Background: Community-acquired Staphylococcus aureus (SA) pneumonia has increased in children, yet few studies have focused on this infection.
Methods: Patients with SA pneumonia (not ventilator-associated) were identified from our surveillance database. Medical records were reviewed; isolates were genotyped by PFGE and Panton-Valentine leukocidin genes detected by polymerase chain reaction.
Results: From August 2001 to April 2009, 117 patients had SA pneumonia. The rate of SA pneumonia per 10,000 admissions increased from 4.81 hospitalizations in year 1 to 9.75 in year 7 (P = 0.04). Methicillin-resistant SA (MRSA) caused 74% and methicillin-susceptible SA (MSSA) caused 26% of the infections. USA300 represented 75/82 (92%) of the MRSA and 14/28 (50%) of the MSSA isolates (P < 0.01). Patients with MRSA were younger (median [range], 0.8 years [0.1–16.9 years]) than patients with MSSA infections (2.5 years [0.2–20.9 years]) (P = 0.008). Clinical presentation was pneumonia with or without effusion in 30, empyema in 72, or lung abscess in 15 cases. Viral coinfections in 18/68 patients tested were associated with respiratory failure (72% vs. 24% [P < 0.001]). Thirty-five children were intubated and 68 had intensive care unit care; 89, 25, and 3 had video-assisted thoracoscopy (VATS), thoracentesis, and lobectomy, respectively. VATS was used more for USA300 than non-USA300 infections (80% vs. 57% [P = 0.03]). In all, 88 children received clindamycin. Improvement or cure occurred in 103 patients (88%), unscheduled visit or readmission related to the same problem in 6, respiratory sequelae in 7, and death in 1 patient.
Conclusions: SA pneumonia increased in frequency over the study years and most were caused by community-acquired MRSA and USA300 isolates. Viral coinfection in 15% of the cases was associated with respiratory failure. Clindamycin is an effective treatment for susceptible-SA pneumonia; VATS was more common in patients with USA300 infections.
From the *Infectious Diseases Section, Department of Pediatrics, Baylor College of Medicine, Houston, TX; and †Infectious Disease Service, Texas Children's Hospital, Houston, TX.
Accepted for publication February 14, 2011.
Supported by an investigator initiated grant from Pfizer (to S.L.K.), and the author has participated on Pfizer advisory committees.
M.A.C.-M. was supported by the Boyd Morse Foundation.
Address for correspondence: Sheldon L. Kaplan, MD, Infectious Disease Service, Texas Children's Hospital, Feigin Center, Ste 1150, 1102 Bates Street, Houston, TX 77030. E-mail: firstname.lastname@example.org.
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