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Updated: May 1, 2026

A Mouse Model of Retinal Ischemia-Reperfusion Injury Through Elevation of Intraocular Pressure
Published on: July 14, 2016
Retinal microvascular damage and vasogenic edema produced by Clostridium perfringens type D epsilon toxin in rats
John W Finnie1, Jim Manavis2, Robert J Casson2
1SA Pathology (Finnie, Manavis), Hanson Institute Centre for Neurological Diseases, Adelaide, South Australia, AustraliaOphthalmic Research Laboratories, South Australian Institute of Ophthalmology (Casson, Chidlow), Hanson Institute Centre for Neurological Diseases, Adelaide, South Australia, AustraliaSchool of Veterinary Science (Finnie), University of Adelaide, Adelaide, South Australia, AustraliaDepartment of Ophthalmology and Visual Sciences (Casson, Chidlow), University of Adelaide, Adelaide, South Australia, Australia john.finnie@health.sa.gov.au.
Abstract:
When the brain is exposed to large circulating levels of Clostridium perfringens type D epsilon toxin (EXT), microvascular damage with resulting severe, generalized, vasogenic edema seems to be principally responsible for the ensuing acute, and frequently fatal, neurologic disorder. However, although the blood-retinal barrier resembles in many respects the blood-brain barrier, retinal changes in livestock with acute epsilon intoxication have not, to the authors' knowledge, been previously reported. In rats given an acute dose of ETX, retinal microvascular endothelial injury led to widespread vasogenic edema as assessed immunohistochemically by marked plasma albumin extravasation. As laboratory rodents are a good model of the domestic livestock disease produced by ETX, it is probable that the latter sustain some visual deficit when exposed to large doses of this potent neurotoxin.

