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 b-lactamases, making
penicillin a useless
antibiotic to treat
staphylococcal infections caused by b-lactamase-producing S aureus.
Methicillin, a semisynthetic
penicillin introduced in 1959, was specifically designed to be resistant to b-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.