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 æm 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 æm, 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.