L08: Pneumonia

Pneumonia is defined as inflammation of the lung parenchyma — the alveoli and terminal airways — most commonly caused by infection. It is classified by the clinical setting (community-acquired vs hospital-acquired vs ventilator-associated), by the causative organism, and by the morphological pattern of inflammation.

Community-acquired pneumonia (CAP) is the most common form. Streptococcus pneumoniae (pneumococcus) is the leading bacterial cause and the organism most responsible for classical lobar pneumonia. Other common CAP pathogens include Haemophilus influenzae (especially in smokers and COPD patients), Mycoplasma pneumoniae (atypical pneumonia), Chlamydophila pneumoniae, and Legionella pneumophila.

Lobar pneumonia, caused predominantly by S. pneumoniae, progresses through four pathological stages. (1) Congestion (day 1–2): vasodilation and protein-rich oedema fluid fills alveoli; bacteria proliferate rapidly. (2) Red hepatisation (day 2–4): alveoli filled with red blood cells, fibrin, and neutrophils; the lobe becomes solid and dark red, resembling liver in texture (hence hepatisation). (3) Grey hepatisation (day 4–8): red cells lyse; lobe becomes grey-white with dense fibrin and macrophages. (4) Resolution (day 8+): macrophages phagocytose debris; fibrin is lysed by proteases; normal aeration is restored. Complications include abscess formation, empyema (pus in the pleural space), and bacteraemia with distant seeding.

Bronchopneumonia is a patchy consolidation centred on bronchioles and spreading to adjacent alveoli. It is caused by a wider range of organisms including Staphylococcus aureus, Klebsiella pneumoniae, and Gram-negative bacilli. It is more common in the very young, very old, and immunocompromised, and in patients with prior lung damage (bronchiectasis, cystic fibrosis).

Atypical (interstitial) pneumonia does not consolidate individual lobes. Instead, inflammation is predominantly in the alveolar walls (interstitium), producing a mononuclear cell infiltrate (lymphocytes, macrophages) with relatively little alveolar exudate. The chest X-ray shows diffuse interstitial infiltrates rather than lobar consolidation. Causative organisms include Mycoplasma pneumoniae, Chlamydophila, Coxiella burnetii (Q fever), and viruses (influenza, RSV, SARS-CoV-2). Clinical features are often disproportionately mild compared with the radiological abnormality.

Diffuse alveolar damage (DAD) is the histological correlate of ARDS (acute respiratory distress syndrome). Triggers include severe pneumonia (viral or bacterial), sepsis, aspiration, and trauma. The pathological hallmark is hyaline membranes: eosinophilic deposits of fibrin and plasma proteins lining alveolar walls, reflecting widespread endothelial and epithelial injury. Type I pneumocytes are destroyed; type II pneumocytes proliferate to attempt repair. The clinical consequence is refractory hypoxaemia and bilateral infiltrates.

Pneumocystis jirovecii pneumonia (PCP) is an AIDS-defining illness occurring when CD4 count falls below 200 cells/µL. P. jirovecii (formerly carinii) is a fungus that causes a distinctive interstitial pneumonia with a foamy "cotton-candy" alveolar exudate on H&E staining. Diagnosis requires BAL with special staining (silver stain identifies the cysts). Treatment is high-dose co-trimoxazole.

RSV (respiratory syncytial virus) is the leading cause of lower respiratory tract infection in infants under 2 years, causing bronchiolitis characterised by small airway inflammation, oedema, and mucus plugging.