Leprosy_Robbins_Teaching , causes and clinical feature.pptx

leprosy, morphology, clinical feature, diagnosis

1. Leprosy (Hansen’s Disease) Chronic infectious disease caused by Mycobacterium leprae Affects skin, peripheral nerves, mucosa of upper respiratory tract, eyes Two major clinical forms: Tuberculoid & Lepromatous

2. Etiology & Transmission Causative agent: Mycobacterium leprae (acid-fast bacillus) Transmission: prolonged close contact, nasal secretions, skin lesions Incubation period: long (2–10 years)

3. Pathogenesis (1/2) Entry: via skin or respiratory mucosa → uptake by macrophages & Schwann cells → survival inside cells due to failure of phagolysosome fusion → host immune response determines disease type

4. Pathogenesis (2/2) Cell-mediated immunity strong → Tuberculoid leprosy CMI weak/absent → Lepromatous leprosy Spectrum of disease: Tuberculoid ← Borderline → Lepromatous

5. Pathology – Tuberculoid Leprosy Gross: few, well-demarcated hypopigmented patches, anesthetic Nerves: thickened, palpable Microscopy: granulomas with epithelioid cells, Langhans giant cells, lymphocytes Few/no bacilli (paucibacillary)

6. Pathology – Lepromatous Leprosy Gross: numerous, symmetric skin lesions (nodules, plaques, diffuse thickening) Facies leonina (lion-like face) Microscopy: sheets of foamy macrophages (lepra cells) filled with bacilli Many acid-fast bacilli (multibacillary)

7. Nerve Pathology Tuberculoid: nerve destruction due to granulomatous inflammation Lepromatous: Schwann cells packed with bacilli, slow destruction Both → anesthesia, deformities, trophic ulcers

8. Clinical Correlation Tuberculoid: localized, few lesions, anesthesia, better prognosis Lepromatous: widespread lesions, nodules, deformities, infectious Borderline: unstable, may shift towards either pole

9. Tuberculoid Leprosy

10. Diagnosis Skin smears/biopsy (AFB stain) Histology (granulomas vs lepra cells) Lepromin skin test: +ve in tuberculoid, –ve in lepromatous