Skip to main content
Elsevier - PMC COVID-19 Collection logoLink to Elsevier - PMC COVID-19 Collection
. 2009 May 18:299–315. doi: 10.1016/B0-72-169377-6/50031-9

Disease Problems of Small Rodents

Thomas M Donnelly
PMCID: PMC7150271

The most challenging medical diagnoses are those made in areas of discovery. All too often, the animal and its condition are familiar, and the diagnosis and treatment are routine. However, some cases involve original investigation in emerging fields of veterinary medicine.

The treatment of rodents as pets is one of these emerging fields, presenting a terrain bristling with complexities for many veterinarians. First among these is the common perception of rodents. Most people do not consider them pets, and they usually are called “vermin.” Moreover, almost all scientists consider rodents experimental tools. Veterinarians are not immune to such prejudices, and some may feel reluctant to examine a fully grown, red-eyed, wheezing rat. Owners of pet rodents often feel the same aversion for unsympathetic veterinarians and as a result travel long distances to see one who understands their needs. A second area of concern is the unfamiliarity of clinical veterinarians with rodent biology. Although much information has been accumulated on wild and laboratory rodents, very little of this information pertains to pet rodents. Geriatric diseases, the pharmacokinetics of common drugs, and the beneficial and harmful effects of human handling, contact, and care are a few of the phantom areas in this field. Yet the spectrum of problems affecting rodents does not differ greatly from that of dogs and cats.

One intent of this chapter is to describe the common diseases of pet rodents seen in practice so that their relative novelty becomes a challenge and not a stumbling block. Another is to inform clinicians about reasonable methods to diagnose common diseases of rodents accurately.

THE DIAGNOSTIC CHALLENGE

Pet Rodent Etiquette

Establishing and familiarizing the veterinary staff with a few simple rules of so-called pet rodent etiquette can make the physical examination a positive and fruitful experience. This preparation leaves the clinician confident and free of undue anxiety that can arise when he or she is presented with a concerned, overprotective owner. The veterinarian should be ready to apply his or her acumen and therapeutic skills toward treating the patient. Establishing clear communication between clinician and owner greatly facilitates the rodent's treatment and recovery.

Scheduling an Appointment

Rats and hamsters are essentially nocturnal animals and are only occasionally active during the day.55 In contrast, gerbils and mice are active during both the night and day.50 Healthy rodents are generally active during the awake part of their normal circadian cycle. When a sleep-deprived, drowsy, and irritable animal is brought to the clinician, subtle signs of diseases may be overlooked. This is especially true with hamsters. When possible, receptionists should schedule appointments for rats and hamsters during early evening hours. Appointment times are not as critical for gerbils and mice. Taking the time to explain the reasoning behind appointment scheduling to clients who are unwilling to make an evening appointment often not only changes their minds but also sets the veterinarian-client relationship off to a good start.

Instruct the client to bring the rodent to the hospital in its own cage. Husbandry and sanitation are essential to taking a good clinical history. Only by seeing the cage, water supply, feed containers, bedding, and food can the clinician understand the environment in which the rodent lives. Clients should be tactfully instructed not to clean the rodent's housing before the appointment because, by doing so, they may inadvertently destroy information important for diagnosis and treatment.

Reception Area

The waiting area for owners with pet rodents should be quiet. Receptionists should avoid planning appointments for natural predators, such as outdoor cats or hunting dogs, when a pet rodent is scheduled for an examination.

The rodent's sense of smell is well developed, and its world is rich in olfactory stimuli and pheromonal cues. Rodents are more sensitive to the effects of heat than cold. Even though wild golden hamsters and gerbils are desert-dwelling animals, their main method of thermoregulation involves escape from the heat by burrowing or seeking cool places. Mice in particular are very sensitive to the effects of heat. Waiting areas for rodents should be kept relatively cool. The dry-bulb temperature range of 64.4° to 78.8°F (18°−26°C), recommended by the National Institutes of Health, is ideal for housing rodents. Also, the opportunity for a habituated rodent to nestle next to the familiar smell of its owner can only be afforded in a quiet and safe waiting area.

Educating clients and receptionists about ways to make a trip to the clinic less stressful is well worth the time investment that it requires. If proper attention is devoted to education, then the veterinarian is likely to see a rodent amenable to examination instead of one ready to fight, flee, or cringe.

Medical History

In reaching a correct diagnosis, facts about the history and nature of a rodent's problem are generally more useful than the clinical history for a companion animal. Skill is required to extract a reliable, unbiased history of a pet's disease. Some owners are good at noticing changes and can provide important information, but others are not.

Find out what owners know about rodents. Have they had rodents as pets before? Where did they obtain their information on caring for their pet? Was it from the Internet, a book, a pet store, or first-hand experience? Books about rodents for owners of all ages are listed in the Suggested Reading section at the end of this chapter. Although these books are generally available, most veterinarians have not seen them. Many of these books are informative about husbandry requirements; however, many provide incorrect or misleading descriptions of diseases. For this reason, the sections on diseases must be carefully evaluated. Knowing your clients' sources of information further helps you assess their ability to provide an accurate history.

Do not become unsettled if an owner appears to know more than you do. Such a client can be very informative, enthusiastic, and willing to take an active role in treatment. When discussing a pet's problem with the owner, communicate on a level commensurate with his or her aptitude and background. Parents often present a sick rodent that belongs to their child, who is often the family member most knowledgeable about the pet's habits and behavior. When obtaining a medical history in these cases, the young owner's presence is invaluable.

Ask neutral questions that do not bias responses. For example, “Tell me about your rat's drinking habits.” Try to avoid direct or leading questions such as, “Have you noticed that your rat is drinking more water?” because they may influence the response. Posing general questions such as, “Anything else?”, “What do you mean?”, or “Tell me more about that” helps encourage the owner to elaborate on his or her responses. Do not be afraid to say, “I'm not sure what you mean,” and never belittle owners' opinions of their pets' illness. Try to obtain answers to the following specific questions:

  • Where did the pet come from? A pet store? A laboratory?

  • How long has the owner had the pet?

  • Are there other pets in the household? If so, are they the same species or another species?

  • What food does the owner give the pet? Where is the food purchased?

  • What food does the pet prefer and what does it actually eat?

  • Where is the food stored and for how long?

  • Who is responsible for feeding and cleaning? How routinely are these tasks performed?

  • How long have the signs of illness been apparent? Who first noticed them and why?

  • Has the pet's condition deteriorated, improved, or remained stable?

Pets isolated from other rodents and household animals and those acquired from a private breeder or laboratory are less likely to have infectious disease than are animals obtained from a pet store.

Many diseases are the result of poor or inappropriate diets. Pet rodents often selectively eat only one ingredient (e.g., sunflower seeds) when offered mixed-seed, vegetable, and fruit diets. In households with children, a regular feeding routine may not occur, and pets are inappropriately fed by doting children. Owners are often ignorant of the availability of specially formulated diets for laboratory rodents. These diets, which are pelleted, are convenient and nutritionally balanced sources of nourishment. However, most diets are only available in 50-lb bags and can only be purchased from wholesale feed distributors. A list of these diets and the feed manufacturers (and their web sites) can be found in the annual Buyer's Guide issue of Lab Animal (see Suggested Reading and Resources). Presently, two feed manufacturers, Oxbow Pet Products (Murdock, NE; www.oxbowhay.com) and Mazuri (St Louis, MO; www.mazuri.com have developed pelleted diets for pet rodents and rabbits. The diets are available in 2-, 5-, 10-, and 50-lb bags by direct order or from selected retail locations. Oxbow has also developed Critical Care, a product used specifically for force-feeding rodents and rabbits that are anorexic because of illness or recovery from surgery.

Clinical Examination

Seeing how a pet rodent is maintained provides information that is helpful in reaching a diagnosis or a reasonable prognosis. Information obtained from a physical examination is limited because of a rodent's size. However, the significance of the rodent's history and husbandry can only be evaluated after thoroughly examining the animal. With appropriate handling and a few specialized but simple pieces of equipment, the major organ systems can be thoroughly reviewed. If the same procedure is followed consistently, it eventually requires less and less time to perform.

Observe the pet rodent in its cage for activity, condition of grooming, and the presence of a head tilt or any discharge. If the rodent is dyspneic or depressed, be extremely careful when handling the animal because it is probably very sick and could die from the stress of a physical examination. Also warn the owner of your guarded prognosis.

Pet rodents that have been frequently and gently handled usually require minimal restraint. Less cooperative patients need to be more firmly restrained, and the use of a towel or even heavy gloves may be required (see Chapter 28). Although pet rodents do not often bite, their nips can be painful and may elicit an unfortunate reflex response from the handler that results in the pet being pitched onto the floor or at a wall. In addition to the potential for traumatic injury that this circumstance entails, the rodent may escape and become harmed.

In general, the first component of the physical examination that I perform is to accurately measure the patient's weight. Weight measurement is essential for calculating appropriate dosages of medications and provides an opportunity for gauging the rodent's temperament before the actual physical examination begins. Rodents are easily weighed in metal or plastic containers placed on a small digital scale or a triple-beam balance.

A binocular loupe and an otoscope are useful to evaluate physical signs. Start at the head, examining first the ears, eyes, and nose for discharge and the oral cavity for dentition. In most rodents except mice, the otoscope allows careful examination of the mouth and ears. Lymph nodes and glands of the head can be observed for size and palpated for consistency. Assessing the head is probably the most time-consuming part of the examination.

Palpate the abdomen for consistency and the presence of unusual masses. However, do not squeeze the animal too hard because overzealous palpation can result in visceral rupture. Examine the anogenital region for discharges and staining of the fur or skin. When a rodent is picked up, it generally urinates and defecates. Have a dipstick ready to perform an immediate urinalysis; feces can be caught in a small tube and examined later, if required. Observe the condition of the fur and assess the body condition in general. Palpate the limbs for tenderness or fractures and pay special attention to the paws, observing the length of the nails and the state of the footpads.

Respiration and heart rates are difficult to measure in rodents because rates are very rapid. Instead, look for signs of dyspnea. A sensitive pediatric stethoscope is useful to auscultate large rodents. Some respiratory infections, such as mycoplasmosis, are clinically silent. These diseases can be better heard than seen; abnormal sounds called “snuffling” in rats and “chattering” in mice are noticeable without a stethoscope.

