Chapter 4

Biology of the Hamster and Hamster disease


4.1 Taxonomy:

Order: Rodentia

Suborder: Myomorpha

Family: Cricetidae 

Types of Hamsters


4.3 Housing Standard for Hamsters:

Cage requirements:

Body weight(gms)

Floor area/animal( 


< 60









> 100


Cage height = six inches

Room temperature: 18-26 C (65-79 F)

Humidity: 40 to 70%

Reference: 22


4.4 Biology of Syrian Hamster (Mesocricetus auratus)

Life Span:

Body Length:

Tail Length:

Adult Weight:


Number of Mammae:

Litter Size:

Weaning Age:

Estrus Cycle:

Duration of Estrus Cycle:

Duration of Estrus:

Gestation Period:


Female Breeding Life:

Male Breeding Life:

Rectal Temperature:


Blood volume:

Heart rate:

Respiratory rate:

Daily food consumption:

Daily water consumption:



Milk composition:


Chromosome number:

Dental formula:

 2-3 years, record 4 years

170-180 mm

12 mm

90-175 gm. NOTE: often female is larger than the male.

12-16 (22 may occur)

6 or 7 (4-15)

about 3 weeks

Polyestrus; all year

4-5 days

4-23 hours

15-18 days (average 15 1/2 days)

8-10 weeks

about 1 year

1 year

97.0o to 102.3o F, average 99.3o F (36.1o to 38.9o C, average 37.4o C)

7.5% of body weight

275-425 beats/minute

33-l27/minute (average 74)

l0-14 gms

7-l0 cc

crystalluria, cream-colored, turbid, pH 8.0

almost black, tubular, firm, about 5 mm long

74% water, 12.6% fat, 9% protein, 3.4% sugar

2n = 44

I l/l, C 0/0, PM 0/0, M 3/3 = 16



Blood collection sites:

Cardiac puncture: under light anesthesia with a 3/8 inch 25-gauge needle, up to 2 ml. can be safety removed from a l00 gm. hamster.

Sever the tip of the tail

Slit the footpad

Orbital sinus


A volume of blood 4.5 to 5% of the body weight can be extracted. This is more blood on a percentage body weight basis than can be collected from any other laboratory animal.

Normal erythrocyte life span:

60-70 days

Erythrocyte size:

6-7 um in diameter

Reticulocyte numbers:

2 to 12.55% (mean of 4.9%)

Lymphocytes: appear in both small and large forms; the large form may have a few azurophilic cytoplasmic granules.

Monocyte: clear blue cytoplasm with fine reddish granules clumped in the indentation of the nucleus.


Granules are large and strongly acidophilic.

Platelet count:

250,000 to 1,000,000/ul (range of those reported)

Plasma protein concentration:

4.5 + 0.73 g/dl (lower than the mouse and rat)


Erythroid ratio: l.7:l.0 


Hematology during hibernation:

Permissive Hibernator (Temp. 5o C (+ or - 2o C) or (41o F - 44.6o F)

RBC, Hb, and PCV increased along with the blood volume.

Hematopoiesis was suppressed (as indicated by a reduction in circulating reticulocytes and failure of a reticulocyte response to massive blood withdrawal; when hibernation was terminated, the long-delayed reticulocyte response took place)

Retardation of RBC senescence and a virtual absence of random erythrocyte destruction associated with an increased potential erythrocyte life span to l60 days

Marked leukopenia. 


4.5 Biology of the Chinese Hamster (Cricetulus griseus)


Striped-back hamster

Length from muzzle to base of tail:

approximately 9 cm

Weight of young adults:

28 to 40 gms.

Weight of older animals:

up to 55 gms.

 Gestation period:

20.5 days (average)

Number of mammae:

8 (i.e. four pairs)

Litter size:

4.8 (average)

Weaning weight for males:

l5.9 to l7 gms.

Weaning weight for females:

15.l to l6.8 gms.


at least 25 days

Weaning age:

21-25 days

Age at puberty of female:

8-12 weeks

Estrus cycle:

4 days

Length of reproductive life:

approximately 1 year

Male breeding life

1 year


Black dorsal stripe (i.e. striped-back hamster)

Dorsal coat color:

ocherous to roan

Ventral coat color:

gray to white

Optimal room temperature:

72o-76o F

Light-dark cycle:

use a reversed illumination for recently weaned litters; 11 hours of da

rkness starting at 7 A.M., and by 9 A.M., the females should come into heat and mate.

