Background and aims The incidence of necrotizing pneumococcal pneumonia has increased over the last two decades. We hypothothesized that increased pneumococcal load or augmented inflammatory cytokine production may lead to destructive pneumococcal lung disease.
Methods This study prospectively enrolled children aged 0–18 years with a diagnosis of community-acquired pneumonia with pleural effusion admitted to 6 medical centres. Children were diagnosed with pneumococcal empyema if the pleural fluid tested positive for quantitative pneumococcal (lytA) detection by real-time polymerase chain reaction (RT-PCR). Pneumococcal empyema cases were further divided into four groups accoring to necrosis severity scaled by radiographic image findings: 0) non-necrosis, 1) mild necrosis, 2) cavitation, and 3) bronchopleural fistula (BPF). Nasopharyngeal and pleural pneumococcal load, as well as proinflammatory cytokines (TNF-α, IL-1β, IL-6, IL-8), Th1-(IL-2, IFN-γ), Th2-(IL-4, IL-10), and Th17-cytokines (IL-17) in the pleural fluid were measured.
Results Serotypes 19A and 3 accounted for 65.3% and 4.2% (respectively) of 72 cases of pneumococcal empyema. In multivariate analysis, pleural pneumococcal density (adjusted odds ratio [aOR], 1.79; 95% confidence interval [CI], 1.03–3.06), and IL-8 (aOR, 2.64; 95% CI, 1.21–5.75) were independent factors associated with the severity of lung necrosis. There was a good correlation between nasopharyngeal and pleural pneumococcal density (ρ = 0.42; p = 0.001). A lytART-PCR pleural density ≥ 50,000 copies/mL had a sensitivity of 88.2% and a specificity of 70.9% for predicting bronchopleural fistula.
Conclusion Evolution of S. pneumoniae toward increased fitness in their interaction with host and exaggerated IL-8 expression are responsible for the increase of necrotizing pneumococcal pneumonia.