For pathogens associated with acute and rapidly transmitting infections, their incidence, abundance and fitness depend not only on their ability to spread through a host population but also on their ability to maintain circulation. This dissertation will explore the conditions required for persistence of acute pathogens and the consequences for the pathogen's life history evolution by constructing models that abstract salient features of infection, transmission and competition dynamics.

We begin with a mechanistic model of within-host dynamics and link it to epidemiological models of disease transmission. The epidemic patterns and population level extinction risk for the pathogen can result in a trade-off, an invasion-persistence trade-off, between pathogen's abilities to spread in the host population and to maintain circulation in the host population. Depending on the shape of the dose-response curve and the host population size, we observe contrasting results—pathogen evolution driving itself to the brink of extinction or existence of evolutionarily stable intermediate pathogen growth rate. Two independent emergences of acute and short-lasting species of Bordetellae, B. pertussis and B. parapertussis as human pathogen, from milder but persistent B. bronchiseptica, can be understood in the light of this trade-off.

In an individual based framework, we extend this model to include structure in the host population, stochasticity in demographic and transmission processes, and explicit competition between pathogen strains. We find that the evolutionary dynamics are strongly influenced by the structure of the host population. When the host interactions are localized, pathogen traits that optimize the recruitment of susceptibles (maximize R₀), are no longer favored. Instead, pathogens that produce larger and longer-lasting epidemics in their local communities (maximize patch-level R ₀) are favored.

We further construct an analytical model that abstracts meta-population epidemic dynamics, and within-patch strain competition. For acute pathogens that reside in locally small host populations that exhibit episodic behavior, a pathogen's ability to compete for susceptibles and its ability to colonize patches are in conflict. We find that migration rate and patch-size affect the meta-population epidemic dynamics, and consequently the frequencies of competition and colonization interactions—the proportion of which determines the evolutionarily stable pathogen traits.