Community-acquired (CA) methicillin-resistant Staphylococcus aureus (MRSA) infection among individuals without healthcare-associated (HA) risk factors was first recognized about a decade ago. It has now emerged as an epidemic that is responsible for rapidly progressive, fatal diseases including necrotizing pneumonia, severe sepsis and necrotizing fasciitis. Unlike HA-MRSA, CA-MRSA are usually pan-susceptible to non-beta-lactam antimicrobials. In addition to novel methicillin resistance genetic cassettes, many CA-MRSA harbor a phage harboring Panton-Valentine Leukocidin (PVL) genes and some data support the idea that PVL is responsible at least in part for the increased virulence of CA-MRSA. The tight association between the novel methicillin resistance cassettes and PVL phage cannot be explained, as they integrate into distinct sites on the S. aureus chromosome. This paper presents the evidence that CA-MRSA isolates are distinct strains emerging de novo from CA-methicillin susceptible isolates rather than from HA-MRSA isolates that have escaped from the hospital setting and that these novel CA-MRSA isolates may be more virulent than HA-MRSA. The second aim is to outline the progress in understanding the role of PVL in CA-MRSA pathogenesis.