Clinical aspects of the Chagas' heart disease

University of Maryland, Baltimore, Baltimore, Maryland, United States
International journal of cardiology (Impact Factor: 4.04). 03/2007; 115(3):279-83. DOI: 10.1016/j.ijcard.2006.03.004
Source: PubMed


Chagas' heart disease, caused by protozoan Trypanosoma cruzi, is a common cause of cardiomyopathy in the Americas. Transmission of T. cruzi occurs through Reduviids, the kissing bugs. Less common ways of transmission are blood transfusion, congenital transmission, organ transplantation, laboratory accident, breastfeeding, and oral contamination. Infestation results in cardiac dysautonomia, myocardial apoptosis, and myocardial fibrosis. In acute phase, death is mostly caused by myocarditis and in chronic phase, it is mostly by irreversible cardiomyopathy. A majority of the patients with Chagas' disease remain in the latent phase of disease for 10 to 30 years or even for life. Specific anti-Chagas' therapy with trypanocide drugs is useful in acute phase but the management of chronic Chagas' heart disease is mostly empirical. The mortality during the acute phase of cardiac Chagas is around 5%. Five-year mortality of chronic Chagas' disease with cardiac dysfunction is above 50%. The clinical aspects of the Chagas' heart disease are concisely reviewed.

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    • "to et al . , 2008 ) . Although acute T . cruzi infection is frequently asymptomatic , severe cases of acute myocarditis and meningoencephalitis can occur in 5% of cases with a 2 – 10% mortality rate ( Medeiros et al . , 2008 ) . Myocardi - tis can be detected in more than 80% of patients presenting with severe symptoms of acute Chagas dis - ease ( Punukollu et al . , 2007 ) . A direct progression from the acute phase to a clinical chronic form of the disease may occur in 5% of cases . Many cases of congenital infection are asymptomatic , although the reported percentage of symptomatic infec - tion in Bolivian newborns was 50% , with a mortality rate of 2 – 13% if left untreated . Clinical manifestations "
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    ABSTRACT: American trypanosomiasis is a parasitic disease caused by the flagellate protozoan Trypanosoma cruzi. Chagas disease is endemic in Latin America, where an estimated 10-14 million people are infected, and an emerging disease in Europe and the USA. Trypanosoma cruzi is transmitted by blood-sucking bugs of the family Reduviidae. Rhodnius prolixus, Panstrongylus megistus, Triatoma infestans, and T. dimidiata are the main vectors in the sylvatic cycle. Non vector-borne transmission includes blood transfusion, congenital and oral transmission, transplantation, and accidental infections. Most cases of acute infection occur in childhood and are usually asymptomatic, although severe myocarditis and meningoencephalitis may occur. Approximately 30% of T. cruzi-infected people will develop the chronic stage of the disease. Chronic chagasic cardiomyopathy is characterized by progressive heart failure, arrhythmias, intraventricular conduction defects, sudden death, and peripheral thromboembolism. Acute exacerbation can occur in individuals with involvement of cellular immunity such as advanced AIDS (acquired immunodeficiency syndrome), and transplant-associated immunosuppression. Neurological involvement may present with encephalitis, meningoencephalitis, or a space-occupying cerebral lesion called chagoma. Chagas disease is a major cause of ischemic stroke in Latin America. Several epidemiological studies have found an association between T. cruzi infection and cardioembolic ischemic stroke. Benznidazole and nifurtimox are the two available trypanocide drugs against T. cruzi.
    Handbook of Clinical Neurology 07/2013; 114:103-23. DOI:10.1016/B978-0-444-53490-3.00007-8
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    • "Microvascular changes are also observed that gradually disrupt cell myocardial contractile response (myocytolysis ) (James et al., 2005; Bern et al., 2007). In patients with severe heart damage, ventricular aneurysm can be produced, a pathognomonic characteristic of cardiac Chagas disease (Punukollu et al., 2007); approximately one-third of these chagasic patients die suddenly , and a greater percentage will succumb due to heart failure. A direct progression from the acute phase to a chronic clinical form of Chagas disease has been recorded in few patients (Prata, 2001). "
