Abstract. The extent of inflammation, fibrosis, and progression of chronic Chagas heart disease (cChHD) was associated with persistence of parasite DNA in cardiac lesions of necropsies or explants from Argentinean cChHD patients. A Trypanosoma cruzi−based polymerase chain reaction showed a positive result in 1) 15% of cardiac sections with less than 10 mononuclear inflammatory cells/high-power field (440×) (MNC/HPF), 89% with 10-19 MNC/HPF, and 100% with more than 20 MNC/HPF (P < 0.0001); 2) 33% with less than 10% fibrosis, 79% with 10-19% fibrosis, and 100% with more than 20% fibrosis (P < 0.01); 3) 25% of specimens from patients classified in Kuschnir groups 0 and I, 70% in group II and 90% in group III (P < .001); and 4) 45% and 90% of the specimens from cChHD patients without or with heart failure, respectively (P < 0.01). These findings stress the role of the parasite in pathogenesis and disease progression of cChHD.

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Abstract. The aim of this work was to investigate the potential usefulness of Trypanosoma cruzi lysate, recombinant protein JL7, and peptides P013, R13, JL18, JL19, and P0β as serological markers for human Chagas disease. We analyzed 228 sera from Brazilian Chagas disease patients classified into four clinical groups and 108 from non-chagasic patients. We defined the diagnostic sensitivity, specificity, and Kappa index measured by enzyme-linked immunosorbent assay (ELISA). As previously described, the highest values of diagnostic parameters were achieved for T. cruzi lysate and JL7; peptide P013 showed high specificity but low sensitivity. The other peptides resulted in lower sensitivity and specificity in our ELISA than T. cruzi lysate and JL7 protein. Antibodies against JL7 protein were mainly detected in sera from patients with severe chagasic cardiomyopathy, compared with those from the indeterminate form, whereas peptides failed to discriminate between the clinical forms of the disease.Chagas disease, caused by the hemoflagellate Trypanosoma cruzi, is a widespread tropical disease affecting at least 8 million people primarily in Latin American countries.1 The acute phase lasts 1 or 2 months and is usually symptomless, 2 however most of the infected individuals enter a life-long chronic phase with its asymptomatic and symptomatic forms. The asymptomatic, also called indeterminate form is characterized by the absence of clinical symptoms. However,~40% of persons with chronic T. cruzi infection develop symptoms of visceral damage, which may include cardiac lesions, digestive alterations, or both clinical manifestations (cardiac plus digestive). 2In the chronic phase, the primary method for diagnosis is the search of antibodies by serological testing, whereas the secondary diagnostic techniques are parasitological tests.1 So far, conventional serological tests include complement fixation, 3,4 indirect immunofluorescence assay (IFA), 5 indirect hemagglutination assay (IHA), 6 direct agglutination with 2-mercaptoethanol (DA-2ME), 7 and enzyme-linked immunosorbent assay (ELISA). [8][9][10] These tests usually use crude or semi-purified parasite preparations, often derived from a stage present only in the insect and in cultures at 26 C (epimastigote) but absent in the human host. Other assays incorporate more defined parasite components, like multiple fusion proteins containing epitopes from various T. cruzi antigens.11-15 Moreover, a rapid immunochromatographic assay (Chagas Stat-Pak, Chembio Diagnostic Systems, Medford, NY) has also been developed by employing a mixture of T. cruzi recombinant antigens, presenting a different degree of performance. [16][17][18] However, in the absence of a true gold standard, it is still necessary to carry out at least two different serological tests to establish a reliable diagnosis of Chagas disease. Indeed, the World Health Organization (WHO) consensus guidelines recommend to perform a third assay or repeat sampling to confirm or exclude the diagnosis if two serological tests ...

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Strategies to construct the physical map of the

Infection with Trypanosoma cruzi develops in three phases: acute, indeterminate or asymptomatic, and chronic phase (with cardiac or digestive manifestations). Moreover, transmission may occur from infected mothers to newborn, the so-called congenital form. In the present study, humoral responses against T. cruzi total extract and against the 13 amino acid peptide named R-13 derived from the parasite ribosomal P protein, previously described as a possible marker of chronic Chagas heart disease, were determined in chagasic patients and in blood bank donors from endemic areas. While in sera from acute phase, only IgM anti-T.cruzi response was observed, both IgM and IgG anti-T. cruzi antibodies were detected in sera from congenitally infected newborns. The percentage of positive response in sera from blood bank donors was relatively high in endemic regions. Antibodies against the R-13 peptide were present in a large proportion of cardiac chagasic patients but were totally lacking in patients with digestive form of Chagas' disease. Furthermore, anti-R-13 positive responses were detected in congenitally infected newborns.

The infusion of certain amino acids, such as serine, alanine, and proline (SAP), has been shown to increase the glomerular filtration rate, whereas branched chain amino acids (BCAA) leucine, isoleucine, and valine fail to modify the glomerular filtration rate. It has been suggested that this effect of amino acids on the glomerular filtration rate is mediated by the action of the hormone glomerulopressin. The purpose of this work was to study the action of SAP and BCAA on glomerulopressin production. Livers isolated from rats were perfused with (i) Krebs-Ringer-Bicarbonate, (ii) SAP, or (iii) BCAA. Results indicate that glomerulopressin production is stimulated by SAP, but inhibited by BCAA.