Abstract
There are approximately 7.8 million people in Latin America, including Chile, who suffer from Chagas disease and another 28 million who are at risk of contracting it. Chagas is caused by the flagellate protozoan Trypanosoma cruzi. It is a chronic disease, where 20%-30% of infected individuals develop severe cardiopathy, with heart failure and potentially fatal arrhythmias. Currently, Chagas disease treatment is more effective in the acute phase, but does not always produce complete parasite eradication during indeterminate and chronic phases. At present, only nifurtimox or benznidazole have been proven to be superior to new drugs being tested. Therefore, it is necessary to find alternative approaches to treatment of chronic Chagas. The current treatment may be rendered more effective by increasing the activity of anti-Chagasic drugs or by modifying the host's immune response. We have previously shown that glutathione synthesis inhibition increases nifurtimox and benznidazole activity. In addition, there is increasing evidence that cyclooxygenase inhibitors present an important effect on T. cruzi infection. Therefore, we found that aspirin reduced the intracellular infection in RAW 264.7 cells and, decreased myocarditis extension and mortality rates in mice. However, the long-term benefit of prostaglandin inhibition for Chagasic patients is still unknown.
Highlights
Chagas disease is caused by Trypanosoma cruzi, a flagellated protozoan transmitted to humans either by transfusion of infected blood, from an infected mother to her child, or by its most important vector, a blood–sucking bug (Triatoma infestans, a.k.a. ‘vinchuca’), which carries the parasite in its contaminated feces
Chagas disease can be diagnosed with greater sensitivity by the detection of T. cruzi specific sequences of DNA by polymerase chain reaction (PCR) reaction (Britto, 2009; Sousa et al, 2009)
In mice infected with T. cruzi, microcirculatory abnormalities include focal vascular constriction, microvascular proliferation, and occlusive platelet thrombi in small epicardial and intramural coronary arteries, which lead to ischemia (Factor et al, 1985; Marin-Neto et al, 2007; MarinNeto and Rassi, 2009; Ramos and Rossi, 1999; Rossi and Ramos, 1996)
Summary
Chagas disease is caused by Trypanosoma cruzi, a flagellated protozoan transmitted to humans either by transfusion of infected blood, from an infected mother to her child, or by its most important vector, a blood–sucking bug (Triatoma infestans, a.k.a. ‘vinchuca’), which carries the parasite in its contaminated feces. While the efficacy of drug treatment has been validated in infected people younger than 16 years of age, it is not known if the same drugs can halt disease progression in adult patients, or if their use can be recommended to those at an indeterminate phase of the disease); v) a dearth of tools in clinical studies to rapidly assess the efficacy of therapeutic treatments being identified by the research community, even if the capacity to do these studies exists (The knowledge and tools for management of the cardiac or digestive symptoms that may result from Chagas disease exists; we know very little about how to make these interventions available to the patients or about the social costs associated with the disease) vi) a deficiency of treatment guidelines that are congruent with regional differences in disease manifestations (WHO, 2007). Sudden death is an occasional complication in patients with severe underlying cardiac involvement, including ventricular aneurysms, which is a characteristic finding in cardiac Chagas (Bestetti and Cardinalli-Neto, 2009; Marin-Neto and Rassi, 2009; Rassi et al, 2009a; Rassi and Rassi, 2009) This set of signs and symptoms are nonspecific to establish the diagnosis of Chagas disease. Chagas disease can be diagnosed with greater sensitivity by the detection of T. cruzi specific sequences of DNA by PCR reaction (Britto, 2009; Sousa et al, 2009)
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