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Public Health Dispatch: Vancomycin-Resistant Staphylococcus aureus --- Pennsylvania, 2002

Please note: The text of this report has been corrected and does not correspond to the official electronic PDF version. An erratum has been published; to view the erratum, please click here.

Staphylococcus aureus is one of the most common causes of hospital- and community-acquired infections (1,2). Since the recognition of vancomycin-resistant enterococci in 1988, the emergence of vancomycin-resistant S. aureus (VRSA) (minimum inhibitory concentration [MIC] >32 µg/mL [3]) has been anticipated. The transfer of the genetic element containing the vanA vancomycin resistance gene from Enterococcus faecalis to S. aureus was demonstrated in the laboratory in 1992 (4); the first clinical infection with VRSA was reported in July 2002 (5). This report describes the second documented clinical isolate of VRSA from a patient.

On September 20, the patient was admitted to a hospital in Pennsylvania and evaluated for a chronic foot ulcer and possible osteomyelitis. A culture of the ulcer grew S. aureus. This isolate was tested for antimicrobial susceptibility by disk diffusion; a vancomycin-agar screen plate (brain heart infusion agar containing 6 µg/mL vancomycin) also was inoculated. Growth on the vancomycin screen plate and a 12 mm zone of inhibition around the vancomycin disk suggested that the isolate had decreased susceptibility to vancomycin. Further testing by Etest® confirmed that the isolate was resistant to vancomycin (MIC=64 µg/mL). Following notification of the Pennsylvania Department of Health (PDH), the isolate was forwarded to CDC, where it was confirmed to be VRSA (vancomycin MIC=32 µg/mL by broth microdilution testing). The isolate contained both the mecA and vanA genes mediating oxacillin and vancomycin resistance, respectively. The isolate was susceptible to chloramphenicol, linezolid, minocycline, quinupristin-dalfopristin, rifampin, and trimethoprim-sulfamethoxazole.

The patient has been discharged from the hospital and is responding to antimicrobial treatment. The patient is receiving home-health care. PDH and CDC are assisting health-care providers investigating this case of VRSA. The goals of this investigation include assessment of infection-control practices in the hospital and home setting and the possibility of transmission of the organism to other patients, health-care providers, and family or social contacts. Previous investigations of VRSA and vancomycin-intermediate S. aureus in the home setting demonstrated no transmission among family or home health-care contacts (5,6).

The presence of vanA in this VRSA suggests that the resistance determinate was acquired from a vancomycin-resistant enterococcus. Development of this VRSA appears to be unrelated to the previous VRSA identified in Michigan (5). However, because both were probably the result of conjugation events, additional VRSA infections are likely to occur. Therefore, clinical microbiology laboratories must ensure that they are using susceptibility testing methods that will detect VRSA and that they are saving potential VRSA for confirmatory testing. In addition, more systematic surveillance for VRSA will enhance the ability of the public health system and the health-care system to rapidly address this resistant pathogen.

The public health response to this VRSA occurrence is ongoing. Using proper infection-control practices and good antimicrobial agent management will help limit the emergence and spread of antimicrobial-resistant microorganisms, including VRSA. CDC recommends contact precautions when caring for patients with these infections, including placing the patient in a private room, wearing gloves and a gown during patient contact, washing hands after contact with the patient and infectious body tissues or fluids, and not sharing patient-care items with other patients. CDC guidelines for preventing spread of VRSA are available at http://www.cdc.gov/ncidod/hip/10_20.pdf.

The isolation of S. aureus with confirmed or "presumptive" vancomycin resistance should be saved and reported through state and local health departments to CDC's Division of Healthcare Quality Promotion, National Center for Infectious Diseases, telephone 800-893-0485.

Reported by: D Miller, V Urdaneta, MD, A Weltman, MD, Pennsylvania Dept of Health. Office of the Director, Div of Healthcare Quality Promotion, National Center for Infectious Diseases; S Park, EIS Officer, CDC.

References

  1. CDC. National Nosocomial Infections Surveillance (NNIS) report, data summary from January 1992--June 2001. Am J Infect Control 2001;29: 404--21.
  2. Lowy F. Staphylococcus aureus infections. N Engl J Med 1998;339: 520--32.
  3. National Committee for Clinical Laboratory Standards. Methods for dilution antimicrobial susceptibility tests for bacteria that grow aerobically. 4th ed. Approved standard, M7-A4. Villanova, Pennsylvania: National Committee for Clinical Laboratory Standards, 1997.
  4. Noble WC, Virani Z, Cree RGA. Co-transfer of vancomycin and other resistance genes from Enterococcus faecalis NCTC 12201 to Staphylococcus aureus. FEMS Microbiol Lett 1992;93:195--8.
  5. CDC. Staphylococcus areus resistant to vancomycin---United States, 2002. MMWR 2002;51:565--7.
  6. Hageman, JC, Pegues DA, Jepson C, et al. Vancomycin-intermediate Staphylococcus aureus in a home health-care patient. Emerg Infect Dis 2001;7:1023--5.

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