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A Study of Hamster Diseases from the Dept. of Comp
Diseases of Hamsters
PAT 707, Pathology of Laboratory Animals II
Prepared by Trenton R. Schoeb
Department of Comparative Medicine
University of Alabama at Birmingham
Winter Quarter 1989-90 Foreword
There are two species of hamsters used as laboratory animals, the Syrian or
golden hamster (Mesocricetus auratus) and the Chinese or gray hamster (Cricetulus
griseus). Golden hamsters are slightly larger, have 22 pairs of chromosomes, and are
usually golden-brown although they can have various other coat colors including
albino. Gray hamsters have gray backs with a black longitudinal stripe, and have 11
pairs of chromosomes. Inasmuch as there is little published information specifically
concerning Chinese hamsters, most of the material presented here applies only to
Syrian hamsters.
Hamsters are not amenable to cesarean derivation. Therefore, in contrast to
contemporary rat and mouse production colonies, hamster colonies are best
considered conventional in quality. Routine health assessments seldom are done, so
there is not much information available on incidence and prevalence of various
conditions among young animals. In one survey (Renshaw et al., 1975), diarrhea,
neoplasms, pneumonia, amyloidosis, polycystic disease, and pregnancy toxemia were
the most common diagnoses. The situation is a little better with respect to aged
hamsters, especially neoplasms in such animals. In one 30-month study (Schmidt et
al., 1983), many animals died at 15 months of age and after of amyloidosis of the
kidneys, liver, and adrenals.
General References
Benirschke K, Garner FM, Jones TC (eds). Pathology of Laboratory Animals. Springer-
Verlag, New York, 1978.
Benjamin SA, Brooks AL. 1977. Spontaneous lesions in Chinese hamsters. Vet Pathol
14:449-462.
McMartin DN. 1979. Morphologic lesions in aging Syrian hamsters. J Gerontol 34:502-
511.
Pour P et al. 1980. Spontaneous tumors and common diseases in three types of
hamsters. JNCI 63:797-811.
Renshaw HW et al. 1975. A survey of naturally occurring diseases of the Syrian
hamster. Lab Anim 9:179-191.
Schmidt RE et al. Pathology of Aging Syrian Hamsters. CRC Press; Boca Raton, FL;
1983.
Seamer J, Chesterman FC. 1967. A survey of disease in laboratory animals. Lab Anim
1:117-139.
Ward BC, Moore W. 1969. Spontaneous lesions in a colony of Chinese hamsters. Lab
Anim Care 19:516-521.
Lymphocytic Choriomeningitis
1. Agent:
An Arenavirus (Arenaviridae). (The name comes from "arena," referring to
"sand," from the electron microscopic appearance of the virions. Related agents
include Lassa, Machupo, and Junin hemorrhagic fever viruses.)
2. Epizootiology:
LCMV is important as a public health hazard. LCM in persons usually is not a
severe disease, but it can be serious. All infected hamsters shed lots of virus in the
urine, and it is readily transmitted. In rodents it is transmitted transplacentally.
3. Pathogenesis & pathology:
The manifestations of LCM infection are dependent on genetically determined
factors of both host and virus. Genovesi and Peters (1987) report that PD4 and NHA
inbred hamsters were highly susceptible, but CB and LSH hamsters were resistant.
Other strains were intermediate in susceptibility. The WE strain of virus was the
most virulent, whereas the Armstrong strain was not virulent for hamsters of any
strain, although the two virus strains were equally immunogenic.
In experimental infections, most neonates and about half of young adults develop
persistent viremia leading to immune complex glomerulopathy and vasculitis
(panarteritis), with lymphocytic inflammatory lesions in the liver, kidney, lung,
pancreas, spleen, meninges, and brain. The other half of young adults and nearly all
adults eventually clear the infection. (LCM is a classic example of immune-mediated
viral disease; immunosuppression decreases severity of lesions.)
4. Diagnosis & control:
Detectable by commercially available serologic tests.
5. References:
Armstrong D et al. 1969. Meningitis due to lymphocytic choriomeningitis virus endemic
in a hamster colony. J Am Med Assoc 209:265-266.
Baum SG et al. 1966. Epidemic nonmeningitic lymphocytic choriomeningitis virus
infection. New Engl J Med 274:934-936.
Biggar RJ et al. 1976. Implications, monitoring, and control of accidental transmission
of lymphocytic choriomeningitis within hamster tumor cell lines. Cancer Res 36:537-
553.
Biggar RJ et al. 1977. Lymphocytic choriomeningitis in laboratory personnel exposed
to hamsters inadvertently infected with LCM virus. J Am Vet Med Assoc 171:829-833.
Bowen GS et al. 1975. Laboratory studies of a lymphocytic choriomeningitis virus
outbreak in man and laboratory animals. Am J Epidemiol 102:233-240.
Genovesi EV, Peters CJ. 1987. Susceptibility of inbred Syrian golden hamsters
(Mesocricetus auratus) to lethal disease by lymphocytic choriomeningitis virus. Proc
Soc Exp Biol Med 185:250-261.
Gregg MB. 1975. Recent outbreaks of lymphocytic choriomeningitis in the United
States of America. Bull World Health Organization 52:549-553.
Hirsch MS et al. 1974. Lymphocytic choriomeningitis virus infection traced to a pet
hamster. New Engl J Med 291:610-612.
Hotchin J et al. 1974. Lymphocytic choriomeningitis in a hamster colony causes
infection in hospital personnel. Science 185:1173-1174.
Lewis AM Jr et al. 1965. Lymphocytic choriomeningitis virus in hamster tumors spread
to hamsters and humans. Science 150:363-364.
