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.