The value of determining rectal temperature is questionable. A rodent is stressed by the examination, and as a result its body temperature increases. Furthermore, it is easy to cause rectal damage and prolapse in these animals because of their small size. Finally, most thermometers are too big to use in pet rodents. However, rectal temperatures can be measured safely by using small, semiflexible temperature probes connected to a digital clinical thermometer. These probes are reusable; are available in polyvinyl chloride, nylon, and Teflon; and range in size from 1 to 3 mm in diameter. They are ideal for monitoring body temperature when performing surgery on pet rodents. A list of manufacturers can be found in the annual Buyer's Guide issue of the journal Lab Animal (see Supplemental Reading and Resources) listed under “Research/Animal Research Equipment/Temperature Probes.”

The clinician can obtain a small amount of blood for a smear and microhematocrit from a hind-limb skin stab, nail-clip, or nick of the tip of the tail (see Chapter 28). Obtaining larger amounts of blood for a complete blood count and biochemical analysis may not be practical because of the quantity and quality of blood required. Rats often have chronic renal disease; a blood urea nitrogen concentration can be estimated by using a blood dipstick, and proteinuria can be detected by urine dipstick analysis.

Technologic advances have made possible electrocardiography and accurate and sensitive recordings of heart rate, respiratory rate, and blood pressure. However, the cost of this equipment may prohibit its use in most small exotic animal practices. Advances in high-resolution film screen combinations that require relatively low radiographic exposures and developments in ultrasound have allowed diagnostic imaging to become a useful, ancillary examination. A 1993 review describes the limitations of diagnostic imaging in small pets.67 The Atlas of Diagnostic Radiology of Exotic Pets contains many excellent radiographs of the anatomy of rodents in health and disease.61

DISEASES

General Comments

Diseases of small rodents seen in practice

The prevalence and type of small rodent diseases seen in practice are quite different from those seen in a research setting. Although this may seem rather obvious, much of the literature describing the maladies of pet rodents has been indiscriminately inferred from conditions seen in laboratory rodents. The diagnosis and treatment of pet rodents involve evaluation and care of an individual animal in a household, not the health management of rodents from a research colony. Derangements likely to be seen in practice include trauma-induced injuries, infectious diseases, and problems related to nutrition and aging; genetic disorders are uncommon. Natural infections that would be considered rare in a laboratory animal colony often are transmitted to rodent pets by other pets and by children; for example, pet animals other than rodents are a major reservoir of dermatophytes,24 and human beings are the main natural host of Streptococcus pneumoniae and Streptococcus pyogenes.41 Rodents used for research are maintained in tightly controlled environments designed to reduce the impact of unwanted variables in animal experiments.18 However, pet rodents generally are exposed to temperature, humidity, and light-cycle changes; a broad range of foods; numerous microorganisms borne by animals and human beings; and various types of handling. As a result, pet rodents exhibit a wider range of physiologic and pathologic responses than do rodents used for research. Consequently, the disease presentation of many pet rodents does not conform to the classic description of the disease.

Veterinarians must be discerning in selecting information about rodents. Research-oriented scientific publications can be more confusing than helpful for small pet practice. Many research articles treat rodents as part of a herd or as experimental tools, and disease is diagnosed at necropsy. Successful diagnosis and resolution of disease are not addressed, and it is in this area that our understanding must be broadened. Fortunately, exceptions to this are now becoming more numerous. Clinical case reports and columns such as “What's Your Diagnosis?” in laboratory animal journals are more numerous and clinically oriented, and several newer publications specifically address problems seen in pet rodents. Some suggested sources of information for veterinarians are listed under Suggested Reading and Resources.

Significant diseases and life spans

Pet mice, rats, gerbils, hamsters, and degus are subject to a limited number of naturally occurring medical problems. The most common, spontaneous outbreaks of disease are caused, or at least stimulated, by shortcomings in feeding and management. Some of these problems, unique to each species, are listed and grouped by the primary organ system affected in Table 29-1 . The average life span of each species is also given. Most problems in these species are dermatopathies, enteropathies, or pneumonia. Certain problems such as malnutrition, hypothermia, and trauma, which are also commonly seen in small exotic animal practice but are not necessarily unique to a species, are not presented.

TABLE 29-1.

Common Problems of Small Rodents Seen in Clinical Practice

SPECIES (AVERAGE LIFE SPAN)
Organ System Mice (1.5–2.5 years) Rats (2–3 years) Hamsters (1.5–2 years) Gerbils (3–4 years) Degus (7–10 years)
Integumentary and mammary gland Alopecia, bite wounds, ectoparasites, mammary neoplasia Ulcerative dermatitis, mammary gland neoplasia Bite wounds, scent gland tumors, cutaneous lymphoma Nasal dermatitis, ventral gland, lesions, tail-slip
Digestive Neonatal enteritis, endoparasites Salivary gland inflammation, incisor overgrowth Diarrhea, enterotoxemia, weight loss Enteritis
Respiratory Chronic respiratory disease Chronic respiratory disease, pneumonia Pneumonia Pneumonia
Urinary Urinary obstruction Chronic renal disease
Reproductive Vaginal discharge, maternal cannibalism
Ocular Red tears Exophthalmos Cataracts
Cardiovascular Atrial thrombosis, congestive heart failure
Endocrine Hyperadrenocorticism Diabetes mellitus
Nervous Epileptic seizures

Prophylaxis for small rodents

Prevention of disease in rodents is far more successful than treatment. Disease prevention is primarily based on common-sense husbandry practices, such as purchasing healthy, genetically sound animals; supplying balanced fresh food appropriate in protein and caloric content; providing clean, fresh water; furnishing adequate shelter that includes shade from direct sunlight; avoiding drafts and excessive temperature or humidity changes; keeping cages clean by preventing the accumulation of excess feces and urine; isolating sick animals from a group for treatment; and protecting vulnerable animals from more aggressive members of their group (e.g., young animals from older animals and male hamsters from female hamsters) or from natural predators living in the same household (e.g., mice from cats). Other sound husbandry practices include housing different species separately to prevent interspecies disease transmission (e.g., rats carry Streptobacillus moniliformis in their nasopharyngeal cavity, which causes septicemia in mice) and reducing obesity by limiting food intake and providing cage accessories that allow play and exploration (e.g., exercise wheels, tunnels, and ramps).

Unlike larger companion animals, pet rodents are not vaccinated. The introduction of ivermectin, although not approved for use in any rodent species, has allowed routine systemic treatment of pet rodents with pinworms and mites.

Dental problems are seen in pet rodents because of their continually erupting teeth. Overgrown incisors are seen most frequently in rats and mice. Specially designed cheek dilators, mouth specula, rongeurs, and filing rasps for treating dental problems are now commonly available (see Chapter 34).

Clinical Signs and Treatment

Mice

Integumentary system and mammary glands

Most of the problems seen in pet mice are associated with the skin. A survey from a large research animal diagnostic laboratory indicated skin disease in mice represents 25% of all cases (for all species) submitted for diagnosis.37 I categorize four groups of skin problems in mice: behavioral disorders, husbandry-related problems, microbiologic and parasitic infections, and idiopathic conditions. Behavioral, husbandry-related, and infectious causes of skin disease are relatively straightforward to diagnose and treat. However, many skin diseases characterized by chronic or ulcerated skin (often secondarily colonized by bacteria) are diagnosed as idiopathic. This group is commonly unresponsive to either topical or systemic treatment, and affected individuals are often euthanatized.

Mice exhibit well-studied social and sexual behavior. Social dominance, a form of behavior relating to the social rank and dominance status of an individual mouse in a group, is manifested as barbering and fighting. Barbering is a unique condition seen in group-housed mice in which the dominant mouse nibbles off the whiskers and hair around the muzzle and eyes of cagemates (Fig. 29-1 ). There are no other lesions, and only one mouse (the dominant one) retains all its fur. Removing the dominant mouse stops barbering; frequently, however, another mouse assumes the dominant role. Barbering is often seen in female mice caged together. Male mice, except littermates raised together from birth, are more likely to fight, often very savagely, and inflict severe bite wounds on one another, especially over the rump, tail, and shoulders.

Figure 29-1.

Figure 29-1

Barbering in a mouse. Barbering is often seen in mice housed in groups, in which the dominant male chews the facial hair and whiskers of his cagemates.

Mechanical abrasion resulting from self-trauma on cage equipment is a form of husbandry-related alopecia. Small patches of alopecia appear on the lateral surfaces of the muzzle. These result from metal feeders that chafe, poorly constructed watering device openings, and metal cage tops. Unlike barbering, dermatitis may also be associated with the alopecic area. Treatment consists of replacing the poorly constructed equipment with nonabrasive equipment.

Individually housed mice can display aberrant stereotypic behavior such as polydipsia and bar chewing that results in mechanical abrasion and alopecia. In this situation, replacing the cage equipment does not help. Instead, provide environmental enrichment toys such as running wheels or hollow tubes. Nursing mice often have ventral abdominal and thoracic alopecia; this is normal and is nearly always associated with the extensive distribution of mammary glands. Absorbent cotton or cotton-wool may wrap around the legs of suckling mice and cause necrosis and sloughing of limb extremities.58

Most infectious causes of alopecia and dermatitis are associated with fur mites. Generalized thinning of the hair, especially on difficult-to-groom areas such as the head and trunk, is seen (Fig. 29-2 ). The coat often appears greasy and, in cases of heavy infestation, mice are noticeably pruritic with self-inflicted dermal ulcers. Three mite species are commonly seen: Myobia musculi, Myocoptes musculinus, and Radfordia affinis. The most clinically significant species is M. musculi, but infestations are usually caused by more than one species. Mites are spread by direct contact with infected mice or infested bedding. Diagnosis is based on identifying adult mites, nymphs, or eggs on hair shafts with a hand lens or a stereoscopic microscope. Adults and nymphs appear pearly white and elongate (being about twice as long as they are wide); eggs are oval and seen attached to the base of hairs or inside mature females.

Figure 29-2.

Figure 29-2

A, Alopecia is commonly associated with mite infestation in mice. B, Noticeable pruritus and self-inflicted dermal ulceration may be observed. Three mite species are commonly seen: Myobia musculi, Mycoptes musculinus, and Rhadfordia affinis.