Parker JC et al. 1976. Lymphocytic choriomeningitis infection in fetal, newborn, and
young adult Syrian hamsters. Infect Immun 13:967-981.
Transmissible Lymphoma
1. Cause:
A unique mammalian viroid has been proposed as the cause by Coggin et al.;
however, recent evidence indicates that the actual cause may be a papovavirus.
2. Epizootiology:
More than half of the hamsters 1 to 21 days old exposed in Coggin's facilities
developed lymphoma. (Between 1975 and 1979, there were 3,749 individual cases.)
Coggin et al. have described several epizootics among their hamsters, and epizootics
also have occurred elsewhere. Transmission is by direct animal to animal contact,
aerosol or ingestion of dried cage litter containing urine and feces. In Coggin's
colony, it was common for more than 25% of newly introduced hamsters to die of
diarrheal disease within 5 weeks after exposure to hamsters carrying the lymphoma
agent.
Coggin's hamsters also had enzootic papovavirus infection.
3. Clinical:
Emaciation, weakness, lethargy, diarrhea, rectal and abdominal bleeding, and
subcutaneous masses. Papillomas also occur in infected colonies.
4. Pathology:
Most lymphomas arise in the large and small intestine and mesenteric nodes.
Other affected organs, in approximate descending order of frequency, include liver,
kidney, thymus, cervical lymph nodes, perirenal lymph nodes, stomach, eye, and
inguinal lymph nodes. Most lymphomas are of B-cell origin, although some are T-cell,
and most are composed of immature lymphoid cells, with rare to frequent mitotic
figures. Some tumors are more pleomorphic, and some were classified as
plasmacytomas.
The cause of the diarrhea is not apparent from published descriptions; intestinal
lesions are characterized as "nonbacterial." In young animals there is watery
intestinal content with intussusceptions in a few hamsters; in adults hemorrhagic
enteritis is common and many affected hamsters have intussusceptions.
Papillomas are histologically typical.
5. Diagnosis & control:
Demonstration of the causative agent is difficult; lymphoma cells are not
permissive for papovavirus replication and no virions are produced. Viral DNA is
present in these cells, but in very small amounts, and it is difficult or impossible to
detect. The papillomas, however, do contain demonstrable virus. The agent is very
resistant and easily transmissible, making control difficult.
6. References:
Ambrose KR, Coggin JH Jr. 1975. An epizootic in hamsters of lymphomas of
undetermined origin and mode of transmission. J Natl Cancer Inst 54:877-880.
Barthold SW et al. 1987. Further evidence for a papovavirus as the probable etiology
of transmissible lymphoma of Syrian hamsters. Lab Anim Sci 37:283-288.
Coggin JH Jr et al. 1978. Horizontally transmitted lymphomas of Syrian hamsters. Fed
Proc 37:2086-2088.
Coggin JH et al. 1981. Unusual filterable oncogenic agent isolated from horizontally
transmitted Syrian hamster lymphomas. Nature 290:336-338.
Coggin JH Jr et al. 1983. B-cell and T-cell lymphomas and other associated diseases
induced by an infectious DNA viroid-like agent in hamsters (Mesocricetus auratus).
Am J Pathol 110:254-266.
Coggin JH Jr et al. 1985. Papovavirus in epitheliomas appearing on lymphoma-bearing
hamsters: lack of association with horizontally transmitted lymphomas of Syrian
hamsters. J Natl Cancer Inst 75:91-97.
Graffi A et al. 1968. Cell-free transmissible leukosis in Syrian hamsters, probably of
viral etiology. Brit J Cancer 22:577-581.
Graffi A et al. 1968. Virus-associated skin tumors of Syrian hamsters: preliminary
note. J Natl Cancer Inst 40:867-873.
Graffi A et al. 1969. Induction of transmissible lymphomas in Syrian hamsters by
application of DNA from viral hamster papovavirus-induced tumors and by cell-free
filtrates from human tumors. Proc Natl Acad Sci USA 64:1172-1180.
Graffi A et al. 1969. Studies on the hamster papilloma and the hamster virus
lymphoma. Comp Leukemia Res Bibl Hematol 36:293-303.
Manci EA et al. 1984. Lymphoma-associated ulcerative bowel disease in the hamster
(Mesocricetus auratus) induced by an unusual agent. Am J Pathol 116:1-8.
Scherneck S et al. 1979. Studies on the DNA of an oncogenic papovavirus of the
Syrian hamster. Virology 96:100-107.
Vasa-Thomas KA et al. 1977. Characterization of immune responses to spontaneous
hamster lymphomas. J Natl Cancer Inst 58:1287-1293.
Miscellaneous Viruses
1. Hamster leukemia virus: A retrovirus.
2. Cytomegalovirus: A herpesvirus, infects salivary glands, no disease known.
Smith MG. 1959. The salivary gland viruses of man and animals (cytomegalic inclusion
disease). Prog Med Virol 2:171-202.
3. Viruses detected serologically, but significance of findings unknown: Sendai
virus, pneumonia virus of mice, SV-5, reovirus type 3, Theiler's GD-VII virus,
Toolan's H-1 virus, and Kilham's rat virus.
Profeta ML et al. 1969. Enzootic Sendai virus infection in laboratory hamsters. Am J
Epidemiol 89:316-324.
Reed JM et al. 1974. Antibody levels to murine viruses in Syrian hamsters. Lab Anim
Sci 24:33-37.
Soret MG, Buthala DA. 1967. Enzootic Sendai virus infection in hamsters. Bacteriol
Proc __:163-164.
Proliferative Ileitis
("Wet-Tail," "Hamster Enteritis," Etc.)
