They can cause a wide spectrum of diseases, including bacteremia, peritonitis, surgical wound infections, urinary tract infections, endocarditis, and a variety of device-related
infections [1–11]. The majority of the enterococcal infections are caused by Enterococcus faecalis. However, in parallel with the increase in nosocomial enterococcal infections, a partial replacement of E. faecalis by Enterococcus faecium has occurred in European and United States hospitals [12–14]http://www.earss.rivm.nl. Molecular epidemiological studies indicated FK228 research buy that E. faecium isolates responsible for the majority of nosocomial infections and hospital outbreaks are genetically distinct from indigenous intestinal isolates [15, 16]. Recent studies revealed intestinal colonization rates with these hospital-acquired E. faecium as high as 40% in hospital wards, while colonization in healthy people appeared to be almost absent [13, 15, 16]. It is assumed that adherence to mucosal surfaces is a key process for bacteria to survive and colonize the GI SCH727965 tract. Intestinal colonization of nosocomial E. faecium strains is a first and key step that precedes clinical infection due to fecal contamination of catheters or wounds, and in the minority of infections, through
bacterial translocation from the intestinal lumen to extraintestinal sites [17, 18]. It is not known which factors facilitate intestinal colonization of nosocomial E. faecium strains. The enterococcal surface protein Esp, located on a putative pathogeniCity island [19, 20], is specifically enriched in hospital-acquired E. faecium and has been identified as a potential virulence gene. Esp is involved in biofilm formation
[21] and its expression is affected by changes in environmental conditions, being highest in conditions that mimic the microenvironment of the human large intestines: 37°C and anaerobioses [22]. Furthermore, in one study, bloodstream isolates of E. faecium enriched with esp had increased adherence to human colorectal adenocarcinoma cells (Caco-2 cells) [23], suggesting a role of Esp in intestinal colonization. In contrast, adherence of E. faecium to Vildagliptin Caco-2 cell lines was not associated with the presence of esp in another study [24]. In E. faecalis, Esp is also located on a pathogeniCity island, although the genetic content and organization of the E. faecium and E. faecalis PAI is different. Esp of E. faecalis is also expressed on the surface of the bacterium [25, 26] and is important in colonization of urinary tract epithelial cells [25]. By using a mouse model, Pultz et al. [27] showed that Esp does not facilitate intestinal colonization or translocation of E. faecalis in mice, however this does not automatically predict a lack function for E. faecium Esp in murine colonization. First data suggest that the function of Esp in both enterococcal species might be different. Esp of E.