Treat mice with mite infestations with ivermectin (0.2 mg/kg SC or PO) twice at 10-day intervals. Alternatively, place a few drops of ivermectin solution (diluted to 1:100 in equal parts of water and propylene glycol for three treatments) on the mouse's head to allow spread by grooming and ingestion.6 Fragrant wood chips such as cedar and pine are high in volatile hydrocarbons and have long been known to have ectoparasiticidal properties. However, the hydrocarbons also induce cytochrome P-450 enzymes in the liver, which increase the metabolism of many common anesthetics and drugs (e.g., the sleep time of pentobarbital is decreased). Fragrant wood chips may also be associated with skin hypersensitivity, so I recommend replacing this type of bedding with paper or recycled paper litter.

Sometimes an owner presents a single pet mouse with clinical signs of mite infestation but with no evidence of mites or known history of recent exposure to other animals. Biopsy samples may be useful in these cases to distinguish active acariasis from dermal hypersensitivity to mites or other allergens such as wood chip bedding. Dermal hypersensitivity to M. musculi is well described in certain inbred strains of mice (B6 and NC) and is characterized by severe pruritus, the presence of fine dandruff all over the body, and occasionally ulcerative dermatitis.23 The prevalence of dermal hypersensitivity in outbred pet mice strains is unknown. In these cases, treat the mouse with ivermectin as if it had clinical acariasis and monitor treatment response. If unresponsive, categorize these mice into the idiopathic group and offer the owner additional diagnostic tests and treatments.

Ringworm is uncommon in pet mice but can be caused by Trichophyton mentagrophytes. Lesions, when present, are most common on the face, head, neck, and tail. The lesions appear scruffy with patchy areas of alopecia and variable degrees of erythema and crusting. Pruritus is usually minimal to absent, and the lesions do not fluoresce under a Wood's lamp.19

Skin swellings are usually tumors or abscesses. Results of fine-needle aspirate often reveal the nature of the contents and allow diagnosis. Three bacterial species, Staphylococcus aureus, Pasteurella pneumotropica, and S. pyogenes, have been isolated as the causes in various well-described cases.15 All are considered opportunistic pathogens and can cause abscesses in other organs (e.g., P. pneumotropica is sometimes associated with conjunctivitis, panophthalmitis, and swollen eye abscesses). Antibiotic therapy with penicillins or cephalosporins, concurrent with drainage and debridement of the abscess, is effective.

Idiopathic skin disease in mice is characterized by ulcerative dermatitis with pruritus. In affected mice, test results for primary ectoparasitic, bacterial, or mycotic infections are negative. Histopathologic and immunofluorescent microscopic examination of selected inbred strains of mice have revealed an underlying vasculitis attributed to immune complex deposits in dermal vessels. In these mice, dietary factors and dysregulated fatty acid metabolism have been implicated in the pathogenesis. Two treatments appear to alleviate or resolve lesions. Gavaging affected mice with 0.1 mL/day of liquid from Derm Caps (DVM Pharmaceuticals, IVAX Corporation, Miami, FL), an essential fatty acid supplement containing omega-3 fatty acids, regressed lesions and resolved pruritus in 10 of 10 affected mice.42 In another report, persimmon leaf extract administered daily for 4 weeks significantly decreased skin lesions, serum immunoglobulin E levels, and scratching behavior in affected mice.48

The most common spontaneous tumors associated with the skin are mammary adenocarcinomas, followed by fibrosarcomas. The incidence of mammary tumors varies according to the mouse strain and the presence or absence of mouse mammary tumor viruses; in some strains, the incidence is as high as 70%.70 In wild and outbred mice, the incidence of fibrosarcoma ranges from 1% to 6%.30 By the time a diagnosis is made, subcutaneous tumors are nearly always malignant and often have ulcerated. Although tumors can be treated by surgical excision, the chance of recurrence is high and the prognosis is poor. Attempts to treat tumors in mice by radiation or chemotherapy have not been reported.

Digestive system

Endoparasites are relatively common in mice. However, only two parasites regularly seen in the digestive tract, the protozoan parasites Spironucleus muris and Giardia muris, are considered pathogenic, even though they are not associated with clinical signs in immunocompetent hosts. A diagnosis is made by demonstrating characteristic trophozoites in wet mounts of fresh intestinal contents or feces. Treatment is metronidazole added to the drinking water (0.04%- 0.10% for 14 days), but it does not completely eliminate the infection.31 In individual pet animals, metronidazole can be compounded into a fruit-flavored suspension and given at dosages used in other rodents.

Pinworms are ubiquitous and considered nonpathogenic. Two are commonly encountered in mice: Syphacia obvelata and Aspicularis tetraptera. The only indication of pinworm infestation often is rectal prolapse from straining. To establish a diagnosis of S. obvelata infestation, make a clear cellophane tape impression of the perianal skin. Adult S. obvelata females deposit ova around the anus. A. tetraptera does not deposit its ova in this area, and fecal smear or flotation is required to confirm a diagnosis. Ivermectin (2 mg/kg PO given twice at a 10-day interval) eliminates pinworms from mice. Ivermectin 1% is diluted 1:9 in vegetable oil to establish a concentration of 1.0 mg/mL; affected mice are dosed with a volume of 0.2 mL/100 g PO.21 The recommended package label dose for mice with ectoparasites (0.2 mg/kg given twice at a 10-day interval) does not eliminate pinworms.34

Diarrhea is not usually seen in adult mice. Digestive disease in adult mice is usually caused by a varying combination of pathogenic and opportunistic infectious agents. Fecal flotation and fresh wet mounts of feces usually yield positive results and do not necessarily give a definitive diagnosis. However, these techniques are sometimes helpful in identifying heavy endoparasite infections. Treatment is generally directed at clinical signs and consists of the judicious use of antimicrobials.

Respiratory system

Diseases of the upper and lower respiratory tracts are common in pet mice and rats. Animals may display sniffling, sneezing, chattering, and labored breathing. If dyspnea is suspected, do not overhandle the animal during clinical examination because it may die. Collecting tracheal and nasal secretions is not recommended; swabbing is highly traumatic, and the disease is generally caused by a mixed viral, mycoplasmal, and bacterial infection. Antibiotic treatment is helpful but usually does not eliminate the disease.

The two most common causes of clinical respiratory disease in mice are Sendai virus and Mycoplasma pulmonis. Sendai virus is associated with an acute respiratory infection in which mice display chattering and mild respiratory distress. Neonates and weanlings may die. Adults generally recover within 2 months. When the disease expression exceeds this pattern, the cause is most likely concurrent mycoplasmal infection. M. pulmonis causes chronic pneumonia, suppurative rhinitis, and occasionally otitis media. Purulent exudate accumulates in inflamed and thickened nasal passages, causing chattering and dyspnea. Survivors develop chronic bronchopneumonia, bronchiectasis, and occasionally pulmonary abscesses (this does not happen in rats). Antibiotic therapy may alleviate clinical signs but does not eliminate the infection. For treatment, enrofloxacin (10 mg/kg) in combination with doxycycline hyclate (5 mg/kg) given every 12 hours PO for 7 days is sometimes helpful.

Urinary system

Urethral obstruction in male mice has been described as a result of infection of the preputial glands with S. aureus and of the bulbourethral glands with P. pneumotropica. Accessory sex gland secretions and, rarely, urolithiasis have also been implicated. Mice often are presented to the veterinarian because they mutilate their penis as a result of these conditions. In addition, occasional injury of the penis is seen in young males from aggressive breeding activity and abrasion on the cage. Treatment involves isolating the affected mouse, cleaning and debriding the affected areas, and treating with antibiotics.

Rats

Integumentary system and mammary glands

Ulcerative dermatitis caused by S. aureus infection results from self-trauma associated with fur mite infestation or, more commonly, scratching of the skin over an inflamed salivary gland. Rats have a remarkable ability to resist infection with S. aureus.18 Treatment consists of clipping the toenails of the hindpaws, cleaning the ulcerated skin, and applying a topical antibiotic. Systemic treatment is rarely necessary.

The most common subcutaneous tumor in rats is fibroadenoma of the mammary glands. The distribution of mammary tissue is extensive, and the tumors can occur anywhere from the neck to the inguinal region (Fig. 29-3 ). Tumors can reach 8 to 10 cm in diameter and develop in both males and females. The surgical technique for tumor removal is straightforward (see Chapter 30), and survival after mastectomy is good if the tumor is benign.32 Adenocarcinomas represent fewer than 10% of mammary tumors in rats. The prevalence of mammary tumors, as well as that of pituitary tumors, is significantly lower in ovariectomized rats than in sexually intact Sprague-Dawley rats.32 However, recurrence of fibroadenomas is common in uninvolved mammary tissue, and often several surgeries are needed. In contrast, mammary tumors in mice are nearly always malignant and often are not amenable to surgical removal.

Figure 29-3.

Figure 29-3

Mammary fibroadenoma in the inguinal region of a female rat.

Ectoparasitic infestation is less common in rats than in mice. Occasionally, the fur mite Radfordia ensifera is seen. Although R. ensifera infestation produces few ill effects, heavy infestation may lead to self-trauma and ulcerative dermatitis. Other mites, including Demodex species, have been described in rats maintained in laboratories75; however, they are seldom seen, and no reports of infestations in pet rats appear in recent literature. Diagnosis and treatment are the same as those for mice.

Avascular necrosis of the tail, or ringtail, is a highly photogenic lesion of rats and probably for this reason is always described in textbooks and articles on diseases of rats. It occurs primarily in young laboratory rats in low-humidity environments and often in rats housed in hanging cages; it is rarely seen in pet animals. If ringtail is diagnosed, treatment involves amputating the tail below the necrotic annular constriction.

Digestive system

Inflammation and edema of the cervical salivary glands is caused by sialodacryoadenitis virus, a coronavirus. Owners of infected rats often describe their pets as having mumps. Sialodacryoadenitis virus infection is highly contagious. It initially causes rhinitis followed by epithelial necrosis and inflammatory swelling of the salivary and lacrimal glands. Cervical lymph nodes also become enlarged. There is no treatment for this disease. Glandular healing follows within 7 to 10 days, and clinical signs subside within 30 days, with minimal residual lesions remaining. During acute inflammation, affected rats are at high risk for anesthesia-related death because of the decreased diameter of the upper respiratory tract lumen; also, ocular lesions such as conjunctivitis, keratitis, corneal ulcers, synechiae, and hyphema can develop from lacrimal dysfunction. The eye lesions usually resolve but occasionally progress to chronic keratitis and megaglobus.

