Pneumonia Pathology
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Direct answer
Consolidation — inflammatory exudate flooding alveoli in place of air — is the pathological core of pneumonia, and its distribution sorts the disease into three patterns. Lobar pneumonia, classically Streptococcus pneumoniae, fills a whole lobe through four stages (congestion, red then grey hepatization, resolution); bronchopneumonia produces patchy centrilobular consolidation around inflamed bronchioles, favouring the old, the young and the debilitated; interstitial pneumonia, the atypical pattern of Mycoplasma, Legionella and viruses, inflames the alveolar septa without exudate. In India, any pneumonia that fails to resolve on adequate therapy demands sputum for acid-fast bacilli and imaging to exclude tuberculosis or an obstructing tumour — the single most examined local rule.
What you must remember
- Lobar stages: congestion (0-24 hours, vascular engorgement), red hepatization (days 2-3, fibrin-rich exudate with erythrocytes, the livery dry cut surface), grey hepatization (days 4-6, fibrin with leucocyte breakdown), resolution (day 7 onward, fibrinolysis and macrophage clearance).
- Organism-pattern map: Streptococcus pneumoniae — lobar; Staphylococcus aureus and Haemophilus influenzae — bronchopneumonia, post-viral; Klebsiella pneumoniae — lobar in alcoholics and diabetics, currant-jelly sputum, abscess-prone.
- Atypical pneumonia: Mycoplasma (school outbreaks, cold agglutinins), Legionella (air-conditioning water, gastrointestinal symptoms, hyponatraemia), Chlamydophila and respiratory viruses; interstitial infiltrate with dry cough.
- Complications: parapneumonic effusion, empyema, lung abscess (especially staphylococcal and klebsiellar), organisation into carnification, bacteraemia, and pneumatoceles in children with staphylococcal infection.
- Physical signs by stage: crackles in congestion, dullness with tubular breath sounds and increased vocal resonance in hepatization, returning crackles in resolution.
- Indian corollary: non-resolving pneumonia means tuberculosis, post-obstructive pneumonia behind a bronchogenic carcinoma, or klebsiellar abscess until excluded.
- Paediatric red flag: staphylococcal pneumonia after influenza produces pneumatoceles, pyopneumothorax and rapid deterioration in a malnourished child.
Reading the four stages at the bedside
A 40-year-old alcoholic arrives with rigors, rust-coloured sputum and a dull right lower zone. Histologically he is in red hepatization: alveoli packed with fibrin, erythrocytes and neutrophils, and the cut lung surface resembles liver — hence the name, and hence the physical signs. Airlessness conducts sound, so bronchial breathing and increased vocal resonance replace the vesicular murmur over the consolidated lobe; a day later the exudate greys as leucocytes break down, and the signs persist unchanged while the patient's outcome is decided. If he survives to the second week without antibiotics, resolution begins: macrophages ingest the debris, plasmin digests the fibrin, and the alveoli re-aerate — with complete anatomical restitution, the point pathologists insist upon. When fibrin persists and organises into fibrous tissue instead, the lobe is carnified: permanently stiff, a surgical consideration. In Klebsiella infection the same lobe swells beyond its boundary, produces a bulging fissure on the radiograph and sloughs into abscesses — the reason alcoholics' pneumonias get a broader, necrosis-prone organism on every differential list.
The non-resolving pneumonia
The examiner's Indian twist is the shadow that stays. A middle-aged smoker's recurrent consolidation in the same segment is post-obstructive pneumonia — the tumour is the diagnosis, the infection only its voice, and bronchoscopy is mandatory. A migrant worker's persistent infiltrate with evening fever and weight loss is tuberculosis until sputum smear, culture or nucleic-acid testing proves otherwise. And a diabetic's cavitating lesion after a bout of pneumonia is a klebsiellar or staphylococcal abscess, needing drainage as much as antibiotics. The rule unifying all three: antibiotics treat the exudate, not the reason it keeps returning.
Frequently asked questions
What are the four stages of lobar pneumonia?
Congestion, red hepatization, grey hepatization and resolution — corresponding to engorgement, fibrino-sanguinous exudate, leucocyte-dominant exudate and fibrinolysis with clearance.
Which organism causes lobar pneumonia with currant-jelly sputum?
Klebsiella pneumoniae, typically in alcoholics and diabetics, prone to abscess formation and a bulging interlobar fissure.
How does bronchopneumonia differ pathologically from lobar pneumonia?
Patchy, centrilobular consolidation centred on acute bronchiolitis affecting multiple lobes, versus confluent exudate filling an entire lobe.
Which organisms cause atypical (interstitial) pneumonia?
Mycoplasma pneumoniae, Legionella pneumophila, Chlamydophila and respiratory viruses — patchy interstitial inflammation without alveolar exudate.
What should be excluded when pneumonia fails to resolve in India?
Pulmonary tuberculosis, post-obstructive pneumonia behind a bronchogenic carcinoma and lung abscess, using sputum acid-fast bacilli testing and bronchoscopy.