Aetiology

Early-onset HAP (<5 days after admission to hospital) is often caused by Streptococcus pneumoniae.[7] Late-onset HAP (>5 days after admission to hospital) is usually caused by microorganisms that are acquired in hospital, most commonly MRSA, Pseudomonas aeruginosa, and other non-pseudomonal gram-negative bacteria.[7] Several of the microorganisms causing HAP have increased antibiotic resistance.[8]

Oropharyngeal commensals (viridans group streptococci, coagulase-negative staphylococci, Neisseria species, and Corynebacterium species) and anaerobic organisms are rare causes of HAP.

HAP due to Legionella pneumophila is sporadic, but more common with serogroup 1 when a water supply is colonised or there is ongoing construction.[9] Viral and fungal aetiologies are also rare, but incidents for each can be relatively high (e.g., if an influenza outbreak occurs or there is Aspergillus in an air duct feeding immunosuppressed patients).[10][11]

Pathophysiology

The most common introduction of bacteria into alveoli is micro-aspiration of oropharyngeal pathogens or leakage of secretions containing bacteria around an endotracheal tube cuff.[12] Other pathways include macro-aspiration (e.g., of vomit), inhalation, haematogenous spread from infected intravenous catheters, direct inoculation (e.g., thoracentesis), and translocation from the gastrointestinal tract.[13] Important factors that predispose patients to the pathways described include the severity of the patient's underlying disease, prior surgery, exposure to antimicrobials, other medications, and exposure to invasive respiratory devices and equipment.[14] Sources of pathogens for HAP include healthcare devices (infected biofilm in the endotracheal tube), the environment (air, water, equipment, and fomites), and the transfer of microorganisms from patient to patient through healthcare workers (poor hand hygiene).[15][16] Finally, sinuses may be potential reservoirs of healthcare-associated pathogens that contribute to HAP.[17]

Bacterial adherence is an essential step in disease production.[18] In patients with HAP, their endogenous flora continue to provide a source for upper airway colonisation. There may be a predilection for gram-negative organisms because there is an increased protease content in saliva and hence a loss of fibronectin from buccal cell surfaces, resulting in increased adherence and colonisation of airway mucosa with gram-negative bacilli. Typically, mucosal cells are coated with fibronectin, which selects for adherence of gram-positive bacteria.[18]

Classification

National Institute for Health and Care Excellence[3][4]

Hospital-acquired pneumonia

  • Pneumonia that develops 48 hours or more after hospital admission and that was not incubating at hospital admission.

    • Pneumonia that develops in hospital after endotracheal intubation (ventilator-associated pneumonia) is excluded from this definition and it is not covered in this topic.

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