DISEASES OF LABORATORY RODENTS
Research Animal Methods- - Fall 2011
Lecture for 10/31/2011
David G. Besselsen, DVM, PhD
University of Arizona - Tucson
Students should also be able to recognize certain infectious agents that, although they are not associated with clinical disease, are frequently encountered in contemporary rodent colonies and have adverse effects on research. Finally, students should be able to recognize the most common non-infectious diseases encountered in the laboratory rodents.
I. MOUSE DISEASES
Mouse Hepatitis Virus (MHV) MHV is a coronavirus RNA virus) that only affects mice. Several MHV strains display tropisms for different tissues but all share the ability to replicate in the liver. Transmission can occur by the fecal-oral route, direct contact, aerosolization, and fomites. There are two major patterns of disease based on the tropism of the virus strain. The respiratory pattern begins in the nasal passages and lungs with dissemination to other organs (including the brain) by the hematogeneous route. Intestinal involvement is minimal, if present at all. The enteric pattern infects the nasal passages and bowel with variable spread to the liver and abdominal lymph nodes. Disease expression is age and strain dependent, ranging from watery diarrhea and high mortality in suckling mice to weight loss and variable death rates in adult mice. Immunodeficient adult nude mice exhibit a progressive wasting disease. MHV is a common contaminant of tumor cell lines and is immunosuppressive in vivo, even if subclinical. Serology (ELISA, IFA) and histology (liver, large intestine) are commonly used for diagnosis. The three most common control measures are to tolerate infection in the colony (it eventually becomes endemic), rederive the colony (by caesarean section or embryo transfer), or restock with clean animals. If MHV-free mice are obtained, strict attention to husbandry is required to prevent reintroduction of the virus. The stop-breeding technique to halt the infection of susceptible weanlings (as is done with Sendai virus) is also an effective way to eliminate the virus.Sendai Virus
Sendai virus is a paramyxovirus (RNA virus) of the parainfluenza type 1 group and is known to infect mice, rats, hamsters, and guinea pigs. Direct contact and airborne transmission, even over distances of 5-6 feet, are known means of spread of the disease. Infections are usually enzootic in a colony and are maintained by horizontal transmission in young rodents. Infected rodents may exhibit labored breathing and decreased fecundity. This virus is immunosuppressive and may predispose to secondary bacterial infections. In clinically apparent infections, signs are variable but may include chattering, mild respiratory distress to labored breathing, and decreased fecundity in adults, deaths (possibly whole litters) in neonates and sucklings, and poor growth in weanling and young adults. Clinical signs are generally not observed in endemically infected colonies. Serology and histology (lungs) are commonly used for diagnosis. In static colonies, the disease will run its course; no latent infections occur. In breeding colonies, cessation of breeding for 60 days, elimination of all suckling mice during this time period, and purposeful mixing of weanlings and adults to insure maximum viral exposure of all susceptible mice will prevent infections of future litters.Mouse Parvoviruses
Minute virus of mice (MVM) and mouse parvovirus (MPV) are two distinct serotypes of parvoviruses (DNA virus) that infect mice. Transmission occurs by fecal-oral and direct contact. Clinical disease in mice has never been documented in natural infections. However, these viruses cause persistent infections and modulate the immune response in mice and are common contaminants of transplanted cell lines and tumors. Serology is used for diagnosis. These viruses can be eliminated by rederivation or depopulation. Disinfection of the environment is extremely important since parvoviruses are very resistant in the environment.Lymphocytic Choriomeningitis (LCM)
LCM virus is an arenavirus (RNA virus). Mice are the primary host for this virus, while hamsters are an important secondary host since they also develop chronic viremia and viruria. Numerous other mammalian species can be infected with LCM virus including rats, guinea pigs, non-human primates, and humans. In mice, in utero or perinatal infections produce a persistent, subclinical infection with life-long viremia and shedding of virus in urine, saliva and milk. In fact, vertical (transovarian and/or transuterine) transmission is considered 100% efficient for mice born to infected dams. Transmission among adult mice and hamsters is horizontal via direct contact. A major source of infection in contemporary laboratory rodent colonies is transplanted rodent tumor cell lines. In mice, persistent, subclinical infections result in modest growth retardation and eventually immune complex glomerulonephritis which is associated with emaciation, ruffled fur, hunched posture, ascites and some deaths. Acuteinfection occurs when the mice are exposed after the first week of life (after the development of immunocompetence).The outcome is either death within a few days or weeks, or recovery with elimination of the virus. Hamsters and other mammals are naturally infected with LCM from exposure to secretions/excretions from infected rodents. Serology and histology (brain) are used for diagnosis. Depopulation is the only recommended control measure due to the zoonotic nature of the virus and since vertical transmission of the virus in mice makes other control measures useless. Public Health Significance: CDC reports human LCM infections; to date, all zoonoses have been linked to exposure to infected mice and hamsters or to accidents associated with in vitro LCM production.
