Trypanosoma evansi: Ultrastructural Cardiac Muscle and Cardiac Microvasculature Changes in Experimental Murine Infections
Tejero, Felix; Arias-Mota, Lourdes Lorena; Roschman-González, Antonio; Finol, Héctor José; Aso, Pedro María.
Acta sci. vet. (Online);
38(3): 279-285, 2010.
Artigo
em Inglês
| VETINDEX
| ID: vti-5085
Resumo
Background: Trypanosoma evansi is the etiologic agent of the equine trypanosomosis, a disease related to the detriment of the extensive bovine farming in the Venezuelan grasslands. Even though macroscopic pathologies such as anemia, pale mucosa, icteric tissues, generalized edema, splenomegaly, liver and renal hypertrophy, abortion, anoestrus, emaciation, lymphadenopathies, striated muscle atrophy as well as epicardiac and endocardiac hemorrhages have been described for infections with the agent, no reports of any heart ultrastructural change in experimental or natural infections induced by Venezuelan T. evansi isolates are available. So, a transmission electron microscopic approach to the problem was needed. This work describes cell features of the cardiac myocyte and the cardiac microvasculature ultrastructure in mice experimentally infected with an equine local isolate of T. evansi, also providing an account of the infection with the mices survival. Materials, Methods & Results: NMRI Mus musculus were inoculated with a Venezuelan T. evansi isolate derived from a naturally infected Equus caballus. From day three post-infection, and every other day until the mices death, one rodent was randomly killed, the heart apex was isosmotically removed and cut in symmetrical blocks, which were fixed, post-fixed, dehydrated, infiltrated, included, sectioned, contrasted and studied by means of transmission electron microscopy, with the subsequent characterization of the cardiac myocyte and the cardiac microvasculature transformations. The evaluation of the micrographs demonstrated ultrastructural time-increasing harmful mitochondrial alterations that included reduction in the number of mitochondria per cell, decrease in mitochondrial dimensions and lessening of the number of cristae per mitochondrion. Myofibrillar destruction, myofilament loss and atrophy were also evident.(...)(AU)
Biblioteca responsável:
BR68.1
Localização: BR68.1
Texto completo