Notes · Community Medicine · 22 October 2026

Leprosy (Hansen's disease)

Definition

• Leprosy, also called Hansen’s disease, is a chronic infectious disease caused by the obligate intracellular bacillus Mycobacterium leprae that primarily involves the skin, peripheral nerves, upper respiratory tract mucosa, and the eyes.

Epidemiology

• Global prevalence has fallen to <1 case per 10 000 population after the introduction of multidrug therapy (MDT) in the 1980s, but India, Brazil and Indonesia together account for >80 % of new cases.
• The disease is endemic in tropical and subtropical regions; the highest incidence is seen in the 15‑35 year age group, with a slight male preponderance (M:F ≈ 1.5:1).
• Household contacts of an untreated patient have a 5‑8 fold higher risk of acquiring the infection.

Aetiology

• Mycobacterium leprae is a slow‑growing, acid‑fast bacillus that cannot be cultured in vitro; it thrives at temperatures of 30‑33 °C, explaining its predilection for cooler body sites such as the skin and superficial nerves.
• Transmission is believed to occur mainly via prolonged respiratory droplets from untreated multibacillary (MB) patients; occasional zoonotic transmission from armadillos has been documented in the Americas.

Pathophysiology

• After inhalation or skin inoculation, bacilli are phagocytosed by macrophages and Schwann cells.
• In susceptible hosts (genetic factors such as HLA‑DR2, low cell‑mediated immunity), the bacilli multiply within these cells, leading to granulomatous inflammation and nerve damage.
• The spectrum of disease reflects the host’s immune response:
  • Tuberculoid (TT) – strong Th1‑mediated immunity, few lesions, low bacterial load.
  • Lepromatous (LL) – weak Th2 response, numerous lesions, high bacterial load.
  • Borderline (BT, BB, BL) – intermediate immune status, unstable disease prone to reactions.
• Nerve involvement results from direct infection of Schwann cells and subsequent demyelination, causing sensory loss, muscle weakness and autonomic dysfunction (e.g., loss of sweating).

Clinical Features

• Skin lesions – hypopigmented or erythematous macules, papules, nodules, or plaques with loss of sensation to light touch, pain and temperature.
• Peripheral nerve involvement – thickened, non‑tender peripheral nerves (e.g., ulnar, common peroneal) with sensory loss in the corresponding dermatome; motor weakness may lead to claw hand or foot drop.
• Sensory loss – early loss of fine touch and temperature, while pain perception may be relatively preserved, predisposing to repeated injuries.
• Eye involvement – lagophthalmos, corneal ulceration, and cataract due to facial nerve palsy and loss of blink reflex.
• Reactional states – acute inflammatory episodes that can worsen nerve damage:
  • Type 1 (reversal) reaction – occurs in borderline forms, characterized by erythema, swelling of existing lesions and new nerve tenderness.
  • Type 2 (erythema nodosum leprosum, ENL) – immune complex–mediated, seen in LL, presents with painful nodules, fever, and systemic symptoms.

Investigations

• Clinical diagnosis remains the cornerstone, based on characteristic lesions and nerve findings.
• Skin smear (slit‑skin smear) – quantitative bacteriological index (BI) expressed on a 0‑6+ scale; useful for classifying MB disease and monitoring treatment response.
• Skin biopsy – histopathology shows granulomas in TT and foamy macrophages packed with acid‑fast bacilli in LL; special stains (Ziehl‑Neelsen, Fite‑Faraco) highlight organisms.
• Serology – anti‑PGL‑1 (phenolic glycolipid‑1) antibody titers correlate with bacterial load but are not routinely used for diagnosis.
• Nerve conduction studies – may document peripheral neuropathy when clinical assessment is equivocal.

