Introduction & Microbiology - Ancient Affliction
- Causative agent: Mycobacterium leprae (Hansen's bacillus).
- Acid-fast, obligate intracellular bacillus; rod-shaped.
- Slow generation time: 12-14 days.
- Optimal growth temperature: 27-33°C (cooler body areas).
- Reservoirs: Humans, nine-banded armadillos.
- Transmission: Primarily respiratory droplets; prolonged close contact.
- Long incubation period: Avg 2-5 years (up to 20 years).
ā Mycobacterium leprae is an obligate intracellular parasite that cannot be cultured on artificial media.

Classification - Spectrum Story
Leprosy is a spectrum based on host Cell-Mediated Immunity (CMI).
-
Ridley-Jopling (R-J) Spectrum:
- Tuberculoid (TT): āCMI, few bacilli. Well-defined lesions, early nerve damage.
- Lepromatous (LL): āCMI, many bacilli. Diffuse lesions, late nerve damage.
- Borderline (BT, BB, BL): Intermediate, unstable forms.
-
WHO Classification (Treatment):
- Paucibacillary (PB): ā¤5 skin lesions AND smear negative. (Mainly TT, BT).
- Multibacillary (MB): >5 skin lesions OR smear positive OR >1 nerve involved. (Mainly LL, BL, BB).

ā CMI is strongest in Tuberculoid (TT) leprosy (few bacilli, localized) and weakest in Lepromatous (LL) leprosy (many bacilli, disseminated).
Clinical Features - Nerve & Skin Tales
- Skin Lesions ("Patches & Plaques")
- One/more hypopigmented or reddish skin patches.
- Definite sensory loss (touch, pain, temperature) within patches.
- Plaques, nodules; skin can be shiny, dry, or thickened.
- Late: Madarosis (eyebrow/eyelash loss), leonine facies (LL).
- Nerve Damage ("Silent Sabotage")
- Thickened, often tender, peripheral nerves (e.g., ulnar, common peroneal, great auricular).
- Sensory loss: Fine touch, pain, temperature affected early.
- Motor loss: Muscle weakness, paralysis leading to deformities (e.g., claw hands, foot drop, lagophthalmos).
- Autonomic dysfunction: Anhidrosis (reduced sweating), dry/cracked skin.

ā The ulnar nerve is the most commonly affected peripheral nerve in leprosy, followed by the common peroneal nerve.
Diagnosis - Unmasking Hansen's
- Slit-Skin Smear (SSS):
- Sites: Earlobes, active lesions. Ziehl-Neelsen (ZN) stain for Acid-Fast Bacilli (AFB).
- Bacteriological Index (BI): Measures bacillary load, graded 0 to 6+.
- Morphological Index (MI): Percentage of solid, uniformly stained (viable) bacilli; MI ā with effective treatment.
- Histopathology (Biopsy): Confirms diagnosis & classifies leprosy type (e.g., granuloma structure, lymphocyte infiltration, bacillary presence).
- Nerve Biopsy: Useful in pure neuritic leprosy when skin lesions are absent.
- PCR: Detects M. leprae DNA; high sensitivity, especially in paucibacillary (PB) or early cases.
ā The Lepromin test (Fernandez and Mitsuda reactions) is negative in lepromatous leprosy (LL, BL) and positive in tuberculoid leprosy (TT, BT), indicating Cell-Mediated Immunity (CMI) status.
Management & Reactions - Healing & Hazards
- MDT Regimens (WHO):
Category Drugs Duration PB Rifa (600mg M) + Dap (100mg D) 6 mo MB Rifa (600mg M) + Dap (100mg D) + Clofa (300mg M, 50mg D) 12 mo SLPB SDR: Rifa (600mg) + Oflox (400mg) + Mino (100mg) Single - Lepra Reactions: MDT always continued.
ā Thalidomide is drug of choice for severe Type 2 lepra reaction (ENL) but is strictly contraindicated in pregnancy due to teratogenicity.
HighāYield Points - ā” Biggest Takeaways
- Caused by Mycobacterium leprae; primarily affects skin and peripheral nerves.
- Spectrum: Paucibacillary (PB) (strong CMI, e.g., TT) to Multibacillary (MB) (poor CMI, e.g., LL).
- Cardinal signs: anesthetic skin lesions, thickened peripheral nerves, positive slit-skin smear (MB).
- Lepra Reactions: Type 1 (Reversal, cell-mediated) and Type 2 (ENL, immune complex).
- Treatment: WHO Multidrug Therapy (MDT) with Rifampicin, Dapsone, Clofazimine.
- Nerve damage is the hallmark, leading to significant disability and deformity.
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