Species declines and extinctions have been recorded across taxa as evidence of an ongoing global biodiversity crisis. Amphibians are at the forefront of these declines with nearly one third of amphibian species estimated to be at risk of extinction. While many factors contribute to population declines and extinctions, the role of disease is of particular concern to amphibians which are hosts to multiple globally distributed pathogens such as the fungal pathogen Batrachochytrium dendrobatidis (Bd), the dsDNA virus, ranavirus and trematode parasites, all of which can affect host populations. Amphibian disease-mediated population declines and extinctions have drawn special attention to the relationships between disease and diversity in general, as an understanding of these relationships is crucial for conservation and management efforts.
Host species vary in their competence (effectiveness of transmission) to specific pathogens. As host diversity increases, so does the likelihood of encountering an especially competent or incompetent host, which can alter disease dynamics in the greater community. Prior examinations of amphibian host diversity suggest that increased host diversity reduces disease risks of Bd and trematodes in some systems but the generality of these effect is still debated. Far less is known about the role of host diversity and ranavirus dynamics. Changes in pathogen diversity also alter disease dynamics, as pathogens interact via their effects on a host and its immune system. In amphibian systems, co-infection often increases disease burdens. although this is not always the case.
Here, using a series of experiments, I examined the interrelationships among diversity and disease in amphibians, with a focus on the Western toad (Anaxyrus boreas) as host. Western toads have experienced range reductions and population declines at high altitude sites in the Oregon Cascade Range.
In chapter two I paired laboratory and outdoor mesocosm experiments to examine the relationships of host diversity with ranavirus. In the laboratory experiment I found that after ranavirus exposure, only the Pacific chorus frog (Pseudacris regilla) experienced increased mortality when exposed to ranavirus. In the mesocosm experiment, like the laboratory study, the addition of ranavirus exposed conspecifics led to reduced host survival. However, in the presence of P. regilla amphibian assemblages experienced nearly complete mortality of all species, including A. boreas and the Cascades frog (Rana cascadae).
In chapter three I examined the effects of host diversity on Bd disease dynamics. Previous laboratory studies in my system suggested a protective effect of diversity on Bd disease risk. In an outdoor mesocosm experiment I found that communities of only A. boreas experienced reduced survival after addition of Bd exposed conspecifics. However when all three host species were present, survival was not different from controls, providing evidence that the reduction of Bd disease risk associated with increased host diversity is robust to changes in scale and ecosystem complexity.
In chapter four I experimentally altered both host and pathogen diversity in a factorial laboratory experiment which elicited a range of responses. I found increased variation in growth in the two days following experimental pathogen exposure, with the direction and strength of the effect modulated by host-pathogen combination. In the absence of other host species A. boreas, had increased mortality when simultaneously exposed to both Bd and trematodes.
This dissertation provides evidence of the impacts of diversity on amphibian disease outcomes and highlights the role of community composition in wildlife disease dynamics. This work suggests that to fully appreciate the dynamics of wildlife disease we must consider all interacting species in a community. I provide evidence that increased host diversity may reduce Bd disease risks in a community, while those same changes to host diversity in ranavirus exposed community can lead to collapse of amphibian populations. Further I have shown differences between laboratory and field experiments that suggest pairing diversity studies at different scales is important in the study of wildlife disease