Management (Current WHO Guidelines, 2023)

• Multidrug therapy (MDT) – the only WHO‑endorsed curative regimen:
  • Paucibacillary (PB) leprosy (≤5 skin lesions, BI negative): Rifampicin 600 mg once monthly supervised + Dapsone 100 mg daily self‑administered for 6 months.
  • Multibacillary (MB) leprosy (>5 lesions or BI positive): Rifampicin 600 mg monthly + Clofazimine 300 mg monthly supervised + Dapsone 100 mg daily + Clofazimine 50 mg daily self‑administered for 12 months.
• Management of reactions – essential to prevent permanent nerve damage:
  • Type 1 reaction – Prednisolone 1 mg/kg/day tapered over 12‑16 weeks; add methotrexate or azathioprine for steroid‑dependent cases.
  • Type 2 reaction (ENL) – Thalidomide 100‑300 mg daily (contraindicated in pregnancy) or high‑dose Clofazimine 300 mg daily; steroids are added for severe systemic involvement.
• Adjunctive measures – daily foot care, protective footwear, physiotherapy, and patient education to avoid injuries.
• Chemoprophylaxis for contacts – Single‑dose Rifampicin (SDR) 10 mg/kg given once to eligible household contacts reduces incidence by ~57 % (WHO 2020 recommendation).

Complications

• Peripheral neuropathy – irreversible sensory loss leading to repeated trauma, ulceration and secondary infections.
• Disabilities – claw hand, foot drop, facial palsy, and lagophthalmos causing corneal blindness.
• Reactions – can cause acute neuritis, leading to permanent nerve function loss if not treated promptly.
• Stigma and psychosocial impact – discrimination may result in isolation, depression, and reduced access to health care.

High‑Yield Exam Points

• M. leprae prefers cool body sites (30‑33 °C) → explains involvement of skin and superficial nerves.
• Ridley‑Jopling classification (TT, BT, BB, BL, LL) is based on the host’s cell‑mediated immunity; TT = strong immunity, LL = weak immunity.
• WHO operational classification (PB vs MB) is based on number of skin lesions and smear result; guides MDT duration (6 months vs 12 months).
• MDT regimen: Rifampicin (once monthly), Dapsone (daily), Clofazimine (daily + monthly) – remember the doses for MB disease.
• Type 1 reaction = delayed‑type hypersensitivity; treat with steroids.
• Type 2 reaction (ENL) = immune‑complex mediated; treat with Thalidomide (if not pregnant) or high‑dose Clofazimine.
• Single‑dose Rifampicin for contacts is a proven chemoprophylaxis strategy.
• Nerve thickening + loss of sensation is pathognomonic; always examine peripheral nerves in suspected cases.
• Disability grading (WHO Grade 0‑2) is used for monitoring and public‑health reporting.

Practice questions

1. A 28‑year‑old man presents with three hypopigmented, anesthetic macules on his forearm and a single thickened ulnar nerve. Slit‑skin smear is negative. According to WHO classification, which regimen should he receive?
   Answer: PB MDT – Rifampicin 600 mg monthly + Dapsone 100 mg daily for 6 months, because he has ≤5 lesions and a negative smear.

2. Which of the following statements about erythema nodosum leprosum (ENL) is FALSE?
   A) It is a type 2 reaction seen mainly in lepromatous leprosy.
   B) Thalidomide is the drug of choice, except in pregnancy.
   C) High‑dose Clofazimine can be used as an alternative to Thalidomide.
   D) Prednisone alone is sufficient to control severe ENL.
   Answer: D — Prednisone alone is often inadequate; Thalidomide or high‑dose Clofazimine is required for severe ENL.

3. A community health worker is planning a leprosy control program. Which intervention has the greatest evidence for reducing new case detection among household contacts?
   A) Monthly vitamin A supplementation.
   B) Single‑dose Rifampicin 10 mg/kg to contacts.
   C) Weekly skin examinations of contacts.
   D) BCG vaccination of contacts.
   Answer: B — Single‑dose Rifampicin given to contacts reduces incidence by about 57 % and is recommended by WHO.

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