JCM Figure table search 04
Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Roberts, J. C.
Right arrow Articles by Murray, B. E.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Roberts, J. C.
Right arrow Articles by Murray, B. E.

 Previous Article  |  Next Article 

Journal of Clinical Microbiology, May 2004, p. 2317-2320, Vol. 42, No. 5
0095-1137/04/$08.00+0     DOI: 10.1128/JCM.42.5.2317-2320.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Molecular Epidemiology of the fsr Locus and of Gelatinase Production among Different Subsets of Enterococcus faecalis Isolates

Jill C. Roberts,1,2,{dagger} Kavindra V. Singh,1,3 Pablo C. Okhuysen,1,3 and Barbara E. Murray1,2,3*

Center for the Study of Emerging and Re-emerging Pathogens,1 Department of Microbiology and Molecular Genetics,2 Division of Infectious Diseases, Department of Internal Medicine, The University of Texas Medical School at Houston, Houston, Texas 770303

Received 24 November 2003/ Returned for modification 21 January 2004/ Accepted 6 February 2004

We examined 215 Enterococcus faecalis isolates and found that neither the two-component regulatory locus fsr (E. faecalis regulator) nor gelatinase production was more common in disease-associated isolates than in isolates colonizing healthy individuals (ca. 60 to 65%). The majority of gelatinase-negative isolates, including 14 endocarditis isolates (of 80 isolates tested), contained the previously described 23.9-kb deletion and lacked fsrA and fsrB. While these findings indicate that neither fsr nor gelatinase is required for E. faecalis to cause infection, this study did not address whether fsr or gelatinase affects the severity of disease, as it does in animal models.

* Corresponding author. Mailing address: Center for the Study of Emerging and Re-emerging Pathogens, University of Texas Medical School—Houston, 6431 Fannin, 1.728 JFB, Houston, TX 77030. Phone: (713) 500-6745. Fax: (713) 500-5495. E-mail: bem.asst{at}uth.tmc.edu.

{dagger} Present address: Center for Biological Defense, University of South Florida, Tampa, FL 33612.

Journal of Clinical Microbiology, May 2004, p. 2317-2320, Vol. 42, No. 5
0095-1137/04/$08.00+0     DOI: 10.1128/JCM.42.5.2317-2320.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:



Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
Antimicrob. Agents Chemother. Clin. Microbiol. Rev.
Clin. Vaccine Immunol. ALL ASM JOURNALS

Copyright © 2004 by the American Society for Microbiology. All rights reserved.