Leprosy

Abstract

Leprosy is a disease associated with great stigma due to the deformities it can produce. It is caused by Mycobacterium leprae. In 2008 a new mycobacteria, M. lepromatosis was recognized as the agent of Lucio leprosy. It is not known how leprosy is transmitted. Only infected people with a defect in their cell-mediated immunity, which is specific for M. leprae, develop the disease. Those with still high immunity will develop tuberculoid leprosy (TT), with a single skin lesion and no detectable bacilli; those with no CMI will develop lepromatous leprosy (LL), with areas of skin infiltrated by foamy histiocytes filled with leprosy bacilli. In between are the borderline patients, borderline tuberculoid (BT), mid-borderline (BB), and borderline lepromatous (BL), with decreasing levels of CMI and increasing bacillary load. For therapy, according to the WHO, patients are divided in paucibacillary (PB) (negative slit-skin smears, i.e. Indeterminate, TT, and BT) and multibacillary (MB) (positive slit-skin smears, i.e. BB, BL, and LL). PB patients are treated with six months of dapsone plus rifampicin; MB patients are treated with 12 months of dapsone plus rifampicin plus clofazimine. Two types of hypersensitivity reactions may occur, type 1 and type 2. Type 1 reaction is considered to be due to a change in the CMI and only happens in borderline patients (BT,BB,BL). It produces inflammation of the skin lesions and/or nerves; the drug of choice for it is prednisone. Type 2 reaction is considered to be due to antigen-antibody deposition in tissues, and only happens in BL and LL patients. The most common presentation is erythema nodosum leprosum, but it may present with fever and inflammation of several organs. The drug of choice for a severe reaction is thalidomide, but in a woman of child-bearing age it is contraindicated and prednisone should be used. Leprosy is a disease that can be easily diagnosed, and with appropriate early therapy can be cured with no sequelae.