Hospital-acquired pneumonia (non COVID-19)

Bacteria cause most cases of HAP and ventilator-associated pneumonia (VAP), especially aerobic gram-negative bacilli such as Pseudomonas aeruginosa, Escherichia coli, Klebsiella pneumoniae, and Acinetobacter species. In addition to methicillin-sensitive Staphylococcus aureus (MSSA), both hospital-acquired and community-acquired strains of MRSA are causing an increasing number of HAP cases.[9][10] Oropharyngeal commensals (viridans group streptococci, coagulase-negative staphylococci, Neisseria species, and Corynebacterium species) and anaerobic organisms are rare causes of HAP. Patients exposed to antimicrobials or to a healthcare facility outside of an acute care hospital may be colonized with multidrug-resistant (MDR) pathogens and are at risk for HAP due to those pathogens (e.g., P aeruginosa and MRSA).[3] MDR pathogens may also reside in intensive care units (ICUs); hence, active surveillance of ICU infections is recommended.[3] HAP in patients in the hospital may be due to pathogens less known for being nosocomial, such as Streptococcus pneumoniae and Legionella species.[11] HAP due to Legionella pneumophila is sporadic, but more common with serogroup 1 when a water supply is colonized or there is ongoing construction.[12] Viral and fungal etiologies are also rare, but incidents for each can be relatively high (e.g., during current coronavirus [COVID-19] pandemic, if an influenza outbreak occurs, or there is Aspergillus in an air duct feeding immunosuppressed patients).[13][14]

The most common introduction of bacteria into alveoli is microaspiration of oropharyngeal pathogens or leakage of secretions containing bacteria around an endotracheal tube cuff.[15] Other pathways include macroaspiration (e.g., of vomit), inhalation, hematogenous spread from infected intravenous catheters, direct inoculation (e.g., thoracentesis), and translocation from the gastrointestinal tract.[16] 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.[17] 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).[18][19] Finally, sinuses may be potential reservoirs of healthcare-associated pathogens that contribute to HAP.[20]

Bacterial adherence is an essential step in disease production.[21] In patients with HAP, their endogenous flora continue to provide a source for upper airway colonization. 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 colonization of airway mucosa with gram-negative bacilli. Typically, mucosal cells are coated with fibronectin, which selects for adherence of gram-positive bacteria.[21]

American Thoracic Society; Infectious Diseases Society of America[1]

Hospital-acquired pneumonia

Acute lower respiratory tract infection acquired after 48 hours of admission to the hospital.

Ventilator-associated pneumonia

Pneumonia that occurs >48 to 72 hours after endotracheal intubation.

Pathophysiology

Classification

American Thoracic Society; Infectious Diseases Society of America[1]