1. Cause:
Not established. It is evident that PI is infectious, because PI is transmissible
via ileal homogenates from affected hamsters, and immune serum from affected
hamsters reacts in immunofluorescence procedures with particulate antigen in
epithelial cells of affected ilea. Further, bacteria morphologically resembling
Campylobacter are identifiable in affected epithelial cells with the Warthin-Starry
stain and by EM, the incidence can be reduced by antibiotic treatment, and the agent
can be retained by a 0.22 ?m filter. The identity of the probably causative
intracellular bacteria is uncertain. Campylobacter jejuni has been isolated from
affected hamsters, but probably does not cause PI, because pure cultures of the
organism do not reproduce the disease, and the disease can be transmitted with
intestinal homogenates that probably are free of C. jejuni. The intracellular bacteria
are reported to react with antisera against Campylobacter spp.; however, results of
studies with monoclonal antibodies indicate that although the organism shares
antigens with bacteria of known Campylobacter species, it does not react with
monoclonal antibodies specific for several known Campylobacter species, including
C. jejuni.
The cecal mucosal hyperplasia reported by Barthold et al. (1978) may be a
different condition. Immune serum from hamsters with PI did not react in FA tests
with cecal epithelium, there were no bacteria in epithelial cells by EM, and tissue
homogenates did not transmit the disease.
There is some evidence that some acute cases of "wet-tail" without ileal
hyperplasia may be caused by invasive E. coli.
Two viruses isolated from affected tissues were lethal (but without specific
lesions) in sucklings: their role, if any, in PI is unknown.
2. Epizootiology:
One of the most common diseases of hamsters, but prevalence unknown. Most
common in weanlings and young adults. Morbidity may be 100% and mortality may be
up to 80%. Infection if not disease should be considered present in most if not all
colonies. Transmission unknown, probably via feces.
3. Clinical signs and pathology:
In natural cases, diarrhea (fecal matting of the perineal fur), dehydration,
stunting.
Normal hamsters orally inoculated with homogenates or supernatants of
homogenates of ilea from affected hamsters developed a spectrum of disease separable
into three syndromes, any or all of which can occur in natural outbreaks. The acute
syndrome occurred 7 to 10 days after inoculation and was characterized by acute
enteritis with profuse, often hemorrhagic, diarrhea. Deaths occurred 24 to 36 hours
after onset. The small intestines were dilated with yellow liquid, blood, or both, and
intussusceptions were common. Microscopically, there was mild catarrhal enteritis
to severe hemorrhagic necrosis of mucosa, but no hyperplasia. Subacutely affected
hamsters (21-30 days after inoculation) were stunted and dehydrated, and had
diarrhea and palpable "rope-like" abdominal masses. Deaths occurred 2 to 7 days
after the onset of diarrhea. The ileum or entire small intestine was thickened and the
mesenteric nodes were enlarged. There were various degrees of mucosal hyperplasia
in the small intestine, sometimes with necrosis and hemorrhage. Hyperplastic mucosal
epithelium penetrated into the tunica muscularis, and there was severe
pyogranulomatous inflammation of ileal wall and serosa. Mesenteric lymph nodes were
hyperplastic and had foci of granulomatous inflammation, and there was
nonsuppurative portal hepatitis. In the chronic syndrome, 1 to 4 months after
inoculation, affected animals had few outward signs of illness, but had palpable ileal
lesions and some died suddenly. These had enlarged ilea with associated peritoneal
adhesions. There was fibrosis and stricture of the ileocecal junction resulting in
severe dilatation of ileum and death in some. Microscopically, there was
pyogranulomatous inflammation and fibrosis. Numerous slightly curved, 0.3 x 1.5 ?m,
rod-shaped bacteria were in the apical cytoplasm of crypt epithelial cells beginning
on the 5th day after inoculation.
4. Diagnosis & control:
Diagnose by signs & lesions. Control measures unknown--no known way to
identify non-infected hamsters.
5. References:
Amend NK et al. 1976. Transmission of enteritis in the Syrian hamster. Lab Anim Sci
26:566-572.
Barthold SW et al. 1978. An outbreak of cecal mucosal hyperplasia in hamsters. Lab
Anim Sci 28:723-727.
Bartlett JG et al. 1978. Antibiotic induced lethal enterocolitis in hamsters. Am J Vet
Res 39:1525-1530.
Boothe AD, Cheville NF. 1967. The pathology of proliferative ileitis of the golden
Syrian hamster. Pathol Vet 4:31-44.
Davis AJ, Jenkins SJ. 1986. Cryptosporidiosis and proliferative ileitis in a hamster.
Vet Pathol 23:632-633.
Frisk CS et al. 1978. Enteropathogenicity of Escherichia coli isolated from hamsters
(Mesocricetus auratus) with hamster enteritis. Infect Immun 20:319-320.
Frisk CS et al. 1980. Hamster (Mesocricetus auratus) enteritis caused by epithelial
cell-invasive Escherichia coli. Infect Immun 31:1232-1238.
Frisk CS, Wagner, JE. 1977. Experimental hamster enteritis: an electron microscopic
study. Am J Vet Res 38:1861-1868.
Frisk CS, Wagner JE. 1977. Hamster enteritis: A review. Lab Anim 11:79-85.
Goldman PM et al. 1972. A preliminary evaluation of Clostridium sp. in the etiology of
hamster enteritis. Lab Anim Sci 22:721-724.
Jackson ST, Wagner JE. 1970. Proliferative ileitis in Syrian hamsters (Mesocricetus
auratus). Lab Anim Digest 6:12-15.
Jacoby RO, et al. 1975. Experimental transmission of atypical ileal hyperplasia of
hamsters. Lab Anim Sci 25:465-473.
