The genus Leishmania comprises a wide range of species, some of which are pathogenic to humans and each of which has a different tissue preference, resulting in one of the three clinical forms of human leishmaniasis: visceral, cutaneous, or mucocutaneous. Although, all pathogenic species are deposited intradermally in the mammalian host upon an infectious sand fly bite, only the viscerotropic strains can leave the skin and reach the internal organs. We assume that Leishmania tissue tropism is not only the result of Leishmania genetic determinism but is also governed by the interaction of the parasite with different vectorial and human host elements. To shed light on these elements and key steps determining the course of the infection, we describe throughout this review the disease's progression from the early stages of infection taking place in the skin to the late stages succeeding in the parasite's visceral dissemination. Hence, we address the question of Leishmania tropism, through providing relevant hypotheses and answers gathered from the literature.
Keywords: Disease progression; Host-parasite interaction; Leishmania; Skin immunity; Tissue tropism; Visceralization.
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