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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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