Pathogenesis of bovine spongiform encephalopathy in sheep

L.J.M. van Keulen, M.E.W. Vromans, C.H. Dolstra, A. Bossers, F.G. van Zijderveld

    Research output: Contribution to journalArticleAcademicpeer-review

    53 Citations (Scopus)

    Abstract

    The pathogenesis of bovine spongiform encephalopathy (BSE) in sheep was studied by immunohistochemical detection of scrapie-associated prion protein (PrPSc) in the gastrointestinal, lymphoid and neural tissues following oral inoculation with BSE brain homogenate. First accumulation of PrPSc was detected after 6 months in the tonsil and the ileal Peyer¿s patches. At 9 months postinfection, PrPSc accumulation involved all gut-associated lymphoid tissues and lymph nodes as well as the spleen. At this time point, PrPSc accumulation in the peripheral neural tissues was first seen in the enteric nervous system of the caudal jejunum and ileum and in the coeliac-mesenteric ganglion. In the central nervous system, PrPSc was first detected in the dorsal motor nucleus of the nervus Vagus in the medulla oblongata and in the intermediolateral column in the spinal cord segments T7¿L1. At subsequent time points, PrPSc was seen to spread within the lymphoid system to also involve all non-gut-associated lymphoid tissues. In the enteric nervous system, further spread of PrPSc involved the neural plexi along the entire gastrointestinal tract and in the CNS the complete neuraxis. These findings indicate a spread of the BSE agent in sheep from the enteric nervous system through parasympathetic and sympathetic nerves to the medulla oblongata and the spinal cord
    Original languageEnglish
    Pages (from-to)445-453
    JournalArchives of Virology
    Volume153
    Issue number3
    DOIs
    Publication statusPublished - 2008

    Keywords

    • disease-specific prp
    • scrapie infection
    • natural scrapie
    • nervous-system
    • prion protein
    • bse agent
    • transmission
    • cattle
    • accumulation
    • mice

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