Chromosome number:

2n = 22 (considered to be inbred)

NOTE: Prior to copulation there is a period of "chasing" characterized by running in circles with the female chasing the male.)


Brittle bristle is limited to females and occurs when they reach maturity; results in alopecia and dry, flaky skin.

Pinnaless: entire litters may be born without the outer ear. 

Uses in Research:

12 hamster species from China, but Cricetulus griseus is the only one widely used in research.

Possible role as a reservoir host for Leishmania donovani. Susceptible to tuberculosis, diphtheria, rabies, influenza, and equine encephalitis. Develop spontaneous hereditary diabetes mellitus. 

References: l, 5, 7.  

4.6 Biology of the European Hamster (Cricetus cricetus) 


Black-bellied hamster, common hamster.

Natural location:

Europe and parts of Russia eastward into Siberia.

Natural habitat:

steppes, plowed land, cultivated fields, and along river banks.


white faces and feet, black abdomens, and reddish-brown backs, white patches may be interposed between the dorsal and ventral markings.

Adult body length:

usually more than 200 mm. with a maximum of 280 mm.


112 to 908 gms.

Life span:

about two years

Gestation period:

l5.5 to l7 days (in captivity or laboratory) l8-21 days (in wild)

Litter size:

4 to l8 (usually 6 to 12)

Natural weaning age:

25 days

Number of mammae:

8 (i.e. four pairs)

Puberty in males:

60 days

Puberty in females:

60-80 days

Estrus cycle:

4-6 days

Rectal temperature:

36.8`C or 98.2`F

Water consumption:

5 ml./l00 gm. body weight

Food consumption:

2.9 gm./l00 gm. body weight in August 1.8 gm./100 gm. body weight in November 

References: l, l5, l9. 


4.7 Biology of the Dwarf Hamster (Phodopus sungorus) 


Djungarian or Zungarian hamster, hairy-footed hamster, small desert hamster.

Natural location:

Siberia, Manchuria, and northern China.

Natural habitat:

somewhat arid regions in stiff grass on plains and sand dunes.


Dark midline dorsal stripe

Dorsal coat color:

grayish to pinkish buff.

Ventral coat color:


Body length:

ll0 mm. (males)90 mm. (females) Weight: approx. 54gms. (males) and 30 gms. (females)

Gestation period:

l9-21 days

Average litter size:


Estrus cycle:

4 days

Weaning age:

20 days

Sexual maturity:

93-95 days 

NOTE: May breed all year, but there are fewer litters being produced in the periods of December-March and July-August. 

References: l, l9. 


