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Antimicrobial Agents and Chemotherapy, February 2000, p. 272-277, Vol. 44, No. 2
0066-4804/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Reversion of the Glycopeptide Resistance Phenotype in Staphylococcus aureus Clinical Isolates

Susan Boyle-Vavra,1,* Sarah K. Berke,1 Jean C. Lee,2 and Robert S. Daum1

The University of Chicago Children's Hospital, Department of Pediatrics, Chicago, Illinois 60637,1 and Channing Laboratory, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 021152

Received 1 June 1999/Returned for modification 14 July 1999/Accepted 29 October 1999

The recent identification of glycopeptide intermediate-resistant Staphylococcus aureus (GISA) clinical isolates has provided an opportunity to assess the stability of the glycopeptide resistance phenotype by nonselective serial passage and to evaluate reversion-associated cell surface changes. Three GISA isolates from the United States (MIC of vancomycin = 8 µg/ml) and two from Japan (MICs of vancomycin = 8 and 2 µg/ml) were passaged daily on nutrient agar with or without vancomycin supplementation. After 15 days of passage on nonselective medium, vancomycin- and teicoplanin-susceptible revertants were obtained from each GISA isolate as determined by broth dilution MIC. Revertant isolates were compared with parent isolates for changes in vancomycin heteroresistance, capsule production, hemolysis phenotype, coagulase activity, and lysostaphin susceptibility. Several revertants lost the subpopulations with intermediate vancomycin resistance, whereas two revertants maintained them. Furthermore, although all of the parent GISA isolates produced capsule type 5 (CP5), all but one revertant tested no longer produced CP5. In contrast, passage on medium containing vancomycin yielded isolates that were still intermediately resistant to vancomycin, had no decrease in the MIC of teicoplanin, and produced detectable CP5. No consistent changes in the revertants in hemolysis phenotype, lysostaphin susceptibility, or coagulase activities were discerned. These data indicate that the vancomycin resistance phenotype is unstable in clinical GISA isolates. Reversion of the vancomycin resistance phenotype might explain the difficulty in isolating vancomycin-resistant clinical isolates from the blood of patients who fail vancomycin therapy and, possibly, may account for some of the difficulties in identifying GISA isolates in the clinical laboratory.

* Corresponding author. Mailing address: University of Chicago Children's Hospital, MC 6054, 5841 S. Maryland Ave., Chicago, IL 60637. Phone: (773) 702-6401. Fax: (773) 702-1196. E-mail address: sboyleva{at}midway.uchicago.edu.

Antimicrobial Agents and Chemotherapy, February 2000, p. 272-277, Vol. 44, No. 2
0066-4804/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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