POLA - 1999

Marti Hanes, DVM

Dept of Lab Animal Resources

University of Texas Health Science Center-San Antonio

San Antonio, Texas 28284


hanes @uthscsa.edu




Syrian hamster (Mesocricetus auratus) (a.k.a. Golden hamster), compact body, short legs, 4 front toes, 5 rear,  6 inches long, 120g, with a short tail, dark ears, and black eyes; may be any color, including Albino. 22 chromosome pairs, females are larger than males.

Chinese hamster (Cricetulus griseus) (a.k.a. gray hamster ) which is shorter, 30-35g, gray dorsal, and with a black stripe down its back. 11 chromosome pairs

European hamster (Cricetus cricetus) (a.k.a. blackbellied hamster)22 chromosome pairs

Armenian hamster (Cricetulus migratorius) (a.k.a. migratory hamster)

Dzungarian hamster (Phodopus sungorus) (a.k.a. Siberian, dwarf, striped hairyfooted hamster) 30-50g,

South African hamster (Mystromys albicaudatus) (a.k.a. white tailed rat)

Most often used are Syrian and Chinese hamsters

Specialized Anatomic and Unique features

·        Cheek pouches in hamster are well developed, are highly distensible evaginations of lateral buccal walls, are used to store and transport food, can be easily evaginated under anesthesia were a common site for experimental tumor implantation and vascular physiology studies; are immunologically privileged sites.

·        Hip or flank glands in hamsters are sebaceous glands with pigmented cells and terminal hairs which secrete during sexual arousal in both sexes and are used for olfactory marking of territory. Testosterone can be converted to Dihydrotestosterone here.

·        Stomach of hamsters has a distinct constriction between the forestomach and glandular stomach and there is almost no lesser curvature resulting in two blind sacs. Pregastric fermentation

·        Cecum- divided into apical and basal portions separated by a semilunar valve, series of 4 valves in the ileocecocolic area.

·        Kidneys have extremely long papillae which extend into the ureters.  water conservation

·        Heart -accessible purkinje network  in addition to S.A. node- useful for conduction experiments

·       Vaginal Discharge-Post ovulatory, dimethyl disulfide, used as breeding tool, can be mistaken for inflammatory exudate. Duplex uterus, 7pr mammae. Females are hyperactive during estrus, and can travel considerable distance

·       Sexual dimorphism:. Male Syrian hamsters have bigger adrenals due to 3x thicker zona reticularis; in most rodents, females have bigger adrenals.

·       Germfree derivation not practical, crossfostering doesn’t work, infants are extremely immature when born, have sharp incisors at birth, and usually will reject others infants

·        Liver- Intranuclear Inclusions, Nonspecific- Cause not definitely known, but thought to be formed by invagination of nuclear membrane with incorporation of some cell cytoplasm. Inclusions are weakly eosinophilic with H&E, PAS-negative, 5-8 microns in diameter, homogeneous or granular, and usually eccentrically located within the nucleus.  The nuclei containing them are frequently enlarged and have an irregular wrinkled profile. Intracytoplasmic Nonglycogenic Present in liver in normal circumstances, but more numerous if there is hepatic damage.  Eosinophilic with H&E, strongly PAS-positive before and after diastase digestion, thus, indicating nonglycogenic character.  Stain intensely with Sudan black, suggesting presence of bound lipids; are also acid-fast with Ziehl-Neelsen.  Usually 2-30 microns in diameter,

·        Trophoblastic Giant Cells. Are derived from the fetal placenta; specifically from the trophoblast ;the epithelial cell layer covering the blastocyst.  The blastocyst erodes the uterine mucosa to establish the hemochorial placenta seen in hamsters, guinea pigs, other rodents, and primates; placenta in hamster called labyrinthine hemotrichorial.  The trophoblastic giant cells are in direct contact with maternal bloodstream.  These cells exhibit remarkable migratory activity, and frequently are found inside mesometrial uterine arteries and ovarian arteries; they apparently only migrate toward arterial blood.  Can be seen three weeks postpartum.

·        Hematology-polychromasia, anisocytosis, RBC 50-78days, heterophils, 60-70% lymphocytes

·        Immunologic tolerance- lack of suppressor T cells, atypical cytotoxic T cells


Animal models of human disease and recent publications  (370,000 used annually)

·       Physiology

·       Infectious

·       Bacterial-Clostridium difficile, Mycobacterium tuberculosis, MB leprae, Camplobacter sp., Corynebactera paulometabuleri

·        Viral- LCM, sheep associated MCV

·       Prion- scrapie

·       Parasitic-Echinococcus multilocularis, Echinostoma, Schistosoma currassoni, Acanthocheilonma viteae, Cestodiasis

