Bacteriocin production augments niche competition by enterococci in the mammalian gastrointestinal tract

The authors develop a mouse model of Enterococcus faecalis colonization to show that enterococci harbouring the bacteriocin-expressing plasmid pPD1 replace indigenous enterococci and have the ability to transfer the plasmid to other enterococci, which enhances the stability of the bacteriocin-expressing bacteria in the gut; this result suggests a therapeutic approach that leverages niche-specificity to eliminate antibiotic-resistant bacteria from infected individuals. Competition defeats multidrug-resistant bacteria Enterococcus faecalis is a normal gut bacterium and is usually harmless, but it can cause a variety of hospital-acquired infections in which its acquisition of antibiotic resistance makes it hard to treat. Nita Salzman and colleagues develop a mouse model of E. faecalis infection and use it to show that enterococci harbouring the bacteriocin-expressing plasmid pPD1 replace indigenous enterococci and have the ability to transfer the plasmid to other enterococci, thereby enhancing the stability of the bacteriocin-expressing bacteria in the gut. However, colonization by a strain in which the plasmid was not passed on resulted in clearance of other enterococci strains from the gut — including those resistant to the antibiotic vancomycin. This result suggests a way of using bacteriocin-producing bacteria as targeted therapeutics designed to clear competing multidrug-resistant strains from infected individuals. Enterococcus faecalis is both a common commensal of the human gastrointestinal tract and a leading cause of hospital-acquired infections 1 . Systemic infections with multidrug-resistant enterococci occur subsequent to gastrointestinal colonization 2 . Preventing colonization by multidrug-resistant E. faecalis could therefore be a valuable approach towards limiting infection. However, little is known about the mechanisms E. faecalis uses to colonize and compete for stable gastrointestinal niches. Pheromone-responsive conjugative plasmids encoding bacteriocins are common among enterococcal strains 3 and could modulate niche competition among enterococci or between enterococci and the intestinal microbiota. We developed a model of colonization of the mouse gut with E. faecalis , without disrupting the microbiota, to evaluate the role of the conjugative plasmid pPD1 expressing bacteriocin 21 (ref. 4 ) in enterococcal colonization. Here we show that E. faecalis harbouring pPD1 replaces indigenous enterococci and outcompetes E. faecalis lacking pPD1