Enterococcus Colonization Project Database

Enterococcus faecium Colonization Factors

Enterococci are common causes of hospital-acquired infection, with many studies citing them as the third most common cause of nosocomial infections. Unlike many other human pathogens, enterococci are part of the normal human bowel flora. In fact, high-level gastrointestinal colonization frequently precedes clinical infection. Factors that promote extensive gastrointestinal colonization by enterococci, other than antimicrobial resistance determinants, remain obscure.

Our overall goal is to determine which factor(s) that transfer from C68, a clinical isolate that represented the most prevalent VRE clone in 11 Cleveland hospitals in 1996, to D344SRF (a non-colonizing strain) confer on the transconjugants the ability to colonize the mouse gastrointestinal tract. Since we know that at least 275 kb of DNA has transferred over to the recipient strain (220 + 40 + 15 kb plasmids) and perhaps more, a comparative genome strategy will inform knockout experiments that will be required to identify the genes and plasmids involved with colonization.

Project Information

Enterococcus faecium Colonization Factors:

Enterococci are common causes of hospital-acquired infection, with many studies citing them as the third most common cause of nosocomial infections. Unlike many other human pathogens, enterococci are part of the normal human bowel flora. In fact, high-level gastrointestinal colonization frequently precedes clinical infection. Factors that promote extensive gastrointestinal colonization by enterococci, other than antimicrobial resistance determinants, remain obscure. Although there are several species within the genus Enterococcus, two species predominate as causes of human clinical infection. Enterococcus faecalis is responsible for roughly 70% of human enterococcal infections, with Enterococcus faecium involved in most of the remainder. E. faecium tends to be more resistant to antibiotics than E. faecalis. In particular, E. faecium are frequently resistant to ampicillin and vancomycin, the two most effective and commonly used agents to treat susceptible enterococcal infections. One E. faecium clonal complex (designated clonal complex 17, or CC17) is responsible for the vast majority of vancomycin-resistant E. faecium outbreaks and clinical infections the world over. CC17 strains are far more likely to be resistant to ampicillin than are other strains, and they are more likely to contain the putative virulence determinants espEfm and hylEfm. CC17 strains are also replete with mobile elements and other segments of DNA that are absent from less pathogenic strains. Our overall goal is to determine which factor(s) that transfer from C68, a clinical isolate that represented the most prevalent VRE clone in 11 Cleveland hospitals in 1996, to D344SRF (a non-colonizing strain) confer on the transconjugants the ability to colonize the mouse gastrointestinal tract. Since we know that at least 275 kb of DNA has transferred over to the recipient strain (220 + 40 + 15 kb plasmids) and perhaps more, a comparative genome strategy will inform knockout experiments that will be required to identify the genes and plasmids involved with colonization.

Project Collaborators

  • Louis B. Rice, Project P.I.: Department of Medicine, Case Western Reserve University, Cleveland, OH.
  • Mark Adams, Department of Genetics, School of Medicine, Case Western Reserve University, Cleveland, OH.
  • Paul Dunman, Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NE.

Funding Information

This sequencing project was supported by the National Institute of Allergy and Infectious Disease, National Institutes of Health funded Genome Sequencing Center for Infectious Diseases at the Broad Institute.