Ectromelia virus, the causative agent of mousepox, is a poxvirus (DNA virus) and is considered one of the most contagious, potentially-lethal diseases of mice. Natural infections occur via the fecal-oral route, urine contamination or by direct contact. Skin abrasions are thought to provide the main route of entry. Inoculation of mice with poxvirus infected tumor cells or serum has also caused disease outbreaks. All mice are susceptible to infection, but the severity of clinical disease varies greatly with the strain of mouse infected. In acute clinical disease, there is high morbidity and high mortality with affected animals exhibiting hunched posture, conjunctivitis and facial swelling. Subacute to chronically infected animals develop a cutaneous vesicular body rash which often progresses to swelling, necrosis and sloughing of the extremities (ectromelia). Deaths are sporadic. Clinical and gross pathology signs are highly suggestive of the disease. Histology (skin, liver) and serology are used to confirm the diagnosis. If the animals are readily available commercially, depopulation is recommended with sanitization of the facility with formalin.
Pasteurella pneumotropica is a gram-negative, short pleomorphic rod with bipolar staining properties and is known to infect mice, rats, gerbils, hamsters, and guinea pigs. Transmission by aerosol, fecal-oral, and contact with infected secretions (including venereal transmission) has been reported. The bacteria is considered an opportunistic pathogen, proliferating in the presence of other respiratory microbial pathogens. The majority of infected rodents show no clinical signs. Upper respiratory infections can manifest as oculonasal discharge, torticollis from otitis media, and/or dyspnea (if mycoplasmal and/or viral respiratory disease are also present). Epidemics of conjunctivitis and panophthalmitis have been reported in weanling mice. Subcutaneous abscesses, mastitis, metritis and accessory sex gland abscesses have also been observed. Cultures of the ocular, skin or glandular tissues usually reveal mixed infections of Pasteurella pneumotropica with Mycoplasma pulmonis or other bacterial flora. Sendai virus and Mycoplasma pulmonis antibody titers are usually detected in rodents with pneumonia. Long-term antibiotic therapy with high doses of Baytril (enrofloxacin) has been reported to eliminate subclinical infections in mice; the efficacy of this antibiotic for elimination of this bacteria from other rodents is unknown. Since intrauterine infection of pups can occur, cesearian rederivation may not eliminate the infection.Helicobacter Hepatitis and Typhlocolitis
Helicobacter hepaticus, H. bilis, and H. cholecystus are recently recognized pathogens of laboratory mice and rats that can induce chronic active hepatitis and typhlocolitis in susceptible strains. Infections are persistent and usually subclinical, although rectal prolapse is occasionally observed. A/J mice infected with H. hepaticus also have an increased incidence of hepatic tumors, and H. hepaticus can alter serum enzyme levels, bile acid profiles, and heat-shock protein expression. Transmission occurs by the fecal-oral route with fomite transmission likely. Diagnosis can be made by serology, polymerase chain reaction (PCR), microaerophilic culture, or histology (liver). An antibiotic-impregnated feed is commercially available and can be used to eradicate H. hepaticus infections in mice and rats, although the effectiveness of this treatment on other Helicobacter species is unknown. Ceaserean rederivation may not be effective since experimental infections of pregnant dams have resulted in transmission of H. hepaticus to mouse feti.
Salmonella typhimurium,and S. enteritidis are gram-negative, toxin-producing, invasive, enteric bacteria that can infect numerous animal species including all laboratory rodent species. The disease is spread by fecal-oral transmission. A common source of infection for laboratory rodents is food, water, or bedding that has been contaminated by infected feces from wild rodents. Clinical signs in acute epizootics may include hunched posture, anorexia, lethargy, diarrhea, and high to sporadic mortality in weanlings, and abortion or sudden death in adults. The disease will eventually become endemic, with periodic cycling of overt disease symptoms such as acute deaths, chronic low fertility, fetal resorption, or abortion. Clinical signs and identification of wild rodent exposure can be suggestive of salmonellosis. Culture and histology of the intestine, liver and spleen provide a definitive diagnosis. Depopulation is the recommended control procedure. Prevention of food, bedding, water, or laboratory rodent contamination by wild vermin and proper sanitizing of cages and watering equipment has virtually eliminated this disease from contemporary laboratory rodent colonies. Public Health Significance: Humans ingesting Salmonella typhimurium contaminated food or water may experience a transient diarrhea. Children or immunocompromised adults may experience more severe disease. The disease in humans is reportable.
