14th Congress of the European Federation of Neurological Societies
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Leprosy
Dr. Abhijit Chaudhuri
Dr. Abhijit Chaudhuri
London, United Kingdom  
Disclosure: I have received consultation fees, speaker fees and support for attending seminars/meetings from: BMJ Group, GLG, Astra Zeneca, Bayer, Schering, Novartis, Teva
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Topic: Other
36 slide(s) – 00:26:10– English –2010-09-26
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Involvement of peripheral nerves by chronicMycobacterium leprae infection is the most characteristic manifestation of leprosy (Hansen’s disease). Leprosy constitutes an important public health problem in the developing world. The most likely portal of entry ofM. leprae is the respiratory tract and the clinical course depends on the strength of the inoculum and host immune response to the bacilli. There are two polar forms of the disease, tuberculoid leprosy and lepromatous leprosy, with a spectrum of intermediate forms (known as borderline or dimorphous leprosy). Tuberculoid leprosy is a localised disease in patients with high resistance, with few bacilli and sharply demarcated skin lesions, and lepromatous leprosy represents the low immunity, systemic infectious form of the disease. The temperature preference ofM. leprae restricts its target to the cooler, exterior tissues of the body. It is in the cool tissues that nerve damage first develops and leads to a temperature-dependent pattern of sensory and motor mononeuropathies. Peripheral nerve involvement occurs in all forms of leprosy (late in lepromatous, early in tuberculoid form) which becomes thickened and tender. Mutilation, deformity and trophic ulcers result commonly from secondary effects of nerve damage. Diagnosis of leprosy is clinical, confirmed by histological demonstration of the weakly acid-fast bacilli in smears obtained by incising a clinically affected area of skin. Dapsone remains one the key anti-mycobacterial agents for the treatment of leprosy, along with rifampicin and clofazimine. The choice and the duration of regimen depends on the bacterial density (paucibacillary or multibacillary) in lesions. Treatmentinduced reactions (lepra reactions) require prompt identification and treatment to avoid damage, and are of two types. Type 1 reactions, which are severe and due to a shift of host-immunity on treatment, require treatment with large doses of steroids. Type 2 reactions (erythema nodosum leprosum) are essentially due to immune complex deposition (Arthus reaction). Variable in severity and symptoms, Type 2 reactions are treated with thalidomide, clofazimine and occasionally with corticosteroids
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