Hamsters (Laboratory) - Pathology
Hamsters are now commonly used in laboratory testing, but for many years other species including mice, rats and guinea pigs were used for studies requiring small easily managed animals. In 1919 the first study using hamsters was undertaken assessing the susceptibility of Chinese hamsters to leishmania. A number of difficulties were encountered including an inability to breed the animals and hamsters were not used again until the 1930s when a Syrian hamster burrow was uncovered by an archaeologist near Aleppo. Nearly all common golden hamster breeds are related to these wild discovered hamsters. Syrian hamsters (Mesocricetus auratus)were used and were found to be easier to breed and had more desirable traits for laboratory testing than Chinese hamsters. Syrian hamsters have gone on to become the most commonly encountered laboratory hamster species with around 500,000 per year currently used in the US. However, approximately ten times more mice and rats are used compared to hamsters.
Strains and Stocks
Although Syrian hamsters Mesocricetus auratus or Golden hamsters are the most commonly encountered laboratory species, a number of other species are also used. These include the Chinese hamster Cricetus cricetus, the Armenian hamster Cricetulus migratorius, the Dzungarian hamster Phodopus sungarus and the South African hamster Mystromyx albicauafus. There are a number of differences between these types of hamster;
|Syrian/Golden||Compact body, short legs, 4 front toes, 5 rear toes, 120g, approximately 15cm long, short tail, dark ears, females larger than males.|
|Chinese||usually grey with a black stripe down its back, 30-35g.|
|European||usually has a black bely|
|Dzungarian||varieties include siberian, dwarf, striped and hairyfooted. 30-35g. Summer coat is brown and winter is white.|
|South African||usually white tailed.|
General Behavioural Characteristics
In particular, Syrian hamsters are solitary and only tolerate company when breeding. Females are easily disturbed and aggressive when lactating or pregnant and in such situations, can be prone to kill other hamsters. Cannibalism is common in stressed primiperous females. Chinese hamsters are particularly pugilistic.
Anatomy and Histology
This section has been included to allow familiarisation with the peculiarities of hamster anatomy to provide a context for some of the disease and pathological headings found below. Therefore only anatomical areas with specific features warranting emphasis have been included below;
Sebaceous glands with pigmented cells and terminal hairs that secrete during sexual arounsal in both sexes. Also used for olfactory territorial marking.
Post-ovulatory dimethyl disulphide is used as a breeding tool by females but is often mistaken for an inflammatory exudate due to its similarity in smell to rotten eggs.
Male Syrian hamsters have much larger adrenal glands than females despite females being generally larger than males.
This is not usually possible in hamsters as infants are extremely immature when born and 'foreign' infants usually do not accept one another.
Extremely long papillae extending into ureters. Very developed water conservation systems.
The Purkinje network and sino-atrial node are easily accessible surgically and is a useful physiological feature for some experiments.
Hamsters have highly distensible evaginations of the lateral buccal walls which are used to store and transport food.
Long duodenum, long jejunum, short ileum, big cecum, long colon.
Distinct constriction between the forestomach and glandular stomach. No lesser curvature of the stomach resulting in two blind sacs. Pregastric fermentation occurs in hamsters.
Apical an basal portions seperated by a semilunar valve. There are a series of 4 valves in the ileocecolic area.
For ease of use, the diseases of hamsters listed below are by body system, or where this is not appropriate in an “Other” category displayed after the body system sections. Those diseases listed below are not exhaustive but rather highlight common diseases encountered with laboratory hamsters.
Fungal infections occur infrequently in hamsters. Trichophyton mentagrophytes and microsporum spp are the most commonly isolated. In Infection may be asymptomatic or show clinical signs including small, patchy alopecia.
Macroscopic pathology includes irregular to circular, crusty, flaky skin lesions with reddened margins.
The mites Demodex criceti and Demodex aurati can have a reasonably high infestation level without clinical signs. Both mites are often found together, although Demodex criceti is considered to be non-pathogenic. Increased incidence has been reported in males an older animals and also as a secondary condition to malnutrition or concurrent disease.
Clinical signs range from none to alopecia, scaly skin, dermatitis and a rough looking coat. Alopecia generally occurs over the rump and back.
Other Mite Infestations
Reproductive Tract Neoplasms
This condition most commonly occurs mainly in female syrian hamsters with risk increasing with age.
Uterine carcinomas are seen in 25% of female neoplasm cases.
Acute bacterial mastitis has been associated with opportunistic infections of β-haemolytic Streptococcus spp. and usually occuring 7-10 days post parturition.