Jacoby RO. 1978. Transmissible ileal hyperplasia. I. Histogenesis and
immunocytochemistry. Am J Pathol 91:433-450.
Jelinek F, Aldova E. 1986. Campylobacteriosis in golden hamsters (Mesocricetus
auratus). Z Versuchstierkd 28:167-171.
Johnson EA, Jacoby RO. 1978. Transmissible ileal hyperplasia. II. Ultrastructure. Am
J Pathol 91:451-468.
Jonas AM et al. 1965. Enzootic intestinal adenocarcinoma in hamsters. J Am Vet Med
Assoc 147:1102-1108.
Kim JCS, Jourden M. 1977. Ultrastructure of proliferative ileitis in hamsters
(Mesocricetus auratus). Lab Anim 11:171-174.
LaRegina M, Lonigro J. 1982. Isolation of Campylobacter fetus subspecies jejuni from
hamsters with proliferative ileitis. Lab Anim Sci 32:660-662.
LaRegina M et al. 1980. Effects of antibiotic treatment on the occurrence of
experimentally induced proliferative ileitis of hamsters. Lab Anim Sci 30:38-41.
Lawson GH et al. 1985. Demonstration of a new intracellular antigen in porcine
intestinal adenomatosis and hamster proliferative ileitis. Vet Microbiol 10:303-313.
Lentsch RH, et al. 1982. Campylobacter fetus subspecies jejuni isolated from Syrian
hamsters with proliferative ileitis. Lab Anim Sci 32:511-514.
McNeil PE et al. 1986. Control of an outbreak of wet-tail in a closed colony of hamsters
(Mesocricetus auratus). Vet Rec 119:272-273.
McOrist S et al. 1989. Early lesions of proliferative enteritis in pigs and hamsters. Vet
Pathol 26:260-264.
McOrist S, Lawson GH. 1987. Possible relationship of proliferative enteritis in pigs and
hamsters. Vet Microbiol 15:293-302.
Sheffield FW, Beveridge E. 1962. Prophylaxis of "wet-tail" in hamsters. Nature
196:294-295.
Stills HF et al. 1987. Utilization of monoclonal antibodies to evaluate the involvement
of Campylobacter jejuni in proliferative ileitis in Syrian hamsters (Mesocricetus
auratus). Infect Immun 55:2240-2246.
Stills HF, Hook RR Jr. 1989. Experimental production of proliferative ileitis in Syrian
hamsters (Mesocricetus auratus) by using an eleal homogenate free of Campylobacter
jejuni. Infect Immun 57:191-195.
Stills HF Jr, Hook RR Jr, Kinden DA. 1989. Isolation of a Campylobacter-like organism
from healthy Syrian hamsters (Mesocricetus auratus). J Clin Microbiol 27:2497-2501.
Thomlinson JR. 1975. "Wet-tail" in the Syrian hamster. A form of colibacillosis. Vet Rec
96:42.
Tomita Y, Jonas AM. 1968. Two viral agents isolated from hamsters with a form of
regional enteritis: a preliminary report. Am J Vet Res 29:445-453.
Wagner JE et al. 1973. Proliferative ileitis of hamsters: electron microscopy of bacteria
in cells. Am J Vet Res 34:249-252.
Clostridiosis
Like rabbits, guinea pigs, and other animals, including people, administration
of antibiotics can result in overgrowth of Clostridium difficile in the cecum and large
intestine, with elaboration of characterisitc toxins. Hamsters are so susceptible that
they are the species most used to study the disease experimentally, and were used
to elucidate the nature of the disease as it commonly occurred in human patients
treated with clindamycin. The disease also can occur spontaneously.
Bartlett JG et al. 1977. Clindamycin-associated colitis due to a toxin-producing species
of Clostridium in hamsters. J Infect Dis 136:701-705.
Fekety R. Antibiotic-associated enterocolitis. In Infectious Diarrheal Diseases:
Current Concepts and Laboratory Procedures; Mellner PD, ed.; Marcel Dekker, Inc.,
New York; 1984; pp. 77-92.
Kim P-H, Iaconis JP, Rolfe RD. Immunization of adult hamsters against Clostridium
difficile-associated ileocecitis and transfer of protection to infant hamsters. Infect
Immun 55:2984-2992, 1987.
Libby JM et al. 1982. Effects of the two toxins of Clostridium difficile in antibiotic-
associated cecitis in hamsters. Infect Immun 36:822-829.
Michelich VJ et al. 1981. Diet as a coadjuvant in development of antibiotic-associated
diarrhea in hamsters (Mesocricetus auratus). Lab Anim Sci 31:259-262.
Rehg JE, Liu YS. 1982. Clostridium difficile typhlitis in hamsters not associated with
antibiotic therapy. J Am Vet Med Assoc 181:1422-1423.
Rifkin GD et al. 1978. Neutralization by Clostridium sordellii antitoxin of toxins
implicated in clindamycin-induced cecitis in the hamster. Gastroenterology 75:422-424.
Small JD. 1968. Fatal enterocolitis in hamsters given lincomycin hydrochloride. Lab
Anim Care 18:411-420.
Toshniwal R et al. 1979. Etiology of tetracycline-associated pseudomembranous colitis
in hamsters. Antimicrob Agents Chemother 16:167-170.
Tyzzer's Disease
Similar to the disease in rats and mice: diarrhea; multifocal necrotizing
cecocolitis, hepatitis, and, in a few cases, myocarditis.
Nakayama M et al. 1976. Typhlohepatitis in hamsters infected perorally with Tyzzer's
organism. Jap J Exp Med 46:309-324.
Takagaki Y et al. 1966. Experimental Tyzzer's disease in different species of
laboratory animals. Jap J Exp Med 36:519-534.
