Patogenesis de las Leishmaniasis / Pathogenesis of Leishmaniasis

RESUMO

At least 15 species of Leishmania produce human disease in different geographic areas of the world. The type o lesion or disease dependes upon many factors such as species and antigencity of the infecting parasite, size of the inoculum, and age and immune response of the host. Once the inoculation has taken place, the incoming from the parasite enters the host macrophages where it transforms in order to cause disease. The macrophage is the target cel of leishmaniasic infection. The equilibrium between destrution of the incoming from the parasite at the site of inoculation and survival of those that are able to transform inside the macrophages determines the development of not of the disease. The lymphokine-activated macrophage should be able to destroy all microorganisms. This process is slow in Leishmanioasis, but is finally acomplished in most cutaneous infections. On the other hand, in visceral leishmaniasis, mucous leishmaniasis and in difusse forms of cutaneous leishmaniasis this degree of inmunologic efficiency is not reached and do not cure spontaneosly. Some species of leishmania resist the digestive action of macrphages despite appropiate lymphokine stimulation. This finding explains the chronicity of the infection with aparently normal infammatory and hypersensitivity response. Hypersensitivity and immunity are not identical. They probably depend of different cell groups, and while immunity protects and is usefull, hypersensitivity is destructive and deletereous to the host.