Macroscopic pathology will include swollen mammary glands and in some cases a mucopurulent exudate. Some females suffering with mastitis may cannabalise their litters.
Amyloidosis causes soluable proteins to polymerise into insoluable fibrils resulting in chronic infections and impaired renal function. This condition frequently in older (>1) female hamsters.
Macroscopic histology includes rough, pale and enlarged kidneys, enlarged adrenal glands and liver at necropsy. Microscopic histopathology may include glomerular hyalinisation, amyloid deposits in tubules and amyloid deposits in other organs including the spleen, liver and adrenals. Microscopic histopathology can be easily visualised with Congo red stain.
Arteriolar Nephrosclerosis (Hamster Nephrosis)
Arteriolar nephrosclerosis is a degenerative disease occurring most commonly in older hamsters, particularly females. Clinical symptoms will include weight loss and polyuria/polydipsia. Some links have been made between this disease and 'Lymphocytic choriomeningitis' virus infections (see below) which results in renal vascular hypertension. Arteriolar nephrosclerosis may also be concurrent with amyloidosis (above).
Macroscopic pathology on necropsy will include irregular kidneys that may be granular or pitted in appearance. Microscopic histopathology will include interstitial fibrosis, basement membrane thickening, tubular dilation with proteinaceous exosinophilic material and renal casts.
Known to occur spontaneously in some inbred strains of Chinese hamster, inherited via a recessive gene. Clinical symptoms include weight loss, glucose intolerance, mild to severe hyperglycemia, polydipsia, polyuria, hypoinsulinemia and ketouria.
Microscopic pathology will include pancreatic islet involution with severe and widespread nuclear pyknotic (irreversible condensation of chromatin in the nucleus of a cell undergoing necrosis or apoptosis), shrunken and eosinophilic cytoplasm with cytoplasmic vacuoles and loss of granules.
Although pneumonia is relatively uncommon in hamsters, it can be caused by a number of bacterial pathogens including Streptococcus pneumoniae, S. agalactiae, Pasturella pneumotropica, Staphylococcus aureus, Klebsiella pneumoniae, Bordetella spp, Corynebacterium paulometabulum and Salmonella spp..
Macroscopic pathology includes respiratory lesions at necropsy.
Atrial thrombosis and congestive heart failure are associated with older female hamsters and occur frequently. Atrial thrombosis is also associated with amyloidosis (see above). Clinical symptoms include dyspnea, tachycardia and cyanosis.
Macroscopic pathology will display a thrombi most commonly in the left atria.
This is an epizootic infection with a high mortality resulting in malformed and missing incisors and is mainly observed among suckling and weaning pups in Syrian hamsters.
Macroscopic pathology will include necrosis and inflammation of the dental pulp with mononuclear leukocytic infiltration of the dental lamina and osteoclasis of the alveolar bone.
Also called 'wet tail'. Enteritis occurs most frequently in 2-3 week old hamsters and results primarily from colonisation of pathogenic bacteria but may signal one of several GI diseases. Enteritis is one of the most common and serious diseases found in laboratory hamsters and has between 20-60% morbidity and up to 90% mortality.
General macroscopic pathology includes ileal thickening and enlargement at the terminal portion with roughened and reddened mucosa and serosa, enlarged mesenteric lymph nodes, peritonitis, flaccid cecum with fetid watery contents and abdominal adhesions. In very advanced cases, small white spots are visible within the ileum together with serosal nodules.
Microscopic histopathology will include hyperplasia of the crypt epithelial cells, migration of immature epithelium into the villi, downward extension of the crypts through the lamina propria, muscularis mucosa, submucosa, Peyer's patches, muscularis externa and serosa. There will be necrosis of epithelial cells to a varying degree with haemorrhage, pyogranulomatous inflammation and crypt microabcesses.
Infectious Causes of Enteritis
Clostridium perfringens, C. difficile and C. spiroforme produce toxins causing oedema, haemorrhage, mucosal dysfunction and necrosis. Clostridial enteritis manifests as 2 syndromes. The first is acute diarrhoea that is likely to have been caused by dietary changes, antibiotic therapy, concurrent diseases or physiological stresses. The second manifestation occurs in older (>6months) hamsters where they slowly loose weight and condition and die without diarrhoea.
Acute diarrhoea is macroscopically diagnosed at necropsy by serosal and mucosal haemorrhages of the cecum and sometimes the lower intestine. Definitive diagnosis for either manifestation is made via bacterial culture. The second manifestation is diagnosed macroscopically via a thickening of the cecal wall containing inflammatory cell infiltrate.
