Pathophysiology of Hospital-Acquired Pneumonia

Abstract

Hospital-acquired pneumonia (HAP) is an important contributor to hospital morbidity, mortality, and increased hospital costs. We review the factors that identify groups of patients that are at risk for HAP, the mechanism by which bacteria enter the lung, and the interaction between bacteria and the host defenses at the cellular level. Mechanical ventilation is the most significant risk factor. Other significant risk factors are discussed and categorized as intervention-related, patient-related, and infection control-related factors. Hospital-associated bacteria such as gram-negative bacilli and S. aureus commonly colonize the oropharynx of hospitalized patients and most commonly cause pneumonia via aspiration into the lung. The lungs are protected from these potential pathogens by physical barriers, mechanical clearance, and at the cellular level by the antimicrobial properties of airway surface fluid and inflammatory cells (e.g., pulmonary macrophages, neutrophils). We review new data indicating that respiratory epithelial cells participate in regulating the inflammatory response. When the host defenses are handicapped in severe illness, hospital-associated bacteria, particularly P. aeruginosa, express multiple virulence factors that can frustrate the crippled host defense mechanisms and propagate lung destruction.

Key Words:

pneumonia - nosocomial - pathophysiology