Grossly, the brain and spinal cord are swollen with congested blood vessels. The histology of acute infections by different viruses is basically similar—variations occur mainly in the severity and distribution of lesions. General features are perivascular and diffuse mononu-clear cell infiltrations, neuronal or glial destruction, and the presence of intranuclear or intracytoplasmic viral inclusions. In meningitis, the subarachnoid space is filled typically with lymphocytes—mostly T-helper cells, fewer T-suppressor/cytotoxic cells, and B cells. In encephalitis and myelitis, the severity of perivascular cuffings varies: The parenchyma, in severe cases, may undergo necrosis (Fig. 6.7). Most viruses have an affinity for the neurons, or for both the neurons and the glial cells. The infected neurons are surrounded by clusters of polymorphonuclear cells, lymphocytes, activated microglial cells, and macrophages. The diseased neurons gradually disintegrate (lysis) and are phagocytosed by macrophages (neuronophagia). Eventually, residual microglial nodules (stars) replace the destroyed neurons (see Fig. 6.7).

Aggregates of viral particles may form inclusion bodies in the nucleus or cytoplasm of surviving neurons and glial cells. Cowdry type A inclusions are large, dense intranuclear eosinophilic bodies surrounded by a clear halo. Cowdry type B inclusions are small, often multiple, and lack a halo. Viral antigens are demonstrated using immunohistologic technique.


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Histologic features of viral meningoencephalitides. A. Mononuclear cell infiltrations in the subarachnoid space and vascular wall. B. Mononuclear cells and activated microglia invade the neurons (neuronophagia). C. Residual glial nodule takes the place of destroyed neurons (Cresyl violet).

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