·       Fungal-Paracoccidiodes brasilensis

·       Protozoal-Leishmania sp. Babesia microti, Cryptospordia

·        Zoonotic- LCM, Hymenolepid tapeworm, Acinetobacter sp

·       Toxicology/ Carcinogenesis - Nitrosoethyl heptlamine(pulmonary adenocarcinoma), DEN(cigarette smoke-leukoplakia), oral hygiene-cheek pouch

·       Reproductive/teratology/birth defects-spermatogenesis

·       Ethanol, neurotoxins

·       Environmental-Triphenyl tin, fly ash, magnetic fields

·       Irritation-cheek pouch

·       Syrian Hamster Embryo (SHE cells)-

·       Respiratory neoplasia

·       Viral oncogenesis

·       Neoplasia-pancreatic, respiratory, viral,

·       Immunology- MHCII, IgA, IgG, histocompatability

·        Behavioral- fighting, cannibalism, reproductive, circadian, melatonin, pheromones, hibernation, harderian gland, hypothermia, stress (tests- fasting, foot shock, immobilization)

·       Nutritional and metabolic - diabetes, glucose, lipid metabolism, anatomy-long duodenum, jejunum, short ileum, big cecum, long colon-

·       Aging/Misc.- polymyopathy, goiter, athlerosclerosis, spontaneous hypertension, ulcer, microopthalia, cardiomyopathy, congestive heart failure, dental  caries,  epilepsy, muscular dystrophy, microcirculation, gall stones, amyloidosis,

·        Strains-   Bio 2.4(agouti)-benign prostatic hypertrophy

·        Bio 14.6-(acromelanic White) cardiomyopathy

·        LSH (golden)-gentle

·        MHA (white)-dental caries

·        PD4(white)-large, placid disposition

Disease Differential lists for hamsters

·         Enteritis; wet tail, diarrhea, constipation-Tyzzer’s, pathogenic E.coli, Clostridium difficile, Campylobacter Cryptosporidium, Salmonella, Giardia,  Chlamydia, cecal mucosal hyperplasia, Proliferative ileitis, cestodiasis, gastric hairballs, ingestion of bedding, intussusception, rectal prolapse, uterine prolapse, dietary change, water deprivation sub clinical-spironeucleus, adenovirus

·         Respiratory Disease, otitis, pneumonia- Sendai, Pasteurella pneumotropica, Streptococcus pneumonia, S. agalactiae, PVM, Mycoplasma pulmonis, congestive heart failure

·         Hepatitis/Hepatic necrosis (white spots on liver)- Leptospirosis, Tularemia, Salmonella, E. coli, Tyzzer’s, Taenia sp, Polycystic liver disease, hepatic cirrhosis, hamster papovavirus

·         Bumps, subcutaneous nodules-( normal-testes, cheek pouches, flank glands), abscesses, hernias, neoplasia, arthropathy, mastitis, impacted cheek pouch, granulomas in skin or lymph nodes

·         Dermatitis- demodicidosis, bedding associated, trauma, cannibalism, protein deficiency, notodres, dermatophyte(/), bacterial-P. pneumotropica, Staph. aureus

·        Ocular -LCM, bacteria, bedding/dust, bite wounds, tooth abscess, trauma

·        Teeth- malocclusion, parvoviral infection, dental caries, periodontal disease

·        CNS-torticollis-encephalitis or inner ear; inco-ordination-insecticide, LCM, tick paralysis, epilepsy; SHN

·        Infertility, infant loss-seasonal quiescence, over use of males, dystocia, mastitis, pseudopregnancy, cannibalism, agalacia, immaturity, stress, reluctance to breed, senescence, starvation, Vit E deficiency in females, cold, prolonged darkness, pair incompatibility, inadequate nesting materials, transparent cage, large fetal load



