Abstract

Ninety-eight deer mice ( Peromyscus maniculatus) were infected with 1 × 10 3 Trypanosoma equiperdum organisms. Infected mice died or were killed between 2 and 202 days after infection and brains were sectioned for light microscopic examination. Although the neuropathology varied in intensity, location and sometimes quality from mouse to mouse, the following pattern of neuropathological development was apparent: brain lesions were not apparent until day 25, and the mildest lesion consisted of meningeal thickening and proliferation of leptomeningeal cells followed by, or concurrent with lymphocyte, macrophage and plasma cell infiltration of the meninges and choroid plexus. The lesions progressed to parenchymal perivascular mononuclear cuffs (as early as day 42) that were often located in subcortical white and basal ganglia areas, although cuffs were seen in all areas of brain. Vacuolation of lower white matter, especially cerebellar white matter, was first seen at day 40 and was an inconstant finding in mice infected longer than 40 days. Trypanosomes were found in arterioles and venules, perivascularly in choroid plexus and meninges, and within brain parenchyma, but their location and presence was inconstant. T. equiperdum infection of deer mice induces a relatively consistent laboratory animal model of human trypanosomal encephalitis.

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