The most common pet and research hamster is the golden or Syrian hamster (Mesocricetus auratus). All Syrian hamsters in captivity appear to have originated from a litter of eight hamsters collected near Aleppo in Syria in 1930. Four of the animals escaped, a male killed one female, and only one male and two females remained. From these three animals, litters were raised that were distributed to Europe and the USA for research and subsequently as pets. In 1971, an additional 12 Syrian hamsters were captured in the field by farmers and imported to the USA.
Syrian hamsters have a head and body length of 170–180 mm and tail length of 12 mm. They range in weight from 110–140 g, and females are larger than males. Wild Syrian hamsters have a light, reddish brown dorsal coat, and the underparts are white. The skin of Syrian hamsters is very loose.
Other species now common as pets are the dwarf hamsters such as the Djungarian (Phodopus sungorus) and Roborovsky (P roborovskii) hamsters. They are small (<100 g body wt), have a docile disposition, do not attempt to bite or run away, thrive in captivity, and make good pets. This discussion primarily deals with diseases of the Syrian hamster.
At least 20 mutations affecting coat color in Syrian hamsters are known. Most are simple recessive traits, four are dominant, and two are sex-linked. Five mutations affect the fur, giving rise to long hair (also known as "teddy bear" hamsters), rex, and satin coats. Length of hair in the longhaired Syrian hamster is influenced by testosterone. Longhaired males from the age of sexual maturity have significantly longer hair than females or castrated males, which display fluffy, shorter hair.
Syrian hamsters possess paired, flank organs in the costovertebral area that are androgen dependent and consist of sebaceous glands, pigmented cells, and terminal hairs. They are larger and heavily pigmented in males and used for territorial marking. All hamsters possess enormous cheek pouches that open inside the lips, extend well back of the shoulders, and when filled with food more than double the width of the animal's head and shoulders.
Adult male Syrian hamsters develop large adrenal glands due to enlargement of the zona reticularis, which is three times the size of that in female hamsters. Like gerbils, Syrian hamsters have a high proportion of erythrocytes with polychromasia.
Female Syrian hamsters are heavier than males and generally are aggressive toward other hamsters. Nonestrous females can behave especially aggressively toward young males and may kill them. The 4-day estrous cycle is characterized by a copious postovulatory discharge on the last day. The discharge is creamy white and has a distinctive odor; it fills the vagina and usually extrudes through the vaginal orifice. Its stringy nature is distinctive, and if touched it can be drawn out as a thread of about 4–6 in. length. Estrus lasts ~1 day, and the gestation period is 16–19 days. The litter size ranges from 2 to 16, with an average of 9. Cannibalism of young accounts for nearly all preweaning mortality. Cold ambient temperatures (<10°C [50°F]), lean diets, and low body weight during pregnancy increase cannibalism. Disturbing the mother by handling the young or nest, and not providing adequate nesting material, warmth, food, or water, often results in cannibalism. Syrian hamsters are prolific breeders, and there may be 3–5 litters/yr. The young are weaned at 20 days and capable of reproducing at 7–8 wk. The lifespan of Syrian hamsters is 2–3 yr.
In the wild, Syrian hamsters live on dry rocky steppes or brushy slopes. They construct shallow burrows. Deep bedding that is appropriate for burrowing is recommended. Cages with at least 40–80 cm of bedding enhance the welfare of Syrian hamsters.
Wild Syrian hamsters are omnivorous, eating many kinds of green vegetation, seeds, fruit, and meat. Exposure to cold stimulates hamsters to gather food, and they will often hibernate at temperatures <5°C (41°F). Syrian hamsters do not fatten before hibernation and will starve unless they waken periodically to eat. Hibernating animals remain sensitive to external stimuli and are usually aroused if handled. Syrian hamsters have prominent depositions of brown fat beneath and between the shoulder blades, in the axilla, and in the neck and perirenal areas.
Syrian hamsters are active chewers and skillful at escaping from their cages. Glass water tubes are contraindicated for Syrian hamsters, because they will readily bite through glass. Stainless steel sipper tubes close to the floor are recommended. Because Syrian hamsters have broad muzzles that often prevent them eating from feed hoppers, feed pellets are placed on the floor of their cage. Hamsters are naturally coprophagic.
