The pathogenesis of epizootic hemorrhagic disease of deer: an electron microscopic study

Ultrastructural studies on capillaries and arterioles from tongue and heart tissues of 3 deer and from a portion of the cerebral hemisphere of a deer experimentally infected with epizootic hemorrhagic disease (EHD) virus revealed striking changes in the vascular endothelial cells. These changes included the focal development of moderately electron-dense materials (viral matrices), aggregations of virus particles and tubules in the cytoplasm. In addition, enlargement of endothelial cells and degenerative changes in some of the endothelial cells were frequently observed. The lumens of affected capillaries and arterioles were often noted to be occluded by fluffy, moderately electron-dense substances or by aggregates of highly electron-dense fibrin which appeared to be adherent to the surface of endothelial plasma membrane. Platelets were frequently present in the capillaries, intermingled with fibrin materials, and appeared either intact or partially or completely degranulated. These observations suggest that viral injury to endothelial cells resulting from EHD virus replication may initiate intravascular thrombosis, and that the hemorrhagic lesion is a manifestation of virus-cell interaction.