Pseudomonas SepticemiaPseudomonas aeruginosa is a water saprophyte that can colonize the intestinal tract of mice and rats following consumption of nonsterile water. A septicemic and endotoxemic syndrome has been reported in colonized mice and rats that have been treated with immunosuppressive drugs or X-irradiation. Although the systemic disease cannot be treated, the syndrome can be prevented by supplying acidified or chlorinated drinking water to rodents scheduled for immunosuppressive therapy. Frequent monitoring or changing of treated water is critical to maintain the proper pH or chlorination.
Staphylococcal FurunculosisStaphylococcus aureus is considered normal flora of the skin and mucous membranes of mice, but is considered a primary pathogen in athymic nude mice. Thymic deficient nude mice, by virtue of the lack of a hair coat and a depleted T-lymphocyte population, develop conjunctivitis and subcutaneous granulomas from which S. aureus can be recovered in pure culture. Inoculation of the bacteria into the skin apparently occurs from grooming or bite wounds, and although the skin usually remains intact, the resultant granuloma progressively enlarges and occasionally spreads subcutaneously to form disfiguring lumps, primarily about the face and head.
PARASITIC DISEASESPneumocystis pneumonia
Pneumocystis carinii is an opportunistic pathogen of the respiratory tract of mice, rats and probably all domestic mammals and man. It is believed to be a protozoan. Transmission occurs by the inhalation of infective cysts. Mice that are immunosuppressed, either by exogenous therapy or by virtue of a hereditary immunological defect, may develop a fatal pneumonia. Affected mice display hunched posture, tachypnea, and weight loss when the pneumonia has consumed a significant portion of the lung. Decreased reproductive efficiency is commonly observed in colonies of immunodeficient mice. Histology of the lungs and polymerase chain reaction are commonly used for diagnosis. Special histochemical stains are needed to visualize the trophozoites and cysts in lung sections. Caesarean rederivation can eliminate P. carinii from a colony. Trimethoprim-sulfa antibiotic combinations are useful for preventing clinical disease in infected colonies of immunodeficient mice but do not eliminate infection.
Fur Mites (Acariasis)
Myocoptes musculinus, Myobia musculi, and Radfordia affinis are host-specific fur mites of mice. Fur mites of other laboratory rodent species include Radfordia ensifera in rats and Chirodiscoides caviae in guinea pigs. Mite transmission occurs by direct contact. Usually no clinical signs are observed, although black-haired mice are thought to have an allergic sensitivity to the mites manifested by pruritus and alopecia progressing to excoriation, ulcerative dermatitis, and disfigurement (see self-mutilation under miscellaneous diseases). On live rodents, plucking hairs from the pelt and examining under a dissecting microscope may reveal mites or eggs (attached to the hair shaft). If the pelt from a recently killed rodent is cooled to room temperature, the mites will crawl up to the tips of the hairs, looking like white specks. Treatments with parasiticides can be used to eliminate mites from infested rodent colonies.
Rodent pinworms display some host-specificity, although some can cross species barriers. In general, Syphacia obvelata and Aspiculuris tetraptera are considered mouse pinworms, Syphacia muris the rat pinworm, Syphacia mesocricetus the hamster pinworm, and Denstomella translucida the gerbil pinworm. Syphacia spp. pinworms deposits eggs in the perianal region while Aspiculuris tetraptera and Denstomella translucida release eggs in the colon which then are passed in fecal pellets. Infestation occurs via ova ingestion. The eggs are very light and have been shown to aerosolize, resulting in widespread exposure. No clinical signs are usually seen, although it has been reported that heavy parasite loads may lead to rectal prolapse or perianal irritation. Heavy parasitism may affect the immunocompetency of the animal. Direct exam of cecal or colonic contents will identify adults, while fecal flotation and tape impression tests of the perianal region will identify eggs. Aspiculuris tetraptera and Denstomella translucida eggs will be missed by tape test alone. Prevention and control of infestation are difficult. Rigid sanitary procedures, use of filter hoods to prevent aerosol transmission, and regular ova examinations with parasiticide treatment of infected animals may control the parasitism. Rederivation will also eliminate the infection. Routine disinfection of animal facilities will not destroy pinworm ova.
