Serratia marcescens shapes cutaneous bacterial communities and influences survival of an amphibian host.

Abstract

Ongoing investigations into the interactions between microbial communities and their associated hosts are changing how emerging diseases are perceived and ameliorated. Of the numerous host-microbiome-disease systems of study, the emergence of chytridiomycosis (caused by Batrachochytrium dendrobatidis, hereafter Bd) has been implicated in ongoing declines and extinction events of amphibians worldwide. Interestingly, there has been differential survival among amphibians in resisting Bd infection and subsequent disease. One factor thought to contribute to this resistance is the host-associated cutaneous microbiota. This has raised the possibility of using genetically modified probiotics to restructure the host-associated microbiota for desired anti-fungal outcomes. Here, we use a previously described strain of Serratia marcescens (Sm) for the manipulation of amphibian cutaneous microbiota. Sm was genetically altered to have a dysfunctional pathway for the production of the extracellular metabolite prodigiosin. This genetically altered strain (Δpig) and the functional prodigiosin producing strain (wild-type, WT) were compared for their microbial community and anti-Bd effects both in vitro and in vivo. In vitro, Bd growth was significantly repressed in the presence of prodigiosin. In vivo, the inoculation of both Sm strains was shown to significantly influence amphibian microbiota diversity with the Δpig-Sm treatment showing increasing alpha diversity, and the WT-Sm having no temporal effect on diversity. Differences were also seen in host mortality with Δpig-Sm treatments exhibiting significantly decreased survival probability when compared with WT-Sm in the presence of Bd. These results are an important proof-of-concept for linking the use of genetically modified probiotic bacteria to host microbial community structure and disease outcomes, which in the future may provide a way to ameliorate disease and address critical frontiers in disease and microbial ecology.