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Instituto de Biofísica Carlos Chagas Filho, Centro de Ciências da Saúde, Universidade Federal do Rio de Janeiro-UFRJ, Rio de Janeiro, RJ, Brazil
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Trypanosoma cruzi, an important zoonotic protozoan that causes Chagas disease, is the focus of this book. There are two major reasons for the significant interest in the study of this protozoan and the disease it causes. First, Chagas disease is an important life-long infection in humans that can be divided into distinct clinical stages: the acute phase, where patient symptoms can vary from asymptomatic to severe; the indeterminate form, which is usually asymptomatic; and the chronic phase, where cardiomyopathy and/or digestive mega syndromes appear. In Latin America, at least 8 million people are infected with T. cruziand 13,000 die each year. In addition, migration patterns are driving the globalization of the disease and there are around 300,000 and 120,000 people infected in the USA and Europe, respectively. Second, T. cruziis an interesting biological model for studying processes such as: (a) cell differentiation, where a non-infective stage transforms into an infective one; (b) cell invasion, where the infective stages are able to penetrate into a mammalian host cell, where they multiply several times and thus amplify the infection; and (c) evasion from the immune system, using several mechanisms.
To better understand the information presented in various chapters of this book, let us review some basic information about T. cruziinfection . Figure 1 shows a general view of the life cycle of T. cruziin both vertebrate and invertebrate hosts . The three basic developmental stages (trypomastigote, amastigote, and epimastigote) are schematically shown in Figure 2a–c, based on images obtained using transmission electron microscopy . The various structures and organelles found in the protozoan are indicated. Figure 3 shows a scheme, where the various phases of the interaction of the trypomastigote form of T. cruziwith a host cell are indicated [1, 2]. The process starts with adhesion of the infective stage to the host cell surface followed by parasite internalization with formation of a parasitophorous vacuole (PV), lysis of the PV membrane, division of amastigotes in the cytoplasm of the host cell, and transformation of amastigotes into trypomastigotes that are then released into the intercellular space.
1.Barrias ES, de Carvalho TM, De Souza W.Trypanosoma cruzi: Entry into mammalian host cells and parasitophorous vacuole formation. Frontiers in Immunology. 2013;4:186. DOI: 10.3389/fimmu.2013.00186
2.Teixeira DE, Benchimol M, Crepaldi PH, De Souza W. Interactive multimedia to teach the life cycle ofTrypanosoma cruzi, the causative agent of Chagas disease. PLoS Neglected Tropical Diseases. 2012;8:e1749
Wanderley de Souza
Reviewed: July 12th, 2019Published: December 18th, 2019