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Antimicrobial Agents and Chemotherapy, January 2001, p. 263-266, Vol. 45, No. 1
0066-4804/01/$04.00+0   DOI: 10.1128/AAC.45.1.263-266.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Disruption of an Enterococcus faecium Species-Specific Gene, a Homologue of Acquired Macrolide Resistance Genes of Staphylococci, Is Associated with an Increase in Macrolide Susceptibility

Kavindra V. Singh,1,2 Kumthorn Malathum,1,2 and Barbara E. Murray1,2,3,*

Center for the Study of Emerging and Re-emerging Pathogens,1 Division of Infectious Diseases, Department of Internal Medicine,2 and Department of Microbiology and Molecular Genetics,3 The University of Texas Medical School at Houston, Houston, Texas 77030

Received 6 July 2000/Returned for modification 24 August 2000/Accepted 25 October 2000

The complete sequence (1,479 nucleotides) of msrC, part of which was recently reported by others using a different strain, was determined. This gene was found in 233 of 233 isolates of Enterococcus faecium but in none of 265 other enterococci. Disruption of msrC was associated with a two- to eightfold decrease in MICs of erythromycin azithromycin, tylosin, and quinupristin, suggesting that it may explain in part the apparent greater intrinsic resistance to macrolides of isolates of E. faecium relative to many streptococci. This endogenous, species-specific gene of E. faecium is 53% identical to msr(A), suggesting that it may be a remote progenitor of the acquired macrolide resistance gene found in some isolates of staphylococci.

* 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) 500-6767. Fax: (713) 500-6766. E-mail: infdis{at}heart.med.uth.tmc.edu.

Antimicrobial Agents and Chemotherapy, January 2001, p. 263-266, Vol. 45, No. 1
0066-4804/01/$04.00+0   DOI: 10.1128/AAC.45.1.263-266.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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