Methicillin-Resistant Staphylococcus aureus Colonization of the Groin and Risk for Clinical Infection among HIV-infected Adults

Philip J. Peters

, John T. Brooks, Sigrid K. McAllister, Brandi Limbago, H. Ken Lowery, Gregory Fosheim, Jodie L. Guest, Rachel J. Gorwitz, Monique Bethea, Jeffrey Hageman, Rondeen Mindley, Linda K. McDougal, and David Rimland

Author affiliations: Centers for Disease Control and Prevention, Atlanta, Georgia, USA (P.J. Peters, J.T. Brooks, S.K. McAllister, B. Limbago, G. Fosheim, R.J. Gorwitz, J. Hageman, L.K. McDougal); Veterans Affairs Medical Center, Atlanta (H.K. Lowery, J.L. Guest, M. Bethea, R. Mindley, D. Rimland); Emory University School of Medicine, Atlanta (D. Rimland)

Abstract

Data on the interaction between methicillin-resistant Staphylococcus aureus (MRSA) colonization and clinical infection are limited. During 2007–2008, we enrolled HIV-infected adults in Atlanta, Georgia, USA, in a prospective cohort study. Nares and groin swab specimens were cultured for S. aureus at enrollment and after 6 and 12 months. MRSA colonization was detected in 13%–15% of HIV-infected participants (n = 600, 98% male) at baseline, 6 months, and 12 months. MRSA colonization was detected in the nares only (41%), groin only (21%), and at both sites (38%). Over a median of 2.1 years of follow-up, 29 MRSA clinical infections occurred in 25 participants. In multivariate analysis, MRSA clinical infection was significantly associated with MRSA colonization of the groin (adjusted risk ratio 4.8) and a history of MRSA infection (adjusted risk ratio 3.1). MRSA prevention strategies that can effectively prevent or eliminate groin colonization are likely necessary to reduce clinical infections in this population.

Methicillin-resistant Staphylococcus aureus (MRSA) infections are a substantial cause of illness and a major public health problem (1). Although MRSA was traditionally considered a health care–associated pathogen, it has emerged worldwide as a notable cause of community-associated skin and soft tissue infections (2). In the United States, MRSA pulsed-field gel electrophoresis (PFGE) type USA300 strains have caused most community-associated MRSA infections (3). High rates of community-associated (4–6) and health care–associated MRSA infections have also been described among HIV-infected persons (7), although the underlying basis for this association is unknown. Proposed mechanisms include immune dysfunction (5,7,8), behavioral risk factors (9), and increased exposure to the health care system (10). The prevalence of MRSA colonization among HIV-infected persons is also high (10%–17%) (11,12), compared with that in the general US population (0.8%–1.5%) (13,14). Colonization with S. aureus is a risk factor for subsequent clinical infection (15,16), and the site of colonization may also be an key risk factor (17). For example, although the anterior nares is considered the primary reservoir of S. aureus (18), MRSA PFGE type USA300 might preferentially colonize the buttocks, genitals, and perineum (17), leading to more infections in these anatomical areas. Improving our understanding of the interaction between MRSA colonization and clinical infection among persons with HIV is necessary so that effective prevention strategies can be developed for this population.