Community-acquired methicillin-resistant Staphylococcus aureus infections

Staphylococcus aureus causes a variety of minor diseases but also is responsible for staphylococcal pneumonia and sepsis, both of which can be fatal. It is thought to be responsible for many of the pneumonia deaths associated with the influenza pandemics of the 20th century. The introduction of penicillin in the 1940s greatly improved the prognosis for patients with severe staphylococcal infections. However, after a few years of clinical use, most staphylococcal strains were able to hydrolyze penicillin by producing beta-lactamases, making penicillin a useless antibiotic to treat staphylococcal infections caused by beta-lactamase-producing S aureus. Methicillin, a semisynthetic penicillin introduced in 1959, was specifically designed to be resistant to beta-lactamase degradation, but resistance developed soon after its introduction into clinical practice. Methicillin-resistant S aureus (MRSA) was first reported in the United Kingdom in 1961, followed by reports from other European countries, Japan, and Australia. The first reported case of MRSA in the United States was in 1968. Currently, MRSA is an important pathogen in nosocomial infections and is a problem in hospitals worldwide, and it is increasingly recovered from nursing home residents with established risk factors. More recently, community-acquired MRSA infections have been documented among healthy individuals with no recognizable risk factors, and it seems clear that community-acquired MRSA (CA-MRSA) strains are epidemiologically and clonally unrelated to hospital-acquired strains. This review focuses on the epidemiology, clinical significance, and virulence markers of CA-MRSA infections.