zoonoses and communicable diseases common to ... - PAHO/WHO

LEPROSY 151lated bacillus produced neither disease nor lesions. The only differences with M.leprae of human origin were negative results to the dopa oxidation and pyridinetests. However, the dopa oxidation test sometimes fails in animals (armadillos) inoculatedexperimentally with human M. leprae (Donham and Leininger, 1977).Results obtained by inoculating mouse foot pads were similar to those derived withM. leprae of human origin, i.e., reproduction of the bacterium in six months up to aquantity similar to that of M. leprae without dissemination from the inoculationpoint (Leininger et al., 1978).Another case of naturally acquired leprosy was discovered in a primate,Cercocebus atys or sooty mangabey monkey (identified in one publication asCercocebus torquatus atys), captured in West Africa and imported to the UnitedStates in 1975 (Meyers et al., 1980, 1981). The clinical picture and histopathologywere similar to man’s and the etiologic agent was identified as M. leprae based onthe following criteria: invasion of the host’s nerves, staining properties, electronmicroscopy findings, inability to grow in mycobacteriologic media, positive dopaoxidation reaction, reactivity to lepromin, patterns of infection in mice and armadillos,sensitivity to sulfones, and DNA homology (Meyers et al.,1985). Simultaneousintravenous and intracutaneous inoculation succeeded in reproducing the infectionand disease in other Cercocebus monkeys. The early appearance of signs (5 to 14months), varying clinical disease forms, neuropathic deformities, bacillemia, anddissemination to various cool parts of the body make the mangabey monkey potentiallythe most complete model for the study of leprosy. It is the third animal speciesreported to be able to acquire leprosy by natural infection (Walsh et al., 1981;Meyers et al., 1983, 1985).The Disease in Man: The incubation period is usually 3 to 5 years, but it can varyfrom 6 months to 10 years or more (Bullock, 1982). Clinical forms of leprosy covera wide spectrum, ranking from mild self-healing lesions to a progressive and destructivechronic disease. Tuberculoid leprosy is found at one end of the spectrum and lepromatousleprosy at the other. Between them are found the intermediate forms.Tuberculoid leprosy is characterized by often asymptomatic localized lesions ofthe skin and nerves. Basically, the lesion consists of a granulomatous, paucibacillary,inflammatory process. The bacilli are difficult to detect, and can be observedmost frequently in the nerve endings of the skin. This form results from activedestruction of the bacilli by the undeteriorated cellular immunity of the patient. Onthe other hand, the humoral response generally involves low titers. Nerve destructioncauses lowered conduction; heat sensibility is the most affected, tactile sensibilityless so. Trophic and autonomic changes are common, especially ulcers on thesole and mutilation of limbs (Toro-González et al., 1983).Lepromatous leprosy is characterized by numerous symmetrical skin lesions consistingof macules and diffuse infiltrations, plaques, and nodules of varying sizes(lepromas). There is involvement of the mucosa of the upper respiratory tract, oflymph nodes, liver, spleen, and testicles. Infiltrates are basically histiocytes with afew lymphocytes. Cellular immunity is absent (negative reaction to lepromin) andantibody titers are high. In this form of the disease, as in the dimorphous, erythemanodosum leprosum (ENL) often appears.The indeterminate form of leprosy has still not been adequately defined from theclinical standpoint; it is considered to be the initial state of the disease. The first