Marti Hanes, DVM
Dept of Lab Animal Resources
University of Texas Health Science Center-San Antonio
San Antonio, Texas 28284
· Mongolian gerbil, jird, clawed jird, sand rat, desert rat , antelope rat (11-15 genera, 100 species)(Meroines unguiculatus, M. libycius, M. shawii , M. tristami); Desert regions of Mongolia and China
· Colors: agouti, black, gray, white, dove, cinnamon, piebald, hairless
· desert dwelling, heat and dehydration resistant, social, burrowing rodents
· Monogamous pairs-affiliative behavior may be due to discrimination of mate’s urine odor, determined by pheromones in parotid saliva, males participate in pup rearing, gerbils prefer mates of similar color
· crepuscular and diurnal, eat all day and night, peak activity at night
· Illegal as pets in Calif.
· ventral marking gland-more prominent in males and they mark more frequently, sebaceous and specialized hair , gonadal control, marking of territory and pup identification (dads care for pups too)
· darkly pigmented scrotum, no preputial glands, furred tail, Harderian glands for chemocommunication and pelage insulation, both sexes have genital papilla, no preputial gland
· large adrenal to body weight, thymus persists for life,
· irregular gestation, 24-26 days, post partum estrus gestation 42 days, 4 teats
ears 3-7 days, hair 7-10 days, eyes 2-3 weeks, begin eating 15 days, wean at 3 wk,
puberty 9-12 wk, lifespan 2-4 years
· Incisors grow continuously, molars are rooted
· Auditory bullae are large, with microscopic adaptation of ear structure
· Incomplete Circle of Willis- susceptible to cerebral schema with common carotid artery ligation- useful in stroke research
· Renal function-Adaptation to urine concentration-papilla and inner medulla>>cortex (2X rat) Renal Bowman’s capsule myofibroblasts in male gerbil kidneys-lamina muscularis unique to Meriones-Water deprived gerbils stabilize at 86% preweight
· Normally lipemic(hypercholestrolemic) on standard diets (AM-obesity, hypertension)
Neonatal-erythrocyte macrocytosis, panleukocytosis, RBC 1/2 of adult
Adult-polychromasia, basophilic stippling reticulocytosis, t1/2 of RBC=10 days,
Males have higher RBC, Hgb, wbc and Lymphocytes( ratio 3:1 of 4:1 over PMN’s) and are physically larger.
· Spontaneous seizures, especially in black gerbils
· Stroke- Circle of Willis incomplete- cerebral ischemia with carotid ligation
· Auditory bullae large- hearing curve close to human
· Endocrine function, water conservation
· Spontaneous epilepsy-2 mo of age, about 1/2 of population
· Hypercholesterolemic (1590 mg/dl), lipemic- hepatic lipidosis, gall stones, lipid metabolism not athersclerosis
· Cardiovascular disease
· Dental research
· Reproductive studies
· Psychology-territorial marking, behavior
· Toxicology-food additives, pesticides, solvents, and heavy metals(lead nephropathology
· Infectious disease research- few of their own, susceptible to other species diseases (e.g. parasitology B. pahangi, B. malayi, Dipetalonema viteae, leshmania, amebiasis, Schistosoma sp. Taenia sp. ad nauseum )
There are no reported naturally occurring viral infections
Experimental studies performed with: Hanta virus, La Cross virus, Tick borne encephalitis virus, Borna virus, Rift Valley fever, pseudorabies, and Encephalomyocarditis virus
· Tyzzer’s Disease, Clostridium piliforme (a.k.a. Bacillus piliformis)
There have been sporadic accounts of Tyzzer’s in gerbil colonies used for research. The gerbil is very susceptible to disease, without the use of immunosuppresion. Young gerbils will become infected following oral inoculation of material from other species. Housing sentinel gerbils on unautoclaved soiled bedding suspected to be contaminated with the organism has been used to detect carriers.
