Infection with different Trypanosoma cruzi populations in rats: myocarditis, cardiac sympathetic denervation, and involvement of digestive organs.
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We tested four isolates of Trypanosoma cruzi to assess parasite virulence and ability to cause myocarditis, cardiac sympathetic denervation, and histopathologic alterations in organs of the digestive system. The susceptibility of rats depends on the population of T. cruzi, with the ABC strain and the CL-Brener clone killing all animals, regardless of the parasitemic pattern. All tested T. cruzi populations caused acute myocarditis, but failed to induce histologic alterations in the intestine. The Cl-Brener and ABC isolates caused esophageal myositis. The myocarditis caused by the ABC, CL-Brener, and Y isolates was severe, but resolution started at the end of the acute phase. In contrast, the Col 1.7 G2 clone induced mild and sustained myocarditis. Our results also showed that T. cruzi populations able to induce severe acute myocarditis caused marked sympathetic denervation, but recovery of normal cardiac histology and innervation occurred. The sustained myocarditis induced by Col 1.7 G2 clone failed to cause sustained denervation. (+info)
Interstitial dendritic cells of the heart harbor Trypanosoma cruzi antigens in experimentally infected dogs: importance for the pathogenesis of chagasic myocarditis.
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Heart sections from 16 mongrel dogs, two normal controls and 14 infected with Trypanosoma cruzi, were submitted to immunohistochemical staining with either rabbit anti-cow S100 Protein monoclonal antibody or rabbit anti-T. cruzi purified specific antibody, using the peroxidase technique to investigate the participation of the interstitial dendritic cells of the heart (IDCs) in myocarditis of Chagas disease. Trypanosoma cruzi antigens were revealed as granular and dense deposits in IDC membrane in the heart of infected dogs both during acute and chronic myocarditis, but not in normal controls. Anti-S100 Protein labeled the IDCs, both in normal and infected dogs and a significant increase in the numbers of IDCs occurred in the myocardium, proportionally to the intensity of the inflammatory infiltration. These findings suggest that IDCs, probably by presenting T. cruzi antigens to immune-competent cells, play an important role in the pathogenesis of Chagas disease. (+info)
Histoplasmosis as a late infectious complication following heart transplantation in a patient with Chagas' disease.
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Infectious complications following heart transplantation are an important cause of morbidity and mortality. Generally, bacterial infections are predominant; however, fungal infections can be responsible for up to 25% of infectious events. We report the case of a patient who presented with histoplasmosis as an infectious complication five years after heart transplantation due to a chagasic cardiopathy. This association has rarely been reported in the international literature. (+info)
Progressive chronic Chagas heart disease ten years after treatment with anti-Trypanosoma cruzi nitroderivatives.
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A randomized ten-year follow-up study involving 91 Chagas patients and 41 uninfected controls was undertaken to determine the effectiveness of nitroderivative therapy. Anti-Trypanosoma cruzi antibodies were consistently lower one year after treatment than 10 years thereafter (P < 0.001). The blood of all treated and 93.7% of untreated Chagas patients yielded polymerase chain reaction (PCR) product from probes annealing to T. cruzi nuclear DNA, indicating active infection. Competitive PCR showed means +/- standard deviations of 20.1+/-22.6 T. cruzi/ml of blood from untreated and 13.8+/-14.9 from treated Chagas patients, but the differences between means were not statistically significant (P > 0.05). Electrocardiograms recorded a gamut of alterations several-fold more frequent in Chagas patients, regardless of treatment, than in uninfected controls (P < 0.001). These results show that nitroderivative therapy for T. cruzi infections is unsatisfactory and cannot be recommended since it fails to eradicate the parasite or change the progression of heart disease in chronic Chagas patients. (+info)
Anti-galectin-1 autoantibodies in human Trypanosoma cruzi infection: differential expression of this beta-galactoside-binding protein in cardiac Chagas' disease.
