Leprosy is one of the oldest diseases and is well acknowledged in the literature of oldest civilization of China, Egypt and India. It is a contagious and disfiguring disease. The etiologic agent of leprosy, Mycobacterium leprae is an intracellular pathogen and was first discovered in 1873 by a Norwegian scientist Dr. Gerhard Armauer Hansen. Generally leprosy affects the peripheral nerves but it also affects the skin and certain other tissues viz., eyes, mucosa of upper respiratory tract, muscle, bone and testes.
The transmission pattern of the disease is still unclear. Some reports provided the information that leprosy is transmission through aerosol route in close contacts. Even the widely advocated methods of spread including person to person contact or contact with respiratory secretions from infected individuals have not been conclusively established so far. The population structure of M. leprae has not been studied yet conclusively. An understanding of transmission dynamics of M. leprae would advance in strategies aimed at breaking the transmission chain of leprosy.
Simple sequence repeats (SSRs) often serve to modify genes with which they are associated. The influence of SSRs on gene regulation, transcription and protein function typically depends on the number of repeats, while mutations that add or subtract repeat units are both frequent and reversible. SSRs thus provide a prolific source of quantitative and qualitative variation. Over the past decade, researchers have found that this spontaneous variation has been tapped by natural and artificial selection to adjust almost every aspect of gene function. These studies support the hypothesis that SSRs, by virtue of their special mutational and functional qualities, have a major role in generating the genetic variation underlying adaptive evolution.