Typical clinical signs include depression, ruffled hair coat, hunched posture, anorexia, and watery diarrhea. Severely affected animals will die within 5 days. Bacteria can be visualized in intestinal enterocytes within 3 days. Extensive hepatic lesions and bacterial antigen will be seen in small intestine and cecum by 5-6 days. Bacterial antigen is demonstrable in muscular tunics and Peyerís patches. The infection is characterized by fecal-oral transmission, and the organism survives in the environment for years.
Pinpoint to 2mm pale foci are usually present on the liver. The small intestine and cecum walls will be edematous, sometimes with ecchymoses. The intestinal contests will be fluid, with varying amounts of blood. The mesenteric lymph nodes may be enlarged and edematous. Liver lesions are frequently more periportal and random, with areas of coagulative to caseous necrosis. There will be variable neutrophilic infiltration as the age of the lesion matures. Within lesser affected hepatocytes on the periphery of the lesions, intracellular bundles of bacilli maybe visualized on H&E stained sections. Older lesions may demonstrate fibrosis and mineralization. Intestinal lesions are most extensive in the jejunum, ileum and cecum, with necrosis and loss of enterocytes of the villar tips. Villar blunting with transmural edema in affected areas will occur. The lamina propria will be expanded by PMN’s and mononuclear cells. Necrosis of intestinal smooth muscle, mesenteric lymph nodes and Peyerís patches have been reported. Bacteria may be present in enterocytes and smooth muscle cells.
Myocardial lesions consist of areas of coagulative myonecrosis with leukocytic infiltration, with collapse of myofibers and mineralization of cell debris. Warthin Starry(silver) , Steiner’s stain (silver) or Giemsa Stain will demonstrate the intercellular bacteria better than H&E. Diffuse suppurative encephalitis is another possible manifestation of infection.
Diagnosis is aided by the presence of bundles of filamentous bacteria peripheral to areas of necrosis in the heart, cecum, and liver. ELISA test is commercially available for detection of anti-Tyzzer’s serum antibodies.
Treatment is unsuccessful; elimination of affected animals, autoclave primary enclosure, reduction of stress are important actions. There is a possibility of interspecies transmission.
· Salmonellosis (Salmonella typhimurium, S. enteritidis, S. sp. group D)
Disease and mortality in young gerbils naturally infected with S. typhimurium have been reported. Clinical signs include, acute high mortality (90%), moderate to severe dehydration, diarrhea, weight loss and leucocytosis with neutrophilia. In the outbreak of group D salmonella, clinical signs included all the above and testicular enlargement.
At necropsy, the gastrointestinal tract is filled with gas and variably tinged fluid. Exudative peritonitis with fibrin may be present. Histologically, the hepatic lesions may vary from foci of leucocytic infiltration to larger areas of coagulative or caseous necrosis with mineralization. Epitheloid macrophages, lymphocytes, and neutrophils complete the paratuberculoid lesions. Crypt abscesses are sometimes seen There may be suppurative orchitis, interstitial pneumonia, and purulent to pyogranulomatous leptomeningitis.
Diagnosis using selective media (lactose-fermenting on MacConkey’s, growth on SS agar), and ruling out Tyzzer’s as a differential. Bacteria may be grown from liver, heart blood, spleen and intestinal contents.
One outbreak was associated with salmonella infected cockroaches (sp) Interspecies transmission, especially with immune compromised individuals is possible.
· Non specific Gastrointestinal disease without determined cause was seen in an aged gerbil colony. Necropsy results include nonsuppurative enteritis, necrotizing enteritis, typhlitis, colitis, gastritis, pancreatitis, and sialoadenitis.