Takasaki Y et al. 1974. Tyzzer's disease in hamsters. Jap J Ext Med 44:267-270.
Zook BC et al. 1977. Tyzzer's disease in Syrian hamsters. J Am Vet Med Assoc 171:833-
836.
Zook BC et al. 1977. Tyzzer's disease in the Chinese hamster (Cricetulus griseus). Lab
Anim Sci 27:1033-1035.
Salmonellosis
Disease similar to that in mice, although one report emphasizes septic pulmonary
thrombophlebitis as a common finding in one epizootic.
Innes JRM et al. 1956. Epizootic Salmonella enteritidis infection causing septic
pulmonary phlebothrombosis in hamsters. J Infect Dis 98:133-141.
Pneumonia
Commonly mentioned in surveys of hamster diseases, but poorly described and
documented. Possible causes include Sendai virus, pneumonia virus of mice,
Streptococcus pneumoniae, & Pasteurella pneumotropica; there are almost certainly
others. Mycoplasma pulmonis has been isolated from the respiratory tract but its
significance in hamsters is not known.
Battigelli MC et al. 1971. Microflora of the respiratory surface of rodents exposed to
"inert" particulates. Arch Intern Med 127:1103-1104.
Hill A. Mycoplasmas of small animals. In Mycoplasmas of Man, Animals, Plants, and
Insects. Bove JM, Duplan JF (eds); INSERM, Paris; 1974; pp. 311-316.
Pearson HE, Eaton MD. 1940. A virus pneumonia of Syrian hamsters. Proc Soc Exp Biol
Med 45:677-679.
Profeta ML et al. 1969. Enzootic Sendai virus infection in laboratory hamsters. Am J
Epidemiol 89:316-324.
Soret MG, Buthala DA. 1967. Enzootic Sendai virus infection in hamsters. Bacteriol
Proc __:163-164.
Miscellaneous Bacterial Diseases
Chute RN et al. 1954. A laboratory epidemic of human-type tuberculosis in hamsters.
Am J Clin Pathol 24:223-226.
Frisk CS et al. 1976. Streptococcal mastitis in golden hamsters. Lab Anim Sci 26:97.
Karbe E. 1987. Disseminated mycobacteriosis in the golden hamster. Zentralbl
Veterinarmed [B] 34:391-394.
Krause T, Kunstyr I, Mutters R. 1989. Characterization of some previously unclassified
Pasteurellaceae isolated from hamsters. J Appl Bacteriol 67:171-175.
Lesher RJ et al. 1985. Enteritis caused by Pasteurella pneumotropica infection in
hamsters. J Clin Microbiol 22:448.
Perman V, Bergeland ME. 1967. A tularemia enzootic in a closed hamster breeding
colony. Lab Anim Care 17:563-568.
Taylor NS et al. 1989. Diversity of serotypes of Campylobacter jejuni and
Campylobacter coli isolated in laboratory animals. Lab Anim Sci 39:219-221.
Parasites
None are important pathogens in laboratory hamsters.
1. Cestodes: Hymenolepis diminuta and H. nana: Usually no signs, but possibly
catarrhal enteritis or obstruction if infestation heavy enough.
Stone WB, Manwell RD. 1966. Potential helminth infections in humans from pet or
laboratory mice and hamsters. Pub Health Reports 81:647-653.
2. Nematodes: Syphacia obvelata (most common), also Aspicularis tetraptera.
Greve JH. 1985. Dentostomella translucida, a nematode from the golden hamster. Lab
Anim Sci 35:497-498.
3. Mites:
1. Demodex aurati: Demodectic or follicular mange. Characterized by alopecia
over rump and back, dry scaly skin, no pruritus. Infestation more common than
disease.
2. D. criceti: Not found in follicles, thought to be nonpathogenic.
3. Ornithonyssus bacoti
4. Notoedres notoedres (ears) and Sarcoptes scabei
Estes PC et al. 1971. Demodectic mange in the golden hamster. Lab Anim Sci
21:825-828.
Nutting WB. 1961. Demodex aurati sp. nov. and D. criceti, ectoparasites of the golden
hamster (Mesocricetus auratus). Parasitology 51:515-522.
Nutting WB, Rauch H. 1958. Demodex criceti N. sp. (Acarina: Demodicidae) with notes
on its biology Parasitology 44:328-333.
Owen D, Young C. 1973. The occurrence of Demodex aurati and Demodex criceti in the
Syrian hamster (Mesocricetus auratus) in the United Kingdom. Vet Rec 92:282-284.
Sarashina T, Sato K. 1986. Demodicosis in the golden hamster. Nippon Juikagu Zasshi
48:619-622.
4. Protozoa: Spironucleus muris, Tritrichomonas muris, Giardia muris, Balantidium
coli and B. caviae, Entamoeba muris.
Wagner JE et al. 1974. Hexamitiasis in laboratory mice, hamsters, and rats. Lab Anim
Sci 24:349-354.
5. General references--parasites:
Wantland WW. 1955. Parasitic fauna of the golden hamster. J Dental Res 34:631-649.
Wantland WW. Parasitology. In The Golden Hamster, Hoffman, Robinson, Magalhaes
(eds); Iowa State Univ Press, 1968; pp. 171-183.
Neoplasms
Incidence of spontaneous neoplasms varies considerably among different
studies. In some cases, 100% of hamsters maintained throughout their normal life
span develop one or more tumors. Common benign neoplasms include intestinal
polyps, adrenal cor-tical adenomas, thyroid adenomas, forestomach papillomas,
and splenic hemangiomas. Common malignancies include lymphomas, leukemias,
intestinal adenocarcinomas and melanomas. Cutaneous neoplasms are uncommon
except for melanomas.
