G. Gudmundsson et Db. Hornick, PATHOPHYSIOLOGY OF HOSPITAL-ACQUIRED PNEUMONIA, Seminars in respiratory and critical care medicine, 18(2), 1997, pp. 99-110
Hospital-acquired pneumonia (HAP) is an important contributor to hospi
tal 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 betwe
en bacteria and the host defenses at the cellular level. Mechanical ve
ntilation 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 b
acteria such as gram-negative bacilli and S. aureus commonly colonize
the oropharynx of hospitalized patients and most commonly cause pneumo
nia via aspiration into the lung. The lungs are protected from these p
otential pathogens by physical barriers, mechanical clearance, and at
the cellular level by the antimicrobial properties of airway surface f
luid and inflammatory cells (e.g., pulmonary macrophages, neutrophils)
. We review new data indicating that respiratory epithelial cells part
icipate in regulating the inflammatory response. When the host defense
s are handicapped in severe illness, hospital-associated bacteria, par
ticularly P. aeruginosa, express multiple virulence factors that can f
rustrate the crippled host defense mechanisms and propagate lung destr
uction.