Abstract
Nosocomial pneumonia, or terminal pneumonia as it was formerly called, results from the repetitive microaspiration of contaminated oropharyngeal secretions into the lungs in the presence of impaired host defenses. This pathophysiologic sequence was suggested by the observations of Osler but clarified by the seminal work of Rouby and colleagues. The enormous impact of antimicrobial agents on the organisms responsible for nosocomial pneumonias was first identified by Kneeland and Price who found that organisms of the normal pharyngeal flora virtually disappeared in terminal pneumonias following administration of these drugs, being replaced by gram-negative bacilli. The remarkable susceptibility of seriously ill patients to becoming colonized by exogenous organisms, even in the absence of antimicrobial therapy, was shown by Johanson et al. These factors, antibiotics and the change in bacterial binding receptors in the airways associated with illness, lead to infections caused by exogenous organisms that are frequently resistant to antimicrobial agents. Clinical findings that usually identify patients with respiratory infections are unreliable for the diagnosis of nosocomial pneumonias as shown by Andrews et al. Invasive techniques, especially the protected specimen brush (PSB) technique, avoid contamination of the specimen by proximal secretions and accurately reflect the bacterial burden of the lung, as first shown by Chastre et al. Quantitation of such specimens serves as an excellent proxy for direct cultures of the lung and are the current gold standard for diagnosis.
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Johanson, W.G., Dever, L.L. Nosocomial pneumonia. Intensive Care Med 29, 23–29 (2003). https://doi.org/10.1007/s00134-002-1589-7
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DOI: https://doi.org/10.1007/s00134-002-1589-7