggression and fighting that can result in the death of one of the pair. Pairhoused gerbils form strong bonds and mate for life (Field and Sibold, 1999).

BASIC ANATOMY AND PHYSIOLOGY

Gerbils are used in various aspects of research based upon some of their unique anatomical and physiological features. They are used extensively to study strokes, dental disease, infectious diseases, epilepsy, and audiogenic disorders, as well as in behavior studies investigating territoriality. Because about 40% of gerbils have an incomplete Circle of Willis (a circle of arteries at the base of the brain critical for blood supply to the brain), ligation of one carotid artery creates cerebral infarcts that allow researchers to study strokes. Gerbils also experience spontaneous epileptic seizures similar to human idiopathic epileptics, and seizure-prone and seizure-resistant strains have been bred for this purpose. 93

94

Exotic Small Mammal Care and Husbandry

bles, though fresh water should always be available when raised in captivity.

REPRODUCTION AND SEXING

Fig. 8.2 Gerbil abdomen with ventral gland located centrally. (Photo courtesy of Dan H. Johnson, DVM, Avian and Exotic Animal Care, Raleigh, NC.) For color detail, please see color plate section.

Both male and female gerbils have a large ventral marking sebaceous gland that should not be confused with a tumor (Fig. 8.2). This gland is twice as large in males when compared to females and produces a musk-scented secretion. Males can be observed rubbing the gland against objects in the environment, which is thought to be a mechanism for marking territory. The adrenal gland of the gerbil is about three times as large as that of the rat when comparing adrenal-to-body weight ratios (Donnelly and Quimby, 2002). The incisor teeth of the gerbil grow continuously throughout life. Gerbils are also prone to periodontal disease and cavities, particularly after 6 months of age (Field and Sibold, 1999). Because gerbils are adapted to the desert, they produce a very small quantity of concentrated urine and require only a small amount of water that can typically be obtained from fruits and vegeta-

Gerbils can be easily sexed by comparing the anogenital distance; as with other rodents the males have a greater distance than females. Males can also be identified by their darkly pigmented scrotum and a prominent genital papilla. Females can be identified by a shorter anogenital distance, a less pronounced genital papilla, and the presence of nipples (which are not present on males). Gerbils will mate for life when pair-housed with their mate. If one mate dies, the other will usually not accept another mate. Harem mating can be used with a single male and 2–3 females in a group, but it is not uncommon for cannibalization of the young by periparturient females. The female gerbil sometimes marks her territory and becomes aggressive after parturition. Males typically reach sexual maturity around 70–84 days of age whereas females usually reach sexual maturity about 30 days after vaginal opening, which occurs at 40–60 days of age (Donnelly and Quimby, 2002). Estrous cycles last 4–6 days with spontaneous ovulation, leaving the female receptive to the male for 12–15 hours. A 14 : 10 hour light : dark cycle allows for most successful breeding, with mating usually occurring at night. Males will typically mate the female multiple times after courtship, indicated by hindlimb thumping. Before parturition, both the male and female will work to prepare the nest and care for the young (Field and Sibold, 1999). Table 8.1 presents the basic biologic profile and physiologic data for gerbils. The gestation period is dependent on the lactation status of the female. The typical gestation period is 24–26 days if the female is not lactating, but is prolonged to 27 days if she is lactating. Females that are bred during the postpartum estrus period can experience delayed implantation, resulting in a gestation period of up to 48 days. The size of the litters can range from three to seven young gerbils, and they will typically nurse for 21 days while consuming solid foods as early as 16 days of

Gerbils

95

Table 8.1 Biological profile. Body weight

Adult male: 65–130 g Adult female: 55–133 g

Rectal temperature

37 °C–39 °C

Body length

95–180 cm

Tail length

100–193 cm

Reproductive data

Gestation length: 24–26 days Weaning: 21–28 days, 12–18 g Estrous cycle length: 4–6 days Polyestrous Litter size: 1–12 (average 5) Birth weight: 3–4 g Fertile postpartum estrus Sexual maturity: 65–85 days Number of mammary glands: 2 pairs (thoracic and inguinal)

Life span

2–5 years

Heart rate

260–600 beats per minute (average 360 bpm)

Respiratory rate

70–120 breaths per minute

Food consumption

5–7 g/day

Water consumption 4–7 mL/day Dental formula

2(I 1/1, C 0/0, P 0/0, M 3/3)

Urine volume

3–4 mL/day

From: Field and Sibold (1999).

age. It is routine to wean animals around day 25 (Donnelly and Quimby, 2002). HOUSING

There are a variety of commercially available housing systems for gerbils. It is most important that it be escape proof with a secure lid because gerbils burrow, gnaw, and can flatten themselves to fit through small spaces. Solid bottom surfaces with adequate bedding are necessary to provide appropriate support and to prevent injury while burrowing. Gerbils should have access to natural resources, such as rocks and sand, and a water bowl to reduce stress and encourage normal marking and foraging behaviors (Field and Sibold, 1999). Cages range considerably in size and should be purchased based upon the number of gerbils being housed together. A single gerbil should have a minimum of 36 square inches and a mating pair should have at least 180 square

inches of floor space. It is recommended that cages be at least 6 inches tall to allow for gerbils to stand as well as burrow. Aquariums make good cages for gerbils because of their smooth surfaces, room for a variety of enrichment devices, and ability to be sanitized. A good rule of thumb is to allow for 5 gallons per gerbil when purchasing a tank (Leck and Johnson-Delaney, 2004). HUSBANDRY

The use of closed-bottom cages requires more frequent cleaning to maintain clean and dry bedding material and prevent ammonia buildup from urine. Because gerbils produce little urine and dry fecal pellets, the cages are easier to clean and do not need to be cleaned as frequently as other small rodents. It is important to check the cage each time it is changed for any areas that may cause injury. As gerbils burrow, scratch, and chew surfaces, they can create sharp edges or areas for escape. Gerbils are adapted to desert climates by burrowing underground; therefore care must be taken to maintain the temperature and humidity so that the cages do not overheat or reach humidity levels >50%. Gerbils can develop a nasal dermatitis at humidity levels >50% (Donnelly and Quimby, 2002). Items of environmental enrichment need to be replaced regularly because gerbils will quickly chew through them. A bowl should also be provided for sand bathing. Gerbils should sand bathe 10–15 minutes several times a week to prevent oil buildup on their coats. NUTRITION

Pellet diets are commercially available for gerbils but should be supplemented with fresh fruits, vegetables (such as carrots, kale, and broccoli), a mixed variety of seeds (no sunflower seeds), and hay. Gerbils will develop high cholesterol levels in their bloodstream if their diet is >4% fat (Donnelly and Quimby, 2002), so high-fat diets and sunflower seeds should be avoided to prevent this. Even though gerbils will consume most of their dietary water requirement from fresh fruits and vegetables, a clean water bottle should always be available.

96

Gerbils will consume 4–7 mL of water daily (Field and Sibold, 1999). The bottle should be maintained on the outside of the cage with the sipper accessible from inside to prevent the gerbils from chewing on the bottle. Food can be provided in a hopper or bowl, and it may need to be placed on the floor of the cage for younger animals to have access during weaning. Gerbils should be monitored for coprophagia, as they do not usually consume their feces unless their diet is nutritionally incomplete (Field and Sibold, 1999).

Exotic Small Mammal Care and Husbandry

worn properly. All items placed in the cage should be nontoxic and able to be sanitized easily.

HANDLING, RESTRAINT, AND PHYSICAL EXAM

Gerbils should be pair-housed whenever possible, to provide companionship. As described earlier, animals should be put together before puberty to prevent aggression. Because gerbils like to burrow and build nests, it is important to provide enough bedding that is deep enough in the cage to allow for this behavior. They will typically dig in the corners of the cage with their forepaws and burrow with their noses. A variety of materials can be included for gerbils to burrow, nest, climb, and chew (Fig. 8.3). There are a variety of commercially available enrichment objects such as running wheels, exercise balls, various toys, and wooden blocks that they can chew on to keep their incisors

Gerbils can be scooped up and held in the palm of the hand with restraint at the base of the tail to prevent jumping, or by the base of the tail in conjunction with the scruff of the neck. The tip of the tail should not be held because it will deglove if the gerbil jumps or moves away quickly (Fig. 8.4). This condition occurs in other rodent species with tails and requires amputation of the exposed portion of the tail. Gerbils will struggle if placed on their back, so they should be maintained in a natural and comfortable position. A physical exam should include the following: assessment of the gerbil’s weight, hydration status (observe the coat quality and presence or absence of a skin tent that persists), and skin condition (for wounds or lesions); examination of the oral cavity for periodontal disease or overgrown teeth; and a systematic observation and palpation of the various body systems. A fecal sample should be tested for parasites or cultured if the gerbil is having diarrhea.

Fig. 8.3 Gerbil in cage with bedding for burrowing and enrichment for climbing and gnawing. (Photo courtesy of Dan H. Johnson, DVM, Avian and Exotic Animal Care, Raleigh, NC.)

Fig. 8.4 Degloved tail tip of gerbil. (Photo courtesy of Dan H. Johnson, DVM, Avian and Exotic Animal Care, Raleigh, NC.) For color detail, please see color plate section.

ENRICHMENT

Gerbils

97

CLINICAL TECHNIQUES

Sample collection—venipuncture Routine blood testing is not practical in gerbils due to the small amount of blood that can be taken and the difficulty in collection. No more than 10% of the animal’s blood volume (a 100-g gerbil will have about 6 mL of blood volume) should be withdrawn at one time or the animal may experience changes in blood pressure and heart function (Field and Sibold, 1999). The life span of a gerbil’s red blood cell is about 10 days, with a rapid turnover (Bihun and Bauck, 2004). Table 8.2 presents the hematologic values for gerbils, and Table 8.3 presents the biochemical values. Blood can be collected from gerbils from various locations depending on the volume of blood required and on whether anesthesia is available for specific techniques. The lateral tail vein, tail tip clip, and toenail clip are methods that can be utilized without anesthesia. The lateral tail vein can be found by applying gentle pressure at the tail base to occlude the vessel. It may be necessary to place the animal in a warm chamber or to immerse the tail in a warm water bath to increase blood flow to the area for easier visualization of the vein. A 25gauge needle can be inserted into the vessel and blood can be withdrawn either in a tuberculin

Table 8.2 Laboratory normal values—complete blood cell count.

syringe or directly into a hematocrit tube. The tail tip and toenail clip can be used to collect smaller amounts of blood (0.1–0.2 mL), should be used only once or twice, and require pressure application to the site until the bleeding stops. If the orbital sinus or cardiac puncture is to be used, the gerbil should be anesthetized (Field and Sibold, 1999; Bihun and Bauck, 2004).

Drug administration Drugs can be administered in the gerbil either intravenously (IV), subcutaneously (SC), intramuscularly (IM), intraperitoneally (IP), or by oral gavage (PO). A 23- to 25-gauge needle should be used for injections if the agent is not too viscous. The lateral tail vein can be used for intravenous injections in the gerbil and can be accessed in the same manner previously described for blood collection. Once the needle is in the tail vein and the drug is administered, the vein will blanch temporarily as the drug enters the vein. A range of 0.2–0.5 mL can be administered IV in this manner. Subcutaneous injections can most easily be administered under the skin over the shoulder blades or the neck. Care should be taken to pull back on the syringe once it is under the skin to confirm that it is not in a blood vessel. A maximum of 1.0–3.0 mL can safely be administered by this route.

Table 8.3 Laboratory normal values—serum biochemical values. Biochemical Parameter

Reference Interval

Hematologic Parameter

Reference Interval

Total protein (g/dL)

4.6–14–7

RBC (×10 cells/μL)

7–10

Albumin (g/dL)

1.8–5.8

Hemoglobin (g/dL)

12.1–16.9

Globulin (g/dL)

0.8–10.0

Hematocrit (%)

41–52

Glucose (mg/dL)

47–137

WBC (×103 cells/μL)

4.3–21.6

Cholesterol (mg/dL)

90–141

Neutrophils (%)

5–34

Blood urea nitrogen (mg/dL)

17–30

Lymphocytes (%)

60–95

Total bilirubin (mg/dL)

0.8–1.6

Monocytes (%)

0–3

Sodium (mEq/L)

143–147

Eosinophils (%)

0–4

Potassium (mEq/L)

3.6–5.9

Basophils (%)

0–1

Chloride (mEq/L)

93–118

Platelets (×10 cells/μL)

400–600

Phosphorus (mg/dL)

3.7–11.2

Total blood volume (mL/kg)

60–85

Calcium (mg/dL)

3.7–6.1

6

3

From: Bihun and Bauck (2004).

From: Bihun and Bauck (2004).

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The quadriceps and gluteal muscles can be used for intramuscular injections in the gerbil. The sciatic nerve runs along the lateral aspect of the hip and hind leg and should be avoided. A maximum volume of 0.1 mL can be administered IM. Intraperitoneal injections are given in either the lower left or right abdominal quadrants when the animal is restrained by the scruff so that the ventrum of the gerbil is exposed. Since gerbils struggle when placed on their backs, they should be restrained in a vertical orientation for this type of injection. After the needle has entered the abdomen, the plunger should be withdrawn to confirm that the needle is not within an abdominal organ. If brown/green liquid from feces, urine, or blood enter the syringe it should be withdrawn and a new needle and syringe used for another attempt. A maximum of 3–4 mL can be administered IP. Oral gavaging requires specialized balltipped gavage needles, and the gerbil can be restrained in the same manner as described for the IP injection. The distance between the mouth and the last rib should be measured so that the length of the needle to be inserted to reach the stomach can be determined. Any resistance noted when inserting the needle may indicate that the needle is in the trachea instead of the esophagus and it should be removed and another attempt made. Once the tip of the needle is in the stomach, the dose can be administered.

Sample collection—cystocentesis Urine samples are difficult to obtain because the gerbil does not generate a significant volume of urine over time. A fecal sample can be collected from the cage or carrier and evaluated for endoparasites. Rectal swabs can be taken for culture if needed in cases of persistent diarrhea.

COMMON DISEASES

The formulary for gerbils is presented in Table 8.4.

Bacterial diseases Tyzzer’s disease: Clostridium piliforme Gerbils are very susceptible to Tyzzer’s disease. They can die suddenly or present with clinical

Exotic Small Mammal Care and Husbandry

signs of disease: rough hair coat, lethargy, and possibly watery diarrhea (Field and Sibold, 1999). Tyzzer’s disease is the most frequently described fatal infectious disease of gerbils (Donnelly and Quimby, 2002). Death may Table 8.4 Formulary. Agent

Dosage (mg/kg)

Acepromazine

DO NOT USE

Route

Amikacin

5–10 q8–12h

IM, SC

Amitraz

1.4 mL/L

Topical

Amoxicillin

DO NOT USE

Ampicillin

DO NOT USE

Atropine

0.05

IM, SC

Buprenorphine

0.05 q8–12h

SC, IM, IV

Ciprofloxacin

10–20 q12h

PO

Dexamethasone

0.1–0.6

IM

Diazepam

5

IP, IM, SC

Doxycycline

2.5 q12h

PO

Enrofloxacin

5–10 q12h

PO, IM

Fenbendazole

20 q24h × 5 days

PO

Gentamicin

5 q24h

IM

Griseofulvin

25 q24h

PO

Isoflurane

To effect

IH

Ivermectin

0.2–0.4 repeat PO in 8–10 days

Ketamine

40–44 8–10 days

IP, IM

Ketamine + diazepam

50 + 5–10

IP

Ketamine + xylazine

50 + 2–10

IM, IP

Neomycin

100 q12h

PO

Oxytetracycline

20 q24h 10 q8h

SC PO

Oxytocin

0.2–3.0 IU/kg

SC, IM

Prednisone

0.5–2.0 q12–24h

PO

Procaine penicillin G

DO NOT USE

Tetracycline

10–20 q8h 2.5 mg/mL

PO PO in drinking water

Trimethoprim sulfamethoxazole

15 q12h

PO

Vitamin K1

1–10

IM

From: Field and Sibold (1999); Leck and Johnson-Delaney (2004).

Gerbils

occur suddenly or after a short period of illness and is associated with liver necrosis. Transmission of the spores is usually by ingestion when in contact with contaminated bedding. Control of the disease requires both environmental decontamination and treatment of affected animals. Infected and exposed animals should be quarantined and environmental areas autoclaved. Some gerbils will respond to treatment with tetracycline/oxytetracycline in drinking water (Field and Sibold, 1999), fluid therapy, and cross-fostering offspring to mice (Donnelly and Quimby, 2002).

“Sore nose” Nasal dermatitis can be seen predominantly in weanlings, with up to 20% of a colony being affected (Field and Sibold, 1999). Secretions from the Harderian gland, porphyrins, are thought to irritate the skin around the nares, resulting in inflammation, hair loss, and a moist dermatitis with a secondary Staphylococcus aureus and/or S. xylosus bacterial infection (Donnelly and Quimby, 2002). The disease may spread to the ventral body surfaces, front legs, and feet if not treated. Environmental stressors that contribute to the disease include overcrowding within the cage and a relative humidity level over 50% (Donnelly, 2004). Some gerbils will present in the same manner but have gotten their lesions as a result of chewing on their wire cages, causing trauma to their face. This is usually referred to as bald nose when there is only hair loss as a result of this trauma (Capello, 2002). Treatment consists of ensuring the bedding is clean, dry, and soft as well as reducing any causes of stress, and elimination of any sharp objects within the cage. Tetracycline in water can also be prescribed if there is bacterial involvement.

Salmonella spp. Salmonella spp. can cause gastrointestinal upset in gerbils and can present with anorexia, lethargy, staining of the perianal region with diarrhea, weight loss, dehydration, unkempt coats, and sometimes with sudden death. Outbreaks can result in the death of many animals in a colony, but more commonly gerbils will develop the clinical signs and recover. If an

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animal tests positive for Salmonella when cultured, it should be eliminated from the colony (Field and Sibold, 1999).

Helicobacter pylori Gerbils, like humans, are susceptible to Helicobacter pylori infection. It can cause severe gastritis and ulceration of the stomach, progressing to gastric adenocarcinoma in 37% of animals in one study (Donnelly and Quimby, 2002).

Abdominal gland disease The large, ventral abdominal marking gland of gerbils can become enlarged due to either infection or neoplasia. Both systemic antibiotics and topical treatment are needed to treat infections, though surgical excision of the gland is usually necessary when antibiotics do not resolve the infection. If a tumor is suspected, then surgical removal of the gland is recommended (Capello, 2002).

Parasitic diseases Cestodes Both Hymenolepis diminuta and H. nana tapeworms can infect gerbils as well as hamsters and people. Hymenolepis diminuta requires a cockroach or grain beetle as an intermediate host, whereas H. nana can have a direct life cycle in addition to the intermediate host. Treatment with niclosamide is usually prescribed as well as education of the owners about the zoonotic potential for the disease.

Nematodes Gerbils have been diagnosed with pinworms (Syphacia obvelata and S. muris), which can be transmitted from rats, mice, and other rodents. Diagnosis can be made by performing a tape test on the perianal region and placing it on a slide to observe the eggs under the microscope. Treatment needs to be both systemic and environmental. An avermectin can be used to rid the gerbil of adult pinworms, and the living environment should be sanitized with chlorinebased agents to remove any eggs. The eggs are very resistant to chemicals, can be challenging to eliminate, and typically will cause reinfection.

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Mites Gerbils can get both demodectic and sarcoptic mange. Demodex in gerbils is caused by Demodex merioni; sarcoptic mange is caused by Sarcoptes scabiei, Notoedres muris, and Myobia musculi. Any area of skin that shows hair loss, broken hairs, or red crusty skin should be examined for the presence of mites. Gerbils will be very itchy if infected with sarcoptic mange, and less itchy, if at all, with demodecosis. A skin scrape can be performed and examined under a microscope to look for mites. A superficial skin scrape will collect sarcoptic mites, though they are difficult to find. Deep skin scrapes are performed for demodecosis and mites are usually easy to locate. If there are any areas of thick crusting, the crusts can be dissolved in potassium hydroxide (KOH) and examined to detect mites. Treatment consists of ivermectin administration either subcutaneously or by mouth at 4- to 7-day intervals. Amitraz can be used topically for demodecosis if the gerbil can be prevented from licking the medicine for at least 30 minutes after it has been applied. (Capello, 2002).

Exotic Small Mammal Care and Husbandry

of seizures and has been found to be an inherited trait. As a result, seizure-prone and seizure-resistant strains have been bred for research. Phenobarbital can be used to treat seizures if severe, but animals usually outgrow the behavior.

Reproductive disorders Cystic ovaries are usually seen in female gerbils over 2 years of age. They will typically present with a distended abdomen and radiography, ultrasound, and fine needle aspirate can be used to confirm the condition. One or both ovaries can be affected and should be surgically removed (Lewis, 2003). When only one ovary is affected, it can be removed without a significant impact on breeding performance (Donnelly and Quimby, 2002).

Neoplasia About 25%–40% of gerbils develop some type of neoplasia by 2–3 years of age. Of the tumors seen in gerbils over 3 years of age, 80% are either squamous cell carcinoma of the ventral marking gland in males or ovarian granulosa cell tumors in females (Donnelly and Quimby, 2002).

Fungal infections When a hairless region is noted, it should also be examined for the presence of a fungal infection. Trichophyton mentagrophytes, Microsporum canis, and M. gypseum are the most common causes of dermatomycosis. Hair samples should be taken from the lesions and cultured, which can take up to 2 weeks to identify a source of infection. The lesions can spread quickly and also be transmitted to people, so care should be taken to wash clothing and skin after handling animals with suspicious lesions. Both systemic treatment with griseofulvin and topical treatment with enilconazole in addition to routine environmental cleaning are usually required to eliminate the disease.

Drug toxicity Gerbils have been shown to have acute, fatal toxicity to the antibiotic dihydrostreptomycin, which is part of a penicillin–dihydrostreptomycin–procaine formulation. A single 50 mg dose of drug resulted in 80%–100% death of 55– 65 g gerbils (Donnelly and Quimby, 2002).

Congenital disorders Some newborn gerbils have been diagnosed with a ventricular septal heart defect. Spontaneous hyperplasia of the seminiferous and epididymal tubules has also been identified in male gerbils between 12 and 30 weeks of age and is considered to be a congenital disorder (Donnelly and Quimby, 2002).

Neurologic diseases

Age-related conditions

Starting at about 2 months of age, about 20%– 40% of gerbils will exhibit seizures. They are stereotypic of epilepsy (tonic–clonic), can be triggered by stress, and last a few minutes. A deficiency in the enzyme cerebral glutamine synthetase has been linked to the development

In addition to neoplasia, other conditions commonly occur in older gerbils. Kidney disease develops in the form of chronic interstitial nephritis, and cysts develop in the cortex of the kidney. Also, cholesteatomas of the ear spontaneously develop and can cause erosion of

Gerbils

bone and infection (Donnelly and Quimby, 2002).

REFERENCES Bihun, Craig, and Bauck, Louise. 2004. Basic Anatomy, Physiology, Husbandry, and Clinical Techniques. In Quesenberry, K.E., and Carpenter, J.W. (eds.). Ferrets, Rabbits, and Rodents: Clinical Medicine and Surgery. Second edition. Saunders, St. Louis, MO, pp. 286–298. Capello, Vittorio. 2002. Common Dermatologic Disorders of Pet Rodents. Exotic DVM 4(1):33–37. Donnelly, Thomas M. 2004. Disease Problems of Small Rodents. In Quesenberry, K.E., and Carpenter, J.W. (eds.). Ferrets, Rabbits, and

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Rodents: Clinical Medicine and Surgery. Second edition. Saunders, St. Louis, MO, pp. 310–312. Donnelly, Thomas M., and Quimby, Fred W. 2002. Biology and Diseases of Other Rodents. In Fox, J.G., Anderson, L.C., Leow, F.M., and Quimby, F.W. (eds.). Laboratory Animal Medicine. Second edition. Academic Press, San Diego, pp. 275–279. Field, Karen J., and Sibold, Amber L. 1999. The Laboratory Hamster & Gerbil: A Volume in The Laboratory Animal Pocket Reference Series. Suckow, M.A. (series ed.). CRC Press, Boca Raton, FL. Leck, Susan, and Johnson-Delaney, Cathy A. 2004. What Every Veterinarian Needs to Know about Gerbils. Exotic DVM 6(5):36–40. Lewis, William. 2003. Cystic Ovaries in Gerbils. Exotic DVM 5(1):12–13.

Hamsters

COMMON BREEDS

There are many breeds of hamsters available, but the Syrian (golden) hamster is the most popular pet (Fig. 9.1). The Chinese (stripedback) and Djungarian (dwarf) are also common household pets. It is common to house hamsters individually because of aggressive behavior between animals. If a pair or colony of hamsters has been together since birth, they may be able to be housed in pairs or small groups but should be watched closely. Hamsters of different species should not be housed together, and the Syrian hamster should be single-housed due to aggression toward other hamsters with the exception of a female in heat. In contrast, dwarf hamsters are more social and can be housed in groups if intro-

Fig. 9.1 Normal hamster in cage. (Photo courtesy of Dan H. Johnson, DVM, Avian and Exotic Animal Care, Raleigh, NC.)

9 duced early in life. The Chinese hamster is similar in size to the dwarf hamster and can sometimes be cohoused, but often they do not get along with other hamsters either and need to be housed alone.

BASIC ANATOMY AND PHYSIOLOGY

Hamsters have a variety of unique anatomical structures and physiologic characteristics. They have four digits on each front paw and five digits on each rear paw. Their 16 teeth consist of a set of upper and lower incisors and three sets of upper and lower molars, all of which are present at birth and are prone to dental caries as a result of the carbohydrate and vitamin content of their diets (Hankenson and Van Hoosier, 2002). (Table 9.1 presents the basic biological profile for hamsters.) Hamsters also have bilateral cheek pouches (Figs. 9.2 and 9.3), an invagination of tissue within both cheeks, where food and bedding materials may be stored. These cheek pouches are considered to be “immunologically privileged” sites—one of the unique immunological features of the hamster. They can be easily everted and the materials removed (Fig. 9.4), which may be necessary if fasting an animal prior to surgery. Like other rodents, hamsters also have Harderian glands associated with their eyes. These glands produce a lipid and porphyrin material that aids in the lubrication of the eyes and lids. Hamsters also have unique sebaceous 103

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Exotic Small Mammal Care and Husbandry

Table 9.1 Biological profile. Body weight

Adult male: 85–130 g Adult female: 95–150 g

Rectal temperature

37°C–38.5°C

Body length

14–19 cm (6–8 inches)

Reproductive data

Gestation length: 16 days Weaning: 21 days, 35–40 g Estrous cycle length: 4 days Polyestrous Litter size: 4–12 (average 7–8) Birth weight: 1–2 g Fertile postpartum estrus Sexual maturity: 56–63 days Number of mammary glands: 6–11 pairs

Life span

1–3 years

Heart rate

286–400 beats per minute (average 332 bpm)

Respiratory rate

33–127 breaths per minute (average 74 bpm)

Food consumption

10–14 g/day

Water consumption

7–10 mL/day

Dental formula

2(I 1/1, C 0/0, P 0/0, M 3/3)

Urine volume

6 mL/day

Fig. 9.3 Isolated hamster cheek pouch. (Photo courtesy of Dan H. Johnson, DVM, Avian and Exotic Animal Care, Raleigh, NC.) For color detail, please see color plate section.

From: Field and Sibold (1999).

Fig. 9.4 Emptying the cheek pouch prior to fasting for surgery. (Photo courtesy of Dan H. Johnson, DVM, Avian and Exotic Animal Care, Raleigh, NC.)

Fig. 9.2 Hamster eating, with bulging cheek pouches. (Copyright Shawn Low, Dreamstime. com.)

glands referred to as flank glands (Fig. 9.5). Flank glands can be found in the upper flank region on both sides of the vertebral column. These can be located in males more easily than in females because the hair over the gland is coarse and the skin is usually a darker pigmented area. These glands should not be mistaken for skin tumors. In females, these glands can also be found on the back but are not as prominent as those found on males. The glands are sebaceous and respond to hormones (testosterone in males and estrogen in females).

