THE MERCK VETERINARY MANUAL
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Gerbils

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Gerbils are also known as jirds or sand rats. Wild Mongolian gerbils are found in Mongolia, adjacent parts of southern Siberia and northern China, and Manchuria. The pet and laboratory gerbil is Meriones unguiculates, commonly known as the Mongolian gerbil. There are 14 species in the genus Meriones. All captive Mongolian gerbils are derived from 20 pairs trapped in eastern Mongolia in 1935.

Externally gerbils are quite ratlike. The head and body length is 95–180 mm and tail length is 100–193 mm. The average weight is 50–55 g in females and 60 g in males. The covering of fur on the tail is short near the base and progressively longer toward the tip. Coloration of upper parts varies from pale, clear yellowish through sandy and gray. The sides of the body are generally lighter than the back.

Gerbils inhabit clay and sandy deserts and are highly resistant to heat stress and dehydration. They are terrestrial and construct simple burrows in soft soil where they spend most of their time.

Biology

Mongolian gerbils have several coat colors. The wild coat color is agouti and is controlled by an autosomal dominant gene. Sandy-colored gerbils are due to a recessive color gene and show a yellow to ginger color on the dorsum and the typical creamy white belly of a wild-type Mongolian gerbil. The dorsal yellow hairs have short black tips, and a light olive green base. A clear demarcation line between dorsal and ventral color is present. Black gerbils are due to an autosomal recessive gene; white albino gerbils with red eyes due to an autosomal recessive gene are also seen.

Gerbils have a large, ventral abdominal marking gland that is androgen dependent. It attains greater size in the male and develops at an earlier age. The gland is used for territorial marking. Females mark their territory following parturition and become more aggressive.

The adrenal cortex produces nearly equal amounts of corticosterone and 19-hydroxycorticosterone. When the adrenal gland weight is compared with body weight, the gerbil adrenal gland is ∼3× the size of the adrenal in the rat. Gerbils have a high proportion of erythrocytes with polychromasia, basophilic stippling, and reticulocytosis.

Male gerbils attain sexual maturity by 70–84 days. Vaginal opening in females occurs between 40–60 days, 30 days before sexual maturity occurs. Gerbils tend to pair bond; when older females lose their mate, getting them to accept another is often impossible. Early-maturing females are more likely to breed successfully on first pairing, and the lifetime fecundity of early-maturing females is more than twice that of their late-maturing littermates.

The gestation period of nonlactating gerbils is 24–26 days, but lactating females have a prolonged gestation of 27 days. If females are bred in the postpartum period, they delay implantation, leading to a gestation as long as 48 days. Litter size is typically 3–7 animals. Young gerbils suckle for about 21 days and begin to eat solid foods at 16 days. In general, day 25 is considered suitable for weaning. The normal lifespan of a gerbil is 2–3 yr.

Husbandry

The diet of wild Mongolian gerbils consists of green vegetation, roots, bulb seeds, cereals, fruit, and insects. Gerbils hoard food and are not normally coprophagic, unless diets lack adequate nutrient value. They thrive on commercially available pelleted rodent diets with 18–20% protein but may have deficiency problems when fed primarily homemade diets, sunflower seeds, or table scraps, which lack specific nutrients. Sunflower seeds are high in fat and low in calcium. Pelleted chow (5 g/day) has been recommended to avoid obesity. Gerbils develop high blood cholesterol concentrations on diets containing more than 4% fat. This is manifest as lipemia and is more pronounced in males.

Gerbils excrete little urine, and fecal pellets are hard and dry. Their cages require less frequent cleaning than other pet and laboratory rodents. Gerbils adapt to a wide range of ambient temperatures. Due to their propensity to develop nasal dermatitis at relative humidities above >50%, a low humidity is advisable.

Gerbils require sandbathing to keep their coats from becoming oily due to Harderian gland nasal excretions that are spread by grooming and sebaceous exudates from the skin. Sandbathing is usually completed within 5 min. The practice not only cleans and grooms the pelage but also deposits lipids on the substrate that act as olfactory signals. Additionally, it has homeostatic consequences. When sandbathing is prevented, accumulating hair lipids mat the pelage, and behavior changes. Sandbath-deprived gerbils increase their frequency of “sand rolls” (the gerbil rolls onto its side or back and returns to its feet within 1 second), decrease grooming, and increase territorial marking, especially in males.

