Clinical Guides
Leprosy (Hansen Disease)
A clinically focused Indian guide to early leprosy diagnosis, revised NLEP multidrug therapy, reaction care, disability prevention and contact management, prepared for mandatory clinical review.
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Leprosy (Hansen Disease)
A clinically focused Indian guide to early leprosy diagnosis, revised NLEP multidrug therapy, reaction care, disability prevention and contact management, prepared for mandatory clinical review.
Summary
Leprosy, or Hansen disease, is a chronic infection caused principally by Mycobacterium leprae that preferentially affects skin, peripheral nerves, eyes and upper-airway mucosa. It is curable. The preventable harm comes largely from delayed recognition, immune-mediated reactions and neuritis that damage nerve function, followed by unnoticed injury to insensitive hands, feet or eyes. A pale or reddish patch with definite sensory loss, a thickened peripheral nerve with sensory or motor impairment, or acid-fast bacilli in a slit-skin smear is a cardinal diagnostic sign. Early disease can be subtle, so absence of dramatic deformity is not reassurance.
India's National Leprosy Eradication Programme provides free diagnosis, multidrug therapy, disability prevention and rehabilitation through the public system. From 1 April 2025, the programme uses rifampicin, dapsone and clofazimine for both paucibacillary and multibacillary disease: six months for PB and twelve months for MB. Under the revised NLEP classification, one to five lesions with no nerve involvement and a negative slit-skin smear are PB; more than five lesions, any involved nerve or a positive smear places the patient in MB. Local programme rules govern blister packs, children, pregnancy, interrupted treatment and referral.
Leprosy reactions are not antimicrobial failure. Type 1 reaction and erythema nodosum leprosum may occur before, during or after MDT; acute neuritis, weakness, sensory deterioration, eye pain or a new reaction can threaten function quickly and requires prompt assessment. MDT usually continues while the reaction is treated under supervision. Household and other eligible contacts need respectful screening and programme-administered post-exposure prophylaxis after exclusions. Diagnosis, notification, contact work, resistance testing and second-line therapy must follow NLEP pathways rather than improvised private regimens.
How Common Is It?
Leprosy remains a substantial Indian public-health problem despite national elimination as defined by registered prevalence below one per ten thousand population. Elimination at that threshold is not eradication, interruption of transmission or absence of disease in every district. The NLEP Annual Report 2024-2025 recorded 100,957 newly detected cases, an annual new case detection rate of 7.00 per 100,000, and 82,297 people under treatment as of 31 March 2025, corresponding to a registered prevalence of 0.57 per 10,000. Among new cases, 63.03 percent were multibacillary, 4.68 percent were children and 1.88 percent had grade 2 disability.
These are programme figures for a defined financial year, not a timeless estimate of biological incidence. Case detection rises when active surveys become more effective and falls when services are disrupted, so change cannot be interpreted without programme context. Child cases indicate recent transmission; grade 2 disability at first diagnosis signals delayed detection. The annual report also shows geographical heterogeneity: most districts met the prevalence threshold, while important high-endemic pockets persisted. A national average therefore cannot guide the probability in a particular village, migrant community or household.
Long incubation, slow progression, stigma, misdiagnosis and access barriers create hidden disease. A patient may delay because a patch is painless, a nerve deficit evolves gradually or the word leprosy threatens relationships and employment. Conversely, not every hypopigmented patch in an endemic area is leprosy. The clinically useful response is skilled skin and nerve examination, prompt confirmation of cardinal signs, active contact work and reliable completion of treatment, coupled with reporting that separates new case detection, registered prevalence, treatment completion, child cases and disability.
Risk Factors
Prolonged close contact with an untreated infectious case increases risk, particularly within households and other settings with sustained exposure. Transmission is believed to occur mainly through respiratory droplets during repeated contact; brief social contact, sharing a room once or touching intact skin does not justify exclusion or panic. Most exposed people do not develop leprosy because host immunity is protective. Genetic susceptibility, intensity and duration of exposure, bacillary burden of the index case and living conditions influence risk, while the incubation period is commonly several years and may be much longer.