·        Proliferative Ileitis (Transmissible Ileal Hyperplasia, “Wet-tail”, proliferative regional enteritis, proliferative bowel disease, terminal ileitis, terminal enteritis, enzootic intestinal adenocarcinoma, atypical ileal hyperplasia, hamster enteritis.)  Is common and important natural disease of hamsters; usually occurs as an epizootic disease of weaning animals with a morbidity of 20-60% and a mortality of affected animals reaching 90%; usually associated with stressful conditions such as transport, overcrowding, surgical procedures, diet, and experimental manipulations. The term wet tail should not be used as it includes all the diseases that cause diarrhea in hamsters, this is a significant cause of disease in pet store animals, and a potential complication to research. Incriminated agents include E coli, Camplobacter sp, and Cryptosporidium, Chlamydia sp., and Camplobacter-like organisms. Clinical signs include are usually confined to younger animals, esp. during the weaning process, and are resistant after 12 weeks. Include lethargy, anorexia, irritability, ruffled hair coat, huddling in corners, fetid watery diarrhea, dehydration, weight loss, drop in body temperature, abdominal distention, and occasionally convulsions. Rectal prolapse or intussusceptions frequently occur. Usually die within 48 hours of appearance of signs; some animals remaining alive become runted, emaciated and cachectic; with perineal soiling.Necropsy: Early see segmentally enlarged terminal ileum with roughened reddened mucosa and reddened serosa; flaccid cecum with fetid watery contents.  Later see more thickening of ileum with small white spots and serosal nodules; then see markedly thickened, rigid, friable terminal ileum with white nodules on serosal side, occasional local fibrinous peritonitis with or without adhesions, occasional intussusception of ileum into cecum,  caseous material in the lumen, and a necrotic mucosa. The opened bowel reveals an abrupt transition of the cranial, normal ileum and caudal cecum with the affected, hyperplastic mucosa.  Microscopically, hyperplasia of crypt epithelial cells, migration of mitotically active, immature epithelium onto the villi, with  elongation, distortion, fusion and widening of villi in terminal ileum. This is followed by downward extention and  penetration of crypts through lamina propria, muscularis mucosa, submucosa and Peyer’s patches, muscularis externa, and the serosa with concomitant necrosis of epithelial cells and development of varying degrees of necrosis and hemorrhage, pyogranulomatous inflammation and crypt microabscesses.  Chronic lesions include fibrous tissue proliferation around false diverticula (not true diverticula because muscle layers penetrated).With silver(Steiner’s, Warthin-Starry) or PAS stains, numerous and characteristic small bacteria can bee seen in the apical cytoplasm of proliferation enterocytes. Macrophages in the lamina propria and submucosa contain abundant PAS+ material in the cytoplasm.  Ultrastructurally, see slightly curved bacilli usually free in cytoplasm near apices of cells.

·        Campylobacter fetus ssp. jejuni has been isolated from outbreaks of proliferative ileitis and from clinically normal animals.   May have watery diarrhea. Hamsters have been somewhat resistant to experimental disease.  Hamsters may shed the organism for several months.  It is a zoonotic threat.

·        Escherichia coli  clinically similar to other causes of diarrhea. Isolates of strains 1056, 1126, 4165 from naturally occurring cases of enteritis were pathogenic when injected into susceptible recipients.  Ligated loop test revealed changes in most weanlings and some adults. The small intestine may contain yellow to dark red fluid material.  histopathological changes include blunting and fusion of villi degeneration and sloughing of enterocytes, PMNs in the lamina propria. But hyperplasia of the intestinal mucosa is not seen.  The mesenteric lymph nodes may have lymphoid hyperplasia or PMN infiltration.  There may be focal coagulative necrosis in the liver with PMNs, and gastric ulcers.  Colitis, typhylitis, intussusception. Ultrastructurally the ileal enterocyte cytoplasm reveal  bacilli.      Enteropathogenic E coli  may play a role in ileal hyperplasia.


·        Clostridium piliforme (Tyzzer’s Disease). (a.k.a. Bacillus pilliformis) Several epizootics have been observed. Gram negative spore forming, 16s ribosomal RNA indicates closed relation to Clostridia sp than Bacillus sp.  Wide host range with interspecies transmission a possibility.  Hamsters infected by contact with affected animals or bedding.  Predisposing factors include intestinal parasitism, poor sanitation, inappropriate feeding. Animals infected with liver homogenates had detectable lesions in the intestine and liver in 3 days. In Syrian hamsters 28% of 64 weanlings became ill with huddled, sleepy appearance and staining of perineum with pale yellow feces; animals died or were moribund within 48 hours.  Gross lesions were variable. The lesions may be confined to either the liver or the intestinal tract.  Multifocal hepatic necrosis may be present.  Intestinal lesion when viable grossly consist of varying  degrees of dilation of the large intestines and occasional reddening of the serosa of the ileum ; the intestines filled with foamy yellow material, gray plaques were occasionally seen in cecal or colonic mucosa.  Several small white spots were occasionally in the liver. Microscopically, hepatic lesions were characterized by foci of coagulative necrosis with peripheral neutrophilic infiltration.  Intracellular bundles of bacteria are best demonstrated at the periphery of hepatic lesions. Lesions in the intestinal tract consist of edema of the lamina propria with PMNs and effacement of the mucosal architecture. There may be extention of inflammation into the muscular tunics.  Typical bacilli are demonstrable in the enterocyes adjacent to affected areas. Focal granulomatous myocarditis has been associated with Tyzzer’s in hamsters. Bacilli are best seen with  Warthin-Starry or Giemsa.  Organisms are long, pleomorphic, and sometimes beaded bacilli; are not generally believed to grow in cell-free media; are Gram-negative and spore forming; and are cultured in chick embryos. Significant cause of morbidity and mortality with interspecies transmission.