Overgrowth of the incisors is common in rats, and their teeth can grow into the nasal cavity (Fig. 29-4 ). See Chapter 34 for further discussion of this problem.

Figure 29-4.

Figure 29-4

Overgrown incisors in a rat. Overgrown teeth can be cut with a high-speed drill.

Respiratory system

Respiratory disease caused by infectious agents is the most common health problem in rats. Three major respiratory pathogens cause overt clinical disease: M. pulmonis, S. pneumoniae, and Corynebacterium kutscheri. Other organisms such as Sendai virus (a parainfluenza virus), pneumonia virus of mice (a paramyxovirus), rat respiratory virus (a hantavirus),46 cilia-associated respiratory (CAR) bacillus, and Haemophilus species are minor respiratory pathogens that by themselves rarely cause overt clinical disease. However, these minor respiratory pathogens interact synergistically as copathogens with the major respiratory pathogens to produce two major clinical syndromes: chronic respiratory disease (CRD) and bacterial pneumonia.

CRD is the best understood multifactorial respiratory infection in rats. M. pulmonis is the major component of CRD, also known as murine respiratory mycoplasmosis. Rats may live 2 to 3 years with CRD. Clinical signs are highly variable, and initial infection develops without any clinical signs. Early signs involve both the upper and the lower respiratory tracts and may include snuffling, nasal discharge, polypnea, weight loss, hunched posture, ruffled coat, head tilt, and red tears.15, 35 Thoracic radiographs may be helpful in the diagnosis of CRD (Fig 29-5 ). The most important aspect of CRD for clinicians is that respiratory mycoplasmosis varies greatly in disease expression because of environmental, host, and organismal factors that influence the host-pathogen relationship. Examples of such factors include intracage ammonia levels; concurrent Sendai virus, coronavirus (sialodacryoadenitis virus), pneumonia virus of mice, rat respiratory virus, or CAR bacillus infection; the genetic susceptibility of the host; the virulence of the Mycoplasma strain; and vitamin A or E deficiency.15 For many years, the standard treatment for laboratory rats was to add tetracycline to sweetened water. However, this treatment is ineffective in rats because blood antibiotic concentrations are below minimum inhibitory concentrations, and pulmonary tissue concentration of tetracycline is noninhibitory. Instead, administer enrofloxacin (10 mg/kg PO q12h for 7 days) in combination with doxycycline hyclate (5 mg/kg PO q12h for 7 days). Although mycoplasma and CAR bacillus are susceptible to this antibiotic therapy, the respiratory viruses are not. In addition, certain strains of rats have a heightened cellular immune response to mycoplasma that aggravates respiratory damage. Therefore, warn owners that antibiotic treatment will not cure CRD but may alleviate clinical signs. Reducing ammonia levels in cages by removing bedding and using clean paper daily may also help. Despite developing high antibody titers to mycoplasma and high antibiotic tissue levels, affected animals typically have persistent M. pulmonis infection. Chronic signs of infection often include middle ear infection (by way of the eustachian tube); ciliostasis and subsequent buildup of lysozyme-rich inflammatory exudate in airways; and, eventually, bronchiectasis and bronchiolectasis from inflammatory damage to the bronchiolar membranes. Abscesses may develop in scattered areas of one or both lungs. In these animals with advanced CRD, reducing ammonia levels in cages and administering bronchodilators and low levels of short-acting corticosteroids are also sometimes helpful in reducing clinical signs.

Figure 29-5.

Figure 29-5

Lateral radiographic view of a 1.5-year-old male rat with chronic respiratory disease. The lungs have multifocal areas of pulmonary infiltrate. The cause of disease is usually multifactorial, involving concurrent infection with Mycoplasma pulmonis, Sendai or other viruses, and cilia-associated respiratory bacillus, as well as management and genetic factors.

Bacterial pneumonia is nearly always caused by S. pneumoniae (Fig. 29-6 ) but seldom develops in the absence of some combination involving M. pulmonis, Sendai virus, or CAR bacillus. Infection with C. kutscheri (Fig. 29-7 ) also results in pneumonia but only in debilitated or immunosuppressed animals. In pet rats, immunosuppression can result from diabetes, neoplasia, or dietary deficiencies. C. kutscheri pneumonia is rare in pet rats. Pneumonia caused by S. pneumoniae can be of sudden onset. Young rats are more severely affected than are older ones, and often the only sign they exhibit is sudden death. Mature rats may demonstrate dyspnea, snuffling, and abdominal breathing. A purulent exudate may be seen around the nares and on the front paws (from wiping of the nostrils). A tentative diagnosis can be based on identifying numerous gram-positive diplococci on a Gram stain of the exudate or in a sample submitted for cytologic examination (Fig. 29-8 ). Severe bacteremia is an important consequence of advanced disease and results in multiorgan abscesses and infarction. Treatment must be aggressive, and the use of beta-lactamase–resistant penicillins such as cloxacillin, oxacillin, and dicloxacillin (all of which can be administered orally) is recommended. There are no published dosages of these drugs for rats, and the dosage is empirical.

Figure 29-6.

Figure 29-6

Fibrinopurulent pneumonia in a rat caused by Streptococcus pneumoniae.

Figure 29-7.

Figure 29-7

Gross appearance of the lungs in a diabetic rat with pneumonia caused by Corynebacterium kutscheri infection. Lobular pneumonia is the result of the hematogenous spread of the organism. Compare the appearance of these lungs with that of the lungs in Fig. 29-6.

Figure 29-8.

Figure 29-8

Photomicrograph of a Giemsa-stained smear from a rat with a nasal exudate. Multiple diplococci characteristic of Streptococcus pneumoniae are visible. The polymorphonuclear cells characteristic of purulent exudate are clearly evident.

Urinary system

Chronic progressive nephrosis (CPN) is the best-known age-related disease of rats. In CPN, the kidneys are enlarged and pale and have a pitted, mottled surface that often contains pinpoint cysts (Fig. 29-9 ). Lesions consist of a progressive glomerulosclerosis and myriad tubulointerstitial disease primarily involving the convoluted proximal tubule (Fig. 29-10 ).27 The most striking change in renal function is a proteinuria level exceeding 10 mg/day that progressively increases in severity with age. The features of CPN are qualitatively similar among different strains of laboratory rats, but the onset, incidence, and severity of the disease vary considerably. The disease occurs earlier and is of greater severity in males than in females; urinary protein excretion averaging 137 mg/day has been documented in 18-month-old male Sprague-Dawley rats, whereas excretion averaging 76 mg/day was reported in female rats of the same age.65 Dietary factors appear to have an important role in the progression of CPN. Restricting calories, feeding diets low in protein (4%-7%), and limiting the source of dietary protein reduce the incidence and severity of CPN. Feeding soy protein (as opposed to casein) and substantially restricting calories reduce the incidence and severity of CPN; feeding low-calorie diets that contain high protein levels does not. Exposure to drugs and chemicals also exacerbates CPN. Treatment is supportive and involves feeding a low-protein diet and administering anabolic steroids.

Figure 29-9.

Figure 29-9

Enlarged, pale kidneys from a rat with chronic progressive nephrosis. Note the pitted, mottled surface containing pinpoint cysts.

Figure 29-10.

Figure 29-10

Photomicrograph of severe glomerulosclerosis in a rat. The proximal tubules are dilated and contain copious amounts of a protein-rich material; this finding indicates the deterioration of glomeruli that fail to filter and retain plasma protein.

Ocular system

The harderian glands of rats are located behind the eyes. They secrete various porphyrins that give the tears a reddish color. Harderian gland secretion increases in response to stress and disease, and the tears dry around the eyes and external nares (the nasolacrimal duct drains into the nasal cavity), resembling crusts of blood (Fig. 29-11 ). Owners commonly report bleeding from the eyes and nose of their pet rats. The porphyrins fluoresce under ultraviolet light and can be readily differentiated from blood with a Wood's lamp. The condition is known as chromodacryorrhea or red tears, and although it is not pathologic, it is a consequence of acute-onset stress such as that caused by pain, illness, or restraint. Red tears often indicate a chronic underlying disease, and their presence warrants a thorough evaluation of the affected pet rat.

Figure 29-11.

Figure 29-11

Red tears in a rat. The color results from porphyrin pigments in the harderian gland secretions, which are visible around the nares (arrows).

Hamsters

Although many types of hamsters live in the wild, only a few types are kept as pets. The most common is the golden or Syrian hamster (Mesocricetus auratus), which has been kept as a pet since the 1940s. Although two other species of hamsters, the common or European hamster (Cricetus cricetus) and the ratlike Chinese hamster (Cricetulus griseus) are used in research, they do not make good pets because of their aggressive nature. However, dwarf hamsters such as the Djungarian (Phodopus sungorus) and Roborovski (Phodopus roborovskii) are being seen increasingly as pets because they have a docile disposition, do not attempt to bite or run away, and do well in captivity. Very few reports of spontaneous diseases in these animals have been published; Cantrell and Padovan have prepared the most complete review to date on this subject.11 The description of diseases refers to Syrian hamsters.

Integumentary system and marking glands

The most common skin problem seen in hamsters is haircoat roughness. This is a nonspecific sign of fighting, aging, and a variety of diseases. Female hamsters are heavier than males and generally are more aggressive, not only toward other hamsters, but also their owners. They can inflict severe bite wounds on cagemates, and nonestrous females can be especially aggressive toward young males and may kill them.

Hamsters have distensible cheek pouches that may be mistaken for lesions by the owner.9 Sometimes the cheek pouches become impacted, and the material must be removed from the pouches with fine forceps. A radiograph of the head often shows the extent of the impaction.61 Predisposing causes of impaction, such as malocclusion of incisors or molars, should be investigated. Male hamsters have large, pendulous testes and pigmented sebaceous flank glands, which clients may mistake for tumors.

