Thesis (Ph.D.) - Indiana University, Biology, 2017Parasites comprise a striking diversity of lifeforms, and probably evolved from free-living organisms many times. It has even been argued that most species on earth are parasites. Parasites can have profound effects on their hosts, and the biology of hosts, in turn, affects the evolution and spread of parasites. My dissertation research examined the effects of parasites on the physiology, behavior, and breeding systems of their hosts, as well as the effects of host physiology and behavior on parasitism. In chapters one and two, I focused on the disease ecology of a natural system: haemosporidian (blood) parasites and an avian host, the dark-eyed junco. In chapter one, I measured the association between junco long-distance migration behavior and infection with haemosporidian parasites. I found that a migrant population of juncos maintains a significantly lower prevalence of haemosporidian parasite infections relative to a closely related and seasonally sympatric sedentary junco population, suggesting that longdistance host migration may be associated with reduced parasitism. In chapter two, I showed that experimental elevation of circulating testosterone levels in hosts does not affect the prevalence of haemosporidian parasite infections in a wild population of juncos, and that haemosporidian infections do not affect host telomere degradation. I also showed that the prevalence of haemosporidian parasite infections increases with host age. In chapters three and four, I used an experimental host-parasite system in the lab to assess how coevolving parasites affect the breeding system of their hosts. In chapter three, I showed that coevolving bacterial parasites (Serratia marcescens) can constrain the spread of self-fertilization into obligately outcrossing populations of nematode (Caenorhabditis elegans) hosts. This result supports the Red Queen hypothesis and contributes to a large body of evidence that antagonistic coevolution between hosts and parasites can maintain biparental sex. Finally, in chapter four, I showed that the presence of parasites (S. marcescens) in the environment does not induce plastic changes in the propensity to outcross in hosts (C. elegans) capable of both outcrossing and self-fertilization, and that coevolutionary interactions with S. marcescens parasites does not cause C. elegans hermaphrodites to evolve a higher propensity to outcross.