Chagas' Disease: Decreased Resistance to Trypanosoma Cruzi Acquired Infection in Offspring of Infected Mice

Yves CarlierLaboratoire de Parasitologie, and IRIBHN Unite Statistique, Facult de Medecine, Universite Libre de Bruxelles, Laboratorium voor Pathologische Anatomie, Universitaire Instelling Antwerpen, Brussels, Belgium

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Maria Teresa RiveraLaboratoire de Parasitologie, and IRIBHN Unite Statistique, Facult de Medecine, Universite Libre de Bruxelles, Laboratorium voor Pathologische Anatomie, Universitaire Instelling Antwerpen, Brussels, Belgium

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Carine TruyensLaboratoire de Parasitologie, and IRIBHN Unite Statistique, Facult de Medecine, Universite Libre de Bruxelles, Laboratorium voor Pathologische Anatomie, Universitaire Instelling Antwerpen, Brussels, Belgium

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Marta OntiveroLaboratoire de Parasitologie, and IRIBHN Unite Statistique, Facult de Medecine, Universite Libre de Bruxelles, Laboratorium voor Pathologische Anatomie, Universitaire Instelling Antwerpen, Brussels, Belgium

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Jocelyne FlamentLaboratoire de Parasitologie, and IRIBHN Unite Statistique, Facult de Medecine, Universite Libre de Bruxelles, Laboratorium voor Pathologische Anatomie, Universitaire Instelling Antwerpen, Brussels, Belgium

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Eric Van MarckLaboratoire de Parasitologie, and IRIBHN Unite Statistique, Facult de Medecine, Universite Libre de Bruxelles, Laboratorium voor Pathologische Anatomie, Universitaire Instelling Antwerpen, Brussels, Belgium

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Viviane De MaertelaerLaboratoire de Parasitologie, and IRIBHN Unite Statistique, Facult de Medecine, Universite Libre de Bruxelles, Laboratorium voor Pathologische Anatomie, Universitaire Instelling Antwerpen, Brussels, Belgium

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The course of Trypanosoma cruzi infection was studied in an experimental model, using the offspring of mice that were chronically infected with T. cruzi. When infected two months after birth, a higher mortality rate in heavily parasitized mice occurred in these offspring than in controls born to uninfected mothers. The harmful maternal influence reached a maximum when offspring were exposed both to prenatal (placental) and postnatal (lactating) influences. It was a reversible phenomenon that led to a T. cruzi-specific failure of the offspring to control the acute phase of the infection. Such features are suggestive of a maternally-induced impairment of the immune response of the offspring.

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