Hamsters

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Fig. 9.6 Ventral view of male (left) and female (right) differentiating genitalia. Fig. 9.5 Bilateral flank glands of the hamster. (Photo courtesy of Dan H. Johnson, DVM, Avian and Exotic Animal Care, Raleigh, NC.)

REPRODUCTION AND SEXING

There are a variety of ways to distinguish male and female hamsters, including observation of the distance between the anus and the genitalia on the abdomen as well as the presence or absence of other organs. Like other rodents, females have a shorter anogenital distance when compared with males. Females will also have the presence of mammae on their abdomen. Male hamsters also have a large posterior scrotum within the anogenital area that produces a rounded appearance in contrast to the more blunt appearance of the female. (See Fig. 9.6.) The internal anatomy of the hamster is similar to that of mice and rats. The male accessory sex organs include the vesicular gland, coagulating gland (anterior prostate), prostate, ampullary glands, and bulbourethral glands. The female has separate vaginal and urinary openings as well as a pair of vaginal pouches on either side of the lower vagina internally (Bihun and Bauck, 2004). The uterus

has two cervical canals that combine to form a single external vaginal opening (Capello, 2001a). Reproductive activity can vary among strains of hamsters as well as with the season. Males and females reach sexual maturity at approximately 12 weeks of age, when they weigh 90–100 g. Although they may exhibit mating behaviors as early as 4 weeks of age, it is unusual for a successful mating to occur before 8 weeks of age. Both sexes exhibit a decline in reproductive success at around 14 months of age (Hankenson and Van Hoosier, 2002). The female hamster has a 4-day estrous cycle, with proestrus, estrus, and metestrus occurring within the first day. During the estrus phase, the female is receptive to the male and exhibits the characteristic lordosis posture with spread hind legs and tail erect. On the second day of the estrous cycle the female enters diestrus, which is marked by the presence of postovulatory discharge within the vagina and vaginal orifice. At this time she is no longer receptive to the male and cannot be mated again for 3 days. Female hamsters can show considerable aggression, and mating should be observed to

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Exotic Small Mammal Care and Husbandry

stores and the light cycle as well (Bihun and Bauck, 2004). The hibernation period typically lasts only 2–3 days but can be as long as 7 days. During this time animals can be aroused if handled as well. HOUSING AND HUSBANDRY

Fig. 9.7 Female hamster with a litter of pups. (Photo courtesy of Dan H. Johnson, DVM, Avian and Exotic Animal Care, Raleigh, NC.) For color detail, please see color plate section.

determine if the female is going to be receptive to the male or harm him. If she is receptive, the pair can be left together until the next light cycle. Once pregnant, the females will exhibit weight gain and abdominal distention at day 10. Although pregnancy can last between 15 and 18 days, the average is 16 days. Pregnant females will start their nesting behavior and will self-groom excessively prior to giving birth. Hamsters can have up to six litters a year with an average of 8–11 pups in a litter (Fig. 9.7). The female should not be disturbed during the first 10 days postpartum to prevent stress that can result in cannibalization of the pups. The cage should not be changed during this time and enough food and water should be placed prior to parturition to last during this period. Pups are typically weaned between 21 and 28 days, after which time the female will resume her estrous cycle. UNIQUE FEATURES OF IMPORTANCE

Hamsters are very active nocturnal animals. It has been shown that females will travel over 4 miles per day on an activity wheel within the cage. In contrast, hamsters also enter hibernation phases. Although hibernation is triggered by cold temperatures (below 40 °F, or 5 °C) it can vary depending on the availability of food

Hamsters can be housed in groups, but they are usually caged separately because of aggression and fighting. Many commercial cages systems are available for hamsters and should be escape-proof and as large as possible. Some wire cages, aquaria, and solid-sided cages with a secure top make good choices. Because hamsters can gnaw through thick wood and aluminum, their habitat should be inspected frequently for areas that might allow them to escape. Cages should be kept in cool, less humid areas of the house particularly in the summer. Many types of cage bedding are available and should be changed every 1–2 weeks. Acceptable types that can be used include hardwood chips, sawdust, paper products, shavings, beet pulp, and corn cobs. Pine and cedar shavings should be avoided because they are dustier and can have sharper edges. They also contain aromatic hydrocarbons that may affect liver enzymes. Hamsters will tend to use one corner of the cage for urination, which can be cleaned more frequently to keep the cage clean. A good depth of bedding should also be provided for hamsters to dig. Cages should contain a water bottle, and food should be provided on the floor of the cage in a corner. The water bottle should have a stainless steel sipper because hamsters can bite through glass. Each animal can consume up to 30 mL of water each day, and the bottle should be placed so that the sipper is low enough for the smallest hamster to reach, including nursing pups. NUTRITION

Hamsters will typically eat for a few minutes and then fast for 2 hours, consuming 10–15 g of food each day. Young hamsters begin to consume solid food around 7–10 days of age, and like many other rodents all hamsters are

Hamsters

coprophagic (Field and Sibold, 1999). The nutritional requirements for hamsters have not been determined, but a commercial rat chow can be provided as the basic diet. Alfalfa cubes can be combined with the basic diet to provide a balance of carbohydrates (60%– 65%), protein (16%–24%), and fat (5%–7%). Soybean meal also provides better nutrition than fish meal that is typically given to other rodents. Corn starch is also a good source of energy that hamsters utilize throughout life. Vitamin E deficiency can be a common nutritional problem in hamsters, leading to muscular dystrophy, heart disease, and fetal death. Most commercial diets have sufficient vitamin E supplementation to prevent these complications (Hankenson and Van Hoosier, 2002).

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Fig. 9.8 Hamster in running wheel for enrichment. (Copyright Kristina0488, Dreamstime. com.)

ENRICHMENT

Because hamsters are so active, they should be provided with sufficient enrichment to allow for such activity. This can be accomplished with a variety of commercially available enrichment wheels and tunnels (Figs. 9.8 and 9.9). Singly housed animals should also be given ample nest building materials as they will create a nest environment. Paper tunnels and tubes (paper towels, toilet paper) and cardboard boxes can also be placed in the cage to provide items for hamsters to climb on and gnaw. HANDLING AND RESTRAINT

Hamsters are nocturnal animals, so they are inactive during the day; care should be taken not to startle them or handle them until they are awake to prevent being bitten. Males are usually easier to handle than females, but regular handling will help to reduce aggressiveness and allow for easier handling. There are a variety of ways to handle and restrain a hamster depending on the reason for manipulating them. If you wish to move them to another cage it is easiest to use a small can or cup. Once placed inside the cage, the hamster will usually get inside the can or cup and can quickly be moved to another cage.

Fig. 9.9 Hamster in tubing enrichment device. (Copyright Alina Cardiae, Dreamstime.com.) For color detail, please see color plate section.

Other methods of restraint vary depending on the temperament of the animal and the amount of restraint required. Some animals can be approached from behind and grasped around the head and shoulders (Fig. 9.10). Additional restraint may be necessary for physical exam or administration of injections and can be effective when grasping the skin at the base of the neck and retaining loose skin in your hand as you close your hand over the back. Be certain to grasp just the skin, and not the body, sufficiently before lifting from the cage.

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Exotic Small Mammal Care and Husbandry

Table 9.2 Laboratory normal values—complete blood cell count. Hematologic Parameter

Reference Interval

RBC (×10 cells/μL)

5–9.2

Hemoglobin (g/dL)

14.6–20

6

Hematocrit (%)

46–52

WBC (×103 cells/μL)

5–10

Neutrophils (%)

10–42

Lymphocytes (%)

50–95

Monocytes (%)

0–3

Eosinophils (%)

0–4.5

Basophils (%)

0–1

Platelets (×10 cells/μL)

300–570

Total blood volume (mL/kg)

65–80

3

From: Bihun and Bauck (2004).

Table 9.3 Laboratory normal values—serum biochemical levels.

Fig. 9.10 Manual restraint technique, grasping skin between the shoulder blades at the base of the neck. (Photo courtesy of Dan H. Johnson, DVM, Avian and Exotic Animal Care, Raleigh, NC.)

CLINICAL TECHNIQUES

Blood can be collected from a variety of locations and the general guideline of collecting no more than 10% of the total blood volume every 2–3 weeks should be followed. Common sites include the jugular vein, cephalic vein, lateral tarsal vein, cranial vena cava, and orbital venous sinus. Other locations used less commonly to obtain blood samples include a toenail or tail clip or a cardiac puncture, which should only be used for terminal procedures. Brief anesthesia may be required to obtain an appropriate blood sample to minimize stress to the animal, and general anesthesia is required for cardiac punctures (Field and Sibold, 1999). Tables 9.2 and 9.3 present reference intervals for hematologic and biochemical values for hamsters.

Biochemical Parameter

Reference Interval

Total protein (g/dL)

5.5–7.2

Albumin (g/dL)

2.0–4.2

Globulin (g/dL)

2.5–4.9

Glucose (mg/dL)

60–160

Cholesterol (mg/dL)

65–148

Blood urea nitrogen (mg/dL)

14–27

Creatinine (mg/dL)

0.4–1.0

Creatine kinase (IU/L)

366–776

Aspartate aminotransferase (IU/L)

43–134

Alaline aminotransferase (IU/L) 22–63 Alkaline phosphatase (IU/L)

6–14.2

Lactate dehydrogenase (IU/L)

134–360

Total bilirubin (mg/dL)

0.24–0.72

Sodium (mEq/L)

124–147

Potassium (mEq/L)

3.9–6.8

Chloride (mEq/L)

92–103

Phosphorus (mg/dL)

4.0–8.2

Calcium (mg/dL)

8.4–12.3

Magnesium (mg/dL)

1.9–2.9

From: Bihun and Bauck (2004).

Hamsters

Various injection sites are also available. Intravenous (IV) injections can be administered in many of the same locations where blood can be drawn and include the following: cephalic vein, jugular vein, lateral tarsal vein, and lingual vein. As with blood collection, brief anesthesia may be required to allow for administration of intravenous injections. Other types of injections can usually be given with appropriate manual restraint. Preferred locations for intramuscular (IM) injections are typically the caudal thighs, but the epaxial muscles may also be chosen. The intrascapular and inguinal areas can be used for subcutaneous (SC) injections as with many other species. Intraperitoneal (IP) injections are typically given in the same manner as other rodents. As with many small rodent species, medications can also be administered orally (PO) utilizing the oral gavage technique, which requires specialized ball-tipped gavage needles. The distance between the mouth and the last rib should be measured so that the length of the needle to be inserted to reach the stomach can be determined (Fig. 9.11). Any resistance noted when inserting the needle may indicate that the needle is in the trachea instead of the esophagus and should be removed and attempted again. Once the tip of the needle is in the stomach, the dose can be administered. It can be difficult to get a urine sample from a hamster because they do not produce large amounts of urine, but they will typically urinate when restrained in an unfamiliar environment. Enough urine can be collected for use on urine reagent strips by manually restraining the hamster over a clean table top or sanitizable surface that will allow easy collection after urination.

COMMON DISEASES

Hamsters are generally healthy animals with a handful of diseases that are most common. They can range from dermatologic problems, diarrhea, respiratory disease, parasites, various forms of neoplasia, metabolic disorders, and conditions associated with the normal aging of a hamster.

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Fig. 9.11 Oral gavage technique for medication administration in many rodent species.

Skin disorders Cutaneous abscesses are often a result of trauma within the cage on sharp objects or as a result of fighting between animals. Various organisms have been associated with cutaneous abscesses and include Staphylococcus aureus, Pasteurella pneumotropica, and Streptococcus spp. Like abscesses in other species, they should be lanced, flushed, and explored to determine the extent of the lesion (Field and Sibold, 1999). Antibiotic therapy may be necessary but should be chosen carefully to avoid creating proliferative enteritis associated with the administration of certain antibiotics. Hamsters are also susceptible to ectoparasitic infections. The presence of demodex mites is a common finding and usually does not cause any lesions except in older, malnourished, or immunocompromised animals. Various species of mites can be found on examination, including the following: demodectic mites (Demodex criceti and D. aurati); ear mites (Notoedres spp.); nasal mites (Spleorodens clethrionomys); and the tropical rat mite (Ornithonyssus bacoti). Animals clinically affected will present with characteristic dry and scaly skin, alopecia of the rump region, and lack of pruritis. Ear mite infection is usually confined to the ears in female hamsters, but it can be found on the feet, nose, tail and genitalia of male hamsters (Hankenson and Van Hoosier, 2002). Diagnosis of most mites can be made with either a hair pluck or skin scraping, but the presence of demodex mites on any skin scraping is not

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always the cause of the lesion and may be simply an incidental finding.

Gastrointestinal diseases Diarrhea is usually seen in young and weanling animals between 4 and 8 weeks of age. There are a variety of causes of diarrhea, commonly referred to as wet tail, and include stress, overcrowding, and infection with various bacteria, viruses, and parasites. Not all causes of diarrhea are treatable, so it is important to select a hamster that does not have a family history of complications associated with diarrhea. It is also important to practice good husbandry and take measures to minimize stress. The classic cause of “wet tail” is infection with Lawsonia intracellularis, a bacterium that weanlings are very susceptible to, and infection carries a 60% morbidity rate and 90% mortality rate within a week of exhibiting signs. Providing supportive therapy with fluid replacement, diet modification, and antibiotic therapy with tetracycline, enrofloxacin, or trimethoprim-sulfa drugs has been successful in reducing mortality in animals. Animals will typically develop resistance by 10–12 weeks of age. Tyzzer’s disease, caused by Clostridium piliforme, also causes diarrhea and death in hamsters. The disease is typically subclinical and results in clinical signs when animals have undergone an environmental change, are under stress, are immunocompromised, or are of weanling age. Infection with this organism does not always result in clinical symptoms, and spores can persist in the environment for up to 2 years. Antibiotic therapy is discussed later in the chapter, but it is significant because the administration of many classes of antibiotics disrupts the normal gut flora of hamsters. This imbalance allows organisms such as Clostridium difficile to overgrow and produce toxins that are lethal to the animal. Antibiotics in hamsters must be carefully selected to avoid this condition. Hamsters can harbor a variety of parasites within their gastrointestinal tract. A fecal swab will reveal a variety of protozoa such as Hexamita spp., Giardia spp., Tritrichomonas muris, and Entamoeba muris. The significance of their presence has not been determined

Exotic Small Mammal Care and Husbandry

because these protozoa can be found in equal numbers in both healthy and sick animals. In addition to protozoa, hamsters can also have pinworms and tapeworms. Hamsters can become infected with three species of pinworms: Syphacia mesocriceti, the hamster pinworm; Syphacia obvelata, the mouse pinworm; and Syphacia muris, the rat pinworm. As with protozoal infection, the significance of disease associated with the presence of these parasites is not known. Due to the possibility of cross-infection from mice and rats to hamsters, though, it is good practice not to house hamsters in the same room as mice or rats and to practice good husbandry. Combination therapy with thiabendazole and piperazine has been used for effective elimination of the mouse pinworm; oral ivermectin in the drinking water is effective against the mouse and the rat pinworm. Rodentolepis nana is the one tapeworm of the hamster that is significant because it is common, though usually animals are asymptomatic, and it has zoonotic potential. The number of parasites in a sample is more clinically relevant than just its presence, because a heavy parasitic burden may cause physical obstruction of the intestinal tract, creating an impaction that could lead to death. Tapeworms can be diagnosed either on fecal exam or observation within the intestinal cavity during surgery or necropsy.

Respiratory diseases Respiratory disease in hamsters is uncommon but can result from infection with Sendai virus, Streptococcal spp. (Streptococcus pneumoniae is most prevalent), Pasteurella pneumotropica, and Corynebacterium spp. Depending on the cause, the animal may have varying degrees of clinical symptoms that include depression, inappetence, oculonasal discharge, respiratory distress, and associated mortality. Sendai virus infection does not usually produce significant clinical symptoms and occasionally causes the death of suckling hamsters. The bacterial infections listed tend to be lethal and cause more severe disease with respiratory distress, nasal and ocular discharge, anorexia, and depression (Hankenson and Van Hoosier, 2002). The hamster is the reservoir host for lymphocytic choriomeningitis virus (LCMV),

Hamsters

which is transmissible to humans. Clinical signs vary greatly depending on several factors: the age of the animal at infection, the dose and route of infection, the immune status of the animal, and the strain of the animal and virus. A chronic progressive wasting disease is seen in about half of all hamsters that are infected as neonates. Adults usually develop subclinical disease that may impact the reproductive success of the animal. If animals are identified with this disease, they should be euthanized because of the zoonotic potential.

Neoplasia Neoplasia is not a common finding in the hamster. Lymphosarcoma is most frequently reported and has been reported to be horizontally transmitted in young, inbred animals. Melanomas, benign intestinal polyps, and mammary gland tumors can also be seen.

Diseases associated with aging A variety of conditions are seen in hamsters as they age (1.5–2 years of age). Amyloidosis is the most noteworthy cause of death in hamsters and can affect all organ systems. Diagnosis of this disease is typically determined postmortem with histopathology of tissues and the use of Congo red stain to confirm its presence. Arteriolar nephrosclerosis is a degenerative disease of aged hamsters and may be seen in conjunction with amyloid deposits within the kidneys. Atrial thrombosis is also an important cause of death in aging hamsters, females more so than males, as it occurs spontaneously and in any chamber of the heart (Field and Sibold, 1999). Two diseases of the liver can also be seen. Polycystic liver disease may have a congenital component and results in the formation of large cysts both within the liver parenchyma and on the surface of the liver. Spontaneous cirrhosis of the liver can also occur and is more likely to be seen in female hamsters.

Nutritional and metabolic disorders Spontaneous hemorrhagic necrosis of the central nervous system occurs in fetal hamsters. It is usually associated with feeding a vitamin E deficient diet and occurs within the last tri-

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mester of pregnancy. Hamsters can also become diabetic. They exhibit Type 1 diabetes mellitus that appears to be associated with certain inbred lines.

TREATMENTS

The formulary for hamsters is presented in Table 9.4.

Anesthesia Hamsters do not have the ability to thermoregulate while anesthetized, so particular attention to keeping them warm is necessary. Inhalant and injectible anesthetics and analgesics can be used in hamsters. Isoflurane, halothane, and methoxyflurane can be used for inhalational anesthesia and will require the use of a face mask or cone or an anesthesia chamber. Atropine sulfate is commonly recommended as a preanesthetic as well, especially with the use of halothane. Injectible anesthetics can also be used effectively in hamsters. Ketamine has variable results when used alone, but when combined with xylazine it can produce sufficient muscle relaxation and a surgical plane of anesthesia. When given intraperitoneally this combination can provide 30–70 minutes of surgical anesthesia. Ketamine and xylazine can also be administered subcutaneously for restraint or nonsurgical procedures, but it will not produce a surgical plane of anesthesia. However, these drugs should not be administered intramuscularly due to the development of muscle necrosis at the injection site. This is also true of telazol and xylazine combinations given intramuscularly. Sodium pentobarbital can be given intraperitoneally as a single agent to achieve a surgical plane of anesthesia lasting 30–45 minutes, or it can be used in combination with ketamine to reduce the total dose of sodium pentobarbital needed. In this instance ketamine should be administered subcutaneously 10 minutes prior to the intraperitoneal injection of sodium pentobarbital.

Analgesia Animals should be monitored closely for signs of pain and distress. Some of the common indi-

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Exotic Small Mammal Care and Husbandry

Table 9.4 Formulary for anesthetics, preanesthetics, analgesics, and antibiotics. Agent

Dosage (mg/kg)

Route

Acepromazine

0.5–1.0

IM, SC

Amikacin

5–10 q8–12h

IM, SC

Amitraz

0.025% solution q4d

Topical

Amoxicillin

DO NOT USE

Ampicillin

DO NOT USE

Atropine

0.2–0.5

IM, SC

Buprenorphine

0.5 q8h

SC

Cimetidine

5–10 q6–12h

PO, SC, IM

Ciprofloxacin

10–20 q12h

PO

Dexamethasone

0.5 q12–24h

IP, IM, SC

Diazepam

3–5

IP, IM

Doxycycline

2.5 q12h

PO

Enrofloxacin

5–15 q12h

PO, IM

Fenbendazole

20–50 q24h × 5 days

PO

Furosamide

2–5 q12h

Gentamicin

3–5 q8–24h

IM, SC

Griseofulvin

25–50 q24h

PO

Isoflurane

To effect

IH

Ketamine

40–150

IM, IP

Ketamine + acepromazine

50–150 + 0.5–1.0

IM

Ketamine + diazepam

50–150 + 2.5–5.0 (diazepam, IP)

IM

Ketamine + medetomidine

100(K) + 0.25(M)

IP

Ketamine + xylazine

50–150 + 5

IM, IP

Metronidazole

20–60 q8–12h

PO

Neomycin

15 q12h

PO

Oxytocin

0.2–3.0 IU/kg

SC, IM

Pentobarbital

60mg/kg

IP

Prednisone

0.5–2.0 q12–24h

PO, SC, IM, IP

Procaine penicillin G

DO NOT USE

Tetracycline

10–12 q8–12h

PO

Vitamin K1

1–10 q8h

IM

From: Capello (2001b); Field and Sibold (1999).

cations that the animal is experiencing pain and/or distress include general characteristics of depression and a reluctance to move, an unkempt appearance from decreased grooming, lack of appetite, increased respiration, an abnormal gait or posture, licking or chewing

of a painful site, and restlessness. There are a variety of analgesics or sedatives that can be given to hamsters, many of which have a short duration of action. Hamsters appear to be resistant to the effects of morphine, however, and its use should be avoided.

Hamsters

Antibiotics Hamsters are sensitive to many antibiotics and they should be used with caution. Enterocolitis can be induced and progress to death with the administration of many antibiotics including ampicillin, penicillin, cephalosporins, erythromycin, lincomycin, oral gentamicin, and vancomycin. The normal gut flora of the hamster consists of mostly Lactobacillus and Bacteroides species and a few coliforms. The administration of certain antibiotics alters the composition of the normal flora of the gut and allows an overgrowth of undesirable bacteria— including Clostridium difficle, which generates toxins that make the animal sick. REFERENCES Bihun, Craig, and Bauck, Louise. 2004. Basic Anatomy, Physiology, Husbandry, and Clinical

113

Techniques. In Quesenberry, K.E., and Carpenter, J.W. (eds.). Ferrets, Rabbits, and Rodents: Clinical Medicine and Surgery. Second edition. Saunders, St. Louis, MO, pp. 286–298. Capello, Vittorio. 2001a. Pet Hamsters: Selected Anatomy and Physiology. Exotic DVM 3(2):23–27. Capello, Vittorio. 2001b. Pet Hamster Medicine and Surgery—Part II: Clinical Evaluation and Therapeutics. Exotic DVM 3(4):33–39. Field, Karen J., and Sibold, Amber L. 1999. The Laboratory Hamster & Gerbil: A Volume in The Laboratory Animal Pocket Reference Series. Editor: Suckow, M.A. (series ed.). CRC Press, Boca Raton, FL. Hankenson, F. Clair, and Van Hoosier, Gerald L., Jr. 2002. Biology and Diseases of Hamsters. In Fox, J.G., Anderson, L.C., Leow, F.M., and Quimby, F.W. (eds.). Laboratory Animal Medicine. Second edition. Academic Press, San Diego, pp. 167–202.

10

Guinea Pigs

Guinea pigs (Cavia porcellus) are popular pets due to their docile temperament and hardiness. If handled gently and frequently while young, they can be very friendly and seem to enjoy human contact. Guinea pigs were domesticated approximately 400 years ago when they were brought from South America to Europe. In their natural habitat, they lived in diverse climates that ranged from mountains to swamps. Their optimal environmental temperature range is 65 °F–79 °F. Guinea pigs are prone to hyperthermia and are more tolerant of cool temperatures than heat (Quesenberry et al., 2004).

a Fig. 10.1 a Coat color variation in guinea pigs. For color detail, please see color plate section.

COMMON BREEDS

Three original breeds were recognized by the American Rabbit Breeders Association (ARBA; www.arba.net), distinguished primarily by hair coat patterns: the American (or English), the Abyssinian, and the Peruvian. The American has short hair, the Abyssinian has whorls, and the Peruvian has long, silky hair. Many coat color variations and patterns have since been described, including white, red, tan, brown, chocolate, black, solid, bicolored, and tricolored (Fig. 10.1a,b). The shorthair, albino English, or Hartley guinea pig is used commonly in biomedical research settings (Harkness et al., 2002).

b Fig. 10.1 b Abyssinian guinea pigs. (Copyright Stefan Andronache, Dreamstime.com.) For color detail, please see color plate section. 115

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Exotic Small Mammal Care and Husbandry

BASIC ANATOMY AND PHYSIOLOGY

Guinea pigs share many traits with members of the order Rodentia, but also have several distinctive characteristics. Like other rodents, they are hindgut fermenters, have gram-positive intestinal flora, exhibit coprophagy, and have open-rooted (hypsodontic) incisors and molars. Guinea pigs are unique in their dietary requirement for vitamin C (Daviau, 1999). Table 10.1 presents the basic biological parameters for guinea pigs. Guinea pigs have stocky bodies. Males generally weigh 900–1,200 g and females 700– 900 g. In captivity, their life span is approximately 5–6 years. They have four digits on the front feet and three on the rear, which require periodic nail clipping. As mentioned previously, their incisors and molars continue to grow throughout their life span. Dental malocclusion and overgrowth is a common clinical problem. Overgrowth of the lower cheek teeth can trap the tongue and traumatize the gingival

tissue. Although many factors contribute to the incidence of malocclusion, there seems to be a strong genetic predisposition, so affected animals should not be bred (Quesenberry et al., 2004). Guinea pigs are monogastric herbivores with a very large cecum, 15–20 cm long, containing up to 65% of the gastrointestinal contents (Harkness et al., 2002). They are coprophagic, typically eating soft cecal feces directly from the anus. The nutritional benefits of coprophagy in guinea pigs have not been fully characterized, though it appears to be important in meeting the nutritional requirements (Quesenberry et al., 2004). REPRODUCTION AND SEX DETERMINATION

Males and females are easily distinguished (Fig. 10.2). Boars have large, obvious testes

Tabel 10.1 Basic biologic parameters. Body weight

Adult male: 900–1,200 g Adult female: 700–900 g Birth weight: 45–115 g

Body temperature

35.9 °C–37.5 °C (96.6 °F–99.5 °F)

Reproductive data

Sexual maturity Female: 6 weeks Male: 10 weeks Nonseasonally polyestrous Estrous cycle: 15–17 days Ovulation: spontaneous Gestation length: 59–72 days Litter size: 2–5 Weaning age: 21 days

Life span (captivity)

5–6 years

Heart rate

240–310 beats per minute

Respiratory rate

42–104 breaths per minute

Food intake

6 g/100 g body weight per day

Vitamin C requirement

10 mg/kg/day

Water intake

10 mL/100 g body weight per day

From: Carpenter (2005); Quesenberry et al. (2004); Riggs (2008).

Fig. 10.2 Differentiation of external genitalia in female (top) and male (bottom) guinea pig.

Guinea Pigs

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a Fig. 10.3 a Normal genitalia of a male guinea pig.

and the penis can be everted from the prepuce using gentle digital pressure (Fig. 10.3a). Sows have a Y-shaped vaginal opening between the urethral orifice and the anus. The vulvar opening is at the intersection of the branches of the “Y”; the anus is located at the base of the “Y” (Fig. 10.3b). Male guinea pigs reach sexual maturity at 3 months of age, females at 2 months of age. Female guinea pigs are nonseasonally polyestrous and spontaneous ovulators. The estrous cycle lasts 15–17 days. The presence of a vaginal plug, a lightcolored solid mass of coagulated semen that falls from the vagina, can be used to confirm mating several hours after breeding (Peters, 1997a). Guinea pigs have a long gestation period ranging from 59 to 72 days (average 68 days). Gentle palpation can detect fetuses as firm swellings in the uterine horns as early as 15 days’ gestation, although it is safer and more reliable at 28–35 days’ gestation. Fetal skeletons can be visualized by radiographs at 6 weeks. Several days prior to parturition, a 2.5to 3.0-cm gap in the pubic symphysis is palpable by placing a finger under the sow in sternal recumbency. If bred after 7 or 8 months for the first time, this separation may be inadequate and result in dystocia (Quesenberry et al., 2004). Guinea pig pups are delivered quickly and generally at night. Newborns are precocious; they are born fully furred with their eyes open.

b Fig. 10.3 b Normal genitalia of a female guinea pig.

