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Access to the article is free, however registration and sign-in are required. Infection by the pathogenic bacterium Staphylococcus aureus can cause a wide range of conditions, from mild skin infections to life-threatening endocarditis, pneumonia, and sepsis. Until recently, severe infections caused by strains that are resistant to multiple drugs including beta-lactam antibiotics (penicillin and cephalosporin)--the so-called methicillin-resistant S. aureus (MRSA) strains--were found exclusively in health-care institutions and hospitals, and strong hygiene procedures were used to prevent transmission and destroy the bacteria. But in 1999, fatal infections caused by MRSA were unexpectedly reported in the community. Since then, the spread of community-acquired MRSA to healthy individuals has been worldwide , resulting in severe fatal infections including fasciitis necroticans ("flesh-eating bacteria"), Waterhouse-Friedrichsen syndrome, and highly lethal necrotizing pneumonia . On page 1130 of this issue, Labandeira-Rey et al. report that MRSA strains that cause necrotizing pneumonia rely on the dual action of a single bacterial toxin that results in the destruction of respiratory tissue and bacteria-engulfing immune cells and exacerbated inflammation. This new understanding may help guide the design of effective therapeutic regimens for S. aureus infections and other infectious respiratory illnesses.

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      Keywords:

      mecA,NSDL,NSDL_SetSpec_BEN,Panton-Valentine leukocidin (PVL),necrotizing pneumonia,methicillin-resistant S. aureus (MRSA) strains,staphylococcal protein A (or SpA),Protein A,adhesion expression,oai:nsdl.org:2200/20110722030127319T

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      English

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      Creative Commons Attribution Non-Commercial Share Alike

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