The animal's overall appearance and behavior, particularly in relation to its cagemates, should be noted. Sick animals are often isolated from others and may show weight loss, hunched posture, lethargy, rough fur, labored breathing, and a loss of exploratory behavior. Early signs of disease involve changes in the color, consistency, odor, and volume 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, and ectoparasites. The oral cavity should be checked for overgrown teeth or impacted cheek pouches. 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.
Syrian hamsters are not normally aggressive but can be provoked if suddenly startled, awakened, or roughly handled. It may be easier to scoop Syrian hamsters up in a small container rather than pick them up directly. Their highly elastic skin should be grasped sufficiently to prevent the animal from biting.
Diarrhea may occur in Syrian 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-wk old Syrian hamsters and results in high mortality. It is caused by the intracellular bacterium Lawsonia intracellularis. Treatment involves correcting life-threatening electrolyte imbalance and dehydration, administering antibiotics, and force feeding. Several antibiotic treatments are recommended, including doxycycline (5–10 mg/kg, PO, bid for 5–7 days), enrofloxacin (10 mg/kg, PO or IM, bid for 5–7 days), and trimethoprim-sulfamethoxazole combination (30 mg/kg, PO, bid for 5–7 days). Symptomatic treatment with bismuth subsalicylate may be given if diarrhea persists. Replacement electrolyte and glucose solutions should be given orally, and electrolyte fluid replacement such as saline or lactated Ringer's solution should be given at a dosage of 20 mL/100 g body wt once daily. Sequelae of proliferative ileitis in surviving Syrian hamsters may include eventual obstruction, intussusception, or rectal prolapse.
Diarrhea in adult Syrian hamsters is associated with Clostridium difficile enterotoxemia and, as in guinea pigs, may occur 3–5 days after administration of antibiotics such as penicillin, lincomycin, or bacitracin.
Tyzzer disease due to Clostridium piliforme is seen in Syrian hamsters and is usually precipitated by stress such as overcrowding, high environmental temperature and humidity, heavy internal and external parasite load, and nutritionally inadequate diets. C piliforme is opportunistic in immunosuppressed animals and not seen in immunocompetent animals.
Bacterial pseudomycetoma has been described in several dwarf hamsters. The treatment is excision.
Hamster polyoma virus (HaPV) is the cause of epizootic lymphoma in young Syrian hamsters and epitheliomas in older enzootically infected hamsters. When first introduced into a naive population of breeding Syrian hamsters, HaPV results in an epizootic of lymphoma, with an incidence as high as 80%. Lymphomas often arise in the mesentery but can arise in the axillary and cervical lymph nodes. Once enzootic in a hamster population, the occurrence of lymphoma declines to a much lower level. Enzootically infected Syrian hamsters develop HaPV skin tumors rather than lymphoma. HaPV lymphoma–affected Syrian hamsters appear thin, often with palpable masses in the abdomen. Often, they have demodectic mange due to either Demodex criceti or D aurati.
Fecal smears of Syrian hamsters are abundant in protozoan organisms. However, their role in enteric disease is speculative, because similar protozoa are found in comparable numbers in both healthy and diseased animals.
Demodex criceti and D aurati are occasionally found on hamsters. Clinical signs consist of mild to moderate alopecia, pruritus, and erythema generally on the dorsal region of the body, the hindlimbs, and face. Additionally, crusts and scaling may be found on physical examination. Skin scrapings confirm the presence of a large number of Demodex spp in various stages of development. Treatment consists of a combination of 1% selenium sulfide shampoo and topical application of selamectin (15 mg/kg, applied once). Hamsters that do not respond to treatment or relapse often have serious underlying disease and typically die within 3 mo. Historically, reports exist of pet hamsters infected with the tropical rat mite Ornithonyssus bacoti (see Mice and Rats as Pets).
Spontaneously occurring dermatophytosis is extremely rare in Syrian hamsters.