Gerbils often stand erect on their hind limbs, so it is important that cages have a solid bottom and the floor-to-lid height is tall enough to allow for this behavior. Pet gerbils kept in inferior cages that are painted with lead paint or made of alloys containing lead have a high potential to develop chronic lead toxicity because of their gnawing behavior and the urine-concentrating ability of their kidneys. Chronically, gerbils become emaciated, livers are small and pigmented, and kidneys are small and pitted. Microscopically, acid-fast inclusions are noted in the proximal collecting tubules and hepatocytes.

Physical Examination

The gerbil's overall appearance and behavior, particularly in relation to its cagemates, should be noted. Sick animals are often isolated from others and may demonstrate weight loss, hunched posture, lethargy, rough fur, labored breathing, and loss of exploratory behavior. Early signs of illness involve changes in the color, consistency, odor, and amount of urine and feces. The perineal area should be checked for fecal or urine stains or discharges from the vulva in females. Fecal samples may be taken for parasite detection and bacterial culture. The fur and skin should be examined for alopecia, fight wounds or other trauma, ectoparasites, and elasticity for evidence of dehydration. The oral cavity should be checked for overgrown teeth. Ears should be examined for discharges or inflammation and eyes for discharges or conjunctivitis. Feet should be examined for sores and overgrown or broken nails. The abdomen should be palpated for masses. The normal body temperature of gerbils is 98–102°F (37–39°C). The respiratory rate and any signs of labored breathing should be noted. The thorax can be auscultated with a pediatric stethoscope.

Gerbil tails are fragile. Animals should only be handled by the base of the tail to avoid damage.

Infectious Diseases

“Facial eczema,” “sore nose,” and nasal dermatitis all describe a common skin condition seen in gerbils. Clinical lesions next to the external nares appear erythematous initially, progress to localized alopecia, and develop into an extensive moist dermatitis. The cause is believed to be increased Harderian gland secretion of porphyrins (similar to chromodacryorrhea in rats), which act as a primary skin irritant. Experimental Harderian gland adenectomized gerbils do not develop nasal or facial lesions. Various staphylococcal species (Staphylococcus aureus and S xylosus) may act synergistically to produce the dermatitis. Stress factors such as environmental humidity >50% or overcrowding cause excessive Harderian gland secretion. Nasal dermatitis infection may extend to the maxillary sinuses. Affected gerbils are anorectic, stop drinking water, lose weight and die. The distribution and nature of the lesions are useful in diagnosis. Accumulated porphyrins fluoresce under ultraviolet light (Wood's lamp). Routine bacteriology yields isolation of pathogenic staphylococci. Treatment includes careful cleaning of the skin lesions and the use of topical (chloramphenicol 1% ophthalmic ointment, tid) or parental antibiotics. (Streptomycin is fatal in gerbils and is contraindicated.) Prevention requires reduction of environmental humidity below 40% and reduction of sources of stress such as overcrowding or sandbath deprivation.

Naturally occurring Tyzzer's disease, an enterohepatic disease caused by the obligately intracellular bacterium Clostridium piliforme, is the most frequently described fatal infection of gerbils. Common clinical and pathologic findings are sudden death or death after a short period of disease, together with the presence of multiple foci of hepatic necrosis. Diarrhea and necrotic lesions in the intestinal tracts are variably present. The probable route of infection is by mouth, as gerbils exposed to infected bedding will contract Tyzzer's disease. Supportive fluids and prophylactic treatment with tetracycline or metronidazole are recommended to reduce mortality in cagemates. Because the bacteria form spores, the housing environment should be thoroughly sanitized and disinfected.

The Mongolian gerbil is susceptible to infection by Helicobacter pylori, which causes severe gastritis, gastric ulceration, and intestinal metaplasia. Gastric adenocarcinoma develops in approximately ⅓ of infected gerbils over 15 mo of age. Clostridium difficile-associated fatal enterotoxemia has been associated with treatment using nutritionally balanced triple-antibiotic wafers (containing amoxicillin, metronidazole, and bismuth) to eliminate naturally occurring Helicobacter infections. Affected animals are reported to die within 7 days of antibiotic treatment.

Naturally occurring viral infections of gerbils are not reported.

