Enterococcal biofilms

Enterococci are among the leading causative agents of nosocomial infections and are infamous for multiresistance to antimicrobial drugs. The vast majority of enterococcal species isolated in the hospital are E. faecalis and E. faecium, which are responsible for difficult-to-treat-infections from indwelling medical devices, (central) venous and urinary catheters and endocarditis. All these types of enterococcal infections are biofilmmediated. Microbial biofilms are populations of microorganisms typically surrounded by an extracellular polymeric substance matrix, and can grow into three-dimensional structures through a complex regulated process. Different enterococcal structural and regulatory genes involved in biofilm formation have been identified and mutants have been tested in animal models. Apart from the surface protein Esp, several other LPxTG containing surface proteins contribute to adhesion and initial biofilm formation. Among the different identified autolysins, coexpression of gelE and sprE tightly regulates eDNA production by fratricide. gelE-sprE is regulated by the fsrABCD locus, which seems to be a global quorum sensing biofilm regulator in E. faecalis. Also two araC-like regulators contained on the E. faecalis and E. faecium pathogenicity islands, polysaccharides, glycolipids, a maltose metabolism bopABCD operon, a putative secreted antigen and several hypothetical genes contribute to enterococcal biofilm formation. Since the majority of the identified enterococcal biofilm associated genes originate from E. faecalis, more future studies on E. faecium are needed. Enterococcal isolates from food have been demonstrated to be biofilm producers, but it is not known whether ingestion of enterococcal biofilm could lead to health problems. Enterococcal strains might be able to inhibit more pathogenic species in multispecies biofilm, but this needs to be more extensively tested.