·        Salmonellosis. S. enteritidis serotypes typhimurium and enteritidis  . Hamsters are very susceptible and disease is frequently a cause of diarrhea. Transmission is probably ingestion of contaminated food and bedding.  Explosive outbreaks of acute salmonellosis are characterized by depression, anorexia, dyspnea, ruffled coat and high mortality.  At necropsy there are multifocal pinpoint areas in the liver, patchy pulmonary hemorrhage and red hilar lymph nodes. Microscopically foci of congestion, hemorrhage, interstitial pneumonia, and erosion and necrosis of the walls of veins and venules with formation of pulmonary phlebothrombosis (partially occluding septic thrombi).  There was focal necrosis in the liver and spleen, and  hepatic venous thrombosis.  Embolic glomerular lesions and focal splenitis may occur.  There were no enteric signs or lesions. Organism may be recovered from the blood, lung and other viscera.  Danger of interspecies transmission. Lesions were reproduced in inoculated hamsters.


·        Antibiotic-associated Enterocolitis (Clostridial Enteropathy)

Lincomycin, clindamycin, ampicillin, vancomycin, erythromycin, cephalosporins, gentamicin, and penicillin.

Profuse diarrhea, with high mortality, occurs within 2-10 days following the oral or parenteral administration of certain narrow spectrum antibiotics.  The predominant bacterial  microflora of the hamster intestine are Lactobacillus  and Bacteriodes.  Following therapy overgrowth with Clostridium difficle  occurs, resulting in acute colitis, diarrhea and death.  In animals treated with vancomycin 100% mortality, oral administration of cecal content from normal animals (yummy) provided some protection.  This alteration of the inhibitory barrier of gram neg anaerobes and other Clostridia, may allow colonization of C. difficile  and elaboration of toxin.

The cecum is distended with fluid contents, with hemorrhage into the gut wall.  Histopathology nmay reveal lesions from mild typhlitis to acute pseudomenbranous typhlitis.  There is effacement of the mucosal epithelium, edema of the lamina propria, leukocyte infiltration, mucosal hyperplasia.  Terminal ileum and colon may be involved.

Anaerobic culture should recover. C difficile, cytotoxicity by cell culture of mouse inoculation, cytotoxin neutralized by antitoxin.


·        Non-antibiotic associated Clostridial Enteropathy- acute onset enteritis has been seen in hamsters w/o history of antibiotic administration.  Necrotizing typhlitis with mucosal damage are characteristic.    C. difficile cytotoxin may be demonstrated in cecal contents of affected hamsters.


·        Cecal Mucosal Hyperplasia -Spontaneous cases of cecal  hyperplasia have been observed in weanling and suckling hamsters. Diarrhea, runting, and high mortality were associated with disease.  At necropsy, ceca are congested, contracted and opaque.  Microscopic changes observed include increased mitotic activity and hyperplasia of enterocytes lining cecal crypts, and focal mucosal erosions.  Bacterial cultures and EM have failed to id an agent. 

·        Leptospirosis- hamsters are susceptible to various species of Leptospirosis. Severe hemolytic disease, jaundice, hemoglobinuria, nephritis, and hepatitis within 4-6 days.

·        Tularemia (Francisella tularensis )  One descriptive report of an acute outbreak in a colony with 100% mortality.  Animals had roughened hair-coats, huddled, and died within 48 hours.  Grossly, lungs were mottled with subpleural hemorrhages; livers were enlarged and pale; spleens were enlarged, one had white foci; the Peyer’s patches were raised and chalky white; mesenteric lymph nodes were enlarged and were chalky white.  Microscopically, there was necrosis of lymphoreticular tissues with variable hemorrhages and bacteremia.  Source of infection not definitely known; contaminated fresh vegetables suspected.


·        Yersinia pseudotuberculosis  Infection is by fecal contamination of food and water by wild rodents and birds.  Chronic emaciation with intermittent diarrhea.  See caseous lesions in mesenteric lymph nodes, spleen, liver, lungs, gallbladder, and intestinal walls.  See intermittent diarrhea.

·        Streptococcus sp. beta-hemolytic streptococci causing acute suppurative mastitis in two hamsters.

·        Streptococcus (Diplococcus) pneumoniae Infections caused pneumonia in one colony.

·        Pasteurella pneumotropica . causing mastitis, and dermal  abscesses midway between the eyes and ears of 13 hamsters which had received whole-body irradiation.

·        Staphylococcus sp. purulent exudate in focal lesions on the skin and feet. , lymphadenitis,

·        Actinomyces bovis . Hamsters bearing tumor transplants in their cheek pouches and receiving long-term cortisone treatment developed abscesses on their lips which contained Actinomyces  organisms.  There is another descriptive report of Actinomyces bovis  caused  purulent pockets of material in a submaxillary gland in with sulfur granules.

·        Mycoplasma pulmonis -Experimental and natural infections have been reported, but role as a pathogen not known.