The average litter size is two to four pups. Birth weight ranges from 60 to 110 g depending on the litter size. Although the normal lactation period is 3 weeks, pups will often start to nibble solid food as early as the end of the first week. Pups require stimulation of the urogenital region for urination and defecation for the first 2 weeks of life. Weaning typically occurs at 21 days or at a weight of 180 g. If orphaned, pups can be fostered to a lactating sow or fed with a formula of evaporated milk mixed with equal parts water. Solid food moistened with formula can be offered at 2 days of age. Sows have a postpartum estrus 2–10 hours after parturition. To prevent accidental pregnancies, it is recommended to remove males after breeding. HUSBANDRY AND NUTRITION

Cages can be constructed of plastic, metal, or wire. Because guinea pigs do not jump or

118

climb, open-topped cages are acceptable. The height of the walls should be at least 10 inches. Solid-bottomed cages are preferable to wire mesh as foot and leg injuries are more common in guinea pigs housed on wire (Quesenberry et al., 2004). Newspapers, shredded paper, wood shavings, and straw are all acceptable bedding materials. Bedding should be changed frequently to prevent a moist environment and to minimize ammonia levels in the cage. Guinea pigs seem to enjoy a shelter or a hide box. Guinea pigs are strict herbivores. The recommended diet for guinea pigs is a pelleted feed, supplemented with grass hay and fresh fruits and vegetables. Obesity is a problem with sedentary pigs, so the amount of pellets fed should be restricted to meet their caloric requirements. The most important factor in a guinea pig’s diet is meeting the dietary requirement for vitamin C. Adult nonbreeding guinea pigs require 10 mg per kilogram per day (mg/kg/day), and it is recommended to feed pregnant guinea pigs up to 30 mg/kg/day (Quesenberry et al., 2004). Vitamin C is labile and is depleted from commercial diets by storage and oxidation within 90 days (Knapka, 1999). Fresh foods high in vitamin C such as leafy greens (kale, parsley, beet greens, chicory, and spinach) should be fed daily. Alternatively, drinking water can be supplemented with vitamin C at 1 g/L and changed daily. Guinea pigs develop strong preferences early in life. Changes in the type of food, appearance or presentation can result in anorexia. Young animals should be presented with different types of pelleted and fresh foods so they become accustomed to a balanced, varied diet.

HANDLING AND RESTRAINT

Most pet guinea pigs are accustomed to handling and are docile and easy to restrain. They generally will sit calmly on a table for examination. If carried, they should be well-supported with two hands (Fig. 10.4). Nervous guinea pigs, or those not used to handling, can be cradled against the handler’s body for stability.

Exotic Small Mammal Care and Husbandry

Fig. 10.4 Manual restraint of a guinea pig. (Photo courtesy of Understanding Animal Research.org.)

PHYSICAL EXAMINATION

Healthy guinea pigs are usually active, curious, and vocal. They should initially be observed in their cage for alertness, activity level, respiratory rate, and character. Weight, body condition, temperature, auscultation of heart and lungs, and abdominal palpation should routinely be assessed. The rectal and urogenital area should be observed for fecal impaction or other abnormalities. Hair coat and skin should be examined for evidence of nutritional deficiencies and ectoparasites, which are common in group-housed guinea pigs acquired from pet stores. Nails should be examined for overgrowth and clipped if needed. Human fingernail clippers or small cat clippers are most effective. The oral cavity should be examined, and the maxillary and mandibular cheek teeth visualized with an otoscope cone or speculum for normal wear and for growth abnormalities. Guinea pigs can find this stressful and care should be taken to minimize struggling, which can result in trauma and fracture of the incisors. CLINICAL TECHNIQUES

Routine blood sampling can be challenging in guinea pigs because peripheral veins are very small. Small volumes can be obtained from the lateral saphenous and cephalic veins using

Guinea Pigs

tuberculin syringes and a 27- or 25-gauge needle. Larger samples can be collected from the jugular vein. The animal should be restrained with forelegs extended over the edge of the table. The site should be shaved to better visualize the vein. Chemical restraint is often necessary to minimize the stress of handling required for this procedure. Cranial vena caval samples can be obtained in anesthetized animals, though risks associated with this procedure include bleeding into the thoracic cavity of the pericardium (Quesenberry et al., 2004). It is safe to withdraw approximately 7%–10% of the total blood volume (7 ml per 100 g body weight). Reference ranges for normal hematology and serum biochemical values can be found in Table 10.2. Guinea pigs are predisposed to a number of urogenital conditions that require urine sampling to aid in a diagnosis. The technique is similar to that for other small animals. The guinea pig is restrained in dorsal recumbency, pressure is applied over the bladder, and cystocentesis is performed with a 25-gauge needle. Parenteral medications are commonly administered either subcutaneously (SC) or intramuscularly (IM). Subcutaneous injections are easily made into a dorsolateral location from the nape of the neck to the flank. Intramuscular injections can be given in the lumbar musculature on either side of midline or into the posterior lateral thigh. Intraperitoneal (IP) injections are administered to the right of midline about 1 inch cranial to the pubic bone. Oral (PO) medications can be administered by syringe into the side of the mouth. PREVENTIVE HEALTH

Guinea pigs are generally very hardy animals. No vaccines are currently recommended for pet guinea pigs. Optimal husbandry and nutrition is generally all that is needed to assure good health. COMMON DISEASES

Guinea pigs, like all rodents, are very susceptible to stress associated with improper nutrition, poor husbandry, or extreme temperatures.

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Table 10.2 Reference ranges for hematology and serum biochemical values for guinea pigs. Value

Reference Interval

RBC (×10 cells/μL)

3.2–8.0

Hemoglobin (g/dL)

10.0–17.2

Hematocrit (%)

32–50

WBC (×103 cells/μL)

5.5–17.5

Neutrophils (%)

22–48

Lymphocytes (%)

39–72

6

Monocytes (%)

1–10

Eosinophils (%)

0–7

Basophils (%)

0.0–2.7

Platelets (×10 cells/μL)

260–740

Total blood volume (mL/kg)

70

3

Total protein (g/dL)

4.2–6.8

Albumin (g/dL)

2.1–3.9

Globulin (g/dL)

1.7–2.6

Glucose (mg/dL)

60–125

Cholesterol (mg/dL)

16–43

Blood urea nitrogen (mg/dL)

9.0–31.5

Creatinine (mg/dL)

0.6–2.2

Aspartate aminotransferase (U/L)

26–68

Alaline aminotransferase (U/L) 25–59 Alkaline phosphatase (U/L)

6–14.2

Total bilirubin (mg/dL)

0.0–0.9

Sodium (mmol/L)

120–152

Potassium (mmol/L)

3.8–7.9

Chloride (mmol/L)

90–115

Phosphorus (mg/dL)

3.0–7.6

Calcium (mg/dL)

8.2–12.0

From: Carpenter (2005); Quesenberry et al. (2004); Riggs (2008).

This can predispose them to a number of diseases. A thorough history should include the source of the guinea pig, cage type and location, frequency of cage changes, diet changes, and contact with other animals. Guinea pigs have been used as laboratory animals for many years and there is an abun-

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dance of information about diseases that are not commonly seen in pet guinea pigs. This discussion will focus on the most commonly encountered diseases in pets. Sick guinea pigs are commonly anorexic and exhibit weight loss. They may have a rough, unkempt appearance with hair sticking up. They typically appear lethargic and disinterested in their surroundings. Clinically apparent nasal or ocular discharge, dull eyes, or diarrhea may be present. They often display a hunched posture and are reluctant to move.

Gastrointestinal diseases Antibiotics with gram-positive spectrum can eradicate the normal intestinal flora in guinea pigs and cause an overgrowth of Clostridium difficile and toxin production. Clinical signs of anorexia, diarrhea, and hypothermia typically appear 1–5 days after antibiotic administration, and they can rapidly progress to death. Antibiotic-associated enterotoxemia is treated symptomatically. Lactated Ringer’s solution, administered subcutaneously, should be provided to support hydration (10 mL/100 g per day). A live-culture yogurt or lactobacillus supplement can be used to support re-establishment of normal gut flora. Antibiotics most often implicated include penicillin, ampicillin, chlortetracycline, clindamycin, erythromycin, and lincomycin. Safe alternatives for guinea pigs are trimethoprim-sulfa, chloramphenicol, and enrofloxacin. Salmonella typhimurium and S. enteritidis are the most common cause of bacterial enteritis in guinea pigs (Quesenberry et al., 2004). The disease is contracted through fecal contamination of food. Symptoms include weight loss, weakness, unkempt hair coat, conjunctivitis, and abortion. Diarrhea is not always present. Fecal cultures are used to diagnose this disease. Prevention consists of thoroughly washing fresh fruits and vegetables, storing food in a sanitary manner, and keeping the cage clean. Recovered animals may become asymptomatic carriers and continue shedding the organism in feces, so treatment is not recommended. Salmonellosis is considered a zoonotic disease (Terrill and Clemons, 1998). Tyzzer’s disease has been reported in guinea pigs. The etiologic agent is Clostridium piliformes. Clinical signs include emaciation,

Exotic Small Mammal Care and Husbandry

watery diarrhea, an unkempt appearance, and sudden death. Young or stressed animals are most often affected. The organism is an intracellular bacteria, so fecal cultures are not diagnostic. A definitive diagnosis is made upon necropsy. The characteristic organisms (“pickup sticks”) are apparent in liver and intestine samples stained with silver stain or H and E (hematoxylin and eosin) (Harkness et al., 2002). Cryptosporosis caused by Cryptosporidium wrairi can cause diarrhea in young or stressed guinea pigs. Clinical signs are weight loss, diarrhea, and death. Organisms can be visualized on direct fecal exam or alternatively by histopathology of small intestinal samples at necropsy. Several species of coccidia have been reported in guinea pigs, though infection does not often cause clinical disease. Eimeria caviae and Balantidium caviae may cause mild diarrhea.

Respiratory disease Guinea pigs are susceptible to pneumonia caused by a number of pathogenic agents. Streptococcal pneumonia can present as an acute or chronic disease. Clinical signs include dyspnea and nasal discharge, otitis media, and metritis. Generalized disease may occur in chronic infections including pleuritis, peritonitis, pericarditis, arthritis, local abscessation, purulent conjunctivitis, hemoglobinuria, and hematuria. Sudden death is often the presentation in acute infections (Peters, 1997b). Bordetella bronchiseptica can be isolated from the respiratory tract of normal guinea pigs and rabbits. Clinical signs of bronchopneumonia include dyspnea, congestion, consolidation, and purulent bronchial exudates (Peters, 1997b). Infected animals are often found dead without obvious antemortem signs (Terrill and Clemons, 1998). Infection is acquired by contact or airborne exposure of other guinea pigs or rabbits. Antibiotics and supportive care may be helpful in treating affected animals.

Reproductive and urogenital disease Urinary calculi are common in boars and sows over 3 years of age. Signs of urolithiasis include

Guinea Pigs

anorexia, hematuria, dysuria, and a hunched posture. Urethral obstruction can be relieved with retrograde flushing. Surgical removal is indicated if this treatment fails or in the case of cystic or ureteral calculi. Mature boars can accumulate a mass of sebaceous material (scrotal plug) in the inguinal area, which can result in secondary infection or obstruction. Treatment consists of soaking with dilute chlorhexidine solution, to remove debris, and antibiotic therapy. Dystocia is not uncommon in the guinea pig. If not bred for the first time prior to 7–8 months of age, the pelvic symphysis will permanently fuse, preventing passage of fetuses during parturition. Obesity, large fetuses, and uterine inertia can all contribute to dystocia (Quesenberry et al., 2004). Pregnancy toxemia is most common 2 weeks before parturition and 2 weeks postpartum. Obese sows are predisposed to this metabolic condition. Diagnosis is based on history, a urine pH of 5 to 6, ketonuria, and hypoglycemia. Clinical signs include lethargy, anorexia, weakness, and incoordination. Treatment, although often unrewarding, includes aggressive fluid therapy (IV or IP), administration of glucose, corticosteroids, and calcium gluconate (Nakamura, 2000).

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Fig. 10.5 Ulcerative pododermatitis in a guinea pig. (Photo courtesy of Dan H. Johnson, DVM, Avian and Exotic Animal Care, Raleigh, NC.) For color detail, please see color plate section.

Cutaneous and dermatological disease Suppurative cervical lymphadenitis affects the cervical lymph nodes, but involvement of other nodes is possible. Streptococcus zooepidemicus, Lancefield’s group C, is the most common etiological agent that is present in the conjunctiva and nasal cavity of normal guinea pigs. Infection occurs when the oral mucosa becomes abraded. The involved nodes form abscesses containing thick, yellowish white suppurative exudates. This condition is treated by surgically draining the abscesses and treating with appropriate antibiotic therapy. Pododermatitis (bumble foot) is commonly seen in guinea pigs, particularly obese animals or those housed on wire-bottomed cages (Fig. 10.5). Lesions are secondarily infected most often with Staphylococcus aureus. Infection can progress to a deep cellulitis and osteomyelitis. Affected animals should be housed on solid-floored cages with soft bedding. Special

Fig. 10.6 Trixacarus caviae infection. (Photo courtesy of Dan H. Johnson, DVM, Avian and Exotic Animal Care, Raleigh, NC.) For color detail, please see color plate section.

consideration to maintaining a sanitary environment is imperative. Treatment consists of surgical debridement of lesions if indicated, antiseptic foot soaks, and appropriate antibiotic and analgesic therapy. Common ectoparasitic infections in guinea pigs include mites (Trixacarus caviae, Chirodiscoides caviae), lice (Gliricola porcelli, Gyropus ovalis), and fleas (Ctenocephalides felis) (Fig. 10.6). Clinical signs are variable, but can include pruritis, excoriations, crusts, and alopecia. Diagnosis is made by skin scrape, although some mites can be seen by the naked eye as dark, moving dots on the hair shaft.

Table 10.3 Guinea pig formulary. Antimicrobial Agents

Dosage (mg/kg)

Route

SC, IM, IV

Antimicrobial Agents Amikacin

10–15 divided q8–24 hrs

Amoxicillin

Do not use

Amoxicillin/clavulanic acid

Do not use

Ampicillin

Do not use

Cephalexin

50 divided q12–24h

PO

Ciprofloxacin

5–15 q12–24h

PO

Clindamycin

Do not use

Doxycycline

2.5 q12h

Enrofloxacin

5–15 q12h

PO, SC, IM

Gentamicin

5–8 divided q8–24h

SC, IM PO

Metronidazole

20 q12h

Penicillin G

Do not use

Trimethoprim-sulfa

15–30 q12h

PO

PO, SC

Antifungal Agents Griseofulvin

15–25 q24h

PO

Lime sulfur dip (2.5%)

Dip q7d for 4–6 treatments

Topical

0.3% solution q7d for 3–6 treatments

Topical PO

Antiparasitic Agents Amitraz Fenbendazole

20 q24h for 5 days

Ivermectin

0.2–0.4 q7–14d

SC

Praziquantel

5–10 repeat in 10 days

PO, SC, IM

Sulfadimethoxine

25–50 q24h for 10 days

PO

Selamectin

6

Topical

Sulfamerazine

1–5 mg/mL

Drinking water

Sulfaquinoxaline

1 mg/mL

Drinking water

Chemical Restraint, Anesthesia, and Analgesia Acepromazine

0.5–1.0

Atipamazole

1

IM SC

Atropine

0.1–0.2

IM, SC

Buprenorphine

0.05 q8–12h

SC

Butorphanol

0.4–2.0 q4h

SC

Carprofen

1–2 q12–24h

PO IM

Diazepam

0.5–3.0

Flunixin meglumine

2.5–5.0 q12–24h

SC

Glycopyrrolate

0.01–0.02

SC

Isoflurane

0.25%–4.0% to effect

Inhalation

Ketamine

22–44

IM

Ketamine + diazepam

20–30 (K)/1–2 (D)

IM

Ketamine + medetomidine

40 (K)/0.5 (M)

IM, IP

122

Guinea Pigs

123

Table 10.3 Continued Antimicrobial Agents

Dosage (mg/kg)

Route

Ketamine + midazolam

5–10 (K)/0.5–1.0 (M)

IM

Ketoprofen

1 q12–24h

SC, IM

Medetomidine

0.3

SC, IM

Midazolam

1–2

IM

Morphine

2–5 q4h

IM

Naloxone

0.01–0.1

SC, IP

Oxymorphone

0.2–0.5 q6–12h

SC, IM

Pentobarbital

30–45

IP

Yohimbine

0.5–1.0

IM, IV

Calcium gluconate

100

IM

Cimetadine

5–10 q6–12h

PO, SC, IM, IV IM, SC, IV

Miscellaneous Agents

Dexamethasone

0.5–2.0

Diphenhydramine

5

SC

Epinephrine

0.003

IV

Furosemide

2–5 q12h

PO, SC

Metoclopramide

0.2–1.0 q12h

PO, SC, IM

Oxytocin

0.2–3.0 IU/kg

SC, IM, IV

Prednisone

0.5–2.2

SC, IM

Vitamin C

50–100 mg/animal q24h (for deficiency)

PO, SC

From: Carpenter (2005); Morrisey and Carpenter (2004).

Trixacarus, Chirodiscoides, and lice can be effectively treated with ivermectin. Fleas can be treated with pyrethrin-based cat flea products or topically administered Selamectin (6 mg/kg; Revolution, Pfizer, Exton, PA) (Quesenberry et al., 2004). Dermatophytosis (ringworm) should be considered in animals that present with alopecia. Trichophyton mentagrophytes and Microsporum canis are most often isolated. Clinical signs include circular lesions with crusting on the face, head, and ears. Diagnosis is made by culture on dermatophyte testing media (DTM). Animals can be asymptomatic carriers of this potentially zoonotic disease.

Barthold, 2007). Clinical signs of vitamin C deficiency include reluctance to move, unkempt hair coat, anorexia, diarrhea, teeth grinding, vocalization, and lameness. Diagnosis is based on history and evidence of radiographic lesions. Treatment should be initiated with vitamin C 50 mg/kg/day IP, IM, or SC, then by diet supplementation. Good sources of vitamin C are fresh cabbage, kale, and oranges. Vitamin C tablets can be added to drinking water at a concentration of 200–400 mg/L and changed daily (Quesenberry et al., 2004).

Musculoskeletal disease

Guinea pigs should be hospitalized only if absolutely necessary. Supportive care should include correcting nutritional deficiencies and correcting dehydration and hypothermia. Replacement fluids can be administered by subcutaneous and intraperitoneal routes, and they should be warmed to avoid contributing to

Guinea pigs are not capable of synthesizing vitamin C and therefore require it in their diet to prevent scurvy (15–25 mg/day). Scurvy causes severe skeletal abnormalities, causes locomotor problems, and predisposes animals to opportunistic bacterial infections (Percy and

CLINICAL TREATMENTS

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hypothermia. Anorectic animals can be fed via syringe or oral gavage with slurried food or critical care diets. Anesthesia should be used in guinea pigs both for procedures that involve more than momentary pain and as chemical restraint agents to minimize stress. Inhalant anesthetics provide excellent control of duration and depth of anesthesia, though endotracheal intubation is difficult in the guinea pig. A face mask with a sealed diaphragm can be adapted for use in guinea pigs. Common anesthetic agents used for guinea pigs are listed in Table 10.3. REFERENCES American Rabbit Breeders Association. www. arba.net/Breeds.htm (accessed November 4, 2009). Carpenter, J.W. 2005. Exotic Animal Formulary. Third edition. Elsevier Saunders, St. Louis, MO, pp. 377–408. Daviau, J. 1999. Clinical Evaluation of Rodents. Veterinary Clinics of North America: Exotic Animal Practice 2(2):429–445. Harkness, J.E., Murray, K.A., and Wagner, J.E. 2002. Biology and Diseases of Guinea Pigs. In Fox, J.G., Anderson, L.C., Loew, F.M., and Quimby, F.W. (eds.). Laboratory Animal Medicine. Second edition. Academic Press, San Diego, CA, pp. 201–246. Knapka, J.J. 1999. Nutrition of Rodents. Veterinary Clinics of North America: Exotic Animal Practice 2(1):153–167.

Exotic Small Mammal Care and Husbandry

Morrisey, J.K. and Carpenter, J.W. 2004. Formulary. In Quesenberry, K.E. and Carpenter, J.W. (eds.). Ferrets, Rabbits, and Rodents: Clinical Medicine and Surgery. Second edition. Saunders, St. Louis, MO, pp. 436–444. Nakamura, C. 2000. Reproduction and Reproductive Disorders in Guinea Pigs. Exotic DVM 2(2):11–17. Percy, D.H., and Barthold, S.W. 2007. Pathology of Laboratory Rodents and Rabbits. Third edition. Blackwell Publishing, Ames, IA, pp. 217–251. Peters, L.J. 1997a. The Guinea Pig: An Overview Part I. In Rosenthal, K.L. (ed.). Practical Exotic Animal Medicine. Veterinary Learning Systems, Trenton, NJ, pp. 156–160. Peters, L.J. 1997b. The Guinea Pig: An Overview Part II. In Rosenthal, K.L. (ed.). Practical Exotic Animal Medicine. Veterinary Learning Systems, Trenton, NJ, pp. 161–168. Quesenberry, K.E., Donnelly, T.M., and Hillyer, E.V. 2004. Biology, Husbandry, and Clinical Techniques of Guinea Pigs and Chinchillas. In Quesenberry, K.E., and Carpenter, J.W. (eds.). Ferrets, Rabbits, and Rodents: Clinical Medicine and Surgery. Second edition. Saunders, St. Louis, MO, pp. 232–244. Riggs, S.M. 2008. Guinea Pigs. In Mitchell, M.A., and Tully, T.N., Jr. (eds.). Manual of Exotic Pet Practice. Saunders, St. Louis, MO, pp. 456–473. Terrill, L.A., and Clemons, D.J. 1998. The Laboratory Guinea Pig. CRC Press, Boca Raton, FL.

Chinchillas

Chinchillas are long-lived rodents that are native to South America, primarily Peru, Argentina, Bolivia, and Chile. The chinchilla is a hystricomorph (hedgehoglike) rodent closely related to guinea pigs, porcupines, and agoutis (Hrapkiewicz et al., 1998). Chinchillas in the wild were valued for their pelts and hunted so intensively that they are now listed on the highly endangered list (Johnson, 2006; Riggs and Mitchell, 2008). The only remaining native population of chinchillas is located in Chile (Merry, 1990; Pinney, 2003). Most captive chinchillas in the United States are descendents of a small group of chinchillas that were imported in the 1920s into California by M.F. Chapman (Quesenberry et al., 2004; Donnelly and Quimby, 2002). This small genetic pool is thought to be the basis for many of the commonly seen diseases (Riggs and Mitchell, 2008). Chinchillas are appealing as pets because they are relatively odor-free, are easy to take care of, and have an easygoing temperament (Hrapkiewicz et al., 1998). COMMON BREEDS

The family Chinchillidae comprises three genera consisting of six species. There are two species of chinchilla that are kept in captivity: Chinchilla laniger (or lanigera; the shorttailed chinchilla) and C. brevicaudata (the long-tailed chinchilla). The most common species kept in the United States is C. laniger (Fig. 11.1).

11 Fig. 11.1 The most common pet species, Chinchilla laniger. (Photo courtesy of Dan H. Johnson, DVM, Avian and Exotic Animal Care, Raleigh, NC.) For color detail, please see color plate section.

BASIC ANATOMY AND PHYSIOLOGY

Chinchillas are nocturnal in the wild but in captivity they readily adapt to being diurnal. Chinchillas have a compact body, large head, delicate limbs, large hairless ears, and a bushy tail. Chinchillas also have large eyes that are sensitive to light; therefore, the light:dark cycle should be 12:12. The long vibrissae aid in locomotion in the dark. They usually weigh between 400 and 700 g and females are typically larger than males. Typical life span in captivity is around 10 years, although chinchillas have been reported to live up to 20 years.

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Table 11.1 Hematologic chinchillas.

parameters

for

Table 11.2 Plasma biochemical parameters for chinchillas.

Hematologic Parameter

Reference Interval

Biochemical Parameter

Reference Interval

PCV (%)

27–55 (avg. 38)

Sodium (mEq/L)

130–170

5–10.7 (avg. 8)

Potassium (mEq/L)

3–7

Hemoglobin (g/dL)

8–15 (avg. 12.7)

Chloride (mEq/L)

105–130

MCV (μm3

32.1–69.2 (avg. 55)

Glucose (mg/dL)

60–125

MCH (mg)

10.4–19.8 (avg. 16.9)

Blood urea nitrogen (mg/dL)

10–40

20–38.5 (avg. 30.7)

Creatinine (mg/dL)

0.8–2.3

RBC (×10 cells/μL) 6

MCHC (%) WBC (×10 cells/μL)

6–16 (avg. 9.57)

Calcium (mg/dL)

8–25

Neutrophils/heterophils (%)

9–78 (avg. 43)

Phosphorus (mg/dL)

4–8

Lymphocytes (%)

10–70 (avg. 60)

Total protein (g/dL)

5–8

Monocytes (%)

0–5 (avg. 2)

Albumin (g/dL)

2.5–4.2

Eosinophils (%)

0–5 (avg. 1)

Globulin (g/dL)

3.5–4.2

Basophils (%)

0–2 (avg. 1)

Creatine kinase (IU/L)

0–300

Platelets (×103 cells/μL)

300–600

Aspartate transferase (IU/L)

15–100

Alkaline phosphatase (IU/L)

10–70

Bilirubin (mg/dL)

0.6–1.3

Cholesterol mg/dL)

40–300

3

From: Donnelly and Quimby (2002); Merry (1990); Quesenberry et al. (2004); Riggs and Mitchell (2008).

Alanine aminotransferase (IU/L) 10–35

Reference intervals for hematologic and biochemical values of chinchillas are presented in Tables 11.1 and 11.2. Chinchillas are social in the wild and can be housed together in captivity, although females may be aggressive toward males during breeding (Hrapkiewicz et al., 1998). Chinchillas do not make much noise but they do emit vocalizations when alarmed, frightened, injured, upset, or content. Chinchillas are shy, quiet, and very agile. They have long hind limbs and feet as well as a long plumed tail that aid in leaping. Chinchillas rarely bite; in fact, their main defense mechanism is flight. If they cannot get away from the perceived threat, they will experience stress that will often result in illness or even death. Chinchillas are a prey species; therefore, they should be kept separate from other pets in the household, including cats, dogs, ferrets, and birds. Chinchillas have four toes on all four feet. Teeth are open-rooted and grow continuously. The dental formula is 2(1/1 incisors, 0/0 canines, 1/1 premolars, and 3/3 molars) for a total of 20 teeth. The gastrointestinal tract is

From: Merry (1990); Quesenberry et al. (2004); Riggs and Mitchell (2008).

long and the cecum is large. Chinchillas, like rabbits, produce night feces that are rich in nitrogen, and they are coprophagic. REPRODUCTION AND SEXING

Female chinchillas are the dominant sex, are generally larger in size, and display higher aggression levels than males (Johnson, 2006). Females have two cervices and two uterine horns (Quesenberry et al., 2004). Chinchillas have one pair of inguinal mammary glands and two pair of lateral thoracic mammary glands. Sexing can be difficult as the external genitalia appear similar. The female’s coneshaped clitoris may be mistaken for a penis (Hoefer and Crossley, 2002; Hrapkiewicz et al., 1998). Sex can generally be determined by anogenital distance (Figs. 11.2 and 11.3).

Chinchillas

127

The distance is about twice as long in the male as in the female. There is no true scrotum in the male and the testicles are located in the inguinal canals. Chinchillas are seasonally polyestrous, generally having two litters between November and May. Interestingly, chinchillas born in the spring reach sexual maturity around 4–6 months of age whereas puberty may not occur until close to 1 year of age for chinchillas born in the fall. The estrous cycle can range from 30 to 50 days. (The basic biological profile for chinchillas is presented in Table 11.3.) Chinchillas are generally housed in polygamous groups or in pairs. Mating is confirmed by the expulsion of a copulatory or vaginal plug. Ovulation is spontaneous. Gestation is the longest of rodent species (approximately

Fig. 11.2 Male chinchilla. (Photo courtesy of Dan H. Johnson, DVM, Avian and Exotic Animal Care, Raleigh, NC.)

