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Mink that were homozygous recessive for the Aleutian gene (aa) were inoculated with Aleutian disease virus (ADV) and simultaneously treated with cyclophosphamide (Cy). Control mink were inoculated with ADV. All mink were injected with bovine serum albumin (BSA) and their anti-BSA antibody response was measured to monitor the influence of drug therapy on the humoral antibody response. Formation of anti-BSA antibody was markedly suppressed and the hypergammaglobulinemia and development of AD lesions was inhibited in the Cy-treated mink. The non-Cy-treated control mink developed characteristic signs and lesions including glomerulonephritis and arteritis. The nontreated ADV-infected mink, but not the Cy-treated ADV-infected mink, had glomerular deposition of C3 and gamma globulin. Both groups had high titers of virus in their blood. These results indicate that the development of ADV lesions can be prevented by immunosuppressive treatment and further implicate host immune mechanisms in the pathogenesis of Aleutian disease.

Primary horse leukocyte cultures were inoculated with 2 or 10 50% tissue culture infective doses (TCID(50)) of equine infectious anemia (EIA) virus per cell, and the titer of cell-associated and fluid-phase virus was determined from 1 to 72 hr postinoculation (PI). Cover slips were collected from 4 to 72 hr PI and stained for EIA viral antigen by the indirect immunofluorescent (FA) technique. Viral replication was detected after a latent period of approximately 18 to 24 hr and reached peak titers of approximately 10(4.5) to 10(6) TCID(50)/0.5 ml from 48 to 72 hr PI. The fluid phase contained 10(1) to 10(2) TCID(50)/0.5 ml more virus than the cells. Viral antigen was first detected by FA from 18 to 24 hr PI. Approximately 75% of the cells contained antigen in their cytoplasm 72 hr PI. The FA technique is a sensitive method for detecting EIA virus in horse leukocyte cultures.

Rabbits were poisoned by the intraperitoneal injection of plasmocid dihydroiodide at a dosage of 80 mg. per kg. body weight. Animals were euthanatized 1, 2, 5, 7, 9, 12, 24 and 48 hours after plasmocid injection and serum and diaphragmatic muscle collected. The serum was examined for its serum glutamic oxalacetic transaminase (SGOT) and creatine phosphokinase (CPK) concentrations. The diaphragm was sectioned and examined for the progression of morphologic alterations. It was found that SGOT and CPK concentrations were similar in their time and duration of elevation and that the serum CPK elevations closely paralleled the occurrence and degree of morphologic muscle degeneration. It appears that CPK is the most specific clinical biochemical test for the detection of muscle necrosis available at this time.