the former with modulate, which emphasizes the need for an inclusive, predictive paradigm for parasite-host interaction. Evolutionary history and mode of transmission will first be considered separately, then integrated using an equation discussed by Antia et al. (1993) and a model proposed by Lenski and May (1994).Transmission is a spatial factor, defined by host density and specific qualitiesof host-parasite interaction, which gives direction to the modulation ofvirulence. Evolution is a temporal factor which determines the extent of themodulation. The selective pressures of the transmission mode act on parasitepopulations over evolutionary time, favoring an equilibrium level of virulence(Lenski and May 1994). DOES COEVOLUTION DETERMINE VIRULENCE? Incongruent evolution is the colonization of a new host species by a parasite. It is widely reported that such colonizations, when successful, feature high virulence due to the lack of both evolved host defenses and parasitic self-regulation (Esch and Fernandez 1993, Toft et al. 1991). Unsuccessful colonizations must frequently occur when parasites encounter hosts with adequate defenses. In Africa, indigenous ruminants experience low virulence from Trypanosoma brucei infection, while introduced ruminants suffer fatal infections (Esch and Fernandez 1993).There has been no time for the new host to develop immunity, or for theparasite to self-regulate. Virulent colonizations may occur regularly inepizootic-enzootic cycles. Sin Nombre virus, a hemmorhagic fever virus, wasepizootic in 1993 after the population of its primary enzootic host,Peromyscus maniculatus, had exploded, increasing the likelihood oftransmission to humans (Childs et al. 1995). Sin Nombre exhibited unusuallyhigh mortality in human populations (Childs et al. 1995), which were beingcolonized by the parasite. It is assumed that coevolution of parasite and hostwill result in decreased virulence (Esch and Fernandez 1993, Toft et a...
