[Cytomegalic inclusion disease in mice. Lesions produced in the generalized form].
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Biomedical subjects
Publications and source records attributed to G Lussier.
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Hexamitiasis was encountered in a breeding colony of C(3)H/HeJ mice. The disease was observed in animals under three weeks of age. It was characterized clinically by retarded development, hunched attitude, lethargy, and in some cases by diarrhea and death. Lesions were noted particularly in the duodenum. The intestinal contents were watery and foamy. Histologically, cyst-like formations due to the dilation of the glands of Lieberkühn were seen together with inflammatory reaction in the lamina propria and sloughing of the epithelium. The infection was controlled by the routine administration of dimetridazole in the drinking water.
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Guinea pigs were immunized with inactivated measles virus. When challenged with live virus by the intradermal route, most of the animals developed an area of erythema within 24 to 48 hours; however, an unexpected feature of the skin-testing was that some of the guinea pigs developed a very severe necrotic reaction by the sixth or seventh day.
Wasting disease was observed in hamsters inoculated at birth with a cell-free bovine leukemic extract. The autopsy and histological examination of the runted hamsters revealed visible lesions in the lymphoid tissues. These lesions consisted mostly in depletion of lympocytes in the spleen and in the cortex of the lymph nodes and in atrophy of the Peper's patches. Thymic lesions were also observed. Anemia and a decrease of circulating lymphocytes were observed in the peripheral blood.
Intranuclear inclusion bodies were observed in the liver cells of 21 of 104 hamsters. The cause of these inclusions remains unknown but they probably represent infoldings of the nuclear membrane in which the cytoplasm has become segregated. An account is given of the age incidence, morphology and histo-chemical features of these inclusions.
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Heparinized blood specimens obtained from two patients in the acute phase of infectious mononucleosis and from a healthy technician were injected intravenously into rhesus monkeys (Macaca mulatta) and the animals were observed for three weeks to one month for clinical, hematological and serological signs of infectious mononucleosis.Splenomegaly was the only definite clinical finding after 12 and 16 days, respectively. There were no definite hematological changes.At autopsy, hyperplasia of the germinal centres of lymphoid follicles, occasional foci of lymphocytic infiltration in the red pulp, and abnormal lymphoid cells in venules or arteries of the spleen were noted.The lesions in the spleen suggest that asymptomatic, presumably viral, infections occur in rhesus monkeys after inoculation with material from patients with infectious mononucleosis.
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Using H-2 recombinant congenic strains of mice, genetic analysis of resistance to murine hepatitis virus type 3 (MHV3)-induced paralysis was performed. It appeared that both H-2K and H-2D, two class I gene regions of the mouse major histocompatibility complex (MHC), can play independent significant roles in the establishment of such resistance.
The symptomatology and histopathological picture were studied in weanling mice inoculated intracerebrally with MCMV and treated with ATS. Increased mortality was observed and fatal encephalopathy developed. Lesions in the brain included areas of necrosis with neuronal degeneration without marked inflammatory cell response until the 21st day after infection. In contrast, the brain of mice inoculated with virus alone or with virus and treated with NSH showed perivascular cuffs and focal infiltration with little or no evidence of loss of neurons. These observations suggest that the degenerative lesions in the brain are directly related to virus multiplication and that the inflammatory response is beneficial rather than detrimental.