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The onset of growth retardation was investigated in fetal lambs following experimental infection of pregnant ewes with Border Disease virus (BDV) on day 53 of pregnancy. Fetuses from control and infected ewes were harvested at weekly intervals between day 60 and day 95 of gestation and morphometric studies were completed on tibial radiographs and tibial growth cartilage metaphyseal junctions. Mean tibial areas were significantly reduced (P < 0.01) in fetuses from infected ewes at 35 and 42 days after infection and growth cartilage metaphyseal junctions were less mature in fetuses from infected ewes at 42 days after infection. Positive immunostaining for BDV antigen was demonstrated in the brains of all fetuses from infected ewes between 14 and 42 days after infection. Attempts to demonstrate BDV antigen in bone proved unsuccessful. It is concluded that intrauterine growth retardation is an early manifestation of BDV infection in lambs and that the process is initiated shortly following infection of the fetus.

Immunogold-silver staining of mixed rat cerebellar neuron/glial cell cultures, using Ranscht monoclonal antibody, resulted in labelling of neuronal processes and oligodendrocytes. This antibody was originally believed to react with galactocerebroside alone, and it was concluded that labelling by it resulted from the presence of myelin [2]. Electron microscopic examination of the cultures did not reveal myelination. Infection of such cultures with rubella virus resulted in a cytopathic effect. This effect was initially characterized as a disaggregation of neuronal processes, and the disruption of a layer of membranous material covering both cell bodies and processes. The virus causes disruption of cultures of pure glial cells, but there is no evidence of virus multiplication or cytopathic effect in pure neuron cultures. The cytopathic effect in mixed neuron/glial cell cultures is concluded to be glial cell mediated.

Degenerative lesions in the spinal cord white matter of 12 English Foxhounds and two Harriers between 3 and 6 years old were associated with a diet composed mainly of ruminant stomachs. Lesions were present throughout the length of the spinal cord and were more severe in ventral and lateral columns than in dorsal columns. Degenerate fibers were accompanied by astrocytic proliferation. Changes suggestive of a primary myelinopathy included vacuolated myelin sheaths around apparently intact axons and thick-thin transitions in myelin sheath thickness. Mixed sensory and motor peripheral nerves and muscle histochemical fiber type profiles appeared normal. Similarities were noted with the changes described in subacute combined degeneration of the spinal cord in human beings, a neuropathy caused by methionine and methylation deficiency in patients with vitamin B12 deficiency. Mean serum methionine levels were significantly lower (P greater than 0.01) and mean liver methionine synthetase levels were significantly greater (P greater than 0.01) in affected dogs restored to a balanced diet than in age-matched controls maintained on the balanced diet. The elevated methionine synthetase levels possibly reflected compensatory reactions to the associated dietary change.

Intraperitoneal inoculation with the M9 mutant of Semliki Forest virus caused focal demyelinating encephalomyelitis in weanling BALB/c and C57BL/6 mice. Demyelination was more severe in BALB/c than in C57BL/6 mice. Virus particles were seen in oligodendrocytes in areas of myelin vacuolation 5 and 7 days post inoculation (DPI). Oligodendrocytes containing virus in BALB/c mice showed hypertrophy and vacuolar degeneration. There was a mononuclear cell infiltrate and lymphocytes and necrotic cells were present in vacuoles in myelin sheaths. Demyelinating plaques containing macrophages laden with myelin debris were most prominent 14 DPI when virus was cleared from the brain. Remyelination of the central type occurred 28 DPI in BALB/c mice. These findings indicate that direct virus-induced injury to oligodendrocytes has a major role in the initiation of inflammation and demyelination in this model system.