OOS 45-8
Amphibian skin microbial community responses to Batrachochytrium dendrobatidis: A time-series experimental approach
All species of plants and animals harbor microbial symbionts and how those communities of microbes are related to the health of their host organisms is largely undetermined. In particular, there is a limited understanding of how symbiotic microbes may mediate the establishment of pathogenic organisms that can cause disease. Amphibian species vary in their ability to tolerate infection with a fungal skin pathogen (Batrachochytrium dendrobatidis, ‘Bd’), and a number of recent studies have demonstrated that certain amphibian skin bacteria can inhibit growth of the pathogen. We conducted an experiment that addresses how skin community responses to the pathogen vary across known susceptible and tolerant amphibian species (n=53 individuals belonging to five species: Anaxyrus boreas, Rhinella marina, Lithobates catesbeiana, Lithobates pipiens, Osteopilus septentrionalis). We used barcoded pyrosequencing reads (Illumina) of ribosomal 16S genes to examine the communities of bacteria at multiple time points before and after exposure to Bd. We used QIIME and UniFrac to analyze community differences among species and treatments over time.
Results/Conclusions
Following QIIME quality filtering, 840 samples yielded sufficient sequences, representing 15 time points across 53 individual amphibians plus controls. Each sample was rarefied to 5,051 sequences per sample and more than a thousand OTUs were classified at the 97% sequence similarity limit. We observed very distinct communities among the five species of amphibians, and the skin communities of the susceptible species (boreal toads) were the most different compared to the two tolerant species (cane toads and bullfrogs). These differences remain constant even after Bd exposure but the volatility of the communities on the susceptible hosts is greater compared to the tolerant hosts, suggesting that the skin communities of tolerant species may be more resilient during infection. We propose that shifts in the abundance of pathogen-inhibiting bacteria following pathogen exposure can play a major role in the disease state of an individual.