The clinical characteristics and virulence factors related to musculoskeletal infections caused by community-acquired, methicillin-resistant Staphylococcus aureus (MRSA) in children are not well-defined.
In this retrospective study, the demographics, hospital course and outcome of children with musculoskeletal infections were reviewed from medical records and by contacting patients or their physicians. Antimicrobial susceptibilities were determined by disk diffusion. Polymerase chain reaction was performed to detect genes encoding for virulence factors. Mann-Whitney, χ2 and Kaplan-Meier tests were used for statistical analysis.
Community-acquired MRSA and community-acquired methicillin-susceptible S. aureus (MSSA) caused musculoskeletal infections in 31 and 28 children, respectively. The median numbers of febrile days after start of therapy were 4 and 1 for MRSA and MSSA patients, respectively (P = 0.001). The median numbers of hospital days were 13 and 8 for the MRSA and MSSA groups, respectively (P = 0.014). At follow-up, 2 patients in the MRSA and 1 in the MSSA group had developed chronic osteomyelitis. pvl and fnbB genes were found in 87 and 90% versus 24 and 64% in the MRSA versus MSSA groups, respectively. (P = 0.00001 and 0.017). Ten patients with pvl-positive strains had complications versus no patients with pvl-negative isolates (P = 0.002).
Febrile days and hospital days were greater in children with musculoskeletal infection caused by MRSA than in those affected by MSSA, but no significant differences were found in the final outcome. pvl and fnbB genes were more frequent in the MRSA than in the MSSA strains. The presence of the pvl gene may be related to an increased likelihood of complications in children with S. aureus musculoskeletal infections.
From the *Baylor International Pediatrics Aids Initiative, Baylor College of Medicine, Houston, TX; †Medical Research Unit in Clinical Epidemiology, Instituto Mexicano del Seguro Social, Durango, Mexico; and the ‡Department of Pediatrics, Baylor College of Medicine and the Infectious Disease Laboratory, Texas Children’s Hospital, Houston, TX
Accepted for publication March 19, 2004.
Supported in part by a grant from Pharmacia, Inc. and by grant D43 TW01036 from the Fogarty International Center of the National Institutes of Health.
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