·        Corynebacterium kutcheri--G+ diptheroid bacillus isolated from the oral flora , esophagus, cecal contents, submaxillary nodes and upper respiratory tract of normal adult Syrian hamsters, possible reservoir host. Giemsa of smear-”Chinese characters”


·        Lymphocytic Choriomeningitis (LCM) (Arenaviridae, Genus Arenavirus).  Wide host range (primates including man, rodents), natural reservoir is wild mouse.  Infection exposure with urine or saliva from  animals shedding virus, including oronasal or skin abrasions.  cage to cage aerosol transmission not impatient part of transmission.  Congenital infection is hamsters occurs, cell culture and transplantable tumors have been contaminated and are a laboratory source of importance.  The disease depends on the age, strain and dose of virus and route. 

Experimentally, newborn hamsters have approximately half clear the virus with lymphocytic infiltration.  The other half will be viremic for 3 mo, viuric for 6mo.  At six months there is chronic wasting, lymphocytic infiltration in the liver, spleen, lung, meninges and brain.  Vasculitis and glomerulitis with antigen and antibody complexes in the arterioles and glomerular basement membranes. 

LCM infected hamsters are the primary source of LCM in humans. Hamster source of infection for man.; infections were contracted from hamsters or infected tumor-cell lines passaged in hamsters. Sequelae post exposure may vary from subclinical infections to influenza like symptoms. Occasional viral meningitis or encephalomyelitis may occur. Diagnosis by serology, IFA , however,  complement fixation tests may be confounded by high anticomplement antibodies in young hamsters.

·        Parvoviral Infection- An epizootic of high mortality with malformed and missing incisors  has been observed among sucking and weaning pups in a breeding colony of Syrian hamsters.  Necrosis and inflammation of the dental pulp  with mononuclear leukocytic infiltration of the dental lamina and osteoclasis of alveolar bone.  Seroconversion to rat Toolan H-1, a parvovirus that has previously been shown to have similar effects in  experimentally infected neonates.

·        Hamster Papovavirus-(HaPV)polyoma- similar to but not identical with the polyoma virus of mice.  It is the cause of Transmissible lymphoma, which can occur in epizootics among young hamsters, and keratinizing skin tumors of hair follicle origin or subclinical infections.  IT is not a papilloma virus.  HaPV is not common, but infection in both European and Syrian hamster colonies have been reported in the US and Europe.  Theorized to have been introduced from wild European hamsters to Syrians. Spread by urine, causes a multisystemic infection with persistence in the kidney and shedding in the urine.  Virus is oncogenic, but tumor formation is a side effect instead of being essential to the life cycle of the virus. Typical of polyoma viruses, the virus can infect cells lytically with virus replication, or transform cells without replication. Lymphomas do not have detectable virus, however HaPV epitheliomas have virus replication in the epithelium (similar to papilloma virus).  Hamsters are susceptible to the oncogenic effects of the virus beyond the neonatal period.

Affected hamsters are thin, with palpable abdominal masses.  Lymphomas in the mesenteric lymph nodes, axillary and inguinal lymph nodes with out involvement of the spleen.  Infiltration of the liver sinusoids, kidney, thymus and other organs occurs.  Cytologically, the tumors are usually lymphoid, but  erythroblastic, myeloid and reticulosarcomas have been seen. Tumors arising in the thymus are T-cell, mesentery are B-call.  Variably differentiated from blastoid to plasmacytoid.    mesenteric masses may involve the intestinal wall, and may exhibit central necrosis.  Skin tumors are non-glaborous areas with keratinizing structures resembling trichofolliculomas.

Epizootic HaPV is unique, lymphoid tumors are otherwise rare in hamsters, and then only seen in aged animals. Trichoepithelioma have not been described in hamsters unless they were associate with HaPV.  Crystalloids can be visualized in the keratinizing epithelium.  No serological test., depopulate.


·        Adenovirus- INIB have been seen in ileal enterocytes in tissues from young (<4wks) hamsters.  Mouse Adenovirus K87 strain antibodies have been detected in hamsters.  Large amphophilic intranuclear inclusions in villar enterocytes, goblet cells and rare cryptal epithelium. Asymptomatic, no inflammation. Virus viable on EM and serology, significance is unknown.


·        Cytomegalovirus (Salivary Gland Virus) (Herpesvirus). Virus is host specific; produces subclinical disease in Chinese hamsters.  Acinar cells  of the submaxillary glands are more affected than ductal cells with intranuclear and occasionally cytoplasmic inclusions, megalocytes and lymphocytic infiltrations

·        Pneumonia Virus of Mice (PVM) (Paramyxovirus).  Natural hosts include hamsters and rats.  Conventional colonies are seropositive without clinical disease. Old literature suggests it was the etiologic agent of interstitial pneumonitis with consolidation, however more temporal significance is unknown.

