Mark D. King, MD, MS; Bianca J. Humphrey, BS; Yun F. Wang, PhD; Ekaterina V. Kourbatova, MD, MPH; Susan M. Ray, MD; Henry M. Blumberg, MD
Acknowledgments: The authors thank Fred Tenover, Linda McDougal, Sigrid McAllister, and Gregory Foshiem at the Centers for Disease Control and Prevention for performing the Panton–Valentine leukocidin and SCCmec analyses and for providing images containing USA-type strains for comparison. They also thank John Boring for his assistance with calculating prevalence ratios and advice on other statistical considerations.
Grant Support: In part by the Emory Medical Care Foundation, the Emory Mentored Clinical Research Scholars Program (National Institutes of Health/National Center for Research Resources [K12 RR 017643]), and the National Institutes of Health/National Institute of Allergy and Infectious Diseases (K23 AI054371).
Potential Financial Conflicts of Interest: None disclosed.
Requests for Single Reprints: Henry M. Blumberg, MD, Division of Infectious Diseases, Emory University School of Medicine, 49 Jesse Hill Drive, Atlanta, GA 30303; e-mail, email@example.com.
Current Author Addresses: Dr. King: Beacon Clinic, 1136 Alpine Avenue, Suite 205, Boulder, CO 80304.
Drs. Ray and Blumberg and Ms. Humphrey: Division of Infectious Diseases, Emory University School of Medicine, 49 Jesse Hill Drive, Atlanta, GA 30303.
Dr. Wang: Department of Pathology and Laboratory Medicine, Emory University School of Medicine, Grady Memorial Hospital, P.O. Box 26248, 80 Jesse Hill Drive, Atlanta, GA 30303.
Dr. Kourbatova: Division of Tuberculosis and Lung Diseases, Samara State Medical University, Pionerskaya Street, 48, 443099 Samara, Russia.
Author Contributions: Conception and design: M.D. King, H.M. Blumberg.
Analysis and interpretation of the data: M.D. King, B.J. Humphrey, Y.F. Wang, E.V. Kourbatova, S.M. Ray, H.M. Blumberg.
Drafting of the article: M.D. King, S.M. Ray, H.M. Blumberg.
Critical revision of the article for important intellectual content: M.D. King, B.J. Humphrey, Y.F. Wang, E.V. Kourbatova, S.M. Ray, H.M. Blumberg.
Final approval of the article: M.D. King, B.J. Humphrey, Y.F. Wang, E.V. Kourbatova, S.M. Ray, H.M. Blumberg.
Statistical expertise: M.D. King, E.V. Kourbatova.
Obtaining of funding: M.D. King, H.M. Blumberg.
Administrative, technical, or logistic support: M.D. King, H.M. Blumberg.
Collection and assembly of data: M.D. King, B.J. Humphrey.
Studies have shown that community-acquired methicillin-resistant Staphylococcus aureus (MRSA) causes S. aureus skin and soft-tissue infection in selected populations.
To determine the proportion of infections caused by community-acquired MRSA, the clinical characteristics associated with community-acquired MRSA, and the molecular epidemiology of community-acquired MRSA among persons with community-onset S. aureus skin and soft-tissue infection.
Active, prospective laboratory surveillance to identify S. aureus recovered from skin and soft-tissue sources.
1000-bed urban hospital and its affiliated outpatient clinics in Atlanta, Georgia.
384 persons with microbiologically confirmed community-onset S. aureus skin and soft-tissue infection.
Proportion of infections caused by and clinical factors associated with community-acquired MRSA among persons with community-onset S. aureus skin and soft-tissue infection. Pulsed-field gel electrophoresis and antimicrobial susceptibility patterns were used to epidemiologically classify community-onset S. aureus infections. Community-acquired MRSA was defined by MRSA isolates that either demonstrated a USA 300 or USA 400 pulsed-field type or had a susceptibility pattern showing resistance only to β-lactams and erythromycin (for isolates not available for pulsed-field gel electrophoresis).
Community-onset skin and soft-tissue infection due to S. aureus was identified in 389 episodes, with MRSA accounting for 72% (279 of 389 episodes). Among all S. aureus isolates, 63% (244 of 389 isolates) were community-acquired MRSA. Among MRSA isolates, 87% (244 of 279 isolates) were community-acquired MRSA. When analysis was restricted only to MRSA isolates that were available for pulsed-field gel electrophoresis, 91% (159 of 175 isolates) had a pulsed-field type consistent with community-acquired MRSA; of these, 99% (157 of 159 isolates) were the MRSA USA 300 clone. Factors independently associated with community-acquired MRSA infection were black race (prevalence ratio, 1.53 [95% CI, 1.16 to 2.02]), female sex (prevalence ratio, 1.16 [CI, 1.02 to 1.32]), and hospitalization within the previous 12 months (prevalence ratio, 0.80 [CI, 0.66 to 0.97]). Inadequate initial antibiotic therapy was statistically significantly more common among those with community-acquired MRSA (65%) than among those with methicillin-susceptible S. aureus skin and soft-tissue infection (1%).
Some MRSA isolates were not available for molecular typing.
The community-acquired MRSA USA 300 clone was the predominant cause of community-onset S. aureus skin and soft-tissue infection. Empirical use of agents active against community-acquired MRSA is warranted for patients presenting with serious skin and soft-tissue infections.
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King MD, Humphrey BJ, Wang YF, Kourbatova EV, Ray SM, Blumberg HM. Emergence of Community-Acquired Methicillin-Resistant Staphylococcus aureus USA 300 Clone as the Predominant Cause of Skin and Soft-Tissue Infections. Ann Intern Med. 2006;144:309–317. doi: 10.7326/0003-4819-144-5-200603070-00005
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Published: Ann Intern Med. 2006;144(5):309-317.
Infectious Disease, MRSA.
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