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Parasites and their Virulence

e digenean D. spathaceum invades the eyes of sticklebacks, increasing the likelihood of successful predation by birds (Milinski 1990). D. dendriticum migrate to the brains of infected ants, causing them to uncontrollably clamp their jaws onto blades of grass, ensuring ingestion by sheep (Esch and Fernandez 1993, Combes 1991). Infection of a mammalian brain by rabies (Lyssavirus spp.) alters the host's behavior, increasing the chance of conflict with other potential hosts, while accumulation of rabies virus in the salivary glands ensures that it is spread by bites (Krebs, J. W. et al. 1995). Horizontally transmitted parasites which target nervous tissue increase transmissibility by modifying the host into a suicidal instrument of transmission. Transmission factors determining parasitic virulence are the spatial element in a spatial-temporal dynamic. Host density directly determines the virulence of parasites which depend upon a single host species (Herre 1993). Virulence may be increased when transmission necessitates insect vectors or consumption of the primary host by another species. Virulence varies inversely with the distance between potential hosts; this distance is magnified when it is measured between different species. THE EQUILIBRIUM MODEL It has been proposed that there is a coevolutionary arms race between parasite and host, as the former seeks to circumvent the defensive adaptations of the latter (Esch and Fernandez 1993). In this view, parasitic virulence is the result of a dynamic stalemate between host and parasite. This exemplifies the red queen hypothesis, which predicts continued stalemate until the eventual extinction of both species. Benton (1990) notes that the red queen hypothesis ignores the potential for compromise in such a system. Snails (Biomphalaria glabrata) resistant to Schistosoma mansoni are at a selective disadvantage due to the costs associated with resistance (Esc...

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