· Staphylococcal Dermatitis( Staphylococcus aureus )
Acute diffuse moist dermatitis has been associated with Staphlococcus aureus infection, and altered temperature >72F and humidity (<50%),The disease is more prevalent in younger gerbils, with a high morbidity and mortality. The disease has been reproduced by inoculation into the nasal area of young gerbils. At necropsy, there maybe a diffuse moist dermatitis and greasy haircoat. The face, nose, feet legs and ventral body surface may exhibit alopecia, erythema and moist brown exudate. Microscopically, a moderate to severe suppurative dermatitis with transepitheial and dermal neutrophils infiltrating into adnexa and deep dermis will be apparent. Acanthosis, hyperkeratosis, and serocellular crust containing cocci maybe present. Fatal cases will have systemic signs including suppurative hepatitis.
A commonly encountered disease in juvenile and adult gerbils characterized by nasal dermatitis and alopecia around the upper lip and external nares. The erythema, alopecia, scabbing, accumulation of reddish-brown porphyrin pigmented exudate, and moist dermatitis may spread to other areas. The disease has been related to Staphylococcus saprophyticus, S. xylosis and S. aureus, but is now temporally related to stress ( loss of cage mate, incompatible mate, anxiety producing overcrowded conditions) resulting in excessive burrowing behavior, and release of retrobulbarly located Harderian secretions. Removal of Harderian glands from affected animals resulted in marked improvement. Housing on sand resulted in marked improvement. Harderian secretions normally bathe the eye and conjunctival sac, are transported down the nasolacrimal duct to the external nares. The secretions are mixed with saliva during grooming during thermoregulatory behaviors. The failure to remove these porphyrin lacrimal gland secretions results in collection causing chemical irritation, and dermatitis. Trauma occurs due to from rubbing and scratching. The condition may be self limiting. Elizabethan collars that prevent grooming increase the nasal dermatitis, animals with bilateral harderian gland adenectomy did not develop the disease. Varying degrees of labial and planum dermatitis may be present, with ulceration, exudation, excoriation and crusting; the forepaws may be involved. Hyperkeratosis, epidermal hyperplasia, melanin pigmentary incontinence, spongiosis, necrosis, neutrophilic infiltration and epidermal abcessation maybe present. DDX; fight wounds, food or water located in area creating trauma, Rx: Remove stressors, clean face, use sandy or clay bedding, ophthalmic ointment.
· Bordetellosis (Bordetella bronchiseptica)-Bordetella infection is a potential problem, but natural infection has not been reported; young gerbils developed severe disease with high mortality when experimentally infected.
· Pasteurella pneumotropica- potential isolate for conjunctivitis, dacroadenitis
· Leptospirosis-Experimental infections are characterized by hemolytic anemia, icterus, and mottled livers. Degeneration of the distal renal tubules and centrolobular hepatocytes, with splenic erythrophagocytosis were seen. Chronic persistent infection developed with nonsuppurative inflammation, fibrosis, and progressively severe renal tubular degeneration and cyst formation. Spirochetes were present in the liver and kidney.
· Demodex-(Demodex meriones, D. aurati or criceti)-Similar to the disease in hamsters may be localized to tail head. Lesions are alopecic, with scale, hyperemia or focal ulceration. Old age and debilitation are important predisposing factors, not important in healthy gerbils. Alopecia, DX: skin scraping, TX: topical acaricde
· Liponyssoides-(Liponyssoides sanguineus) an ectoparasite of laboratory and wild house mice. no lesions
· Giardiasis-Not been reported as a natural infection, gerbils are highly susceptible to Giardia. . Trophozoites can be found in the upper small intestine, or throughout the bowel.
· Spironucleus muris, Tritrichomonas sp and Entamoeba sp-maybe found in the cecum and large intestine- may serve as reservoir for other species, seen in 22/141 in aged colony.
none cause clinical problems. Syphacia
obvelata , S. muris- susceptible to contract infection with mouse and rat
pinworms. Dentostomella translucida-
anterior small intestine, seen in 4/141 gerbils in aged colony.
