Staphylococcus aureus, particularly methicillin-resistant S. aureus (MRSA), is a major human pathogen. MRSA can cause skin and soft tissue infections (SSTIs), as well as pneumonia, bacteremia, and sepsis (1). The majority of MRSA infections are caused by only a small number of clones. For example, the major clones in the United Kingdom are epidemic MRSA 15 (EMRSA-15) (clonal complex 22 [CC22] and sequence type 22 [ST22]) and EMRSA-16 (CC30 and ST36), whereas in Japan, Hungary, and the United States, the predominant clones are ST5-staphylococcal cassette chromosome mec element (SCCmec) II, ST239-SCCmec III, and ST8-SCCmec IV, respectively (1, 2). In China, the major clones are ST239-SCCmec III and ST5-SCCmec II, while ST59 is the third most common ST (3).MRSA infections can be caused by either health care-associated (HA) MRSA or community-associated (CA) MRSA. However, CA-MRSA is phenotypically and genotypically different from HA-MRSA (4). CA-MRSA is believed to mainly cause SSTIs in healthy persons without risk factors for MRSA acquisition, and it rarely causes necrotizing pneumonia (5, 6). CA-MRSA typically harbors SCCmec type IV (21 to 24 kb) or V (28 kb) and is less resistant to non--lactam antibiotics. HA-MRSA persists in hospitals, causes cutaneous and invasive infections, and usually contains larger SCCmec, such as types I (34 kb), II (53 kb), or III (67 kb); thus, the resistance of HA-MRSA isolates is not restricted to -lactam antibiotics, and these pathogens are often resistant to multiple types of drugs (1).Panton-Valentine leukocidin (PVL), a bicomponent poreforming cytotoxin assembled by LukS-PV and LukF-PV, has been demonstrated to have a significant function in the pathogenesis of MRSA by targeting polymorphonuclear cells, monocytes, and macrophages (7). Epidemiological studies have revealed that the PVL genes are carried mainly by CA-MRSA (8). However, PVL genes carried by HA-MRSA strains have also been described (9, 10). In China, an analysis conducted between 2005 and 2006 of 702 MRSA isolates from 18 teaching hospitals in 14 cities showed that the carriage rate of PVL genes in MRSA strains was 2.3%, and all PVL-positive isolates were considered to be HA-MRSA based on patient medical records (11). In a teaching hospital in Wenzhou, 11.9% of the HA-MRSA isolates were PVL positive (12). The risk of the prevalent PVL-positive HA-MRSA strains is a se-