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The pathogenesis of Chagas' disease has been subject of active research and still remains to be ascertained. Galectin-1 (Gal-1), a member of a conserved family of animal beta-galactoside-binding proteins, localized in human heart tissue, has been suggested to play key roles in immunological and inflammatory processes. In the present study we demonstrated the occurrence of anti-Gal-1 autoAb in sera from patients in the acute and chronic stages of Chagas' disease (ACD and CCD) by means of ELISA and Western blot analysis. We found a marked increase in the level and frequency of Ig E anti-Gal-1 antibodies in sera from patients with ACD, but a low frequency of Ig M anti-Gal-1 immunoreactivity. Moreover, Ig G immunoreactivity to this beta-galactoside-binding protein was found to be correlated with the severity of cardiac damage in CCD, but was absent in nonrelated cardiomyopathies. We could not detect immunoreactivity with Trypanosoma cruzi antigens using a polyclonal antibody raised to human Gal-1 and no hemagglutinating activity could be specifically eluted from a lactosyl-agarose matrix from parasite lysates. Moreover, despite sequence homology between Gal-1 and shed acute phase antigen (SAPA) of T. cruzi, anti-Gal-1 antibodies eluted from human sera failed to cross-react with SAPA. In an attempt to explore whether Gal-1 immunoreactivity was originated from endogenous human Gal-1, we finally investigated its expression levels in cardiac tissue (the main target of Chagas' disease). This protein was found to be markedly upregulated in cardiac tissue from patients with severe CCD, compared to cardiac tissue from normal individuals. (+info)
Predictors of unfavourable prognosis in chronic Chagas' disease.
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The aim of this study was to detect clinical predictors of left ventricular dysfunction, left ventricular dilatation and apical aneurysm on echocardiography, all known as independent predictors of lethal outcome for patients with chronic Chagas' disease. Seventy-four patients with a positive complement-fixation test for Chagas' disease participated; 44 (59%) had left ventricular dysfunction, 41 (55%) left ventricular dilatation and 15 (20%) apical aneurysm. A stepwise logistic regression analysis showed that systolic blood pressure (P < 0.001) and male sex (P < 0.001) were independent predictors of left ventricular dilatation on echocardiography. A receiver-operating characteristic curve provided a systolic blood pressure of 120 mmHg with a sensitivity of 70% and a specificity of 63% to predict left ventricular dilatation. The combination of male sex and systolic blood pressure of 120 mmHg had a sensitivity of 56% and a specificity of 91% to predict left ventricular dilatation. In a separate stepwise logistic regression analysis, left ventricular systolic dysfunction was independently predicted by systolic blood pressure (P = 0.006) and New York Heart Association functional class (P = 0.01). Receiver-operating curves provided a blood pressure of 120 mmHg with a sensitivity of 72% and a specificity of 59% to predict left ventricular dysfunction, whereas a New York Heart Association functional score of 2 predicted left ventricular systolic dysfunction with a sensitivity of 78% and a specificity of 50%. The combination of New York Heart Association functional class and a systolic blood pressure of 120 mmHg predicted left ventricular dysfunction with a sensitivity of 59% and a specificity of 77%. The apical aneurysm was independently predicted by myocardial necrosis on the resting ECG, but only with a sensitivity of 20%. Hence, echocardiographic markers of cardiac mortality and sudden cardiac death in Chagas' disease can be independently predicted by clinical examination. This may be useful for screening high-risk chagasic patients. (+info)
Four cases of acute chagasic myocarditis in French Guiana.
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The authors report four cases of acute chagasic myocarditis which had been diagnosed and treated in Cayenne, French Guiana, in the past 6 years. This French territory, which has the highest standard of living in South America, should be considered an area of risk for sporadic Chagas disease with epidemiologic features similar to those of the disease found in dense Amazon forest areas. Appropriate measures must be taken to screen and promptly manage Chagas disease in the French Guiana population. (+info)
Modulation of chagasic cardiomyopathy by interleukin-4: dissociation between inflammation and tissue parasitism.
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Chronic chagasic cardiomyopathy (CChC) is characterized by an inflammatory reaction which may eventually lead to heart enlargement, arrythmia, and death. As described herein, interleukin-4-deficient mice mount increased specific T helper (Th) 1 immune responses when infected with Trypanosoma cruzi, as compared to wild-type mice. Interestingly, these mice had reduced parasitism and mortality and exacerbated inflammation in their hearts, demonstrating a clear dissociation between inflammation and parasite load. The modulation of these phenomena so as to maximize host and parasite survivals may depend on a fine balance between Th responses, in which a Th1 response will, on one hand, control parasitism and, on the other hand, enhance heart inflammation throughout the course of the infection. (+info)