4.8 References

  • l. Aeromedical Review Selected Topics in Laboratory Animal Medicine, Vol. 24 "The Hamster." USAF School of Aerospace Medicine, Brooks Air Force Base, Texas, 1975.
  • 2. Alleva, J. J., Alleva, F. R. and Lipien, M. W. "Use of vaginal concretions of calcium carbonate to detect ovulation in hamsters." Lab An Sci 26:57-62, l976.
  • 3. Arrington, L. R., Platt, J. K. and Shirley, R. L. "Protein requirements of growing hamsters." Lab An Care l6:492-496, l966.
  • 4. Arrington, L. R., Ammerman, C. B. and Franke, D. E. "Protein requirement of hamsters fed a natural diet." Lab An Sci 29:469-471, l979.
  • 5. Avery, T. L. "Observations on the propagation of Chinese hamsters." Lab An Care l8:l5l-l59, l968.
  • 6. Emminger, A., Reznik, G., Rezink-Schuller, H. and Mohr, U. "Differences in blood values depending on age in laboratory-bred European hamsters (Cricetus cricetus)." Lab Animals 9:33-42. 1975.
  • 7. Festing, M. F. W. "Hamsters" in the UFAW Handbook on the Care and Management of Laboratory Animals, Churchill Livingstone, London, l972.
  • 8. Ford, D. J. "Influence of diet pellet hardness and particle size on food utilization by mice, rats and hamsters." Lab Animals 11:241-246, l977.
  • 9. Fox, J. G., Cohen, B. J. and Loew, F. M. Laboratory Animal Medicine. Chapter 5, Academic Press Inc., N.Y., 1984.
  • 10. Frisk, C. S., Wagner, J. E. and Kusewitt, D. F. "Unusual aggressive behavior in the male golden hamster." Lab An Sci 27:682-684, 1977.
  • 11. Harkness, J. E. Wagner, J. E., Kusewitt, D. F. and Frisk, C. S. "Weight loss and impaired reproduction in the hamster attributable to an unsuitable feeding apparatus." Lab An Sci 27:ll7-ll8, l977.
  • l2. Harkness, J. E. and Wagner, J. E. The Biology and Medicine of Rabbits and Rodents, Lea & Febiger, Philadelphia, l983.
  • 13. Hoffman, R. A., Robinson, P. F. and Magalhaes, H. The Golden Hamster, Its Biology and Use in Medical Research Research, The Iowa State University Press, Ames, l968.
  • 14. Meshorer, A. "Leg lesions in hamsters caused by wood shaving." Lab An Sci 26: 827-829, l976.
  • 15. Schalm, O. W. , Jain, N. C. and Carroll, E. J. Veterinary Hematology, 3rd ed., Lea & Febiger, Philadelphia, pp.256-258, l975.
  • 16. Silverman, J. and Chavannes, J. "Biological values of the European hamster (Cricetus cricetus)." Lab An Sci 27:641-645, l977.
  • 17. Standards for the Breeding, Care and Management of Syrian Hamsters, Institute of Laboratory Animal Resources, National Research Council, Washington, D.C., l960.
  • 18. Takahashi, M., Pour, P., Althoff, J. and Donnelly, T. "The pancreas of the Syrian hamster (Mesocricetus auratus) I. Anatomical Study." Lab An Sci 27:336-342, l977.
  • l9. Walker, E. P. Mammals of the World, 3rd ed., The Johns Hopkins University Press, Baltimore, pp. 8l5-8l9, l975.
  • 20. Warner, R. G. and Ehle, F. R. "Nutritional idiosyncrasies of the golden hamster (Mesocricetus auratus)." Lab An Sci 26: 670-673, l976.
  • 21. Williams, C. S. F. Practical Guide to Laboratory Animals, The C. V. Mosby Co., St. Louis, pp. 26-34, l976.
  • 22. N. I. H. Guide for the Care and Use of Laboratory Animals. NIH Publication No. 85-23; Revised 1985.






4.10.1 BACTERIAL DISEASES Proliferative Ileitis:

Other names for this disease include "wet-tail", regional enteritis, terminal iletis, enzootic intestinal adenocarcinoma, atypical ileal hyperplasia, and hamster enteritis. It is an acute to chronic disease of unknown etiology. The disease occurs primarily in hamsters at near the weanling age (3 to 8 weeks). The morbidity rate ranges from 25 to 60% and the mortality rate can go as high as 90%. Although the etiology is unknown, several agents are suspected as having a role in the disease: one or more coliform serotypes, Campylobacter spp., E. coli, Bacillus piliformis and Proteus vulgaris.

A. Transmission:

Fecal-oral route.

B. Predisposing factors:

Include improper diet, exposure to infected animals, shipment stress, overcrowding, and lack of fresh water. Certain strains of hamsters may be more susceptible than others, i.e., long-haired fawn and teddy bear. (They are Syrian golden hamsters which have long hair and look like teddy bears.)

C. Clinical Signs:

Both acute, subacute,and chronic forms occurs. The acute disease is manifested by lethargy, anorexia, irritability, ruffled hair, diarrhea, dehydration, emaciation and death within 48 hours. The moist feces strain the base of the tail. the subacute syndrome is characterized by diarrhea, retarded growth, with death being the final result. In the chronic form, the signs range from emaciation and cacchexia to a lack of clinical signs, normal growth rates, occasional deaths and palpable abdominal masses.

D. Gross Lesions:

Chronic lesions are most obvious in the ileum and terminal jejunum. The ileal mucosa is thickened causing the gut to be enlarged. The intestine is congested, often ulcerated, and contains a yellow fluid. Intussusceptions may occur during the acute or chronic stages. Perforation of the gut wall and subsequent peritonitis may develop. Surviving hamsters may develop strictures, diverticula, multifocal hepatic abscesses, and adhesions. 

E. Histopathology:

Hyperplasia of the intestinal mucosa is the primary sign. The epithelium of the crysts contains many immature cells and mitotic figures. Migrating leukocytes are seen near the base of the villi. The villi undergo coagulation necrosis as the disease progresses and secondary bacterial invasion causes the accumulation of purulent exudate in the crypts and formation of microabsesses in the intestinal wall.

