Many bacterial pathogens are exquisitely adapted to host parasitization. Their niche is primarily determined by the biochemical milieu of the host. As such, pathogens are selected to exhibit environmentally responsive and adaptive molecular traits which allow adherence, entrance, and rep-lication within the host (7, 26). One major set of selective forces which operates to shape the phenotype of the bacterial pathogen is the host immune system. The host immune response following contact with the pathogen is itself adaptive and seeks to eliminate or restrict bacterial replication. Thus, successful bacterial pathogens must be able to avoid or adapt to evolving host defenses. However, in order to persist within a niche over long periods of time, the pathogen not only must be able to survive within an individual host but also must be able to infect other hosts. To achieve ecologic success (ie, persistence in its niche within the host popu-lation), pathogens require mechanisms both for survival within hosts and transmission between hosts. The set of immune responses in the host population, which are determined by major histocompatibility complex (MHC) polymorphism and attendant antigen-specific T-and B-cell re-sponses, thus are a set of selective forces which act on the population of bacteria.

The evolutionary important quantity on which natural selection acts to shape the genotype-phenotype of a patho-gen is its basic reproductive rate, Ro (20). Ro is an epidemiologic concept and defines the average number of secondary infections an infected host produces in a fully susceptible population. Ro must equal or exceed 1 if the pathogen is to invade and persist in a host community. Natural selection will tend to maximize Ro for a given pathogen, and microbial attributes which enhance Ro are selected. This includes genes which encode attributes which enhance transmission or extend the duration of host infectivity. Because infectious discharges and other pathophysiologic changes in the in-fected host can substantially enhance transmission, patho-gen-induced disease may be viewed as one of the important mechanisms for between-host survival (19). Pathogens which reduce thelife span and/or affect the fertility of individualhosts may also exert selection on host populations (9). Over evolutionary time, pathogens can select host traits that reduce the impact of microbial patho-gens on host life span and fertility (1, 12, 18). Thus, success-ful pathogens can be seen to be engaged in a dynamic coevolutionary interaction with their host population. Two