Abstract
Chagas disease (ChD), also known as American trypanosomiasis, is caused by the trypanosomatid protozoan Trypanosoma cruzi (T. cruzi) that in its natural life-cycle is transmitted through triatomine vectors. Parasitological studies are useful to confirm acute cases, while the diagnosis of chronic T. cruzi infection relies on serological methods. There is no vaccine to prevent the infection, and the treatment is restricted to nifurtimox and benznidazole; and hence, new effective drugs with lower side-effects are urgently needed. The current review updates the facts and phenomena related to ChD, which is becoming an emerging health problem in non-endemic areas too, making the disease a grave global concern.
Highlights
American trypanosomiasis is caused by the protozoan hemoflagellate, Trypanosoma cruzi (T. cruzi), and is mostly transmitted to humans by triatomine bugs
T. cruzi is restricted to South America, Central America, and parts of North America (Mexico and southern United States), and according to estimates by the World Health Organization (WHO), 10 million people are chronically infected with the parasite, and > 10,000 deaths per year are caused by Chagas disease (ChD) [1]
The parasite has six Discrete Typing Units (DTUs), namely, T. cruzi I (TcI) and T. cruzi II (TcII), having DTUs IIa to IIe [3,4,5]; T. cruzi-I, predominating in the sylvatic transmission cycle, has been associated with human disease in Mexico and Central America, while T. cruzi-II prevails in the domestic transmission cycle in most of South America, including Argentina [3]
Summary
American trypanosomiasis is caused by the protozoan hemoflagellate, Trypanosoma cruzi (T. cruzi), and is mostly transmitted to humans by triatomine bugs. The parasite has six Discrete Typing Units (DTUs), namely, T. cruzi I (TcI) and T. cruzi II (TcII), having DTUs IIa to IIe [3,4,5]; T. cruzi-I, predominating in the sylvatic transmission cycle, has been associated with human disease in Mexico and Central America, while T. cruzi-II prevails in the domestic transmission cycle in most of South America, including Argentina [3]. Herrera et al reported the predominance of T. cruzi I in silvatic as well as domestic cycles of the disease in some countries of South America, Central America and in Mexico [11], while in Brazil, T. cruzi II (DTU IIb) and hybrids (DTU IId) induce the indeterminate and cardiac forms of ChD. The macrophages, which generally become attacked by the infective T. cruzi trypomastigotes, are recognized as one of the first cell types encountered by the parasite during natural infection, because of the fact of recognition of T. cruzi by macrophages through numerous Toll like receptors and lectin receptors; during initial replication, CD8+ T cell infiltration become delayed facilitating parasite survival [16]
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