Methicillin-resistant Staphylococcus aureus (MRSA) was initially confined to hospitals, but in the late 1970s appeared in the community in the USA, primarily among intravenous drug users. In the 1990s, community MRSA (cMRSA) strains appeared in multiple areas of the world, and spread extensively. Initially, there were problems with the definition of 'community-acquired', which was exacerbated by the fact that if a time-based definition was used without stratification for risk factors, patients with healthcare-associated MRSA would be counted. Some cMRSA strains have entered the hospital environment to cause outbreaks of infection, which has added to the difficulty in separating the two types. cMRSA strains usually possess genes for Panton-Valentine leukocidin (PVL), which is associated with furunculosis and necrotizing pneumonia, and sometimes possess other virulence genes such as those for toxic shock syndrome or exfoliative toxins. Antimicrobial resistance to commonly used topical and oral agents is now appearing in certain cMRSA strains, which is complicating therapy. While cMRSA strains are usually susceptible to most non-beta-lactam antimicrobials, there is a lack of clinical trial data indicating which drugs have superior clinical efficacy. DNA fingerprinting methods have become more sophisticated over the last decade, and have determined that cMRSA strains have probably arisen from virulent methicillin-susceptible strains, most likely by horizontal transfer of methicillin-resistance genes from coagulase negative staphylococci to S. aureus on a limited number of occasions, and these clones have spread extensively throughout the world by person-to-person transmission. In Australia, the dominant cMRSA clones are the Western Australia, Oceania and Queensland strains.