· Cestodiasis- severe infections have been reported, dehydration, diarrhea with mucus, coinfection with salmonella sp. H. diminuta seen at necropsy in small intestine. DX: smears of intestinal mucosa or H&E sections of small intestine- eggs and cysticercoids seen. Hymenolepsis nana -zoonotic potential- direct life cycle
Spontaneous, audiogenic, do not TX with diphenylhydantoin-fatal
Stress related, begins around 2mo of age, frequent handling of weanlings decreases the incidence, though it can approach 40-80% at 10 mo and persist through life. Autosomal dominant with variable penetrance. Clinical signs include vibrissae and ear twitching, motor arrest, myoclonic jerks, clonic-tonic seizures, vestibular aberrations and death. No histopathologic lesions are seen. The seizures may last from 30 sec to 2 min. The refractory period may be several days. A protective effect in the wild has been proposed. There are seizure prone and seizure sensitive strains available. DDX: encephalitis, poisoning, toxemia, trauma
· General-starvation, water deprivation-sudden weight loss, perineal mucus, sudden death, cannibalism diet-sunflower seeds high in fat, low in calcium incomplete diet
· Barbering-usually tolerate crowding, but if not grouped together before maturity may barber or fight, abscesses can be seen on tail area. Other causes of alopecia include malnurishment and rubbing on equipment.
· Degloving tail-Chilling, overheating, inappropriate handling, sometimes bare area will just slough off, otherwise, amputate at level of breakage, and suture.
· Malocclusion-Lack of opposing occlusal contact results in incisor overgrowth , most often due to loss of upper incisors. Molar teeth are rooted and do not grow.
· Periodontal Disease and Dental Caries- Maintained on standard pelleted feed will develop severe progressive periodontal disease starting at 6 mo, with tooth loss in 2 years. Dental caries are enhanced with a cariogenic diet.
Toxic and Metabolic Disorders
· Streptomycin toxicity- A direct neuromuscular blocking effect is seen with streptomycin at excessive doses. Inhibition of acetylcholine release results in acute toxicity characterized by depression, ascending flaccid paralysis, coma and death within minutes after administration.
· Lead Toxicity- Potential for natural exposure in pets is high do to the gnawing behaviors. The urine concentrating ability of the kidneys exacerbates the toxicity. Chronically , gerbils become emaciated, livers are small and pigmented, kidneys are small and pitted. Acid Fast inclusions are seen the proximal collecting tubules, and hepatocytes. Lipofuscin pigment in the liver is seen in hepatocytes and Kupffer cells.. Microcytic, hypochromic anemia with more than normal stippling is seen.
· Amyloidosis_- NOT RARE, 16% of 141 aged animals necropsied demonstrated amyloid, all affected animals were over 10 mo of age. It was found in the spleen, liver, lymph node, interstitium of the exocrine pancreas, adrenal, heart, and intestines. In the past, generally associated with chronic inflammatory disease such as experimental filiarial infections. Clinically, see weight loss, dehydration, anorexia and death.
· Obesity and Diabetes__About 10% of gerbils on laboratory diet become obese. Reduced glucose tolerance, elevated insulin, hyperplastic or degenerative lesions of the endocrine pancreas may be seen. Lipemia occurs with as little as 4-6% fat in the diet. Increased LDL, hepatic lipidosis and gallstones have been seen in gerbils.
· Hyperadrenocortism/Cardiovascular Disease of Breeding Gerbils _A disease complex only seen in breeding animals, not virgins. It is attributable to hyper adrenalcorticalism, and linked to diabetes and obesity. They develop mild to severe plaques of intimal and medial extracellular matrix with mineralization especially in the aorta, mesenteric, renal, and peripheral arteries. The aortic plaques may be visible at necropsy. Breeding animals have elevated triglycerides, enlarged islets, hepatic lipidosis, thymic involution, adrenal hemorrhage, adrenal lipid depletion and occasional functional pheochromocytomas._
· Focal Myocardial Degeneration-male breeders will have an increased incidence of focal myocardial necrosis and fibrosis. 50% may have lesions related to ischemia. Report of nonspecific myocarditis/ endocarditis with thrombosis(atrial and pulmonary microthrombi).