Fig. 11.3 Female chinchilla. (Photo courtesy of Dan H. Johnson, DVM, Avian and Exotic Animal Care, Raleigh, NC.)

Table 11.3 Biological profile. Body weight

Adult male: 400–600 g Adult female: 400–700 g

Body temperature

98.6 °F–100.4 °F (37 °C–38 °C)

Body length

25–35 cm (10–14 inches)

Reproductive data

Gestation length: 105–118 days (average 111 days) Weaning age: 6–8 weeks Estrous cycle length: 30–50 days (average 40 days) Seasonally polyestrous (November to May) Spontaneous ovulation Litter size: 1–6 (average 2) Birth weight: 30–60 g Newborns are precocious and fully furred Fertile postpartum estrus Sexual maturity: 6–10 months

Life span (captivity)

10–20 years

Heart rate

100–150 beats per minute

Respiratory rate

45–80 breaths per minute

Food consumption

10–21 g/day

Water consumption

65–130 mL/day

From: Hoefer and Crossley (2002); Hrapkiewicz et al. (1998); Johnson (2006); Kahn (2007); Lawson (2001); Quesenberry et al. (2004); Riggs and Mitchell (2008).

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Exotic Small Mammal Care and Husbandry

111 days). Chinchillas are placentophagic and dystocia is uncommon (Johnson, 2006). Female chinchillas do not make a nest. Females have a postpartum estrus within a few days after parturition. The average litter size is two although this may vary between one and six. Chinchillas are precocious; that is, they are born fully furred, with teeth and open eyes. Solid foods can be consumed at 1 week of age and weaning generally occurs at 6 to 8 weeks of age.

UNIQUE FEATURES OF IMPORTANCE

The body of the chinchilla is covered with dense fur that can contain 60–90 loosely attached hairs from each root (Lyon, 2003; Hoeffer and Crossley, 2002). Chinchillas have long vibrissae located on each side of the upper lip that are used for navigation in the dark (Hoeffer and Crossley, 2002). Another distinct feature is that chinchillas have short front legs and large, powerful back legs. The front legs are used for support and to hold food whereas the rear legs are invaluable for jumping.

Fig. 11.4 Enriched chinchilla cage. (Photo courtesy of Dan H. Johnson, DVM, Avian and Exotic Animal Care, Raleigh, NC.)

HOUSING, HUSBANDRY, NUTRITION, AND ENRICHMENT

Due to the activity level and agility of the chinchilla, a large amount of space is required for housing. The cage should be at least 2 m × 2 m × 1 m with a nesting box. Multilevel cages are ideal because chinchillas like to climb and jump (Fig. 11.4). Placement of small platforms within the enclosure on which they can perch is also suggested. Wire cages are recommended as chinchillas like to chew and can readily destroy plastic caging. The cage floor should be solid and covered with wood shavings or newspapers. If wire flooring is used care must be taken to ensure a small-gauge mesh is used as limb and feet injuries can occur if the openings in the flooring are too large. Cedar and pine shavings should be avoided as bedding materials because they contain aromatic oils that can irritate the skin and respiratory tract (Riggs and Mitchell, 2008). A hide box should

Fig. 11.5 Chinchilla in PVC tubing provided as enrichment. (Photo courtesy of Dorcas P. O’Rourke, DVM, East Carolina University, Greenville, NC.)

be provided and can be made of any solid material that is easily sanitized or discarded. Polyvinyl chloride (PVC) pipes are ideal because they are easily sanitized and are commercially available in a variety of shapes and diameters. Four-inch T- or Y-shaped PVC pipes (Fig. 11.5) are ideal in providing a hiding place (Kahn, 2007).

Chinchillas

Enrichment can consist of hanging wooden toys, large solid-surface running wheels, wooden sticks and chew toys, or even empty paper towel rolls. In addition, Johnson (2006) suggests offering pumice stones, lava, and rough cement perches marketed for birds. Wooden enrichment items made from conifer woods such as cedar should be avoided. Commercially available enrichment for rabbits and guinea pigs may be suitable for chinchillas as well. Many chinchilla owners allow for daily exercise and play time in a supervised environment; however, areas should be free of electrical cords and other hazards. Cage temperature should be maintained between 50 °F and 68 °F. Chinchillas do not like damp environments and are prone to heat stroke if the environmental temperature exceeds 86 °F. Humidity should be maintained around 40%. If the environment is dry and located away from drafts, chinchillas can tolerate low temperatures (Hrapkiewicz et al., 1998). Access to a dust bath should be provided at least several times a week if not daily; however, exposure should be limited to 5–30 minutes. Chinchillas that do not have access to a dust bath can develop matted fur. Commercial chinchilla dust (Fuller’s earth) is available, although homemade dust baths can be made from talcum powder and corn starch. Playground sand is not recommended. The dust should be approximately 1 inch deep in a dishpan or other container large enough for the chinchilla to roll around in. Remove dust bath after bathing has occurred as excessive use of a dust bath can cause conjunctivitis. Chinchillas are monogastric hindgut fermenting herbivores and should be fed a diet high in fiber. Chinchillas typically eat at night and ingest more than 70% of their daily food intake during the evening hours (Johnson, 2006; Quesenberry et al., 2004). Commercial pelleted chinchilla food is available and should be provided in a sturdy dish. The formula is similar to rabbit, guinea pig, and rodent diets (Donnelly and Quimby, 2002) although the pellets are longer than rabbit or guinea pig pellets to allow the chinchilla to hold the pellets as it eats. Pellets should be provided in a ceramic, metal, or heavy plastic dish. Pellets should be supplemented with goodquality hay (e.g., oat, timothy, or orchard

129

grass) and fresh leafy green vegetables (e.g., kale, collard greens, and mustard greens). Hay can be provided ad libitum either in loose form in a hay rack or cube form directly on the cage floor. Corn and cabbage should be avoided as they cause flatulence and are hard on the digestive system. Treats, including grains, raisins, and fruits, should be limited as these can lead to obesity and digestive tract upsets. Sugary or starchy treats should be avoided at all times. As with most other animals, any changes in diet should be made gradually to prevent anorexia or gastrointestinal stasis. Water should be provided ad libitum in a cagemounted water bottle or heavy water bowl. HANDLING AND RESTRAINT

Chinchillas are easy to hold and do not bite; however, they may nip if they become stressed. A hand-tamed chinchilla will usually willingly come out of its cage. Place one hand under the abdomen or around the scruff of the neck and place the other hand around the base of the tail (Figs. 11.6 and 11.7). Care should be taken to avoid rough handling or grasping the fur as this can lead to fur slip, a condition in which the fur is released resulting in the loss of fur. Chinchillas should never be picked up by their ears. If the chinchilla is known to bite, two people should hold it.

Fig. 11.6 Chinchilla restraint. (Drawing courtesy of Ian Thomas.)

130

Fig. 11.7 Chinchilla restraint. (Drawing courtesy of Ian Thomas.)

Exotic Small Mammal Care and Husbandry

collected. If necessary, the ear vein can be used to collect a small volume but should not be utilized for repeated sampling. To prevent collapse of these small veins, use a tuberculin syringe and a 25- to 27-gauge needle. The jugular vein can be used to collect a large volume of blood but anesthesia or chemical restraint is generally recommended. The cranial vena cava can be used as a venipuncture site but there is a risk of bleeding into the pericardial sac or thoracic cavity (Donnelly and Quimby, 2002). Other potential sites for venipuncture include femoral, dorsalis penis, lateral abdominal, and tail vein (Lyon, 2003). A minimal sample can be obtained from a toenail clip or via a foot puncture using a sterile needle (Hrapkiewicz et al., 1998).

Sample collection—cystocentesis PHYSICAL EXAM

Initial exam should involve observation of the chinchilla in the transport cage. Movements, demeanor, and breathing rate as well as overall condition of the fur should be noted. A healthy chinchilla will be alert to its surroundings, have bright eyes, and a twitching nose. The hair coat should be soft and smooth and the tail will likely be erect. Weight and rectal temperature should be obtained and recorded. The veterinarian should observe fur, skin, and mucous membranes followed by auscultation of the heart and lungs. The abdomen should be palpated along with observation of the genitalia. The oral cavity should be examined last because this is stressful to the chinchilla and is likely to require restraint by a second person. In some cases, anesthesia may be required if the chinchilla is difficult to restrain or appears to be experiencing pain (Riggs and Mitchell, 2008). (See Table 11.4 for anesthetic agents used in chinchillas.) The teeth of the chinchilla are normally yellow because of a deposit of iron on the enamel (Donnelly and Quimby, 2002). CLINICAL TECHNIQUES

Sample collection—venipuncture Venipuncture can be difficult in chinchillas. The cephalic and lateral saphenous veins can be accessed but only a small volume can be

Urine samples can be obtained from performing cystocentesis with a 25-gauge needle directly into the bladder. Samples can also be obtained by free catch or floor catch. Urine is typically yellow to amber in color and may be darker depending on the diet. Pigments (e.g., porphyrins) in the urine can be mistaken for hematuria but this can be ruled out by the absence or presence of blood cells on a direct smear (Riggs and Mitchell, 2008). Some calcium carbonate crystals may be observed during sediment examination on normal chinchilla urine (Lyon, 2003). Normal urine values for chinchillas are presented in Table 11.5.

PREVENTIVE HEALTH

Vaccinations Routine vaccinations for infectious diseases are not required for chinchillas, but an annual physical exam is recommended. Because obesity is a problem in pet chinchillas, weight should be monitored frequently. Some veterinarians suggest a biannual examination to assess weight and dental health and to perform nail trimming. Owners should alert their veterinarian immediately to any changes in behavior, eating or elimination habits, and physical characteristics (Pinney, 2003). Veterinarians should ask owners about the animal’s housing environment (including cage size and type, bedding, cleaning frequency, temperature, exercise) and

Table 11.4 Anesthetic and analgesic agents used in chinchillas. Agent

Dosage

Route

Acepromazine

0.5–1.0 mg/kg

IM

Acepromazine + ketamine

(A) 0.5 mg/kg + (K) 40 mg/kg

IM

Acepromazine + ketamine + atropine

(A) 0.5 mg/kg + (K) 10 mg/kg + (At) 0.05 mg/kg

IM

Acetaminophen

1–2 mg/mL in drinking water

Alphadolone-alphaxalone (Saffan)

20–30 mg/kg

IM

Aspirin

100–200 mg/kg q6–8h

PO

Atropine

0.05–0.10 mg/kg

SC, IM

Buprenorphine

0.05 mg/kg q8–12h

SC, IV

Butorphanol

0.2–2.0 mg/kg q4h

SC, IM

Carprofen

4 mg/kg q24h

SC

Diazepam

2.5 mg/kg

IP

Fentanyl-droperidol (Innovar-Vet)

0.20 mL/kg

IM

Flunixin meglumine

1–2.5 mg/kg

IM

Glycopyrrolate

0.01–0.02 mg/kg

SC, IM

Halothane

2%–5% induction 2%–3% maintenance

Inhalation

Isoflurane

2%–5% induction 2%–4% maintenance

Inhalation

Ketamine

20–40 mg/kg

IM

Ketamine + acepromazine

(K) 40 mg/kg + (A) 0.5 mg/kg

IM

Ketamine + diazepam

(K) 20–40 mg/kg + (D) 1–2 mg/kg (K) 20 mg/kg + (D) 5 mg/kg

IM IM, IP

Ketamine + midazolam

(K) 5–10 mg/kg + (M) 0.5–1.0 mg/kg

IM

Ketamine + midazolam + atropine

(K) 10–15 mg/kg + (M) 0.5 mg/kg + (A) 0.05 mg/kg

IM

Ketamine + xylazine

(K) 30–40 mg/kg + (X) 4–8 mg/kg

IM

Ketoprofen

1 mg/kg q12–24h

IM, SC

Meperidine

20 mg/kg

IM, SC

Midazolam

1–2 mg/kg

IM, SC

Morphine

2–5 mg/kg

IM

Pentobarbital

30 mg/kg 40 mg/kg

IV IP

Tiletamine/zolazepam (Telazol)

20–40 mg/kg

IM

Xylazine

2–10 mg/kg

IM

Yohimbine

2.0 mg/kg

IM

From: Hawk and Leary (1999); Hoefer and Crossley (2002); Hrapkiewicz et al. (1998); Riggs and Mitchell (2008).

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diet because these items are the main causes of illness.

Endoparasites and ectoparasites Chinchillas can become infested with a number of ectoparasites and endoparasites. (Antiparasitic agents used in chinchillas are presented in Table 11.6.) Diagnosis can be made by using fecal flotation or direct fecal smears. Fleas can be found by inspecting and combing the hair. Mites can be identified from skin scrapes or tape test.

COMMON DISEASES

Choking Like other rodent species, chinchillas cannot vomit. This can lead to choking if the animal ingests an object, such as bedding or treats, which is too large to swallow. Signs are dyspnea, anorexia, pawing at the mouth, and excessive salivation. Confirmation of obstruction can be made by radiograph or palpation (Lyon, 2003).

Malocclusion Table 11.5

Normal urine values.

Color

Yellow to slightly red or amber

Turbidity

Usually cloudy

pH

8.0–9.0 (avg. 8.5)

Protein

Negative to trace

Glucose

Negative

Ketones

Negative

Bilirubin

Negative

Urobilinogen

0.1–1.0 mg/dL

Nitrates

Negative

Blood

Negative

Specific gravity

Usually >1.045

From: Lyon (2003); Merry (1990).

A common problem in chinchillas is malocclusion, or slobbers, which can occur in the incisors, premolars, or molars (Lyon, 2003). Malocclusion can be hereditary or can be caused by a lack of hard items to chew on. Clinical signs include weight loss, drooling, anorexia, halitosis, decrease in fecal volume, and pawing at the mouth. Teeth may be trimmed with scissors or toenail clippers. Because malocclusion is a hereditary condition, chinchillas with malocclusion should not be bred.

Ringworm Trichophyton mentagrophytes is a common cause of ringworm in the chinchilla, although Microsporum canis and M. gypseum can also occur. Lesions can appear anywhere on the body but typically occur as small, scaly areas

Table 11.6 Antiparasitic agents used in chinchillas. Agent

Dose

Route

Carbaryl 5% powder

Dust q7d for 3 weeks

Topical

Fenbendazole

20 mg/kg q24h for 5 days

PO

Ivermectin

0.2–0.4 mg/kg q7days for 3 weeks

PO, SC

Metronidazole

10–60 mg/kg q12h for 5 days

PO

Piperazine citrate

100 mg/kg q24h for 2 days

PO

Praziquantel

5–10 mg/kg, repeat in 10 days

PO, SC, IM

Pyrethrin powder

Dust q7d for 3 weeks

Topical

Sulfamerazine

1 mg/mL in drinking water

Sulfadimethoxine

10–15 mg/kg q12h

PO

Thiabendazole

50–100 mg/kg q24h for 5 days

PO

From: Hoefer and Crossley (2002); Hrapkiewicz et al. (1998).

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133

of alopecia on the ears, nose, and feet (Donnelly, 2004; Hrapkiewicz et al., 1998). Diagnosis is determined after assessment of hair and skin samples as well as dermatophyte culture. Captan antifungal power can be added to the dust bath powder to help control the spread of infection. Oral griseofulvin, as well as ketoconazole, itraconazole, and terbinafine have been used to successfully treat this condition. Lime sulfur dips have also been found to be a successful treatment (Hrapkiewicz et al., 1998; Hoefer and Crossley, 2002). Antimicrobial and antifungal agents used in chinchillas are presented in Table 11.7.

Conjunctivitis Conjunctivitis can be caused by irritation of the eyes resulting from dust baths, poorly ventilated housing, or dirty and damp bedding. Ophthalmic ointment can be administered. Dust baths should not be provided during this time and owners should concentrate on improving housing and husbandry conditions (Hrapkiewicz et al., 1998).

Fur ring Fur rings (hair rings) can accumulate around the penis and under the prepuce in male chinchillas (Fig. 11.8). This hair affects breeding

Table 11.7 Antimicrobial and antifungal agents used in chinchillas. Agent

Dosage

Route

Amikacin

2 mg/kg q8h

SC, IM, IV

Captan powder (Orthocide)

1 tsp/2 cups dust, add to dust bath

Topical

Cephalosporin

25–100 mg/kg q6h

PO

Chloramphenicol

30–50 mg/kg q12h

PO, SC, IM, IV

Chlortetracycline

50 mg/kg q12h

PO

Ciprofloxacin

5–20 mg/kg q12h

PO

Doxycycline

2.5 mg/kg q12h

PO

Enrofloxacin

2.5–15 mg/kg q12h

SC, IM, PO

Gentamicin

2–4 mg/kg q8h

SC, IM, IV

Griseofulvin

25 mg/kg q24h for 30–60 days

PO

Itraconazole

5 mg/kg q24h

PO

Ketoconazole

10–40 mg/kg q24h

PO

Lime sulfur dip

Dilute 1:40 with water, dip q7d for 6 weeks

Topical

Neomycin

15 mg/kg q24h

PO

Oxytetracycline

50 mg/kg q12h 1 mg/mL in drinking water

PO

Sulfadimethoxine

25–50 mg/kg q24h for 10–14 days

PO

Sulfamerizine

1 mg/mL drinking water

Sulfamethazine

1 mg/mL drinking water

Tetracycline

0.3–2 mg/mL drinking water 50 mg/kg q8–12h

PO

Trimethoprim-sulfa

15–30 mg/kg q12h

PO, IM, SC

Tylosin

10 mg/kg q24h

PO, SC, IM

From: Hawk and Leary (1999); Hoefer and Crossley (2002); Hrapkiewicz et al. (1998); Riggs and Mitchell (2008).

134

Exotic Small Mammal Care and Husbandry

Fig. 11.8 Fur ring removed from a male chinchilla. (Photo courtesy of Dan H. Johnson, DVM, Avian and Exotic Animal Care, Raleigh, NC.)

Fig. 11.9 Fur slip in a chinchilla. (Photo courtesy of Dan H. Johnson, DVM, Avian and Exotic Animal Care, Raleigh, NC.) For color detail, please see color plate section.

ability and can cause infection, irritation, paraphimosis, and damage to the penis (Hrapkiewicz et al., 1998). This condition occurs more commonly in breeding males but can occur in nonbreeding males as well. Clinical signs associated with fur ring include excessive grooming of the prepucial area, straining to urinate, lethargy, and decreased appetite. Males should be routinely checked for the presence of a hair ring. To remove, apply sterile lubricant to the area and roll the ring of fur off the penis. The use of anesthesia may aid in this process (Donnelly, 2004).

ors in the environment such as loud noises, feeding proper diet, improving housing conditions, and offering environmental enrichment devices. Johnson (2006) indicates chinchillas exhibiting fur chewing behaviors have been shown to have skin and adrenal histopathologic changes consistent with hyperadrenocorticism. Fur chewing can also lead to development of trichobezoars for which treatments include feline laxatives, fluid therapy, pineapple juice (which contains proteolytic enzymes), and increased dietary fiber (Lyon, 2003).

Enteritis Fur slip Fur slip (Fig. 11.9) is the chinchilla’s ability to release a large patch of fur when frightened or attacked. Fur slip is a natural defense mechanism intended to leave potential predators with nothing but a mouthful of hair (Pinney, 2003). Hrapkiewicz et al. (1998) report it may take up to 5 months for the hair to grow back. Gentle handling and a quiet environment should lessen the chances of this occurring.

Disruption in the digestive system can result in anorexia, diarrhea, mucoid enteritis, bloat, ileus, and rectal prolapse (Hoefer and Crossley, 2002). Enteritis is common in chinchillas and often involves Pseudomonas spp., Pasteurella spp., Proteus spp., Salmonella spp., and Escherichia coli (Merry, 1990). Causes can include abrupt change in diet, overcrowding and stress, antibiotics, and low-fiber diets. Treatment includes supportive care, antibiotics, and analgesics.

Fur chewing

Pseudomonas

Another common condition involving the hair is fur chewing or barbering. The cause of this is unknown but possible causes include boredom, dietary deficiencies, and heredity, as well as environmental stressors including overcrowding. Treatments include reducing stress-

Chinchillas are highly susceptible to Pseudomonas aeruginosa. Contaminated drinking water is generally the source; however, effective treatment can be accomplished by the use of gentamicin. Chlorination of the drinking water or acidifying the water to a pH of 2.5–3

Chinchillas

seems to help prevent infection (Hrapkiewicz et al., 1998). Symptoms include enteritis, conjunctivitis, otitis, pneumonia, mesenteric lymphadenopathy, dermal pustules, and metritis.

Listeriosis Chinchillas are also susceptible to infections with Listeria monocytogenes; however, exposure in pet chinchillas is unlikely (Lyon, 2003). All ages are affected and both enteric and encephalitic forms of the disease are seen. Clinical signs are vague but include general malaise, anorexia, depression, ataxia, diarrhea, circling, convulsions, and paralysis. Death typically occurs within 48–72 hours after onset of symptoms. Treatment includes tetracycline or chloramphenicol but generally treatment is not successful.

Respiratory disease

135

TREATMENTS

Intravenous (IV) catheters can be placed in the peripheral veins, but this can be difficult due to the small size of the veins. A jugular cutdown can be performed under anesthesia to place a 24-gauge indwelling catheter. Supplemental fluids can be administered subcutaneously (SC) in the loose skin of the neck and upper back. Medications can be given by intramuscular (IM) or subcutaneous injection. Intramuscular injections should be given in small volumes into the lumbar muscles or the rear leg. Subcutaneous injections, with a maximum volume of 8 mL per site, can be given in the upper back or neck area. Oral (PO) medications can be

Table 11.8 chinchillas.

Miscellaneous

agents

used

in

Agent

Dosage

Route

Atropine

0.05–0.2 mg/kg

SC, IM

Calcium-EDTA

30 mg/kg q12h

SC

Cimetidine

5–10 mg/ kg q6–12h

IM, PO, SC

Cisapride

0.1–0.5 mg/ kg q8–12h

PO

Dexamethasone

0.5–2.0 mg/kg

IM

Trauma

Diphenhydramine

1–2 mg/kg q12h

PO

Trauma-induced fractures of the tibia are common (Donnelly, 2004). Fractures commonly occur when a leg is caught in an opening in a wire cage or by improper handling. The tibia is a thin, fragile bone and splints and bandages do not give adequate stability for healing.

Doxapram (Dopram)

5–10 mg/kg

IP, IV

Epinephrine

0.2 mg/kg prn

IV, IT, IV, IC

Furosemide

1–4 mg/kg q4–6h

IM

Lactated Ringer’s

50–100 mL/ kg q24h

SC, IV

Metoclopramide

0.2–1.0 mg/ kg q8h

SC

Oxytocin

0.2–3.0 IU/kg

SC, IM, IV

Prednisone

0.5–2.2 mg/kg

SC, IM

Sucralfate

25–100 mg/ kg q8–12h

PO

Bordetella spp., Streptococcus spp., Pasteurella spp., and Pseudomonas aeurginosa can all cause respiratory disease in chinchillas. Predisposing factors include environmental conditions such as overcrowding, poor ventilation, and high humidity, as well as stress in general. Symptoms include depression, dyspnea, nasal discharge, and anorexia (Hrapkiewicz et al., 1998).

Bite wounds Chinchillas are quite capable of inflicting severe and fatal injuries on each other (Johnson, 2006). Chinchillas that are group-housed can have secondary abscesses that develop from bite wounds. Bite wounds and subsequent abscesses may occur if the female bites an unacceptable mate (Donnelly, 2004). Streptococcus spp. and Staphylococcus spp. are generally involved but can be successfully treated with antibiotics based on culture and sensitivity testing (Hrapkiewicz et al., 1998).

Vitamin B complex 0.02–0.2 mL/kg

SC, IM

Vitamin K

1–10 mg/kg prn

IM

Yohimbine

2.0 mg/kg

IP, IM

From: Hoefer and Crossley (2002); Hrapkiewicz et al. (1998); Riggs and Mitchell (2008).

136

given to chinchillas by placing tablets or liquids in food treats such as raisins. The intraperitoneal (IP) route can be used for injecting volumes up to 10 mL. The use of antibiotics is common because many of the diseases are bacterial in origin; however, the microflora in chinchillas is mainly gram-positive, and certain antibiotics can cause severe changes in the gastrointestinal tract bacterial population. Antimicrobials with a selective gram-positive spectrum, such as ampicillin, erythromycin, clindamycin, and lincomycin should not be used in treating disease in chinchillas. Recommended antibiotics include broad spectrum antibiotics for short periods of time as they do not upset the normal flora of the gastrointestinal tract (Hrapkiewicz et al., 1998). Miscellaneous agents used in chinchillas are presented in Table 11.8. REFERENCES Donnelly, T.M. 2004. Disease Problems of Chinchillas. In Quesenberry, K.E., and Carpenter, J.W. (eds.). Ferrets, Rabbits, and Rodents: Clinical Medicine and Surgery. Second edition. Saunders, St. Louis, MO, pp. 255–265. Donnelly, T.M., and Quimby, F.W. 2002. Biology and Diseases of Other Rodents. In Fox, J.G., Anderson, L.C., Loew, F.M., and Quimby, F.W. (eds.). Laboratory Animal Medicine. Second edition. Elsevier Science, San Diego, CA, pp. 286–291. Hawk, C.T., and Leary, S.L. 1999. Formulary for Laboratory Animals. Second edition. Iowa State University Press, Ames, IA.

Exotic Small Mammal Care and Husbandry

Hoefer, H.L., and Crossley, D.A. 2002. Chinchillas. In Meredith, A., and Redrobe, S. (eds.). BSAVA Manual of Exotic Pets. Fourth edition. BSAVA, Quedgeley, Gloucester, UK, pp. 65–75. Hrapkiewicz, K., Medina, L., and Holmes, D.D. 1998. Chinchillas. In Clinical Laboratory Animal Medicine: An Introduction. Iowa State University Press, Ames, IA, pp. 117–133. Johnson, D.J. 2006. Miscellaneous Small Mammal Behavior. In Bays, T.B., Lightfoot, T., and Mayer, J. Exotic Pet Behavior. Saunders Elsevier, St. Louis, MO, pp. 263–279. Kahn, C.M. 2007. The Merck/Merial Manual for Pet Health. Home Edition. Merck & Co., Whitehouse Station, NJ, pp. 873–886. Lawson, P.T. 2001. ALAT Training Manual. Sheridan Books, Chelsea, MI. Lyon, T. 2003. The Chinchilla. In Ballard, B., and Cheek, R. (eds.). Exotic Animal Medicine for the Veterinary Technician. Iowa State Press, Ames, IA, pp. 239–246 Merry, C.J. 1990. An Introduction to Chinchillas. Vet. Tech. 11(5):315–322. Pinney, C.C. 2003. Chinchillas. In The Complete Home Veterinary Guide. Third edition. McGraw-Hill Professional, New York, pp. 483–492. Quesenberry, K.E., Donnelly, T.M., and Hillyer, E.V. 2004. Biology, Husbandry, and Clinical Techniques of Guinea Pigs and Chinchillas. In Quesenberry, K.E., and Carpenter, J.W. (eds.). Ferrets, Rabbits, and Rodents: Clinical Medicine and Surgery. Second edition. Saunders, St. Louis, MO, pp. 232–244. Riggs, S.M., and Mitchell, M.A. 2008. Chinchillas. In Mitchell, M.A., and Tully, T.N., Jr. (eds.). Manual of Exotic Pet Practice. Saunders, St. Louis, MO, pp. 474–492.

Degus

COMMON BREEDS

The degu, Octodon degus, is native to northern and western Chile and belongs to the same order as the chinchilla and guinea pig (Fig. 12.1). They are commonly referred to as trumpet-tailed rats and brush-tailed rats based upon their brown-grey coat and prominent black tail tip. Degus were imported to the United States in 1964, where they have become household pets and research subjects. Due to their social nature with people and other degus, their diurnal sleep patterns, relatively long life span, and low incidence of naturally occurring disease, they make wonderful pets. Their use in research has mainly focused on circadian behavior as a model for human sleep/wake cycles, the development of diabetes mellitus, the formation of cataracts, and drug tolerance (Donnelly and Quimby, 2002).

