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Pathophysiology of pneumonia

Pneumonia is an acute inflammation of the lung (pneumonitis) caused by infection. The infectious agent may be bacterial, mycobacterial, viral, fungal, or parasitic. Health care professionals must remember that pneumonia is an umbrella term for a group of syndromes caused by various agents resulting in inflammation and sequelae.

Microbes regularly enter airways, but many factors prevent colonization:

mucous entrapment
ciliary clearance
immune surveillance
intact epithelial barrier
secreted factors such as:
- secretory IgA
- surfactant proteins (SP-a, SP-d)
- defensins

Disrupting or overwhelming these defense mechanisms can allow microbes to colonize the lungs, resulting in pneumonia.

Disruption of mucociliary clearance:

airway obstruction (CF, COPD, chronic bronchitis, neoplasm)
ciliary dysfunction (Kartagener, smoking, ciliostatic factors)

Disruption of intact epithelial barrier:

injury (e.g., pulmonary edema, intubation) or infection (e.g., viral respiratory infection such as influenza, SARS-CoV-2, etc.)

Factors that increase morbidity:

altered consciousness
debility
dysphagia
intubation

Decreasing immune function:

immune suppression (transplant, HIV)
evading host immunity (IgA proteases, encapsulation)

Aspiration of nasopharyngeal secretions or other fluids can overwhelm the upper airway defense mechanisms and lead to infection. Some organisms (e.g., tuberculosis and influenza) are transmitted via inhalation of microorganisms released into the air. Still, others colonizing endotracheal tubes that bypass the upper airway defenses.

Macrophages in the lower airways and alveoli recognize pathogens and set off an intense immunologic and inflammatory response.
Inflammatory cytokines, white blood cells, and edema flood the alveoli and bronchi causing consolidation of the lungs.
Ventilation/perfusion (V/Q) mismatching occurs with resultant hypoxemia.
The infection may spread to the bloodstream (bacteremia and sepsis), pleura (empyema),or other organs (e.g., meningitis).

The four phases of Pneumonia

Phase 1: Congestion: usually occurs within the first 24 hours of pneumonia. Patients will experience vascular engorgement, intra-alveolar fluid, and multiple bacteria. The lungs will be very heavy and red. Capillaries in the alveolar walls become congested, and the infection will spread to the hilum and pleura. During this stage, a person will experience coughing and deep breathing (Jain et al., 2020).

Phase 2:

Red hepatization occurs a few days after congestion; the lungs will be red, firm, and airless with a resemblance to the liver. Alveolar capillaries will be engorged with blood, and vascular congestion will persist. During the red hepatization stage, the alveoli will contain many erythrocytes, neutrophils, desquamated epithelial cells, and fibrin.

Phase 3: Gray hepatization late consolidation occurs 2 to 3 days following red hepatization and lasts for 4 to 8 days. The red cells have been broken down and appear gray with liver-like consistency due to fibrinopurulent exudate, progressive disintegration of red blood cells, and hemosiderin. The macrophages begin to appear.

Phase 4: Resolution and restoration of the pulmonary architecture start by the eighth day. The enzymatic action begins centrally and spreads peripherally, which liquefies the previous solid fibrinous content and eventually restores aeration. Macrophages are the predominant cells that contain engulfed neutrophils and debris. (Pahal et al., 2020)

References

Jain, V., Vashisht, R., Yilmaz, G., et al. (2020). Pneumonia Pathology. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020. Available from: https://www.ncbi.nlm.nih.gov/books/NBK526116/

Ostergaard L, Huniche B, Andersen PL. Relative bradycardia in infectious diseases. J Infect. 1996 Nov;33(3):185-91

Pahal, P., Rajasurya, V. & Sharma, S. (2020). Typical Bacterial Pneumonia. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; Available from: https://www.ncbi.nlm.nih.gov/books/NBK534295/