Syphacia obvelata, the mouse pinworm, and Dentostomella translucida, an oxyurid, are found in Mongolian gerbils. Pet store gerbils often are infected with mouse pinworms. D translucida is commonly found in the small intestine of both research and pet gerbils. There is an average of 4 parasites/animal, but no clinical signs are associated with the infection.

Infections with dwarf tapeworms, Hymenolepis diminuta and Rodentolepis (Hymenolepis) nana, are reported in pet gerbils. Dehydration and mucoid diarrhea are often presenting signs. R nana has a direct life cycle and may potentially infect humans if ingested. Recommended treatment is niclosamide fed at 10 mg feed/100 g body wt for two 7-day periods separated by 1 wk. Also effective are thiabendazole (0.33% mixed in the feed for 7–14 days) or praziquantel (5–10 mg/kg, IM, SC, or PO, repeated in 10 days).

There have been no reports of naturally occurring or experimental dermatophyte infections in the Mongolian gerbil. Other fungal infections in Meriones spp are exceedingly rare.

Metabolic and Nutritional Disorders

Gerbils develop spontaneous, insidious periodontal disease after 6 mo on standard laboratory rodent diets. On the same diets, ∼10% of the animals became obese, and some show decreased glucose tolerance, elevated serum immunoreactive insulin, and diabetic changes in the pancreas and other organs.

Traumatic Injuries

Thin skin covers the tail of the gerbil. Unlike rats or mice, if a gerbil is picked up by the tip of its tail, the skin will often slip off leaving a raw, exposed tail that eventually becomes necrotic and will shed. If the tail skin is lost, the bare tail must be surgically amputated where the skin ends.

Neoplasia

Spontaneous neoplasia has been reported primarily in laboratory colonies of Mongolian gerbils. A 25–40% incidence of neoplasia in gerbils usually occurs after 2–3 yr of age. 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 >3 yr old. The ventral marking gland tumors invade locally and can metastasize to lymph nodes and lung. Adrenocortical tumors, cutaneous squamous cell carcinoma, malignant melanoma, and renal and splenic hemangiomas are the next most commonly reported tumors. Numerous other tumors including duodenal and cecal adenocarcinoma, hepatic lymphangioma, hemangioma and cholangiocarcinoma, splenic and renal hemangioma, uterine leiomyoma and hemangiopericytoma, ovarian teratoma, testicular teratoma, and malignant melanoma have been reported. However, the total incidence of these tumors was <5%.

Case reports of spontaneous tumors in pet gerbils include infiltrative craniopha-ryngioma, histiocytic sarcoma, systemic mastocytosis, malignant melanoma, and astrocytoma.

Miscellaneous Disorders

A fatal syndrome of acute toxicity is produced in Mongolian gerbils following the injection of penicillin-dihydrostreptomycin-procaine combination. The toxicity is due to the dihydrostreptomycin component. A dose of 50 mg of dihydrostreptomycin causes 80–100% mortality in gerbils weighing 55–65 g.

Approximately 20–40% of gerbils develop reflex, stereotypic, epileptiform (clonic-tonic) seizures from around 2 mo of age. Animals seize in response to sensory stimulation and forced exploratory behavior, but the incidence and severity of their seizures are variable; the seizures generally pass in a few minutes, may be mild or severe, and have no lasting effects. Although the incidence and severity of seizures often decreases with age, certain subsets of adult gerbils do not improve with age but progressively worsen. The susceptibility is seen in selectively bred lines, but may occur in pet gerbils. Seizures may be suppressed in genetically predisposed gerbils if they are frequently handled during the first 3 wk of life. Anticonvulsant therapy is unnecessary.

Cystic ovaries occur frequently in Mongolian gerbils. Cysts range in size from 1–50 mm in diameter. Removal of affected ovaries does not significantly affect reproductive performance. Females with 1 ovary are slightly inferior in fertility compared with normal females; a general decline in fertility may be evident in older females.

Ventricular septal defects are seen occasionally in newborn gerbils.

In addition to neoplasia (see Neoplasia of Ferrets), aged gerbils have a high incidence of chronic glomerulonephropathy and focal myocardial degeneration and fibrosis, especially in males. Aural cholesteatomas occur in 50% of gerbils >2 yr of age. Cholesteatomas in the ear canal displace the tympanum into the middle ear. Compression and secondary infection result in bone necrosis and inner ear destruction. Clinical signs include head tilt.

Last full review/revision July 2011 by Thomas M. Donnelly, BVSc, DACLAM

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