II. Lymphocytic Choriomeningitis (LCM) Virus
III. Salmonellosis
A. Rodentolepis nana is the dwarf tapeworm and Hymenolepis diminuta is the rat tapeworm. Both tapeworms are capable of infecting mice. The incidence of parasitism is rare.
B. Transmission: Rodentolepis nana and Hymenolepis diminuta can be transmitted by an indirect mode with cockroaches, grain beetles, or fleas as intermediate hosts. Rodentolepis nana can also be transmitted by direct ingestion of hexacanth ova or by autoinfection in which the entire life cycle occurs in the host's small intestine (complete life cycle in 14 to 16 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. Pathology: Rodentolepis nana adults range from
25 to 40 mm long and less than l 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 without hooks on the scolex. These tapeworms may
migrate up the pancreatic and biliary ducts. Since R. nana can complete
its life cycle without an intermediate host, strobelocerci may be observed
within the lamina propria of the small intestine.
E. Diagnosis: Visualization of the tapeworm in the small
intestine during necropsy, recovery of hexacanth ova by fecal flotation
or microscopic visualization of segmented parasites or encysted larvae
in histological sections of the small intestine villi are methods of diagnosis.
F. Treatment: Niclosamide at 10 mg/100 gm body weight should be crushed and given in powdered feed for two treatments at 7 day intervals. Praziquantel, at the equivalent of the cat dose, has been used, but the efficacy of treatment has not been documented.
G. Control: Cockroaches should be eliminated and infected animals treated or eliminated.
Public Health Significance: Humans are susceptible to infections with R. nana; since autoinfection can occur, a heavy parasite load may quickly develop.
II. Lymphocytic Choriomeningitis (LCM) Virus
A. Etiology: LCM virus is an arenavirus (RNA virus).
B. Transmission: In utero or perinatal infections (within 1 day post-partum) produce a persistent, subclinical infection. If a mouse is infected at any time after 24 hours of age, antibody production occurs. Virus is continually shed in urine, saliva and milk but antibody is difficult to detect due to low production and to binding with virus to cause circulating antibody-virus complexes. Incidence of disease is rare in commercial breeding colonies. A major source of infection is transplanted mouse (hamster) tumors or cell lines . Vertical (transovarian and/or transuterine) transmission is known to occur and is considered an efficient means of transmission to mice delivered by infected dams.
C. Clinical Signs: Two types of infections are known to occur. The persistent tolerant form results when the infection is acquired in utero or within a few days after birth. There is life-long viremia and shedding of virus. There is modest growth retardation, and at 7-10 months of age, immune complex glomerulonephritis occurs and is associated with emaciation, ruffled fur, hunched posture, ascites and some deaths. The second, nontolerant (acute) infection occurs when the mice are exposed after the first week of life. Viremia develops, but there is no shedding of virus. The outcome is either death within a few days or weeks, or recovery with elimination of the virus.
D. Pathology: Gross lesions vary from none to focal visceral
necrosis and splenomegaly. Histological examination of the brain reveals
lymphocytic infiltration of the meninges, choroid plexus, and of submeningeal
and subchoroid perivascular spaces.
In tolerant mice, perivascular lymphoid infiltrates of viscera and
immune-complex glomerulonephritis may be observed. Please note that these
lesions are also common in inbred strains of mice that are prone to development
of autoimmune disease.
E. Diagnosis: ELISA tests may reveal serum antibodies. PCR of kidney or brain from infected mice or of biological samples will identify virus. Virus isolation can be frustrating since LCM does not induce cytopathic effect. Bioassays include suckling mouse inoculation (footpad injection with infected neural tissue with swelling in 5-9 days or cerebral injection with development of neurological signs) or adult mouse inoculation (inject with whole blood and observe clinical signs or antibody titers in 2 weeks confirming the diagnosis).
F. Treatment: None.
G. Control: Eliminate colony since vertical transmission of the virus makes control measures less effective.
Public Health Significance: CDC reports human LCM infections. Most recent LCM virus exposures have been linked to exposure with experimental infection studies in immunocompromised research mice, or to research bench accidents.
A. Etiology: Salmonella are Gram-negative, toxin-producing, invasive, enteric bacteria. The most common serotype of Salmonella enterica to infect mice is serovar Typhimurium.
B. Transmission: The disease is spread by fecal-oral transmission. Food, water, and bedding may be contaminated by infected feces from wild mice. The incidence of salmonellosis is rare in research mice, and uncommon with sporadic epizootics in mice from colonies raised for pet or zoo industries.
C. Clinical Signs: Disease in susceptible colonies may be manifest only as acute death with no clinical signs of infection. Moderate morbidity characterized by hunched posture, anorexia, lethargy, and high to sporadic mortality may be observed in weanlings and in females in late gestation. Diarrhea may or may not be present. The disease will become endemic, with periodic cycling of overt disease symptoms such as acute deaths, chronic low fertility, fetal reabsorption, or abortion.
D. Pathology: In acute deaths, the spleen may be enlarged
2 to 3 times normal size. Lesions in the small intestine consist of mucosal
congestion and edema with thrombosis of the mesenteric vasculature.
In sub-acute infections, multiple white to yellow foci occur in the liver,
spleen is enlarged, and mesenteric lymph nodes may be enlarged and edematous
(left photo). Histopathological examination may reveal multifocal
necrotizing splenitis and hepatitis, with necrotic foci often accompanied
by colonies of bacteria (arrow in right photo).
. 
E. Diagnosis: The history of the disease outbreak, decreased fecundity in breeding colonies, gross lesions, and identification of wild rodent exposure can be suggestive of salmonellosis. A definitive diagnosis is determined by culture of liver and spleen (in acute cases), feces, mesenteric lymph node, and ileal homogenates (in subacute cases) on selective media such as selenite, brilliant green and MacConkey's agar with serotyping of the isolate.
F. Treatment: Since the carrier state can not be successfully eliminated with antibiotic therapy, elimination of the animal or animals in the colony is suggested. Restock only after extensive sanitation has been performed.
G. Control: Aggressive husbandry improvement procedures should be aimed at prevention of food, bedding, water, or mouse contamination by wild vermin, and proper sanitizing of cages and watering equipment.
Public Health Significance: Humans ingesting Salmonella contaminated food or water may experience a transient diarrhea. Children or immunocompromised adults may experience more severe disease. The disease in humans is reportable.
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