Fig. 12.1 Profile of a normal degu. (Copyright Daniel Rajszczak, Dreamstime.com.) For color detail, please see color plate section.

12 BASIC ANATOMY AND PHYSIOLOGY

Degus have been classified in the suborder Hystricognathi or “porcupine-like rodents” because of their similar skull and jaw muscle structures. The “figure 8” appearance of their cheek teeth places them within the genus Octodon. Their incisors are open-rooted and very powerful. Degus have five toes on each foot, four of which have sharp claws and are well developed for burrowing, and a thumb on each foreleg that is much shorter. Degus are classified as hindgut fermenters with a functioning cecum. Their spleen has a glandular appearance from the unusual cuboidal shape of the endothelium of the sinusoids (Donnelly and Quimby, 2002). Their adrenal glands are relatively large when compared with other rodents. Female degus have four pairs of mammary glands that are accessible when the mother lies on top of the pups to allow them to nurse on their backs. The inguinal canal remains open throughout the life of the male degu. They have intra-abdominal testicles located within two separate hemiscrotal sacs, which are not well developed. Castration can be performed either by a laparotomy or through a prescrotal open technique. Care must be taken to ligate the inguinal canal to prevent herniation of bowel, urinary bladder, and abdominal fat (Capello, 2005).

137

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Exotic Small Mammal Care and Husbandry

Table 12.1 Biological profile and normal physiologic values. Body weight

Adult: 170–300 g

Rectal temperature

101.8 °F (37.9 °C)

Body length

12.5–19.5 cm

Tail length

10.5–16.5 cm

Reproductive data

Gestation length: 87–93 days (average 90 days) Weaning age: 4–6 weeks Captive breeding season: year-round Induced ovulation Litter size: 1–10 (average 6–7) Litters per year: 2–3 Birth weight: 14 g Newborns are precocious and fully furred. Sexual maturity: 3–6 months

Life span (captivity)

5–8 years (maximum 10 years)

Dental Formula

2(I 1/1, C 0/0, P 1/1, M 3/3)

Fig. 12.2 Ventral abdomen of female (left) and male (right) degu genitalia. (Photo courtesy of Dan H. Johnson, DVM, Avian and Exotic Animal Care, Raleigh, NC.) For color detail, please see color plate section.

REPRODUCTION AND SEXING

As in many species, anogenital distance is used to determine the sex of a degu. The anogenital distance of the male is about twice that of the female (Fig. 12.2). Males do not have a scrotum since the testicles are located intra-abdominally. The prepuce of the male is considerably larger than the clitoris of the female, both located ventral to the anus. The penis can be externalized by proximally manipulating the prepuce (Johnson, 2002). Animals in captivity will likely breed yearround and females can have more than one litter per year. Degus reach sexual maturity between 45 days and 20 months, averaging 6 months (Donnelly and Quimby, 2002). Breeding is most successful when the female is 4–9 months of age and weighs less than 250 g. Estrus lasts only about 3 hours, during which time the vaginal membrane opens. Females are induced ovulators, requiring stimulation from the spicules on the tip of the male’s penis for release of the ova. Mating is brief, typically around 10 seconds, and results in the formation of a vaginal plug. The appearance of a “red ring” can be seen early in pregnancy when the vaginal membrane reopens, producing a red discharge (Johnson, 2002). Degus have a relatively long gestational period, 97–93 days, due to allantochorionic

From: Donnelly and Quimby (2002); Johnson (2002).

subplacentation. Litters typically contain seven pups but can range from one to 10 young. Though the young are considered to be precocious, they are not always born fully haired or with their eyes open. Both the male and female participate in caring for the young by huddling to keep them warm. The mother typically lies on top of the pups while they are on their backs to allow them to nurse, usually 25 minutes at a time. Pups will nurse between 14 and 28 days and typically are weaned at 4–6 weeks of age (Johnson, 2002). The basic biological profile for degus is presented in Table 12.1. HOUSING AND HUSBANDRY

Degus are very social animals that create an elaborate system of burrows in nature. In captivity they should be pair- or group-housed. It is rare for fighting to occur, even with new introductions to the colony. Degus should be housed in large multilevel cages with various elements of environmental enrichment such as branches, a nesting box, and running wheels. Many bedding materials can be used to line the

Degus

a

139

b

Fig. 12.3 (a and b) Examples of variations in dust-bathing arrangements. (Figure 12.3a copyright Daniel Rajszczak, Dreamstime.com; Fig. 12.3b photo courtesy of Dan H. Johnson, DVM, Avian and Exotic Animal Care, Raleigh, NC.)

cage, including hay, paper products, and wood shavings (Johnson, 2002). Degus have some unique husbandry needs. Like chinchillas, degus take dust baths and should have the opportunity to do so twice weekly for 10–15 minutes each time in dust material 2–3 inches in depth (Fig. 12.3a,b). While degus do not have significant water intake, special care must be taken to change the bottles at least three times weekly to prevent Pseudomonas infection. In research facilities it is not uncommon to provide treated (acidified) water in addition to performing frequent water bottle changes. NUTRITION

In captivity, degus are fed a mixture of commercial rodent and guinea pig diets supplemented with hay and vegetables (Johnson, 2002; Hromanik, 2003). Treats such as sweet potatoes, seeds, peanuts, and vegetables are also given. To prevent obesity, care must be taken not to overfeed pet degus. The development of diabetes has been associated with foods that elevate blood sugar, and such foods should be avoided (Donnelly and Quimby, 2002). These include but are not limited to fruits, foods that contain molasses or honey,

cereals, and raisins (Johnson, 2002). Degus with diabetes as a result of obesity or diet often develop cataracts within four weeks (Donnelly, 2004). ENRICHMENT

Environmental enrichment is imperative for these social creatures. Self-mutilation and aggression can result when social and physical enrichment are not provided (Johnson, 2002). Because of this need for social interaction, degus should be housed in pairs or small groups as well as participate in human interactions. A variety of physical enrichment can be provided in the cage in the form of toys, wheels, and branches or shelves for climbing. HANDLING, RESTRAINT, AND PHYSICAL EXAM

Because degus are so good-natured and interact well with humans, it is not difficult to handle and restrain them. They can be easily supported with two hands or held in an encircling grip (Fig. 12.4) to allow for examination as well as be scruffed if needed (Johnson, 2002). Nylon fishnets can be used to transfer or carry

140

Exotic Small Mammal Care and Husbandry

Table 12.2 Laboratory normal values (CBC). Hematologic Parameter

Reference Interval

RBC (×106 cells/μL)

7–8

Hemoglobin (g/dL)

11–12

Hematocrit (%)

27–40

WBC (×10 cells/μL)

3–8

Neutrophils (×10 cells/μL)

0.8–5.5

Lymphocytes (×103 cells/μL)

1.2–4.2

Monocytes (×10 cells/μL)

0.07–0.16

Eosinophils (×10 cells/μL)

0.13–0.62

Basophils (×10 cells/μL)

0.03–0.16

Platelets (×103 cells/μL)

435–475

3

3

3

3

Fig. 12.4 Proper handheld restraint of a degu. (Photo courtesy of Dan H. Johnson, DVM, Avian and Exotic Animal Care, Raleigh, NC.)

3

From: Johnson (2002).

COMMON DISEASES

Degus are very healthy and thrifty animals, with a low occurrence of diseases. The formulary for degus is presented in Table 12.3.

Infectious diseases

Fig. 12.5 Degloved tail of a degu requiring surgical correction. (Photo courtesy of Dan H. Johnson, DVM, Avian and Exotic Animal Care, Raleigh, NC.) For color detail, please see color plate section.

them as well. Care must be taken to avoid holding the degu by the tail. They will spin and create a degloving injury by slipping from the handler and leaving behind the skin of the tip of the tail. This situation requires amputation of the exposed tail tip and is common in many rodents (Fig. 12.5). The hematologic and serum chemistry values for degus are similar to those of guinea pigs and rats. Table 12.2 contains published data specific for degu complete blood cell count (CBC) values.

Degus are susceptible to Pseudomonas infection if proper sanitation of water bottles is not maintained. There are also reported cases of Giardia spp. detected by enzyme-linked immunosorbent assay (ELISA) in a colony of adults and pups with fatal diarrhea (Donnelly and Quimby, 2002). A few intestinal parasites, including the Trichuris bradleyi whipworm have also been found in degus. Klebsiella pneumoniae infection resulting in a case of acute suppurative bronchopneumonia has been described in a degu as well (Donnelly and Quimby, 2002).

Metabolic disease In addition to diabetes that results from diets that create elevated blood sugar, degus also develop spontaneous diabetes mellitus. It has been associated with pancreatic islet cell amyloidosis, which can be associated with

Table 12.3 Degu formulary. Agent

Dosage (mg/kg)

Route

Acepromazine

0.5–1.0

IM

Amikacin

2 q8h

IM, SC, IV

Amitraz

As per package directions

Topical

Amoxicillin

DO NOT USE

Ampicillin

DO NOT USE

Atropine

0.05

IM, SC

Cephalosporin

25–100 q6h

PO

Chlorotetracycline

50 q12h

PO

Dexamethasone

0.5–2.0

IV, IP, IM, SC

Diazepam

1–2

IP, IM

Doxycycline

2.5 q12h

PO

Enrofloxacin

5–10 q12h

PO, SC, IM

Fenbendazole

20 q24h × 5 days

PO

Furosamide

5–10 q12h

Gentamicin

2 q8h

Griseofulvin

25 q24h × 28–40 days

PO

Isoflurane

To effect

IH

Ivermectin

0.2–0.4, repeat in 7–14 days

PO

Ketamine

44

IP

Ketamine + acepromazine

40 + 0.5

IM

Ketamine + diazepam

20–40 + 1.0–2.0

IM

Ketamine + xylazine

35 + 5

IP

Metoclopramide HCl

0.5 q8h

SC

IM, SC, IV

Neomycin

15 q12h

PO

Orthocide antifungal powder

1 tsp/2 c dust

Mix in dust bath

Oxytocin

0.2–3.0 IU/kg

SC, IM, IV

Pentobarbital

30 35–40

IV IP

Prednisone

0.5–2.0

PO, SC, IM

Procaine penicillin G

DO NOT USE

Sulfamethazine

1 mg/mL

PO in drinking water

Tetracycline

50 q12h 0.3–2.0 mg/mL

PO PO in drinking water

Thiabendazole

50–100 × 5 days

PO

Trimethoprim sulfadiazine

30 q12h

IM, SC

Vitamin B1

0.02–0.2 mL/kg 1 mg/kg

IM, SC PO in feed

Vitamin K1

1–10

IM

From: Johnson (2002). Clinically, dosages of drugs listed here have been used safely in degus; however, most are based on anecdotal use rather than pharmacodynamic data.

141

142

cytomegalovirus as well as alpha cell crystals with the presence of a herpes-type virus (Donnelly and Quimby, 2002).

Trauma There has been one report of a tibial fracture in a 3-month-old degu. It was able to be repaired by medullary fixation (Beregi et al., 1994).

Neoplasia A variety of neoplasms have been documented in degus, though very few cases overall have been reported. The most common tumor described in degus is hepatocellular carcinoma, reported in four animals between 5 and 6 years of age (Donnelly, 2004). Other types of tumors noted include a bronchoalveolar carcinoma with metastasis to the liver and kidneys, one reticulum cell carcinoma with cervical lymph node involvement that created compression of the trachea resulting in the death of the animal, splenic hemangiomas, and a mesenteric lipoma (Donnelly and Quimby, 2002).

Ocular disease Cataract formation in degus has been associated with the development of diabetes but also has been noted to occur naturally.

Exotic Small Mammal Care and Husbandry

REFERENCES Beregi, A., Felkai, F., Seregi, J., and Sarosi, L. 1994. Medullary fixation of a tibial fracture in a three-month-old degu (Octodon degus). Vet. Rec. 134:652–653. Capello, Vittorio. 2005. Prescrotal Open Technique for Neutering a Degu. Exotic DVM 6(6):29–31. Donnelly, Thomas M. 2004. Basic Anatomy, Physiology, Husbandry, and Clinical Techniques. In Quesenberry, K.E., and Carpenter, J.W. (eds.). Ferrets, Rabbits, and Rodents: Clinical Medicine and Surgery. Second edition. Saunders, St. Louis, MO, p. 312. Donnelly, Thomas M., and Quimby, Fred W. 2002. Biology and Diseases of Other Rodents. In Fox, J.G., Anderson, L.C., Leow, F.M., and Quimby, F.M. (eds.). Laboratory Animal Medicine. Second edition. Academic Press, San Diego, pp. 284–286. Hromanik, Dawn. 2003. Exotic Animal Nutrition: Application of Hay Science. Exotic DVM 5(4):40–41. Johnson, Dan. 2002. What Veterinarians Need to Know about Degus. Exotic DVM 4(4):39–42.

Hedgehogs

13

Hedgehogs are small mammals with bodies that are covered with spines except on their faces and ventral abdomen. They are members of the order Erinaceomorpha, family Erinaceidae, and subfamily Erinaceinae. Hedgehogs’ natural habitats are found across the African, Asian, and European continents. Hedgehogs are illegal in some cities and states, and permits are required in some areas. Potential hedgehog owners are encouraged to check local ordinances, laws, and regulations prior to obtaining a pet hedgehog (Pinney, 2003; Johnson-Delaney, 2008). COMMON BREEDS

Hedgehogs are classified based on ear length, skull morphology, and the shape and pattern of their spines (Heatley, 2008). There are many different species, including Algerian, African, European, Pruner’s, long-eared or Egyptian, and Ethiopian or desert hedgehog (Jones, 2003). The two most common hedgehog species that are kept as pets are the central African hedgehog, Atelerix albiventris, and the European hedgehog, Erinaceus europaeus. The central African hedgehog is also known as the white-bellied, four-toed, or African pygmy hedgehog (Ivey and Carpenter, 2004). The African pygmy hedgehog is native to West and Central Africa. The African pygmy hedgehog is the most common species in the US pet market (Fig. 13.1). Common quill colors include the standard colored quill known as salt and pepper and the all-white quill, which is also referred to as snowflake (Heatley, 2008).

Fig. 13.1 African pygmy hedgehog. (Photo courtesy of Lucinda Prevost.)

BASIC ANATOMY AND PHYSIOLOGY

The hedgehog’s spines, which extend along its head and back, are a deterrent to predators. A second defensive mechanism is the hedgehog’s ability to roll into a tight ball (Fig. 13.2) to protect the vulnerable underbelly, feet, and face. These areas are typically covered with a soft, fine white hair. Most hedgehogs have five toes; however, the African pygmy hedgehog only has four toes on the hind foot and is known as the four-toed hedgehog. Hedgehogs have strong, powerful legs but do not have a tail (Jones, 2003). An unusual anatomic feature of the hedgehog is a distally fused radius and ulna (Heatley, 2008). Adult African hedgehogs are 5 to 8 inches in length whereas the European hedgehogs are 143

144

Exotic Small Mammal Care and Husbandry

Table 13.2 Hedgehog biological profile. Body weight

African (male) 800–1,200 g African (female) 250–400 g European (male) 500–600 g European (female) 400–800 g Birth weight 8–18 g

Body length

17–25 cm (7–9 in)

Body temperature (rectal)

African 36.1 °C–37.2 °C (97 °F–99 °F) European 35.1 °C (95.2 °F)

Reproductive data

Sexual maturity: Male 6–8 months Female 2–6 months Ovulation: induced Gestation length: 34–37 days Litter size: 1–7 pups (avg. 3) Weaning age: 4–6 weeks of age; start eating solid food at 3 weeks Reproductive life span: Female: 2–3 years Male: throughout life

Life span (captivity)

3–8 years (may live to 10 years of age)

Heart rate

180–280 beats per minute

Respiratory rate

25–50 breaths per minute

Fig. 13.2 Balled-up hedgehog. (Photo courtesy of Dan H. Johnson, DVM, Avian and Exotic Animal Care, Raleigh, NC.) For color detail, please see color plate section. Table 13.1 vocalizations.

African

pygmy

hedgehog

Sound

Description

Inaudible sounds

Hedgehogs can hear and make sounds in the 40–90 kHz range (above the human hearing range).

Snorting, grunting, These are warning or aggressive hissing, huffing sounds that are made by sharp vibrating exhalations through the nostrils. These are generally emitted when the animal encounters another animal, is disrupted, or when it is in the act of rolling up. Clucking

This is high-pitched contact call made from the dam to the neonates. It can also be made by males during courtship.

Screaming

This is a severe distress call given when the animal is in pain or distress.

Twittering, whistling

This is a high-pitched sound made by neonates. Whistling stimulates contact by the dam.

Snuffling

This noise is made as hedgehogs look for food.

From: Heatley (2008).

12 to 14 inches long. Hedgehogs have a welldeveloped sense of smell. The relatively small eyes indicate the need to depend on olfactory and auditory cues (Heatley, 2008). African

From: Carpenter (2005); Heatley (2008); Ivey and Carpenter (2004); Johnson-Delaney (2008); Jones (2003); Tully and Mitchell (2001).

pygmy hedgehog vocalizations are outlined in Table 13.1. Because hedgehogs are omnivores, they have stronger jaws and their teeth are more blunt than most insectivores. (The biological profile for hedgehogs is presented in Table 13.2.) The dental formula of the African pygmy hedgehog is 2(3/2 incisors, 1/1 canines, 3/2 premolars, 3/3 molars) for a total of 36 teeth. The incisors are sharp, the canines are small, and the molars and premolars are flat and broad (Jones, 2003). The deciduous teeth appear around 18–23 days of age and permanent teeth erupt at 7–9 weeks of age. REPRODUCTION AND SEXING

Gender can be determined from the external anatomy: males have a longer anogenital dis-

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tance than females (Fig. 13.3). The male has a prepuce located midway along the ventral abdomen. The male does not have a scrotum but the testicles are perceptible by palpation. Hedgehogs are polygamous and females are capable of breeding at a young age. Hedgehogs are polyestrous and the mating season occurs year-round. The male courtship consists of enticing the female to mate by squeaking, hissing, nudging, and running in circles around her. The male should be removed if the female becomes aggressive, but reintroduction can be attempted at a later time. The male should also be removed after breeding occurs as his presence may lead to cannibalism of the young. The male does not perform a role in the care or rearing of the offspring. The female has a bicornuate uterus and a single cervix. Females are spontaneous ovulators and are sexually mature at 2 months; however, breeding should not occur before 6 months of age. After copulation a vaginal plug will be present and the female will not allow further attempts at mating. Gestation is between 34 and 37 days and average litter size is three. A female hedgehog is attentive to her offspring but may cannibalize or abandon them if she is stressed or disturbed after parturition. Baby hedgehogs are born blind and deaf, with eyes and ears fully functioning at 14–20 days of age (Pinney, 2003). Young hedgehogs have “nest spines,” which are just under the skin and emerge within hours after birth. These spines are shed at 1 month of age

Fig. 13.3 Male and female (Drawing courtesy of Ian Thomas.)

hedgehog.

and are replaced with permanent spines. Weaning generally occurs between 4 and 6 weeks of age. UNIQUE FEATURES OF IMPORTANCE

Hedgehogs are nocturnal, territorial, and solitary except during courtship and when raising offspring. In captivity, hedgehogs can become dormant during periods of prolonged environmental temperature stress, including excessive heat or cold, but they do not hibernate. The dormancy usually lasts for a few weeks but is not a continual state. This dormancy period leads to decreased metabolic rate and makes the hedgehog more susceptible to infection; therefore, environmental temperatures should be kept relatively stable to prevent this from occurring. Hedgehogs also exhibit a unique behavior known as anting or self-anointing (Fig. 13.4).

Fig. 13.4 Self-anting (anointing). (Photo courtesy of Dan H. Johnson, DVM, Avian and Exotic Animal Care, Raleigh, NC.) For color detail, please see color plate section.

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This behavior occurs when a hedgehog encounters a novel substance in its environment, licks, tastes, or chews the new substance and produces thick, frothy saliva, which is then applied to its spines. Self-anointing is a normal behavior thought to play a role in attracting mates, marking territory, communication among conspecifics, reducing skin parasites, or as a defense mechanism. Hedgehogs curl into a ball, extend their spines, puff up, and emit a hissing sound when they feel threatened. The spines are modified hairs composed of keratin that have sharp tips but are not barbed. The penetration of a spine through the skin of a handler may cause an allergic reaction. Heatley (2008) reports an average adult hedgehog has approximately 5000 spines.

HOUSING AND HUSBANDRY

Because hedgehogs are solitary in the wild and can be territorial, individual housing is recommended. Caging material should be smoothwalled and high enough to prevent escape, because hedgehogs are agile climbers. Many owners find glass aquariums or heavy plastic storage bins are suitable. A wire cover to prevent escape is suggested. Minimum recommended floor space should be 2’ × 3’ for each hedgehog (Ivey and Carpenter, 2004). Floors should be solid, as wire mesh may cause toe or foot trauma. Bedding should be kept clean and dry. Appropriate absorbent materials such as shredded newspaper, aspen shavings, hay, or crushed corncobs may be used as bedding substrate. Bedding should be approximately 3 inches deep to allow for digging and exploration. Owners should avoid using fabric as a bedding material as the fibers may be eaten or can become entangled in the feet, resulting in necrosis and possible amputation (Heatley, 2008). Aromatic wood shavings, especially cedar, should be avoided because they can lead to dermatitis of the feet and ventral surface. Bedding should be spot changed daily and changed completely on a frequent basis to prevent dermatitis and other problems associated with poor sanitation. Hedgehogs need a nest box slightly larger than the body size of the hedgehog. The box

Exotic Small Mammal Care and Husbandry

should contain smooth sides and be easily sanitized or replaceable. Suitable nest or hide boxes include cardboard or wooden boxes, polyvinyl chloride (PVC) tubes, or flowerpots. Because hedgehogs are nocturnal, owners should be aware they will likely be more active at dusk and dawn. Other cage accessories can include a solid-surface exercise wheel and litter pan. Open wire exercise wheels should not be used as they may cause damage to the limbs. Cage temperature should be 75 °F–85 °F (24 °C–30 °C). Placement of a heating pad under a portion of the cage can help accommodate this temperature range. The hedgehog cage should be located in an area free from drafts or direct sunlight. Because hedgehogs are frightened by loud noises and bright lights, place the cage away from noisy areas in the house. Low humidity, less than 40%, is preferred. A hygrometer and thermometer can be placed in the cage to aid in monitoring environmental conditions within the enclosure. Water should be provided ad libitum and can be provided in a sipper tube or in a heavy crock dish. Owners may also want to provide a shallow tub or pan with warm water for swimming (Tully and Mitchell, 2001).

NUTRITION

In the wild, hedgehogs are insectivores and omnivores. The ideal diet should be low in fat and high in protein. Commercial formulations are available but most are based on cat formulations. Food should not be provided ad libitum as this can lead to obesity, a common problem in captive hedgehogs. Johnson-Delaney (2002) suggests a nightly meal of two tablespoons of dry, reduced-calorie cat food or a mixture of dry and canned food or a good insectivore diet. Also one to two tablespoons of thawed mixed frozen vegetables sprinkled with a vitamin-and-mineral powder can be offered. Several times a week each hedgehog can be offered three to five insects and a one- or two-teaspoon offering of baby food meats or stews, hard-boiled egg, mealworms, pinky mice, horsemeat, or other various worms and insects. Hedgehog weight should be monitored to avoid overeating and to prevent obesity. Pinney (2003) warns snails or slugs

Hedgehogs

should not be fed due to potential parasites that may be harmful to hedgehogs. Ivey and Carpenter (2004) suggest the majority of the diet should consist of a commercially prepared hedgehog food. In addition, approximately one or two teaspoons of various moist foods (canned dog or cat food, low-fat cottage cheese, or cooked meat or egg) and one-half teaspoon of fruit or vegetables (apple, pear, berries, banana, grape, leafy greens, peas, tomatoes, squash, beans, or cooked carrots) may be given. Acceptable treats can be provided three to four times a week and include mealworms, crickets, and earthworms. Waxworms are high in fat and should be avoided. Milk causes diarrhea in hedgehogs and should not be included in the diet. Hard items such as raw carrots, nuts, and seeds can become wedged in the roof of the mouth and should not be provided to hedgehogs. Caloric intake and nutritional requirements vary based on gender, age, reproductive status, and activity level. The diet should be reviewed and adjusted as these factors change.

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Fig. 13.5 Hedgehog cage. (Photo courtesy of Lucinda Prevost.)

ENRICHMENT

Hedgehogs can be placed into a large escapeproof enclosure for exercise. Solid exercise wheels provide exercise and enrichment opportunities. Other enrichment items that may be of interest to hedgehogs include swimming tubs, toys, climbing structures, straw or hay, and cardboard tubes (Fig. 13.5).

Fig. 13.6 Normal hedgehog during physical examination. (Photo courtesy of Dan H. Johnson, DVM, Avian and Exotic Animal Care, Raleigh, NC.)

HANDLING, RESTRAINT, AND PHYSICAL EXAM

Even the tamest hedgehogs tend to roll up into a ball when a physical exam or other procedure is attempted (Ivey and Carpenter, 2004). Hedgehogs accustomed to being handled will likely submit to a physical exam (Figs. 13.6 and 13.7) without curling into a ball; however, isoflurane can be used with those that resist handling. Anesthesia in the hedgehog can be induced in an induction chamber and then maintained using a small mask (Tully and Mitchell, 2001). Hedgehogs rarely bite, but adult males may hiss (Johnson-Delaney, 2008).

Fig. 13.7 Hedgehog restraint. (Photo courtesy of Dan H. Johnson, DVM, Avian and Exotic Animal Care, Raleigh, NC.)

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Physical exams should be performed at least annually or semiannually, and fecal analysis is recommended. A brief examination may be performed while the animal moves around in its transport cage, but a thorough physical examination often requires chemical restraint (Table 13.3). CLINICAL TECHNIQUES

Sample collection—venipuncture Isoflurane is commonly used for anesthetic induction and maintenance. Premedication with atropine may lessen or prevent hypersalivation and is recommended. Injectable drugs such as ketamine, midazolam, xylazine, diazepam, tiletamine/zolazepam, and medetomidine can be used but recovery times are longer than with inhalants. Potential blood collection sites include the cephalic vein, lateral saphenous vein, jugular vein, and cranial vena cava. Small (1 mL or less) blood samples can be obtained from the cephalic, lateral saphenous, and femoral veins. Johnson-Delaney (2008) indicates a toenail clip can be used to collect a sample sufficient for several hematocrit tubes and a blood smear.

Drug administration Subcutaneous (SC) injections can be given in either the spiny or furred areas of the body. Fluids or drugs that are administered under the spiny skin may not be absorbed as readily as in the furred skin. Large volumes up to 100 mL/kg can be injected subcutaneously (Johnson-Delaney, 2008). Common intramuscular (IM) injection sites are the thigh and mantle (obicularis). Oral (PO) medications can be difficult to administer but injection into mealworms may be an alternate way to provide oral administration. Radiographic detail is hampered by the presence of the spines, and the use of anesthesia is usually necessary for proper positioning.

Sample collection—cystocentesis Urine can be collected for urinalysis by placing the hedgehog in a clean container (free-catch method). Urine can also be collected via cystocentesis performed via a ventral percutaneous

Exotic Small Mammal Care and Husbandry

approach or by catheterization under anesthesia (Heatley, 2008). PREVENTIVE HEALTH

Vaccination Currently, there are no recommended vaccines for pet hedgehogs; however, an annual or semiannual physical examination and fecal analysis is recommended. Heatley (2008) recommends a fecal culture for Salmonella spp. and a dermal fungal culture for households in which elderly adults or young children are present. Hedgehogs typically mask signs of illness so owners should be diligent in observing their hedgehog daily. Any changes in hedgehog behavior, eating or elimination habits, or physical characteristics should be brought to the immediate attention of a veterinarian.