Ashbal R. 1945. Spontaneous transmissible tumors in the Syrian hamster. Nature
155:907.
Brownstein DG, Brooks AL. 1980. Spontaneous endometrial neoplasms in aging Chinese
hamsters. JNCI 64:1209-1214.
Chesterman FC, Pomerance A. 1965. Cirrhosis and liver tumours in a closed colony of
golden hamsters. Brit J Cancer 19:801-811.
Crowley LV. 1970. A diffuse plasma-cell disease in a golden hamster. Vet Pathol
7:135-138.
Deerberg F et al. 1987. Spontaneous mortality and incidence of spontaneous tumours
in Han:CHIN hamsters. Z Versuchstierkd 29:129-143.
Dunham LJ et al. 1975. Argyrophilic carcinoids in two Syrian hamsters (Mesocricetus
auratus). J Natl Cancer Inst 54:507-513.
Ernst H et al. 1989. Spontaneous tumours of the European hamster (Cricetus cricetus
L.). Z Versuchstierkd 32:87-96.
Fabry A. 1985. The incidence of neoplasms in Syrian hamsters with particular
emphasis on intestinal neoplasia. Arch Toxicol [Suppl] 8:124-127.
Ferm VH. 1967. The use of the golden hamster in experimental teratology. Lab Anim
Care 17:452-462.
Fortner JG et al. 1961. Transplantable tumors of the Syrian (golden) hamster. Part I.
Tumors of the alimentary tract, endo-crine glands and melanomas. Cancer Res 21:161-
___.
Fortner JG et al. 1961. Transplantable tumors of the Syrian (golden) hamster. Part II.
Tumors of the hematopoietic tissues, genitourinary organs, mammary glands and
sarcomas. Cancer Res 21:199-___.
Fortner JG. 1957. Spontaneous tumors, including gastrointestinal neoplasms and
malignant melanomas in the Syrian hamster. Cancer 10:1153-1156.
Franks LM, Chesterman FC. 1957. Adrenal degeneration and tumor formation in the
golden hamster following treatment with stilbestrol and methylcholanthrene. Brit J
Cancer 11:105-111.
Homburger F. Pathology of the Syrian hamster. In Progress in Experimental Tumor
Research, Vol. 16. S Karger, Basel, 1972.
Homburger F. The Syrian hamster in toxicology and carcinogenesis research. In
Progress in Experimental Tumor Research, Vol. 24. S Karger, Basel, 1979.
Homburger F. 1983. Background data on tumor incidence in control animals (Syrian
hamsters). Prog Exp Tumor Res 26:259-265.
Jelinek F. 1989. Intestinal lymphomas in golden hamsters (Mesocricetus auratus). Z
Versuchstierkd 32:123-128.
Kaspareit-Rittinghausen J, Deerberg F. 1988. Spontaneous neoplasms of the seminal
vesicles in aged Han:Chin hamsters (Cricetulus criseus). Lab Anim 22:127-130.
Kesterson JW, Carlton WW. 1970. Multiple malignant neoplasms in a golden hamster.
A case report and literature survey. Lab Anim Care 20:220-225.
Kim JCS, Mangkoewidjojo S. 1977. Malignant melanoma metastatic to the lung in a pet
hamster. Lab Anim 11:125-127.
Murthy ASK, Russfield AB. 1966. Evidence for three types of benign adrenal tumors
in Syrian hamsters. Arch Pathol 81:140-145.
Ninomiya H, Nakamura T, Yamazaki K. 1988. Chondrosarcoma of the mandible and falx
cerebri in a Chinese hamster (Cricetulus griceus): report of a case. Jikken Dobutsu
37:317-320.
Port CD, Richter WR. 1977. Eosinophilic leukemia in a Syrian hamster. Vet Pathol
14:283-286.
Pour P et al. 1976. Spontaneous tumors and common diseases in tow colonies of Syrian
hamsters. III. Urogenital system and endocrine glands. J Natl Cancer Inst 56:949-961.
Pour P et al. 1976. Spontaneous tumors and common diseases in tow colonies of Syrian
hamsters. II. Respiratory tract and digestive system. J Natl Cancer Inst 56:937-948.
Pour P et al. 1976. Spontaneous tumors and common diseases in tow colonies of Syrian
hamsters. IV. Vascular and lymphatic systems and lesions of other sites. J Natl Cancer
Inst 56:949-961.
Pour P et al. 1976. Spontaneous tumors and common diseases in two colonies of Syrian
hamsters. I. Incidence and sites. J Natl Cancer Inst 56:931-935.
Robinson FR. Hamster, Part III of naturally occurring neoplastic disease. In
Handbook of Laboratory Animal Science, Vol. III. Melby EC Jr, Altman NH (eds); CRC
Press, Boca Raton, FL; 1976; pp. 253-270.
Saunders GK, Scott DW. 1988. Cutaneous lymphoma resembling mycosis fungoides in
the Syrian hamster (Mesocricetus auratus). Lab Anim Sci 38:616-617.
Saunders GK, Scott DW. 1988. Cutaneous lymphoma resembling mycosis fungoides in
the Syrian hamster (Mesocricetus auratus). Lab Anim Sci 38:616-617.
Schmidt RE et al. Pathology of Aging Hamsters. CRC Press, Boca Raton, FL; 1983.
Shrader RE. 1946. Adrenal medullary tumor (pheochromocytoma) in the golden
hamster (Cricetus auratus). Cancer Res 6:504-___.
Turosov VS et al (eds). Pathology of Tumours in Laboratory Animals, Vol. III. Tumours
of the Hamster. International Agency for Research on Cancer, Lyon, 1982.
