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15 January 2005

Volume 40, Number 2
Clinical Infectious Diseases 2005;40:280–285
© 2004 by the Infectious Diseases Society of America. All rights reserved.
1058-4838/2005/4002-0013$15.00
DOI: 10.1086/426894
ANTIMICROBIAL RESISTANCE INVITED ARTICLE

Inducible Clindamycin Resistance in Staphylococci: Should Clinicians and Microbiologists be Concerned?

James S. Lewis II1,2 and

James H. Jorgensen3

1Pharmacy Service, University Health System, and Departments of 2Clinical Pharmacy and Pharmacology and 3Pathology, University of Texas Health Science Center, San Antonio, Texas

The increasing incidence of a variety of infections due to Staphylococcus aureus—and, especially, the expanding role of community‐associated methicillin‐resistant S. aureus (MRSA)—has led to emphasis on the need for safe and effective agents to treat both systemic and localized staphylococcal infections. Unlike most previously noted strains of health care–associated MRSA, community‐acquired MRSA isolates are often susceptible to several non–β‐lactam drug classes, although they are usually not susceptible to macrolides. Several newer antimicrobial agents and a few older agents are available for treatment of systemic staphylococcal infections, but use may be limited by the relatively high cost of these agents or the need for parenteral administration. Inexpensive oral agents for treatment of localized, community‐acquired MRSA infection include clindamycin, trimethoprim‐sulfamethoxazole, and newer tetracyclines. Clindamycin has been used successfully to treat pneumonia and soft‐tissue and musculoskeletal infections due to MRSA in adults and children. However, concern over the possibility of emergence of clindamycin resistance during therapy has discouraged some clinicians from prescribing that agent. Simple laboratory testing (e.g., the erythromycin‐clindamycin “D‐zone” test) can separate strains that have the genetic potential (i.e., the presence of erm genes) to become resistant during therapy from strains that are fully susceptible to clindamycin.

Received 7 July 2004; accepted 1 September 2004; electronically published 21 December 2004.

Reprints or correspondence: Dr. James H. Jorgensen, Dept. of Pathology, University of Texas Health Science Center, 7703 Floyd Curl Dr., San Antonio, TX 78229 ().

George M. Eliopoulos, Section Editor

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