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As a consequence of Triatoma infestons eradication in Argentina, Chile, Uruguay and Brazil, these countries are considered free from Trypanosoma cruzi vectorial transmission, but the adaptation of wild triatomine species to human dwellings and recolonization by surviving insects after spraying deserve a continuing follow up. Considering an endemic area of Chagas disease in northeast Brazil, João Costa in Piauí, T. brasiliensis, T. pseudomaculata and, more rarely, T. sordida were collected in domestic and peridomestic habitats to evaluate the blood source and the infection rate by T. cruzi. The major hosts of all triatomines were birds, rodents, dogs and marsupials. The RAPD analysis of specimens of the predominant species, T. brasiliensis, showed a very homogeneous pattern of peridomestic and domestic populations that differed from that of T. brasiliensis collected in another county, 50 km away. Only T. brasiliensis colonized human dwellings, and 5.6% of the bugs were infected with T. cruzi that belonged to T. cruzi groups I and II, according to the biochemical and molecular characterizations. Our results emphasize the importance of maintaining vector surveillance and control programs.
Chagas disease, caused by the obligate unicellular parasite Trypanosoma cruzi, presents itself in a diverse collection of clinical manifestations, ranging from severe, fatal heart and digestive tract pathologies to unapparent or minor alterations that do not compromise survival. Over the years, a number of mechanisms have been proposed to explain the pathogenesis of chagasic tissue lesions, all of which have faced some criticism or been received with skepticism. This article excludes the autoimmunity hypothesis for Chagas disease because it has been extensively reviewed elsewhere, and summarizes the various alternative hypotheses that have been advanced over the years. For each of these hypotheses, an outline of its main tenets and key findings that support them is presented. This is followed by the results and comments that have challenged them and the caveats that stand on their way to wider acceptance. It is hoped that this writing will draw attention to our shortcomings in understanding the pathogenesis of Chagas disease, which, unfortunately, continues to figure among the most serious health problems of the American continent.
The Yucatan Peninsula of Mexico is endemic with Chagas disease. The main vector responsible for Trypanosoma cruzi transmission is Triatoma dimidiata which is abundant in domestic, peridomestic and sylvan cycles. The abundance of vectors favours T. cruzi transmission and is a high risk for developing chronic chagasic cardiomyopathy (CCC). In the past 10 years, little information was available on parasite seroprevalence and the prevalence of CCC in the Yucatan Peninsula. In the present work, we studied two Mayan communities with a high abundance of T. dimidiata and a random serial sample of 233 patients with an altered electrocardiogram or cardiac failure admitted to the Regional Hospital. A homemade enzyme-linked immunosorbent assay and indirect immunofluorescence standardized techniques were used to detect anti-T. cruzi IgG. In addition, Mayan volunteers were monitored by electrocardiography. In the Mayan communities, 4.8% (3/63) subjects were positive for T. cruzi antibodies none of them presented electrocardiographic alterations, however in seronegative subjects were detected right or left ventricle hypertrophy in 25% (16/63). A remarkable finding was that 90% of the Mayan population recognized the vector and 65% of them had experienced contact with triatomines bites. At the Regional Hospital 0.42% (1/233) were positive for T. cruzi antibodies showing compatible diagnosis with CCC; the most frequent pathology in this population was hypertension in 65% (151/233) and the less frequent was dilated myocardiopathy 6% (14/233). In conclusion, the prevalence of T. cruzi infection and CCC can be considered low in Yucatan, Mexico.
Eighteen strains of Trypanosoma cruzi isolated from two species of triatomines in the state of Paraná, Brazil, were characterized molecularly using three strategies: RAPD (randomly amplified polymorphic DNA) with four primers, analysis of the D7 polymorphic region of the 24Sα rDNA, and RFLP (restriction fragment length polymorphism) of region 5′ of the mitochondrial gene COII (cytochrome oxidase subunit 2). The phenogram constructed with the RAPD data showed that only three strains isolated from Panstrongylus megistus collected in the Municipality of Arapongas were grouped together in a sub-branch. None of the other 15 strains could be clustered according to triatomine species or geographical origin. The strains were grouped with the T. cruzi I reference sample, indicating closer association with the sylvatic transmission cycle of T. cruzi in the state of Paraná. However, analyses of the rDNA and COII gene polymorphisms revealed the presence of populations from both T. cruzi I and II major lineages. In half of the analyzed triatomines, we found parasites from both lineages coinfecting the same bugs. Of these, most (6/9) were isolated from Triatoma sordida, and 3/9 from Panstrongylus megistus. These results contribute to a better comprehension of the ecoepidemiology of Chagas’ disease in Paraná, and raise questions about the role of studies of polyclonal population dynamics for controlling the transmission of T. cruzi to humans in this region.
The objective of this study was to investigate if there is specific host-parasite association in Chilean populations of Trypanosoma cruzi. For this purpose, two groups of parasites were analyzed, one from chronic chagasic patients, and the other from Triatoma infestans triatomines in three regions of the country. The first group consisted of four types of samples: parasites from peripheral blood of non-cardiopathic T. cruzi infected patients (NB); parasites from their corresponding xenodiagnosis (NX); parasites from peripheral blood of T. cruzi infected cardiopathic patients (CB) and parasites from their xenodiagnostics (CX). The T. infestans sample in turn was from three regions: III, V and M (Metropolitan). The genetic differentiation by the Fisher exact method, the lineage distribution of the samples, the molecular phylogeny and the frequency of multiclonality were analysed. The results show that not only are the groups of T. cruzi clones from Chagas disease patients and vectors genetically differentiated, but also all the sub-groups (NB, NX, CB and CX) from the III, V and M regions. The analysis of lineage distribution was concordant with the above results, because significant differences among the percentages of TcI, TcIII and hybrids (TcV or TcVI) were observed. The phylogenetic reconstruction with these Chilean T. cruzi samples was coherent with the above results because the four chagasic samples clustered together in a node with high bootstrap support, whereas the three triatomine samples (III, V and M) were located apart from that node. The topology of the tree including published T. cruzi clones and isolates was concordant with the known topology, which confirmed that the results presented here are correct and are not biased by experimental error. Taken together the results presented here are concordant with a specific host-parasite association between some Chilean T. cruzi populations.
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The scope of this work is the presentation of new theories concerning the role of complement (C) in the resistance of high organism to the infection caused by protozoa. The mechanisms protecting of Entamoeba histolytica, Leishmania spp., Trypanosoma cruzi, Toxoplasma gondii and Naegleria fowleri from the action of C are also described.
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