We report here an electron microscopic study of selected nervous system tissues from pigs infected experimentally with the agent of bovine spongiform encephalopathy (BSE). Generally, the ultrastructural neuropathology of BSE-affected pig brain resembled that of BSE-affected cattle brain. Spongiform change, in the form of membrane-bound vacuoles separated by septae into secondary chambers, dominated the pathology. Numerous astrocytic processes were visible in close conjunction with elongated microglial cells. Neuronal degeneration presented as either dystrophic neurites or by the formation of autophagic vacuoles. Altered subcellular organelles: mitochondria, electron-dense bodies, autophagic vacuoles, neurofilaments and “branching-cisterns” accumulated in abnormal neurites. Autophagic vacuoles appeared as neuronal cytoplasm of increased electron-density sequestrated by intracytoplasmic membranes. Tubulovesicular structures were numerous, particularly in the cerebellum. Unusual crystalloids were observed in the white matter. In conclusion, experimental BSE in pigs demonstrated ultrastructural pathology in keeping with that observed in other spongiform encephalopathies.
http://www.termedia.pl/Review-article-U ... 4,0,1.html
Review article Ultrastructural findings in pigs experimentally infected with bovine spongiform enc
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你吃豬肉能安心嗎?
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stockk
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stockk
- V2
- 文章: 2501
- 註冊時間: 週五 3月 18, 2011 8:58 am
Re: 你吃豬肉能安心嗎?
http://www.plosone.org/article/info:doi ... ne.0003017
Abstract Top
Background
Human variant Creutzfeldt-Jakob Disease (vCJD) results from foodborne transmission of prions from slaughtered cattle with classical Bovine Spongiform Encephalopathy (cBSE). Atypical forms of BSE, which remain mostly asymptomatic in aging cattle, were recently identified at slaughterhouses throughout Europe and North America, raising a question about human susceptibility to these new prion strains.
Methodology/Principal Findings
Brain homogenates from cattle with classical BSE and atypical (BASE) infections were inoculated intracerebrally into cynomolgus monkeys (Macacca fascicularis), a non-human primate model previously demonstrated to be susceptible to the original strain of cBSE. The resulting diseases were compared in terms of clinical signs, histology and biochemistry of the abnormal prion protein (PrPres). The single monkey infected with BASE had a shorter survival, and a different clinical evolution, histopathology, and prion protein (PrPres) pattern than was observed for either classical BSE or vCJD-inoculated animals. Also, the biochemical signature of PrPres in the BASE-inoculated animal was found to have a higher proteinase K sensitivity of the octa-repeat region. We found the same biochemical signature in three of four human patients with sporadic CJD and an MM type 2 PrP genotype who lived in the same country as the infected bovine.
Conclusion/Significance
Our results point to a possibly higher degree of pathogenicity of BASE than classical BSE in primates and also raise a question about a possible link to one uncommon subset of cases of apparently sporadic CJD. Thus, despite the waning epidemic of classical BSE, the occurrence of atypical strains should temper the urge to relax measures currently in place to protect public health from accidental contamination by BSE-contaminated products.
證實靈長類的獼猴也會 人類那跑得掉
日本歐洲和美國一樣有狂牛症跟台灣大不同 .禁了沒多大好處
台灣豬吃溲水.容意被感染
台灣要是進口造成台灣豬隻感染 台灣整個豬農產業可能會毀於一旦
不死也半條命. 禍害可大了
Abstract Top
Background
Human variant Creutzfeldt-Jakob Disease (vCJD) results from foodborne transmission of prions from slaughtered cattle with classical Bovine Spongiform Encephalopathy (cBSE). Atypical forms of BSE, which remain mostly asymptomatic in aging cattle, were recently identified at slaughterhouses throughout Europe and North America, raising a question about human susceptibility to these new prion strains.
Methodology/Principal Findings
Brain homogenates from cattle with classical BSE and atypical (BASE) infections were inoculated intracerebrally into cynomolgus monkeys (Macacca fascicularis), a non-human primate model previously demonstrated to be susceptible to the original strain of cBSE. The resulting diseases were compared in terms of clinical signs, histology and biochemistry of the abnormal prion protein (PrPres). The single monkey infected with BASE had a shorter survival, and a different clinical evolution, histopathology, and prion protein (PrPres) pattern than was observed for either classical BSE or vCJD-inoculated animals. Also, the biochemical signature of PrPres in the BASE-inoculated animal was found to have a higher proteinase K sensitivity of the octa-repeat region. We found the same biochemical signature in three of four human patients with sporadic CJD and an MM type 2 PrP genotype who lived in the same country as the infected bovine.
Conclusion/Significance
Our results point to a possibly higher degree of pathogenicity of BASE than classical BSE in primates and also raise a question about a possible link to one uncommon subset of cases of apparently sporadic CJD. Thus, despite the waning epidemic of classical BSE, the occurrence of atypical strains should temper the urge to relax measures currently in place to protect public health from accidental contamination by BSE-contaminated products.
證實靈長類的獼猴也會 人類那跑得掉
日本歐洲和美國一樣有狂牛症跟台灣大不同 .禁了沒多大好處
台灣豬吃溲水.容意被感染
台灣要是進口造成台灣豬隻感染 台灣整個豬農產業可能會毀於一旦
不死也半條命. 禍害可大了