Household contacts, neighbours and regular social contacts defined by the national programme deserve symptom enquiry and a head-to-toe skin and nerve screen, then periodic advice or follow-up. Children with a new diagnosis are a particularly important signal to search for an infectious source. Overcrowding, poverty, migration, remote residence and weak access do not biologically define the disease but can increase delayed detection and incomplete follow-up. Stigma itself is a risk factor for harm because it drives concealment. Contact tracing must therefore preserve consent and confidentiality; public disclosure can cause discrimination without improving care.
Risk of disability is not the same as risk of acquiring infection. Existing nerve function impairment, multibacillary disease, delayed diagnosis, recurrent reactions, neuritis, eye involvement, plantar ulceration and inability to perform self-care increase the likelihood of lasting impairment. Reactions can occur during or after successful MDT, and rifampicin resistance is a separate concern in relapse, treatment failure or selected surveillance cases. Previous dapsone monotherapy, irregular or inadequate therapy and retreatment histories must be documented. Neither BCG vaccination nor single-dose rifampicin gives absolute protection, so contacts must still be taught the early signs and where to return.
Diagnosis
Leprosy can be diagnosed when at least one cardinal sign is present: definite loss of sensation in a hypopigmented or reddish skin lesion; a thickened or enlarged peripheral nerve with sensory, motor or autonomic impairment in its distribution; or acid-fast bacilli demonstrated in a slit-skin smear. Do not label an uncertain pale patch solely from appearance. Equally, do not wait for deformity or a positive smear when a cardinal clinical sign is clear.
History
Ask when each patch, nodule or swelling began; whether it changed; itch or pain; altered heat, pinprick or light-touch sensation; numbness, burning, electric pain, weakness, dropping objects, foot slap, repeated burns or wounds; eye redness, pain or reduced vision; nasal blockage or epistaxis; fever and tender nodules. Record household or prolonged contact, place of residence, previous leprosy diagnosis, full MDT or monotherapy exposure, missed doses, release-from-treatment date and reaction therapy. Ask sensitively about pregnancy, tuberculosis symptoms, medicines and psychosocial harm.
Examination
Examine the entire skin in good light with consent and privacy. Describe lesion number, morphology, border, infiltration, symmetry, surface, hair and sweating. Test sensation methodically, comparing normal skin. Palpate relevant peripheral nerves for thickening or tenderness and document motor, sensory and autonomic function of eyes, hands and feet. Look for lagophthalmos, corneal risk, clawing, foot drop, ulcers and visible disability. Tender nerves, new weakness or reaction signs are urgent.
Investigations
Slit-skin smear supports classification and is cardinal when bacilli are seen, but a negative result does not exclude PB disease. Skin or nerve biopsy can resolve difficult differentials when interpreted with clinical findings. Routine serology is not recommended as a stand-alone diagnostic test. In relapse, suspected treatment failure or selected AMR surveillance, use the NLEP referral network for smear, biopsy and molecular resistance testing; do not send poorly collected samples or infer resistance from a reaction.
Differential Diagnosis
Vitiligo produces sharply depigmented, often chalk-white macules with normal sensation, sweating and nerve examination; leprosy lesions are commonly hypopigmented or erythematous and may be anaesthetic. Pityriasis versicolor has fine scale, favours the upper trunk and can be supported by potassium-hydroxide microscopy. Pityriasis alba is a mildly scaly facial condition in children without nerve deficit. Post-inflammatory hypopigmentation follows eczema, trauma or infection and retains sensation. Tinea corporis usually has an active scaly margin and itch. None should be distinguished by colour alone: sensory testing and nerve examination change the differential.
