Immunological Alterations in Chagas’ Disease

Abstract

Chagas’ disease is caused by infection with Trypanosoma cruzi, a flagellate parasite discovered in Brazil by Carlos Chagas (1909), who described (1911) the clinical, pathological and epidemiological features of the disease that was to bear his name. The T. cruzi life cycle is a complex one, with several stages of development in vertebrate and invertebrate hosts. In the vertebrates, T. cruzi undergoes intracellular multiplication (amastigote). The emerging nonmultiply- ing trypomastigotes are found in the bloodstream of the infected vertebrates. In the invertebrate (insect) host, the life of T. cruzi is characterized by mor-phological transformations that take place along the digestive tract. Different strains of T. cruzi show differences in morphology during their life cycles (Brener, 1971). The most usual mode of transmission is by means of the invertebrate (hematophagus) intermediary host (Hoare, 1972). After feeding on the infected vertebrates, bloodstream trypomastigotes differentiate in the digestive tracts of the Triatoma bugs. Metacyclic forms of the parasite, eliminated in the insect feces, are considered responsible for infection in the vertebrate host (Zeledon, 1977).