Leprosy is caused by Mycobacterium leprae. The main targets of its attack are peripheral nerves and skin. Most people who are infected with M. leprae develop a subclinical infection and recover naturally without ever having signs or symptoms of the disease. Few people develop the disease, leprosy. The immunological spectrum of leprosy depends upon the response of the host to the invading bacillus. The immuno-competent type of Tuberculoid leprosy represents one end of the spectrum and the immuno-deficient type of Lepromatous leprosy, the other. The intervening type of Borderline leprosy has components of both Tuberculoid and Lepromatous types. Since leprosy affects about 15 million people in the world, with a quarter of them presenting deformities and disabilities, it poses, by far, the major cause of peripheral neuropathy in the world today. While very few countries are entirely exempt from leprosy, the bulk of the disease is concentrated at present in the continents of Africa, Asia and South America. It also occurs, but less commonly, in the islands of the Pacific, the Mediterranean, the countries bordering the Mediterranean, Adriatic and Black Seas, and the northern regions of Australia. In Australia leprosy is uncommon in the European population and is found mainly in Aborigines. In the Northern Territory, with approximately 650 registered and living Aboriginal leprosy patients, considerable attention has been given during the last two decades to the early detection and treatment of the disease.
The leprosy control project has been made more effective by initiating a programme aimed at the prevention and correction of deformities . The overall result has been a steady decline in the incidence of the disease, while the physiotherapy and reconstructive surgery programmes have helped to effectively reduce the backlog of deformity caused by the disease many years ago. Aetiology of Deformity Deformity in leprosy has been classified according to its pathogenesis as primary and secondary . Primary deformity is attributed directly to the disease process initiated by Mycobacterium leprae. Secondary deformity is the consequence of primary damage to nerves. Some of the deformities are of mixed aetiology. Primary deformity includes transient, cosmetic deformities occurring during the active phase of the disease: like raised or hypopigmented patches, nodular infiltration chiefly of the face and ears, and occasionally osteitis of the small bones of the hands and feet. These deformities usually subside with proper treatment of the disease. The more permanent cosmetic deformities include loss of eyebrows, excess of skin of the face and ears, and the various deformities of the nose . These are corrected by cosmetic surgery with good results. Primary deformity, due to leprosy neuritis, is encountered in the face, hands and feet, and follows a definite and predictable anatomical pattern. The facial and trigeminal nerves are involved in the face. While bilateral facial paralysis is rare, unilateral facial paralysis is found in about two percent of leprosy patients and selectively affects the zygomatic branch causing a lagophthalmos.