Search for: All records

Abstract Symbiotic interactions can determine the evolutionary trajectories of host species, influencing genetic variation through selection and changes in demography. In the context of strong selective pressures such as those imposed by infectious diseases, symbionts providing defences could contribute to increase host fitness upon pathogen emergence. Here, we generated genome‐wide data of an amphibian species to find evidence of evolutionary pressures driven by two skin symbionts: a batrachochytrid fungal pathogen and an antifungal bacterium. Using demographic modelling, we found evidence of decreased effective population size, probably due to pathogen infections. Additionally, we investigated host genetic associations with infection status, antifungal bacterium abundance and overall microbiome diversity using structural equation models. We uncovered relatively lower nucleotide diversity in infected frogs and potential heterozygote advantage to recruit the candidate beneficial symbiont and fight infections. Our models indicate that environmental conditions have indirect effects on symbiont abundance through both host body traits and microbiome diversity. Likewise, we uncovered a potential offsetting effect among host heterozygosity–fitness correlations, plausibly pointing to different ecological and evolutionary processes among the three species due to dynamic interactions. Our findings revealed that evolutionary pressures not only arise from the pathogen but also from the candidate beneficial symbiont, and both interactions shape the genetics of the host. Our results advance knowledge about multipartite symbiotic relationships and provide a framework to model ecological and evolutionary dynamics in wild populations. Finally, our study approach can be applied to inform conservation actions such as bioaugmentation strategies for other imperilled amphibians affected by infectious diseases. 

Abstract Molecular technologies have revolutionized the field of wildlife disease ecology, allowing the detection of outbreaks, novel pathogens, and invasive strains. In particular, metabarcoding approaches, defined here as tools used to amplify and sequence universal barcodes from a single sample (e.g., 16S rRNA for bacteria, ITS for fungi, 18S rRNA for eukaryotes), are expanding our traditional view of host–pathogen dynamics by integrating microbial interactions that modulate disease outcome. Here, I provide an analysis from the perspective of the field of amphibian disease ecology, where the emergence of multi-host pathogens has caused global declines and species extinctions. I reanalyzed an experimental mesocosm dataset to infer the functional profiles of the skin microbiomes of coqui frogs (Eleutherodactylus coqui), an amphibian species that is consistently found infected with the fungal pathogen Batrachochytrium dendrobatidis and has high turnover of skin bacteria driven by seasonal shifts. I found that the metabolic activities of microbiomes operate at different capacities depending on the season. Global enrichment of predicted functions was more prominent during the warm-wet season, indicating that microbiomes during the cool-dry season were either depauperate, resistant to new bacterial colonization, or that their functional space was more saturated. These findings suggest important avenues to investigate how microbes regulate population growth and contribute to host physiological processes. Overall, this study highlights the current challenges and future opportunities in the application of metabarcoding to investigate the causes and consequences of disease in wild systems. 

North American salamanders are threatened by intercontinental spread of chytridiomycosis, a deadly disease caused by the fungal pathogenBatrachochytrium salamandrivorans(Bsal). To predict potential dispersal ofBsalspores to salamander habitats, we evaluated the capacity of soil microbial communities to resist invasion. We determined the degree of habitat invasibility using soils from five locations throughout the Great Smoky Mountains National Park, a region with a high abundance of susceptible hosts. Our experimental design consisted of replicate soil microcosms exposed to different propagule pressures of the non-native pathogen,Bsal, and an introduced but endemic pathogen,B. dendrobatidis(Bd). To compare growth and competitive interactions, we used quantitative PCR, live/dead cell viability assays, and full-length 16S rRNA sequencing. We found that soil microcosms with intact bacterial communities inhibited bothBsalandBdgrowth, but inhibitory capacity diminished with increased propagule pressure.Bsalshowed greater persistence thanBd. Linear discriminant analysis (LDA) identified the family Burkolderiaceae as increasing in relative abundance with the decline of both pathogens. Although our findings provide evidence of environmental filtering in soils, such barriers weakened in response to pathogen type and propagule pressure, showing that habitats vary their invasibility based on properties of their local microbial communities. 

Microbiomes are major determinants of host growth, development and survival. In amphibians, host-associated bacteria in the skin can inhibit pathogen infection, but many processes can influence the structure and composition of the community. Here we quantified the shifts in skin-associated bacteria across developmental stages in the striped newt (Notophthalmus perstriatus), a threatened salamander species with a complex life history and vulnerable to infection by the amphibian chytrid fungusBatrachochytrium dendrobatidisand ranavirus. Our analyses show that pre-metamorphic larval and paedomorphic stages share similar bacterial compositions, and that the changes in the microbiome coincided with physiological restructuring during metamorphosis. Newts undergoing metamorphosis exhibited microbiome compositions that were intermediate between paedomorphic and post-metamorphic stages, further supporting the idea that metamorphosis is a major driver of host-associated microbes in amphibians. We did not find support for infection-related disruption of the microbiome, though infection replicates were small for each respective life stage.