Myocardiocyte Ultrastructure and Morphometrical Analysis in Hamsters Experimentally Infected with<i>Trypanosoma cruzi</i>

Colmanetti, Francisco Humberto; Teixeira, Vicente de Paula Antunes; Rodrigues, Maria Laura Pinto; Chica, Javier Emílio Lazo; Reis, Marcio R. C.; Santos, Vitorino Modesto dos

doi:10.1080/019131290923974

Cited by 12 publications

(9 citation statements)

References 24 publications

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“…The ultrastructural pathology data are similar to previous results concerning cardiac myocytes in hamsters and mice experimentally infected with T. cruzi (6, 26), “derrengadera” by T. evansi in wild horse skeletal muscle fibers (1), and in mice parasitized with T. gondii (3). In advanced Chagas’ disease patients, capillary damage also has been reported in skeletal muscle (5).…”

Section: Discussionsupporting

confidence: 88%

Ultrastructural Study on Tissue Alterations Caused by Trypanosomatids in Experimental Murine Infections

Finol

Roschman-González

2014

Front. Public Health

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The ultrastructural study in different tissues of mice experimentally infected with isolates of Trypanosoma evansi, Trypanosoma cruzi, and Leishmania mexicana reveals changes in cardiac myocytes, skeletal muscle fibers, and hepatic, adrenal, kidney, and spleen cells. Some of these changes were cytoarchitectural and others consisted of necrosis. Alterations in the microvasculature were also found. The mononuclear cell infiltrate included neutrophils, eosinophils, and macrophages. This work shows that diverse mice tissues are important target for trypanosomatids.

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Section: Discussionsupporting

confidence: 88%

Ultrastructural Study on Tissue Alterations Caused by Trypanosomatids in Experimental Murine Infections

Finol

Roschman-González

2014

Front. Public Health

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“…An experimental model of chronic Trypanosoma cruzi infection in Syrian hamsters has been described, which mimics human CCC in many aspects, including progressive left ventricular (LV) systolic dysfunction and dilation starting about 4 months after T. cruzi inoculation …”

Section: Introductionmentioning

confidence: 99%

Histopathological Correlates of Global and Segmental Left Ventricular Systolic Dysfunction in Experimental Chronic Chagas Cardiomyopathy

Oliveira

Romano

Carvalho

et al. 2016

JAHA

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BackgroundChronic Chagas cardiomyopathy in humans is characterized by segmental left ventricular wall motion abnormalities (WMA), mainly in the early stages of disease. This study aimed at investigating the detection of WMA and its correlation with the underlying histopathological changes in a chronic Chagas cardiomyopathy model in hamsters.Methods and ResultsFemale Syrian hamsters (n=34) infected with 3.5×104 or 105 blood trypomastigote Trypanosoma cruzi (Y strain) forms and an uninfected control group (n=7) were investigated. After 6 or 10 months after the infection, the animals were submitted to in vivo evaluation of global and segmental left ventricular systolic function by echocardiography, followed by euthanasia and histological analysis for quantitative assessment of fibrosis and inflammation with tissue sampling in locations coinciding with the left ventricular wall segmentation employed at the in vivo echocardiographic evaluation. Ten of the 34 infected animals (29%) showed reduced left ventricular ejection fraction (<73%). Left ventricular ejection fraction was more negatively correlated with the intensity of inflammation (r=−0.63; P<0.0001) than with the extent of fibrosis (r=−0.36; P=0.036). Among the 24 animals with preserved left ventricular ejection fraction (82.9±5.5%), 8 (33%) showed segmental WMA predominating in the apical, inferior, and posterolateral segments. The segments exhibiting WMA, in comparison to those with normal wall motion, showed a greater extent of fibrosis (9.3±5.7% and 7±6.3%, P<0.0001) and an even greater intensity of inflammation (218.0±111.6 and 124.5±84.8 nuclei/mm², P<0.0001).ConclusionsIsolated WMA with preserved global systolic left ventricular function is frequently found in Syrian hamsters with experimental chronic Chagas cardiomyopathy whose underlying histopathological features are mainly inflammatory.

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“…Many mammal species are susceptible to infection by T. cruzi, including mice, 8 -10 rats, [11][12][13] hamsters, 14,15 pigs, 16 -19 dogs, 14,16,20 and primates. 21,22 In mice, the species most frequently used for experimental T. cruzi infection, clinical manifestations vary depending on the lineage of the animal and the strain of the parasite.…”

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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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Myocardiocyte Ultrastructure and Morphometrical Analysis in Hamsters Experimentally Infected withTrypanosoma cruzi

Cited by 12 publications

References 24 publications

Ultrastructural Study on Tissue Alterations Caused by Trypanosomatids in Experimental Murine Infections

Ultrastructural Study on Tissue Alterations Caused by Trypanosomatids in Experimental Murine Infections

Histopathological Correlates of Global and Segmental Left Ventricular Systolic Dysfunction in Experimental Chronic Chagas Cardiomyopathy

Cavia porcellus as a Model for Experimental Infection by Trypanosoma cruzi

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