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.; Associate Editor(s)-in-Chief: Alejandro Lemor, M.D. [1]


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.


Adapted from CDC[1]

Image obtained from Wikimedia Commons
  • Bacteria may invade the lower respiratory tract by micro- or bolus-aspiration of oropharyngeal organisms, inhalation of aerosols containing bacteria, or, less frequently, by hematogenous spread from a distant body site.
  • Bacterial translocation from the gastrointestinal tract had been hypothesized as a mechanism for infection; however, its occurrence in patients with health-care-associated pneumonia has not been shown.
  • Of the plausible routes, micro-aspiration is believed to be the most important for both health-care-associated and community-acquired pneumonia.
  • In studies using radioisotope tracers, 45% of healthy adults were found to aspirate during sleep[2].
  • Persons with abnormal swallowing, such as those who have depressed consciousness, respiratory tract instrumentation and/or mechanically assisted ventilation, gastrointestinal tract instrumentation or diseases, or who have just undergone surgery, especially thoracic and/or abdominal surgery, are particularly likely to aspirate.
  • The high incidence of Gram-negative bacillary pneumonia in hospitalized patients appears to be the result of factors that promote colonization of the pharynx by Gram-negative bacilli and the subsequent entry of these microorganisms into the lower respiratory tract.
  • Although aerobic Gram-negative bacilli are recovered infrequently or are found in small numbers in pharyngeal cultures of healthy persons, colonization dramatically increases in patients with acidosis, alcoholism, azotemia, coma, diabetes mellitus, hypotension, leukocytosis, leukopenia, pulmonary disease, or endotracheal or nasogastric tubes in place, and in patients given antimicrobial agents.
  • Oropharyngeal or tracheobronchial colonization by Gram-negative bacilli begins with the adherence of the microorganisms to the host's epithelial cells.
  • Adherence may be affected by multiple factors related to the bacteria (e.g., presence of pili, cilia, or capsule, or production of elastase or mucinase), host cell (e.g., surface proteins and polysaccharides), and environment (e.g., pH and presence of mucin in respiratory secretions).
  • Studies indicate that certain substances (e.g., fibronectin) can inhibit the adherence of Gram-negative bacilli to host cells.
  • Conversely, certain conditions (e.g., malnutrition, severe illness, or post-operative state) can increase adherence of gram-negative bacteria.
  • In addition to the oropharynx, the stomach has been postulated to be an important reservoir of organisms that cause health-care-associated pneumonia, although the exact role of the stomach in the causation of health-care-associated pneumonia, specifically VAP, has been critically investigated and debated.
  • The stomach's role may vary depending on the patient's underlying condition(s) and on the prophylactic or therapeutic interventions that the patient receives.
  • In healthy persons, few bacteria entering the stomach survive in the presence of hydrochloric acid at pH<2.
  • However, whe gastric pH increases from the normal levels to >4, microorganisms are able to multiply to high concentrations in the stomach.
  • This can occur in patients with advanced age, achlorhydria, ileus, or upper gastrointestinal disease, and in patients receiving enteral feeding, antacids, or histamine-2 (H-2) antagonists.
  • The contribution of other factors, such as duodeno-gastric reflux and the presence of bile, to gastric colonization in patients with impaired intestinal motility also has been suggested.

Ventilator-associated Pneumonia

  • Ventilator-associated pneumonia is primarily caused by the endotracheal or tracheostomy tube allowing free passage of bacteria into the lower segments of the lung in a person who often has underlying lung or immune problems.
  • Bacteria travel in small droplets both through the endotracheal tube and around the cuff.
  • Often, bacteria colonize the endotracheal or tracheostomy tube and are embolized into the lungs with each breath.
  • Bacteria may also be brought down into the lungs with procedures such as deep suctioning or bronchoscopy.
  • Whether bacteria also travel from the sinuses or the stomach into the lungs is, controversial.
  • However, spread to the lungs from the blood stream or the gut is uncommon.
  • Once inside the lungs, bacteria then take advantage of any deficiencies in the immune system (such as due to malnutrition or chemotherapy) and multiply.
  • A combination of bacterial damage and consequences of the immune response lead to disruption of gas exchange with resulting symptoms.

Major Points for Pathogenesis of Adults with Hospital-Acquired, Ventilator-Associated, and Healthcare-Associated Pneumonia [3]

  • 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)
For Level of evidence and classes click here.


  1. Template:Cite web url= guidelines.pdf
  2. Huxley EJ, Viroslav J, Gray WR, Pierce AK (1978). "Pharyngeal aspiration in normal adults and patients with depressed consciousness". Am J Med. 64 (4): 564–8. PMID 645722.
  3. "Guidelines for the management of adults with hospital-acquired, ventilator-associated, and healthcare-associated pneumonia". American Journal of Respiratory and Critical Care Medicine. 171 (4): 388–416. 2005. doi:10.1164/rccm.200405-644ST. PMID 15699079. Retrieved 2012-09-13. Unknown parameter |month= ignored (help)

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