Finnie John W, Manavis Jim, Casson Robert J, Chidlow Glyn
SA 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
SA 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.
J Vet Diagn Invest. 2014 May;26(3):470-472. doi: 10.1177/1040638714530127. Epub 2014 Apr 16.
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.
当大脑暴露于循环中高水平的产气荚膜梭菌D型ε毒素(EXT)时,微血管损伤以及由此导致的严重、全身性血管源性水肿似乎是随后发生的急性且常常致命的神经疾病的主要原因。然而,尽管血视网膜屏障在许多方面类似于血脑屏障,但据作者所知,急性ε中毒家畜的视网膜变化此前尚未见报道。给大鼠急性注射ETX后,视网膜微血管内皮损伤导致广泛的血管源性水肿,通过显著的血浆白蛋白外渗进行免疫组织化学评估可证实这一点。由于实验啮齿动物是ETX所致家畜疾病的良好模型,因此当家畜暴露于大剂量这种强效神经毒素时,很可能会出现一些视觉缺陷。