Abstract
A brief review of the life cycle of T. cruzi and the clinical manifestations and epidemiology of Chagas disease will facilitate an understanding of the public health problem caused by this organism. T. cruzi is a protozoan hemoflagellate that has a complex life cycle involving several parasite stages in hematophagous reduviid bugs and mammalian hosts (1, 2) . Epimastigotes multiply in the midgut of the insect vector and transform to infective insect-derived metacyclic trypomastigotes in the hindgut. Transmission to humans occurs when metacyclic trypomastigotes in bug feces contaminate mucous membranes, conjunctivae or breaks in the skin and enter host macrophages and other cells. There, insect-derived metacyclic trypomastigotes transform into amastigotes, the proliferating form in the mammalian host. After several cycles of intracellular multiplication, amastigotes differentiate into bloodform trypomastigotes, which are then released as the host cell ruptures. Bloodform trypomastigotes penetrate adjacent cells and also spread hematogenously to distant tissues, especially cardiac muscle. After the acute phase of the infection is controlled by immune mechanisms, the parasite persists in low numbers for the life of the host, alternating asynchronously between intracellular amastigotes and circulating bloodform trypomastigotes.
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Kirchhoff, L.V. (1992). Perspectives on Chagas Disease in Latin America and the United States. In: Walker, D.H. (eds) Global Infectious Diseases. Springer, Vienna. https://doi.org/10.1007/978-3-7091-3449-8_13
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DOI: https://doi.org/10.1007/978-3-7091-3449-8_13
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