Premium
Pathogenesis of brain damage produced in sheep by Clostridium perfringens type D epsilon toxin: a review
Author(s) -
FINNIE JW
Publication year - 2003
Publication title -
australian veterinary journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.382
H-Index - 59
eISSN - 1751-0813
pISSN - 0005-0423
DOI - 10.1111/j.1751-0813.2003.tb11474.x
Subject(s) - clostridium perfringens , pathogenesis , toxin , microbiology and biotechnology , clostridium , medicine , biology , pathology , bacteria , genetics
Microvascular endothelial damage by the epsilon toxin of Clostridium perfringens type D appears to be the fundamental cause of cerebral parenchymal injury and lesions occur in a seemingly dose‐ and time‐dependent manner. Large doses of circulating toxin produce a severe, generalised, vasogenic cerebral oedema and an acute or peracute clinical course to death. With lower doses of toxin, or in partially immune sheep, focal necrosis, often bilaterally symmetrical, occurs in certain selectively vulnerable brain regions, which appear to become fewer as the toxin dose is reduced. These cases follow a more protracted clinical course, but death is the usual outcome. The precise pathogenesis of the focal brain damage found in subacutely intoxicated sheep is unresolved, but several possible mechanisms are discussed.