Clostridium perfringens Type D Epsilon Toxin Causes Blood–Retinal Barrier Microvascular Damage and Diffuse Retinal Vasogenic Oedema

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.