Leprosy is a disease of peripheral sensory nerves that results from infection with Mycobacterium leprae, which was first detected in Bergen, Norway, in 1873 by Dr. Armauer Hansen. It can be effectively treated with long-term multidrug therapy. In 2006, more than 250,000 new cases of leprosy were reported to the World Health Organization. Many infected individuals have self-healing indeterminate lesions. Others with initially indeterminate lesions proceed to develop leprosy that can be classified along a clinical and immunologic spectrum from paucibacillary or tuberculoid leprosy to multibacillary or lepromatous leprosy. Most patients fall somewhere between these 2 polar forms of the disease and are classified, using pathology-based criteria developed by Ridley and Jopling (1966), as borderline tuberculoid, midborderline, and borderline lepromatous. The paucibacillary form is associated with strong M. leprae-specific cell-mediated immunity (CMI), whereas the multibacillary form is notable for the lack of antigen-specific CMI. The prevalence of paucibacillary versus multibacillary leprosy varies in different populations. M. leprae cannot be cultured in vitro and grows slowly in the footpads of mice, the liver and spleen of armadillos, and in some nonhuman primates. A genetic component to leprosy susceptibility has long been suspected. While contact with a multibacillary patient increases the relative risk of acquiring disease, most new patients have no known contact with other patients. For further information, see reviews by Fitness et al. (2002), Mira (2006), Moraes et al. (2006), Scollard et al. (2006), and Alter et al. (2008). [from
OMIM]