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Although enterococci are normal commensals of the gastrointestinal tract of humans and many mammals, they have emerged as important pathogens causing nosocomial infections, including urinary tract, bloodstream, wound and surgical-site infections, in addition to their long-recognized importance as a cause of infective endocarditis (Murray, 1990). The binding of Enterococcus faecalis to heart valves and to various biomaterials (Joyanes et al., 1999; Toledo-Arana et al., 2001; Mohamed et al., 2004; Seno et al., 2005) and medical devices (Keane et al., 1994; Dautle et al., 2003; Sandoe et al., 2003) is the presumed initiating factor that then allows subsequent formation of a biofilm. Biofilm formation in E. faecalis has been reported to be influenced by various genes such as esp, initially reported by Toledo-Arana et al. (2001). Gelatinase, which strongly influences virulence in models of peritonitis, endocarditis (Singh et al., 1998, 2005), endophthalmitis (Engelbert et al., 2004) and in vitro translocation (Zeng et al., 2005), has been reported to influence biofilm formation (Mohamed et al., 2003, 2004; Hancock & Perego, 2004; Kristich et al., 2004). Other E. faecalis genes such as epa, atn (Mohamed et al., 2004), bop (Hufnagel et al., 2004), salA and salB (Mohamed et al., 2006) have also been shown to influence biofilms. Biofilm production has been shown to be regulated by quorum-sensing systems in several important pathogens, including fsr in E. faecalis, which was shown to have a pronounced effect on biofilms (Hancock & Perego, 2004; Mohamed et al., 2003, 2004; Pillai et al., 2004).

Influence of the fsr locus on biofilm formation by Enterococcus faecalis lacking gelE