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Leprosy (Hansen’s disease) 

Leprosy (Hansen’s disease)

Leprosy (Hansen’s disease)

Diana N.J. Lockwood


July 30, 2015: This chapter has been re-evaluated and remains up-to-date. No changes have been necessary.


Caution on use of thalidomide to treat Type 2 (ENL) reactions.

Updated on 28 Nov 2013. The previous version of this content can be found here.
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date: 24 April 2017

Leprosy is a chronic granulomatous disease caused by Mycobacterium leprae, an acid-fast intracellular organism not yet cultivated in vitro. It is an important public health problem worldwide, with an estimated 4 million people disabled by the disease. Transmission of M. leprae is only partially understood, but untreated lepromatous patients discharge abundant organisms from their nasal mucosa into the environment.

Clinical features

These are determined by the degree of cell-mediated immunity towards M. leprae, with tuberculoid (paucibacillary) and lepromatous leprosy (multibacillary) being the two poles of a spectrum: (1) tuberculoid—well-expressed cell-mediated immunity effectively controls bacillary multiplication with the formation of organized epithelioid-cell granulomas; (2) lepromatous—there is cellular anergy towards M. leprae with abundant bacillary multiplication. Between these two poles is a continuum, varying from the patient with moderate cell-mediated immunity (borderline tuberculoid), through borderline, to the patient with little cellular response, borderline lepromatous.

Presenting symptoms—most commonly (1) anaesthesia—ranging from a small area of numbness on the skin due to involvement of a dermal nerve, to peripheral neuropathy with affected nerves tender and thickened; (2) skin lesions—most commonly macules or plaques; tuberculoid patients have few, hypopigmented lesions that are anaesthetic; lepromatous patients have numerous, sometimes confluent lesions.

Other manifestations—these include (1) type 1 (reversal reactions)—occur in borderline patients; characterized by acute neuritis and/or acutely inflamed skin lesions; often occur in the first 2 months after starting treatment; (2) type 2 (erythema nodosum leprosum reactions)—occur in up to 50% of patients with lepromatous leprosy; (3) neuritis—silent neuropathy is an important form of nerve damage, causing lifelong morbidity; (4) eye disease—blindness occurs in at least 2.5% of patients.


This is made by recognition of typical skin lesions or thickened peripheral nerves, supported by the finding of acid-fast bacilli on slit skin smears that should be taken from at least four sites (earlobes, and edges of active lesions).


There are six main principles of treatment: (1) stop the infection with chemotherapy—first-line antileprosy drugs are rifampicin, clofazimine, and dapsone, given in combination and duration as determined by whether disease is paucibacillary or multibacillary; these are highly effective in killing bacilli but may not halt nerve damage; (2) treat new nerve damage—a 6-month course of steroids should be given to those with nerve damage for less than 6 months; (3) treat reactions—steroids are likely to be required; (4) educate the patient about leprosy; (5) prevent disability; and (6) support the patient socially and psychologically—patients with leprosy the world over are frequently stigmatized; words such as ‘leper’ should be avoided; the disease can be referred to as ‘Hansen’s disease’.


Vaccination with bacille Calmette–Guérin (BCG) can provide some protection against leprosy (20–80% in different trials).

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