NEOPLASTIC DISEASESMammary Tumors
Mammary adenocarcinomas (malignant) are the one of the two most common neoplasias of mice and may be located nearly anywhere in the subcutaneous region due to the extensive distribution of mammary tissue in the mouse. They are induced by mouse mammary tumor viruses (retroviruses). These viruses can be transmitted vertically by passage through the placenta or in the milk. Grossly the tumor is soft, fleshy, and well vascularized. It may contain necrotic tissue and/or blood-filled cysts. Mammary tumors may be surgically removed, but the prognosis is poor due to the anaplastic, invasive nature of the tumors in mice.
LymphomasLymphomas are the other most common spontaneous neoplastic disease of mice, incidence of which is dependent on the strain of mouse. Lymphocytic, lymphoblastic, and follicular center cell lymphomas and histiocytic sarcomas are commonly observed. C-type viral particles (retrovirus) have been observed in murine lymphomas.
Malocclusion is a condition caused by overgrown teeth as a result of trauma, bacterial infection, or genetic factors. Malocclusion is observed only in incisor teeth in mice, rats, hamsters, and gerbils, while premolar and molar malocclusion are most common in guinea pigs (remember: histrichomorph rodents have hypsodont cheek teeth!). Clinical signs of malocclusion can include hypersalivation, weight loss, teeth-grinding, depression and emaciation. Treatment consists of clipping overgrown teeth every 2 to 3 months.
Fight woundsMice (particularly males) may fight and can inflict severe wounds upon each other. These usually are located on the face, back, and genital areas. If tail biting occurs, the tail may become gangrenous and slough. The wounds may become infected and develop into abscesses. Prevention is by separating the offending animals.
For some reason (possibly boredom or overcrowding), a female mouse may develop a fur-chewing vice and chew the hair off a cage mate or her litter. This usually involves the hair over the nasal and orbital regions or the dorsal cervical area. The exposed skin is intact and normal in appearance. The only cure for barbering, if the client considers it a problem, is to separate the animals or remove the mouse that has not been barbered.
Self-mutilationSeveral inciting factors can induce a pruritic dermatitis which often can progress to self-mutilation from excessive scratching. The scratching can lead to excoriation and ulceration of the skin of the neck and subsequent inoculation of the wounds with environmental bacteria contaminating the feet. The resulting dermatitis evokes a more intense scratching reflex until a large ulcerative pustular dermatitis results from the self-mutilating activity. Potential inciting factors include otitis media (middle ear infection), fur mite infestation, and chemical irritation (from the use of tweezers disinfected with germicidal solutions for transfer of mice between sterile microisolation cages). Black pigmented strains of mice (particularly C57BL/6 and C57BL/10) frequently develop a severe ulcerative dermatitis as they age through a similar pathogenesis that is incited by an immune-mediated mechanism.
II. RAT DISEASES
VIRAL DISEASESRat Coronavirus (RCV) Infection
RCV is a coronavirus (RNA virus) that is also referred to as sialodacryoadenitis virus (SDAV). The virus is highly contagious and is spread by aerosol, direct contact, and fomites. No latent infection or carrier state occurs. The disease is not fatal, and is generally subclinical. The rats may exhibit a porphyrin oculonasal discharge. The submaxillary salivary gland may be palpably enlarged due to sialoadenitis. Dacryoadenitis may cause exophthalmos, which can lead to keratitis and corneal ulcers. Symptomatic rats are at a greater risk for inhalation anesthesia. Clinical signs, serology, and histology (salivary and Harderian glands) are used for diagnosis. Cessation of all breeding activity in a production colony for 60 days and concomitant removal of all suckling and weanling animals or intentional exposure of these young rats by frequent mixing will eliminate the infection in the colony.
Rat ParvovirusesKilham rat virus (KRV), H-1 virus, and rat parvovirus (RPV) are distinct serotypes of parvoviruses (DNA virus) which infect rats. Transmission occurs by fecal-oral and direct contact. Some strains of KRV and H-1 can be transmitted in utero. Clinical disease in rats is rare, but sometimes KRV manifests as a central nervous system hemorrhage, cerebellar hypoplasia, and/or decreased reproduction secondary to embryonic death. These viruses cause persistent infections, modulate the immune response in rats, and are common contaminants of transplanted cell lines and tumors. Serology and gross pathology (when present) are used for diagnosis. These viruses can be eliminated by ceaserean rederivation or depopulation. Since some strains can be transmitted in utero, serology must be performed following rederivation to ensure elimination of these viruses. Disinfection of the environment is extremely important since parvoviruses are very resistant in the environment.
