Tripomastigotes de sangre y de cultivo celular de Trypanosoma cruzi Y.: II.- Patologíade la enfermedad de Chagas en ratones Balb/c

Rossell, Raiza Aragort De; Rodrı́guez, Ana; Jesús, Rosa De; Calcagno, Marina; Segnini, Zulay Maizo De; Díaz, Sergio

doi:10.4067/s0716-07202000000300002

Cited by 3 publications

(2 citation statements)

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“…These megasyndromes are coupled with gastrointestinal motility disturbances in patients with Chagas disease (Madrid et al 2004; Madrid and Defilippi 2006). Mega-organ syndromes and associated symptoms are also exhibited in animal models of Chagas disease (Postan et al 1986; 1987; Scremin et al 1999; De Rossell et al 2000; Boczko et al 2005). Recently, in separate studies, we demonstrated decreased intestinal motility in T. cruzi (Y strain) infected Swiss Webster mice (de Oliveira et al 2008) and intestinal dilation in T. cruzi (Brazil strain) infected C57Bl/6 mice (Ny et al 2008).…”

Section: Introductionmentioning

confidence: 99%

The role of selenium in intestinal motility and morphology in a murine model of Typanosoma cruzi infection

Souza

Sieberg

et al. 2010

Parasitol Res

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Infection with Trypanosoma cruzi causes mega-syndromes of the gastrointestinal (GI) tract in humans and animals. In the present study, we employed magnetic resonance imaging to noninvasively monitor the effect of selenium supplementation on alterations in the GI tract of T. cruziinfected mice. CD1 mice infected with T. cruzi (Brazil strain) exhibited dilatation of the intestines similar to that we recently reported in infected C57Bl/6 mice. The average intestine lumen diameter increased by 65% and the increase was reduced to 29% in mice supplemented with 2 ppm selenium in the drinking water. When supplemented with 3 ppm selenium in chow the lumen diameter was also significantly reduced although the difference between the infected and infected supplemented mice was smaller. Intestinal motility in infected mice fed with selenium-enriched chow was increased

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Section: Introductionmentioning

confidence: 99%

The role of selenium in intestinal motility and morphology in a murine model of Typanosoma cruzi infection

Souza

Sieberg

et al. 2010

Parasitol Res

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“…Mice exhibit many of the functional, pathologic, and immunologic alterations observed in human infection, including cardiomyopathy and mega-organ syndromes 5,11–14. Mori and others15 used x-ray methods to investigate GI tract abnormalities in T. cruzi –infected mice.…”

Section: Introductionmentioning

confidence: 99%

A Magnetic Resonance Imaging Study of Intestinal Dilation in Trypanosoma cruzi–infected Mice Deficient in Nitric Oxide Synthase

Ny¹,

Li²,

Mukherjee³

et al. 2008

The American Journal of Tropical Medicine and Hygiene

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Infection with Trypanosoma cruzi causes megasyndromes of the gastrointestinal (GI) tract. We used magnetic resonance imaging (MRI) to monitor alterations in the GI tract of T. cruzi-infected mice, and to assess the role of nitric oxide (NO) in the development of intestinal dilation. Brazil strain-infected C57BL/6 wild-type (WT) mice exhibited dilatation of the intestines by 30 days post-infection. Average intestine lumen diameter increased by 72%. Levels of intestinal NO synthase (NOS) isoforms, NOS2 and NOS3, were elevated in infected WT mice. Inflammation and ganglionitis were observed in all infected mice. Intestinal dilation was observed in infected WT, NOS1, NOS2, and NOS3 null mice. This study demonstrates that MRI is a useful tool to monitor intestinal dilation in living mice and that these alterations may begin during acute infection. Furthermore, our data strongly suggests that NO may not be the sole contributor to intestinal dysfunction resulting from this infection.

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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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Tripomastigotes de sangre y de cultivo celular de Trypanosoma cruzi Y.: II.- Patologíade la enfermedad de Chagas en ratones Balb/c

Cited by 3 publications

References 0 publications

The role of selenium in intestinal motility and morphology in a murine model of Typanosoma cruzi infection

The role of selenium in intestinal motility and morphology in a murine model of Typanosoma cruzi infection

A Magnetic Resonance Imaging Study of Intestinal Dilation in Trypanosoma cruzi–infected Mice Deficient in Nitric Oxide Synthase

Cavia porcellus as a Model for Experimental Infection by Trypanosoma cruzi

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