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Infect. Immun. doi:10.1128/IAI.00375-08
Copyright (c) 2008, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

A Functional Collagen Adhesin Gene, acm, in Clinical Isolates of Enterococcus faecium Correlates with the Recent Success of this Emerging Nosocomial Pathogen

Division of Infectious Diseases, Department of Internal Medicine; Center for the Study of Emerging and Re-emerging Pathogens; Department of Microbiology and Molecular Genetics, University of Texas Medical School, Houston, Texas 77030

^* To whom correspondence should be addressed. Email: bem.asst{at}uth.tmc.edu.

	Abstract

Enterococcus faecium has recently evolved from a generally avirulent commensal into a multi-drug resistant healthcare associated pathogen causing difficult-to-treat infections, but little is known about the factors responsible for this change. We previously showed that some E. faecium express a cell-wall anchored collagen adhesin, Acm. Here, we analyzed 90 E. faecium isolates (99% acm⁺) and found that the Acm protein was detected predominantly in clinically-derived isolates, while the acm gene was present as a transposon interrupted pseudogene in 12 of 47 isolates of non-clinical origin. A highly significant association between clinical (versus fecal or food) origin and collagen adherence (P 0.0003) was also demonstrated and levels of adherence were highly correlated (r = 0.879) with the amount of cell surface Acm detected by whole-cell ELISA and flow cytometry. Thirty-seven of 41 sera from patients with E. faecium infections showed reactivity with recombinant Acm, while only 4 of 30 community and hospitalized control group sera reacted (P 0.0003); importantly, antibodies to Acm were present in all 14 E. faecium endocarditis patients' sera. Although pulsed-field gel electrophoresis indicated that multiple strains expressed collagen adherence, multilocus sequence typing demonstrated that the majority of collagen adhering isolates, as well as 16 of 17 endocarditis isolates, are part of the hospital-associated E. faecium genogroup referred to as clonal complex 17 (CC17) that has emerged globally. Taken together, our findings support the hypothesis that Acm has contributed to the emergence of E. faecium and CC17 in nosocomial infections.

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