ainable in somefraction of parasite-host interactions, many hosts (such as B. Glabrata)cannot participate indeterminately. An alternative explanation for the reducedvirulence of congruently evolved hosts and parasites is the prudent parasitehypothesis (Esch and Fernandez 1993), in which parasitic virulencedecreases in response to host mortality. Parasites which are too virulent drivetheir hosts, and themselves, to extinction. Parasites which are less virulentpersist in the host population. The prudent parasite hypothesis helps toaccount for the variation in coevolutionary outcome by linking host populationdynamics with virulence, but it fails to describe the individual selective forceswhich modulate virulence over time. The prudent parasite hypothesis servesas the theoretical framework in which the factors determining parasiticvirulence can be synthesized. Antia et al. (1993) and Lenski and May (1994)propose a tradeoff between transmissibility and induced host mortality whichpredicts that parasites will evolve toward a level of virulence which strikes anequilibrium in the parasite-host system. Equilibrium models suggest that P.intestinalis, which evolved a higher (yet appropriate) level of virulence in itshost (Ebert 1994), is a prudent parasite. Antia et al. (1993) use an equationdeveloped by May and Anderson in 1983 to examine the tradeoffs inparasite-host interaction: Ro = (BN) / (a + b + v). Ro is the net reproductiverate of a parasite, B is the rate parameter for transmission, N is host density,a is the rate of parasite induced host mortality, b is the rate ofparasite-independent host mortality and v is the rate of recovery of infectedhosts. Parasite populations grow when transmission or host density increase,when host mortality decreases or when hosts recover slowly. Studies haveestablished a positive correlation between transmissibility (B) and hostmortality (a) (Ebert 1994, Antia et al. 1993, Lenski and May 1994). Parasitepopula...
