Enterococcal surface protein Esp is not essential for cell adhesion and intestinal colonization of Enterococcus faecium in mice.

BACKGROUND

Enterococcus faecium has globally emerged as a cause of hospital-acquired infections with high colonization rates in hospitalized patients. The enterococcal surface protein Esp, identified as a potential virulence factor, is specifically linked to nosocomial clonal lineages that are genetically distinct from indigenous E. faecium strains. To investigate whether Esp facilitates bacterial adherence and intestinal colonization of E. faecium, we used human colorectal adenocarcinoma cells (Caco-2 cells) and an experimental colonization model in mice.

RESULTS

No differences in adherence to Caco-2 cells were found between an Esp expressing strain of E. faecium (E1162) and its isogenic Esp-deficient mutant (E1162Deltaesp). Mice, kept under ceftriaxone treatment, were inoculated orally with either E1162, E1162Deltaesp or both strains simultaneously. Both E1162 and E1162Deltaesp were able to colonize the murine intestines with high and comparable numbers. No differences were found in the contents of cecum and colon. Both E1162 and E1162Deltaesp were able to translocate to the mesenteric lymph nodes.

CONCLUSION

These results suggest that Esp is not essential for Caco-2 cell adherence and intestinal colonization or translocation of E. faecium in mice.