Presented by Gui Becker, University of Alabama
Abstract: Anthropogenic habitat disturbance and climate change are fundamentally altering patterns of disease transmission and immunity across the vertebrate tree of life. Here, we link habitat disturbance, warming temperatures and droughts to shifts in host-microbial interactions and pathogen pressure through spatially oriented field studies and experimental manipulations. We focus on amphibians, a group that stands apart from other vertebrates as the most threatened taxon, and as primary hosts to the most host-generalist of known pathogens of vertebrates, the waterborne fungus Batrachochytrium dendrobatidis (Bd). In the first study, we consider habitat split, an overlooked type of habitat fragmentation that disrupts spatial connectivity between terrestrial and aquatic habitats. We demonstrate that habitat split is associated with increased pathogen infection intensity in amphibians during the summer breeding season, likely by restricting movement during overwintering, preventing the mild pathogen exposures needed to develop acquired immunity. In the second study, we tracked microhabitat conditions and Bd dynamics in terrestrial-breeding frogs over an annual cycle coinciding with a drought, revealing that low rainfall was the best predictor of spikes in Bd infection loads and mortality among heavily infected hosts. In the last study, we found that warming-related fitness depression appeared more closely linked to changes in ecological community interactions than to direct thermal stress. We used replicated bromeliad microecosystems to show warming effects on tadpole gut microbiome dysbiosis mediated through biotic community interactions. Warming shifted environmental bacteria and arthropod community composition, with linkages to changes in microbial recruitment that promoted dysbiosis and stunted tadpole growth. These results, combined, indicate that global change stressors may intensify disease through mechanisms spanning altered movement patterns to disruption of the host microbiome, facilitating spillover infections and shifting disease dynamics from enzootic to epizootic.