Van Hoosier GL et al. Spontaneous tumors of the Syrian hamster: Observations in a
closed breeding colony and a review of the literature. In Defining the Laboratory
Animal; National Academy of Sciences, Washington, DC; 1971; pp. 450-473.
Yube Y. 1972. Spontaneous tumors in hamsters: Incidence, morphology,
transplantation, and virus studies. Gann 63:329-336.
Pregnancy Toxemia
Not ketosis, but similar to eclampsia of women. Hamsters dying of the condition
have disseminated intravascular coagulation with fibrin thrombi in capillaries,
especially those of the glomeruli, which can result in ischemic tubular degeneration
or even cortical necrosis. Incidence unknown, but mortality is probably high.
Galton M. 1966. Thrombosis in the pregnant Syrian hamster. Trans NY Acad Sci 28:423-
438.
Galton M, Slater SM. 1965. Naturally occurring fatal disease of the pregnant golden
hamster. Proc Soc Exp Biol Med 120:873-876.
Richter AG et al. 1984. Pregnancy toxemia (eclampsia) in Syrian golden hamsters. J Am
Vet Med Assoc 185:1357-1358.
Amyloidosis
A common age-related disease; cause unknown. Amyloid deposits around
capillaries, especially those of the glomeruli, spleen, liver, and adrenals. Some have
nephrotic syndrome with generalized edema. Especially common in experimental
chronic infectious diseases such as leishmaniasis and tuberculosis.
Crowell WA, Votava CA. 1975. Amyolidosis induced in hamsters by a filarial parasite
(Dipetalonema viteae). Vet Pathol 12:178-185.
Gellhorn A et al. 1946. Amyloidosis in hamsters with leishmaniasis. Proc Soc Exp Biol
Med 61:25-30.
Gleiser CA et al. 1971. Amyloidosis and renal paramyloid in a closed hamster colony.
Lab Anim Sci 21:197-202.
Glenner GG. 1980. Amyloid deposits and amyloidosis. New Engl J Med 302:1283-1292,
1333-1343.
Gruys E et al. 1979. Deposition of amyloid in the liver of hamsters. An enzyme-
histochemical and electron microscopic study. Lab Anim 13:1-9.
Jakob W. 1971. Spontaneous amyloidosis of animals. Vet Pathol 8:292-306.
Mezza LE et al. 1984. Characterization of spontaneous amyloidosis of Syrian hamsters
using the potassium permanganate method. Lab Anim Sci 34:376-380.
Murphy JC et al. 1984. Nephrotic syndrome associated with renal amyloidosis in a
colony of Syrian hamsters. J Am Vet Med Assoc 185:1359-1362.
Russfield AB, Green MN. 1965. Serum protein patterns associated with amyloidosis in
the Syrian hamster. Am J Pathol 46:59-69.
Chronic Nephropathy
Similar to progressive nephropathy of rats; characterized by interstitial fibrosis
and dilated tubules filled with protein in early stages. Later, glomeruli become
sclerotic. There can be various amounts of amyloid present; whether or not it is
related is unknown. As in rats, high-protein diets increase the severity of the
disease. Also described is arteriolar nephrosclerosis.
Burek JD et al. 1988. Spontaneous renal disease in laboratory animals. Int Rev Exp
Pathol 30:231-319.
Feldman DB et al. 1982. Growth, kidney disease, and longevity of Syrian hamsters
(Mesocricetus auratus) fed varying levels of protein. Lab Anim Sci 32:613-618.
Slauson DO et al. 1978. Arteriolar nephrosclerosis in the Syrian hamster. Vet Pathol
15:1-11.
Slauson DO, Hobbs CH. 1975. Spontaneously occurring arteriolar nephrosclerosis in
the Syrian hamster. Fed Proc 34:878.
Polycystic Disease
A common age-related disease. Rare in hamsters less than 1 year old, but
otherwise resembles congenital polycystic disease of man. One to many, up to several
mm cysts in liver, epididymis, ovary, adrenal, seminal vesicles, renal pelvis,
endometrium, and esophagus (approximate order of decreasing frequency); one
hamster can have cysts in one or many tissues. Cysts contain amber fluid and have
flat epithelial lining. Cause unknown.
Gleiser CA et al. 1970. A polycystic disease of hamsters in a closed hamster colony.
Lab Anim Care 20:923-929.
Somvanshi R et al. 1987. Polycystic liver disease in golden hamsters. J Comp Pathol
97:615-618.
Atrial Thrombosis
Common cause of death in old hamsters. More common in left atrium.
Respiratory signs. Pulmonary edema and effusion. May be accompanied by DIC.
Dodds WJ et al. 1975. Atrial thrombosis and consumption coagulopathy in aged Syrian
hamsters. Fed Proc 34:221.
Dodds WJ et al. 1977. Spontaneous atrial thrombosis in aged Syrian hamsters. II.
Hemostasis. Thrombosis Hemostasis 38:457-464.
McMartin DN. 1977. Spontaneous atrial thrombosis in aged Syrian hamsters. I.
Incidence and pathology. Thrombosis Hemostasis 38:447-456.
McMartin DN, Dodds WJ. 1982. Atrial thrombosis in aged Syrian hamsters. Animal model
of human disease. Am J Pathol 107:227-229.
Sichuk G et al. 1965. Influence of sex hormones on thrombosis of the left atrium in
Syrian (golden) hamsters. Am J Physiol 208:465-470.
Wechsler SJ, Jones J. 1984. Diagnostic exercise: a case of atrial thrombosis and
consumptive coagulopathy in a hamster. Lab Anim Sci 34:137-139.
Hemorrhagic Necrosis of the Central
Nervous System of Fetal Hamsters
Not an important natural disease; results from vitamin E deficiency.
