Necrotising pneumonia, Staphylococcus aureus and Panton-Valentine leukocidin: a review of pathogenesis, clinical features, and management

Necrotizing pneumonia, particularly that caused by Staphylococcus aureus, is a severe and often fatal form of pneumonia. The virulence factor Panton-Valentine leukocidin (PVL) has been strongly implicated in the pathogenesis of severe S. aureus infections, including necrotizing pneumonia, by causing leukocyte destruction and tissue necrosis.

This article is a comprehensive review synthesizing existing literature on the epidemiology, microbiology, clinical presentation, radiological features, pathology, and management strategies for necrotizing pneumonia, with a particular focus on PVL-positive S. aureus infections. It integrates findings from case reports, case series, and observational studies to describe the disease spectrum and current understanding.

PVL-positive S. aureus is a major cause of severe necrotizing pneumonia, often affecting young, previously healthy individuals. Clinical presentation is typically rapid and severe, characterized by fever, hemoptysis, and respiratory failure, with radiographic evidence of multifocal infiltrates, cavitation, and pleural effusions. Mortality rates remain high, often exceeding 50%, despite aggressive antimicrobial therapy and supportive care, highlighting the need for early recognition and targeted interventions. The review emphasizes the importance of early suspicion for PVL-positive S. aureus in severe community-acquired pneumonia.

PCCM fellows should maintain a high index of suspicion for PVL-positive S. aureus necrotizing pneumonia in young, otherwise healthy patients presenting with severe, rapidly progressive pneumonia, especially with hemoptysis or cavitation, and consider empiric therapy including agents active against MRSA and PVL-producing strains.

As a review article, it is limited by the quality and heterogeneity of the primary studies included. Specific treatment recommendations may evolve over time with new evidence, and the exact prevalence of PVL-positive strains varies geographically. The retrospective nature of many included studies means causal links are inferred rather than proven.