F. Treatment:

Tetracycline hydrochloride at a dose of 400 mg/L of drinking water has been reported as successful. Erythromycin at 20 mg/kg has also been successful. Supportive treatment for dehydration with Lactated Ringer's solution given subQ (5% to l5% of body weight) and Koapectate l-2 ml for diarrhea may be effective. 

G. Control:

The disease is difficult to limit in a group of infected animals. High sanitary standards, absence of stresses, and cage filter covers may reduce the severity of an outbreak. Salmonellosis

A. Etiological Agent:

Salmonella typhimurium, Salmonella enteriditis - a gram (-) toxin producing enteric bacilli.

B. Transmission:

Fecal-oral; food, water, bedding may be contaminated by infected feces from wild rodents.

C. Clinical Signs:

The disease may only be manifested as acute death. Diarrhea is usually not present but pregnant females will abort.

D. Gross Pathology:

Necrotizing foci are seen in the liver and spleen but the main lesion is a septic, partially occluding phlebothrombosis in the lungs. It is seen in hamsters, but not in other laboratory animals. This may be accompanied by a bronchopeumonia. Enteric signs do not dominate the clinical picture.

NOTE: Phleobothrombosis - Thrombosis occurring in veins in the absence of inflammation may be termed phlebothrombosis. 

E. Histopathology:

There are focal areas of interstitial pneumonia and lobular collapse. The most significant lesion involves the veins and venules in which are seen septic, partially occluding thrombi that adhere to the walls with underlying necrosis and erosion.

F. Diagnosis:

Is based on necropsy signs, culture of organism on various selective media and serotyping.

G. Treatment:

No specific treatment because antibiotics do not successfully eliminate the carrier state. In a colony situation, elimination of the colony is suggested.

H. Control:

Aggressive sanitation procedures should be aimed at preventing contamination of food, bedding or water by wild vermin. Also proper sanitation of cages and water equipment is required.

I. Public Health Significance:

Humans ingesting Salmonella typhimurium contaminated food or water experience a transient diarrhea. Tyzzer's Disease (Similar to disease in rats and mice):

A. Etiological Agent:

Bacillus piliformis - a gram (-) obligate intracellular rod. Forms spores and is motile by peritrichous flagella.

B. Transmission:

Most likely fecal-oral ingestion of the spores. Predisposing factors to disease include age (commonly 3 to 7 weeks of age) and physiological stresses such as concurrent disease, experimental manipulations, poor housing conditions, or corticostroid administration.

C. Clinical Signs:

Death may be the only indication of infection. Other possible signs may include anorexia, hunched posture, rough hair coat, diarrhea, dehydration, emaciation.

D. Gross Pathology:

The classical lesions of this disease are focal hepatic necrosis and serosal hemorrhage and edema in the ileocecocolic region of the gut. In addition to these, other lesions reported have included: multiple white masses on the surface of the heart and colon, the latter of which was dilated with a yellow foamy material and had a reddened mucosa.

E. Histopathology:

Foci of hepatic necrosis surrounded by inflammatory cells. Myocardial lesions consist of foci of necrosis surrounded by inflammatory cells. Colonic lesions consist of focal necrosis of epithelial cells.

F. Diagnosis:

Diagnosis is made by demonstration of the bacillus in the hepatocytes bordering necrotic liver foci with Giemsa, PAS, or silver stains or by impression smear of the liver stained with new methylene blue (nests of organisms). The organisms can also be found in similarly stained myocardial fibers and intestinal epithelial cells.

G Treatment:

Oxtetracyline at 0.l mg/ml water for 30 days has been reported to abate an epizootic.

H. Control:

Avoidance of stress, elimination of sick animals, and strict sanitation may help prevent outbreaks. Tularemia:

Causative agent is Franciscella tularensis. It is a G (-), pleomorphic, nonmotile, nonsporeforming coccobacillus. This is a rare disease in hamsters although animals raised in areas with tick infestations are more likely to contract this disease. Clinical signs include anorexia, depression, ataxia and death. Necropsy findings include pulmonic congestion and consolidation, foci of hepatic necrosis, and splenic congestion. Diagnosis is made on recovery of the organism. Tetracycline is effective in treatment. Humans are very susceptible and appropriate precaution should be taken to avoid contamination of skin lesions; i.e., it is a zoonotic disease. Pasteurella:

