Staff Publications

Staff Publications

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    'Staff publications' is the digital repository of Wageningen University & Research

    'Staff publications' contains references to publications authored by Wageningen University staff from 1976 onward.

    Publications authored by the staff of the Research Institutes are available from 1995 onwards.

    Full text documents are added when available. The database is updated daily and currently holds about 240,000 items, of which 72,000 in open access.

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Record number 371539
Title TSE pathogenesis in cattle and sheep
Author(s) Keulen, L.J.M. van; Bossers, A.; Zijderveld, F.G. van
Source Veterinary Research 39 (2008)4. - ISSN 0928-4249 - 12 p.
Department(s) CVI - Division Virology
CVI - Divisie Bacteriologie en TSE's
Publication type Refereed Article in a scientific journal
Publication year 2008
Keyword(s) bovine spongiform encephalopathy - follicular dendritic cells - scrapie-infected sheep - gut epithelial monolayers - disease-specific prp - natural scrapie - prion protein - immunohistochemical detection - lateral transmission - lymphoid-tissues
Abstract Many studies have been undertaken in rodents to study the pathogenesis of transmissible spongiform encephalopathies (TSE). Only a few studies have focused on the pathogenesis of bovine spongiform encephalopathy (BSE) and scrapie in their natural hosts. In this review, we summarize the most recent insights into the pathogenesis of BSE and scrapie starting from the initial uptake of TSE agents and crossing of the gut epithelium. Following replication in the gut-associated lymphoid tissues (GALT), TSE agents spread to the enteric nervous system (ENS) of the gut. Infection is then carried through the efferent fibers of the post-ganglionic neurons of the parasympathetic and sympathetic nervous system to the pre-ganglionic neurons in the medulla oblongata of the brain and the thoracic segments of the spinal cord. The differences between the pathogenesis of BSE in cattle and scrapie in sheep are discussed as well as the possible existence of additional pathogenetic routes.
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