Increase of the USA300 clone among community-acquired methicillin-susceptible Staphylococcus aureus causing invasive infections

Background: Methicillin-resistant Staphylococcus aureus (MRSA) USA300 is a predominant cause of community-acquired (CA) infection in the United States. We compared clinical characteristics of children with USA300 versus non-USA300 CA-methicillin-susceptible S. aureus (CA-MSSA) invasive infections at Texas Children's Hospital (TCH). Methods: Medical records were reviewed from children with invasive CA-MSSA infections at TCH between August 1, 2001 and September 30, 2006. Isolates were characterized by pulsed-field gel electrophoresis and polymerase chain reaction for Panton-Valentine leukocidin genes (pvl). Results: Invasive CA-MSSA infections increased from 14 in year 1 to 36 in year 5 (5-year total = 122 patients). Among the CA-MSSA isolates available for typing in the 5-year period, USA300 MSSA strains increased from 14% (2 of 14) to 35% (11 of 31) (P = 0.03). USA300 MSSA strains were more likely than non-USA300 MSSA strains to be nonsusceptible to erythromycin [66% (19 of 29) versus 28% (25 of 88); P < 0.01]. Osteomyelitis cases increased from 43% (6 of 14) in year 1 to 67% (24 of 36) in year 5. The majority of pvl(+) MSSA isolates were USA300 (71% (25 of 35); only 5% (4 of 82) of pvl(-) MSSA isolates were USA300. Patients with osteomyelitis caused by pvl+ isolates had significantly higher mean values for erythrocyte sedimentation rate at admission (P = 0.005) and erythrocyte sedimentation rate maximum value (P = 0.002), maximum C-reactive protein (P = 0.04), and absolute neutrophil count at presentation (P = 0.04) compared with patients whose isolates were pvl-. Conclusions: USA300 accounted for a growing proportion of CA-MSSA isolates among children and was associated with increased numbers of invasive CA-MSSA infections at TCH, especially osteomyelitis. Associations were found in CA-MSSA osteomyelitis between pvl and increased concentrations of systemic inflammatory markers in patients.