Abstract
Leprosy is a unique and enigmatic disease. It is one of the few diseases to have been known in ancient and medieval times, and it was one of the first diseases to be linked to a specific infectious agent, Mycobacterium leprae (M. leprae), in 1873. 1 Yet even now, the organism cannot be cultured in vitro, and important gaps persist in our understanding of its biology and epidemiology. 2 In particular, although contact with a known case of leprosy is a major risk factor in contracting the disease, scientists are not certain how the organism is transmitted from one individual to another, nor do they know when, throughout the period of incubation and clinical disease, an individual is particularly infectious.3 These limitations have prevented the development of highly effective leprosy control measures, and there is little evidence that the transmission of the disease has been significantly reduced in recent years, despite efforts made toward that goal.4 As a bacterial infection, leprosy is susceptible to treatment with antibiotics; therefore, much has changed in the management of the disease over the last 50 years.5 The effective treatment of leprosy with chemotherapeutic agents began in the early 1950s with the introduction of dapsone. However, at least 10 years of treatment were required for multibacillary cases, and lifelong treatment was often advised for those individuals with the highest bacillary counts. In the early 1980s, the introduction of multidrug regimens, all of which included the potent bactericidal drug rifampicin, allowed the length of treatment to be cautiously reduced-to a fixed period of 24 months by the early 1990s and to a fixed period of only 12 months by the end of that decade.6 For the individual patient, multidrug therapy (MDT) meant a relatively rapid and effective cure.
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