Granulomatous disorders include cutaneous tuberculosis, sarcoidosis, granuloma annulare, deep fungal infection and leishmaniasis. Nodular multibacillary disease can resemble lymphoma, leukaemic infiltration, secondary syphilis or disseminated fungal infection. Diffuse infiltration with loss of eyebrows raises lepromatous leprosy but also needs evaluation for endocrine, inflammatory and infiltrative causes. A biopsy is valuable when morphology and cardinal signs disagree.
Pure neuritic leprosy may mimic diabetic or nutritional polyneuropathy, entrapment neuropathy, vasculitis, hereditary neuropathy and trauma. Leprosy often affects selected superficial nerves asymmetrically, with thickening, tenderness, focal sensory loss, weakness and autonomic skin change, but no single pattern is perfectly specific. Acute nerve pain or loss may be a reaction rather than new infection.
During treatment, new erythematous swollen lesions and nerve symptoms may be a type 1 reaction; crops of tender nodules with systemic illness suggest erythema nodosum leprosum. Relapse more often evolves gradually after adequate treatment, while reaction can occur before, during or after MDT. Drug eruption, dapsone hypersensitivity, haemolysis, hepatitis and intercurrent infection can mimic or accompany reaction. The distinction requires timing, nerve-function comparison, smear or biopsy where indicated and specialist review; it must not be made by stopping MDT as a diagnostic trial.
Management
Register and classify the case through the current NLEP pathway, document baseline lesion count, nerve involvement, disability grade, eye-hand-foot function and smear results when performed, then begin the correct multidrug blister regimen promptly. Since 1 April 2025, Indian public facilities use rifampicin, dapsone and clofazimine for both PB and MB disease, with six months for PB and twelve months for MB. Explain supervised monthly and self-administered components, expected clofazimine pigmentation, adherence, warning adverse effects and the difference between cure of infection and slower recovery of nerve damage. MDT should not be interrupted simply because a reaction develops.
At every contact, repeat focused nerve-function and eye assessment rather than merely count tablets. Acute neuritis, type 1 reaction or erythema nodosum leprosum requires prompt grading and treatment. Significant nerve-function loss is commonly treated with a supervised prednisolone course after screening for contraindications and relevant infections; dosing, taper and monitoring must follow the current NLEP or referral protocol. Severe or recurrent ENL may need additional specialist agents. Thalidomide has major teratogenic and regulatory hazards and must never be casually prescribed.
Prevent disability from day one. Teach daily inspection of insensitive hands and feet, soaking and skin care where advised, protective footwear, safe cooking and work practices, wound care, exercises and when to report redness, swelling, blister, ulcer or eye symptoms. Refer for physiotherapy, occupational support, MCR footwear, ulcer care, splints, reconstructive surgery and psychosocial help as needed.
With consent and confidentiality, list eligible contacts, screen them for active leprosy and contraindications, and provide programme-administered single-dose rifampicin PEP where eligible. Notify in accordance with the current Indian requirement and record in Nikusth. Counselling must state that treatment rapidly reduces infectiousness, ordinary social contact is safe, and exclusion from family, school or work is harmful and unnecessary.
Prescribing Information
The revised NLEP adult regimen is rifampicin 600 mg once monthly, clofazimine 300 mg once monthly plus 50 mg daily, and dapsone 100 mg daily. PB treatment is six months and MB treatment twelve months under programme definitions. For children aged ten to fourteen years, the public NLEP table lists rifampicin 450 mg monthly, clofazimine 150 mg monthly plus 50 mg on alternate days, and dapsone 50 mg daily. For children below ten years or below 40 kg, weight-based and partial-blister arrangements require the exact current programme instruction; do not extrapolate an adult pack.
