Pathogenesis of BSE

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Abstract
Before the emergence of bovine spongiform encephalopathy (BSE) and recognition of its zoonotic potential, the major example of the transmissible spongiform encephalopathies (TSEs) of animals was scrapie of sheep. But there is no evidence that scrapie transmits naturally to any species other than sheep and goats. The pathogenesis of scrapie has been studied most in experimental laboratory rodent species. In most experimental models of scrapie, after peripheral non-neural routes of infection, replication of the agent can first be detected in lymphoreticular system (LRS) tissue. When the route of introduction of agent into the body is localized, initial involvement will be in LRS tissue draining the infection site. Thereafter, there is a striking amplification of the agent in the LRS and spread by lymphatic/haematogenous routes, giving widespread dissemination in the LRS. This precedes replication in the CNS, but is not the means by which infection reaches the CNS. There is now substantial evidence from experimental models of scrapie that involvement of the CNS is by peripheral nervous system (PNS) pathways. In some models employing oral exposure the earliest localized LRS replication is in the gut-associated lymphoid tissue (GALT) and autonomic PNS routing to the CNS has been implicated. However, the relative importance of different routes of spread of TSEs within the body is determined by a number of host- and agent-dependent factors and, therefore, generalizations from an experimental model to a natural disease across a species barrier may not be appropriate. With the occurrence of BSE and recognition of its food-borne route of transmission via meat and bone meal, has come greater awareness of the probable importance of the oral route of infection in ruminant species affected by TSEs. In consequence, studies have increasingly focused on the natural host species to examine pathogenetic events.