Digestive system

The most common problems seen in pet hamsters are enteropathies. Diarrhea may occur in hamsters of any age and is known as wet-tail, although this euphemism is frequently used to describe the disease in young hamsters. Proliferative ileitis is the most significant intestinal disease of 3- to 10-week-old hamsters and results in a high mortality rate. It is caused by the intracellular bacterium Lawsonia intracellularis, which is also responsible for proliferative enteropathy in pigs and ferrets.43, 57 Treatment must be aggressive and involves correcting any life-threatening electrolyte imbalance, administering antibiotics, and force-feeding. Several antibiotic treatments are recommended, including tetracycline hydrochloride (400 mg/L of drinking water for 10 days), tetracycline (10 mg/kg PO q12h for 5-7 days), enrofloxacin (10 mg/kg PO or IM q12h for 5-7 days), and trimethoprim-sulfa combination (30 mg/kg PO q12h for 5-7 days). Symptomatic treatment with bismuth subsalicylate may be given if diarrhea persists. Give replacement electrolyte and glucose solutions orally, and administer electrolyte replacement fluids such as saline or lactated Ringer's solution at a dose of 20 mL/100 g q24h. Offer liquid food such as pureed baby spinach, apples, carrots, and lettuce mixed in equal parts with a slurry made from rodent pellets, or offer a nutritional supplement such as Critical Care (Oxbow Pet Products). Adding 1 tablespoon of honey to the feed mixture may make it more palatable. If the hamster does not eat, force-feed small amounts of liquid feed. Potential sequelae to proliferative ileitis in surviving hamsters are obstruction, intussusception, or rectal prolapse (see Chapter 30).16

Diarrhea in adult hamsters is associated with enterotoxemia caused by Clostridium difficile and may develop 3 to 5 days after treatment with antibiotics such as penicillin, lincomycin, or bacitracin. Bovine antibodies against toxigenic C. difficile administered orally will protect hamsters against experimental antibiotic-associated enterotoxemia.47

Tyzzer's disease (Clostridium piliforme, previously known as Bacillus piliformis) was described in hamsters and gerbils obtained from a pet store supplier.51 In this outbreak, hamsters and gerbils had a high mortality rate but the rats and mice did not. Affected rodents were depressed and dehydrated and had scruffy coats and diarrhea; many animals had no clinical signs before death. The authors concluded that the clinical outbreak was precipitated by severe stress, including that caused by overcrowding, high environmental temperature and humidity, heavy internal and external parasite load, and nutritionally inadequate diets, despite the prophylactic treatment of drinking water with oxytetracycline. Tyzzer's disease, first recognized in 1917 in a colony of Japanese waltzing mice by Tyzzer at Harvard,72 is frequently listed in laboratory animal textbooks as an intestinal disease of rodents and other animals. However, the actual prevalence of the infection in rodents is unknown. The report concerning the pet store illustrates the opportunistic nature of C. piliforme in immunosuppressed animals. The disease is not seen in healthy immunocompetent animals.

Weight loss is seen in aged hamsters and is often associated with hepatic and renal amyloidosis. One research report described amyloidosis in 88% of hamsters older than 18 months of age.26 In long-term research studies, amyloidosis is described as the principal cause of death in laboratory hamsters, with a higher incidence, increased severity, and earlier age of onset in female hamsters than in male hamsters.62 Social stress induced by crowding correlates with the incidence of disease.25 In pet hamsters, the incidence and clinical signs of amyloidosis have not been described and, because overcrowding is usually not a problem, the incidence may be low. However, if the condition is present, clinicians should expect edema and ascites caused by hypoproteinemia of hepatic and renal origin. If amyloidosis is diagnosed in a pet hamster, the prognosis is poor and treatment supportive.

Respiratory system

In one survey, 6 of 14 laboratories in the United States reported pneumonia as the second most common clinical condition in hamsters after diarrhea.60 An earlier survey conducted in Germany noted respiratory infections in 8% of all clinical conditions in hamsters.45 Histologic evidence of bronchopneumonia resembling bacterial pneumonia and of interstitial pneumonia resembling viral pneumonia has been described, but there are no reports of observed clinical cases. Consequently, other authors have stated that respiratory disease is uncommon in hamsters.28 The true prevalence remains to be established.

Purulent rhinitis associated with pneumonia and sticky eyelids has been described in hamsters and is associated with a poor prognosis.38 Bacterial pneumonias, especially those caused by Streptococcus species, may be inadvertently transmitted by children to pet hamsters. Rapid diagnosis can be made by identifying the characteristic gram-positive diplococci on a Gram stain of a sample of nasal and ocular discharges. Follow-up culture and treatment with chloramphenicol (chloramphenicol palmitate, 50 mg/kg PO q8h; chloramphenicol succinate, 30 mg/kg IV or IM q8h) are recommended until antibiotic sensitivity results are available.2

Reproductive system

Female hamsters have a 4-day estrous cycle that ends with a copious postovulatory discharge. The discharge is creamy white and has a distinctive odor; it fills the vagina and usually extrudes through the vaginal orifice (female hamsters have three orifices: urinary, genital, and anal). Its stringy nature is distinctive, and if touched it can be drawn out as a thread of about 4 to 6 inches in length. Owners often describe the discharge as pus and mistakenly believe it to be abnormal.

Pyometra has been observed clinically, although rarely, in pet hamsters. A tentative diagnosis is made by ultrasound examination of the abdomen, and ovariohysterectomy is the treatment of choice.

In group-housed laboratory female hamsters, cannibalism of young accounts for about 95% of all preweaning mortality.60 Other factors such as cold ambient temperatures (< 50°F [10°C]), lean diets, and low body weight (especially during pregnancy) appear to increase cannibalism.63, 64 Instruct the owners of pet hamsters to give the mother ample food and water and to leave her alone in a quiet, warm place for at least 1 or preferably 2 weeks. Disturbing the mother by handling the young or nest and not providing adequate nesting material, warmth, food, or water often results in litter desertion and cannibalism.

Cardiovascular system

Atrial thrombosis has been described in aging research hamsters,33 and in certain strains the incidence is high (up to 73%).12 Most thromboses develop in the left atrium from heart failure and lead to a consumptive coagulopathy (Fig. 29-12 ). Although the incidence does not differ between the sexes in aged hamsters, atrial thrombosis occurs on average at a younger age in females (13.5 months) than in males (21.5 months).12 Aged pet hamsters have clinical signs of cardiomyopathy such as hyperpnea, tachycardia, and cyanosis. Untreated hamsters typically die within 1 week after these signs are evident. The endocrine status of the animal and especially the amount of circulating androgens influence the incidence of atrial thrombosis. Thus castration of male hamsters is linked to an increase in the prevalence of atrial thrombosis.66

Figure 29-12.

Figure 29-12

Thrombosis in the atria of the heart of a hamster caused by cardiomyopathy.

(Courtesy Heidi L. Hoefer, DVM.)

Cardiomyopathy should be suspected in aged pet hamsters (older than 1.5 years) that present clinically with signs of tachypnea, lethargy, anorexia, and cold extremities. Diagnosis is based on clinical signs and results of radiography and ultrasonography of the heart. Treatment of heart disease is symptomatic and involves empirical use of digoxin, diuretics, angiotensin-converting enzyme inhibitors, and prophylactic anticoagulants. Recommended dosages for hamsters are available for some of these drugs; otherwise, extrapolate dosages from those used in ferrets and closely monitor the response. Verapamil, a calcium antagonist, administered at a dose increasing from 0.25 mg to 0.50 mg SC q8h over a 4-week period, prevented severe myocardial lesions in untreated 2-month-old inbred female myopathic hamsters.39

Endocrine system

Surveys of spontaneous lesions in laboratory hamsters describe a high incidence of adrenocortical hyperplasia and adenoma.62 However, despite extensive histopathologic study, there has been only one clinical report of hyperadrenocorticism, or Cushing's disease, in three hamsters, with high serum cortisol concentrations documented in only one of the three animals.5 Hamsters with clinical signs resembling those of Cushing's disease are occasionally seen in practice (Fig. 29-13 ). Diagnosis is based on documenting classic signs seen in dogs, such as a history of polydipsia, polyuria, and polyphagia; clinical signs of alopecia and hyperpigmentation; and high concentrations of plasma cortisol and serum alkaline phosphatase. Reference values of cortisol concentrations are low compared with those of other species and range from 0.5 to 1.0 μg/dL in normal males and females.76 Hamsters may secrete both cortisol and corticosterone56; therefore, at present, meaningful measurement of plasma cortisol concentrations in hamsters is empirical. If hyperadrenocorticism is suspected, the cause, such as hypersecretion by a functional tumor, primary adrenal hyperplasia, or excess adrenocorticotropic hormone production, often is more difficult to determine. Hamsters respond to exogenous adrenocorticotropic hormone stimulation.76 In the clinical report of the three hamsters, one hamster that was treated with metyrapone (8 mg PO q24h for 1 month) responded well; another hamster treated with o,p′-DDD (mitotane) (5 mg PO q24h for 1 month) did not improve and was then given a similar dose of metyrapone, also without success.4 Further research needs to be done on this syndrome.

Figure 29-13.

Figure 29-13

Generalized alopecia associated with adrenocortical hyperplasia in a hamster.

Ocular system

Exophthalmos is common in hamsters. It is usually a result of ocular infection or trauma to the periorbital area, or it occurs iatrogenically during restraint. Hamsters with sialodacryoadenitis (caused by cytomegalovirus infection) may develop keratoconjunctivitis sicca, exophthalmos, and subsequent proptosis. Occasionally, a hamster's eye is displaced forward if the caregiver restrains the animal too tightly by holding the skin at the back of the neck. If the hamster is treated soon after the exophthalmos occurs, then the prognosis for saving the eye is good. Cleanse the ocular area gently with an ophthalmic wash, and lubricate the eye with sterile ophthalmic lubricant. Gently retract the lid margins around the globe until the eye returns to its normal position. Treat the eye with an antibiotic ophthalmic ointment for a minimum of 7 to 10 days. Occasionally, tarsorrhaphy is needed to prevent recurrence. Enucleation may be necessary if the eye cannot be replaced or if it has been severely traumatized.

Neoplasia

Lymphoma is the most common neoplasm in Syrian hamsters. Clinicians see three variations. In older hamsters, lymphoma is the most frequently observed neoplasm of the hematopoietic system.71 These tumors are often multicentric, involving the thymus, thoracic lymph nodes, mesenteric lymph nodes, superficial lymph nodes, spleen, liver, and other sites. Cytology of the tumors is variable. A second variation, cutaneous lymphoma, which resembles mycosis fungoides, an epidermotropic T-cell lymphoma in humans, is seen in adult hamsters.29 Lethargy, anorexia, weight loss, patchy alopecia, and exfoliative erythroderma have been described in affected animals. Pathologists have noted dense infiltrates of neoplastic lymphocytes in the dermis, with extension into the epidermis. The third variation is an epizootic of lymphoma in young hamsters. The causative agent is hamster polyomavirus (HaPV).4 When HaPV is first introduced into a naive population of breeding hamsters, an epizootic of lymphoma, with an incidence as high as 80%, can result. Once enzootic in a hamster population, the occurrence of lymphoma declines to a much lower level. Enzootically infected hamsters develop HaPV skin tumors rather than lymphoma. Hamsters with HaPV lymphoma appear thin, often with palpable abdominal masses. Tumors often arise in the mesentery but can arise in the axillary and cervical lymph nodes. The tumors are often lymphoid, but erythroblastic, reticulosarcomatous, and myeloid types occur. Anecdotal reports of chemotherapy in hamsters have been based on protocols using drugs that can be administered subcutaneously, orally, or intraperitoneally at dosages used in other small animals.

