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Leprosy is a chronic granulomatous disease caused by Mycobacterium leprae and principally acquired during childhood or young adulthood. The skin, mucous membrane of the upper respiratory tract, and peripheral nerves are the major sites of involvement in all forms of leprosy. The clinical manifestations, natural history, and prognosis of leprosy are related to the host response, and the various types of leprosy (tuberculoid, lepromatous, etc.) represent the spectra of the host's immunologic response (cell-mediated immunity).


The clinical spectrum of leprosy depends exclusively on variable limitations in the host's capability to develop effective cell-mediated immunity (CMI) to M. leprae. The organism is capable of invading and multiplying in peripheral nerves and infecting and surviving in endothelial and phagocytic cells in many organs. Subclinical infection with leprosy is common among residents in endemic areas. Presumably the subclinical infection is handled readily by the host's CMI response, Clinical expression of leprosy is the development of a granuloma; and the patient may develop a "reactional state," which may occur in some form in >50% of certain groups of patients. The granulomatous spectrum of leprosy consists of

1. a high­resistance tuberculoid response (TT)
2. a low­or absent-resistance lepromatous pole (LL)
3. a dimorphic or borderline region (BB) and two intermediary regions:
4. borderline lepromatous (BL)
5. borderline tuberculoid (BT)

In order of decreasing resistance, the spectrum is TT, BT, BB, BL, LL.

Immunologic Responses Immune responses to M. leprae can produce several types of reactions associated with a sudden change in the clinical status.

Lepra Type 1 Reactions (Downgrading and Reversal Reactions): Individuals with BT and BL develop inflammation within existing skin lesions. Downgrading reactions occur before therapy; reversal reactions occur in response to therapy. Type 1 reactions can be associated with low-grade fever, new multiple small "satellite" maculopapular skin lesions, and/or neuritis.

Lepra Type 2 Reactions (Erythema Nodosum Leprosum, ENL): Seen in half of LL patients, usually occurring after initiation of antilepromatous therapy, generally within the first 2 years of treatment. Massive inflammation with erythema nodosum-like lesions.

Lucio's Reaction: Individuals with diffuse LL develop shallow, large polygonal sloughing ulcerations on the legs. The reaction appears to be either a variant of ENL or secondary to arteriolar occlusion. The ulcers heal poorly, recur frequently, and may occur in a generalized distribution. Generalized Lucio's reaction is frequently complicated by secondary bacterial infection and sepsis.


* one or more hypopigmented (lighter than your normal skin color) skin lesions that have decreased sensation to touch, heat, or pain
* numbness or absent sensation in the hands and arms, or feet and legs
* skin lesions that do not heal after several weeks to months

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