Methicillin-resistant Staphylococcus aureus (MRSA) was described in 1961, shortly after the introduction of methicillin, and outbreaks of MRSA were reported in the early 1960s [1,2]. Since that time, MRSA has spread worldwide, and the prevalence of MRSA has increased in both healthcare and community settings. For example, the prevalence of methicillin-resistance among S. aureus isolates in intensive care units in the United States is 60 percent , and more than 90,000 invasive infections due to MRSA occurred in the United States in 2005 .
Methicillin resistance is mediated by PBP-2a, a penicillin binding protein encoded by the mecA gene that permits the organism to grow and divide in the presence of methicillin and other beta-lactam antibiotics. The mecA gene is located on a mobile genetic element called staphylococcal chromosome cassette (SCCmec). (See "Microbiology of methicillin-resistant Staphylococcus aureus".)
A single clone probably accounted for most MRSA isolates recovered during the 1960s; by 2004, six major MRSA clones emerged worldwide, labeled as SCCmec I-VI [5-9]. Dissemination of resistance was mediated by horizontal transfer of the mecA gene and related regulatory sequences .
The epidemiology and clinical manifestations of MRSA infection in adults will be reviewed here. Prevention, control, and treatment of MRSA infections in adults are discussed separately. (See "Prevention and control of methicillin-resistant Staphylococcus aureus in adults" and "Treatment of invasive methicillin-resistant Staphylococcus aureus infections in adults" and "Treatment of skin and soft tissue infections due to methicillin-resistant Staphylococcus aureus in adults".)
Healthcare-associated methicillin-resistant S. aureus (HA-MRSA) and community-associated methicillin-resistant S. aureus (CA-MRSA) differ with respect to their clinical and molecular epidemiology.