Tutorial 09: Pneumonia (Clinical Pathology)

This tutorial applies knowledge of pneumonia pathology to clinical scenarios, focusing on diagnosis, classification, and complications. Pneumonia is inflammation of the lung parenchyma caused by infection. Classification guides empirical antibiotic choice: community-acquired (CAP), hospital-acquired (HAP — onset ≥48 h after admission), and ventilator-associated pneumonia (VAP).

Lobar pneumonia, most commonly caused by Streptococcus pneumoniae, produces the classic four-stage pathological sequence: congestion → red hepatisation → grey hepatisation → resolution. Clinically this correlates with: day 1–2 (fever, cough, pleuritic chest pain as visceral pleura is inflamed), days 2–4 (classic clinical pneumonia with productive cough and rusty sputum — haemoptysis from red hepatisation), days 4–8 (fever persisting as grey hepatisation continues), then resolution (cough clears, chest X-ray clears). Chest X-ray shows lobar consolidation (air bronchogram sign — airways visible against consolidated alveoli). The Gram stain of sputum shows Gram-positive diplococci.

Bronchopneumonia produces patchy bilateral opacities centred on airways on CXR. Sputum may grow multiple organisms. It is more common in debilitated patients: the elderly (reduced cough reflex, impaired mucociliary clearance), post-operative patients (atelectasis from poor ventilation), patients with impaired consciousness (aspiration risk), and immunocompromised.

Atypical pneumonia, caused by Mycoplasma pneumoniae, Chlamydophila pneumoniae, Legionella pneumophila, and viruses, classically presents with a "walking pneumonia" phenotype: gradual onset, dry (non-productive) cough, systemic features (headache, myalgia) out of proportion to respiratory symptoms, and diffuse interstitial infiltrates on CXR. Mycoplasma produces cold agglutinins (IgM autoantibodies that agglutinate red cells at 4°C) in ~50% of cases, causing autoimmune haemolytic anaemia. Legionella is associated with water cooling towers, causes severe multi-organ pneumonia (Pontiac fever or Legionnaires' disease), and requires urinary antigen testing for diagnosis (since it fails to grow on standard media).

ARDS (diffuse alveolar damage) can complicate severe pneumonia, sepsis, or aspiration. Pathologically: hyaline membranes (fibrin + plasma proteins) coat alveolar walls; type I pneumocyte necrosis; type II hyperplasia. Clinical criteria (Berlin definition): acute onset, bilateral infiltrates, P/F ratio <300 (PaO₂/FiO₂), and absence of cardiac failure/fluid overload as primary cause. Management: lung-protective ventilation (tidal volumes 6 mL/kg ideal body weight), prone positioning, and treatment of underlying cause.

Aspiration pneumonia results from inhalation of oropharyngeal or gastric contents, introducing anaerobic bacteria (Bacteroides, Fusobacterium, Peptostreptococcus) into the lung. It preferentially affects the dependent lobes (right lower lobe most commonly, as the right main bronchus is more vertical). Gastric acid causes a chemical pneumonitis before bacteria proliferate; patients may progress to lung abscess (cavitating lesion with air-fluid level on CXR) requiring prolonged antibiotics and postural drainage.

Pneumocystis jirovecii pneumonia (PCP) in an HIV-positive patient with a CD4 count below 200/µL presents as progressive dyspnoea, dry cough, and bilateral perihilar ground-glass infiltrates on CT. LDH is often markedly elevated. BAL with silver stain (Grocott methenamine silver, GMS) demonstrates the characteristic cysts and trophic forms. Co-trimoxazole (trimethoprim-sulfamethoxazole) at high doses is first-line treatment; adjunctive corticosteroids are given when PaO₂ is below 70 mmHg.