II. Lymphocytic Choriomeningitis (LCM)
III. Salmonellosis
A. Etiology: Hymenolepis nana (dwarf tapeworm) and
Hymenolepis
diminuta infect hamsters with a moderate rate of incidence.
Hymenolepis
nana adults range from 25 to 40 mm long and less than 1 mm wide and
have an armed rostellum (see photo). Hymenolepis diminuta
adults
range from 20 to 60 mm in length and 3 to 4 mm wide with no hooks on the
scolex. 
B. Transmission: Hymenolepis nana and Hymenolepis diminuta can be transmitted indirectly with cockroaches, beetles, or fleas as intermediate hosts. Hymenolepis nana can also be transmitted by direct ingestion of hexacanth ova and autoinfection in which the entire life cycle occurs in the small intestine without ingestion of ova (direct life cycle is 14 to 16 days).
C. Clinical Signs: Usually there are no external signs of infection. Impactions have been reported with heavy infections resulting in intestinal obstruction.
D. Diagnosis: Diagnosis can be made by fecal flotation
and examination for hexacanth ova (see photo), direct examination of intestines
with a dissecting microscope, or histopathological examination of the small
intestine. 
E. Treatment: Niclosomide (Yomesan) at 10 mg/100 gm body weight given in a treatment at 7 day intervals is effective but not currently available in the U.S. Thiabendazole at 0.33% crushed and mixed in pulverized feed for 7 to 14 days have been effective. Praziquantel at 5.1 -11.4 mg/kg IM, SQ or PO (repeat in 10 days) can be used in both hamsters and gerbils.
F. Control: Cockroaches should be eliminated and infected animals killed or treated.
Public Health Significance: People become infected with H. nana from contact with the ova; since autoinfection can occur, a heavy parasite load may quickly develop.
II. Lymphocytic Choriomeningitis Virus (LCM)
A. Etiology: LCM is a RNA virus of the arenavirus group. Incidence of infection and spontaneous disease is rare. Most reported human cases have been associated with infected hamsters.
B. Transmission: In utero or perinatal infections (within 1 day post-partum) may produce a subclinical persistent infection or a chronic, progressive wasting disease. The virus is intermittently shed in urine and saliva with the concomitant production of antibody. Approximately half the infected hamsters will clear the infection. If infected as young adults, antibody production and persistent viruria and viremia continue for up to 6 months. The natural reservoir for LCM is the wild rodent population. Transmission occurs via urine and saliva, traumatized skin, conjunctiva, respiratory passages, or congenital contamination. In research involving hamsters, a common route of infection is the transplantation of LCM-contaminated tumors.
C. Clinical Signs: Usually there are no clinical signs. Wasting syndrome and death may occur in hamsters with persistent infections. Signs can include convulsions, decreased growth, and inactivity. Decreased reproduction has been reported in chronically infected females.
D. Pathology: Gross lesions vary and if present, may include splenomegaly, swollen or shrunken, pitted kidneys, lymphadenopathy, hepatomegaly. Gross lesions alone are not diagnostic. Microscopic lesions include lymphocytic meningitis, chronic glomerulonephropathy, widespread vasculitis, and marked lymphocytic infiltration of the viscera.
E. Diagnosis: Diagnosis is based partly upon the lymphocytic infiltration of the meninges, choroid plexuses, and of submeningeal and subchoroid perivascular spaces. ELISA tests are used to detect serum antibodies to LCM. PCR of fresh hamster tissue or transplantable cells/fluids can be used to diagnose persistent or acute infections. Injection of hamster blood or tissues into LCM-free mice will produce clinical signs and antibody titers in 2 weeks.
F. Control: All hamsters at risk for infection from horizontal and vertical transmission should be euthanatized and evaluated for diagnostic examinations. Major efforts to disinfect cages and equipment once the hamsters have been eliminated should be immediately employed. The wild rodent population should be controlled.
Public Health Significance: People are susceptible to LCM virus, and experience flu-like symptoms and occasional nonsuppurative meningitis. Past reports of zoonosis have linked human infections to exposure to infected pet hamsters.
A. Etiology: Salmonella enterica serovars Typhimurium and Enteritidis are Gram-negative, invasive enteric bacteria. Incidence of infection and disease is low.
B. Transmission: Food, water and bedding may be contaminated by infected feces from wild rodents.
C. Clinical Signs: The disease may only be manifest as acute death. Clinical signs are seen primarily in pregnant or recently delivered females and infant or weanling hamsters. Diarrhea is usually not present but pregnant females may abort and become cachexic.
D. Pathology: Fluid-filled small intestine and cecum may be observed in young hamsters. The lungs have a patchy hemorrhagic and partly grayish appearance. Small white foci are seen in the liver. The most significant lesion is septic, partially occluding thrombosis of pulmonary venules with underlying necrosis and erosion of the vessel walls. There are focal areas of interstitial pneumonia and lobular collapse. Thrombosis of liver venules and multifocal necrosis of the liver, lymph nodes and spleen are found.
E. Diagnosis: Recovery of Salmonella sp. from fecal or lesioned organ cultures is diagnostic. Use of enriched or selective media, and collection of feces and lymph node or liver homogenates from multiple animals enhances the opportunities to recover Salmonella, especially when the disease has become enzootic.
F. Control: Treatment is not recommended, and elimination of colony animals is recommended. 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.
Public Health Significance: Humans ingesting Salmonella contaminated
food or water experience a transient diarrhea.
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