Mycoplasma pulmonis is a microbial organism that lacks a cell wall and causes chronic progressive respiratory disease in mice and rats. Transmission by aerosol, fecal-oral, and contact with infected secretions (including venereal transmission) has been reported. Most infections are subclinical. Adverse environmental factors, such as high cage ammonia levels, and/or the acquisition of primary viral or bacterial respiratory pathogens, activate subclinical mycoplasmal infections. Sites of predilection in the host are the nasopharynx, middle ear, lung, and uterus. Signs of overt disease include oculonasal discharge and otitis media, followed by labored breathing, anorexia, and hunched posture occur. Other clinical signs include snuffling, chattering, head tilt, anorexia/weight loss, rough hair coat, hunched posture, and reduced fertility. In addition to clinically apparent disease, subclinical infections can adversely affect research by impairing respiratory function and the immune system. Diagnosis is made by serology, culture, or histology (lungs). Other respiratory pathogens such as Pasteurella pneumotropica and Sendai virus are frequently identified along with Mycoplasma pulmonis. Depopulation is recommended to eliminate the disease. Since intrauterine infection of pups can occur, ceasarian derivation may not eliminate the infection.
Tyzzer's DiseaseClostridium piliforme is a gram-negative, obligate intracellular, spore-forming rod that infects mice, rats, hamsters, gerbils, guinea pigs, rabbits, cats, dogs, horses, and possibly humans. Transmission occurs via fecal-oral route by ingestion of spores, which may remain in the environment for a year or more. Factors which predispose to overt clinical disease include the immune status, age (sucklings, weanlings), and strain of the rodent host, and physiological stresses such as concurrent microbial infections, experimental manipulations, poor housing conditions, or corticosteroid administration. Gerbils are unique among the laboratory rodents in that they develop clinical disease in the absence of stressful predisposing factors. Anorexia, hunched posture, ruffled, rough hair coat, watery diarrhea, pasting of feces around perineum, inactivity, and sudden death are common clinical signs. Since the organism cannot be propagated on artificial media, diagnoses are made by serology or histology (liver, intestine). Avoidance of stress and strict sanitation help prevent outbreaks in infected colonies. Depopulation is the current recommendation for eliminating the disease.
NEOPLASTIC DISEASESMammary Fibroadenoma
This is the most common tumor of rats. Because of the extensive mammary tissue present in rats, tumors may be found practically anywhere - behind the shoulder blades, at the base of the tail, etc. Tumors may occur in males as well as in females. The tumors, which appear as subcutaneous lumps, may be quite extensive. Ulceration and subsequent dermatitis occur frequently. Tumors are usually encapsulated and benign. With surgical removal, the prognosis is good, although recurrence in another location is not uncommon. The progression of either the glandular or fibrous component to malignancy is rare.Large Granular Lymphocyte Leukemia (Fischer Rat Leukemia)
A spontaneous leukemia with circulating atypical lymphocytes containing azurophilic cytoplasmic granules has been reported in aged Wistar Furth (WF) and Fischer 344 (F344) rat strains with an incidence of 17%-25% in aged rats. This leukemia is one of the most common neoplasms in aged F344 rats and is frequently referred to as Fischer Rat Leukemia. Clinically, leukocytosis with up to 90% atypical lymphocytes and anemia are observed. Splenomegaly, hepatomegaly and lymphadenopathy are seen at necropsy. Tissue enlargement is due to massive infiltration by neoplastic lymphocytes. Leukemic cells are thought to be of natural killer (NK) cell origin.
MISCELLANEOUS DISEASESHeat Exhaustion Rats have a limited ability to regulate body temperature with the primary thermoregulatory mechanism being tail vein dilation or constriction. Predisposing factors to heat exhaustion are ambient temperatures above 28oC (85oF), high humidity (about 80%), poor ventilation and overcrowding. The rats salivate profusely to wet the hair coat for cooling, and water consumption increases. Death from heat exhaustion can be diagnosed from a history of high temperature, lack of water (or empty water bottles), saliva soaked chins, hyperemia of lungs and mesenteric vessels, and hemorrhage in the thymus.
RingtailInsufficient environmental humidity (<20%), elevated temperatures, and drafts predispose this condition. Annular constriction of the tail or tail sloughing may be observed in weanling rats. Diagnosis is made on clinical signs and a history of low environmental humidity. There is no treatment for affected rats. Tail stumps usually heal without complication. Prevention of ringtail is accomplished by providing sufficient environmental humidity, reducing drafts, and maintaining room temperatures between 70-74°F.