· Chronic Nephropathy - usually seen in gerbils over 1 year of age. Clinically find polyuria, polydipsia, weight loss, Necropsy-shrunken and pitted kidneys with fibrosis. In a recent publication, 16% of 141 animals necropsied had chronic lymphocytic and plasma cystic interstitial nephritis, 18% had chronic tubular nephrosis with eosinophilic proteinaceous casts in the lumina, and some had cellular casts. The tubular epithelium was atrophic. Fourteen percent had chronic glomerulopathy consisting of variably increased mesangeal matrix, dilated Bowman’s spaces, and shrunken glomeruli. Glomerulosclerosis was present in 6%, glomerular/interstitial amyloid was present in 9%. Pyelonephritis, urethral obstruction, hydronephrosis, nephrocalcinosis, cystitis and urethritis seen in aged gerbils
· Hepatic Degeneration- Multifocal hepatocellular degeneration and necrosis were present in 26% of 141 animals in an aged gerbil colony. Lesions consisted of discrete foci of necrosis with minimal inflammatory response. Unknown etiology, non specific. May also see telangectasia, fatty change, hepatitis in aged gerbils.
· Infertility- various causes, ovarian cysts, incompatibility, sexual immaturity, senescence, overcrowding, pesticide/toxin ingestion, nutritional deficiencies, environmental disturbances, very low ambient temperatures and systemic disease. Aged males may demonstrate orchitis, prostatitis, testicular mineralization.
· Cystic Ovaries-20% of aged females >400 days . Cysts vary from 1-50mm in diameter. Ovulation and corpus luteum formation continue to occur, but may get abdominal swelling, infertility, and decreased littersize. Aged report in females was biased, because the cysts were palpated and animals culled and not submitted for necropsy, only had 6/73 females. Aged females also exhibited metritis, dystocia, cystic endometrial hyperplasia, myometrial mineralization.
· Ocular Proptosis-Aged gerbils may develop a protruding nictitating membrane, protrusion of the bulbar conjunctiva with proptosis.
In general the spontaneous incidence is low, increasing in gerbils over 2yr of age. Low incidence of mammary, pulmonary and pituitary tumors.
· Aural Cholesteatoma-spontaneous cholesteatomas occur in 50% of gerbils over 2yr age. They are composed of masses of tympanic membrane origin keratinized epithelial cells, which displace the tympanum into the middle ear. Compression and secondary infection result in bone necrosis and inner ear destruction. Clinical signs include head tilt, gerbils rarely get primary otitis media because of the vertical orientation of the eustachian tubes. Aged colony reported in 1995 only 6%, but study culled animals with bilateral lesions and did not submit for necropsy.
· Ovarian tumors-ovarian granulosa cell tumor are frequently bilateral and fleshy to lobulated masses. Thecal cell tumors, dysgeriminomas, leiomyomas and luteal cell tumors have been identified. aged females_cystic to lobulated massed, with granulosa cells as the predominant cell type. In an aged colony, 6/73 females had granulosa cell tumors, 1/73 thecal cell, 1/73 dysgerminoma, 1/73 undifferentiated carcinoma.
· Vascular tumors - Renal hemangiomas (5% of 141 animals) and hemangiosarcomas were reported in aged gerbils (1.5%), with metastasis to the lung. splenic hemangiomas
· Cutaneous Tumors- sebaceous gland adenoma and carcinomas, squamous cell carcinomas of the ear, melanomas, basal cell tumor
Marking gland adenocarcinomas-Are characterized by enlarged glands with irregular features. Microscopically there is marked anisocytosis, cytoplasmic volume and staining properties are altered,_ the cytoplasm may be granular to vacuolar._also see squamous cell carcinomas
· Adrenal cortical tumors- adenomas and carcinomas
· Other tumors reported-uterine adenocarcinomas, fibrosarcomas, pancreatic cell adenoma, leiomyomas, thymoma, cecal adenocarcinoma, Hodgkin’s like lymphoma, osteosarcoma, exorbital lacrimal gland adenoma