Gerbils

Integumentary system and marking glands

Facial eczema, sore nose, and nasal dermatitis all describe a common skin condition seen in gerbils. Clinical lesions adjacent to the external nares appear erythematous initially; these lesions progress to localized alopecia and then to an extensive moist dermatitis (Fig. 29-14 ). The cause is believed to be an increase in the secretion of porphyrins by the harderian gland (as in chromodacryorrhea in rats), which act as a primary skin irritant. Various staphylococcal species (S. aureus and S. xylosus) may act synergistically to produce the dermatitis.10, 68 Stress may cause excessive harderian gland secretion. Two examples of stress are overcrowding and exposure to an environmental humidity of greater than 50% (in this case, the coat stands out and appears matted instead of lying sleekly against the body). Gerbils require sandbathing to keep their coats from becoming oily. Keeping the gerbil in a dry environment, cleaning its face, and providing soft clay or sand bedding instead of abrasive wood chip bedding usually alleviate the problem. Use topical or parenteral antibiotics (except streptomycin) in gerbils with severe dermatitis.

Figure 29-14.

Figure 29-14

Sore nose (facial eczema, nasal dermatitis) in a gerbil. This condition may result from an increase in harderian gland secretion complicated by infection with Staphylococcus species.

The tail of gerbils is covered by thin skin. Unlike rats or mice, if a gerbil is picked up by the tip of its tail, the skin often slips off, leaving a raw, exposed tail that eventually becomes necrotic and sheds (Fig. 29-15 ). If the tail skin is lost, surgically amputate the bare tail where the skin ends. The tail usually sloughs if it is left untreated. When picking up a gerbil, avoid grasping the tail unless it is gently held at the base. The best holding technique involves placing the palm of the hand over the gerbil's back and encircling the body with thumb and fingers. Gerbils bite if they are not handled securely, despite the claim in many reviews that they rarely bite human handlers regardless of provocation.

Figure 29-15.

Figure 29-15

One normal (bottom) and two (top) gerbil tails with varying degrees of tail-slip. Tail-slip can result from the restraint of a gerbil by its tail.

Gerbils have large, ventral, abdominal marking glands that are androgen dependent (Fig. 29-16 ). Owners may mistake this normal ventral gland for a tumor. In aged animals, the gland may become infected or neoplastic. Local debridement and topical antibiotic ointments are indicated for treatment of infected glands. Do a wide excisional biopsy if you suspect a tumor such as adenocarcinoma.

Figure 29-16.

Figure 29-16

Ventral marking glands on a male gerbil.

Digestive system

Naturally occurring Tyzzer's disease is the most frequently described fatal infectious disease of gerbils.13, 36, 51, 59, 77 In reported cases, common findings were sudden death or death after a short illness and the presence of multiple foci of hepatic necrosis. Diarrhea and gross and microscopic lesions in the intestinal tract were variably present. Experimentally induced Tyzzer's disease in gerbils has confirmed that these animals are extremely susceptible to infection74; the probable route of infection is oral. Gerbils exposed to infected bedding contract the disease.

Gerbils will develop spontaneous, insidious periodontal disease if fed a standard rat or mouse diet for more than 6 months.73 On the same diet, approximately 10% of animals become obese, and some may even develop diabetes. Various pelleted commercial diets are available that are suitable for rats, mice, hamsters, and gerbils.

Central nervous system

Approximately 20% to 40% of gerbils develop reflex, stereotypic, epileptiform (clonic-tonic) seizures beginning at 2 months of age. The susceptibility is inherited, seen in selectively bred lines, and is caused by a deficiency in cerebral glutamine synthetase.40 There is no treatment. Most animals outgrow the behavior with time. The seizures generally pass in a few minutes; they may be mild or severe and have no lasting effects.

Reproductive system

Cystic ovaries are reported to occur frequently in laboratory Mongolian gerbils.54 Removal of the affected ovary is recommended.

Tumors and aging

After 2 to 3 years of age, approximately 25% to 40% of gerbils develop neoplasia.49, 73 Squamous cell carcinoma of the sebaceous ventral marking gland in males and ovarian granulosa cell tumor in females account for 80% of tumors seen in animals older than 3 years. Besides neoplasia, older gerbils have a high incidence of chronic interstitial nephritis.8 Aged gerbils have a remarkable propensity for the development of aural cholesteatoma, a nonneoplastic keratinizing epithelial mass that occurs in the middle ear and mastoid region, erodes bone, and invades the labyrinth and the cranial cavity.14

Degus

Degus, or trumpet-tail rats, are native to Chile. Taxonomically, they are in the same diverse order as guinea pigs and chinchillas. Degus have been used as laboratory animals for 20 years, but there are very few reports on naturally occurring diseases. One report describes a 3-month-old pet degu with a tibial fracture that was repaired by medullary fixation.7 Like chinchillas, captive degus must be provided with a dust bath twice a week.1 Although degus do not drink much water, owners should change water bottles regularly to prevent bacterial overgrowth. The testicles of male degus are intraabdominal and the method of castration is by laparotomy.20

Integumentary system

Clinicians should not hold degus by the tail because they will spin like a top, leaving the veterinarian holding only the skin. Degus familiar with their owners do not show this behavior and tail shedding is uncommon.1

Endocrine and ocular system

Degus develop spontaneous diabetes mellitus caused by amyloidosis of Langerhans islets. Cellular infiltration of Langerhans islets induced by cytomegalovirus, alpha cell crystals with the presence of a herpes-type virus, and foods such as guinea pig chow or fresh fruit that increase blood glucose concentrations are also associated with the development of diabetes in degus.22, 53, 69 Owners should feed degus a commercial rodent diet supplemented with vegetables. Like prairie dogs, it is easy to overfeed degus and obesity is likely to occur. No treatments have been described for diabetic degus.

Degus can develop cataracts within 4 weeks of the onset of diabetes.17 A congenital cataract unrelated to diabetes has also been described.78

Neoplasms

Various neoplasms have been described in degus. Hepatocellular carcinoma is the most frequently described; however, there have been only four reported cases in animals 5 to 6 years of age.50, 52 Other reported tumors include bronchioloalveolar carcinoma,3 reticulum cell sarcoma,52 splenic hemangioma,52 lipoma,52 rhabdomyosarcoma,50 and transitional cell carcinoma.44

Medication and antibiotic therapy in pet rodents

Because of the small size of pet rodents, even pediatric-strength medications often must be diluted for use in these species. Knowing the precise weight of the animal, diluting medications, and administering medications with a tuberculin or insulin syringe will increase dosing accuracy. Medication often is given by mixing it into feed or water. However, rats do not drink if they find the taste of their water objectionable. Ball-ended dosing needles are ideal for gavage, but always carefully calculate the volume of the dose and depth of penetration when using the dosing needle to prevent gastric rupture. Intravenous injections are difficult to administer; intraperitoneal injection (for anesthetics), intramuscular, or subcutaneous injections are commonly substituted.

Exercise caution when administering antibiotics to rodents. Streptomycin and procaine are toxic in mice; nitrofurantoin causes neuropathologic lesions in rats; and gerbils cannot tolerate dihydrostreptomycin and streptomycin. Hamsters are similar to guinea pigs in their susceptibility to clostridial enterotoxemia when they are given penicillins, erythromycin, or lincomycin. Many antibiotics are added to the drinking water of pet rodents, but the water must contain high concentrations and fresh solutions must be prepared daily to achieve therapeutic levels. As an example, tetracycline is often added to the drinking water of rats and mice at a dose of 5 mg/mL for the treatment of respiratory mycoplasmosis. Rats often do not drink the medicated water because of its unpleasant taste. Some researchers add sugar to the water to encourage drinking, but such supplementation is controversial.

Antibiotics that are apparently safe to use in rodents (especially guinea pigs and hamsters) include enrofloxacin, ciprofloxacin, trimethoprim-sulfa combinations, and chloramphenicol. Other sulfonamides, tetracycline, and piperacillin should be used sparingly in hamsters, and ampicillin and amoxicillin should be avoided (see Chapter 28). Many compounding pharmacies can now prepare medications in flavored syrups or treats that are palatable to rodents.

Client Education

Most clients purchase books on pet rodents in pet stores and often rely on the recommendations of the pet store owner before asking for advice from a veterinarian. Unfortunately, many of the available owner's manuals are not familiar to veterinarians. Having some knowledge about pet rodents from these handbooks, clients often raise questions about what they have read, and clinicians may not appear well informed from the client's perspective if they are unfamiliar with their references. The rodent owners then often return to the pet store owner for guidance; unless their animals are very sick, the owners do not return to the veterinarians for advice on husbandry and diseases. At this point, the prognosis for very ill pets is poor.

Familiarity with the pet hobbyist literature breaks the cycle of mistrust and ignorance. Many hobby books on pet rodents are highly entertaining and informative about the husbandry and biology of the animals. However, the medical information in these books should be carefully reviewed by the veterinarian. Purchasing some of these books and then recommending them to pet rodent owners is an effective method of educating clients and establishing a good rapport with them. The books are generally less expensive than veterinary textbooks and are written for a range of age groups (e.g., children and parents) and levels of interest. Barron's Educational Series and Dorling Kindersley are two reputable publishers of readily available books. TFH Publications, another reputable publisher, no longer publishes. Access www.tfh.com for availability of titles.

