Abstract
The American trypanosomiasis, Chagas’ disease, affects about 20 million people in Central and South America. The causative agent is a parasitic flagellate, Trypanosoma cruzi, which has a complex life cycle, involving a replicative form, the amastigote, and a nonreplicative form, the bloodstream trypomastigote, in the mammalian host. There is also a replicative form, the epimastigote, and a nonreplicative form, the infective metacyclic trypomastigote, in the insect vector (Brener, 1973). Although at present all these developmental stages can be obtained in axenic culture (Contreras et al., 1985) or in mammalian cell culture (Andrews and Colli, 1982), or from infected mammals (Gutteridge et al., 1978), most metabolic and enzymological studies so far have been performed with cultured epimastigotes, presumably identical to those naturally present in the insect vector. Comparative studies using epimastigotes, amastigotes, and bloodstream trypomastigotes (Gutteridge and Rogerson, 1979) suggest that, at variance with African trypanosomes (Opperdoes, 1987), the different developmental stages of T. cruzi have qualitatively similar metabolic characteristics.
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Cazzulo, J.J. (1992). Energy Metabolism in Trypanosoma cruzi . In: Avila, J.L., Harris, J.R. (eds) Intracellular Parasites. Subcellular Biochemistry, vol 18. Springer, Boston, MA. https://doi.org/10.1007/978-1-4899-1651-8_7
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