It is rare to see overt disease caused by Pasteurella pneumotropica. Infections are usually latent and clinical signs do no manifest themselves unless the animal is stressed or another disease process becomes prominent. Clinical signs can include chattering, loud respiration, weight loss, cutaneous abscesses, conjunctivitis, and mastitis. Pulmonary lesions are the primary finding on necropsy. Suppurative reactions may also be seen in the tympanic bullae, orbital glands, uterus, skin, mammary gland, cervical lymph nodes, and the urinary system. Diagnosis is made through recovery of the organism by culture. Antibiotics used in treatment are chloromycetin and ampicillin. Streptococcus:

Diseases in this category are caused by beta hemolytic Streptococci (Lancefield Group C, species S. zooepidemicus). The main clinical syndrome is subcutaneous abscesses with occasional pneumonic involvement. Diagnosis is made by recovering the organism from the affected tissue. Treatment is initiated based on antibiotic susceptibility of the organism. Pseudomonas aeruginosa

Pseudomonas spp. usually cause inapparent infections in the gastrointestinal tract or may cause subcutaneous abscesses. Diagnosis is made via recovery of the organism. Treatments with the appropriate antibiotic.

Pseudomonas becomes pathogenic in immunosuppressed or x-irradiation treated hamsters. Hard to elimate. Acidify water to pH 2.5, chlorinate to l0 p.p.m., or both.


4.10.2 PARASITIC DISEASES Protozoa Spironucleus muris (Hexamita)

A. Etiological Agent:

Spironucleus muris is a flagellated protozoan that dwells on the mucosal surface of the small intestine.

B. Transmission:

Ingestion of infective cysts is the primary mode of transmission. A carrier stage occurs in adults. It is transmissible to rats and mice.

C. Clinical Signs:

Weanling animals appear to be the most susceptible and develop the more acute form. The animals are usually smaller in size, depressed, and have abdominal distention. Diarrhea is evidenced by a sticky fecal mass in the perianal area. Dehydration and anorexia follow with a moderate mortality rate (0-25%). Adults display a more chronic form whose signs include weight loss and listlessness; diarrhea is uncommon.

D. Gross Pathology:

The small intestines (the anterior portion) are often dilated and filled with gassy catarrhal fluid contents. The mucosa may be reddened but autolysis rapidly ensues.

E. Diagnosis:

Direct smears of the contents reveal fast darting protozoa. Histological examination of the small intestine will reveal the protozoa in the crypts and along surface of the villous epithelium.

F. Treatment:

Dimetridazole (l% solution or l gm/L drinking water) has been reported to reduce mortality. Tritrichomonas muris & Giardia muris

A. Transmission:

The main route of infection is ingestion of the organism which is passed in feces of the infected animal.

B. Clinical Signs:

No clinical signs have been attributed directly to these organisms. Diarrhea is often associated with both organisms; however, it is believed that the diarrheal state merely provides them with the optimum growth environment.

C. Gross Pathology:

No specific pathology. Tritrichomonas is most commonly found in the lower small intestine and cecum while Giardia is found primarily in the jejunum.

D. Treatment:

No specific treatment and, in colony situations, none is attempted.

E. Control:

Colonies maintained behind a barrier and derived via Cesarian section are usually Giardia and Tritrichomonas free. Tapeworms:

A. Etiological agent:

Hymenolepis nana (dwarf tapeworm) and Hymenolepis diminuta (rat tapeworm).

B. Transmission:

Hymenolepis nana and Hymenolepis diminuta can be transmitted by an indirect mode with cockroaches, beetles, or fleas as intermediate hosts. Hymenolepis nana can be transmitted by direct ingestion of hexacanth ova or by autoinfection in which the entire life cycle occurs in the small intestine without ingestion of ova (complete life cycle is l4-l6 days).

C. Clinical Signs:

Usually there are no external signs of infection. However, catarrhal enteritis, diarrhea, emaciation, and chronic weight loss may occur with heavy infestations.

D. Gross Pathology:

Hymenolepis nana adults range from 25-40 mm long and less than l mm wide and have an armed rostellum. Hymenolepis diminuta adults range from 20-60 mm in length and 3-4 mm wide with no hooks on the scolex. Often the tapeworms migrate up the pancreatic and biliary ducts.

E. Diagnosis:

Fecal flotation and examination for hexacanth ova, direct examination of intestines, histopathological examination.

F. Treatment:

Niclosamide at l0 mg/l00 gm body weight given in two treatments at 7 day intervals or 0.33% active niclosamide in the feed for 7 days.

