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At present (2000) there is no convincing evidence that the HIV-positive state has any significant effect on the normal course of leprosy. The course of most infections in patients with lepromatous leprosy (including tuberculosis) does not differ from similar infections in patients who do not have leprosy. The exception is strongyloidiasis, which may become a serious complication. The reverse may not be true; leprosy may hasten the onset of AIDS in HIV-positive patients. Even though there is no well-established association of HIV and leprosy, and the evidence is not complete, it is entirely possible that the HIV epidemic may adversely affect the control of leprosy, as well as the way in which the disease behaves in individuals. Perhaps, in the future, this may be another section of the leprosy saga which has changed.

Leprosy has been transmitted in the laboratory to hamsters, mice, and the nine-banded armadillo, and more recently to rhesus, sooty mangabey, and African green monkeys. The progress of the disease in these animals is very similar to that of human leprosy. Chimpanzees in cages have become infected after contact, but the importance of leprosy in nonhuman primates is not yet established. Another indeterminate relationship is that between simian immunodeficiency and leprosy. It seems probable that rhesus monkeys that are SIV-positive have increased susceptibility to leprosy.

Somewhat similar mycobacterial infections occur in other animals, specifically in water buffalo, cattle, wood pigeons, certain frogs, freshwater snails, rats, and Mexican platyfish: none of these organisms affect man. Susceptibility to leprosy varies; Caucasians are apparently the most susceptible, then (in descending order) Asians, Indians, and Blacks. Leprosy does not give immunity to other diseases; in fact it may lower the host resistance. Despite the fact that leprosy bacilli are found in placentas and in the breast milk of lepromatous mothers, the disease is rare in infancy. It has, however, been known to occur in very young infants, even when the mother had no clinical history or evidence of leprosy. There is some geographic variation as to its occurrence in childhood: in Madras, India, 20% of patients are under the age of 10 years, while in the southern United States only 3% of patients are below this age. Generally, in endemic areas, children account for 20%-30% of all detected cases, but even if untreated, not all will develop active or persistent disease. Whether this is a genetic susceptibility or acquired immunity is controversial. Hospital statistics show that the disease is more common in men, but outpatient figures show that it occurs more commonly in females. In children the ratio is equal. There is an equally unsolved variation in the incidence of the two varieties, lepromatous and tuberculoid leprosy. In Asia, 50% of leprosy is the lepromatous form, whereas in Africa, it is less than 10%. There is some evidence that certain individuals, if they do get leprosy, will develop the lepromatous pattern and that this may be genetically determined.

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