Endoparasites and ectoparasites Skin diseases, including fungal disease, fleas, ticks, and mites, are common. Endoparasites include nematodes, cestodes, trematodes, and protozoans. Endoparasites can be diagnosed by finding parasitic ova or protozoa in a direct fecal smear or in a fecal flotation. Routine direct fecal parasite exams and fecal flotation can be used to diagnose internal parasites. Isospora erinacei and Eimeria rastegaiv are common coccidian parasites found in hedgehogs. Common nematodes include flukes (Brachylaemus erinacei), lungworms (Crenosoma striatum), tapeworms (Hymenolepis erinacei), and intestinal nematodes (Capillaria erinacei). Antiparasitic agents used in hedgehogs are presented in Table 13.4.

Dental health Dental and gum diseases, such as gingivitis and periodontitis, can be prevented by feeding an appropriate diet and by routine teeth brushing. Tartar-control treats marketed for dogs and cats may help loosen tartar. Nails should be trimmed regularly as they can quickly become overgrown or ingrown. A complete blood count, ECG, and chemistry panel are recommended for geriatric hedgehogs. Individual hedgehogs can be identified with microchips or application of a nontoxic paint applied to a few spines.

Table 13.3 Chemical restraint, anesthetic, and analgesic agents used in hedgehogs. Agent

Dosage

Use/comments

Acepromazine

0.1–1.0 mg/kg SC, IM, PO

Sedative; can combine with ketamine; hypotension may occur if used alone; atropine pretreatment may alleviate this effect

Atipamezole (Antisedan, Pfizer)

0.3–1.0 mg/kg IM

Reversal of medetomidine

Atropine

0.01–0.05 mg/kg SC, IM

Preanesthetic to avert hypersalivation

Buprenorphine (Buprenex, Reckitt & Colman)

0.01 mg/kg SC, IM q6–8h 0.01–0.50 mg/kg SC, IM q6–12h

Analgesia Analgesia

Butorphanol (Torbugesic, Fort Dodge)

0.2–0.4 mg/kg SC, IM q6–8h 0.3–0.5 mg/kg IM 1.0 mg/kg IM

Analgesia Analgesia

Diazepam

0.5–2.0 mg/kg IM

Mild sedation; may be given with ketamine for anesthesia; anticonvulsant

Enflurane

To effect

Induction and maintenance of anesthesia

Flunixin meglumine (Banamine, Schering-Plough)

0.03 mg/kg IM q8h 0.3 mg/kg SC q24h

Nonsteroidal anti-inflammatory

Halothane

To effect

Rarely used, isoflurane preferred

Isoflurane

3%–5% induction

Anesthetic of choice; generally occurs in an induction chamber or mask By mask or endotracheal tube

0.25%–3.5% maintenance Ketamine

5–25 mg/kg IM

Sedation; narcosis; anesthesia; do not use in neck where there is brown fat, may use in combination with diazepam or xylazine; prolonged, rough recovery

Ketamine (K) /diazepam (D)

(K) 5–20 mg/kg + (D) 0.5–2.0 mg/kg IM

Anesthesia; do not use in neck where there is brown fat

Medetomidine (Domitor, Pfizer)

0.05–0.10 mg/kg IM 0.2 mg/kg SC

Light sedation; reverse with atipamezole Heavy sedation; reverse with atipamezole

Medetomidine (M) / ketamine (K)

(M) 0.1 kg/kg + (K) 5 mg/ kg IM

Anesthesia; (M) can be reversed with atipamezole (0.3–0.5 mg/kg IM)

Medetomidine (M) / ketamine (K) / fentanyl (F)

(M) 0.2 mg/kg + (K) 2 mg/ kg + (F) 0.1 mg/kg SC

Anesthesia; good muscle relaxation; (M) can be reversed with atipamezole (1 mg/kg IM) and (F) can be reversed with naloxone (0.16 mg/kg IM)

Meloxicam

0.2 mg/kg PO, SC q24h

Analgesia

Naloxone

0.16 mg/kg IM

Reversal of fentanyl

Sevoflurane

To effect

Anesthesia

Tiletamine/zolazepam (Telazol, Fort Dodge)

1–5 mg/kg IM

Sedation; anesthesia; narcosis; prolonged, rough recovery

Xylazine

0.5–1.0 mg/kg IM

Anesthesia; may be administered with ketamine

Yohimbine

0.5–1.0 mg/kg IM

Reversal of xylazine

From: Carpenter (2005); Heatley (2008); Johnson-Delaney (2008).

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Table 13.4 Antiparasitic agents used in hedgehogs. Agent

Dosage

Use/comments

Amitraz (Mitaban, Pharmacia & Upjohn)

0.3% topical q7d × 2–3 weeks

Mites (Caparinia, ivermectin-resistant Chorioptes); may dilute; use with caution

Fenbendazole

10–15 mg/kg PO q14d × 2–3 treatments 5–30 mg/kg PO q24h × 5 days 25 mg/kg PO q10d

Nematodes

Fipronil

1 spray/hedgehog

Fleas, mites; safety unknown

Imidacloprid

½ puppy/kitten dose monthly, topical

Fleas

Ivermectin

0.2 mg/kg PO, SC q14d × 3 treatments

Mites (Caparinia); nematodes; a pyrethrinbased shampoo q7d × several treatments is often needed concurrently for full response Ectoparasites

0.2–0.4 mg/kg PO, SC q10– 14d × 3–5 treatments 0.5 mg/kg PO, SC q14d × 3 treatments

Nematodes (Crenosoma, Capillaria) Nematodes

Mites; resistance to the lower doses of ivermectin has been noted

Levamisole (1%)

10 mg/kg SC, repeat q48h; repeat prn q14d

Nematodes, including lungworms

Lufenuron

½ puppy/kitten dose monthly

Fleas

Mebendazole

<500 g BW—25 mg q12h >500 g BW—50 mg/kg × 5 days, repeat after 2–3 weeks

Capillaria, Crenosoma, Brachylaemus, Hymenolepsis, Physaloptera

Metronidazole

25 mg/kg PO q12h × 5 days

Intestinal protozoa

Permethrin (1%)

Topical

Mites; apply once with fine mist; treat animal and bedding

Praziquantel (Droncit, Bayer)

7 mg/kg PO, SC, repeat q14d

Cestodes, trematodes

Selamectin (Revolution, Pfizer)

6 mg/kg topically

Ectoparasites (fleas, mites)

Sulfadimethoxine

2–20 mg/kg PO, SC, IM q24h × 2–5 days, off 5 days, on 2–5 days 10 mg/kg PO q24h × 5–7 days

Coccidia

100–200 mg/kg SC q24h × 3 days

Coccidia

Sulfadimidine

Coccidia

From: Carpenter (2005); Heatley (2008); Johnson-Delaney (2008).

COMMON DISEASES

Obesity Obesity (Fig. 13.8) is one of the most common medical problems seen in pet hedgehogs. Obesity is due to overeating, feeding an improper diet, lack of exercise, or cold ambient temperature. Clinical signs include weight gain, listlessness, and lameness. The diet should be

evaluated and factors such as portion control and elimination or reduction in the amount of snacks should be considered.

Dental disease Typical signs of gingivitis and periodontitis are drooling, loss of appetite, and weight loss. These dental diseases may be prevented by daily brushing. Treatment includes profes-

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and acute death. Long-term prognosis is poor but hedgehogs can be maintained short-term with furosemide, enalapril, and digoxin.

Salmonellosis Several strains of salmonella occur in hedgehogs; therefore, owners should assume all hedgehogs can carry and transmit the pathogen. To reduce the risk of salmonella transmission, owners should wash their hands with soap and water after handling their pet or their cages and bedding. Pets should not be handled in food preparation areas nor should they be held close to your mouth. Antimicrobial agents used in hedgehogs are presented in Table 13.5.

Trauma Wounds and fractures can be caused from other hedgehogs or other pets in the household. Trauma can also be attributed to falls or being stepped on. Fig. 13.8 Obese hedgehog. (Photo courtesy of Dan H. Johnson, DVM, Avian and Exotic Animal Care, Raleigh, NC.) For color detail, please see color plate section.

sional veterinary dental cleaning and antibiotics, if necessary. Drooling associated with anting behavior is normal and should not cause alarm.

Dermatitis (chorioptic mange mites, fungal, bacterial) Skin parasites can be identified and treated. A review of the environmental and sanitary conditions should be performed to help eliminate and control parasites. Clinical signs include flaky skin, broken quills, and irritability (Pinney, 2003). Antifungal agents used in hedgehogs are presented in Table 13.6.

Liver disease Neoplasia Neoplasia in hedgehogs is typically signaled by nodules or masses on or under the skin, ulcerations, foul breath, drooling, anorexia, diarrhea, weight loss, and abdominal enlargement. There is an increased incidence of tumors in hedgehogs greater than 3 years of age and oral squamous cell carcinomas are common. Mammary gland and uterine tumors are common in females and are almost always malignant.

Heart disease Dilated cardiomyopathy is commonly observed in pet hedgehogs and generally affects older hedgehogs. Clinical signs include dyspnea, weight loss, heart murmur, decreased activity,

Liver diseases, including hepatitis, hepatosis, hepatic lipidosis, and neoplasia, can be due to chronic obesity, fatty diet, liver toxins, chronic bacterial infection, or genetic predisposition. Clinical signs include diarrhea, loss of appetite, weight loss, or even death.

Respiratory disease Pneumonia and rhinitis can be bacterial, fungal, or viral in etiology. Fluid therapy, oxygen therapy, and antibiotic or antifungal agents are treatment options. Signs include difficulty breathing, congestion, and sneezing. Predisposing factors for upper and lower respiratory tract infection include dusty or unsanitary bedding, malnutrition, and concurrent disease (Ivey and Carpenter, 2004).

Table 13.5

Antimicrobial agents used in hedgehogs.

Agent

Dosage

Use/comments

Amikacin

2.5–5.0 mg/kg IM q8–12h

Amoxicillin Amoxicillin/clavulanic acid (Clavamox, Pfizer) Ampicillin

15 mg/kg PO, SC, IM q12h 12.5 mg/kg PO q12h

Make sure animal is hydrated; do not use in renal disease Broad spectrum, palatable Broad spectrum, palatable

Cetiofur (Naxcel, Pharmacia & Upjohn) Cephalexin (Keflex, Dista) Chloramphenicol

20 mg/kg SC q 12–24h

Chlorhexidine (Nolvasan, Fort Dodge) Chlorhexidine shampoo (Hexadene, Virbac) Ciprofloxacin Clindamycin (Antirobe, Pharmacia & Upjohn) Enrofloxacin (Baytril, Bayer) Erythromycin

Gentamicin Gentamicin ophthalmic drops, ointment Metronidazole Mupirocin (2%) (Bactroban, GlaxoSmithKline) Nystatin, neomycin, thiostrepton, triamcinolone cream (Panalog, Fort Dodge) Oxytetracycline

10 mg/kg SC, PO, IM q12–24h

25 mg/kg PO q8h 30 mg/kg IM q12h 30–50 mg/kg IV q12h 50 mg/kg PO, SC, IM q12h 0.1–0.05% dilution, topical prn to affected area 2%–3% shampoo

Wound treatments; soaking; use at proper dilution Bacterial and fungal dermatitis

5–20 mg/kg PO q12h 5.5–10.0 mg/kg PO q12h

Broad-spectrum antibiotic Anaerobes, dental disease

2.5–5.0 kg/kg PO, IM q12h 5–10 mg/kg PO, SC, IM q12h 10 mg/kg PO, IM q12h

Broad spectrum: respiratory/GI/systemic Start at low end of dose Penicillin-resistant gram-positive cocci; Mycoplasma spp., Pasteurella spp., and Bordetella spp. infections; well-accepted Rarely indicated Corneal abrasions or conjunctivitis. Use as in dog or cat. Anaerobes Flagellates; infection Traumatic skin lesions or bacterial dermatitis Bacterial or mycotic dermatitis; allergic dermatopathy; anti-inflammatory; long-term use may slow healing Bordetella; administer in food × 5–7 days; broad spectrum Gram-positive cocci

2 mg/kg SC, IM q8h Topical to conjunctiva or cornea q8h 20 mg/kg PO q12h 25 mg/kg PO q12h × 5 days Topical to cutaneous lesions q12–24h Topical to cutaneous lesions q12–24h 25–50 mg/kg PO q24h

Penicillin G Piperacillin Spiramycin Sulfadimethoxine

40,000 IU/kg SC, IM q24h 10 mg/kg SC q8–12h 15 mg/kg PO × 8 days 2–20 mg/kg PO, SC, IM q24h

Terramycin ophthalmic ointment

Topical to conjunctiva or cornea

Thiabendazole, dexamethasone, neomycin solution (Tresaderm, Merial) Trimethoprim/sulfa Triple antibiotic ophthalmic ointment Tylosin (Tylan, Elanco)

Topical to cutaneous lesions or ear canal q12h prn 30 mg/kg PO, SC, IM q12h Topical to conjunctiva or cornea 10 mg/kg PO, SC q12h

From: Carpenter (2005); Heatley (2008); Johnson-Delaney (2008). 152

Gram-positive rods; enterobacteria; many resistant strains; not recommended Gram-positive infection Palatable to most hedgehogs Acute salmonellosis; bacteriostatic

Gingivitis Coccidiosis; gram-negative bacteria; may have slight nephrotoxicity Corneal abrasions or conjunctivitis; use as in dog or cat Bacterial or mycotic dermatitis; otitis externa; anti-inflammatory Respiratory infections; palatable Corneal abrasions or conjunctivitis, use as in dog or cat Mycoplasma; Clostridium; do not give IM as it causes muscle necrosis

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Table 13.6 Antifungal agents used in hedgehogs. Agent

Dosage

Use/comments

Chlorhexidine (Nolvasan, Fort Dodge)

2%–3% shampoo

Dermatophytosis

Enilconazole (Imaverol, Janssen)

Topical q24h

Dermatophytosis, dilute 1 : 50

Griseofulvin (microsize)

25 mg/kg PO q12h 50 mg/kg PO q24h × 14–21 days

Skin, deep mycoses; daily long-term therapy

Itraconazole (Sporonox, Ortho Biotech)

5–10 mg/kg PO q12–24h

Systemic mycoses

Ketoconazole

10 mg/kg PO q24h × 6–8 weeks

Mycoses; daily long-term use; best absorbed in acid environment

Lyme sulfur

2.5% q5–7days Topical

Dermatophytosis

Nystatin

30,000 IU/kg PO q8–24h

Superficial yeast infections

Tincture of iodine 2%

Topical

Dermatophytosis

From: Carpenter (2005); Heatley (2008); Johnson-Delaney (2008).

Table 13.8 Hedgehog complete blood count reference ranges.

Fig. 13.9 Hedgehog with wobbly hedgehog syndrome. (Photo courtesy of Dan H. Johnson, DVM, Avian and Exotic Animal Care, Raleigh, NC.) Table 13.7 Hedgehog serum biochemistry reference ranges. Blood urea nitrogen

13.3–15.0 mmol/L

Potassium

3.6–5.1 mmol/L

Sodium

132–138 mmol/L

Calcium

2.0–2.3 mmol/L

Phosphorus

2.0–3.8 mmol/L

Alanine aminotransferase (ALT)

39.7–68.9 IU/L

Serum glucose

81.5–116.1 mg/dL

Total bilirubin

0–0.1 mg/dL

Creatinine

0.2–0.4 mg/dL

From: Johnson-Delaney (2008); Tully and Mitchell (2001).

Hematocrit

28.0%–38.5% (avg. 36%)

Hemoglobin

9.9–13.2 g/dL

Neutrophils

1.6–2.8 × 103/mL

Lymphocytes

3.72–6.14 × 103/mL

Eosinophils

0.36–2.4 × 103/mL

Monocytes

0–0.084 × 103/mL

Basophils

0.096–0.45 × 103/mL

Platelets

230–430 × 103/mL

Serum protein

5.1–7.2 g/100 mL

Serum calcium

9.5–10.9 mg/dL

Albumin

3.4–3.6 g/dL

MCH

16.8–23.4 pg

MCHC

33.3–35.2 g/dL

MCV

49.1–53.2

RBC

4.4–7.64 × 106/mL

Reticulocytes

8%–15%

WBC

5.8–21 × 103/mL

From: Heatley (2008); Johnson-Delaney (2008); Jones (2003); Tully and Mitchell (2001).

Wobbly hedgehog syndrome Hedgehogs are affected by a neurodegenerative disease called wobbly hedgehog syndrome (WHS; Fig. 13.9). The prevalence of this disease in captive African hedgehogs is around 10% (Garner and Graesser, 2006). The onset of clinical signs can occur between 1 and 36

Table 13.9 Miscellaneous agents used in hedgehogs. Agent

Dosage

Use/comments

Atropine

0.05–0.2 mg/kg IM, SC

Bradycardia

Calcium glubionate

23 mg/kg PO q12–24h

Palatable

Calcium gluconate (10%)

0.5–50 mg/kg IM

Fracture repair, hypocalcemia

Cimetidine

10 mg/kg PO q8h

Treatment of gastric ulcers

Depo-Medrol

1.0–5.0 mg/kg SC, IM

Anti-inflammatory

Dexamethasone

0.1–1.5 mg/kg IM 1.0–4.0 mg/kg SC, IM, IV

Inflammation; allergies Shock

Doxapram

2–10 mg/kg IV, IP

Respiratory stimulant

Enalapril (Enacard, Merck)

0.5 mg/kg PO q24h

Vasodilator; heart failure; cardiomyopathy

Epinephrine

0.003 mg/kg IV

Cardiac arrest

Erythropoietin (Epogen, Amgen)

100 U/kg SC q48–72h

Chronic anemia

Flunixin meglumine (Banamine, Schering-Plough)

0.03 g/kg IM q8h 0.3 mg/kg SC q24h

Arthritis; chronic inflammation Arthritis; chronic inflammation

Furosemide

2.5–5.0 mg/kg PO, SC, IM q8h

Edema; diuretic

Glycopyrrolate

0.01–0.02 mg/kg SC

Bradycardia

Hyaluronidase (Wydase, Wyeth)

100–150 U/L

Add to SC fluids; facilitates fluid absorption in SC fat

Iron dextran

25 mg/kg IM

Anemia

Lactobacilli

½ tsp/kg q24h

Restore gastrointestinal flora

Lactulose

0.3 mL/kg PO q8–12h

Hepatic disease; encephalopathy; constipation

Methylprednisolone

1–2 mg/kg SC

Anti-inflammatory

Metoclopramide

0.2–0.5 mg/kg PO, SC

Antiemetic; gastrointestinal motility enhancer

Prednisolone

2.5 mg/kg PO, SC, IM q12h prn 10 mg/kg SC, IM

Allergies Shock

Sucralfate (Carafate, Hoechst Marion Roussel)

10 mg/kg PO q8–12h

Gastrointestinal ulcers

Theophylline

10 mg/kg PO, IM q12h

Bronchodilator

Vitamin A

400 IU/kg IM q24h × 10 days

Skin disorders; excessive quill loss; rule out infections

Vitamin B complex

1 mL/kg SC, IM

CNS signs; paralysis of unknown origin; anorexia; use small animal formulation

Vitamin C

50–200 mg/kg PO, SC q24h

Vitamin C deficiency; infections; gingival disease; support of recovery from all infections; can use 1 g ascorbic acid/L drinking water (change daily)

Vitamins, multiple

<1 drop/kg PO q24h

Subclinical deficiency; hand-rearing orphans

From: Carpenter (2005); Heatley (2008); Johnson-Delaney (2008).

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Hedgehogs

months of age. Clinical signs include falling to one side, scoliosis, seizures, tremors, exophthalmos, muscle atrophy, dysphagia, wasting, and paresis; however, these signs are not specific to WHS. Garner and Graesser (2006) suggest WHS may be an inherited disease influenced by diet, environmental factors, or infectious agents.

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veterinarian experience and animal’s overall status should be considered along with the available reference values (Tables 13.7 and 13.8) to diagnose and treat illness or disease conditions in the exotic pet species. Miscellaneous agents used in hedgehogs are presented in Table 13.9. REFERENCES

Musculoskeletal disease Musculoskeletal disease can manifest in lameness or a reluctance to move or walk. Common causes are overgrown nails, foot infections, obesity, fractures, and arthritis. Corneal ulcers and other ocular injuries occur frequently in hedgehogs. Treatment may be difficult to administer. The loss of vision in one or both eyes does not appear to impact hedgehogs’ ability to move around their cages.

TREATMENTS

Fluid administration Fluids can be administered via the cephalic vein using an insulin syringe or 26-gauge needle. This route generally requires anesthesia. Fluids can also be administered via intraosseous catheter. The catheter can be placed in the proximal or distal tibia or the trochanteric fossa of the proximal femur (Heatley, 2008). Fluids can be administered subcutaneously, intravenously (IV), or intraperitoneally (IP). LABORATORY NORMAL VALUES

A true reference range for African hedgehogs, consisting of data obtained from healthy animals, is not available; however, values from both ill and healthy animals have been used to construct the reference range tables that are currently available (Heatley, 2008). Therefore,

Carpenter, James W. 2005. Exotic Animal Formulary. Third edition. Saunders, St. Louis, MO, pp. 358–373. Garner, M.M., and Graesser, D. 2006. Wobbly Hedgehog Syndrome. Exotic DVM 8(3):57–59. Heatley, J.J. 2008. Hedgehogs. In Mitchell, M.A., and Tully, T.N., Jr. (eds.). Manual of Exotic Pet Practice. Saunders, St. Louis, MO, pp. 433–455. Ivey, E., and Carpenter, J.W. 2004. African Hedgehogs. In Quesenberry, K.E., and Carpenter, J. (eds.). Ferrets, Rabbits, and Rodents: Clinical Medicine and Surgery. Second edition. Saunders, St. Louis, MO, pp. 339–353. Johnson-Delaney, C. 2002. Other Small Mammals. In Meredith, A. and Redrobe, S. (eds.). BSAVA Manual of Exotic Pets, Fourth edition. BSAVA, Quedgeley, Gloucester, UK, pp. 108–112. Johnson-Delaney, C. 2008. What Veterinarians Need to Know About Hedgehogs. Exotic DVM 9(1):38–44. Jones, M.D. 2003. The Hedgehog. In Ballard, B., and Cheek, R. (eds.). Exotic Animal Medicine for the Veterinary Technician. Iowa State Press, Ames, IA, pp. 255–261. Pinney, C.C. 2003. Hedgehogs. In The Complete Home Veterinary Guide. Third edition. McGraw-Hill Professional, New York, pp. 501–508. Tully, T.N., Jr., and Mitchell, M.A. 2001. A Technician’s Guide to Exotic Animal Care. AAHA Press, Lakewood, CO, pp. 179–186.

Sugar Gliders

Sugar gliders (Petaurus breviceps) are small, nocturnal marsupial mammals native to Australia, New Guinea, and Tasmania (Fig. 14.1). Although sugar gliders have been kept in homes and zoos for many years, they are just becoming popular as a domestic pet. This popularity has led to a corresponding rise in the frequency of veterinary visits. COMMON BREEDS

Petaurus breviceps is a member of the Petauridae family. Petaurus means “rope dancer” or “tightrope walker,” and breviceps means “short headed.” There are seven subspecies of sugar gliders: P. breviceps breviceps; P. breviceps

Fig. 14.1 Sugar glider. (Photo courtesy of Dan H. Johnson, DVM, Avian and Exotic Animal Care, Raleigh, NC.) For color detail, please see color plate section.

14 longicaudatus; P. breviceps ariel; P. breviceps flavidus; P. breviceps tafa; P. breviceps papuanus; and P. breviceps biacensis, also known as the biak glider (Franklin, 2005). BASIC ANATOMY AND PHYSIOLOGY

The coloration of sugar gliders is blue-gray agouti fur on the back and sides, with a white or cream color on the chest, throat, and underbelly. There is a black stripe that extends from the nose to the base of the tail. There are black rings around the eyes that extend to the ears (Fig. 14.2). The fur is soft and silky to the touch. The head is wedge-shaped and, since sugar gliders are nocturnal, they have large,

Fig. 14.2 Sugar glider. (Photo courtesy of Judi Fox.)

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Fig. 14.4 Patagium. (Drawing courtesy of Ian Thomas.) Fig. 14.3 Sugar glider grasping plant. (Photo courtesy of Judi Fox.) For color detail, please see color plate section.

protruding, widely spaced eyes. The ears are large, erect, and hairless thus providing the sugar glider with a sharp sense of hearing. Sugar gliders have five toes on their hind feet, with an opposable first digit and syndactyly (fusion) of the second and third digits (Ness and Booth, 2004). The fused digits form a “hair comb” that is used to groom their coat (Tully and Mitchell, 2001). All digits contain a claw except the inner opposable first digit on the hind feet, which is used for grasping branches (Kelsey-Wood, 1996) (Fig. 14.3). The bushy tail is approximately as long as the body length and is used as a rudder during gliding. According to Kahn (2007), sugar gliders can glide up to 148 feet by using their tail to balance and steer. The tail is weakly prehensile and can coil around items. Sugar gliders have a large gliding membrane called a patagium (Fig. 14.4) that stretches from the outside tip of the fifth digit of the forelimb to the inside of the first digit of the hind limb on each side. REPRODUCTION AND SEXING

Determining the gender of sugar gliders is fairly easy. Males have a bifurcated (forked) penis located in the cloaca and a pendulous cloacal scrotum located cranial to the penis. The males have a frontal scent gland on top of their head that is often reported as a bald spot. Females

Fig. 14.5 Marsupial versus placental mammal reproductive tract. (Drawing courtesy of Ian Thomas.)

(Fig. 14.5) have a ventral abdominal pouch containing two mammae, two uteri, and two long lateral vaginal canals as well as a median or central vaginal canal. Both sexes have a cloaca, which is a common opening to the gastrointestinal tract, urinary duct, and reproductive tracts (Franklin, 2005). The biological profile of sugar gliders is presented in Table 14.1. Sugar gliders breed easily in captivity. Abdominal masses in the female sugar glider may indicate pregnancy. Litter size is generally one or two young, called joeys. Gestation is 15–17 days; once the joeys are born they instinctively find their way to the pouch, where they will remain for about 70 days. The young will venture out from the pouch but will return for protection and nursing for up to two months. Dystocia is rare in marsupials because the fetus is expelled early in gestation; however, marsupials are susceptible to other reproduc-

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Table 14.1 Biological profile. Body weight

Adult male: 110–160 g Adult female: 95–135 g Birth weight: 0.2 g

Body temperature

96.5 °F–97.9 °F (35.8 °C–36.6 °C)

Body length

16–21 cm (avg. 17 cm)

Tail length

16.5–21 cm (avg. 19 cm)

Reproductive data Sexual maturity Female: 8–12 months Male: 12–15 months Estrous cycle: 29 days in length Gestation length: 15–17 days Litter size: 1–2 (usually 2) Pouch emergence: 60–74 days Weaning age: 110–120 days Average life span in captivity: 10–15 years Seasonally polyestrous Polygynous (dominant male breeds with mature females in colony) Life span (captivity)

9–12 years

Heart rate

200–300 beats per minute

Respiratory rate

16–40 breaths per minute

Food consumption 15%–20% body weight/day From: Carpenter (2005); Johnson-Delaney (2002); Kahn (2008); Rivera (2003); Tully and Mitchell (2001).

tive problems with the most common being pouch eviction. Causes of eviction include overcleaning of the pouch by the dam, an overexcited or stressed dam, and overcrowding of the fetus. Accidental ejection of the fetus can occur in a dam if there is loss of muscle tone in the wall of the pouch (Carboni and Tully, 2008). The joey can be replaced into the pouch and a thin strip of surgical tape can be placed over the pouch opening to prevent ejection. The dam should be relocated to a quiet, dark area to give her time to calm down. UNIQUE FEATURES OF IMPORTANCE

Males have frontal, sternal, and urogenital scent glands. The frontal scent gland (Fig. 14.6)

Fig. 14.6 Frontal scent gland. (Photo courtesy of Dan H. Johnson, DVM, Avian and Exotic Animal Care, Raleigh, NC.)

is often mistaken as alopecia in adult males. The dominant male in the family group uses scent to mark other members of the family as well as their territory. Sugar gliders use scent as a way to communicate. Females also have scent glands and have a well-developed pouch, or marsupium, where the young are raised. Sugar gliders do not have the characteristic eupubic bones that support the pouch in many marsupial species. Sugar gliders are social and make an assortment of sounds. They can yap, buzz, drone, hiss, and scream (Bays et al., 2006). They quietly chatter, alert other sugar gliders with a yapping alarm call, and produce a high-pitched cry when angry. During periods of extreme cold temperature or food scarcity, sugar gliders can conserve their energy by going into torpor (a state of lowered physiological activity characterized by reduced metabolism, heart rate, respiration, and body temperature) for up to 16 hours per day. HOUSING

In the wild sugar gliders live in trees and sleep in nests during the day. They live in family units; as the unit increases in size, the mature young adults leave the family and seek mates from other units to make new families (KelseyWood, 1996). In captivity sugar gliders should be housed in pairs or larger groups (Fig. 14.7).

