Abstract
Until recently, Staphylococcus aureus—associated pulmonary infections have been indistinguishable with respect to the toxin-associated genes in the strains associated with each case. The recent emergence and worldwide spread of community-acquired methicillin-resistant S. aureus (CA-MRSA) clones containing the genes encoding Panton-Valentine leukocidin (PVL) has led to an increase in the number of pulmonary lung infections associated with PVL-positive CA-MRSA and the recognition of more-specific clinical conditions. The diffusion of CA-MRSA within certain communities is now impressive. In Texas, for example, 76% of infections due to community-acquired S. aureus at Texas Children's Hospital (Houston) are caused by MRSA [1, 2].