A genetic approach has been used to define the molecular basis for the different patterns of virulence and central nervous system cell tropism exhibited by reovirus types 1 and 3. Intracerebral inoculation of reovirus type 3 into newborn mice causes a necrotizing encephalitis (without ependymal damage) that is uniformly fatal. Animals inoculated with reovirus type 1 generally survive and may develop ependymal cell damage (without neuronal necrosis) and hydrocephalus. Using recombinant clones derived from crosses between reovirus types 1 and 3, we have been able to determine that the SI genome segment is responsible for the differing cell tropism of reovirus serotypes and is the major determinant of neurovirulence. The type 1 S1 genome segment is responsible for ependymal damage with subsequent hydrocephalus; the type 3 SI genome segment is responsible for neuronal necrosis and neurovirulence. We postulate that these differences are due to the specific interaction of the al outer capsid polypeptide (the protein coded for by the SI genome segment) with receptors on the surface of either ependymal cells or neuronal cells.

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Sprague-Dawley rats have a marked age-related susceptibility to Haemophilus influenzae type b that does not correlate with serum bactericidal activity. Eighty percent of 5-day-old animals that survive to 48 h after an intraperitoneal inoculation of a mean lethal dose of bacteria have histologically documented meningitis. Animals surviving the inoculations as infants manifest cerebral dysfunction as adults. This model should facilitate experimental study of bacterial meningitis.

Telencephalic white matter of the neonatal kitten frequently contained diffuse astrogliosis or focal necrosis (sometimes including the thalamus and the caudate) following a single intraperitoneal injection of Escherichia coli lipopolysaccharide. No evidence for a disseminated intravascular coagulopathy was found. Telencephalic lesions in neonatal monkey and rabbit were also hemorrhagic. Enhanced karyorrhexis of glial nuclei was presented in the telencephalic white matter of the neonatal rat. In the kitten, a delay in the generation of macrophages and hypertrophic astrocytes occurs following transient neonatal endotoxemia. Marked weight loss and temperature fluctuation are prominent systemic effects. Large hemispheric cavitary lesions are not accompanied by obvious neurological deficits in the kitten.