Parasite immunity: Leishmania and Schistosoma

Published on September 29, 2022   30 min

Other Talks in the Series: The Immune System - Key Concepts and Questions

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Hello again. My name is Catarina Gadelha. I'm a reader in molecular cell biology at the University of Nottingham. My research topic is host-parasite interactions, with a particular focus on the cell surface receptors and ligands that enable these interactions. In this part of the lecture, we will look at leishmaniasis and schistosomiasis.
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Leishmaniasis is caused by several species of the genus Leishmania, all transmitted between mammalian hosts by female sandflies. Following a period of incubation, different species cause different clinical manifestations ranging in severity from self-curing cutaneous lesions to life-threatening visceral disease. The outcome, as usual, is determined by parasite and host genetics.
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Cutaneous leishmaniasis, caused by Leishmania major or L. tropica is usually limited to an ulcer that self heals over several months, but can also lead to scarring and disfigurement. Mucocutaneous leishmaniasis is caused by species of the Viannia group: Leishmania braziliensis or L. guyanensis. It is characterized by destructive lesions of the nasal septum, lips, and palate, and it's caused by a strong immunopathological response. Visceral leishmaniasis, caused by Leishmania donovani in Asia and Africa, or Leishmania infantum in the Mediterranean, the Middle East, Central Asia, and Latin America is the most severe form of the disease. Usually fatal unless treated. Post-kala-azar dermal leishmaniasis is a skin manifestation that occurs in otherwise healthy people after treatment of visceral leishmaniasis. Table one in this publication of the journal Lancet,
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Parasite immunity: Leishmania and Schistosoma

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