Host ontogeny and parasites: Implications for epidemic size, stage structure, sex, and population dynamics

A central goal in ecology is to understand the factors that drive variation in the abundance and distribution of species. The field of community ecology has made great strides in uncovering the mechanisms driving much of this variation. Still, natural systems frequently behave quite differently than simple models often anticipate. This model-nature contrast suggests that our models lack key biology. I demonstrate that current models miss key features of population and disease dynamics because they overlook parasites and stage-specific traits of hosts.;Chapters I-III connect asymmetric effects of parasites on larger adult hosts to changes in the stage, stability, and reproductive structure of host populations (as shown over multi-year field surveys and multiple mesocosm experiments). First, to identify the mechanisms linking parasites, host traits, and population-level changes we built a stage-structured model of disease. The model revealed that parasites altered key relationships between juveniles and adults (resource competition). These relationships drove dynamic feedbacks between resources and resource-dependent life history traits (reproduction and development) and altered population structure and stability. Next, in Chapter III, across a multi-year field survey and a field-deployed mesocosm experiment, hosts appeared to increase population-level allocation to sex during fungal epidemics. Using a combination of field patterns, experiments, and a size-based model of infection risk, we eliminated one hypothesis (that males were resistant and escaped culling from parasites). Instead, infected female hosts shifted energetic allocation from asexual to sexual reproduction.;Finally, Chapter IV, examined habitat-disease links through direct effects on parasites/hosts and indirect effects on non-host species that drove disease. Multi-year field surveys and an in-situ experiment revealed that a potent environmental constraint (UVR) was overwhelmed by indirect effects from (1) food-web links yielding net parasite gains due to lower densities of UVR-sensitive predators of parasites; (2) community composition of hosts, and (3) host stage structure.;Together, this research highlights that parasites play a role in structuring natural populations and host population structure shapes parasite epidemics. Ultimately, theory that explicitly considers parasites and stage-specific host traits within a larger food web context can yield new insight into the forces that govern variation across natural populations.