Pulmonary infections and community associated methicillin resistant Staphylococcus aureus: a dangerous mix?

The incidence of complicated pneumonias in children is increasing with a concurrent increase in the incidence of community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA) infections. CA-MRSA is distinct from hospital associated MRSA [HA-MRSA] in regards to its genotype, epidemiology, and clinical course. Unlike HA-MRSA, CA-MRSA often strikes young, previously healthy children. Pneumonias caused by CA-MRSA have a rather distinct presentation. Because of its pore-forming toxins, namely Panton-Valentine leukocidin (PVL) and alpha-hemolysin, extensive necrotizing disease with corresponding hypoxaemia and hypercarbia is common. Other features include multilobar disease, leucopenia, haemoptysis, and high mortality rates. A previous influenza-like illness or skin and soft tissue infection [SSTI] often precede the development of pneumonia due to CA-MRSA. Vancomycin is recommended as first-line empiric therapy for suspected CA-MRSA infections. However, vancomycin is not an ideal agent for the treatment of pneumonia given its poor concentrating ability in alveolar fluid. Linezolid and clindamycin have also been used in the treatment of CA-MRSA pneumonia and ongoing research is looking for alternative antimicrobials. Recent studies have continued to report a lack of correlation between nasal colonization and active infections due to CA-MRSA. Given that the role of nasal colonization in CA-MRSA infection is not clear, the utility of decolonization treatment has been a point of debate. Finally, patients with cystic fibrosis are becoming increasingly colonized with MRSA as opposed to MSSA. There is some accumulating evidence that patients with MRSA show a more rapid deterioration in their degree of obstructive disease as measured by forced expiratory volume in one second (FEV(1)). However, it still is not clear whether MRSA is a marker for worsening disease or whether it actually is a cause of disease progression in cystic fibrosis. More longitudinal data is needed to understand how MRSA colonization impacts the course of disease in cystic fibrosis.