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Journal of Antimicrobial Chemotherapy (2003) 52, 864-868
© 2003 The British Society for Antimicrobial Chemotherapy

Antibacterial susceptibility of a vancomycin-resistant Staphylococcus aureus strain isolated at the Hershey Medical Center

Bülent Bozdogan1, Duygu Esel1,*, Cynthia Whitener2, Frederick A. Browne2 and Peter C. Appelbaum1,§

Departments of 1 Pathology and 2 Medicine, Hershey Medical Center, 500 University Drive, Hershey, PA 17033, USA

Received 14 August 2003; returned 22 August 2003; revised 26 August 2003; accepted 28 August 2003

Staphylococcus aureus strain HMC3 isolated at the Hershey Medical Center, was resistant to vancomycin (VRSA) through the presence of the vanA resistance gene; it also contained mecA, erm(A), erm(B), tet(K) and aac(6')-aph(2''), conferring resistance to licensed ß-lactams, macrolides, tetracycline and aminoglycosides. HMC3 also had alterations in GyrA and GrlB and was resistant to available quinolones. Experimental drugs with low MICs (<2 mg/L) for VRSA HMC3 included cephalosporins BAL9141 and RWJ-54428; glycopeptides oritavancin and dalbavancin; the lipopeptide daptomycin; the glycolipodepsipeptide ramoplanin; new fluoroquinolones WCK 771 A, WCK 1153, DK-507k and sitafloxacin; and the DNA nanobinder GS02-02. These agents were all bactericidal as were trimethoprim/sulfamethoxazole and teicoplanin (MIC 4 mg/L). Oxazolidinones linezolid and ranbezolid; the injectable streptogramin quinupristin/dalfopristin; DNA nanobinders GS2-10547 and GS02-104; peptide deformylase inhibitors NVP-PDF713 and GS02-12; tetracycline derivative tigecycline; the antifolate iclaprim; mupirocin and fusidic acid were all active in vitro but bacteriostatic.

Keywords: S. aureus, VRSA, antimicrobial susceptibilities, mechanisms of resistance

* Present address. Erciyes Üniversitesi Tip Fakültesi, Mikrobiyoloji BD, Kayseri, Turkey.

§ Corresponding author. Tel: +1-717-531-5113; Fax: +1-717-531-7953; E-mail: pappelbaum{at}psu.edu


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