·        Sendai Virus (Paramyxovirus).Sendai infections are widespread, confirmed clinical disease is scarce. There are reports of mortality in newborn Syrian and Chinese hamsters, and they are regarded as natural hosts. Mild necrotizing bronchiolitis and focal interstitial pneumonia can be seen.

·        Other virus- Syrian hamsters will seroconvert to mouse encephalomyelitis virus (GDVII), reo 3, SV5, paramyxovirus, and rat parvoviruses.  There is an endogenous oncovirus, as well as a in vivo sensitivity of newborn hamsters to oncogenic viruses.





Spontaneous  confirmed infection have not been reported.


·        Spironucleus (Hexamita) muris.-Normal flora, found in small intestine and cecum transmit by ingestion.  Non pathogenic to hamsters, dubious pathogenic to mice.  Organisms have six anterior and two posterior flagella ; are pyriform 7-9 m long and 2-3 wide, normally feed on intestinal bacteria and usually viewed as incidental finding.  However, under unusual circumstances may see mucosal damage and clinical signs.  also may see the flagellates in the peripheral blood of hamsters with enteritis.  Transmission to rats and mice.  May alter macrophage activity and immune response in the mouse.


·        Giardia muris , G . mesocricetus Common in some hamster colonies; found in small intestine, usually asyptomatic non-pathogenic  however suggested to be responsible in part of chronic intestinal amyloidosis, with diffuse infiltration of the intestinal lamina propria with plasma cells and lymphocytes, and mural fibrosis. Causes enteritis in mice; transmit by ingestion. Wet mount from the duodenal region reveals pear shaped organisms with characteristic rolling, tumbling movement.  H&E stained sections reveal pear shaped ellipsoidal organisms attached to the brush border of the enterocytes.    Organisms may be seen I the inter villar spaces, crypts of the duodenum, extending to the villar tips. Has 8 flagella, is pyriform, has a large sucking disc on anterior ventral side, and has two nuclei.  Cysts are thick walled ovoid  and more easily visualized with Giemsa or phase contrast and have four nuclei.  Unknown level of threat to humans., possible interspecies transmission.

·        Encephalitozoon cuniculi  infection described in a study of transplantable plasmacytoma of hamsters.

·        Balantidium coli. Rare in hamsters; found in cecum and colon, usually non-pathogenic but occasionally causes enteritis and diarrhea (also in man



Pinworms-Diagnosis by perianal eggs retrieved from cellophane tape impression smears, fecal float, cecal smears at necropsy.

·        Syphacia mesocriceti  (hamster pinworm) not as common as S.oblevata. differences are minor morphology

·        Syphacia obvelata (Mouse pinworm), in cecum and lesser extent colon; direct L.C.; eggs laid around anus; autoinfection occurs; esophageal bulb round; eggs flat on one side; small cervical alae; mild enteritis with heavy infection

·        Syphacia muris (Rat pinworm) infection was experimental;

·        Aspiculuris tetraptera (Mouse pinworm). no documented evidence that hamsters are susceptible.

·        Trichosomoides nasalis (Europe). In nasal mucosa;.



·        Hymenolepis sp.  Relatively common when compared to mice and rats., usually asymptomatic. Diagnosis is by identification of eggs in fecal samples, crush preps of intestinal contents, or histology

·        H. nana (dwarf tapeworm); is the smaller even than H.  diminuta  found in lower small intestine. With direct life cycle get quick immunity because of tissue phase.

·        Hymenolepis diminuta. Not common; need intermediate host. (flour beetle, moth, flea); cause acute catarrhal enteritis or chronic enterocolitis.  Is zoonotic if ingest Intermediate host.

·        Hymenolepis microstoma. Uncommon; found in duodenum, bile duct, gallbladder, and liver; can get inflammation and necrosis; intermediate host. are flour beetles and fleas.

·        Cysticercus fasciolaris (Taenia taeniaeformis). Larval stage of dog and cat tapeworm; see cyst in liver. Contaminated food with feces from definitive host.





ACARIASIS  Male hamsters usually have a larger mite load.  Skin scrapings cleared with 10%KOH or NaOH.

·        Demodex sp.  mites are common in animal facilities. Syrian hamsters born to infected suckling dams acquire the infection during the suckling period. Are generally of low pathogenicity, and clinical signs rarely occur.  Older animals and those hamsters subjected to experimental stressors may develop alopecia, over the back neck and hindquarters.  Denuded areas are nonpuritic, dry and scaling.

·        D.criceti  Found usually in the epidermal pits  with sparing of the dermis. No tissue reaction or pigmentation;

·        Demodex aurati  Found in hair follicles and  in pilosebaceous units. hair follicles may be dilated with mites.

·        Sarcoptes scabei. Itch mite, sarcoptic mange mite; rare in hamsters; only in epidermis; burrows in epidermis; papular dermatitis with pruritus and selfmutilation.

