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Pathogenesis of BSE.

G A H Wells1

  • 1Veterinary Laboratories Agency, New Haw, Addlestone, Surrey KT15 3NB, UK.

Veterinary Research Communications
|October 11, 2003
PubMed
Summary
This summary is machine-generated.

Scrapie pathogenesis in rodents shows initial agent replication in lymphoreticular system (LRS) tissue, followed by spread via peripheral nervous system (PNS) pathways to the central nervous system (CNS). Generalizing findings requires caution due to host- and agent-dependent factors.

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Area of Science:

  • Veterinary Neurology
  • Infectious Diseases
  • Prion Biology

Background:

  • Scrapie was the primary animal transmissible spongiform encephalopathy (TSE) before bovine spongiform encephalopathy (BSE).
  • Natural scrapie transmission is limited to sheep and goats.
  • Experimental models in rodents are crucial for studying scrapie pathogenesis.

Purpose of the Study:

  • To elucidate the pathogenesis of scrapie, particularly the routes of agent spread within the host.
  • To understand the initial sites of replication and pathways to the central nervous system (CNS).
  • To assess the relevance of experimental findings to natural TSE infections in ruminants.

Main Methods:

  • Studies primarily utilized experimental rodent models of scrapie.

Related Experiment Videos

  • Infection routes included peripheral non-neural exposures.
  • Pathogenesis was investigated by tracking agent replication in various tissues, including lymphoreticular system (LRS) and nervous system tissues.

    • Main Results:

    • Following peripheral infection, scrapie agent replication is first detected in lymphoreticular system (LRS) tissues.
    • Significant agent amplification occurs in the LRS, with dissemination via lymphatic/hematogenous routes.
    • Evidence suggests the CNS is infected via peripheral nervous system (PNS) pathways, potentially involving the gut-associated lymphoid tissue (GALT) and autonomic nervous system in orally infected models.

    Conclusions:

    • Scrapie pathogenesis in experimental models involves initial LRS replication and subsequent CNS invasion via PNS pathways.
    • Host and agent factors influence TSE spread, limiting direct extrapolation from models to natural infections.
    • Increased awareness of BSE transmission highlights the importance of the oral route in ruminant TSEs, prompting focus on natural host studies.