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    ABSTRACT: Chagas disease is a parasitic infection caused by the protozoan Trypanosoma cruzi, a flagellated organism that is transmitted mainly to humans through the infected feces of triatomine kissing bugs (vector transmission in endemic areas) or by transfusion of infected blood, donations of infected organ, or transmission from an infected mother to her child at birth. Chagas disease was first described in 1909 by the Brazilian physician Carlos Chagas, and due to the parasite's distribution throughout North, Central and South America, the disease is commonly known as American trypanosomiasis. However, this disease is now present in non-endemic countries such as Canada, the United States of America, and several countries in Europe (principally Spain). Moreover, Chagas disease was recently designated by the World Health Organization as one of the main neglected tropical diseases. The aim of this review is to summarize the research efforts recently described in studies conducted in Mexico on Chagas disease. In this country, there are no existing vector control programs. In addition, there is no consensus on the diagnostic methods for acute and chronic Chagas disease in maternity wards and blood banks, and trypanocidal therapy is not administered to chronic patients. The actual prevalence of the disease is unknown because no official reporting of cases is performed. Therefore, the number of people infected by different routes of transmission (vector, congenital, blood transfusion, organ transplantation, or oral) is unknown. We believe that by promoting education about Chagas disease in schools starting at the basic elementary level and including reinforcement at higher education levels will ensure that the Mexican population would be aware of this health problem and that the control measures adopted will have more acceptance and success. We hope that this review sensitizes the relevant authorities and that the appropriate measures to reduce the risk of infection by T. cruzi are undertaken to provide the Mexican people a better quality of life.
    Acta tropica 04/2013; 127(2). DOI:10.1016/j.actatropica.2013.04.007 · 2.27 Impact Factor
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    • "In about one third of these patients the infection leads to a symptomatic chronic phase, characterized by cardiac and/or digestive implications, and less often alterations in the central nervous system (Matsuda et al., 2009; Tanowitz et al., 2009; Rassi and Rassi, 2010). Clinical manifestations are associated to morbidity and cardiac involvement is the main cause of death in the chronic stage of the disease (Prata, 2001; Dutra et al., 2005; Punukollu et al., 2007). To date, a protective vaccine against this infection is inexistent and the efficacy of the current and rather toxic anti-parasitic chemotherapy is under consideration in patients in the chronic phase of the disease (Marin- Neto et al., 2009). "
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    ABSTRACT: The protozoan parasite Trypanosoma cruzi is the etiological agent of Chagas disease. To date, no vaccine is available for protection against T. cruzi infection. The CD8(+) T cells immune response against specific antigens has shown to efficiently control the spread of the parasite in murine experimental infection. However, data concerning CD8(+) response in Chagas patients are still restricted to a few epitopes. We have studied the existence of immunodominant CD8(+) T cell epitopes in the paraflagellar rod proteins 2 and 3 (PFR2 and PFR3) from T. cruzi in a mouse model, and analyzed their recognition by cytotoxic T lymphocytes from Chagas disease patients. Immunization of C57BL/6-A2/K(b) transgenic mice with plasmids coding for the fusion proteins PFR2-HSP70 and PFR3-HSP70 induced a specific CTL response against two PFRs epitopes (PFR2(449-457) and PFR3(481-489)), and showed specific lysis percentages of 24 and 12, respectively. Moreover, the PFR2(19-28), PFR2(156-163), PFR2(449-457), PFR3(428-436), PFR3(475-482) and PFR3(481-489) peptides were observed to have a high binding affinity to the HLA-A*02:01 molecule. Remarkably, these HLA-A*02:01-binding peptides are successfully processed and presented during natural infection by T. cruzi in the context of MHC class I as evidenced by using peptide-pulsed K562-A2 cells as antigen presenting cells. The T cells from Chagas disease chronic patients specific for PFR2/PFR3 selected CD8(+) epitopes showed a pro-inflammatory cytokine secretion profile (IFN-γ, TNF-α and IL-6). A positive Granzime B secretion was observed in three out of 16 patients in response to PFR2(156-163) and PFR2(449-457) peptides, two out of 11 patients in response to PFR2(19-28) peptide and one out of 14 and 11 patients in response to PFR3(428-436) and PFR3(481-489) peptides, respectively. The PFRs-specific cytotoxic activity in purified PBMC was only detected in patients in the indeterminate phase of the disease.
    Molecular Immunology 06/2012; 52(3-4):289-98. DOI:10.1016/j.molimm.2012.05.021 · 2.97 Impact Factor
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