Chronic GlomerulonephropathyA chronic disease frequently observed in aged rats that results in renal insufficiency and often renal failure. Presumptive diagnosis is made by blood chemistry analysis and the characteristic small, pitted kidneys at necropsy. Histology confirms the diagnosis. Dietary restriction (particularly protein intake) has been shown to delay the onset and decrease the severity of this disease.
III. HAMSTER DISEASES
BACTERIAL DISEASESProliferative ileitis
The disease in hamsters is caused by an intracellular bacteria closely related if not identical to Lawsonii intracellularis, which causes a similar disease in domestic swine. Previous names for these closely-related organisms include campylobacter-like organism (CLO), Ileal-symbiont Intracellularis, and Ileobacter intracellularis. The disease is transmitted via direct fecal-oral contact and fomite contamination. Acute disease is manifest by lethargy, anorexia, irritability, ruffled hair, diarrhea, dehydration, and death. Moist feces stains the base of the tail. The disease occurs primarily in weanling hamsters, but has been noted in adult animals debilitated by concurrent disease. Diagnosis is made primarily by recognition of characteristic gross and histologic lesions consisting of greatly thickened ileal and/or cecal walls from mucosal epithelial hyperplasia. Verification of the causative agent can be accomplished by a polymerase chain reaction (PCR) assay. Depopulation or rederivation are effective means to eliminate the infection.
Clostridial TyphlitisAcute diarrheal disease associated with variable morbidity and high mortality may result from infections with Clostridium perfringens, C. difficile, and/or C. spireforme in hamsters and guinea pigs. These anaerobic bacteria produce toxins that cause edema, hemorrhage, and occasionally mucosal dysfunction and necrosis. The typhlitis occurs in hamsters and guinea pigs experiencing immunosuppression from concurrent infectious or metabolic disease, or cecal bacteria dysbiosis from chronic antibiotic therapy or nutritional imbalance. The disease is tentatively diagnosed at necropsy when serosal and mucosal hemorrhages are observed. Definitive diagnosis can be made by the identification of the bacteria in anaerobic cultures, detection of toxins in cecal filtrates, and histology. Treatment and control are targeted at control of infectious and environmental stressors, and cessation of antibiotic treatments.
PARASITIC DISEASESTapeworms (Cestodiasis)
Hymenolepis nana is the dwarf tapeworm and Hymenolepis diminuta is the rat tapeworm; both can infect mice, rats, hamsters, and gerbils. Transmission occurs indirectly with cockroaches, grain beetles, or fleas as intermediate hosts. Hymenolepis nana can also be transmitted by direct ingestion of hexacanth ova or by autoinfection in which the entire life cycle occurs in the host's small intestine. Usually there are no external signs of infection, however, catarrhal enteritis, diarrhea, emaciation and chronic weight loss may occur with heavy infestations. Visualization of the tapeworm in the small intestine during necropsy, recovery of hexacanth ova by fecal flotation, or microscopic visualization of parasites in histological sections of the small intestine villi are methods of diagnosis. Control includes parasiticide treatment or elimination of infected animals and elimination of cockroaches. Public Health Significance: Humans are susceptible to infections with H. nana. Since autoinfection can occur, a heavy parasite load may quickly develop.
Demodex criceti and Demodex aurati are mange mites of hamsters that can also infect gerbils. High incidence of infestation occurs without clinical signs. The two species of mites are generally found together. Demodex criceti is considered non-pathogenic, has a shorter body length and is found in the epidermis. Demodex aurati, the more pathogenic mite, is longer that Demodex criceti, and is found in the pilosebaceous component of the skin. Demodex infestations are thought to be spread by direct contact. Clinical signs can range from none to alopecia, dry, scaly, scabby dermatitis, and rough hair coat. Alopecia generally occurs over the rump and back. Predisposing factors are necessary for the development of clinical signs and include malnutrition, concurrent systemic disease, and age. Skin scrapings of alopecic skin and histopathology are used for diagnosis. Since demodicosis is generally secondary to immunosuppression, sources of stress should be eliminated to reduce clinical disease.
MISCELLANEOUS DISEASESFight Wounds
Fight wounds in hamsters are common. Animals will attack each other, often for no apparent cause. Many times attacks occur when food and water are in short supply. Also females will attack males during mating. Males will fight briefly when first placed in new environments as a means of establishing social dominance. Subcutaneous abscesses are a frequent sequelae.
Cannibalism of litters by female hamsters and mice are common if disturbed after parturition. To avoid cannibalism, nest material should be placed in the cage prior to parturition and the hamster or mouse should not be disturbed for several days after parturition.
