Staphylococcus aureus Colonization and Infection in New York State Prisons
Departments of 1Medicine and 2Pathology, Columbia University, College of Physicians and Surgeons, Division of Infectious Diseases, 3Columbia University–School of Nursing, and 4New York State Department of Correctional Services, New York, New York; 5Center for Social Epidemiology and Population Health, School of Public Health–University of Michigan, Ann Arbor
Methicillin‐resistant Staphylococcus aureus is increasingly responsible for staphylococcal outbreaks in prison. There is limited information on the source of the outbreak strains, risk factors for infection, and transmission of these strains within a prison. We conducted a survey to determine the prevalence of nasal colonization with S. aureus in 2 New York State prisons. S. aureus isolates from clinical cultures collected from all New York State prisons during a 6‐month period were compared with the colonizing strains. Analyses were conducted to determine whether prison‐level characteristics were associated with colonization or infection with S. aureus. The colonization rate was 25.5% (124/487); 10.5% of the isolates were methicillin resistant, all were staphylococcal chromosomal cassette (SCC)mec type IV, and 61.5% were Panton Valentine leukocidin (PVL) positive. Surprisingly, 21.6% of the methicillin‐susceptible isolates were also PVL positive. Of the clinical isolates, 48.3% were methicillin resistant, with 93.1% of the latter being SCCmec type IV and 48.3% being PVL positive. The predominant clone was USA 300. Prison‐level risk factors for infection included the proportion of inmates with drug offenses, the length of inmate stay, and the jail from which inmates originated. This study suggests that both new and long‐term inmates act as sources of S. aureus strains, with the more virulent of the latter preferentially being selected as pathogens.
Received 18 January 2007; accepted 13 April 2007; electronically published 10 August 2007.
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. Infection Control and Hospital Epidemiology 30:1, 4-8Online publication date: 1-Jan-2009.
Online publication date: 1-Oct-2008.
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Online publication date: 1-Sep-2008.
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Online publication date: 1-Jul-2008.
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Potential conflicts of interest: none reported.
Financial support: Pfizer Pharmaceuticals (grant 2005‐0858 to F.D.L. and E.L.L.); National Center for Research Resources, National Institutes of Health (grant P20 RR020616 to E.L.L. and F.D.L., in support of the Center for Interdisciplinary Research on Antimicrobial Resistance).





