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Pathogenesis of experimental scrapie.

R H Kimberlin¹, C A Walker

¹AFRC & MRC Neuropathogenesis Unit, Edinburgh, UK.

Ciba Foundation Symposium

|January 1, 1988

Summary

Scrapie pathogenesis involves the lymphoreticular system (LRS) before the central nervous system (CNS), with slow spread limiting disease progression. This study explores the mechanisms behind the slow development of scrapie infections.

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Area of Science:

Neuroscience
Infectious Diseases
Pathogenesis Research

Background:

Understanding unconventional slow infections like scrapie relies on animal models.
Scrapie pathogenesis in peripheral inoculation models involves the lymphoreticular system (LRS) before the central nervous system (CNS).

Purpose of the Study:

To elucidate the pathogenesis of experimental scrapie, focusing on the sequential involvement of the LRS and CNS.
To investigate the mechanisms contributing to the slow progression of scrapie disease.

Main Methods:

Studies utilized experimental scrapie models in mice and hamsters with non-neural peripheral injections.
Pathogenesis was tracked through the lymphoreticular system (LRS) and central nervous system (CNS) involvement.

Main Results:

Infection spreads hematogenously to the LRS, then via autonomic nerves to the CNS.
Long-lived cells in the LRS are crucial; neuroinvasion and CNS spread likely use neuronal pathways.
Disease onset correlates with functional damage in CNS target areas, not just initial infection.
Infectivity plateaus in LRS and CNS precede neuroinvasion and clinical disease, indicating restricted replication.

Conclusions:

The slow progression of scrapie is attributed to limited cell-to-cell spread from LRS to CNS.
Restrictions on neuronal spread and replication within the brain further contribute to the disease's slowness.

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