OOS 23-4
The effects of host density on amphibian chytridiomycosis

Tuesday, August 11, 2015: 9:00 AM
342, Baltimore Convention Center
Cheryl J. Briggs, Dept. of Ecology, Evolution & Marine Biology, University of California, Santa Barbara, Santa Barbara, CA
Roland A. Knapp, Sierra Nevada Aquatic Research Laboratory, University of California

Chytridiomycosis, the disease caused by the amphibian chytrid fungus, Batrachochytrium dendrobatidis, has had devastating effects on amphibians worldwide, with numerous species extinctions documented in recent decades and many more at risk of Bd-caused declines. However, the outcome of infection with Bd varies among amphibian species and among populations of the same species. Some species/populations experience epizootic dynamics with high levels of mortality and rapid population declines, while other species/populations experience enzootic dynamics with sublethal infections and population persistence. Both of these outcomes are occurring in populations of mountain yellow-legged frogs (Rana muscosa/Rana sierrae) in high elevation lakes in the California Sierra Nevada. One factor potential contributing to the different infection outcomes is host density. A common modeling result is that infectious diseases are predicted to have larger effects at high host densities (if increasing host density increases the transmission rate). We tested this prediction in the Sierra Nevada/mountain yellow-legged frog system through analysis of the patterns of infection and disease outcome in field surveys of hundreds of frog populations, and through frog translocation experiments in which frogs were moved from high-density to low-density lakes. We used individual-based models to explore the mechanisms underpinning the observed results. 


Contrary to our prediction, we found that host density did not affect either the intensity of Bd infection or the impact of the pathogen on the host population. This lack of host density effect occurred in both the field surveys of natural populations and in the frog translocation experiments. Our models suggest that this result could be explained by the presence of a pathogen reservoir and/or pathogen transmission that is dominated by self-reinfection. These results have important implication for control strategies designed to mitigate the effects of this fungal pathogen on threatened amphibian species, because they suggest that strategies aimed at reducing transmission through reducing susceptible host density are likely to be unsuccessful.