·        Notoedres notodres. Found in the stratum corneum, with scabby lesions of the ears, nose, feet, perineum.

·        Notodres cati-outbreak reported

·        Speleorodens clethrionomys- nasal mite infestation detected in three breeding colonies in Europe

·        Ornithonyssus bacoti (tropical rat mite); troublesome pest of lab animals; can debilitate and cause death from chronic blood loss; can infect man; vectors of many microorganisms.

·        Ornithonyssus sylvarium (northern fowl mite); a bloodsucker, usually on plumage of chickens; hamsters are incidental hosts; entire L.C. on host.


MYIASIS  rare cases of Wohlfahrtia vigil  (flesh fly),Sarcophaga hemorrhoidalis (flesh fly), Musca domestica (house fly). cause dermal myiasis; infestation with maggots if wild or when no screens. Flesh fly females are I and lay larvae in open wounds and fetid sores; larvae develop in 4-7 days, pupate for four days; full life cycle is two weeks; larvae are voracious and often actively invade healthy tissue.




Reported incidence of spontaneous malignant neoplasms in Syrian hamsters is about 4%, with marked variation in individual colonies, reflecting the influence of both genetic and environmental influences. 

Majority are endocrine or alimentary and benign.

Adrenocortical adenomas one of most frequent.

Cutaneous lymphoma (mycosis fungoides)-epidermotropic in adults, lethargy, weight loss, patch alopecia, exfoliative erythroderma.  Dense infiltrates of neoplastic lymphocytes in the dermis with extention into the epidermis. The most common malignant tumor is the lymphosarcoma , often involving the thymus, thoracic lymph nodes, mesenteric lymph nodes, superficial lymph nodes, spleen, liver, and others. with variable cell types.

Other reported tumors have included: gastrointestinal tract, and skin appendages, glioblastoma,  astrocytoma, medulloblastoma, ependymoma, pineocytoma mesothelioma induced by asbestos,.

Newborn hamsters commonly used in vivo to screen for potentially oncogenic viruses. syrian polyoma virus <30 days. Chinese hamsters have high incidence of endomyometrial neoplasms


·        Pregnancy toxemia.  Reported to occur in some colonies; in one report said to resemble human eclampsia with associated renal cortical necrosis.

·        Diabetes mellitus.  Occurs spontaneously in some inbred strains of Chinese hamsters; inherited by recessive gene, Clinically hamsters demonstrate weight loss, glucose intolerance, mild to severe hyperglycemia,  polydipsia, polyuria, hypoinsulinemia, ketonuria.  Microscopically, many islet exhibit involution with progressively severe and widespread nuclear pyknotic , shrunken and more eosinophilic cytoplasm with cytoplasmic vacuoles and loss of granules.

·        Arteriolar Nephrosclerosis (Hamster Nephrosis)- degenerative renal disease important disease of aging hamsters.  More frequent in females. Similar to progressive glomerulonephropathy in aged rats.  Animals experience weight loss and polyuria, polydipsia.   A chronic viral association with LCM has been suggested due to the lymphoplasmocytic interstitial component.  Renal vascular hypertension, and antigen antibody antigen complex deposition has also been proposed as causes .Amyloidosis may be concurrent.  Affected kidneys are irregular, granular, rough, pate, and pitted.  Glomerular changes are characterized by segmental to diffuse thickening of basement membranes, with deposition of eosinophilic matrix, and frequently obliteration of normal structure. Degeneration of renal tubules is characterized by atrophy, flattening of cells or  regeneration with poorly differentiated epithelium.  Interstitial fibrosis, basement membrane thickening, tubular dilation with proteinaceous eosinophilic material and casts, fibrinoid change in renal arteries, mild inflammatory response.  A significant case of death and morbidity in older hamsters. 


·        Polycystic Disease (Polycystic liver disease). Liver cysts are of varying size up to 2cm , single or multiple, subcapsular and parenchymal, have a thin wall, and contain light to straw colored fluid; similar cysts can occur in epididymus, seminal vesicles, pancreas, endometrium , ovaries and adrenals. Liver cysts are lined by cuboidal epithelium that becomes flattened in larger cysts; occasionally the epithelium is continuous with bile duct epithelium.; cysts maybe multiple and separated by fibrous bands.  Adjacent tissues may demonstrate pressure atrophy, hemosiderin deposition, bile duct proliferation and lymphocytic inflammation.  Considered to be congenital in origin due to either failure of fusion of interlobular and intralobular ducts, or failure of redundant ducts to atrophy. Usually incidental findings at necropsy

·        Amyloidosis  Commonly seen in normal aging hamsters (over 1 year of age) and in animals with chronic infections.  The disease may vary in incidence among colonies, females most common, 5mo-15mo of age. Clinically a increase in serum albumin is accompanied by an increase in serum globulins.  Can be experimentally caused by casein injections, and suppressed in females with injection of androgens.

