668 • CID 2008:46 (1 March) • Sievert et al.
M A J O R A R T I C L E
Vancomycin-Resistant Staphylococcus aureus
in the United States, 2002–2006
Dawn M. Sievert,1,2James T. Rudrik,1Jean B. Patel,2L. Clifford McDonald,2Melinda J. Wilkins,1
and Jeffrey C. Hageman2
1Michigan Department of Community Health, Lansing; and
2Centers for Disease Control and Prevention, Atlanta, Georgia
(See the editorial commentary by Tenover on pages 675–7)
This report compares the clinical characteristics, epidemiologic investigations, infection-control
evaluations, and microbiologic findings of all 7 of the cases of vancomycin-resistant Staphylococcus aureus (VRSA)
infection in the United States during the period 2002–2006.
Epidemiologic, clinical, and infection-control information was collected. VRSA isolates underwent
confirmatory identification, antimicrobial susceptibility testing, pulsed-field gel electrophoresis, and typing of the
resistance genes. To assess VRSA transmission, case patients and their contacts were screened for VRSA carriage.
Seven cases were identified from 2002 through 2006; 5 were reported from Michigan, 1 was reported
from Pennsylvania, and 1 was reported from New York. All VRSA isolates were vanA positive and had a median
vancomycin minimum inhibitory concentration of 512 mg/mL. All case patients had a history of prior methicillin-
resistant S. aureus and enterococcal infection or colonization; all had several underlying conditions, including
chronic skin ulcers; and most had received vancomycin therapy prior to their VRSA infection. Person-to-person
transmission of VRSA was not identified beyond any of the case patients. Infection-control precautions were
evaluated and were consistent with established guidelines.
Seven patients with vanA-positive VRSA have been identified in the United States. Prompt
detection by microbiology laboratories and adherence to recommended infection control measures for multidrug-
resistant organisms appear to have prevented transmission to other patients.
Staphylococcus aureus and Enterococcus species are
gram-positive, human commensal bacteria. S. aureus is
commonly found on theskin and inthenaresofhealthy
people. Enterococci are normally present in the human
intestines. Both of these bacteria are opportunistic
pathogens and have been among the most common
causes of nosocomial infections [1, 2]. During the past
2 decades, these bacteria have developed resistance to
commonly prescribed antimicrobial agents. Methicil-
lin-resistant S. aureus (MRSA) infection first emerged
in the United States in the 1970s, and by the 1990s,
Received 15 August 2007; accepted 31 October 2007; electronically published
30 January 2008.
The findings and conclusions in this report are those of the authors and do not
necessarily represent the views of the Centers for Disease Control and Prevention.
Reprints or correspondence: Dr. Dawn M. Sievert, Div. of Healthcare Quality
Promotion, Centers for Disease Control and Prevention, 1600 Clifton Rd., MS A-
24, Atlanta, GA 30333 (DSievert@cdc.gov).
Clinical Infectious Diseases 2008;46:668–74
? 2008 by the Infectious Diseases Society of America. All rights reserved.
MRSA was considered to be endemic in most large
urban medical centers [3, 4]. Vancomycin-resistant en-
terococci (VRE) were first reported in a US hospital in
1989 and rapidly became a common cause of health
care–associated infections [5–7]. Although vancomycin
could no longer be used to treat the growing number
of VRE infections, it remained the only uniformly ef-
infections [8–10]. In 1992, Noble et al.  demon-
strated that conjugal transfer of the vanA gene, which
mediates vancomycin resistance, from VRE to MRSA
on the skin surface of hairless mice could be achieved,
creating vancomycin-resistant S. aureus (VRSA). In an
era of increasing rates of VRE and MRSA infection, the
prospect of this transfer occurring spontaneously in
vivo was of serious concern. In 1997, the first case of
vancomycin-intermediate S. aureus infection was re-
ported from Japan . However, the mechanism of
resistance was not mediated by vanA but rather by a
change in cell physiology caused by genetic mutations
and altered expression of certain genes, resulting in a
by guest on February 2, 2016
674 • CID 2008:46 (1 March) • Sievert et al.
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