In the early 1980s Anderson and May showed that parasite virulence (host mortality rate when infected) and parasite transmission are positively correlated because of their joint dependence on host exploitation (e.g. replication rate). This correlation often results in maximum parasite fitness at intermediate virulence, which has important implications for both parasite evolution and transmission. Anderson and May's observation has led to nearly four decades of work on the ecology and evolution of host-parasite interactions, which focuses on making either general predictions for a range of simplified host-parasite systems or detailed predictions for a single host-parasite system. Yet, despite decades of research, we know comparatively little about parasite evolution and transmission in heterogeneous and/or small host populations. Additionally, much previous work has distanced itself from empirical data, either by outpacing the collection of data or under-utilizing available data. My work focuses on the evolution and transmission of parasites in heterogeneous host populations; I rely on tradeoff theory, but adopt a case-study approach to maximize the use of empirical data. Using West Nile virus infections of birds I show that a continent-wide strain displacement event cannot be explained by current data (Chapter 2), and that transmission in heterogeneous host communities can be estimated using data from citizen scientists, laboratory experiments, and phylogenetic comparative analysis (Chapter 3). Using Myxoma virus infection of European rabbits, I show that tradeoff theory can help us to understand parasite evolution in host populations with heterogeneous secondary infection burden (Chapter 4). In Chapter 5 I show that poorly evolved parasites invading new host populations experience transient evolution away from optimal virulence. In addition to my biological focus, I emphasize clarity and rigor in statistical analyses, including the importance of appropriate uncertainty propagation, as well as reproducible science. / Thesis / Doctor of Philosophy (PhD) / In their work in the late 1970s and early 1980s, Anderson and May demonstrated that pathogen induced host harm and pathogen transmission ability are intimately linked. This work clearly showed that pathogens maximize their reproductive potential by causing some harm their hosts, contrary to the established belief that pathogens shouldn't harm their hosts at all. I extend this work to study pathogen evolution and transmission in heterogeneous host populations, using two model host-pathogen systems: birds infected with West Nile virus, and European rabbits infected with the myxoma virus, as well as a general model for the evolution of poorly adapted pathogens in small host populations. I show that pathogen transmission in heterogeneous host populations can be estimated using citizen science data, that pathogen transmission is lower in heterogeneous populations, and that pathogens invading naive host populations may experience short-term evolution to higher-than-optimal virulence, increasing infection burden.
| Identifer | oai:union.ndltd.org:mcmaster.ca/oai:macsphere.mcmaster.ca:11375/24586 |
| Date | January 2019 |
| Creators | Kain, Morgan |
| Contributors | Bolker, Benjamin, Biology |
| Source Sets | McMaster University |
| Language | English |
| Detected Language | English |
| Type | Thesis |
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