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Journal of Bacteriology, August 2005, p. 5709-5718, Vol. 187, No. 16
0021-9193/05/$08.00+0     doi:10.1128/JB.187.16.5709-5718.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Molecular Characterization of a Widespread, Pathogenic, and Antibiotic Resistance-Receptive Enterococcus faecalis Lineage and Dissemination of Its Putative Pathogenicity Island

Sreedhar R. Nallapareddy,1,2 Huang Wenxiang,1,2,{dagger} George M. Weinstock,3,4 and Barbara E. Murray1,2,3*

Division of Infectious Diseases, Department of Internal Medicine,1 Center for the Study of Emerging and Re-emerging Pathogens,2 Department of Microbiology and Molecular Genetics, University of Texas Medical School,3 Human Genome Sequencing Center, Baylor College of Medicine, Houston, Texas 770304

Received 21 March 2005/ Accepted 25 May 2005

Enterococcus faecalis, a common cause of endocarditis and known for its capacity to transfer antibiotic resistance to other pathogens, has recently emerged as an important, multidrug-resistant nosocomial pathogen. However, knowledge of its lineages and the potential of particular clones of this species to disseminate and cause disease is limited. Using a nine-gene multilocus sequence typing (MLST) scheme, we identified an evolving and widespread clonal complex of E. faecalis that has caused outbreaks and life-threatening infections. Moreover, this unusual clonal complex was found to contain isolates of unexpected relatedness, including the first known U.S. vancomycin-resistant enterococcus (E. faecalis strain V583), the first known penicillinase-producing (Bla+) E. faecalis isolate, and the previously described widespread clone of penicillinase producers, a trait found in <0.1% of E. faecalis isolates. All members of this clonal cluster (designated as BVE for Bla+ Vanr endocarditis) were found to contain a previously described putative pathogenicity island (PAI). Further analysis of this PAI demonstrated its dissemination worldwide, albeit with considerable variability, confirmed its association with clinical isolates, and found a common insertion site in different clonal lineages. PAI deletions, MLST, and the uncommon resistances were used to predict the evolution of the BVE clonal cluster. The finding of a virulent and highly successful clonal complex of E. faecalis with different members resistant to the primary therapies of choice, ampicillin and vancomycin, has important implications for the evolution of virulence and successful lineages and for public health monitoring and control.

* Corresponding author. Mailing address: Div. Infectious Diseases, Dept. Internal Medicine, Center for the Study of Emerging and Re-emerging Pathogens, University of Texas Medical School at Houston, 6431 Fannin Street, MSB 2.112, Houston, TX 77030. Phone: (713) 500-6745. Fax: (713) 500-6766. E-mail: bem.asst{at}uth.tmc.edu.

{dagger} Present address: Department of Infectious Diseases, Chongqing University of Medical Sciences, Chongqing, China 400016.

Journal of Bacteriology, August 2005, p. 5709-5718, Vol. 187, No. 16
0021-9193/05/$08.00+0     doi:10.1128/JB.187.16.5709-5718.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



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