Rifampicin can cause hepatitis, thrombocytopenia, flu-like reactions and orange-red body fluids and is a potent enzyme inducer that interacts with hormonal contraception, anticoagulants, antiretrovirals and many other medicines. Monthly intermittent dosing makes unplanned repeat doses hazardous. Dapsone may cause dose-related haemolysis, methaemoglobinaemia, agranulocytosis, hepatitis or the potentially fatal dapsone hypersensitivity syndrome; assess anaemia risk and G6PD status according to local protocol and clinical context. Clofazimine commonly causes red-brown to dark skin discolouration and dryness; high cumulative exposure can cause serious gastrointestinal toxicity. Explain expected pigmentation in advance rather than letting it destroy adherence.
Leprosy reactions are immune events, so additional anti-inflammatory prescribing is separate from MDT. Prednisolone requires a documented indication, baseline infection and metabolic assessment, gastric or bone protection when appropriate, and serial nerve-function monitoring. ENL management is specialist-led; thalidomide is tightly controlled and contraindicated in pregnancy because of profound teratogenicity.
Suspected relapse or resistance must enter the NLEP AMR referral network. Do not add a lone drug, recycle irregular rifampicin or invent a second-line combination. WHO second-line advice exists, but India-specific molecular results, prior exposure, pregnancy and programme supply determine the regimen. The 2018 WHO guideline explicitly found insufficient direct evidence for benefits and harms of drug-resistant regimens and based those recommendations on expert opinion. That limitation increases, rather than reduces, the need for molecular confirmation, specialist interpretation, pharmacovigilance and programme-authorised treatment.
When to Refer
Refer immediately or the same day for new nerve pain with weakness or sensory loss, tender enlarged nerves, lagophthalmos, red or painful eye, reduced vision, acute foot drop or wrist drop, rapidly progressive reaction, severe ENL, ulcer with spreading infection, suspected osteomyelitis or systemic illness. Nerve function can be lost over a short period and waiting for the next monthly blister visit is unsafe. Continue indicated MDT unless a qualified clinician identifies a serious drug reaction or another specific reason to hold it.
The NLEP pathway sends difficult-to-diagnose cases, complicated disease, reactions and grade 2 disability requiring reconstructive care to district hospital or higher services. Refer when cardinal signs are uncertain, lesions are atypical, pure neuritic disease is suspected, biopsy or slit-skin smear expertise is needed, a child has disease, or pregnancy complicates classification or reaction treatment. Eye involvement needs ophthalmology; significant motor deficit, contracture or recurrent ulcer needs DPMR, physiotherapy, orthotics or surgical assessment. Mental-health crisis, family exclusion, threatened employment or violence is also a legitimate referral need.
Seek urgent specialist and pharmacovigilance advice for jaundice, widespread rash, fever with facial oedema, mucosal involvement, dyspnoea or cyanosis, severe anaemia, unusual bruising, abdominal pain with vomiting, or another possible serious MDT adverse reaction. Suspected relapse, non-response after verified adherence, a rising bacillary index where serial smear is appropriate, or prior irregular monotherapy needs an AMR-capable reference pathway rather than empiric extension.
Contacts with a suspicious patch or nerve symptom are potential cases, not PEP candidates until assessed. Contacts with tuberculosis symptoms, significant rifampicin interaction or another programme exclusion need evaluation. A referral is complete only when the receiving facility, appointment, transport, records and interim safety-net are clear.
Red Flags
New motor weakness is the highest-priority functional red flag: difficulty closing an eye, thumb opposition loss, finger clawing, wrist drop, foot drop or repeated tripping may represent active neuritis. New sensory loss, severe nerve tenderness or pain, hot swollen lesions and oedematous hands or feet also demand urgent reaction assessment. An eye that is red, painful, photophobic or losing vision, or lagophthalmos with corneal exposure, can deteriorate irreversibly. Teach patients to report function change immediately rather than wait for a deformity.
Type 1 reaction often causes inflammation of existing lesions, oedema and neuritis, especially in borderline disease. Type 2 reaction or ENL produces tender erythematous nodules and may include fever, malaise, neuritis, arthritis, orchitis, iridocyclitis or other systemic involvement. Reactions can occur before diagnosis, during MDT or after release from treatment. They are not evidence that MDT has failed and do not justify automatic retreatment, but severe reaction, recurrence or corticosteroid dependence needs expert management.
