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MOLECULAR EPIDEMIOLOGY |
School of Biomedical Sciences, Curtin University of Technology, Perth, Western Australia and *Department of Microbiology, Faculty of Medicine, Kuwait University, PO Box 24923, Safat 13110, Kuwait
Corresponding author: Dr E. E. Udo (e-mail: EDET{at}hsc.kuniv.edu.kw).
Received 12 June 2000; revised version received 8 Nov. 2000; accepted 16 Nov. 2000.
Abstract
A total of 128 MRSA isolates from a burns unit in 1992 and 1997 was studied by resistotyping, plasmid analysis and pulsed-field gel electrophoresis (PFGE) of SmaI-digested chromosomal DNA to ascertain whether a clone of MRSA had persisted in the unit or whether different clones had been introduced at different times. All the MRSA isolates produced ß-lactamase and had high MICs to methicillin (>2565mumg/L). All were resistant to tetracycline, kanamycin, cadmium acetate and mercuric chloride. Most were resistant to gentamicin, neomycin, erythromycin, chloramphenicol, trimethoprim, ciprofloxacin, propamidine isethionate and ethidium bromide, and were susceptible to minocycline, vancomycin and teicoplanin. None of the 1992 isolates was resistant to mupirocin, but 56% and 19% of the 1997 isolates expressed high- and low-level mupirocin resistance, respectively. Many of the 1997 isolates had acquired a 38-kb plasmid encoding high-level mupirocin resistance. The 1992 isolates had two main PFGE patterns; 82% of them belonged to PFGE pattern 1. The 1997 isolates had PFGE pattern 1, the same as the majority of the 1992 isolates. All MRSA isolates from both years carried the mecA gene in the same SmaI fragment. These findings demonstrated that a clone of MRSA that was prevalent in the burns unit in 1992 had persisted and became the predominant clone in 1997.
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