at mycobacterium leprae was responsible for leprosy, it was necessary to isolate the organism, grow it outside of the host, and inoculate and infect another, healthy creature (Brody, 1974, p. 22). This was not done, but Hansen's theory was widely accepted despite this. Although it is difficult to trace the path of infectivity because of the disease's long latency period, leprosy was labeled "decidedly contagious" (Brody, 1974, p. 23). Of course, the natural susceptibility of the host, the response of the cellular immune system, plays an important role in the risk of infection, but it was believed that the risk of infections was "in direct proportion to the intimacy of contact between infected and healthy persons" (Brody, 1974, p. 24).
The incubation period for leprosy is anywhere between three and eight years. The first signs of the disease are usually neurological: areas of numbness, enlarged nerves, altered skin texture, anesthetization, and slight paralysis (Brody, 1974, p. 25). Although the bacterium affects the nervous system, it does not "live" in the nerve cells. The bacterium produces a reaction that causes the demyelination of the nerves. The first stage of the disease is called indeterminate. The disease then progresses in one of two directions, toward the tuberculoid or the lepromatous kind ("Leprosy in the Indian", 1987, January-February, p. 5). The tuberculoid form is usually benign, and the prognosis is good as a result of an effective tissue response against the bacilli. Lepromatous leprosy is malignant because the tissue defense cannot overcome the bacilli (Brody, 1974, p.26).
The skin lesions associated with leprosy are of two types, macular and infiltrated (Brody, 1974, p. 27). Macular lesions are described as "circumscribed, nonelevated alterations in the color of the skin of any size or shape" (Brody, 1974, p. 27). Lepromatous macules appear in the early stages, are scattered symmetrically, are s...