Thesis (Ph.D.) - Indiana University, Biology, 2016The dilution effect is an intriguing, emerging pattern in the community ecology of disease. This pattern links losses of species diversity with elevated disease risk across a wide variety of human, wildlife, and plant disease systems. However, the dilution effect remains controversial. In most cases, it is unclear which ‘diluter’ taxa drive the pattern, when and how they reduce disease, and why disease dilution can depend on the metric of disease being considered (e.g., infection prevalence vs. density of infected hosts). Here, I develop a predictive, mechanistic framework for the dilution effect in a zooplankton-fungus model system. I uncover which diluters drive this pattern, how and when they reduce disease, and how different mechanisms reduce each metric of disease. In chapter one, I detect a correlation between diversity and disease in nature, but reveal that this pattern is driven by a key diluter taxa. The focal host here and throughout, Daphnia dentifera, is a dominant planktonic grazer in many North American freshwater lakes. It often experiences autumnal epidemics caused by the virulent fungus Metschnikowia bicuspidata. Epidemics are smaller in lakes with higher zooplankton diversity, supporting a dilution effect pattern. However, path models reveal that one key diluter taxa (i.e., “small spore predators”), Ceriodaphnia sp., drives this pattern by biasing the index of diversity. Furthermore, these key diluters strongly reduce disease themselves, even though their impacts are embedded within a complex food web. Thus, these diluters drive the dilution effect pattern in nature, especially in lakes with smaller refuges, more intense fish predation, and fewer insect predators. In chapter two, I bring these key competitor/diluters into the laboratory and test whether they reduce the size of experimental epidemics in focal hosts. At the local scale, these competitor/diluters could reduce disease by consuming parasites (reducing encounters between focal hosts and parasites, without becoming infected), or competing with focal hosts for resources (lowering focal host density, and hence inhibiting density- dependent disease transmission). In a multi-generational mesocosm experiment, presence of competitor/diluters successfully reduces disease. However, in two additional case studies, the dilution effect fails and becomes irrelevant. Parameterized mechanistic models suggest that variation in focal hosts traits drives these divergent outcomes. Thus, while diluters can reduce disease at the local scale, their impacts are not guaranteed to support a dilution effect. In chapter three, I predict variation among these experimental outcomes from two focal host traits: competitive ability and disease risk. In a second mesocosm experiment, the strength of dilution (i.e., magnitude of reduced disease) is strongest for focal hosts with higher disease risk. However, diluters’ reduction of disease fades as focal hosts become more resistant. Disease dilution is also strongest for focal hosts that compete more weakly, since competitor/diluters become more numerous. Finally, path models reveal that diluters’ consumption of parasites reduces infection prevalence, but competition with focal hosts reduces the density of infected hosts. Thus, this framework, centered on variation in focal host traits, predicts how and when diluters reduce each metric of disease (infection prevalence vs. density of infected hosts). Finally, in chapter four, I grapple with the dangers of competition and disease for focal hosts interacting with competitor/diluters and parasites. In an eco-evolutionary mesocosm experiment, the combination of competition and disease dramatically lowers density of focal hosts, despite benefits of disease dilution. Nevertheless, rapid evolution of higher competitive ability in diverse populations of focal hosts buffers their densities from these negative impacts of competition and disease. Epidemics even accelerate this evolutionary response. However, while these rapidly evolving host populations maintain higher overall densities, they also maintain higher densities of infected hosts (especially when competitor/diluters are absent). Thus, rapid evolution of focal hosts can fundamentally alter costs and benefits of local interactions among focal hosts, parasites, and competitor/diluters. Although the dilution effect may remain controversial, my dissertation delineates several paths forward. I uncover which diluters drive a dilution effect pattern in nature, and emphasize the need to identify key diluter taxa in other disease systems. I discover how and when diluters reduce disease, and highlight the importance of focal host traits in regulating outcomes of the dilution effect. I reveal that different mechanisms can reduce infection prevalence and density of infected hosts, and stress the importance of a mechanistic framework for predicting these outcomes. Finally, I introduce rapid host evolution as an eco-evolutionary frontier of dilution effect research. Together, these four chapters develop and test a mechanistic framework for the dilution effect. This framework greatly increases power of the dilution effect paradigm.