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The kineto plastid protozoan parasite Trypanosoma cruzi is the causative agent of human Chagas’ disease, and it is endemic in regions of Latin America where it has become a major public health problem, constituting one of the largest parasitic disease burdens [1]. T. cruzi has a complex life cycle in which different developmental forms are present in both vertebrate and invertebrate hosts [2]. Three forms are well described: 1. amastigotes (dividing form found in the cytoplasm of the vertebrate host cell; 2. trypomastigotes (invasive form); and 3. epimastigotes (extracellular and replicating form found in the invertebrate host). In the vertebrate host, the replication of intracellular T. cruzi is responsible for the main pathologies associated with chronic Chagas’ disease [3]. The establishment of the parasite inside the host cells is key to the success of the infection and the progression of the disease. The drugs which are most frequently used for the treatment of Chagas’ disease are nitroheterocyclic compounds: Nitrofuran (Nifurtimox) and nitroimidazoles such as Benznidazole, discovered over three decades ago which induce drastic toxic effects in the vertebrate [1]. New therapeutic compounds are needed, mainly because the major limitation of anti-T. cruzi chemotherapeutics in the chronic phase of Chagas’ disease is their low efficiency
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