| dc.description.abstract | Pathogen spillover to novel hosts represents a huge selective event, and can result in rapid evolutionary changes in both the pathogen and the host. However, it is seldom possible to identify which specific host characteristics are under selection following emergence, nor understand the evolutionary repercussions of these changes. In the early 1990’s, Mycoplasma gallisepticum emerged in North American house finches (Haemorhous mexicanus) following a jump from poultry. Previous studies monitoring disease spread and response to infection provided details of temporal and geographic patterns of host history of exposure, including evidence of the evolution of resistance in populations with a long history of exposure. In this thesis, I explore the specific host responses that were subject to selection following disease emergence in coevolved, relative to unexposed populations and evaluate how this led to the qualitative disease dynamics previously observed. In chapter one, I show that susceptibility to infection must be equal in both susceptible and resistant host genotypes in order for selection to occur, with mortality avoidance most likely driving the mode and tempo of rapid selection on resistance and virulence evolution observed in this system. In the second chapter, I find limited evidence for a protective benefit of a commonly measured immune component: systemic antibody, and show other important immune processes that are involved in host resistance, including an avoidance of immune manipulation. Findings presented here demonstrate the importance of the specific mechanism of host responses in determining evolutionary trajectories. | en_GB |