·        Kidneys, adrenals and liver  when affected are enlarged and  pale. Can also be seen in the lungs, spleen, stomach, intestines, ovaries, testes, and epididymides. Grossly appears white, with Lugol’s solution turns brown color, and with added dilute sulfuric acid turns a blue color.    Deposition of eosinophilic homogeneous material in glomeruli of kidneys, around splenic lymphoid follicles, cortices of the adrenals, and around portal triads in the liver with variable involvement of the sinusoids. Microscopically, with H&E is amorphous, slightly pink material with “apple-green” birefringence when stained with Congo Red and is yellow with Thioflavin T.  See massive deposition of amyloid with leishmanial infections, tuberculosis, treatment with DES and with certain tumors. Clinically similar to nephrosis, significant liver and adrenal function occur very late in the disease.

·        Atrial Thrombosis and congestive heart failure.  Occurs frequently in older female hamsters, and is often associated with amyloidosis. Thrombi most commonly seen in left atria only (87%).  Changes in coagulation parameters and fibrinolytic factors are consistent with a consumptive coagulopathy, blood stasis due to myocardial insufficiency probably is a major contributor to the pathogenesis.  Disease recognized by development of  dyspnea, tachycardia, and cyanosis due to congestive heart failure.  A firm to friable thrombus adherent to adjacent endocardium is present in the left atrium, with variable extention into other chambers of the heart. There is bilateral ventricular hypertrophy,  with pulmonary edema and pleural effusion. Thrombi maybe moderately organized.  Myocardial changes when present are characterized by nuclear hypertrophy, vacuolation of the cytoplasm, fiber atrophy, interstitial fibrosis.  Concurrent medial degeneration and calcification of coronary arteries. Valvular myxomatous or fibrotic change. Occasionally, some inflammation in heart wall but not significant

·        Age related vascular changes - fibrinoid degeneration of arterioles, cerebral mineralization,

·        Spontaneous Hemorrhagic Necrosis of the CNS of Fetal Hamsters.  (SHN). Most likely due to Vitamin E deficiency in dams.   Recognized in fetal hamsters during last trimester and newborn hamsters.  Animals are stillborn, weak or cannibalized. Grossly, see hemorrhage or edema in calvarium and spinal canal Microscopic changes most extensive in the forebrain-proencephalon, with symmetrical subependymal vascular degeneration, and edema with hemorrhage in the adjacent neuropil. Intraventricular hemorrhage has been observed. Lesions may proceed posteriorly and deeper into the neuropil of the brain.  When the process is severe, it may affect the spinal cord, but usually spares the cerebellum . There may be  thinning and dissolution of developing cortical mantles and neuropil.  Retina and internal ear may become edematous and exhibit some necrosis. Myopathy in some fetuses.  Cardiomyopathy in some dams.  Appears that disorder of the capillary bed is primary lesion.  Vitamin E reduces incidence and severity, and corn oil or linoleic acid increases incidence and severity. It is alleviated by Vit E supplementation.

·        Hepatic Cirrhosis.  Incidence has been high in some colonies; up to 20% reported; seen in older animals and more in females.  Grossly, see uniform nodularity in all lobes.  Microscopically, see extensive periportal proliferation of hyalinized fibrous connective tissue with proliferation of bile ducts, nodular hepatocellular regeneration with concurrent degeneration and necrosis, and lymphocytes and neutrophils.

·        Bedding Associated Dermatitis- Chinese and Syrian hamster leg lesions related to wood shavings.  Foot pads with degeneration and atrophy of the digits.  Necrotic areas with ulceration may spread to the shoulders.  Microscopically, pieces of wood shavings are present in the lesions with pyogranulomatous inflammation.  Mulitnucelated giant cells may be present around migrating wood particles. Doe not appear to be a problem with mice and rats, DDX: trauma, cannibalism

·        Dental disease- malocclusion (molars are rooted, incisors missalign with trauma.)

-experimental models of periodontal disease, spontaneous is uncommon

-dental caries experimental with microbial and dietary induction



·        Behavior- Syrian hamsters are solitary creatures that don’t enjoy each other’s company except when breeding.  They are easily disturbed and agitated.  females are aggressive, especially when lactating or pregnant, prone to fight and kill others.  Cannibalism is common, especially when stressed, primiparous females.  Some neonates may survive with limb amputation.  Chinese hamsters are more pugilistic.  Hamsters are nocturnal, with high activity, several miles on a exercise wheel within 24 hrs.  Active chewers and adept escape artists. Permissive rather than obligatory hibernators . Maybe induced with low temp, short days, solitude, adequate to abundant  food stores and nest materials.  High temperature low water may stimulate estivation, animals will loose weight and increase brown fat stores, reproductive activity ceases with atrophy,  pseudohibernation-sensitive to touch