• Kristina G Hultén, Sheldon L Kaplan, Linda B Lamberth, Katherine Slimp, Wendy A Hammerman, Maria Carrillo-Marquez, Jeffrey R Starke, James Versalovic, and Edward O Mason.
• Departments of Pediatrics, Baylor College of Medicine, Texas Children's Hospital, Houston, 77030, USA. khulten@bcm.tmc.edu
• Infect Control Hosp Epidemiol. 2010 Feb 1; 31 (2): 183-90.

ObjectiveTo document the introduction of the methicillin-resistant Staphylococcus aureus (MRSA) USA300 clone into a children's hospital. Current molecular epidemiology of infections due to the USA300 strain of MRSA in the pediatric healthcare setting remains obscure.DesignRetrospective study of patients with hospital-acquired S. aureus infection during the period from August 1, 2001, through July 31, 2007, at Texas Children's Hospital in Houston.MethodsPatients with hospital-acquired S. aureus infection from whom an isolate was available for molecular analysis were included. Clinical information was obtained from patient medical records and the electronic hospital information system. S. aureus isolates underwent antimicrobial susceptibility testing, pulsed-field gel electrophoresis, and polymerase chain reaction testing for staphylococcal cassette chromosome (SCC) mec, agr, the diamine N-acetyltransferase gene, and the Panton-Valentine leukocidin genes (pvl).ResultsOf 242 patients with hospital-acquired S. aureus infection, 147 (61%) had methicillin-susceptible S. aureus infection. Of the 95 MRSA isolates causing hospital-acquired infection, 69 (73%) were USA300 isolates, and that rate did not increase over time. Skin and soft tissue infection (P < .001), onset of infection less than 10 days after admission (P = .007), and lack of comorbidities (P < .001) were associated with hospital-acquired MRSA infection caused by the USA300 strain, compared with other isolates (hereafter referred to as non-USA300 isolates). Nine of 10 patients with a S. aureus infection at the time of death were infected with a non-USA300 strain. USA300 carried SCCmec IV, agr I, the diamine N-acetyl transferase gene, and pvl. USA300 isolates were more susceptible to clindamycin, gentamicin, and trimethoprim-sulfamethoxazole than were other non-USA300 isolates (P < .01).ConclusionsIn our patient population, the annual numbers of observed cases of hospital-acquired S. aureus infection have remained constant. USA300 was the most common clone and, compared with other non-USA300 MRSA isolates, was associated with skin and soft tissue infection, early onset of infection after admission, and greater susceptibility to antimicrobial agents.

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