E. coli is transmitted via direct contact, fecal-oral and fomite transmission. Predisposing factors include a high carbohydrate diet, stress, overcrowding and lack of fresh water. Clinical signs include yellow watery diarrhoea that mats around the tail.
Microscopic pathology includes lesions in the small intestine and cecum together with serosal oedema. There will also be submucosal oedema and effacement of enterocytes colonised by bacteria in the small intestine or cecum. Often there is no inflammatory cell inflitrate in the lamina propria or submucosa.
Causative agents include Campylobacter coli, Campylobacter fetus and chlamydial organisms transmitted via fecal-oral or fomite contamination. Clinical signs include lethargy, anorexia, diarrhoea, dehydration and death. Moist faeces often stains the base of the tail. Ileitis primarily occurs in hamsters of between 3 to 10 weeks.
Macroscopic pathology will include yellow to dark red fluid within the small intestine and mesenteric lymph node hyperplasia. There may also be focal coagulative necrosis in the liver.
Microscopic pathology includes lesions in the ileum and cecum and serosal haemorrhage. The ileum is often also thickened. Intestinal segments will have mild to moderate segmental hyperplasia of the mucosa. Intestinal crypts will appear elongated with marked proliferation of enterocytes and often goblet cells. Lymphoid hyperplasia may be seen together with leukocytes near the base of the villi. Diagnosis is primarily made via histolology.
The incidence of salmonellosis in hamsters is low. Salmonella enterica is the common causative agent and is associated with contaminated food and bedding. Diarrhoea may be haemorrhagic, cause septicaemia and can also cause sudden death. Clinical signs are primarily seen in pregnant females or infants.
Macroscopic pathology includes fluid filled small intestine and cecum. The lungs may have a patchy haemorrhagic appearence. Small white foci are visible in the liver. The most significant macroscopic pathology is a septic lesion partially occluding thrombosis of pulmonary venules. Multifocal necrosis of the liver, lymph nodes and spleen may also be visible.
This is caused by clostridium piliforme. Infected hamsters exhibit a hunched posture and rough hair coats with or without diarrhoea.
Macroscopic pathology is widespread and includes enterocolitis with oedema, hyperemia of the large intestines, lymphadenitis and multifocal liver necrosis.
The hamster pinworms Syphacia mesocricetus, syphacia obvelata and syphacia muris are capable of inflicting heavy parasitic loads, although incidence of infection is low. Transmisson of infection occurs through ova ingetion and the eggs have also been shown to aerosolise increasing potential infection risks.
Heavy parasitic loads may lead to rectal prolapse or perianal irritation. Macroscopic pathology will show thickened GI tract and pinworms are recognised as white hair-like nematodes in the cecum.
Rodentolepis nana (dwarf tapeworm) or Hymenolepis diminuta are common although usually asymptomatic. Heavy infections may cause enteritis, intestinal impaction and abcesses within the mesentric lymph nodes.
Macroscopic pathology will show thickened and inflamed intestines.
Although this is rarely reported in hamsters, Francisella tularensis causes acute septicemia and has a high morbidity and mortality rates. Death occurs with 48hrs of onset.
Macroscopic pathology includes haemorrhagic lungs, enlarged and necrotic liver and spleen, prominent Peyer's patches and enlarged mesenteric lymph nodes.
This is a zoonotic pathogen.
Yersinia pseudotuberculosis is usually the result of fecal contamination of food or water and leads to acute septicemia and intermittent diarrhoea.
Macroscopic pathology includes lesions in the mesenteric lymph nodes, spleen, liver, lungs, gallbladder and intestinal walls.
Also called cholangiohepatitis, the cause of this pathology is thought to be from a Helicobacter species called H. cholecysticus. Affected hamsters display no clinical signs.
Macroscopic pathology includes bile duct hyperplasia, pericholangial fibrosis and centrilobular pancreatitis.
Lymphocytic Choriomeningitis Virus (LCM)
LCM is an RNA virus from the arenavirus group and is rare in hamsters, although most reported human cases have been associated with infected hamsters. In utero or perinatal infections may facilitate chronic infection resulting in a progressive wasting disease affecting the liver, spleen, lung, meningies and brain. Approximately 50% of hamsters will clear the infection.
A common route of infection of LCM in research laboratories is via the transplantation of LCM-containing tumours. Macroscopic pathology may include splenomegally, swollen or shrunken pitted kidneys and hepatomegally. Microscopic pathology may include lymphocytic meningitis, chronic glomerulonephropathy, widespread vasculitis and widespread lymphocytic infiltration.