Biofilm dispersion in Enterococcus faecalis is mediated by nutrient step-change and intra-species signaling

Enterococcus faecalis is a Gram-positive intestinal commensal and opportunistic pathogen capable of causing serious infections, including urinary tract infections, endocarditis, and wound infections. A major contributor to its persistence during infection is the ability to form biofilms on host tissues and medical devices. Biofilm cells have higher phenotypic tolerance to antimicrobial treatment than planktonic bacteria. While mechanisms governing biofilm assembly in E. faecalis have been widely studied, the processes that regulate biofilm dispersion, the final stage of the biofilm life cycle, remain poorly understood. In this study, we found that dispersion is triggered by a tenfold step-change increase in nutrient availability and by cell free supernatant (CFS) of E. faecalis OG1RF cultures. Cells released from biofilms regain sensitivity to antibiotics similar to planktonic cells but maintain a high potential for adherence. We characterized the glycosyltransferase epaOX, which contributes to the structure of the enterococcal polysaccharide antigen as necessary for nutrient step-change induced dispersion, CFS induced dispersion, and adhesion of dispersed cells. Supplementation of epaOX mutant CFS with galactose and N-acetylgalactosamine was sufficient to restore CFS induced dispersion. Together these data suggest that dispersion in OG1RF occurs with fast kinetics, affects antibiotic sensitivity and is regulated in part by known virulence factors.