G. Control:

Cockroaches should be eliminated and infected animals treated.

H. Public Health Significance:

Humans are susceptible to Hymenolepis nana infections and, since autoinfection can occur, a heavy parasite load may quickly develop. Pinworms:

A. Etiological Agent:

Syphacia mesocriceti, Syphacia obvelata.

B. Transmission:

Syphacia deposit their eggs in the perianal region. Transmission of infection occurs via ova ingestion. The eggs are very light and have been shown to aerosolize, resulting in widespread exposure. Syphacia muris may occur in colonies maintained in the same rooms as rats.

C. Clinical Signs:

No signs are usually seen. It has been reported that heavy parasite loads may lead to rectal prolapse or perianal irritation.

D. Gross Pathology:

Pinworms are easily recognized as white hairlike nematodes in the cecum.

E. Diagnosis:

Direct exam of cecal contents, fecal flotation and perianal tape test will identify adults and eggs, respectively.

F. Treatment:

If treatment is desired, piperazine (4-7mg/ml water) for 3-l0 days is effective.

G. Control:

Many times Syphacia infection is merely a transient problem and persists only if infected mice or rat colonies are nearby. If this is not the case, prevention and control of infection are often difficult. Rigid sanitary procedures, use of filter hoods to prevent aerosol transmission and regular ova examinations with treatment may control the parasitism. Syphacia obvelata can infect man so excreta from an infected colony should be handled with caution. Mange:

A. Etiological Agent:

Demodex criceti and Demodex aurati

B. Transmission:

Generally thought to be direct contact. Several reports state that the mite is much more common than the finding of clinical mange would indicate. Several predisposing factors are necessary for the development of clinical signs: malnutrition, intercurrent systemic disease, and age.

C. Clinical Signs:

Clinical signs can range from none to alopecia, dry, scaly, scabby dermatitis and rough hair coat.

D. Gross Pathology:

The mites are generally found together. Demodex criceti is generally considered non-pathogenic, has a shorter body length and is found in the epidermis. Demodex aurati is the more pathogenic, is longer than Demodex criceti, and is found in the pilosebaceous component of the skin.

E. Diagnosis:

Skin scrapings.

F. Treatment:

l-5.5% Ronnel and propylene glycol daily for 5 weeks. Goodwinol ointment.

G. Control:

Relatively uncommon; adequate nutrition and good husbandry. Ear Mange Mite:

A. Etiological Agent:

Notoedres spp.

B. Transmission:

Presumably by direct contact.

C. Clinical Signs:

In females, only the ears are affected, but in the males lesions can occur on the ear, nose, genitalia, tail, and feet. Lesions appear as papilloma-like horny excrescences and yellowish crusts.

D. Gross Pathology:

Scaly dermatitis especially of the ears.

E. Diagnosis:

Skin scraping.

F. Treatment:

Topical application of a 25% solution of tetraethylthiuram monosulfide (TetmosolR) every 2 to 3 days for 4 treatments or dipping in a 0.5% solution of lindane once or twice within a 6-7 day interval. 

4.10.3VIRAL DISEASES Lymphocytic Choriomeningitis (LCMV):

RNA virus belongs to the genus Arenavirus and the family Arenaviridae.

A Transmission:

In utero or perinatal infections (within l day post partum) produce a subclinical persistent infection. The virus is continually shed in urine and saliva but no antibody titer is produced. This is called a persistent tolerant infection (PTI). If infected any other time, antibody production occurs. The natural reservoir for LCMV is the wild rodent population. Transmission occurs via urine and saliva, via traumatized skin, the conjunctiva, or respiratory passages. Arthropod vectors and dust may be vehicles for transmission. In research involving hamsters, a common route is the transplatantion of LCMV-contaminated tumors.

B. Clinical Signs:

Usually there are no clinical signs other than a wasting syndrome and death. Rare signs may include meningitis, convulsions, decreased growth, and reluctance to move.

C. Gross Pathology:

Gross lesions vary widely. Some of the lesions seen are splenomeglay, fatty liver, pleural exudates, splenic necrosis, hepatic necrosis, and necrosis of lymph nodes.

D. Histopathology:

Microscopic lesions include lymphocytic infiltration of the meninges, focal necrosis with mononuclear cell infiltrate in many organs and lymphosarcomatous accumulations of reticular cells and lymphocytes in the liver and mesenteric lymph nodes.

