Hospital-acquired pneumonia pathophysiology

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Editor(s)-in-Chief: C. Michael Gibson, M.S., M.D. ; Philip Marcus, M.D., M.P.H.

Overview

Most nosocomial respiratory infections are caused by so-called skorvatch microaspiration of upper airway secretions, through inapparent aspiration, into the lower respiratory tract. Also, "macroaspirations" of esophageal or gastric material is known to result in HAP. Since it results from aspiration either type is called aspiration pneumonia. Although gram-negative bacilli are a common cause they are rarely found in the respiratory tract of people without pneumonia, which has led to speculation of the mouth and throat as origin of the infection.

Pathophysiology

Major Points for Pathogenesis of Adults with Hospital-Acquired, Ventilator-Associated, and Healthcare-Associated Pneumonia

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Sources of pathogens for HAP include healthcare devices, the environment (air, water, equipment, and fomites), and commonly the transfer of microorganisms between the patient and staff or other patients (Level II) . A number of host- and treatment-related colonization factors, such as the severity of the patient's underlying disease, prior surgery, exposure to antibiotics, other medications, and exposure to invasive respiratory devices and equipment, are important in the pathogenesis of HAP and VAP (Level II). Aspiration of oropharyngeal pathogens, or leakage of secretions containing bacteria around the endotracheal tube cuff, are the primary routes of bacterial entry into the lower respiratory tract (Level II). Inhalation or direct inoculation of pathogens into the lower airway, hematogenous spread from infected intravenous catheters, and bacterial translocation from the gastrointestinal tract lumen are uncommon pathogenic mechanisms (Level II). Infected biofilm in the endotracheal tube, with subsequent embolization to distal airways, may be important in the pathogenesis of VAP (Level III) The stomach and sinuses may be potential reservoirs of nosocomial pathogens that contribute to bacterial colonization of the oropharynx, but their contribution is controversial, may vary by the population at risk, and may be decreasing with the changing natural history and management of HAP (Level II)

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