In older Syrian hamsters, lymphoma is the most frequently observed neoplasm of the hematopoietic system. It is multicentric and commonly affects lymphatic organs. Cutaneous lymphoma, resembling mycosis fungoides (an epidermotropic T-cell lymphoma in people), is seen occasionally in adult Syrian hamsters. Affected animals show anorexia, weight loss, and patchy alopecia. Cutaneous lymphoma can be misdiagnosed as hyperadrenocorticism (Cushing disease), because affected hamsters initially show patchy alopecia and dermal hyperpigmentation. However, cutaneous lymphoma shows rapid progression of the disease, with mean time from presentation to euthanasia ~10 wk. Adenomas of the adrenal gland are common in Syrian hamsters, but few reports exist of confirmed clinical Cushing disease in hamsters.
Melanomas, not only of the flank organ but also of the skin, are frequently reported in Syrian hamsters. There is a striking 10:1 male:female melanoma ratio.
Djungarian hamsters showed a high prevalence of neoplastic disease (5 times greater than Syrian hamsters), and most tumors are integumental (eg, mammary tumors, atypical fibromas, and papillomas).
Atrial thrombosis occurs in aging Syrian hamsters with an incidence of up to 70%. Most thromboses develop in the left atrium secondary to heart failure and lead to a consumptive coagulopathy. Although the incidence does not differ between the sexes near the end of their respective lifespans, atrial thrombosis occurs on average at a younger age in females (13.5 mo) than in males (21.5 mo). Aged Syrian hamsters present with clinical signs of cardiomyopathy such as hyperpnea, tachycardia, and cyanosis. In untreated Syrian hamsters, death usually follows within a week after these signs are evident. The incidence of atrial thrombosis is influenced by the endocrine status of the animal, especially by the amount of circulating androgens. Thus, the castration of male Syrian hamsters is linked to an increase in the prevalence of atrial thrombosis.
Weight loss is seen in older Syrian hamsters and often associated with hepatic and renal amyloidosis. It is the principal cause of death in longterm research studies. Females have a higher incidence (80% among hamsters >18 mo old), increased severity, and earlier age of onset of amyloidosis than males. There is a correlation between social stress induced by crowding and amyloidosis in laboratory Syrian hamsters. Not surprisingly, it is infrequently reported in pet Syrian hamsters, in which overcrowding is not a problem.
Degenerative renal disease also occurs more frequently in older female Syrian hamsters. Affected kidneys are pale and granular. Microscopically, glomerular changes vary from thickening of the basement membrane to glomerular obliteration. Amyloid deposition occurs frequently as a concurrent event.
Polycystic liver disease is seen in Syrian hamsters >1 yr of age. The lesions are due to developmental defects of the bile duct and are not associated with clinical signs. At necropsy, numerous thin-walled cysts may be seen.
Syrian hamsters have a reputation as carriers of lymphocytic choriomeningitis virus (LMCV), a rodent-borne virus that can cause substantial neurologic disease, particularly among prenatal and immunocompromised people. The common house mouse, Mus musculus, is the natural host and principal reservoir of LCMV. People are typically infected through close proximity to wild mice and their droppings. However, three of the largest outbreaks of LCMV infection in the USA were attributable to hamsters obtained from a single supplier in the late 1970s. More recently, individual cases of LCMV infection have been epidemiologically linked to hamsters among organ transplant recipients. Although the risk of hamsters transmitting LCMV to the general population may be overstated, a German survey of persons in contact with pet hamsters confirmed an increased risk of LCMV infection, especially in city dwellers, younger age groups, and females. Transplacental infection occurs in the fetus of women who develop viremia during the first and second trimesters. The virus acts as a neuroteratogen, causing chorioretinopathy, hydrocephalus, microcephalus, lissencephaly, and potentially fetal death. The relative risk posed by hamsters should be considered among transplant recipients and pregnant women, because infected animals may remain clinically unaffected by LCMV and can transmit the virus for at least 8 mo. When apparent, LCMV infection in hamsters is characterized by wasting. Early signs are decreased activity and appetite and unkempt coat. Later signs include weight loss, hunched posture, blepharitis, convulsions, and eventually death.
Last full review/revision September 2015 by Thomas M. Donnelly, BVSc, DVP, DACLAM, DABVP(ECM)