Leprosy is a chronic infectious disease caused by Mycobacterium leprae (M. leprae). It affects human skin and the peripheral nerve systems, as well as eyes and other systems, resulting in a variety of disabilities associated with leprosy. According to the report by World Health Organization (WHO), over 200,000 affected people (mainly in Asia and Africa) were registered annually and leprosy still constitutes a public health problem today. Leprosy control in China has been successfully achieved in 1981, but it has not been eliminated in several regions according to the WHO leprosy elimination criterion (< 1 case per 10,000 population), primarily in Yunnan, Guizhou, Sichuan, Tibet, and Hunan Provinces. Here, we reported the epidemiological trends and management of leprosy in Yuxi, Yunnan Province from 1952 to 2008. A total of 2223 leprosy cases with detailed diagnosis and treatment data were analysed. The overall prevalence rate of leprosy in the Yuxi region presented a roughly unimodal distribution between 1952 and 2008, with a peak (9.27 per 10,000 population) in 1965. With the introduction and ubiquitous coverage of the WHO multi-drug therapy (MDT) in this area, leprosy elimination was achieved in 1992. Overall, the age distribution of patients changed dramatically over years, and there were only two childhood cases between 1995 and 2008 (both in 1998). Nearly half of the total cases (49.1%) were classified as multibacillary leprosy. In recent years, the majority of cases (>80%) were detected by passive approaches, and there is an increasing tendency to find multibacillary leprosy patients. The results provide an overall profile of our 57-year effort regarding leprosy control in the Yuxi region. The trend and unique feature in detection of new cases in recent years suggested that the transmission of leprosy has stopped in the area or, at least, dramatically declined. M. leprae is an unculturable pathogen with an exceptionally eroded genome. The high level of inactivation of gene function in M. leprae, including many genes in its metabolic pathways, has led to a dependence on host energy production and nutritional products. We hypothesized that host cellular powerhouse - the mitochondria - may affect host susceptibility to M.
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