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Fig. 14.7 Pair of sugar gliders. (Photo courtesy of Judi Fox.)

In captivity there are many aspects of housing that must be taken into consideration including the following: 1. Space—the enclosure should be as spacious as possible to allow for exercise (Fig. 14.8). Ideally the cage will be taller than it is wide, to simulate the sugar glider’s natural arboreal environment. Space should allow for separate sleeping, feeding, and drinking areas. The minimum space required for a single-housed sugar glider is 20 × 20 × 30 inches (Kahn, 2007). 2. Accessibility—the enclosure should be made so it can be easily accessed and cleaned. The more accessible the cage, the more easily the enclosure can be cleaned and maintained. 3. Security—the housing enclosure should be secure so the sugar gliders cannot escape. Caging material should contain openings less than 0.5 inch in size. Latches should not be accessible or easily opened by the cage occupants. Kahn (2007) recommends the use of a lock to ensure security. 4. Safety—the enclosure should not contain sharp metal protrusions or other materials that could injure the sugar glider. Enclosure should not be made of galvanized wire due to possibility of heavy metal poisoning. 5. Temperature control—temperature should be relatively constant. Do not place cage near heating or air-conditioning vents. Cage temperature range should be should be 65 °F-75 °F, and rapid temperature fluctuations should be avoided.

Fig. 14.8 Sugar glider cage. (Photo courtesy of Judi Fox.)

Fig. 14.9 Sugar glider enrichment. (Photo courtesy of Judi Fox.) For color detail, please see color plate section.

6. Furnishings—natural wood branches, including pear, apple, and willow, can be used for climbing and perching (Fig. 14.9). The use of branches from almond, apricot, cherry, peach, or black walnut trees should

Sugar Gliders

Fig. 14.10 Sugar glider in nest box. (Photo courtesy of Dan H. Johnson, DVM, Avian and exotic Animal Care, Raleigh, NC.) For color detail, please see color plate section.

be avoided (Kahn, 2007). Branches should not be placed directly over food or water dishes. A nestbox should be provided for sleeping and should be located near the top of the cage (Fig. 14.10). Bottles or open bowls can be used for providing water. Separate food containers should be provided for dry and moist or wet foods.

HUSBANDRY

Food should be provided in one evening meal, whereas fresh water should be provided ad libitum. Food and water dishes should be washed daily and uneaten food should be discarded. Cage bars, perches, platforms, and branches should be cleaned regularly with a dilute bleach solution. Sugar gliders cannot be litter trained as they urinate and defecate at random. Fecal matter should be removed daily and the entire floor covering (shredded paper products or wood shavings) should be replaced weekly. Shredded newspaper, cedar wood shavings, and pine wood shavings should not be used as they can cause toxicity. NUTRITION

The sugar glider is an omnivore, meaning both plant and animal foods are necessary for a bal-

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anced diet. Protein, grain, fruits, and vegetables are the main components of a sugar glider diet. Food can be dry, semimoist, moist, or live. Drastic changes in diet should be avoided, and new foods should be introduced in small increments. Feeding time should be consistent. Exact amounts will depend on the age and breeding status of each individual but generally the diet should consist of 25%–35% protein, 65%–75% fruit, vegetable, and grain (KelseyWood, 1996). Enclosures containing more than one sugar glider should be provided with multiple food and water stations to allow each animal to access and obtain food and water. Fresh fruits such as apple, apricot, banana, cantaloupe, cherry, date, fig, grape, melon, orange, peach, pear, persimmon, pineapple, plum, prune, raisin, and strawberry can be offered. Preferred vegetables include asparagus, bean, beet, broccoli, carrot, cauliflower, celery, chives, cress, lentils (dried), lettuce, dandelion, parsley, peas, potato (boiled), soybean, spinach, tomato, and turnip. Suggested seeds and nuts are almond, Brazil nut, cashew nut, canary seed, hazelnut, peanut (unsalted), millet, pine nut, rice (boiled), safflower, semolina, sunflower, sweet corn, and tonic bird seed blocks (Kelsey-Wood, 1996). Protein sources can include beef, beef extracts, canned cat or dog foods, crickets, cheese, egg, hamburger, mealworms, poultry, sausage, and whitefish. Feeding fatty meats should be avoided, and invertebrates should be obtained from a pet store or a commercial breeder. Johnson-Delaney (1998, 2000) offers a successful captive sugar glider diet based on field research and consultation with various zookeepers, veterinarians, and naturalists (Table 14.2). It is recommended to feed fresh portions in the evening and to chop items together to reduce selection of favorite foods. Treats should be limited to 5% of daily consumption and include meats, diced fruits with multiple vitamin/mineral powder, bee pollen, crickets, worms, and various insects. Booth (2000) also offers a suitable captive sugar glider diet that is outlined in Table 14.3. The owner should present a total of 15%–20% of body weight daily. One diet from each group should be selected each day. Booth

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Table 14.2 Successful captive sugar glider diet (Johnson-Delaney).

Table 14.3 Suitable diet for captive sugar gliders (Booth).

Leadbeater’s Mixture = 50% of diet: 150 mL warm water 150 mL honey 1 shelled hard-boiled egg 25 g high-protein baby cereal 1 tsp vitamin and mineral supplement

Offer a total of 15%–20% of body weight per day. Select one diet from each group each day. Sugar gliders will benefit from an effort to provide a regular supply of vitamin- and mineral-enriched insects.

Mix warm water and honey. In a separate container, blend egg until homogenized. Gradually add honey–water mixture, then vitamin powder, then baby cereal, blending after each addition until smooth. Keep refrigerated until served. Insectivore/carnivore diet from commercial food manufacturer (Reliable Protein Products, Mazuri, or ZuPreem) = 50% of diet

Group 1: Insects

75% moths, crickets, beetles 25% fly pupae, mealworms

Meat mix

Commercial small carnivore or insectivore mix

Group 2: Nectar mix

1.5 cups fructose 1.5 cups sucrose (brown sugar) 0.5 cup glucose made up to 2 L with warm water Commercially available mixes have the advantage of balanced vitamin and mineral additives

Dry lorikeet mix

4 cups rolled oats 1 cup wheat germ 1 cup brown sugar 0.5 cup glucose 0.5 cup raisins or sultanas

Treat foods can include various chopped fruits; bee pollen, and vitamin and mineral supplement. From: Johnson-Delaney (1998, 2000).

Group 3: Fruits and vegetables

Select from diced apple, nectarine, melons, grapes, raisins, sultana, figs, tomato, sweet corn kernels, sweet potato, beans, shredded carrot, and butternut pumpkin

Greens

Mixed sprouts Lettuce, broccoli, and parsley Corn kernels, sultanas Vitamin and mineral supplement at manufacturer’s directions

Fig. 14.11 Sugar glider enrichment—perch. (Photo courtesy of Judi Fox.) From: Booth (2000).

(2000) recommends sugar gliders be provided a regular supply of vitamin/mineral-enriched insects. ENRICHMENT

The housing enclosure should provide the sugar glider with options for enrichment and stimulation. Enrichment toys can include commercially available rodent, large bird, or cat toys. Bird toys such as swings, ladders,

bells, and perches can easily interest sugar gliders (Fig. 14.11). Bones can be provided for chewing, and pieces of PVC pipe cut to an appropriate size can provide hours of play. Branches placed in the cage will allow sugar gliders to climb and exercise. Sugar gliders should be removed from their cage daily to allow for interaction with humans, although sugar gliders should never be left unattended outside their cage (Kahn, 2007).

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Table 14.4 Agents used for chemical restraint, analgesia, and anesthesia in sugar gliders. Agent

Dosage

Route

Atropine

0.01–0.02 mg/kg

SC, IM

Butorphanol (Torbugesic, Fort Dodge)

0.5 mg/kg q8h

IM

Butorphanol/acepromazine

(B) 1.7 mg/kg + (A) 1.7 mg/kg

PO

Diazepam

0.5–1.0 mg/kg

IM

Enflurane

To effect

Inhalational

Flunixin meglumine (Banamine, Schering-Plough)

0.1–1.0 mg/kg q12–24h

IM

Glycopyrrolate

0.01–0.02 mg/kg

SC, IM, IV

Isoflurane

5% induction 1%–3% maintenance

Inhalational Inhalational

Ketamine

20 mg/kg (follow with isoflurane)

IM

Ketamine/acepromazine

(K) 10 mg/kg + (A) 1 mg/kg

SC

Sevoflurane

1%–5%

Inhalational

From: Carpenter (2005); Ness and Booth (2004).

HANDLING, RESTRAINT, AND PHYSICAL EXAM

Conducting a thorough physical examination of the sugar glider can be a challenge as they are not tolerant of palpation and auscultation (Carboni and Tully, 2008). Visual observation of overall appearance as well as respiration can be achieved from a distance without actually handling the animal. Manual restraint is best tolerated by sugar gliders that are frequently handled or that have been hand-raised. The handler should be cautious because the glider may bite and try to escape. The best way to manually restrain a sugar glider is to hold the head between the thumb and middle finger and use the index finger to restrain the top of the head. The body can then be placed in the palm of the restrainer’s hand. More fractious sugar gliders can be restrained with a cloth bag. Owners should be requested to give consent for inhalational (isoflurane) anesthesia in order to perform a more complete physical examination (Fig. 14.12; Table 14.4).

Fig. 14.12 Sugar glider inhalational anesthesia. (Photo courtesy of Dan H. Johnson, DVM, Avian and Exotic Animal Care, Raleigh, NC.)

CLINICAL TECHNIQUES

Reference intervals for biochemical and hematologic values are presented in Tables 14.5 and 14.6.

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Table 14.5 Sugar glider serum biochemistry reference ranges.

Table 14.6 Sugar glider hematology values. Hematocrit

39.7%–53%

Hemoglobin

13.9–17.1 g/dL

Erythrocytes

7–17.8 × 106/μL

0.1–0.8 mg/dL

Mean corpuscular hemoglobin concentration

30–37 g/dL

Calcium

4.0–11 mg/dL

Mean corpuscular hemoglobin

18.2–20.6 pg

Phosphorus

3.8–6.0 mg/dL

Mean cell volume

58–62 μm3

Potassium

3.3–5.9 mEq/L

White blood cells

2.1–12.2 × 103/μL

Chloride

105–107 mEq/L

Neutrophils

0.2–3.0 × 103/μL

Sodium

135–145 mEq/L

Lymphocytes

1.6–9.6 × 103/μL

Alanine aminotransferase (ALT)

37–111 IU/L

Monocytes

0–3.0 × 103/μL

Aspartate aminotransferase (AST)

7–179 IU/L

Eosinophils

0.02–0.16 × 103/μL

Alkaline phosphatase

152–212 IU/L

Basophils

0–0.04 × 103/μL

Creatinine phosphokinase (CPK)

210–589 IU/L

Plasma proteins

5.6–6.9 g/dL

Cholesterol

159–162 mg/dL

Albumin

3.0–4.8 g/dL

Globulin

1.5–3.6 g/dL

Platelets

105–220 × 103/μL

Glucose

76–232 mg/dL

Blood urea nitrogen

18–24 mg/dL

Creatinine

0.2–1.1 mg/dL

Total bilirubin

From: Carpenter (2005); Kahn (2008); Ness and Booth (2004); Tully and Mitchell (2001).

From: Carpenter (2005); Kahn (2008); Ness and Booth (2004); Tully and Mitchell (2001).

Sample techniques—venipuncture Small-volume blood samples can be obtained from the cephalic, lateral saphenous, femoral, ventral coccygeal, or lateral tail vein or from the medial tibial artery (Johnson-Delaney, 2002). Larger blood samples (up to 1 mL in adults) can be obtained from the jugular or cranial vena cava while under general anesthesia. A 0.5- to 1-mL syringe and a 27- to 30gauge needle should be used for blood collection. A blood volume up to 1% of total body weight can be safely collected. Blood collection can be facilitated with the use of an inhalant anesthetic. Rivera (2003) describes the techniques for blood collection. Jugular vein blood collection: place the glider in dorsal recumbency with forelimbs positioned caudally. Moisten fur along the jugular groove and apply gentle pressure at the thoracic inlet. Insert needle at 30 °–45 ° angle in the jugular groove and apply negative pressure as the needle is advanced. The syringe will fill with blood when the jugular vein is penetrated.

Cranial vena cava blood collection: place the glider in dorsal recumbency with forelimbs extended caudally. Insert needle at the angle formed by the first rib and the manubrium. Aim the needle toward the contralateral hip joint at a shallow angle. Suction should be applied as the needle is advanced, and the syringe will fill with blood as the vessel is penetrated. Do not probe for the vessel with the needle, rather withdraw and retry. Medial tibial artery blood collection: Extend the hind limb with the medial aspect exposed. Moisten fur and visualize the artery, which runs from the stifle to the tarsus. Insert the needle at a 30 ° angle and apply suction. Apply gentle pressure after blood collection to prevent formation of a hematoma. Radiographic techniques are similar to those used in other companion animals. Gas anesthesia, mainly isoflurane and sevoflurane, is commonly used. Radiographs are particularly valuable in diagnosing pneumonia (Kahn, 2007).

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Sample collection—cystocentesis and fecal sample

Drug administration Injections can be given in a variety of routes and sites. Intravenous (IV) injections are difficult and require general sedation. Sites for IV injections are the cephalic and lateral saphenous veins. Intramuscular (IM) injections should be given in the epaxial muscles of the neck and upper thorax, or in the biceps, triceps, or quadriceps muscles. Subcutaneous (SC or SQ) injections should be given along the dorsal midline of the thorax. Care should be taken to not inject into the patagium.

Urine for urinalysis can be collected from the bottom of the cage in a small syringe, collected in a sterile container during manual expression, or via cystocentesis. To perform cystocentesis, sedate the animal and isolate the bladder. Insert a 25- or 27-gauge needle with a 0.5- to 1.0-mL syringe directly into the bladder and withdraw urine. Fecal material can be collected from the cage floor for fecal flotation and direct fecal smear.

Table 14.7 Antiparasitic agents used in sugar gliders. Agent

Dosage

Route

Carbaryl powder (5%)

Use sparingly

Topical or in nest boxes

Febantel/pyrantel pamoate

(F) 15 mg/kg + (P) 14.4 mg/kg

PO

Fenbendazole

20–50 mg/kg q24h × 3 days

PO

Ivermectin

0.2 mg/kg, repeat in 10–14 days

SC

Metronidazole

25 mg/kg q12h

PO

Oxfendazole

5 mg/kg single dose 10–20 mg/kg

PO PO

Pyrethrin powder

Use products safe for kittens

Topical

From: Carpenter (2005); Ness and Booth (2004).

Table 14.8 Antimicrobial and antifungal agents used in sugar gliders. Agent

Dosage

Route

Amoxicillin

30 mg/kg divided q12–24h × 14 days 30 mg/kg q24h

IM, PO IM, PO

Amoxicillin/clavulanic acid (Clavamox, Pfizer)

12.5 mg/kg divided q12–24h

PO, SC

Cephalexin

30 mg/kg divided q12–24h

PO, SC

Ciprofloxacin

10 mg/kg q12h

PO

Enrofloxacin (Baytril, Bayer)

5 mg/kg q12h

PO, SC, IM

Gentamicin

2 mg/kg divided q12–24h

SC, IM

Itraconazole

5–10 mg/kg q12h

PO

Lincomycin

30 mg/kg q24h × 7 days

IM

Metronidazole

25 mg/kg q12h × 7–10 days

PO

Trimethoprim/sulfamethoxazole

15 mg/kg q12h 50–57 mg/kg q24h

PO PO

From: Carpenter (2005); Ness and Booth (2004).

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PREVENTIVE HEALTH

Vaccinations are not currently required for sugar gliders, although tetanus toxoids may be considered. An annual or semiannual physical exam, fecal analysis, and review of diet and husbandry are recommended. Nails should be trimmed periodically. Nonbreeding male sugar gliders should be neutered to prevent development of scent glands. Coccidia and Giardia have been identified in sugar gliders (Ness, 1999). Diagnosis is based on the visualization of oocysts or trophozoites in a fecal sample. Sulfadimethoxine is recommended for treatment of coccidia; metronidazole is recommended for Giardia. Antiparasitic, antimicrobial, and antifungal agents used in sugar gliders are presented in Tables 14.7 and 14.8. COMMON DISEASES

Many diseases and disorders that occur in sugar gliders are directly related to nutrition and infectious agents (Kahn, 2007).

Exotic Small Mammal Care and Husbandry

gliders (Ness and Booth, 2004). A diet containing low calcium and vitamin D3 and high phosphorus is believed to cause this disease. A diet consisting of fruit and muscle meat can lead to a predisposition to nutritional osteodystrophy. Clinical signs are acute hindlimb paresis or hindlimb paralysis. Treatment options include cage rest, diet correction, supplementation of calcium and vitamin D3, and parenteral calcium.

Trauma Incidents of trauma in sugar gliders in captivity can occur from attacks from other household pets; these injuries can be fatal due not only to the trauma but also because of the potential infection associated with the bite (Ness and Booth, 2004). Household accidents, including falling into toilet bowls, being stepped on, being shut in a door or window, crashing into furnishings and walls, burning from landing on lamps or light bulbs, and chewing on electrical cords, can also cause trauma to sugar gliders. Ophthalmic injuries (mainly conjunctivitis and corneal scratches) are common due to their protruding eyes. Lacerations are also quite common.

Obesity Obesity is often seen in sugar gliders fed an inadequate diet high in fats and proteins (Rivera, 2003). The owner should be educated on proper feeding and nutritional requirements of the sugar glider. Obesity can also be attributed to lack of exercise. Obesity can lead to cardiac, hepatic, and pancreatic disease.

Dental disease Tartar buildup associated with carbohydraterich diets is common. Treatment includes teeth cleaning as needed. Prevention includes feeding insects with a hard exoskeleton to reduce tartar buildup.

Stress-related diseases Malnutrition Malnutrition is regularly observed in sugar gliders fed an inadequate diet. Malnutrition leads to other diseases, including hypoproteinemia, anemia, and hypocalcemia. Clinical signs are mostly nonspecific and can include lethargy, weakness, pale mucous membranes, dehydration, and cachexia. Treatment includes feeding an adequate diet and supportive care.

Nutritional osteodystrophy Nutritional osteodystrophy, also known as metabolic bone disease or nutritional secondary hyperparathyroidism, is one of the most common diseases that afflict captive sugar

Stressed sugar gliders are prone to develop behavioral problems. Clinical signs include alopecia, self-inflicted wounds, cage pacing, cannibalism, coprophagia (eating fecal material), trichophagia (fur biting), lignophagia (wood or shavings chewing), polyuria (excess urination), polydipsia (excess drinking), and hyperphagia (overeating). Identification and subsequent reduction or elimination of the stressors must occur in order to correct the behavioral problems. Kelsey-Wood (1996) lists the prime stressors as lack of housing space, incorrect diet, lack of climbing facilities, overcrowding, aggression by cage mates, poor hygiene, excess and sudden noises or disturbances, temperature fluctuations, and close proximity to stress-

Sugar Gliders

167

Table 14.9 Miscellaneous agents used in sugar gliders. Agent

Dosage

Route

Calcitonin

50–100 IU/kg

Calcium glubionate

150 mg/kg q24h

PO

Calcium glycerophosphate/lactate

7 mg/kg

IM

Cisapride

0.25 mg/kg q8–24h

PO, IM

Dexamethasone

0.1–0.6 mg/kg 0.5–2.0 mg/kg

SC, IM, IV SC, IM, IV

Metoclopramide

0.05 mg/kg q6–12h prn

PO, SC, IM

Vitamin A

50–5000 IU/kg

IM

Vitamin B complex

0.02–0.2 mL/kg

SC, IM

From: Carpenter (2005).

Fig. 14.13 Fluid therapy in a sugar glider prepared for surgery. (Photo courtesy of Dan H. Johnson, DVM, Avian and Exotic Animal Care, Raleigh, NC.)

ors located outside the cage such as household pets or children.

Neoplasia Neoplasia is common in sugar gliders, with lymphoid neoplasia listed as the most common tumor reported. Other tumors have been found in the liver, kidney, spleen, pouch, jaw, and lymph nodes (Kahn, 2007). TREATMENTS

Miscellaneous agents used in sugar gliders are presented in Table 14.9.

Fluid therapy is administered by routes commonly used in other small animals and includes intraosseous (IO), oral (PO), and subcutaneous routes (Fig. 14.13). Subcutaneous fluids should be administered along the dorsal midline of the thorax (Ness and Booth, 2004). Fluids should not be administered into the patagium as this can cause discomfort and distress to the sugar glider. Intraosseous fluids should be administered through an intraosseous catheter placed in the proximal femur. Fluid volume up to 10% of the sugar glider’s body weight may be administered (Tully and Mitchell, 2001).

REFERENCES Bays, T.B., Lightfoot, T., and Mayer, J. (eds.). 2006. Exotic Pet Behavior: Birds, Reptiles, and Small Mammals. Saunders, St. Louis, MO, pp. 328–340. Booth, R.J. 2000. General Husbandry and Medical Care of Sugar Gliders. In Bonagura, J.D. (ed.). Kirk’s Current Veterinary Therapy XIII Small Animal Practice. WB Saunders, Philadelphia, PA, pp. 1157–1163. Carboni, D., and Tully, T.N., Jr. 2008. Marsupials. In Mitchell, M.A., and Tully, T.N., Jr. (eds.). Manual of Exotic Pet Practice. Saunders, St. Louis, MO, pp. 299–325. Carpenter, J.W. 2005. Exotic Animal Formulary. Third edition. Elsevier Saunders, St. Louis, MO, pp. 347–358.

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Franklin, J. 2005. Natural History of the Sugar Glider (Petaurus breviceps). Exotic Mammal Medicine & Surgery. 3(2):7–9. Johnson-Delaney, C. 1998. Feeding Sugar Gliders. Exotic DVM 1(0):4. Johnson-Delaney, C. 2000. Medical Update for Sugar Gliders. ICE Proceedings 2(3):91–93. Johnson-Delaney, C. 2002. Other Small Mammals. In Meredith, A., and Redrobe, S. (eds.). BSAVA Manual of Exotic Pets. Fourth edition. BSAVA, Quedgeley, Gloucester, UK, pp. 102–106. Kahn, C.M. 2007. The Merck/Merial Manual for Pet Health. Home Edition. Merck & Co., Whitehouse Station, NJ. Kahn, C.M. 2008. The Merck Veterinary Manual. Ninth edition. Merck & Co., Whitehouse Station, NJ. Available at http://www.merckvetmanual.com/mvm/index.jsp (accessed September 2, 2008).

Exotic Small Mammal Care and Husbandry

Kelsey-Wood, D. 1996. Sugar Gliders as Your New Pet. TFH Publications, Neptune, NJ. Ness, R.D. 1999. Clinical Pathology and Sample Collection of Exotic Small Mammals. Veterinary Clinics of North America: Exotic Animal Practice 2(3):591–620. Ness, R.D., and Booth, R. 2004. Sugar Gliders. In Quesenberry, K.E., and Carpenter, J. (eds.). Ferrets, Rabbits, and Rodents: Clinical Medicine and Surgery. Second edition. Saunders, St. Louis, MO, pp. 330–338. Rivera, S. 2003. Other Species Seen in Practice. In Ballard, B., and Cheek, R. Exotic Animal Medicine for the Veterinary Technician. Iowa State Press, Ames, IA, pp. 269–272. Tully, T.N., Jr., and Mitchell, M.A. 2001. A Technician’s Guide to Exotic Animal Care. AAHA Press, Lakewood, CO, pp. 187–192.

Opossums

The Virginia opossum (Didelphis virginiana) is a marsupial that can be found in most of the United States east of the Rocky Mountains and on the West Coast (Figs. 15.1 and 15.2). It lives in habitats ranging from deciduous forests to farmland, and it prefers environments near marshes or streams. Although considered by some to be a nuisance in residential areas,

Fig. 15.1 Adult Didelphis virginiana. (Copyright Teekaygee, Dreamstime.com.) For color detail, please see color plate section.

15 others find “house possums” to be enjoyable pets, especially if hand-reared. Ownership of these wild animals is regulated or restricted by some states. BASIC ANATOMY AND PHYSIOLOGY

The dental formula in Virginia opossums is 2(5/4 incisors, 1/1 canines, 3/3 premolars, 4/4 molars). They have a prehensile tail that is used by young opossums to hang from trees. On their rear feet opossums have an opposable hallux, which acts like a thumb and facilitates grasping branches and climbing. The urogenital tract of female marsupials is very distinct from that of placental mammals. The cloaca is a common opening for the genitourinary tract and gastrointestinal tract. Opossums have mar-

Fig. 15.2 Juvenile Didelphis virginiana. For color detail, please see color plate section. 169

170

Table 15.1

Exotic Small Mammal Care and Husbandry

Basic biologic parameters.

Body weight

Adult male: 4–5 kg Adult female: 2 kg Birth weight: 2 g

Body length (including tail)

91 cm

Body temperature

32.2 °C–35.0 °C (90 °F–95 °F)

Reproductive data

Sexual maturity: 6–12 months Females polyestrous Estrous cycle: 23–28 days Ovulation: Spontaneous Gestation length: 12–13 days Litter size: 8–20 embryonic young Weaning age: 10–12 weeks

Life span (captivity)

7 years

Heart rate

70–228 beats per minute

Respiratory rate

25–40 breaths per minute

Food intake

150–200 g/day

Water intake

100–150 mL/day

From: Bergin (1986); Johnson-Delaney (2005).

supial bones, a fur-lined abdominal pouch, and 13 mammae (Carboni and Tully, 2009). Both males and females have cloacal glands that secrete a whitish, oily secretion. The basic biological parameters of opossums are presented in Table 15.1. Opossums are nocturnal. They are generally solitary, nonaggressive animals. When threatened, opossums will fake death, or “play possum,” to avoid attack from predators (Johnson-Delaney, 2005). REPRODUCTION AND SEXING

Females are easily distinguished from males by the presence of an abdominal pouch. Males have a forked glans penis posterior to the scrotum (Johnson-Delaney, 2005). (See Fig. 15.3.) The mating period is from January to July in warmer climates. Signs of estrus in female opossums include excessive salivating and rubbing or marking behavior. Males make a “clicking” sound when they detect females in estrus (Johnson-Delaney, 2005). Babies are

Fig. 15.3 Differentiation of male (left) and female (right) juvenile opossums.

born 13 days after mating. The dam prepares the pouch for the young by cleaning it in the days prior to parturition. After birth, the fetus will climb through the mother’s fur to the abdominal pouch or mammae (Carboni and Tully, 2009). Opossums generally raise 2 litters per year. The final litter size ranges from 1 to 15, but averages around 10 (Wildlife Medical Clinic, 2009). They remain in the pouch for 7–8 weeks and are weaned at approximately 5 months of age (Fig. 15.4). Spaying or neutering pet opossums is recommended to reduce the incidence of urogenital infections in females and odor and scent marking behavior in males. Male opossums can be neutered as performed for sugar gliders. A step-by-step reference for spaying female opossums can be found in Capello (2006). HOUSING AND HUSBANDRY

Opossums have been maintained in pairs or groups. Individuals or breeding pairs can be

Opossums

171

Fig. 15.4 Abdominal pouch with litter. (Photo courtesy of Dan H. Johnson, DVM, Avian and Exotic Animal Care, Raleigh, NC.) For color detail, please see color plate section.

housed in cages with a floor area of 45 cm × 75 cm and a sloping roof 80 cm at its highest end and 35 cm at its lowest (Bergin, 1986). Standard rabbit cages are also appropriate. A nest box should be provided. Standard rodent or rabbit bedding material is suitable for opossums. They normally live in a wide temperature range (50 °F–86 °F) but 72 °F is considered optimal (Johnson-Delaney, 2005). HANDLING AND RESTRAINT

It is advisable to wear heavy gloves and use towels when restraining opossums. A firm grasp of the head and the base of the tail is required to restrain the animal (Fig. 15.5). Opossums have very sharp teeth and may bite if not properly restrained. Opossums can be successfully restrained by methods used for fractious cats such as a “cat bag” or wrapping it up in a towel (Carboni and Tully, 2009).