Drug red flags include fever, rash, facial swelling, lymphadenopathy, jaundice or organ dysfunction after dapsone; breathlessness, cyanosis or marked anaemia suggesting methaemoglobinaemia or haemolysis; thrombocytopenic bleeding or hepatitis associated with rifampicin; and persistent severe abdominal symptoms on clofazimine. Stop or continue individual drugs only through an urgent clinician-led plan because both uncontrolled toxicity and fragmented monotherapy cause harm.
Public-health red flags include a child case, grade 2 disability at diagnosis, multiple linked cases, relapse after adequate therapy and suspected drug resistance. Social danger also matters: expulsion from home, school refusal, job loss, self-harm thoughts or forced disclosure require active safeguarding and counselling. Leprosy does not justify routine isolation, separate utensils or denial of ordinary contact once treatment is organised.
Indian Clinical Context
The National Leprosy Eradication Programme is a centrally supported programme under the National Health Mission. It integrates free diagnosis, MDT, contact screening, post-exposure prophylaxis, disability prevention, rehabilitation and reporting through public facilities from primary care to medical colleges and central institutes. The programme website states that the revised three-drug regimen for both PB and MB disease became effective nationwide on 1 April 2025 and that leprosy was declared notifiable in 2025. Local clinicians should confirm the operational notification route and use Nikusth or the state workflow rather than assuming that a referral centre will report on their behalf.
Classification is now operationally strict. PB requires one to five skin lesions, no involved nerve and a negative smear; more than five lesions, any involved nerve or a positive smear is MB. This differs from older learning material that treated limited nerve involvement or a two-drug PB pack differently. A current Indian answer should not reproduce the superseded regimen. Where lesion count, nerve status and smear disagree, use the category that prevents undertreatment and obtain programme advice.
NLEP services extend beyond tablets. ASHAs support suspect referral, contact survey and adherence; district hospitals manage difficult diagnosis, reactions, ulcers and disability; medical colleges and institutes provide advanced diagnosis, reconstructive care and AMR support. Single-dose rifampicin PEP is for eligible contacts after consent and screening, not for unassessed community distribution. The index patient's confidentiality and preference about disclosure must shape contact work.
The word 'elimination' has caused damaging complacency. India's 2024-2025 report still records child cases, disability and endemic pockets, so clinicians must retain examination skill. Use person-first, non-stigmatising language; explain curability and rapid reduction of infectiousness on MDT. No law, programme target or epidemiological label justifies segregation or discrimination.
NMC Competency Mapping
Leprosy spans Dermatology, Microbiology, General Medicine, Community Medicine, Ophthalmology, Orthopaedics, Physical Medicine and Rehabilitation, Pharmacology and AETCOM. DR9.1 is the direct dermatology anchor commonly used for aetiology, clinical features and management. Microbiology learning covers M. leprae biology, acid-fast demonstration, inability to culture routinely in artificial media, host immunity and clinicopathological spectrum. Community Medicine covers NLEP, case definitions, surveillance, contact examination, PEP, disability indicators and stigma reduction. Institutions must verify current code wording and performance level against the official 2024 NMC curriculum rather than copy an unofficial competency list.
A graduating learner should examine a patch for morphology and definite sensory loss, palpate accessible nerves appropriately, test mapped sensory and motor function, inspect eyes, hands and feet and assign a disability grade under supervision. They should identify one cardinal sign, distinguish PB from MB under the revised Indian classification, select six- versus twelve-month MDT, and explain why both groups now receive three drugs. A student must also recognise acute neuritis, type 1 reaction and ENL and understand that reaction can occur despite effective antimicrobial treatment.