Keeler RF et al. 1975. Occurrence of spontaneous hemorrhagic necrosis of the central
nervous system in fetal hamsters. Teratology 11:21-30.
Keeler RF, Young S. 1978. Multifactorial contributions to the etiology of spontaneous
hemorrhagic necrosis of the central nervous system of fetal hamsters. Teratology
17:285-292.
Keeler RF, Young S. 1979. Role of vitamin E in the etiology of spontaneous
hemorrhagic necrosis of the central nervous system of fetal hamsters. Teratology
20:127-132.
Margolis G, Kilham L. 1975. Spontaneous hemorrhagic necrosis of the central nervous
system of fetal hamsters. J Neuropathol Exp Neurol 34:88-89.
Margolis G, Kilham L. 1976. Hemorrhagic necrosis of the central nervous system. A
spontaneous disease of fetal hamsters. Vet Pathol 13:250-263.
Young S, Keeler RF. 1978. Hemorrhagic necrosis of the central nervous system of fetal
hamsters: litter incidence and age-related pathological changes. Teratology 17:293-
302.
Inherited Myopathies
Not important natural diseases, but potentially useful animal models. Best
studied is skeletal and cardiac dystrophy in BIO 14.6 strain. It is a progressive,
autosomal recessive condition with onset at 60-120 days. Affected hamsters have
shortened life spans. Not all muscles are equally affected; limb adductors are most
severely, and earliest, affected. Histology: degeneration, necrosis, regeneration,
fibrosis, fatty change. Resembles Duchenne's muscular dystrophy in several
respects, but mode of inheritance is different. (DMD is X-linked recessive.)
Distribution of lesions also is different. (The heart is not affected in DMD). In
hamsters, congestive heart failure is the usual cause of death. Pathogenesis is
unknown.
Bajusz E, Jasmin G. 1972. Hereditary disease model of congestive cardiomyopathy:
studies on a new line of Syrian hamsters. Fed Proc 31:621.
Gertz EW. 1973. Animal model of human disease: myocardial failure, muscular
dystrophy. Cardiomyopathic Syrian hamster. Am J Pathol 70:151-154.
Homberger F et al. 1963. Further morphologic and genetic studies on dystrophy-like
primary myopathy of Syrian hamsters. Fed Proc 22:195.
Homberger F et al. 1965. The early histopathological lesion of muscular dystrophy in
the Syrian golden hamster. J Pathol Bacteriol 89:133-138.
Homberger F et al. 1966. Hereditary dystrophy-like myopathy. The histopathology of
hereditary dystrophy-like myopathy in Syrian hamsters. Arch Pathol 81:302-307.
York CM et al. 1983. Cardiac carnitine deficiency and altered carnitine transport in
cardiomyopathic hamsters. Arch Biochem Biophys 221:526-533.
Progressive Hind-Limb Paralysis
Sex-linked, occurs in males; BIO 12.14 strain. A degenerative peripheral
neuropathy. Not a good model of amyotrophic lateral sclerosis as once proposed.
Trophoblastic Emboli
Supposedly fairly common in pregnant hamsters; proposed as animal model.
Burek JD. 1979. The pregnant Syrian hamster as a model to study intravascular
trophoblasts and associated maternal blood vessel changes. Vet Pathol 16:553-566.
Diabetes Mellitus in Chinese Hamsters
Boquist L. 1969. Pancreatic islet morphology in diabetic Chinese hamsters. Acta Pathol
Microbiol Scand 75:399-414.
Meier H, Yerganian GA. 1959. Spontaneous hereditary diabetes mellitus in Chinese
hamsters (Cricetulus griseus). I. Pathologic findings. Proc Soc Exp Biol Med 100:810-
815.
Miscellaneous References
Badiola J et al. 1983. Pathologic features of leptospirosis in hamsters caused by
Leptospira interrogans serovars hardjo and szwajizak. Am J Vet Res 44:91-99.
Doi K et al. 1987. Age-related non-neoplastic lesions in the heart and kidneys of
Syrian hamsters of the APA strain. Lab Anim 21:241-248.
Elwell MR, Frenkel JK. 1984. Acute toxoplasmosis in hamsters and mice: measurement
of pathogenicity by fever and weight loss. Am J Vet Res 45:2663-2667.
Frenkel JK. 1972. Infection and immunity in hamsters. Prog Exp Tumor Res 16:326-367.
Fujita H, Orita Y. 1988. An inner ear anomaly in golden hamsters. Am J Otolaryngol
9:224-231.
Gaertner DJ et al. 1987. Muscle necrosis in Syrian hamsters resulting from
intramuscular injections of ketamine and xylazine. Lab Anim Sci 37:80-83.
Hamilton JM et al. 1983. Cholangiofibrosis in the Syrian golden hamster. Vet Rec
112:359-360.
Kajdacsy-Balla A et al. 1987. Animal model of human disease: syphilis in the Syrian
hamster. A model of human venereal and congenital syphilis. Am J Pathol 126:599-___.
Kunstyr I et al. 1987. Spontaneous pathology of the European hamster (Cricetus
cricetus). Malocclusion, dysplastic and inflammatory processes on the jaws. Z
Versuchstierkd 29:171-180.
Nixon CW. 1972. Hereditary hairlessness in the Syrian golden hamster. J Hered 63:215-
___.
van den Ingh TS, Hartman EG. 1986. Pathology of acute Leptospira interrogans
serotype icterohemorrhagiae infection in the Syrian hamster. Vet Microbiol 12:367-376.
Sans-Coma V et al. 1988. Origin of the left main coronary artery from the pulmonary
trunk in the Syrian hamster. Am J Cardiol 62:159-161.
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