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The kallikrein-kinin system in experimental Chagas disease: a paradigm to investigate the impact of inflammatory edema on GPCR-mediated pathways of host cell invasion by Trypanosoma cruzi.

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Chronic chagasic myocarditis (CCM) depends on Trypanosoma cruzi persistence in the myocardium. Studies of the proteolytic mechanisms governing host/parasite balance in peripheral sites of T. cruzi infection revealed that tissue culture trypomastigotes (TCTs) elicit inflammatory edema and stimulate

[Familial Chagas' disease. A case with acute pulmonary edema and a possibly congenital case of Chagas' disease].

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Comparison of Noninvasive Cardiac Test Strategies for Newly Diagnosed Chagas Disease in a Non-Endemic Zone

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Chagas disease is an emerging infectious disease in Europe and other non-endemic areas, mainly owing to migration from endemic areas. We aimed at investigating the value of advanced echocardiography (ECHO) and cardiac magnetic resonance (CMR) in patients newly diagnosed with Chagas disease to

Late reactivation of Chagas' disease presenting in a recipient as an expansive mass lesion in the brain after heart transplantation of chagasic myocardiopathy.

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BACKGROUND Chagas' disease is endemic in many Latin American countries. In the last decades, millions of people from these countries have migrated to the United States, changing the scenario of acute Chagas' disease associated with blood transfusion in North America. RESULTS We report the case of a

Are maternal re-infections with Trypanosoma cruzi associated with higher morbidity and mortality of congenital Chagas disease?

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BACKGROUND Comparing two surveys performed in Bolivia in 1992-1994 and 1999-2001, we reported a significant decrease in the proportions of severe and mortal forms of congenital Chagas disease. This might be due to a reduction of vectorial density (VD) in maternal residence area, raising the question

Prenatal diagnosis of congenital Chagas' disease (American trypanosomiasis).

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The prenatal diagnosis of congenital transmission of Chagas' disease in a pregnant woman with the indeterminate form of the disease is reported. Sonography revealed fetal hydrops at 31 weeks' gestation. Anti-Trypanosoma cruzi IgM and IgG antibodies were negative in the fetal blood sampled by

Fatal acute Chagas disease by Trypanosoma cruzi DTU TcI, Ecuador.

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Chagas disease is caused by the haemoflagellate protozoan Trypanosoma cruzi. Currently, T. cruzi recognizes seven discrete typing units (DTUs): TcI to TcVI and Tcbat. The genetic diversity of T. cruzi is suspected to influence the clinical outcome. Acute clinical manifestations, which

On an acute case of Chagas disease in a region under vector control in the state of São Paulo, Brazil.

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No vector transmitted cases of Chagas disease had been notified in the state of São Paulo since the 1970s. However, in March, 2006, the death of a six-year-old boy from the municipality of Itaporanga was notified to the Center for Epidemiological Survey of the São Paulo State Health Secretariat: an

Right ventricular endomyocardial biopsy in chronic Chagas' disease.

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Right ventricular endomyocardial biopsy was used to study myocardial involvement in 42 patients with chronic Chagas' disease. Patients were divided into three groups: group A included 16 patients with normal ECGs, normal chest x-rays, and no symptoms; group B included 15 patients with abnormal ECGs

Right ventricular endomyocardial biopsy in undetermined form of Chagas' disease.

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Right ventricular endomyocardial biopsy was carried out in thirty three patients with undetermined form of Chagas' disease. Fragments obtained by this method were analysed under light microscopy with hematoxilin-eosin, and Masson trichromic stains. Thirteen (39.4%) patients showed normal myocardial

Cardiac magnetic resonance in Chagas' disease.

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American trypanosomiasis (Chagas' disease [CD]) caused by Trypanosoma cruzi is endemic in Latin America, where it is one of the leading causes of death. The involvement of the heart is crucial in the patients' prognosis. Besides lymphocytic myocarditis, cardiomyopathy is associated with several

Mast Cell Coupling to the Kallikrein-Kinin System Fuels Intracardiac Parasitism and Worsens Heart Pathology in Experimental Chagas Disease.

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During the course of Chagas disease, infectious forms of Trypanosoma cruzi are occasionally liberated from parasitized heart cells. Studies performed with tissue culture trypomastigotes (TCTs, Dm28c strain) demonstrated that these parasites evoke neutrophil/CXCR2-dependent microvascular leakage by

[Emergencies in patients with Chagas' disease in Buenos Aires city, Argentina].

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The objective of this work was to evaluate the most frequent causes of emergency in patients with Chagas disease. Between January 1998-January 1999, individuals with Chagas disease inside the shock-room of Santojanni Hospital in Buenos Aires city, were included in a prospective study. For the

Myocardial changes in acute Trypanosoma cruzi infection. Ultrastructural evidence of immune damage and the role of microangiopathy.

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Histological and ultrastructural studies of the hearts of dogs sacrificed 18 to 26 days after intraperitoneal inoculation with 4 x 10(5) blood forms of the 12 SF strain of Trypanosoma cruzi/kg of body weight disclosed myocarditis characterized by parasitic invasion of some myocytes, damage and

Fatal acute Chagas disease in a chimpanzee.

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BACKGROUND Chagas disease (CD) or American trypanosomiasis is caused by a hemoflagellate protozoan, Trypanosoma cruzi. This organism has been isolated from more than 100 mammalian species and several insect vectors demonstrating a wide host distribution and low host specificity. METHODS A

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