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PNEUMONIA & SUPPURATIVE LUNG DISEASES

Dr. Thin Thin Win @ Safiya Yunus

Department of Pathology, PPSP

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PNEUMONIA

Definition

Inflammation of the lung parenchyma (alveoli) resulting consolidation or hardening of lung parenchyma

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Etiology

Caused by varieties of infectious agent such as bacteria, viruses, fungi, mycoplasma etc:…

Mostly bacterial pneumonia - (Pneumococci, Klebsiella pneumoniae, Staphylococci, Streptococci, H.influenzae, Pseudomonas aeruginosa) – Community acquired acute pneumonia

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Etiology

Result whenever pulmonary defense mechanism are impaired or resistance of host is lowered

Pulmonary defense mechanism –

1. cough reflex

2. mucociliary apparatus

3. phagocytic alveolar macrophages

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Clearing mechanism can be interfered with many factors:

1. Loss or suppression of cough reflex - aspiration of gastric contents in coma, anesthesia, neuromuscular disorders, drugs, chest pain – aspiration pneumonia

2. Injury to mucociliary apparatus – cigarette smoking, inhalation of hot or corrosive gases, viral infection, genetic disorders

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Clearing mechanism can be interfered with many factors:

3. Interfered phagocytic/ bactericidal action of alveolar macrophages

– alcohol, smoking, anoxia, O2 intoxication

4. Pulmonary congestion & edema

5. Accumulation of secretions

– cystic fibrosis & bronchial obstruction

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Aetiology & antomical pattern of pneumonia

Community acquired acute pneumonia

Community acquired atypical pneumonia

Aetiology Bacteria Virus

Mycoplasma

Clamydia

Anatomical involvement

Lobar pneumonia

Bronchopneumonia

Interstitial pneumonia

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Lobar pneumonia

Consolidation of a large portion of a lobe or an entire lobe

(whereas patchy consolidation in bronchopneumonia)

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Lobar pneumonia Bronchopneumonia

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A closer view of the lobar pneumonia demonstrates the distinct difference between the upper lobe and the consolidated lower lobe.

                                 

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Uniformly consolidated lower lobe in lobar pneumonia ( gray hepatization) – lower lobe become airless, liver like texture, gray white

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4 stages of inflammatory response in lobar pneumonia

Congestion Red hepatization Gray hepatization Resolution

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Stage of congestion

Lung – heavy, boggy, red Vascular engorgement Intra-alveolar fluid with few neutrophils & often

numerous bacteria

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Stage of red hepatization

Massive confluent exudation with red cells, neutrophils and fibrin filling the alveolar spaces

Gross – lobe appear distinctly red, firm & airless with liver-like consistency

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Stage of red hepatization

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Stages of gray hepatization

Progressive disintegration of red cells Macrophages replace PMN with fibrin

deposition Persistence of fibrinosuppurative

exudates Gross – grayish brown, dry surface

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Stages of gray hepatization

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Stage of resolution

Consolidated exudates within alveolar spaces undergoes progressive enzymatic digestion to produce a granular, semi fluid debris

Resorbed & ingested by macrophages, coughed up or organized by fibroblasts growing into it

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Stage of resolution (by organization)

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Bronchopneumonia

Patchy consolidation of lung May be one lobe or multilobar Frequently bilateral & basal

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Bronchopneumonia

Gross Lesions - 3 to 4 cm in diameter Slightly elevated, dry, granular, gray-red to

yellow Poorly delimited at margin

Histology Suppurative, neutrophil-rich exudates that fills

bronchi, bronchioles and adjacent alveolar spaces

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At higher magnification, the pattern of patchy distribution of a bronchopneumonia is seen.

                                 

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Bronchopneumonia

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Community acquired atypical pneumonia (Viral and Mycoplasma Pneumonia)Interstitial pneumonia

Morphology

Patchy or whole lobe Bilateral or unilateral Red-blue, congested & subcrepitant Pleuritis or pleural effusion is infrequent

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Community acquired atypical pneumonia (Viral and Mycoplasma Pneumonia)

Histology Inflammatory reaction in interstitial

tissue, virtually within the walls of alveoli Alveolar septa – widened, edematous

with mononuclear infiltrates of L, H, P & N in acute cases

Alveoli – free of exudates Pink hyaline membrane in alveolar walls

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Chronic Pneumonia

Localized lesion in Immunocompetent patient

Granulomatous inflammation → Mycobacterium tuberculosis, Fungal infection (Histoplasmosis, Blastomycosis, Coccidioidomycosis, Aspergillosis)