IV. GERBIL DISEASES
BACTERIAL DISEASESNasal Dermatitis (Sorenose)
The precise cause of this disease is unknown, but stress and secondary bacterial infections are thought to play important roles. Stresses such as overcrowding, weaning, and environmental variations are thought to cause an increased secretion of porphyrin-containing fluid from the Harderian gland, and accumulation of these secretions around the external nares and eyes may result in irritation, self-induced trauma, and secondary bacterial infections. Alopecia, erythema, focal dermatitis, and frequent scab and ulcer formation are all features of the typical case. The perinasal area is normally affected most severely, at least in early cases. The periocular region frequently becomes involved in more chronic cases. A well-established, moist, ulcerative dermatitis can spread to involve the remainder of the head, the forelimbs, and the ventrum of the chest and abdomen. Diagnosis relies on clinical signs. This disease is normally self-limiting when the predisposing stress factor has been removed.
The gerbil displays spontaneous epileptiform seizures. These seizures may be precipitated by sudden stress, handling, or introduction to a novel environment. Incidence of this syndrome is about 20% in natural populations. The condition appears to be inherited, and both seizure-resistant and seizure-sensitive strains have been developed by selective breeding. Inbred animals can have up to 100% incidence. Seizures vary in severity from mild hypnotic episodes characterized by cessation of activity and twitching of the pinnae and vibrissae, to severe myoclonic convulsions followed by tonic extensor rigidity. Post-seizure fatality occurs in less than 1% of affected animals. There is no permanent damage. Seizure onset occurs at 2 to 3 months of age with seizure incidence and severity increasing with age until the animal reaches six months of age. A refractory period of up to five days can follow more severe seizures. Research has shown that the seizure response can be almost completely suppressed in genetically predisposed animals if they are frequently stimulated by handling during the first three weeks of life.
Fractures of the tail vertebrae, and slipping of the tail skin can all occur with improper handling. This usually involves picking up animals by the distal portion of the tail. Surgical amputation with supportive post-surgical care may be necessary when large amounts of tissue are compromised. Such injuries may be prevented by handling animals by the base of the tail.
V. GUINEA PIG DISEASES
BACTERIAL DISEASESBordetella Pneumonia
Bordetella bronchisepticais a small, gram-negative, non-lactose fermenting rod. The organism can be carried by rats, rabbits, dogs, cats, swine, and primates. A carrier state can also occur in the guinea pig. Transmission between animals is by direct contact, aerosolization, and contaminated fomites. Acutely infected guinea pigs may exhibit sneezing, nasal discharge, anorexia, weight loss, conjunctivitis, dyspnea, and death. Stillbirths and abortions may occur in pregnant females. Young animals are more severely affected, and mortality can reach 100% in immunologically naive juveniles. Clinical signs, gross lesions and histology are used to make a presumptive diagnosis. Culture and gram staining of impression smears provide diagnostic confirmation of the disease. Antibiotics may be beneficial in treatment of clinical cases (but beware of antibiotic-induced Clostridial typhlitis!).
Cervical Lymphadenitis (Lumps)
Streptococcus zooepidemicus has been isolated from the majority of affected animals. Bite wounds or respiratory aerosols are the major vehicles for transmission. Aerosolized organisms may invade conjunctival, genital, and oral mucosal surfaces. The organism probably exists as a normal inhabitant of the upper respiratory tract and produces an opportunistic infection in injured mucosal surfaces. The organism initially infects cervical lymph nodes, which become enlarged and develop abscesses. Abscesses may spontaneously rupture with time. Affected animals may show no other signs except nonspecific symptoms of pyrexia or anorexia immediately prior to rupture. Other regional lymph nodes or, rarely, the middle ear and respiratory passages may become involved. Diagnosis is based on clinical presentation and culture of the organism from lesions. Spread of the organism through a colony can be controlled by culling or isolating affected animals prior to lymph node rupture. Limiting the amount of coarse feed may aid in decreasing the incidence.
This disease is seen most frequently in guinea pigs housed on rough, unsanitized wire floors. Lesions occur on the palmar and plantar surfaces of the feet and consist of granulomatous cellulitis or chronic, fibrous granulomas with or without an exudative crust, of the feet. Staphylococci have often been isolated from these lesions, probably as secondary invaders. The best treatment is to transfer the affected animal to a solid floored cage with dry shredded paper bedding. Resolution of advanced lesions despite local and parenteral therapies is uncommon. Soaking the feet in astringents or tamed iodine solutions and bandaging the feet may be beneficial in severe cases.
