Abstract
Clostridium perfringens type D epsilon toxin (ETX) causes severe retinal microvascular endothelial injury in the rat. The resulting blood-retinal barrier (BRB) breakdown leads to increased vascular permeability, which was detected immunohistochemically by the extravasation of plasma albumin as a vascular tracer, and ensuing severe, diffuse, vasogenic retinal oedema. This microvascular damage was also confirmed by a loss of endothelial barrier antigen, a marker of an intact BRB in rats. Since similar microvascular lesions are found in EXT-exposed laboratory rodent and sheep brains, and the BRB resembles the BBB, they are also likely to occur in the eyes of naturally epsilon-intoxicated sheep and goats, but this remains to be determined. Moreover, while retinal oedema is a common and important component of many human and veterinary ocular disorders, more effective treatments are required. Accordingly, the retinal vasogenic oedema reliably and reproducibly induced by ETX in rats provides a useful model in which to study the pathogenesis of retinal oedema development and evaluate its prevention or amelioration by putative pharmacological interventions.