van Keulen Lucien J M, Bossers Alex, van Zijderveld Fred
Department of Bacteriology and TSE's, Central Institute for animal Disease Control , Wageningen University and Research Centre, 8203 AA Lelystad, the Netherlands.
Vet Res. 2008 Jul-Aug;39(4):24. doi: 10.1051/vetres:2007061. Epub 2008 Feb 8.
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.
已经在啮齿动物身上开展了许多研究，以研究传染性海绵状脑病（TSE）的发病机制。只有少数研究关注牛海绵状脑病（BSE）和羊瘙痒病在其自然宿主中的发病机制。在本综述中，我们总结了从TSE病原体的最初摄取和穿过肠道上皮开始，对BSE和羊瘙痒病发病机制的最新见解。在肠道相关淋巴组织（GALT）中复制后，TSE病原体扩散到肠道的肠神经系统（ENS）。然后，感染通过副交感神经系统和交感神经系统节后神经元的传出纤维，传播到脑延髓和脊髓胸段的节前神经元。文中讨论了牛BSE和羊瘙痒病发病机制之间的差异，以及可能存在的其他致病途径。