Prescribing competence includes the supervised and daily components of rifampicin, clofazimine and dapsone, major adverse effects, interactions, adherence and pharmacovigilance. It does not authorise unsupervised corticosteroid tapers, thalidomide or second-line AMR regimens. Public-health competence includes consent-based contact listing, exclusion of active disease before PEP, notification, Nikusth recording and referral. Communication assessment should reject labels, isolation advice and fear-based counselling. Learners should be able to tell a patient that leprosy is curable, ordinary contact is safe, nerve warning signs need urgent return, and disability prevention continues after MDT completion.
Key Exam Pearls for NEET PG
Mycobacterium leprae is an acid-fast, obligate intracellular bacillus with tropism for macrophages and Schwann cells; it prefers cooler sites. It cannot be grown on routine artificial culture media. Mouse footpad and nine-banded armadillo are classic experimental models. The spectrum reflects cell-mediated immunity: tuberculoid disease has strong CMI, few well-defined anaesthetic lesions, asymmetric nerve involvement, low bacillary load and lepromin positivity; lepromatous disease has poor CMI, numerous symmetric lesions, diffuse infiltration, high bacillary load and lepromin negativity. Lepromin is for immunological classification and prognosis, not diagnosis.
Know the three cardinal signs: definite sensory loss in a pale or reddish patch; thickened peripheral nerve with functional impairment; acid-fast bacilli on slit-skin smear. Fite-Faraco staining demonstrates lepra bacilli in tissue. Globi and a high bacteriological index suggest multibacillary disease. Type 1, or reversal, reaction is a delayed hypersensitivity change with inflamed existing lesions and neuritis, often in borderline disease. Type 2 reaction is immune-complex-mediated ENL with tender nodules and systemic manifestations; Lucio phenomenon is associated with diffuse lepromatous disease.
For current India questions, PB means one to five lesions, no nerve involved and negative smear. MB means more than five lesions, one or more nerves involved, or positive smear. From April 2025 both receive rifampicin, dapsone and clofazimine: PB for six months, MB for twelve. Clofazimine causes pigmentation; dapsone causes haemolysis, methaemoglobinaemia and hypersensitivity; rifampicin induces hepatic enzymes and colours secretions.
Continue MDT during most reactions while treating the immune complication. New nerve-function impairment makes a reaction urgent. Relapse is not synonymous with reaction and suspected resistance needs molecular referral. Eligible screened contacts may receive single-dose rifampicin under the programme. National elimination below one per ten thousand is not eradication, and child cases remain evidence of recent transmission.
Frequently Asked Questions
Is leprosy highly contagious through ordinary daily contact?
No. Most people are naturally resistant, and transmission usually requires prolonged close exposure to an untreated infectious case. Leprosy is not spread by brief touch, sharing meals or sitting beside someone. Effective MDT rapidly reduces infectiousness. Contact screening should be respectful and confidential, never used to justify segregation, separate utensils or exclusion from work or school.
How is paucibacillary disease classified and treated in India now?
Under the NLEP protocol effective from 1 April 2025, PB disease has one to five skin lesions, no involved peripheral nerve and a negative slit-skin smear. It receives rifampicin, dapsone and clofazimine for six months. Any involved nerve, more than five lesions or a positive smear moves classification to MB and the treatment duration to twelve months.
Does a leprosy reaction mean that multidrug therapy has failed?
Usually not. Reactions are immune inflammatory episodes that may occur before, during or after effective MDT. They can inflame lesions and injure nerves, so new pain, tenderness, sensory loss, weakness or eye symptoms need urgent assessment. MDT generally continues while the reaction is treated, unless a clinician identifies serious drug toxicity or another specific reason to change it.
Can every household contact take single-dose rifampicin without examination?
No. SDR-PEP is a programme intervention for eligible contacts after consent, screening for active leprosy and tuberculosis, and assessment of contraindications, interactions and recent rifampicin exposure under the current protocol. A contact with a suspicious patch or nerve symptom needs diagnostic assessment, not prophylaxis. PEP reduces risk but does not replace education or future symptom review.
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