E. Diagnosis:

Diagnosis is based partly upon the lymphocytic infiltration of the meninges, choroid plexus, and in submeningeal and subchoroid perivascular spaces. Complement fixation tests may reveal serum antibodies if present. Infected neural tissue can be injected into suckling mouse footpads (get swelling in 5-9 days) or cerebrum (neurological signs).

F. Treatment: None.

G. Control:

Eliminate colony since vertical transmission is possible. Control of wild rodent population.

H. Public Health Significance:

Humans are susceptible to LCM virus. Reports have linked human infections primarily to exposure to infected hamsters. Parvovirus Infection:

DNA VIRUS; Genus-Parvovirus, Family-Parvovridae.

A. Etiological Agents:

Toolan's H-l Virus, Kilham Rat Virus, Minute Virus of Mice.

B. Transmission:

Can be transmitted across the placenta, by ingestion and by droplet. The virus is present in feces, urine, and saliva. The virus may lay latent for long periods of time and is probably activated by the presence of rapidly proliferating tissues and appropriate helper virus. Adult animals are not as susceptible as neonates. All reported infections have been associated with tumor transplantation or experimental inoculation. No natural disease in hamsters has been reported.

C. Clinical Signs:

In neonatal animals, signs include flattened faces, improperly formed incisors or no incisors, protruding tongues, a type of Down's syndrome appearance, fragile bones, cerebellar hypoplasia, and hepatitis

D. Diagnosis:

Diagnosis is based on clinical signs and the presence of titers as determined by complement fixation or hemagglutination inhibition.




Eliminate the colony, and repopulate with freshly purchased stock. Always test tumors prior to transplantation. Other viral Diseases:

Hamsters are generally susceptible to these diseases from being in close proximity to colonies of other species of animals, especially mice and rats. Sendai Virus:


Occurs as an acute epizootIc. Clinical signs include dyspnea, chattering, and variable death. Pathological signs are the same as seen in mice, i.e., interstitial pneumonitis, peribronchiolar infiltrates, filling of bronchioles, and accumulation of macrophages and giant cells. If animals survive the acute phase, there is complete resolution within a month. Mouse Hepatitis Virus:


Mortality is most severe in suckling animals. Clinical signs include jaundice, spasticity. incoordination, and tremors. Pathological lesions are hepatic necrosis, splenomegaly, distended intestinal tract and obstipation with dry feces. There is no treatment. Control is achieved by eliminating the colony.


Old age diseases are more common in hamsters 3 years old or older. Osteoarthritis:

Rather than a primary inflammation, osteoarthitis is essentially a degenerative condition of joint cartilage with reactive and hypertrophic changes in underlying bone.This disease is seen only in aged animals. It is mainly characterized by deformity about the knee. There is sclerosis and dislocation of the bone with fibrillation of the ligaments and fibrosis of the synovial membrane. End Stage Kidneys:

Generally this is thought to be synonymous with amyloidosis, a condition which occurs with great frequency in hamsters (88%). The condition is often found concurrent with a polycystic disease. Pathological signs include glomerular hyalinization, amyloid deposits in the tubules, and amyloid deposits in various other organs such as spleen, liver, and adrenals.


Amyloid is a hyaline material characterized by deposition intercellulary rather than in cells, and by specific staining reactions with iodine, methyl violet, congo red, silver and thioflavine-T. Amyloid stains orange red (light microscopy) and shows a green birefringence (polarization microscopy) when stained with congo red. It stains purple red with methyl or crystal violet (metachromatic stain), mahogany brown with iodine and dark brown to black with silver stain. Thioflavine-T causes yellow fluorescence of amyloid in ultraviolet light. The exact chemical composition of amyloid is unknown. Hepatic Cirrhosis:

The disease is seen in older hamsters and is more common in females. The cause is unknown, but toxic factors in the diet are a possibility. Grossly, there is fairly uniform nodularity of all liver lobes. Microscopically, there is periportal proliferation of hyalinized connective tissue with bile duct proliferation. Also, there is nodular hepatocellular regeneration with concurrent degeneration and necrosis. Lymphomas due to a Mammalian Viroid:

This syndrome is caused by a horizontally transmitted mammalian viroid (a non-encapsidated, DNAse sensitive, low M.W., disease causing, self replicating, naturally infectious nucleic acid). Disease is characterized by the appearance of lymphomas in 50-90% of exposed young hamsters.


