ABSTRACT
Trypanosoma cruzi, the causative agent of Chagas’ disease, is classified as an intracellular parasite, in reference to its preferential location for development within the mammalian host. The term “intracellular” also refers to the escape strategies that it have evolved in order to deal with the effector or killing mechanisms of the hosts phagocytes, the cell that the amastigote form of this parasite is very adept at living in. In fact, parasite escape mechanisms underscore the relevant host defenses that are important for maintaining pathogen numbers in check. These effector mechanisms and T. cruzis preference for the very cell that is supposed to destroy it must be reconciled with the pathology and clinical presentations of infections caused by this parasite. Most patients infected with T. cruzi survive the acute infection and progress to the so-called indeterminate phase. O f these, less than 30% develop the clinical complications of chronic disease such as carditis and organomegally. The different outcomes of the initial infec tion reflect the stochastic nature of the interplay between parasite and host, which is affected by their genetic makeup.
