h and Fernandez 1993). A high level of virulence persists in the system because the snail cannot afford to mount an adequate defense. The arms race hypothesis assumes that the host population can successfully counter increasing parasitic virulence with resistance over an extended period of time. Although an arms race may be sustainable in some fraction of parasite-host interactions, many hosts (such as B. Glabrata) cannot participate indeterminately. An alternative explanation for the reduced virulence of congruently evolved hosts and parasites is the prudent parasite hypothesis (Esch and Fernandez 1993), in which parasitic virulence decreases in response to host mortality. Parasites which are too virulent drive their hosts, and themselves, to extinction. Parasites which are less virulent persist in the host population. The prudent parasite hypothesis helps to account for the variation in coevolutionary outcome by linking host population dynamics with virulence, but it fails to describe the individual selective forces which modulate virulence over time. The prudent parasite hypothesis serves as the theoretical framework in which the factors determining parasitic virulence can be synthesized. Antia et al. (1993) and Lenski and May (1994) propose a tradeoff between transmissibility and induced host mortality which predicts that parasites will evolve toward a level of virulence which strikes an equilibrium in the parasite-host system. Equilibrium models suggest that P. intestinalis, which evolved a higher (yet appropriate) level of virulence in its host (Ebert 1994), is a prudent parasite. Antia et al. (1993) use an equation developed by May and Anderson in 1983 to examine the tradeoffs in parasite-host interaction: Ro = (BN) / (a + b + v). Ro is the net reproductive rate 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 rat...
