Gastrointestinal manifestations of chagas' disease

Oliveira, Ricardo Brandt de

doi:10.1016/s0002-9270(98)00151-8

Cited by 129 publications

(82 citation statements)

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“…This geographical pattern is thought to be linked to differences in the predominant T. cruzi genotypes (51,192). Gastrointestinal Chagas' disease usually affects the esophagus and/or colon, resulting from damage to intramural neurons (83,84,199). The effects on the esophagus span a spectrum from asymptomatic motility disorders through mild achalasia to severe megaesophagus (83).…”

Section: Chronic T Cruzi Infectionmentioning

confidence: 99%

“…Gastrointestinal Chagas' disease usually affects the esophagus and/or colon, resulting from damage to intramural neurons (83,84,199). The effects on the esophagus span a spectrum from asymptomatic motility disorders through mild achalasia to severe megaesophagus (83). Symptoms include dysphagia, odynophagia, esophageal reflux, weight loss, aspiration, cough, and regurgitation.…”

Section: Chronic T Cruzi Infectionmentioning

confidence: 99%

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Trypanosoma cruzi and Chagas' Disease in the United States

et al. 2011

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SUMMARY Chagas' disease is caused by the protozoan parasite Trypanosoma cruzi and causes potentially life-threatening disease of the heart and gastrointestinal tract. The southern half of the United States contains enzootic cycles of T. cruzi , involving 11 recognized triatomine vector species. The greatest vector diversity and density occur in the western United States, where woodrats are the most common reservoir; other rodents, raccoons, skunks, and coyotes are also infected with T. cruzi. In the eastern United States, the prevalence of T. cruzi is highest in raccoons, opossums, armadillos, and skunks. A total of 7 autochthonous vector-borne human infections have been reported in Texas, California, Tennessee, and Louisiana; many others are thought to go unrecognized. Nevertheless, most T. cruzi -infected individuals in the United States are immigrants from areas of endemicity in Latin America. Seven transfusion-associated and 6 organ donor-derived T. cruzi infections have been documented in the United States and Canada. As improved control of vector- and blood-borne T. cruzi transmission decreases the burden in countries where the disease is historically endemic and imported Chagas' disease is increasingly recognized outside Latin America, the United States can play an important role in addressing the altered epidemiology of Chagas' disease in the 21st century.

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Section: Chronic T Cruzi Infectionmentioning

confidence: 99%

Section: Chronic T Cruzi Infectionmentioning

confidence: 99%

Trypanosoma cruzi and Chagas' Disease in the United States

et al. 2011

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“…[11][12][13][14][15] Vagal denervation is thought to play an important pathogenic role in gastrointestinal Chagas disease, and abnormal responses on autonomic stimuli were strongly associated with the digestive form of the disease in one study. 16,17 However, the contribution of autonomic dysfunction to the pathophysiology of Chagas cardiomyopathy is less welldefined, and its significance in the absence of other cardiac findings is controversial. 18,19 Although risk factors for T. cruzi infection have been studied in a number of rural settings, there are few data from urban foci of transmission.…”

Section: Introductionmentioning

confidence: 99%

Autonomic Dysfunction and Risk Factors Associated with Trypanosoma cruzi Infection among Children in Arequipa, Peru

Bowman¹,

Kawai²,

Gilman³

et al. 2011

The American Society of Tropical Medicine and Hygiene

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Chagas disease affects an estimated 8 million people in Latin America. Infected individuals have 20–30% lifetime risk of developing cardiomyopathy, but more subtle changes in autonomic responses may be more frequent. We conducted a matched case-control study of children in Arequipa, Peru, where triatomine infestation and Trypanosoma cruzi infection are emerging problems. We collected data on home environment, history, physical examination, electrocardiogram, and autonomic testing. Signs of triatomine infestation and/or animals sleeping in the child's room and household members with Chagas disease were associated with increased infection risk. Electrocardiogram findings did not differ between cases and controls. However, compared with control children, infected children had blunted autonomic responses by three different measures, the Valsalva maneuver, the cold pressor test, and the orthostatic test. T. cruzi-infected children show autonomic dysfunction, although the prognostic value of this finding is not clear. Sustained vector control programs are essential to decreasing future T. cruzi infections.

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“…The digestive form of Chagas disease ranges from mild motility disorders to mega syndromes, most commonly involving the esophagus and/or colon. 5 The immunologic, physiologic, and pathologic mechanisms of chronic Chagas disease are complex. 6 Serologic testing often shows discordant results, current treatment requires the use of toxic drugs with suboptimal efficacy in chronic infection, and no vaccines for Chagas disease currently exist.…”

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confidence: 99%

Cavia porcellus as a Model for Experimental Infection by Trypanosoma cruzi

Castro-Sesquen

Gilman

Yauri

et al. 2011

The American Journal of Pathology

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The guinea pig (Cavia porcellus) is a natural reservoir for Trypanosoma cruzi but has seldom been used as an experimental infection model. We developed a guinea pig infection model for acute and chronic Chagas disease. Seventy-two guinea pigs were inoculated intradermally with 10 4 trypomastigotes of T. cruzi strain Y (experimental group); 18 guinea pigs were used as control group. Eight animals from the experimental group and two from the control group were Chagas disease, caused by the protozoan parasite Trypanosoma cruzi, is one of the most important parasitic infections of the Americas. Despite successful vector control programs in many countries, the disease remains a major public health problem in Latin America, with 8 to 10 million people currently infected, an annual incidence of 65,000 new cases in 15 countries, and 14,000 deaths associated with the infection per year. 1 Transmission to the mammalian host occurs when a T. cruzi-infected triatomine vector deposits infectious trypomastigotes in feces during a blood meal and the parasites invade through the bite wound or intact mucosal membranes. 2 Trypomastigotes can infect virtually any nucleated cell, where they transform to amastigotes and replicate in the host cell cytoplasm. Amastigotes convert back to trypomastigotes inside the cell and then rupture the cell and circulate in the bloodstream. After weeks, the host immune response usually controls the acute infection but does not completely clear the parasite. This results in lifelong chronic infection of the host.The initial weeks after T. cruzi infection are characterized by a high-level parasitemia and symptoms that vary from mild nonspecific febrile illness to life-threatening myocarditis and/or meningoencephalitis. 2 Acute symptoms and detectable parasitemia resolve spontaneously within 2 to 3 months, and the infected individual passes into the chronic phase of the disease. Nearly all individuals in the early period of chronic infection are asymptomatic and are said to have the indeterminate form of the disease. In most individuals, the infection remains silent for life and is detectable only by anti-T. cruzi serologic tests and, in a proportion of individuals, by molecular Supported by NIH training grant in infectious and tropical diseases 5 T35 AI065385 and NIH grant 1R01AI087776-01.

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Gastrointestinal manifestations of chagas' disease

Cited by 129 publications

References 0 publications

Trypanosoma cruzi and Chagas' Disease in the United States

Trypanosoma cruzi and Chagas' Disease in the United States

Autonomic Dysfunction and Risk Factors Associated with Trypanosoma cruzi Infection among Children in Arequipa, Peru

Cavia porcellus as a Model for Experimental Infection by Trypanosoma cruzi

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