. "Appendix D-7: The Prospects for Immunizing Against Mycobacterium leprae." New Vaccine Development: Establishing Priorities: Volume II, Diseases of Importance in Developing Countries. Washington, DC: The National Academies Press, 1986.
The following HTML text is provided to enhance online
readability. Many aspects of typography translate only awkwardly to HTML.
Please use the page image
as the authoritative form to ensure accuracy.
New Vaccine Development: Establishing Priorities, Volume II, Diseases of Importance in Developing Countries
the organism in the nine-banded armadillo and on studies of localized infection in mice. A new report on laboratory-induced leprosy in monkeys suggests that mangabey monkeys may provide an important nonhuman primate model in which to study the transmission and pathogenesis of the disease (Wolf et al., 1985).
The waxy coat and cell wall structure of M. leprae are similar to those of other acid-fast bacilli, including M. tuberculosis, but DNA hybridization studies indicate that M. leprae has a rather distant taxonomic relationship to other known mycobacteria. M. leprae is thought to grow very slowly in vivo, with a doubling time of between 7 and 14 days (Shepard and McRae, 1965).
HOST IMMUNE RESPONSE
Antibodies against M. leprae are found in patients with all stages of the disease and may be most prevalent in those with lepromatous leprosy. There is a remarkable inverse correlation between the histopathological classification of disease severity in leprosy and the level of cell-mediated immune responses. Patients at the tuberculoid end of the spectrum have cell-mediated immunity and few bacilli; patients at the lepromatous end exhibit no cell-mediated immunity to M. leprae and high bacillary loads (Bloom and Godal, 1983).
DISTRIBUTION OF DISEASE
Leprosy is found in virtually all tropical and subtropical countries. A third of all cases occur in Southeast Asia, and the remainder occurs primarily in Africa and South America. At one time, the disease existed in epidemic form in Norway and in other parts of Europe and the Mediterranean, but for reasons not entirely clear it has been largely eliminated from Europe (Irgens, 1980; Sansarricq, 1981, 1982).
Disease Burden Estimates
Considerable disagreement and uncertainty exist regarding the epidemiology of leprosy infection, transmission, and pathogenesis (Fine, 1982). The estimates given below relate to clinically symptomatic cases of disease, that is, where permanently impaired neurological function or tissue damage is apparent.
The Special Programme for Research and Training in Tropical Diseases (SPRTTD, 1985) conservatively estimates the global prevalence of leprosy to be 10.6 million cases, the vast majority of which are in developing countries. Information on incidence is scant, but several studies suggest that the annual incidence roughly approximates one-tenth of existing prevalence (Noordeen, personal communication, 1984). On