Leprosy, also called Hansen disease, is a chronic infection of the skin and peripheral nerves caused by the slow-growing bacteria Mycobacterium leprae and Mycobacterium lepromatosis. It is curable with WHO-supplied multidrug therapy taken over 6 to 12 months, and is far less contagious than commonly believed — over 95% of people are naturally immune.

Leprosy (ICD-10: A30) is a chronic granulomatous infection of the skin, peripheral nerves, mucosal surfaces, and eyes caused by Mycobacterium leprae and the closely related M. lepromatosis. The organism is an acid-fast obligate intracellular pathogen that has the longest doubling time of any known bacterium (12-14 days) and a 5-7 year incubation period on average, ranging from 9 months to 20+ years. The disease unfolds along a spectrum determined by the host's cell-mediated immune response, classified by Ridley and Jopling into tuberculoid (TT), borderline tuberculoid (BT), mid-borderline (BB), borderline lepromatous (BL), and lepromatous (LL) forms, plus an indeterminate early form.

The key symptoms of Leprosy are: Hypopigmented or reddish skin patches with sensory loss — the patient cannot feel light touch or pinprick over the lesion, a finding present in over 90% of paucibacillary cases., Thickened peripheral nerves palpable as firm cords, most often the ulnar nerve at the elbow, the common peroneal nerve at the fibular head, and the greater auricular nerve in the neck., Numbness and tingling in hands and feet, often in a glove-and-stocking distribution in advanced multibacillary disease., Loss of eyebrows and eyelashes (madarosis) and diffuse infiltration of facial skin (leonine facies) in lepromatous disease., Painless ulcers, burns, or injuries on hands and feet from undetected trauma due to sensory neuropathy., Foot drop, claw hand, or wrist drop from motor nerve involvement — late signs of established nerve damage., Nasal stuffiness, nosebleeds, and eventual collapse of the nasal bridge in lepromatous disease with mucosal involvement..
Diagnosis is primarily clinical, anchored on the WHO three-sign rule: a definite diagnosis requires one or more of (1) a hypopigmented or reddish skin lesion with definite loss of sensation, (2) thickening or enlargement of one or more peripheral nerves with associated motor or sensory deficit, or (3) demonstration of acid-fast bacilli on slit-skin smear. Any of these signs alone is sufficient in an endemic context. Slit-skin smear is performed at 4-6 sites (earlobes, forehead, suspect lesions) by making a small superficial incision and scraping dermal tissue for Ziehl-Neelsen staining. Positive smears confirm multibacillary disease; negative smears do not exclude paucibacillary leprosy. Skin biopsy with histopathology is the reference standard, showing the characteristic perineural infiltrate, granulomas in tuberculoid forms, or foamy macrophages (Virchow cells) packed with acid-fast bacilli in lepromatous forms. PCR for M. leprae DNA has 80-95% sensitivity and is increasingly available in reference labs; it is particularly useful in pure neural leprosy where biopsy is challenging. Nerve function assessment — including monofilament testing of hands and feet, voluntary muscle testing of the small muscles of the hand and foot, and palpation of named peripheral nerves — is essential at diagnosis and serially through treatment. The Ridley-Jopling spectrum is determined by clinical features plus histology; for treatment, the WHO paucibacillary/multibacillary classification suffices. Distinguish leprosy from vitiligo (no sensory loss), tinea versicolor (positive KOH preparation), sarcoidosis (no nerve thickening), and post-inflammatory hypopigmentation (history of prior dermatitis).
All suspected leprosy should be evaluated by an infectious disease specialist, dermatologist, or designated leprosy clinic. In endemic countries, national leprosy programs provide free MDT and management. Pure neural leprosy, leprosy reactions, drug resistance, and ocular involvement require specialist input. Disability-prevention programs benefit from physiotherapist and ophthalmologist involvement throughout treatment and the first 2 years afterward.
Find specialists →Skin lesions begin to fade within 4-8 weeks of starting MDT and continue to improve over 6-12 months. Nerve function in untreated cases often improves modestly with MDT alone, but established damage may persist. Patients are no longer infectious within days of the first rifampicin dose. Type 1 reactions resolve over 12-24 weeks with prednisolone tapers; Type 2 ENL may persist or recur for years and requires individualized long-term management. Clofazimine pigmentation fades 6-12 months after stopping treatment. Disability that remains 2 years after completing MDT is typically permanent and is addressed through rehabilitation and reconstructive surgery.
Seek out a dermatologist or infectious disease physician with leprosy experience, ideally in or affiliated with a national leprosy control program. In the US, the National Hansen's Disease (Leprosy) Program (Baton Rouge, LA) is the federal referral center and provides free consultation and medications. WHO-endorsed centers exist in every endemic country. Continuity matters because MDT extends over months and nerve function must be monitored for at least 2 years post-treatment.
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Prognosis is excellent with timely MDT. Cure rates exceed 98% in completed paucibacillary and multibacillary courses, and patients become non-infectious within days of starting rifampicin. Relapse occurs in under 1% of cases over 10 years post-treatment. Nerve damage is the major source of long-term disability; damage present at diagnosis often does not fully reverse, but early MDT and timely management of reactions prevent most new damage. WHO data show approximately 6% of patients globally present with Grade 2 (visible) disability at diagnosis — the operational marker of delayed detection. Leprosy reactions remain a challenge: Type 1 reversal reactions occur in 20-30% of multibacillary patients, often during the first year of MDT, and Type 2 ENL occurs in 20-50% of lepromatous patients, sometimes recurrently for years. Mortality directly from leprosy is rare in modern practice. Quality of life is heavily influenced by stigma, particularly in cultures with strong historical association; community-based rehabilitation programs and inclusion in mainstream healthcare have substantially reduced this over the past two decades. With sustained access to MDT and early diagnosis, WHO maintains the goal of zero new pediatric Grade 2 disability cases by 2030 as part of its global leprosy strategy.
Regular exercise is encouraged with attention to protecting insensate limbs. Swimming, cycling, and walking in protective footwear are excellent. Avoid bare-foot activities, high-impact exercises that could cause unnoticed foot injury, and prolonged gripping that may damage insensate hands. Physiotherapist-guided range-of-motion exercises preserve joint function and prevent contractures.
Medically reviewed by AIHealz Medical Editorial Board · May 13, 2026