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A partir de quatro fontes do século XVI, são relatadas algumas ocorrências sugestivas de leishmaniose tegumentar americana (LTA) no território andino. A reinterpretação dessas fontes permite enfocar o velho tema da origem da espundia ou leishmaniose de forma mucosa (LM). O artigo reforça a hipótese de que a LM tenha se originado na área amazônica ocidental em tempos arqueológicos por intermédio de migrações humanas, depois ascendido à selva alta e, posteriormente, às terras quentes interandinas, pelos limites da Bolívia e do Peru com o Brasil. As migrações dos mitmaq ou mitimaes contribuíram para sua intensificação durante o império inca. Tais fatos se desenvolvem no contexto histórico e social da queda do império inca e da instalação da colônia espanhola.

Background. Tegumentary leishmaniasis and leprosy display similar spectra of disease phenotypes, which are dependent on cell-mediated immunity to specific antigens. Diffuse cutaneous leishmaniasis and lepromatous leprosy represent the anergic end of the spectrum, whereas mucocutaneous leishmaniasis and tuberculoid leprosy are associated with marked antigen-specific cellular immune response. Methods. We characterized and compared the cell-mediated response to Leish mania and Mycobacterium leprae antigens in a patient with an intriguing association of mucocutaneous leishmaniasis with lepromatous leprosy, which are at opposite ends of the immunopathological spectra of these diseases. This was done by performance of skin tests and by assessment of the cell proliferation and cytokine production of peripheral blood mononuclear cells (PBMCs). Results. Strong skin-test reactions and PBMC proliferation were observed in response to Leish mania antigens but not to M. leprae antigens. The stimulation of PBMCs with Leish mania and M. leprae antigens induced comparable levels of tumor necrosis factor-α, interleukin-5, and interleukin-10. However, the interferon-γ response to Leishmanici antigens was remarkably high, and that to M. leprae antigens was almost nil. Conclusions. We found that concomitant leprosy and tegumentary leishmaniasis can produce opposite polar forms associated, respectively, with absent or exaggerated cell-mediated immune responses to each pathogen. This suggests that independent mechanisms influence the clinical outcome of each infection. Moreover, interferon-γ appears to play a major role in the clinical expression of these intracellular infections. [ABSTRACT FROM AUTHOR]

Background: Tegumentary leishmaniasis and leprosy display similar spectra of disease phenotypes, which are dependent on cell-mediated immunity to specific antigens. Diffuse cutaneous leishmaniasis and lepromatous leprosy represent the anergic end of the spectrum, whereas mucocutaneous leishmaniasis and tuberculoid leprosy are associated with marked antigen-specific cellular immune response., Methods: We characterized and compared the cell-mediated response to Leishmania and Mycobacterium leprae antigens in a patient with an intriguing association of mucocutaneous leishmaniasis with lepromatous leprosy, which are at opposite ends of the immunopathological spectra of these diseases. This was done by performance of skin tests and by assessment of the cell proliferation and cytokine production of peripheral blood mononuclear cells (PBMCs)., Results: Strong skin-test reactions and PBMC proliferation were observed in response to Leishmania antigens but not to M. leprae antigens. The stimulation of PBMCs with Leishmania and M. leprae antigens induced comparable levels of tumor necrosis factor- alpha , interleukin-5, and interleukin-10. However, the interferon- gamma response to Leishmania antigens was remarkably high, and that to M. leprae antigens was almost nil., Conclusions: We found that concomitant leprosy and tegumentary leishmaniasis can produce opposite polar forms associated, respectively, with absent or exaggerated cell-mediated immune responses to each pathogen. This suggests that independent mechanisms influence the clinical outcome of each infection. Moreover, interferon- gamma appears to play a major role in the clinical expression of these intracellular infections.

Drawing from four sixteenth-century sources, the article reports some apparent incidents of American Tegumentary Leishmaniasis within the territory of the Andes. Reinterpretation of these sources affords a look at the longstanding issue of the origin of espundia,or mucosal Leishmaniasis (ML). The study reinforces the hypothesis that ML originated in the western Amazon region, from there climbing into the high forests and later into hot inter-Andean lands via Bolivia's and Peru's borders with Brazil, above al through human migration. dating to archeological times, this process intensified during the Inca period under the social policies of the mitmaq or mitimaes. These events transpired within the historical and social context of the fall of the Inca Empire and the advent of Spanish colonization.