Copyright (c) 2024 Revista médico científica
This work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License.
Leishmaniasis is a disease caused by parasites of the Kinetoplastid order, Trypanosomatidae family and Leishmania genus. Approximately 12 million people are infected with Leishmania and around 350 million live at risk zones. The parasite can exist in two morphological stages: the amastigote and the promastigote. The amastigotes live in intracellular vacuoles mainly in monocytes and macrophages. The Leishmania vectors belong to the Phlebotomus genus (Old World) and to the Lutzomyia genus (New World). When the vectors bite human beings, they inject the metacyclic promastigotes (infective form for humans). The main parasite surface molecules are lipophosphoglycan, glycoprotein 63 and glycosylinositol phospholipid. There are two main clinical forms of Leishmaniasis: cutaneous (localized, diffuse and mucocutaneous) and visceral. Multiple components of the innate and adaptative immune responses participate in the host’s defense against Leishmania. The interaction between the parasite and the immune system is very complex and determines the clinical expression of the disease. Mucocutaneous leishmaniasis (hyperergic pole) and diffuse cutaneous leishmaniasis (anergic pole) are the polar manifestations of a spectrum of clinical manifestations that depend on the immune response against the parasite. Localized cutaneous leishmaniasis is in the center of the spectrum. Leishmania has developed numerous strategies to evade the immune response including the inhibition of macrophage function and the alteration of the intracellular signaling pathways.