REFERENCES

  • 1.Altmann D, Schwendenwein I, Wagner K. Zu biologie, haltung, ernahrung und erkrankungen des degus (Octodon degus) Erkrankungen Der Zootiere. 1994;36:277–292. [Google Scholar]
  • 2.Anderson NL. Pet rodents. In: Birchard SJ, Sherding RG, editors. Saunders Manual of Small Animal Practice. 2nd ed. WB Saunders; Philadelphia: 1999. pp. 1512–1538. [Google Scholar]
  • 3.Anderson WI, Steinberg H, King JM. Bronchioloalveolar carcinoma with renal and hepatic metastases in a degu (Octodon degus) J Wildlife Dis. 1990;26:129–131. doi: 10.7589/0090-3558-26.1.129. [DOI] [PubMed] [Google Scholar]
  • 4.Barthold SW, Bhatt PN, Johnson EA. Further evidence for papovavirus as the probable etiology of transmissible lymphoma of Syrian hamsters. Lab Anim Sci. 1987;37:283–288. [PubMed] [Google Scholar]
  • 5.Bauck L, Orr JP, Lawrence KH. Hyperadrenocorticism in three teddy bear hamsters. Can Vet J. 1984;25:247–250. [PMC free article] [PubMed] [Google Scholar]
  • 6.Baumans V, Havenaar R, van Herck H. The effectiveness of Ivomec and Neguvon in the control of murine mites. Lab Anim. 1988;22:243–245. doi: 10.1258/002367788780746368. [DOI] [PubMed] [Google Scholar]
  • 7.Beregi A, Felkai F, Seregi J. Medullary fixation of a tibial fracture in a three-month-old degu (Octogon degus) Vet Rec. 1994;134:652–653. doi: 10.1136/vr.134.25.652. [DOI] [PubMed] [Google Scholar]
  • 8.Bingel SA. Pathologic findings in an aging Mongolian gerbil (Meriones unguiculatus) colony. Lab Anim Sci. 1995;45:597–600. [PubMed] [Google Scholar]
  • 9.Bivin WS, Olsen GH, Murray KA. Morphophysiology. In: Van Hoosier GL, McPherson CW, editors. Laboratory Hamsters. Academic Press; Orlando: 1987. pp. 9–41. [Google Scholar]
  • 10.Bresnahan JF, Smith GD, Lentsch RH. Nasal dermatitis in the Mongolian gerbil. Lab Anim Sci. 1983;33:258–263. [PubMed] [Google Scholar]
  • 11.Cantrell CA, Padovan D. Biology, care, and use in research. In: Van Hoosier GL, McPherson CW, editors. Laboratory Hamsters. Academic Press; Orlando: 1987. pp. 369–387. [Google Scholar]
  • 12.Carlton WW. Proceedings of the ILSI Histopathology Seminar on the Cardiovascular System of Laboratory Animals. International Life Sciences Institute; Orlando: 1991. Spontaneous cardiac lesions. [Google Scholar]
  • 13.Carter GR, Whitenack DL, Julius LA. Natural Tyzzer's disease in Mongolian gerbils (Meriones unguiculatus) Lab Anim Care. 1969;19:648–651. [Google Scholar]
  • 14.Chole RA, Henry KR, McGinn MD. Cholesteatoma: spontaneous occurrence in the Mongolian gerbil Meriones unguiculatis. Am J Otol. 1981;2:204–210. [PubMed] [Google Scholar]
  • 15.Committee on Infectious Diseases of Mice and Rats, Commission on Life Sciences, National Research Council . Infectious Diseases of Mice and Rats. National Academy Press; Washington, DC: 1991. [Google Scholar]
  • 16.Cunnane SC, Bloom SR. Intussusception in the Syrian golden hamster. Br J Nutr. 1990;63:231–237. doi: 10.1079/bjn19900110. [DOI] [PubMed] [Google Scholar]
  • 17.Datiles MBD, Fukui H. Cataract prevention in diabetic Octodon degus with Pfizer's sorbinil. Curr Eye Res. 1989;8:233–237. doi: 10.3109/02713688908997564. [DOI] [PubMed] [Google Scholar]
  • 18.Donnelly TM, Rush EM, Lackner PA. Ringworm in small exotic pets. Semin Avian Exotic Pet Med. 2000;9:82–93. [Google Scholar]
  • 19.Donnelly TM, Stark DM. Susceptibility of laboratory rats, hamsters, and mice to wound infection with Staphylococcus aureus. Am J Vet Res. 1985;46:2634–2638. [PubMed] [Google Scholar]
  • 20.Fehr M, Schanen H, Grof D. Anatomical basics and description of a method of castration in the degus [in German] Kleintierpraxis. 1994;39:837–840. [Google Scholar]
  • 21.Flynn BM, Brown PA, Eckstein JM. Treatment of Syphacia obvelata in mice using ivermectin. Lab Anim Sci. 1989;39:461–463. [PubMed] [Google Scholar]
  • 22.Fox JG, Murphy JC. Cytomegalic virus-associated insulitis in diabetic Octodon degus. Vet Pathol. 1979;16:625–628. doi: 10.1177/030098587901600520. [DOI] [PubMed] [Google Scholar]
  • 23.Friedman S, Weisbroth SH. The parasitic ecology of the rodent mite, Myobia musculi. IV. Life cycle. Lab Anim Sci. 1977;27:34–37. [PubMed] [Google Scholar]
  • 24.Georg LK: Animal ringworm in public health. Washington, DC, US Department of Health, Education, and Welfare, 1960, Report No 727.
  • 25.Germann PG, Kohler M, Ernst H. The relation of amyloidosis to social stress induced by crowding in the Syrian hamster (Mesocricetus auratus) Zeitschrift fur Versuchstierkunde. 1990;33:271–275. [PubMed] [Google Scholar]
  • 26.Gleiser CA, Van Hoosier GL, Sheldon WG. Amyloidosis and renal paramyloid in a closed hamster colony. Lab Anim Sci. 1971;21:197–202. [PubMed] [Google Scholar]
  • 27.Gray JE. Chronic progressive nephrosis, rat. In: Jones TC, Mohr U, Hunt RD, editors. Urinary System. Springer-Verlag; Berlin: 1986. pp. 174–178. [Google Scholar]
  • 28.Harkness JE. A practitioner's guide to domestic rodents. American Animal Hospital Association; Denver: 1993. [Google Scholar]
  • 29.Harvey RG, Whitbread TJ, Ferrer L. Epidermotropic cutaneous T-cell lymphoma (Mycosis fungoides) in Syrian hamsters (Mesocricetus auratus). A report of six cases and the demonstration of T-cell specificity. Vet Derm. 1992;3:13–19. doi: 10.1111/j.1365-3164.1992.tb00138.x. [DOI] [PubMed] [Google Scholar]
  • 30.Heider K, Eustis SL. Tumors of the soft tissues. In: Turusov VS, Mohr U, editors. Tumours of the mouse. 2nd ed. International Agency for Research on Cancer; Lyon: 1994. pp. 611–631. [Google Scholar]
  • 31.Herweg C, Kunstyr I. Effect of intestinal flagellate Spironucleus [Hexamita] muris and of dimetridazole on intestinal microflora in thymus-deficient (nude) mice. Zentralblatt fur Bakteriologie, Parasitenkunde, Infektionskrankheiten and Hygiene, Abteilung, 1, Originale A. 1979;245:262–269. [PubMed] [Google Scholar]
  • 32.Hotchkiss CE. Effect of surgical removal of subcutaneous tumors on survival of rats. J Am Vet Med Assoc. 1995;206:1575–1579. [PubMed] [Google Scholar]
  • 33.Hubbard GB, Schmidt RE. Noninfectious diseases. In: Van Hoosier GL, McPherson CW, editors. Laboratory Hamsters. Academic Press; Orlando: 1987. pp. 169–178. [Google Scholar]
  • 34.Huerkamp MJ. Correspondence [letter] Lab Anim Sci. 1990;40:5. [PubMed] [Google Scholar]
  • 35.Kohn DF, Barthold SW. Biology and diseases of rats. In: Fox JG, Cohen JB, Loew FM, editors. Laboratory Animal Medicine. Academic Press; Orlando: 1984. pp. 91–122. [Google Scholar]
  • 36.Koopman JP, Mullink JW, Kennis HM. An outbreak of Tyzzer's disease in Mongolian gerbils (Meriones unguiculatus) Z Versuchstierkd. 1980;22:336–341. [PubMed] [Google Scholar]
  • 37.Krogstad AP, Franklin CL, Besch-Williford CL: An epidemiological and diagnostic approach to murine skin lesions [abstract]. Proceedings of the 52nd American Association for Laboratory Animal Science National Meeting, Baltimore, 2001, p 94.
  • 38.Kuntze A. Diseases of guinea-pigs and golden hamsters important in practice. [German.] Monatshefte fur Veterinarmedizin. 1992;47:143–147. [Google Scholar]
  • 39.Kuo TH, Ho KL, Wiener J. The role of alkaline protease in the development of cardiac lesions in myopathic hamsters: effect of verapamil treatment. Biochem Med. 1984;32:207–215. doi: 10.1016/0006-2944(84)90074-7. [DOI] [PubMed] [Google Scholar]
  • 40.Laming PR, Cosby SL, O'Neill JK. Seizures in the Mongolian gerbil are related to a deficiency in cerebral glutamine synthetase. Comp Biochem Physiol C. 1989;94:399–404. doi: 10.1016/0742-8413(89)90088-1. [DOI] [PubMed] [Google Scholar]
  • 41.Lancefield RC. Group A streptococcal infections in animals—natural and experimental. In: Wannamaker LW, Matsen JM, editors. Streptococci and Streptococcal Diseases. Academic Press; New York: 1972. pp. 313–326. [Google Scholar]
  • 42.Lawson GA, Sato A, Schwiebert RS, et al: The efficacy of Derm Caps in the treatment of ulcerative dermatitis in C57BL/6 mice and related strains [abstract]. In Proceedings of the 52nd American Association for Laboratory Animal Science National Meeting, Baltimore, 2001, p 78.
  • 43.Lawson GHK, Gebhart CJ. Proliferative enteropathy. J Comp Pathol. 2000;122:77–100. doi: 10.1053/jcpa.1999.0347. [DOI] [PubMed] [Google Scholar]
  • 44.Lester PA, Rush HG, Sigler RE: Renal transitional cell carcinoma and choristoma in a degu (Octodon degu). In Proceedings of the 52nd American Association for Laboratory Animal Science National Meeting, Baltimore, 2001, p 99. [PubMed]
  • 45.Lindt VS. Uber krankheiten des syrischen goldhamsters (Mesocricetus auratus) Schweizer Archiv fur Tierheilkunde. 1958;100:86–97. [Google Scholar]
  • 46.Livingston RS, Simmons JH, Purdy GA, et al: Serologic diagnosis of rat respiratory virus (RRV) infection [abstract]. In Proceedings of 52nd American Association for Laboratory Animal Science National Meeting Baltimore, 2001, p 70.
  • 47.Lyerly DM, Bostwick EF, Binion SB. Passive immunization of hamsters against disease caused by Clostridium difficile by use of bovine immunoglobulin G concentrate. Infect Immun. 1991;59:2215–2218. doi: 10.1128/iai.59.6.2215-2218.1991. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 48.Matsumoto M, Kotani M, Fujita A. Therapeutic effects of persimmon leaf extract on atopic eczema in NC/Nga mice. [Japanese.] Nippon Eiyo Shokuryo Gakkaishi [J Jap Soc Nutrition Food Sci] 2001;54:3–7. [Google Scholar]
  • 49.Matsuoka K, Suzuki J. Spontaneous tumors in the Mongolian gerbil (Meriones unguiculatus). [Japanese.] Exp Anim. 1995;43:755–760. [PubMed] [Google Scholar]
  • 50.Montali RJ. An overview of tumors in zoo animals. In: Montali RJ, Migaki G, editors. The Comparative Pathology of Zoo Animals. Smithsonian Institution Press; Washington, DC: 1980. pp. 531–542. [Google Scholar]
  • 51.Motzel SL, Gibson SV. Tyzzer disease in hamsters and gerbils from a pet store supplier. J Am Vet Med Assoc. 1990;197:1176–1178. [PubMed] [Google Scholar]
  • 52.Murphy JC, Crowell TP, Hewes KM. Spontaneous lesions in the degu (Rodentia, Hystricomorpha: Octodon degus) In: Montali RJ, Migaki G, editors. The Comparative Pathology of Zoo Animals. Smithsonian Institution Press; Washington, DC: 1980. pp. 437–444. [Google Scholar]
  • 53.Najecki D, Tate B. Husbandry and management of the degu. Lab Anim. 1999;28:54–62. [Google Scholar]
  • 54.Norris ML, Adams CE. Incidence of cystic ovaries and reproductive performance in the Mongolian gerbil, Meriones unguiculatus. Lab Anim. 1972;6:337–342. doi: 10.1258/002367772781006176. [DOI] [PubMed] [Google Scholar]
  • 55.Nowak RM. Walker's Mammals of the World. 6th ed. The Johns Hopkins University Press; Baltimore: 1999. [Google Scholar]
  • 56.Ottenweller JE, Tapp WN, Burke JM. Plasma cortisol and corticosterone concentrations in the golden hamster (Mesocricetus auratus) Life Sci. 1985;37:1551–1558. doi: 10.1016/0024-3205(85)90188-2. [DOI] [PubMed] [Google Scholar]
  • 57.Peace TA, Brock KV, Stills HF., Jr Comparative analysis of the 16S rRNA gene sequence of the putative agent of proliferative ileitis of hamsters. Int J Syst Bacteriol. 1994;44:832–835. doi: 10.1099/00207713-44-4-832. [DOI] [PubMed] [Google Scholar]
  • 58.Percy DH, Greenwood JD, Blake B. Diagnostic exercise: sloughing of limb extremities in immunocompromised suckling mice. Contemp Top Lab Anim Sci. 1994;33:66–67. [PubMed] [Google Scholar]
  • 59.Port CD, Richter WR, Moise SM. Tyzzer's disease in the gerbil (Meriones unguiculatus) Lab Anim Care. 1970;20:109–111. [PubMed] [Google Scholar]
  • 60.Renshaw HW, Van Hoosier GL, Jr, Amend NK. A survey of naturally occurring diseases of the Syrian hamster. Lab Anim. 1975;9:179–191. doi: 10.1258/002367775780994592. [DOI] [PubMed] [Google Scholar]
  • 61.Rübel GA, Isenbügel E, Wolvekamp P. Atlas of Diagnostic Radiology of Exotic Pets. WB Saunders; Philadelphia: 1991. [Google Scholar]
  • 62.Schmidt RE, Eason RL, Hubbard GB. Pathology of Aging Syrian Hamsters. CRC Press; Boca Raton: 1983. [Google Scholar]
  • 63.Schneider JE, Wade GN. Effects of maternal diet, body weight and body composition on infanticide in Syrian hamsters. Physiol Behavior. 1989;46:815–821. doi: 10.1016/0031-9384(89)90042-5. [DOI] [PubMed] [Google Scholar]
  • 64.Schneider JE, Wade GN. Effect of ambient temperature and body fat content on maternal litter reduction in Syrian hamsters. Physiol Behavior. 1991;49:135–139. doi: 10.1016/0031-9384(91)90244-i. [DOI] [PubMed] [Google Scholar]
  • 65.Short BG, Goldstein RS. Nonneoplastic lesions in the kidney. In: Mohr U, Dungworth DL, Capen CC, editors. Pathobiology of the Aging Rat. International Life Sciences Institute Press; Washington, DC: 1992. pp. 211–225. [Google Scholar]
  • 66.Sichuk G, Bettigole RE, Der BK. Influence of sex hormones on thrombosis of the left atrium in Syrian (golden) hamsters. Am J Physiol. 1965;208:465–470. doi: 10.1152/ajplegacy.1965.208.3.465. [DOI] [PubMed] [Google Scholar]
  • 67.Silverman S. Diagnostic imaging of exotic pets. Vet Clin North Am Small Anim Pract. 1993;23:1287–1299. doi: 10.1016/s0195-5616(93)50156-0. [DOI] [PubMed] [Google Scholar]
  • 68.Solomon HF, Dixon DM, Pouch W. A survey of staphylococci isolated from the laboratory gerbil. Lab Anim Sci. 1990;40:316–318. [PubMed] [Google Scholar]
  • 69.Spear GS, Caple MV, Sutherland LR. The pancreas in the degu. Exp Mol Pathol. 1984;40:295–310. doi: 10.1016/0014-4800(84)90047-9. [DOI] [PubMed] [Google Scholar]
  • 70.Squartini F, Pingitore R. Tumours of the mammary gland. In: Turusov VS, Mohr U, editors. Tumours of the Mouse. 2nd ed. International Agency for Research on Cancer; Lyon: 1994. pp. 47–100. [Google Scholar]
  • 71.Strauli P, Mettler J. Tumours of the haematopoietic system. In: Tursusov VS, editor. Tumours of the Hamster. International Agency for Research on Cancer; 1982. [Google Scholar]
  • 72.Tyzzer EE. A fatal disease of the Japanese waltzing-mouse caused by a spore-bearing bacillus (Bacillus piliformis N. sp.) J Med Res. 1917;37:307–338. [PMC free article] [PubMed] [Google Scholar]
  • 73.Vincent AL, Rodrick GE, Sodeman WA., Jr The pathology of the Mongolian gerbil (Meriones unguiculatus): a review. Lab Anim Sci. 1979;29:645–651. [PubMed] [Google Scholar]
  • 74.Waggie KS, Ganaway JR, Wagner JE. Experimentally induced Tyzzer's disease in Mongolian gerbils (Meriones unguiculatus) Lab Anim Sci. 1984;34:53–57. [PubMed] [Google Scholar]
  • 75.Walberg JA, Stark DM, Desch C. Demodicidosis in laboratory rats (Rattus norvegicus) Lab Anim Sci. 1981;31:60–62. [PubMed] [Google Scholar]
  • 76.Wardrop KJ, Van Hoosier GL. The hamster. In: Loeb WF, Quimby FW, editors. The Clinical Chemistry of Laboratory Animals. Pergamon Press; New York: 1989. pp. 31–39. [Google Scholar]
  • 77.White DJ, Waldron MM. Naturally-occurring Tyzzer's disease in the gerbil. Vet Rec. 1969;85:111–114. doi: 10.1136/vr.85.5.111. [DOI] [PubMed] [Google Scholar]
  • 78.Worgul BV, Rothstein H. Congenital cataracts associated with disorganized meridional rows in a new laboratory animal the degu (Octodon degus) Biomedi Express. 1975;23:1–4. [PubMed] [Google Scholar]

