- The causes of the global biodiversity crisis are varied and complex. Anthropogenic threats may act in isolation, or interact additively or synergistically with each other or with natural stressors to affect sensitive taxa. The recent emergence of many infectious diseases in wildlife has brought attention to the role of disease in population declines and species extinctions. Both abiotic and biotic components of the environment may mitigate or exacerbate effects of pathogens on their hosts through direct or indirect mechanisms. The effects of the environment on host-pathogen dynamics are complex, context-dependent, and in need of further examination.
One particularly sensitive group, amphibians, is at the leading edge of the sixth mass extinction. The emerging infectious disease (EID) chytridiomycosis, caused by the fungal pathogen Batrachochytrium dendrobatis (Bd), is implicated in population declines and extinctions of amphibians globally. My disseration addresses questions pertaining to environmental influences on disease dynamics of Bd. As described in chapter 1, various abiotic and biotic components of the environment may affect host-pathogen dynamics of Bd, resulting in changes to the dynamics of Bd transmission and spread.
Chapter 2 examines the influence of an abiotic factor, the insecticide (carbaryl) and three different assemblages of larval Pacific treefrogs (Pseudacris regilla) and Cascades frogs (Rana cascadae) on host-pathogen dynamics of Bd within a community context. I found separate effects of each treatment on amphibian growth and development, but no interactive effects among the treatments. However, Bd appeared to reduce phytoplankton abundance and increase periphyton biomass, an unexpected result that merited further investigation.
One possible explanation for the results described in chapter 2 is that zooplankton might consume Bd zoospores, the infective stage of the pathogen, a hypothesis that I examine in chapter 3. I conducted laboratory experiments and confirmed the presence of Bd zoospores in the gut of Daphnia sp. through quantitative PCR and visual inspection. I discuss conservation implications of this finding.
To determine whether predation on Bd zoospores by zooplankton could reduce infection in amphibians, I conducted a mesocosm experiment, which is described in chapter 4. I found complex effects on species interactions: competition between larval Cascades frogs and zooplankton for phytoplankton resources reduced phytoplankton concentration, zooplankton abundance, and survival of amphibians. These effects were diminished in the presence of Bd, suggesting that zooplankton may have at least partially substituted Bd zoospores for phytoplankton in their diet, thus stimulating competitive release. However, competitive effects between zooplankton and larval amphibians overshadowed indirect positive benefits of zooplankton predation on Bd zoospores.
In chapter 4, competitive effects between zooplankton and larval amphibians for phytoplankton suggested that host-pathogen dynamics might be affected by the host’s supply of resources. Chapter 5 describes a mesocosm experiment that examined how eutrophication might affect Bd-infected Pacific treefrogs and other members of the aquatic community. Nutrient additions caused increased algal growth, which benefitted herbivorous larval amphibians. Larvae exposed to Bd altered their growth, development, and diet, and allocated resources differently than unexposed individuals. However, nutrient supplementation did not alter the response of larval amphibians to Bd.
As described in chapter 6, consideration of hosts and pathogens as functional members of the ecological communities in which they exist can lead to important insights in host-pathogen dynamics. My PhD research may contribute to control measures for the emerging infectious disease chytridiomycosis.