Fig. 15.5

Manual restraint.

PHYSICAL EXAM

Opossums have a lower metabolic rate and body temperature than most mammals. The normal range is from 90 °F–99 °F. SAMPLE COLLECTION

Blood can be collected from the lateral tail vein in younger animals using a blind approach to the ventral aspect of the tail. Alternatively, the cephalic or saphenous veins can be accessed (Johnson-Delaney, 2005). Reference intervals for hematologic and biochemical values for opossums are presented in Table 15.2.

NUTRITION DRUG ADMINISTRATION

Opossums are omnivores. They can be fed a good quality dog or cat food in captivity, supplemented by vegetables and fruits. Live foods, such as mealworms and crickets, can be used to supplement their diet. Obesity is a common problem in captive opossums, so lower-fat foods are recommended.

Drug administration is performed as in other small mammal species. Intramuscular injections can be given in the large muscle mass in the thighs and arms. Intravenous injections can be given in the pouch veins or lateral tail veins. Subcutaneous injections and fluid administra-

172

Exotic Small Mammal Care and Husbandry

Table 15.2 Reference ranges for hematology and serum biochemical values for Didelphis virginiana.

Table 15.3

Formulary for Didelphis virginiana.

Agents Value

Reference Interval

Dosage (mg/kg)

Route

Antimicrobial Agents

RBC (×106 cells/μL)

3.3–6.5

Enrofloxacin

2.5–5.0 q12–24h

PO, IM, SC

Hemoglobin (g/dL)

8.3–17.9

Gentamicin

1.5–2.5 q12h

PO, IM, SC

Griseofulvin

20 q24h × 30–60 days

PO

Sulfadimethoxine

5–10 q12–24h

PO

Trimethoprim-sulfa

10–20 q12–24h

IM, PO

Hematocrit (%) WBC (×103 cells/μL)

28–51 3.9–22.9

Neutrophils (%)

11–67

Lymphocytes (%)

13–82

Chemical Restraint, Anesthesia, and Analgesia

Monocytes (%)

0–8

Eosinophils (%)

0–3

Atropine

0.02–0.04

IM, SC

Basophils (%)

0–3

Butorphanol

0.1–0.5 q6–8h

IM, SC, PO

Diazepam

0.5–2.0

IM, PO, IV

Total protein (g/dL)

3.8–8.0

Albumin (g/dL)

0.2–0.9

Globulin (g/dL)

3.7–7.1

Flunixin meglumine 0.1–1.0 q12–24h

SC, IM

Glycopyrrolate

0.01–0.02

IM, IV, SC

Ketamine

30–50

IM

2–3(K)/0.05– 0.1(M)

IM

Glucose (mg/dL)

64–145

Cholesterol (mg/dL)

80–203

Ketamine + medetomidine

Blood urea nitrogen (mg/dL)

23–60

Medetomidine

0.1

SC, IM

Meloxicam

0.2 q24h

PO, SC

Creatinine (mg/dL) Aspartate aminotransferase (U/L) Alaline aminotransferase (U/L) Alkaline phosphatase (U/L) Total bilirubin (mg/dL) Sodium (mmol/L)

0.4–7.3 250–339 68

Miscellaneous Agents Cisapride

0.25 q8–24h

PO, IM

Dexamethasone

0.2 q12– 24h (antiinflammatory); 0.5–2.0 (shock)

IM, SC, IV

Furosemide

1–5 q6–12h

SC, IM, PO

Metoclopramide

0.05–0.1 q6–12h

PO, SC, IM

Prednisone

0.1–0.2 q24h

IM, SC, PO

137 0.1–0.8 101–155

Potassium (mmol/L)

3.1–6.1

Phosphorus (mg/dL)

2.1–8.2

Calcium (mg/dL)

9.6–11.2

From: Johnson-Delaney (2005).

From: Johnson-Delaney (2005).

tion can be given in the intrascapular area. Oral suspension can be administered by syringe or by incorporating it in fruit that they will readily consume. COMMON DISEASES

Opossums carry diseases such as leptospirosis, tuberculosis, relapsing fever, tularemia, spotted fever, toxoplasmosis, coccidiosis, trichomonia-

sis, and Chagas disease. (See Table 15.3 for the opossum formulary.) They are definitive hosts for at least three species of Sarcocystis (S. neurona, S. falcatula, and S. speen) and serve as a reservoir for S. neurona, the etiologic agent of equine protozoal myeloencephalitis (EPM) in horses, in the southeastern United States (Dubey et al., 2001). They are often heavily parasitized. They are also susceptible to infestation with fleas, ticks, mites, and lice. Opossums are hosts for cat and dog fleas, especially in urban environments (UC IPM Online, 2009).

Opossums

REFERENCES Bergin, T.J. 1986. Monotremes and Marsupials Husbandry. In Fowler, M.E. (eds.). Zoo and Wild Animal Medicine. Second edition. WB Saunders, Philadelphia, PA, pp. 563–566. Capello, V. 2006. Surgical Technique for Neutering the Female Virginia Opossum. Exotic DVM 8(2):31–36. Carboni, D., and Tully, T.N. 2009. Marsupials. In Mitchell, M.A., and Tully, T.N., Jr. (eds.). Manual of Exotic Pet Practice. Saunders, St. Louis, MO, pp. 299–325. Dubey, J.P., Black, S.S., Rickard, L.G., Rosenthal, B.M., Lindsay, D.S., Shen, S.K., Kwok, C.H., Hurst, G., and Rashmir-Raven, A. 2001. Prevalence of Sarcocystis neurona sporocysts in

173

opossums (Didelphis virginiana) from rural Mississippi. Veterinary Parasitology 95(2–4):283–293. Johnson-Delaney, C.A. 2005. What Every Veterinarian Needs to Know About Virginia Opossums. Exotic DVM 6(6):38–43. UC IPM Online. 2009. Statewide Integrated Pest Management Program, Agriculture and Natural Resources, University of California. Available at http://www.ipm.ucdavis.edu/PMG/PESTNOTES/pn74123.html (accessed September 9, 2009). Wildlife Medical Clinic. 2009. Opossums. College of Veterinary Medicine, University of Illinois at Urbana-Champaign. Available at http://vetmed. illinois.edu/wmc/opossums.html (accessed September 9, 2009).

Index

Note: Page numbers in italics refer to Figures; those in bold to Tables. allergic sensitivities, 43 alopecia, in ferrets, 68 analgesia, for hamsters, 111–112 anesthesia for ferrets, 67 for guinea pigs, 124 for hamsters, 108, 111 for hedgehogs, 147 for sugar gliders, 163, 163 bacterial diseases, 23–40. See also specific diseases chlamydial infections, 37–38 enteric infections, 29–32 mycoplasmic infections, 40 respiratory infections, 32–37 ricksettsial infections, 38–40 systemic infections, 23–29 bacterial enteritis in guinea pigs, 120 in rabbits, 55 bartonellosis, 37–38 bedding, 14–15. See also under specific animals biochemical analysis, reference ranges for in chinchillas, 126 in ferrets, 66 in gerbils, 97 in guinea pigs, 119 in hamsters, 108 in hedgehogs, 153 in mice, 75 in opposums, 172 in rabbits, 53 in rats, 88

in sugar gliders, 164 bite wounds, 42–43 in chinchillas, 135 in mice, 79 blood collection. See under specific animals blood values. See biochemical analysis; hematologic analysis bordetellosis, 36 in guinea pigs, 120 in rabbits, 56 breeding, 4. See also under specific animals brucellosis, 23–24 cages. See housing; husbandry campylobacteriosis, 29–30 canine distemper virus (CDV), in ferrets, 70 cannibalization, of young in hamsters, 106 in hedgehogs, 145 catheterization of chinchillas, 135 of ferrets, 67, 72 of hedgehogs, 148, 155 of rabbits, 52 of sugar gliders, 167 cat scratch disease. See bartonellosis cheek pouches, in hamsters, 103, 104 chinchilla(s), 125–136 anatomy and physiology of, 125–126, 127 bedding for, 128

behavior of, 17, 126 bite wounds in, 135 blood collection from, 130 blood values for, 126 breeding in, 127–128 breeds of, 125 cages for, 128 choking in, 132 conjunctivitis in, 133 diet of, 129 drug dosages for, 131, 132, 133, 135 dust baths for, 129 endoparasites in, 132 enrichment strategies for, 17, 19, 128, 129 enteritis in, 134 formularies for, 131, 132, 133, 135 fur chewing in, 134 fur ring in, 133–134, 134 fur slip in, 134, 134 handling of, 129, 129 housing for, 128, 128 husbandry of, 128–129 listeriosis in, 135 malocclusion in, 132 neonates, 128 nutrition of, 129 physical examination of, 130 pseudomonas in, 134–135 reference ranges for, 126 reproduction in, 127–128 respiratory diseases in, 135 restraint of, 129, 129, 130 ringworm in, 132–133 sexing of, 126–127, 127 175

176

trauma in, 135 treatments for, 135–136 urinalysis, reference ranges for, 132 urine collection from, 130 venipuncture in, 130 circadian rhythms, 4–5 conjunctivitis in chinchillas, 133 in rabbits, 56 crepuscular mammals, 7, 12–13 cryptosporidiosis, 45–46 in guinea pigs, 120 cystocentesis in chinchillas, 130 in gerbils, 98 in guinea pigs, 119 in hedgehogs, 148 in rats, 88 in sugar gliders, 165 degu(s), 137–142 anatomy and physiology of, 137, 138 bedding for, 138–139 behavior of, 15, 137 blood values for, 140 breeding in, 138 breeds of, 137 cages for, 138–139 castration of, 137 diet of, 139 diseases of, 140–142 drug dosages for, 141 dust baths for, 139, 139 enrichment strategies for, 15, 17–18, 139 formularies for, 141 handling of, 139–140, 140 housing for, 138–139 husbandry of, 138–139 metabolic diseases in, 140–142 neonates, 138 neoplastic diseases in, 142 nutrition of, 139 ocular diseases in, 142 pseudomonas in, 140 reference ranges for, 140 reproduction in, 138 restraint of, 139–140, 140 sexing of, 138, 138 trauma in, 142 dermatologic diseases. See also specific diseases in guinea pigs, 121–123 in hamsters, 109–110 in hedgehogs, 151 in mice, 79

Index

in rabbits, 57–58 dermatophytosis (ringworm), 40–41 in guinea pigs, 123 in rabbits, 57 diet. See nutrition diseases. See specific diseases dust baths for chinchillas, 129 for degus, 139, 139 ectoparasites in chinchillas, 132 in ferrets, 67–68 in guinea pigs, 121–122 in hamsters, 109–110 in rats, 89 ehrlichiosis, 38 endoparasites in chinchillas, 132 in ferrets, 67–68 in hedgehogs, 148 in rats, 89 enrichment strategies, 11–19. See also under specific animals assessment for, 11 definition of, 11 enteritis in chinchillas, 134 in rabbits, 55 in rats, 90 erysipeloid, 32 ethogram, 11 feeding. See nutrition ferret(s), 61–72 adrenal disease in, 68–69, 68, 69 anatomy and physiology of, 61–63 anesthesia for, 67 bedding for, 63 behavior of, 16, 61, 65 blood collection from, 66–67 blood values for, 66 breeding in, 62 breeds of, 61 cages for, 63–64 canine distemper virus (CDV) in, 70 cardiac diseases in, 70 catheterization of, 72 cystocentesis in, 67 diet of, 64 drug administration in, 67 drug dosages for, 71 ectoparasites in, 67–68 endoparasites in, 67–68

enrichment strategies for, 16, 18, 64–65, 64 fluid administration in, 72 formularies for, 71 gastrointestinal diseases in, 69–70 handling of, 65–66, 65, 67 helicobacteriosis in, 69 housing for, 63 husbandry of, 63–64 lymphosarcoma in, 69 mites in, 67–68 neonates, 62 neoplastic diseases in, 68–69 neutering of, 62, 68 nutrition of, 64 nutritional support for, 72 physical examination of, 65–66 proliferative bowel disease (PBD) in, 69 reference ranges for, 66 reproduction in, 62 restraint of, 65–66, 65, 67 sexing of, 61–62, 62 treatments for, 70–72 vaccinations in, 67 venipuncture in, 66 fractures. See trauma fungal diseases, 40–41. See also specific diseases gastrointestinal diseases in ferrets, 69–70 in guinea pigs, 120 in hamsters, 110 in mice, 76–78 in rabbits, 53–56 gerbil(s), 93–101 abdominal gland disease in, 99 anatomy and physiology of, 93–94, 95 bacterial diseases in, 98–99 bedding for, 95–96 behavior of, 15, 93 blood collection from, 97 blood values for, 97 breeding in, 94–95 breeds of, 93 cages for, 95 congenital diseases in, 100 diet of, 15, 95–96 diseases of, 98–101 drug administration in, 97–98 drug dosages for, 98 enrichment strategies for, 15, 17–18, 95, 96, 96

Index

formularies for, 98 fungal diseases in, 100 handling of, 96 helicobacteriosis in, 99 housing for, 95 husbandry of, 95 mites in, 100 nasal dermatitis (“sore nose”) in, 99 nematodes in, 99 neonates, 94–95 neoplastic diseases in, 100 neurologic diseases in, 100 nutrition of, 15, 95–96 parasitic diseases in, 99–100 physical examination of, 96 reference ranges for, 97 reproduction in, 94–95 reproductive diseases in, 100 restraint of, 96 salmonellosis in, 99 sexing of, 94 tapeworms in, 99 toxicity in, 100 Tyzzer’s disease in, 98–99 venipuncture in, 97 guinea pig(s), 115–124 anatomy and physiology of, 116, 116 anesthesia for, 124 behavior of, 16, 115 bedding for, 118 blood collection from, 118–119 blood values for, 119 breeding in, 117 breeds of, 115 cages for, 117–118 cystocentesis in, 119 dermatologic diseases in, 121–123 dermatophytosis (ringworm) in, 123 diet of, 15, 116, 118 diseases of, 119–123 drug administration in, 123–124 drug dosages for, 122–123 ectoparasites in, 121–122 enrichment strategies for, 15, 17–18 formularies for, 122–123 gastrointestinal diseases in, 120 handling of, 118 housing for, 117–118 husbandry of, 117–118 malocclusion in, 116 mites in, 121–123

177

musculoskeletal diseases in, 123 neonates, 117 nutrition of, 15, 116, 118 physical examination of, 118 pododermatitis in, 121, 121 pregnancy toxemia in, 121 reference ranges for, 119 reproduction in, 117 reproductive diseases in, 120–121 respiratory diseases in, 120 restraint of, 118, 118, 119 salmonellosis, 120 sexing of, 116–117, 116, 117 treatment in, 123–124 hamster(s), 103–113 amyloidosis in, 111 analgesia in, 111–112 anatomy and physiology of, 103–104, 104 anesthesia for, 111 antibiotics for, 113 bedding for, 106 behavior of, 15, 103 blood collection from, 108–109 blood values for, 108 breeding in, 105–106 breeds of, 103 cages for, 106 cannibalization of young, 106 cheek pouches in, 103, 104 common breeds, 103 dermatologic diseases in, 109–110 diet of, 15, 106–107 diseases of, 109–111 drug administration in, 109, 109, 113 drug dosages for, 112 ectoparasites, 109–110 enrichment strategies for, 15, 17–18, 107, 107 flank glands in, 103–104, 105 formularies for, 112 gastrointestinal diseases in, 110 handling of, 107 Harderian glands, 103 hibernation in, 106 housing for, 106 husbandry of, 106 lymphocytic choriomeningitis (LCM) in, 110–111 metabolic diseases in, 111 mites in, 109–110 neonates, 106

neoplastic diseases in, 111 nutrition of, 15, 106–107 pinworms in, 110 reference ranges for, 108 reproduction in, 105–106 respiratory diseases in, 110–111 restraint of, 107, 108 sexing of, 105, 105 treatments for, 111–113 Tyzzer’s disease in, 110 urine collection in, 109 “wet tail” infection in, 110 handling, 8. See also under specific animals; see also restraint under specific animals hedgehog(s), 143–155 African pygmy hedgehog, 143–144, 143 anatomy and physiology of, 143–144, 144 anesthesia for, 147 bedding for, 146 behavior of, 17, 145–146 blood collection from, 148 blood values for, 153 breeding in, 145 breeds of, 143 cages for, 146 cardiac disease in, 151 cystocentesis in, 148 dental disease in, 148, 150–151 dermatologic diseases in, 151 diet of, 146–147 diseases in, 150–155 dormancy in, 145 drug administration in, 148 drug dosages for, 150, 152, 153, 154 endoparasites in, 148 enrichment strategies for, 17, 18–19, 147, 147 fluid administration in, 155 formularies for, 150, 152, 153, 154 handling of, 147–148 housing for, 146, 147 husbandry of, 146 liver disease in, 151 mites in, 151 musculoskeletal disease in, 155 neonates, 145 neoplastic diseases in, 151 neurologic diseases in, 153–155 nutrition of, 146–147

178

obesity in, 150, 151 parasitic diseases in, 148, 151 physical examination of, 147–148 reference ranges for, 153, 155 reproduction in, 145 respiratory diseases in, 151 restraint of, 147–148 salmonellosis in, 151 self-anting in, 145–146, 145 sexing of, 144–145, 145 teeth of, 144 trauma in, 151 treatment in, 155 urine collection in, 148 vaccinations in, 148 venipuncture in, 148 vocalizations of, 144 wobbly hedgehog syndrome in, 153, 153–155 helicobacteriosis, 31–32 in ferrets, 69 in gerbils, 99 in mice, 78 hematologic analysis, reference values for in chinchillas, 126 in degus, 140 in ferrets, 66 in gerbils, 97 in guinea pigs, 119 in hamsters, 108 in hedgehogs, 153 in mice, 75 in opposums, 172 in rabbits, 53 in rats, 88 in sugar gliders, 164 hemorrhagic fever w/ renal syndrome (HFRS), 41–42 housing, 5–14. See also under specific animals air quality in, 8–9 bedding for, 14–15 illumination in, 7 macroenvironment, 5 microenvironment, 5 noise in, 7 as nonsocial enrichment, 13–14 overcrowding and isolation in, 8 temperature/humidity control in, 6–7 ventilation in, 7 husbandry, 22. See also under specific animals Hymenolepsis diminuta and H. nana, 46–47

Index

in gerbils, 99 in rats, 89 leptospirosis, 27–28 in rodents, 27 listeriosis, 27 in chinchillas, 135 lyme disease (borreliosis), 28–29 lymphocytic choriomeningitis (LCM), 42 in hamsters, 110–111 in mice, 79 malocclusion, 4 in chinchillas, 132 in guinea pigs, 116 in rabbits, 4, 50 melioidosis, 32 mice, 73–80 anatomy and physiology of, 73, 73 bedding for, 74 behavior of, 15, 73 bite wounds in, 79 blood collection from, 76 blood values for, 75 breeding in, 74 breeds of, 73 cages for, 74 dermatologic diseases in, 79 diet of, 74 diseases of, 76–79 drug administration in, 76, 76 drug dosages for, 77–78 enrichment strategies for, 15, 17–18, 74 formularies for, 77–78 gastrointestinal diseases in, 76–78 handling of, 75 Harderian glands in, 73 helicobacteriosis in, 78 housing for, 74 husbandry of, 74 lymphocytic choriomeningitis (LCM) in, 79 mites in, 79 neurologic diseases in, 79 nutrition of, 74 physical examination of, 75–76 pinworms in, 78 preventative health in, 76 reference ranges for, 75 reproduction in, 74 respiratory diseases in, 78–79 restraint of, 75, 75 salmonellosis in, 78 sexing of, 73–74, 74

Tyzzer’s disease in, 78 urine collection from, 76 mites in gerbils, 100 in guinea pigs, 121–123 in hamsters, 109–110 in hedgehogs, 151 in mice, 79 in rabbits, 57–58, 58 in rats, 89 murine typhus, 39–40 mycoplasmosis, 40 in mice, 78–79 in rats, 90 nematodes (capillariasis), 46 in gerbils, 99 in hedgehogs, 148 in rats, 89 neonates, 4. See also under specific animals neoplastic diseases in degus, 142 in ferrets, 62, 68–69 in gerbils, 99, 100 in hamsters, 111 in hedgehogs, 151 in rabbits, 56 in rats, 90 in sugar gliders, 167 neurologic diseases in gerbils, 100 in hedgehogs, 153–155 in mice, 79 in rabbits, 57 nutrition, 6, 9. See also under specific animals as enrichment strategy, 15 for supplementation, 15 obesity in hedgehogs, 150 in opposums, 171 in sugar gliders, 166 opposum(s), 169–173 anatomy and physiology of, 169–170, 170 bedding for, 171 blood collection from, 171 blood values for, 172 breeding in, 170 breeds of, 169 cages for, 170–171 diet of, 171 diseases of, 172 drug administration in, 171–172 drug dosages for, 172 formularies for, 172

Index

handling of, 171 housing for, 170–171 husbandry of, 170–171 neonates, 170, 171 nutrition of, 171 obesity in, 171 physical examination for, 171 reference ranges for, 172 reproduction in, 170 restraint of, 171, 171 sexing of, 170, 170 spaying and neutering of, 170 parasitic diseases, 43–47. See also specific diseases helminthic, 46–47 protozoan, 43–46 pasteurellosis, 36 in rabbits, 56 physical examination. See under specific animals pinworms in hamsters, 110 in mice, 78 in rabbits, 56 in rats, 89 Pneumocystis carinii, 44–45 pseudomonas, 34 in degus, 140 rabbit(s), 49–59 anatomy and physiology of, 49–50, 50 bedding for, 51 behavior of, 16, 49 blood collection from, 52 blood values for, 53 breeding in, 50–51 breeds of, 49 cages for, 51–52 catheterization of, 52 cystocentesis in, 52 dermatologic diseases in, 57–58 diet of, 15, 52 drug administration in, 53 drug dosages for, 54–55 enrichment strategies for, 16, 18, 52 enteritis in, 55, 56 fecal examination in, 52 formularies for, 54–55 gastric stasis syndrome in, 53–55 gastrointestinal diseases in, 53–56 gastrointestinal tract in, 50 handling of, 49, 49, 52 housing for, 51–52

179

husbandry of, 51–52 malocclusion in, 50, 50 mites in, 57–58, 58 myiasis in, 58 neonates, 51 neurologic diseases in, 57 nutrition of, 15, 52 pasteurellosis in, 56 physical examination of, 52 pinworms in, 56 radiography in, 53–55 reference ranges for, 53 reproduction in, 50–51 reproductive diseases in, 56–57 respiratory diseases in, 56–57 restraint of, 49, 49, 52 scent glands in, 49 sexing of, 50, 51 sore hocks in, 49, 57 spaying and neutering of, 50 splay leg in, 57 teeth of, 50 Tyzzer’s disease in, 56 ulcerative pododermatitis in, 49, 57 urinalysis, reference ranges for, 53 rabbit fever. See tularemia radiography in rabbits, 53–55 in sugar gliders, 164 rat(s), 81–92 anatomy and physiology of, 82–83, 83 bedding for, 84 behavior of, 15, 81 blood collection from, 87, 88 blood values for, 88 breeding in, 83 breeds of, 81 cages for, 83–83 cystocentesis, 88 diet of, 84 drug administration in, 88 drug dosages for, 85–86, 91 ectoparasites in, 89 endoparasites in, 89 enrichment strategies for, 15, 17–18, 84, 84 enteritis in, 90 formularies for, 85–86, 91 handling of, 84–87 Harderian glands in, 82, 90 housing for, 83–84 husbandry of, 83–84 mites in, 89 neoplastic diseases in, 90 nutrition of, 84

physical examination of, 87 pinworms in, 89 porphyrin staining in, 90 preventative health in, 88–89 reference ranges for, 88 reproduction in, 83 respiratory diseases in, 90 restraint of, 84–87, 87 sexing of, 82, 83 teeth of, 82, 83, 87 treatments for, 90, 92 Tyzzer’s disease in, 90 ulcerative dermatitis in, 90 urine collection from, 88 venipuncture in, 87 rat bite fever, 35–36 reference ranges. See under specific animals reproduction, 4. See also under specific animals reproductive diseases in gerbils, 100 in guinea pigs, 120–121 in rabbits, 56–57 respiratory diseases in chinchillas, 135 in ferrets, 70 in guinea pigs, 120 in hedgehogs, 151 in mice, 78–79 in rabbits, 56–57 in rats, 90 restraint, 8. See also under specific animals; see also handling under specific animals rickettsial pox, 39 ringworm. See dermatophytosis Rocky Mountain spotted fever (RMSF), 38–39 rodent(s), enrichment strategies for, 15, 17–18. See also under specific animals salmonellosis, 30–31 in gerbils, 99 in guinea pigs, 120 in hedgehog, 151 in mice, 78 in rats, 90 sexing. See under specific animals sore hocks. See ulcerative pododermatitis Staphylococci, 34–35 in guinea pigs, 121 in hamsters, 109 in mice, 79 in rats, 90

180

Streptococci, 33–34 in guinea pigs, 120, 121 in hamsters, 109, 110 in mice, 79 in rats, 90 sugar glider(s), 157–168 anatomy and physiology of, 157–158, 159 anesthesia in, 163, 163 bedding for, 161 behavior of, 17, 159 blood collection from, 164 blood values for, 164 breeding in, 158–159 breeds of, 157 cages for, 160–161, 160 cystocentesis in, 165 dental diseases in, 166 diet of, 161–162, 162 diseases of, 166–167 drug administration in, 165 drug dosages for, 163, 165, 167 enrichment strategies for, 17, 18, 160–161, 160, 162, 162 fluid administration in, 167 formularies for, 163, 165, 167 handling of, 163 housing for, 159–161, 161 husbandry of, 160–161 malnutrition in, 166 neonates, 158–159 neoplastic diseases in, 167 nutrition of, 161–162, 162

Index

nutritional osteodystrophy in, 166 obesity in, 166 patagium in, 158, 158 physical examination of, 163 preventative health in, 166 radiography in, 164 reference ranges for, 164 reproduction in, 158–159 restraint of, 163 scent glands in, 159, 159 sexing of, 158 trauma in, 166 treatment in, 167 urine collection from, 165 venipuncture in, 164 vocalizations in, 159 thermo-neutral zone (TNZ), 6 thigmotaxis, 12 toxicosis, 8 toxoplasmosis, 43–44 transportation. See handling; restraint under specific animals trauma in chinchillas, 135 in degus, 142 in hedgehogs, 151 in sugar gliders, 166 tuberculosis, 25–26 tularemia (rabbit fever), 32–33 tumor(s). See neoplastic diseases typhus-like disease, 40 Tyzzer’s disease in gerbils, 98–99

in in in in in

guinea pigs, 120 hamsters, 110 mice, 78 rabbits, 56 rats, 90

ulcerative pododermatitis in guinea pigs, 121, 121 in rabbits, 49, 57 urinalysis, reference values for in chinchillas, 132 in rabbits, 53 vaccinations, for ferrets, 67 venipuncture in chinchillas, 130 in ferrets, 66 in gerbils, 97 in hedgehogs, 148 in rats, 87 in sugar gliders, 164 viral diseases, 41–42. See also specific diseases wobbly hedgehog syndrome, 153–155, 155 yersinosis, 24–25 zoonotic diseases, 21–47 bacterial, 23–40 definition of, 21 fungal, 40–41 parasitic, 42–47 transmission of, 21–22 viral, 41–42