Staphylococcus aureus is a cause of hospital- and community-acquired infections (1,2). In 1996, the first clinical isolate of S. aureus with reduced susceptibility to vancomycin was reported from Japan (3). The vancomycin minimum inhibitory concentration (MIC) result reported for this isolate was in the intermediate range (vancomycin MIC=8 µg/mL) using interpretive criteria defined by the National Committee for Clinical Laboratory Standards (4). As of June 2002, eight patients with clinical infections caused by vancomycin-intermediate S. aureus (VISA) have been confirmed in the United States (5,6). This report describes the first documented case of infection caused by vancomycin-resistant S. aureus (VRSA) (vancomycin MIC >32 µg/mL) in a patient in the United States. The emergence of VRSA underscores the need for programs to prevent the spread of antimicrobial-resistant microorganisms and control the use of anti-microbial drugs in health-care settings. In June 2002, VRSA was isolated from a swab obtained from a catheter exit site from a Michigan resident aged 40 years with diabetes, peripheral vascular disease, and chronic renal failure. The patient received dialysis at an outpatient facility (dialysis center A). Since April 2001, the patient had been treated for chronic foot ulcerations with multiple courses of antimicrobial therapy, some of which included vancomycin. In April 2002, the patient underwent amputation of a gangrenous toe and subsequently developed methicillin-resistant S. aureus bacteremia caused by an infected arteriovenous hemodialysis graft. The infection was treated with vancomycin, rifampin, and removal of the infected graft.
In June, the patient developed a suspected catheter exit-site infection, and the temporary dialysis catheter was removed; cultures of the exit site and catheter tip subsequently grew S. aureus resistant to oxacillin (MIC >16 µg/mL) and vancomycin (MIC >128 µg/mL). A week after catheter removal, the exit site appeared healed; however, the patient’s chronic foot ulcer appeared infected. VRSA, vancomycin-resistant Enterococcus faecalis (VRE), and Klebsiella oxytoca also were recovered from a culture of the ulcer. Swab cultures of the patient’s healed catheter exit site and anterior nares did not grow VRSA. To date, the patient is clinically stable, and the infection is responding to outpatient treatment consisting of aggressive wound care and systemic antimicrobial therapy with trimethroprim/sulfamethoxazole.
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