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The parasitic protozoan Trypanosoma cruzi is the causative agent of Chagas’ disease which affects some 20–30 million people in Central and South America [1]. During its life cycle, the parasite undergoes a number of morphologic and physiologic changes as it passes between two hosts, a reduviid bug and man. Epimastigote or noninfectious forms are found in the midgut of the insect. In the hindgut they change to infectious metacyclic trypomastigotes which are deposited, via the insect feces, on an individual’s skin. Soon after entry through a break in the skin or via a mucous membrane, the trypomastigotes invade host cells, replicate as amastigotes, and convert back to trypomastigotes. When the cell ruptures, these forms are released in the bloodstream. Here, they either spread to surrounding tissues or enter the circulation and are taken up by the hematophagous reduviid. In the insect’s gut, they convert to replicating epimastigotes and the cycle is completed [1]. The most striking change occurs as epimastigotes convert to trypomastigotes. In contrast to epimastigotes, trypomastigotes are infectious to man, do not replicate, are resistant to complement mediated lysis and express high levels of neuraminidase [1–4]. The basis for these metabolic and antigenic changes is directly linked to differential gene expression. |