PARASITIC DISEASESLice (Pediculosis)
Gliricola porcelli and Gyropus ovalis may occasionally cause partial alopecia and pruritus in select animals. They tend to distribute themselves over the dorsum and perineum of the host. Control is by repeated use of parasiticides.
Sarcoptic Mange (Scabies)
Trixacarus caviae is a sarcoptic mange mite of the guinea pig. This parasite occasionally can cause an intense pruritus leading to self-mutilation, abnormal behavior, debility, and death. Diagnosis is by skin scraping and identification of the mite. Control can be achieved by treating with parasiticides. Public Health Significance: Trixacarus may cause scabies in humans.
MISCELLANEOUS DISEASESHypovitaminosis C (Scurvy)
Guinea pigs lack the hepatic enzyme 1-glucuronolactone oxidase, which is essential for the conversion of glucose to ascorbic acid (Vitamin C). Vitamin C is involved in many biochemical processes in the body including the synthesis of collagen and intracellular ground substance. If vitamin C is not supplemented in the diet or if the animal is anorexic, scorbutic lesions will rapidly develop. Scurvy is characterized by frequent vocalizations, weakness, anorexia, diarrhea, flaky to ulcerative skin lesions, stiffness, reluctance to move, petechia of the mucous membranes, subcutaneous hemorrhages and death in two to three weeks due to starvation or secondary infection. Other nonspecific but suspicious indications may include rough hair coat, delayed wound healing, teeth grinding, inactivity, stillbirths, and chronic disease. A diagnosis can be made by dietary history, gross pathology, and serum ascorbate levels. Necropsy findings may include hemorrhages in muscle, fascia, articular cartilage, periosteum, and gingiva. The daily requirement of ascorbic acid is 15 mg/day, and this amount can be provided through supplemental feeding of a handful of cabbage or kale, a green pepper, a quarter of an orange, etc. Pregnant females should receive 30 mg/day. Vitamin C supplemented pellet rations have an average shelf life of 90 days from the milling date when stored in a cool, dry place.
Pregnancy ToxemiaThis syndrome is similar to the problem seen in ewes. It normally occurs in older, obese females. Other predisposing factors include sudden dietary changes, lack of exercise, and environmental stress. Obese, aged males may develop a similar toxemia. The syndrome usually starts during the last two weeks of gestation or the first week post-partum. Following an acute onset, death may occur within 24 hours. When not immediately fatal, common findings include depression, lassitude, anorexia, dyspnea, convulsions, and stillbirths. The urine contains high levels of ketone and protein. Diagnosis is based upon history, clinicecropsy. The condition is best prevented by supplying an adequate amount of digestible energy during late gestation and lactation, and maintaining animals in a non-obese condition. A commercial producer will not keep any female offspring as replacement breeders if produced by a sow that developed pregnancy ketosis.
This syndrome is frequently seen in pet guinea pigs allowed to graze outdoors at temperatures greater than 70o or 75o F. Coma, rapid shallow respiration, pale mucous membranes, slobbering, and high rectal temperature can all be seen clinically. Guinea pigs are extremely susceptible to heat stroke, and even transport in an air-conditioned car has been reported to result in over heating and coma.
Dystocia may be caused by abnormally large or malformed fetuses, unusually large litters, or abnormal presentations. It most commonly occurs in primiparous dams older than six months of age due to the fusion of the pelvic symphysis by that age. In this presentation, Cesarian section is indicated to save the dam and/or pups. Occasionally, when uterine inertia is the only problem, contractions can be reinitiated with the administration of 1 unit of oxytocin subQ. In the young animal, the symphysis normally disjoins at 2 to 24 hours prepartum. This change is easily palpable and is used as an indicator of impending parturition in the guinea pig.
VI. GENERAL REFERENCESBaker, DJ. 1998. Natural pathogens of laboratory mice, rats, and rabbits and their effects on research. Clinical Microbiology Reviews 11(2):231-266.Bhatt, P.N., Jacoby, R.O., Morse, H.C., New, H.E. (Eds.) Viral and Mycoplasmal Infections of Laboratory Rodents. Academic Press, 1984.
Harkness J. E. and Wagner, J. E. The Biology and Medicine of Rabbits and Rodents. 4th edition. Lea and Febiger, 1994. Lindsey JR, GA Boorman, MJ Collins, et al. 1991. Infectious diseases of mice and rats. National Academy Press, Washington, D.C.
Percy, D.H. and Barthold S.W. Pathology of Laboratory Rodents and Rabbits, Iowa State University Press, 1993.
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