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Antimicrobial Agents and Chemotherapy, February 2004, p. 473-476, Vol. 48, No. 2
0066-4804/04/$08.00+0     DOI: 10.1128/AAC.48.2.473-476.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Reemergence of Macrolide Resistance in Pharyngeal Isolates of Group A Streptococci in Southwestern Pennsylvania

Michael Green,1* Judith M. Martin,1 Karen A. Barbadora,1 Bernard Beall,2 and Ellen R. Wald1

Department of Pediatrics, Division of Allergy, Immunology and Infectious Diseases, Children's Hospital of Pittsburgh, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania,1 Respiratory Diseases Branch, Centers for Disease Control and Prevention, Atlanta, Georgia2

Received 22 July 2003/ Returned for modification 24 September 2003/ Accepted 14 October 2003

We previously reported on the emergence of macrolide-resistant pharyngeal isolates of group A streptococci (GAS) in our community. The purpose of the present study was to track longitudinal trends in macrolide resistance in these isolates in southwestern Pennsylvania. Testing for susceptibility to erythromycin and clindamycin was performed for all pharyngeal GAS isolates recovered at the Children's Hospital of Pittsburgh and a local pediatric practice between September 2001 and May 2002. Macrolide resistance phenotypes and genotypes were determined by double-disk diffusion and PCR, respectively. Strain relatedness was determined by field inversion gel electrophoresis and emm gene sequence typing. A total of 708 isolates of GAS were recovered during the study period; 68 (9.6%) were macrolide resistant, while all isolates were sensitive to clindamycin. The monthly prevalence of macrolide resistance ranged from 0 to 41%. Only 21 of 573 (3.7%) strains recovered from September 2001 through March 2002 were macrolide resistant. A sudden increase in the rate of macrolide resistance (47 of 135 isolates [35%]) was seen in April and May 2002. Sixty-two isolates demonstrated the M phenotype (resistance to macrolide antibiotics), and six isolates demonstrated the MLSB phenotype (resistance to most macrolide, lincosamide, and streptogramin B antibiotics); these isolates were confirmed to be mef(A) and erm(A), respectively. Three unique mef(A) clones and four unique erm(A) clones were identified among the resistant isolates. The MIC at which 50% of isolates are inhibited (MIC50) for the mef(A) strains was 16 µg/ml, while the MIC50 for erm(A) strains was 8 µg/ml. The finding of high levels of macrolide resistance among pharyngeal isolates of GAS for a second successive year in our community raises the concern that this problem may be more common in the United States than was previously appreciated. Longitudinal surveillance of isolates from multiple centers is needed to define the prevalence of antimicrobial agent-resistant GAS in the United States.

* Corresponding author. Mailing address: University of Pittsburgh School of Medicine, Division of Allergy, Immunology and Infectious Diseases, Children's Hospital of Pittsburgh, 3705 Fifth Ave., Pittsburgh, PA 15213. Phone: (412) 692-7438. Fax: (412) 692-8499. E-mail: greemd{at}chp.edu.

Antimicrobial Agents and Chemotherapy, February 2004, p. 473-476, Vol. 48, No. 2
0066-4804/04/$08.00+0     DOI: 10.1128/AAC.48.2.473-476.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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