Two papers by our research group were published today in the journal, Proceedings of the National Academy of Sciences (PNAS). Both papers are open access and can be downloaded from the PNAS web site (Vredenburg et al. paper; Briggs et al. paper). These papers represent more than a decade of research by our group on the role of the amphibian chytrid fungus (Batrachochytrium dendrobatidis - Bd) in driving the decline of mountain yellow-legged frogs in the Sierra Nevada.
The first paper (by Vredenburg, Knapp, Tunstall, and Briggs) describes the frog-Bd dynamics in detail for the first time and provides a critical insight into how Bd outbreaks might be controlled. Bd was absent from the three study basins at the inception of the research but invaded the basins in 2004-2005. Following its initial arrival Bd spread through the basins at 0.6 km per year, eventually infecting all mountain yellow-legged frog populations.
Within 1-2 years of its first detection in a frog population, the population began to show evidence of severe chytridiomycosis (the disease caused by Bd). Frog die-offs and population crashes occurred when infection intensities (amount of Bd on a frog's skin) reached a critical threshold. The fact that a disease threshold exists is important because it provides a target for intervention strategies, strategies designed to prevent infection intensities from surpassing this threshold. One strategy, clearing frogs of Bd using an anti-fungal drug, was tested in two of the study basins in 2009 and preliminary results are promising. We'll be conducting additional tests in 2010, one designed to investigate whether clearing frogs of Bd early in an epidemic can actually prevent the epidemic from occurring.
Although most frog populations are extirpated following Bd epidemics, a few persist despite ongoing chytridiomycosis. Scientists have suggested that this persistence could be a consequence of selection for reduced susceptibility of frogs or reduced virulence of Bd. In the Briggs et al. paper, we use a mathematical model to demonstrate that neither of these changes are necessary to explain the long-term persistence of infected frog populations in the presence of Bd. Instead, this outcome could be solely the result of density-dependent host-pathogen dynamics. Under this scenario, epidemics are the result of Bd invading naive frog populations existing at their naturally high densities. This allows the production of vast numbers of zoospores (the infective stage of Bd) that overwhelm any frog defenses and causes massive frog die-offs. Most populations are extirpated but frogs in a few populations survive by chance alone. In these populations, zoospore density is kept low by low frog numbers, and frogs are able to tolerate the resulting low Bd infection intensities. As a consequence frog populations persist at low densities with Bd over the long term.
This model assumes no role for an adaptive immune response by frogs against Bd. Although this is consistent with our current knowledge of the frog-Bd interaction, a series of experiments we are currently conducting will provide clearer insights into the existence of any such response.
For the first time in several years I feel like we are making substantial progress toward understanding and potentially controlling chytridiomycosis. Let's hope our advances haven't come too late.
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