Please use this identifier to cite or link to this item: https://hdl.handle.net/2440/5505
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dc.contributor.authorFinnie, J.-
dc.date.issued2004-
dc.identifier.citationAnaerobe, 2004; 10(2):145-150-
dc.identifier.issn1075-9964-
dc.identifier.issn1095-8274-
dc.identifier.urihttp://hdl.handle.net/2440/5505-
dc.description.abstractAlthough the epsilon toxin of Clostridium perfringens type D produces disease in many species of domestic livestock, neurological disturbance is more common and better studied in sheep. High levels of circulating toxin, especially in lambs, cause cerebral microvascular endothelial damage with disruption of the blood-brain barrier leading to a severe, diffuse vasogenic oedema and an acute or peracute clinical course to death. With lower toxin levels, or in partially immune sheep, a focal, bilaterally symmetrical encephalomalacia sometimes occurs in selectively vulnerable brain regions after a more protracted clinical course, but the pathogenesis is uncertain.-
dc.language.isoen-
dc.publisherAcademic Press Ltd-
dc.source.urihttp://dx.doi.org/10.1016/j.anaerobe.2003.08.003-
dc.titleNeurological disorders produced by Clostridium perfringens type D epsilon toxin-
dc.typeJournal article-
dc.identifier.doi10.1016/j.anaerobe.2003.08.003-
pubs.publication-statusPublished-
dc.identifier.orcidFinnie, J. [0000-0003-2277-1693]-
Appears in Collections:Aurora harvest 5
Pathology publications

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