SUGGESTED READING AND RESOURCES

Children

  1. Step by Step Series: Chinchillas; Gerbils; Guinea Pigs; Hamsters; Dwarf Rabbits; Rabbits. TFH Publications (www.tfh.com), paperback, 64 pp.
  2. Barron's Young Pet Owners Guides: Taking Care of Your Gerbils; Guinea Pig; Hamster; Rabbit. Barron's Educational Guides, Hauppauge, NY, paperback, 32 pp.
  3. Dorling-ASPCA Pet Care Guides for Kids: Guinea Pigs; Hamster; Rabbit. Houghton Mifflin, Boston, hardback, 32 pp.

Adults

  1. Complete Introduction (KW) Series: Chinchillas; Gerbils; Guinea Pigs; Hamsters; Rabbits. TFH Publications (www.tfh.com), hardback, 128 pp.
  2. Proper Care Series: Gerbils; Guinea Pigs; Dwarf Rabbits; Fancy Rats. TFH Publications (www.tfh.com), hardback, 256 pp.
  3. Barron's Complete Pet Owners Manuals: Chinchillas; Degus; Dwarf Hamsters; Gerbils; Guinea Pigs; Hamsters; Mice; Prairie Dogs; Rats; Fancy Rats; Rabbits; Dwarf Rabbits. Barron's Educational Guides, Hauppauge, NY, paperback, 64-104 pp. Since 1999, all publications in the Complete Pet Owners Manuals are written by experienced veterinarians. These books have good husbandry and basic disease sections and are the best value for their price.

Veterinary Resources

Exotic DVM

Zoological Education Network

PO Box 541749

Lake Worth

FL 33454-1749

800-946-4782

www.exoticdvm.com

Lab Animal

345 Park Ave South, 10th floor

New York, NY 10010-1707

www.labanimal.com

This site has an online subscription form for the United States. For subscriptions to other parts of the world go to: www.agenda-rm.co.uk/subscription_form.pdf

Association of Exotic Mammal Veterinarians (AEMV)

PO Box 396

Weare, NH 03287-0396

www.aemv.org


Articles from Ferrets, Rabbits, and Rodents are provided here courtesy of Elsevier

RESOURCES