Direct animal to animal contact, aerosol or ingestion of dried cage litter containing contaminated urine and feces.

Clinical Signs:

Emaciation, weakness, lethargy, diarrhea, rectal and abdominal bleeding and subcutaneous masses.

Most lymphomas are B-cell type, but some are T- cell type. Most arise in large and small bowel and mesenteric nodes. Most are composed of immature lymphoid cells with rare to frequent mitiotic figures.


(l)Am J. Pathol ll0: 254-266, l983.

(2)Nature 290: 336-338, l98l. Atrial thrombosis:

Etiology and pathogenesis are related to myocardial degeneration causing cardiac failure.


Amer. J.Path. l07 (2):227-229 (l982). Diabetes Mellitus:

A spontaneous hereditary disease in hamsters (especially Chinese) not associated with obesity. There is great variety

in the severity of the disease. Early in the disease, pancreatic beta cells are still abundant but are either agranular or in various stages of glycogen storage. Laterin the disease, the beta cells have pyknotic nuclei and cytoplasm is shrunken. This process continues until the islet cells disappear. Neoplasms:

The incidence of naturally occurring tumors is high in the golden hamster and the numbers increase with the age of the animals. The incidence is generally higher in females due to the greater number of reproductive tract neoplasms. By far, endocrine related tumors are the most common. Some of the more common benign tumors are intestinal polyps, adrenal cortical adenomas, thyroid adenomas, fore stomach papilloma, and splenic hemangioma. The most common malignant tumors are lymphomas and leukemias, adenocarcinoma of the intestinal tract, and melanomas. Multiple primary tumors are common. Uterine carcinomas are seen in 25% of female neoplasm cases. Also in females, leiomyomas and leiomyosarcomas can be caused by long term androgen/estrogen administration.

4.10.5 MISCELLANEOUS DISEASES Nutritional Deficiencies:

Hamsters are subject to a number of vitamin and mineral deficiencies if not fed an adequate ration. Some examples are:

Deficiency Signs

l. Vitamin D Paresis, inactivity, crawls


2. Vitamin E Muscular Dystrophy


3. Vitamin B Complex Alopecia, poor growth, rough hair coat, death


4. Phosphorus Along with Vitamin D produces rickets


5. Fat Free Diet-Low in Gall stones Cholesterol


6. High Protein diet Chronic nephritis (feed (l8-24%)low protein 6-l2% diet to revent occurrence)

All of these can be corrected by adding the missing component to the diet and ensuring the animal continues on an adequate nutritional plane. Rough Handling

Rough handling by owners can induce gastric ulcers within 24 hours of the stressful event. Fight Wounds:

Fight wounds in hamsters are not an uncommon finding. Animals will attack each other, often for no apparent cause. Many times this will occur when food and water are in short supply. Also, females will attack males during mating. Thirdly, males will fight briefly as a means of establishing social dominance when first placed in new environments. If two adult males are housed together for the first time, they may even castrate one another. Cannibalism:

Cannibalism of litters by mothers is also common if she is disturbed after parturition. Recommendations to owners to avoid this should include placing litter in the cage for nest building 2 days prior to parturition and do not disturb the cage for 9-l0 days after parturition, except to give feed and fresh water as needed. Do not change or move the cage. Drug Susceptibilities:

Hamsters are susceptible to a number of the common antibiotics. Some examples are: dihydrostreptomycin (0.25 ml), lincocin (l0 mg/kg), erythrocin (30 mg/kg), and penicillin (l00,000 units). Vancomycin and clindamycin are also toxic. These antibiotics if fed to hamsters may result in overgrowth of gram negative enteric bacteria with subsequent development of enterocolitis, endotoxemia and/or septicemia. Can be fatal to majority of treated animals within a few days after treatment. Pregnancy Toxemia:

It occurs in hamsters, but it does not resemble ketosis ofguinea pigs and ewe. It is similar to eclampsia* of pregnant women. Resembles a generalized schwartzman relation with fibrin thrombosis of capillaries including glomeruli leading to renal cortical necrosis and/or ischemic tubular lesions. Morbidity and mortality unknown---probably highly fatal.


Hyperadrenalism involving mineral cortico-steroids and glucocorticosteroids appears to produce some features of accompanying pregnancy, but enzymes of the placenta normally suppress or inactivate certain of the effects of the adrenal hormones. Ischemic placental lesions may interfere with this mechanism and result in preeclampsia or eclampsia with convulsions.


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