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Antimicrobial Agents and Chemotherapy, February 2003, p. 568-576, Vol. 47, No. 2
0066-4804/03/$08.00+0     DOI: 10.1128/AAC.47.2.568-576.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Morphological and Genetic Differences in Two Isogenic Staphylococcus aureus Strains with Decreased Susceptibilities to Vancomycin

Andrea Reipert,1 Kerstin Ehlert,2 Thomas Kast,3 and Gabriele Bierbaum1*

Institut für Medizinische Mikrobiologie und Immunologie, Universität Bonn, D-53105 Bonn,1 Abteilung Anti-Infektiva, Pharma Forschungszentrum, Bayer AG, D-42096 Wuppertal,2 Abteilung Biochemie, Max-Planck-Institut für Entwicklungsbiologie, D-72076 Tübingen, Germany3

Received 29 August 2002/ Returned for modification 25 September 2002/ Accepted 15 November 2002

Many VISA (vancomycin intermediately resistant Staphylococcus aureus) strains are characterized by increased cell wall biosynthesis and decreased cross-linking of the peptide side chains, leading to accumulation of free D-alanyl-D-alanine termini in the peptidoglycan, which act as false target sites for vancomycin. A spontaneous mutant of methicillin-resistant VISA strain SA137/93A (vancomycin MIC [E-test], 8 µg/ml), called SA137/93G, showed increased resistance to vancomycin (MIC [E-test], 12 µg/ml). Analysis of the resistance profile of the mutant revealed a loss of ß-lactam resistance with a concomitant increase in resistance to glycopeptides. In both strains, cell wall thickness was 1.4-fold greater than that of control isolates. However, cross-linking of the cell wall was drastically lower in SA137/93A than in SA137/93G. The sensitivity of strain SA137/93G to ß-lactams was due to loss of the ß-lactamase plasmid and a deletion that comprises 32.5 kb of the methicillin resistance cassette SCCmec, as well as 65.4 kb of chromosomal DNA. A spontaneous mutant of SA137/93G with higher sensitivity to vancomycin displayed a cell wall profile similar, in some respects, to that of an fmhB mutant. Results described here and elsewhere show that the only feature common to all VISA strains is a thickened cell wall, which may play a central role in the vancomycin resistance mechanism.

* Corresponding author. Mailing address: Institut für Medizinische Mikrobiologie und Immunologie, Universität Bonn, Sigmund-Freud-Strasse 25, D-53105 Bonn, Germany. Phone: 49-228-287-9103. Fax: 49-228-287-4808. E-mail: Bierbaum{at}mibi03.meb.uni-bonn.de.

Antimicrobial Agents and Chemotherapy, February 2003, p. 568-576, Vol. 47, No. 2
0066-4804/03/$08.00+0     DOI: 10.1128/AAC.47.2.568-576.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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