Forma cardiaca da Trypanosomiase Americana

Evolution of the clinical and epidemiological knowledge about Chagas disease 90 years after its discovery

“…With respect to the clinical aspects, we cite the etiology of endemic goiter, the nervous forms and the pluriglandular manifestations. Later studies (Azevedo 1933) demonstrated that endemic goiter was concomitant with the trypanosomiasis and not depending on the latter, as Chagas himself eventually admitted when he said that this was "an open question deserving study and insight" (Chagas 1934, Lobo et al 1962. Even the possibility that in some patients already presenting thyroid deficiency or miopraxis there might be a more marked hypothyroidism at the beginning of the acute phase, which disappeared with remission of this phase, as reported by Chagas, was not confirmed.…”

“…In 1922, Chagas again devoted his attention to the cardiac form in a study of 63 patients in an article published with Eurico Villela (Chagas & Villela 1922), which has become a classic. They established the primacy of this form of the disease by stating that it represents "the characteristic par excellence of American trypanosomiasis".…”

“…They added that "despite this, a large number of cases remain in a tolerance state for many years, with affected individuals being able to work". Chagas (1928a) later added that when myocarditis is incipient the patients can devote themselves to any type of work and can live to an old age.…”

Chagas Disease in Mexico: Report of 14 Cases of Chagasic Cardiomyopathy in Children

“…Autonomic disorders with rhythm alterations and sudden death have been described, or death by progressive myocardial insufficiency resulting in asystole (Chagas 1911;Chagas and Villela 1922). While the pathogenesis of the chronic disease is not fully understood yet, a growing consensus suggests that parasite persistence is required for lesion development; it is not known whether tissue damage is caused by parasiterelated factors, by the activation of an immunopathological process, or by autoimmune mechanisms (Cunha-Neto et al 2011).…”

Étude histopathologique des glandes salivaires de souris au cours de l’infection avecTrypanosoma cruzi

“…The alterations induced by T. cruzi in the salivary glands have been described by Chagas and Villela (1922) in chagasic patients with megaesophagus. In these patients the impairment of free passage of food in the esophagus may cause a reflex stimulation of the salivary glands, with consequent increased production of saliva and hypertrophy of the gland (Correia Neto, 1935 ;Vieira and Hadler, 1961).…”