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Complication of pneumonia

1. Abscess formation

- due to tissue destruction & necrosis

2. Pleuritis, Pleural effusion, Empyema

- spread of infection to pleura cavity

causing intra-pleural fibrinosuppurative

reaction

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Complication of pneumonia

3. Organization of exudates

- convert portion of lung into solid tissue with fibrous scar

4. Bacterial dissemination

- to heart valves, pericardium, brain, kidneys, spleen, joints resulting metastatic abscesses, endocarditis, meningitis, suppurative arthritis

5. Septicemia

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Clinical features

Abrupt onset of high fever with chills Productive cough Mucopurulent sputum Pleuritic pain & friction rub Radiologic appearance

- well circumscribed radio-opacity in LP

- focal opacities in BP

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SUPPURATIVE LUNG DISEASES

Bronchiectasis Lung abscess Empyema

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BRONCHIECTASIS

Definition Disease characterized by permanent

dilatation of bronchi & bronchioles caused by destruction of the muscle & elastic tissue, resulting from or associated with chronic necrotizing infection

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Etiology

Obstruction & infection – major cause

- obstruction (mucus, tumor, FB) → impaired normal clearing mechanism → pooling of secretion distal to obstruction → inflammation of airways

Severe infection → necrotizing fibrosis and eventually dilatation of airways

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Etiology

Congenital or hereditary

- cystic fibrosis

- intralobular sequestration of the lung

- immunodeficiency state

- primary ciliary dyskinesia

- Kartagener syndrome

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Morphology

Lower lobes, bilaterally Vertical air passages Most severe in more distal bronchi &

bronchioles

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Gross

Airways – dilated, up to 4 times Long, tube-like enlargement of airways

→ cylindrical bronchiectasis Fusiform or saccular distension →

saccular bronchiectasis Dilated airways can be followed directly

out to pleural surfaces On C.S → cysts filled with

mucopurulent secretions

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Bronchiectasis

Bronchial tubes are extremely dilated with thicken, fibrotic wall. Adjacent lung is almost completely destroyed

Dr TTW (2009) 37Focal area of dilated bronchi with bronchiectasis.

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Histology

Full-blown, active case → intense acute & chronic inflammatory exudation within the walls of bronchi & bronchioles

Desquamation of lining epithelium Extensive areas of necrotizing

ulceration

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Clinical course

Cor pulmonale Lung abscess Metastatic brain abscesses Amyloidosis

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LUNG ABSCESS

Definition

A local suppurative process within the lung, characterized by necrosis of lung tissue

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Etiology & Pathogenesis

Oropharyngeal surgical procedures, sinobronchial infection, dental sepsis, bronchitis

Aerobic & anaerobic streptococci , Staphylococcus aureus, GN organisms

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Mechanisms

Aspiration of infective material in acute alcoholism, coma, anesthesia, sinusitis, gingivodental sepsis, debilitation - cough reflexes depressed

Antecedent primary bacterial infection - post-pneumonic abscess, fungal infection, bronchiectasis

Septic embolism Neoplasia Miscellaneous

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Morphology

Size -few mm to large cavities of 5-6 cm Single or multiple Abscess due to aspiration → more

common on right ( more vertical right main bronchus ) and more single

Abscess from pneumonia or bronchiectasis → usually multiple, basal, diffusely scattered

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Morphology

Cavity filled with suppurative debris If communication with air passage →

partially drain → air-containing cavity Continued infection → large, fetid,

green-black, multilocular cavities (gangrene of the lung)

Suppurative destruction of lung parenchyma within central area of cavitation

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Seen here are two lung abscesses, one in the upper lobe and one in the lower lobe of this left lung.

Dr TTW (2009) 46abscessing bronchopneumonia in which several abscesses with irregular, rough-surfaced walls are seen within areas of tan consolidation.

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• Old pulmonary abscess cavity. • Multiloculated with delicate strands of fibrous tissue crossing the space. • No evidence of acute inflammation in the wall • Fairly normal surrounding lung.

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Course

Most resolve with antimicrobial therapy Extension of infection into pleural cavity

→ empyema Hemorrhage Septic emboli → brain abscess,

meningitis Secondary amyloidosis

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EMPYEMA

Collection of pus in pleural cavity Suppurative pleuritis Presence of purulent pleural exudates Characterized by loculated, yellow-

green, creamy pus composed of neutrophils admixed with other leukocytes

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Etiology

Contiguous spread of organisms from intrapulmonary infection

Lymphatic dissemination Haematogenous dissemination Direct extension of infection below

diaphragm (subdiaphragmatic or liver abscess) especially on right side

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Clinical course

May resolve by antibiotics

Obliterate pleural space or envelope the lungs → embarrass pulmonary expansion

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