Community-Associated Methicillin-Resistant Staphylococcus aureus as a Cause of Health Care--Associated Infection

Abstract

From 1975 through 1980, MRSA infection spread to hospitals in previously unaffected areas of the United States, and the number of institutions reporting cases of MRSA infection increased considerably [1], From 1983 through the early 1990s, the prevalence of health care-associated (HA) MRSA infection increased dramatically, and it continued to increase more gradually during the latter half of the 1990s [2, 3]. In 1998, Herold et al. [4] reported an alarming increase in the occurrence of community-associated (CA) MRSA infection among young children with none of the typical risk factors associated with HA MRSA. Within a few years, CA MRSA strains became widely disseminated, accounting for 15%-74% of S. aureus skin and soft-tissue infections seen in emergency departments [5-8]. A recent population-based study of invasive MRSA infection found that 26.6% of infections had onset during a hospitalization, 58.4% were community-onset infections among individuals with previous health care exposures, and 13.7% were CA infections [9]. CA MRSA strains typically have PFGE patterns (e.g., USA300 or USA400) that differ from HA MRSA strains, are staphylococcal cassette chromosome mec type IV or V, produce Panton-Valentine leukocidin (PVL), and are susceptible to most non-/3-lactam antibiotics [6, 10, 11]. The predominant CA MRSA strain in the United States is multilocus sequence type 8 (ST8):USA300:staphylococcal cassette chromosome mec type IVa, whereas the predominant CA MRSA strains in Europe and Oceania are ST80 and ST30, respectively [ 12, 13] . All predominant CA MRSA strains produce PVL, which is strongly associated with the propensity of these organisms to cause skin and soft-tissue infection, necrotizing fasciitis, and necrotizing pneumonia and with the ability of such strains to spread rapidly [14, 15]. USA300 also carries genes for molecular variants of enterotoxins K and Q and a novel arginine catabolic mobile element that encodes an arginine deiminase pathway and oligopeptide permease system, which may contribute to the epidemiological and clinical virulence of USA300 [14]. CA MRSA strains have been introduced into hospitals by the 15%-23% of patients who require hospitalization for management of their infections [7, 8] and most likely by other colonized patients who require hospital admission for other purposes. In 2003, Saiman et al. [16] reported one of the first recognized outbreaks involving transmission of a CA MRSA strain in a health care facility. Subsequently, a number of nosocomial outbreaks, often