Trypanosoma cruzi

Trypanosoma cruzi

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Brief Summary

The protozoan parasite Trypanosoma cruzi causes Chagas disease in humans. Trypanosoma cruzi is transmitted to humans by blood-sucking triatomine assassin bugs (Reduviidae: Triatominae). The discovery of the cause of Chagas disease and the identification of the vector (as well as many important later related discoveries) is credited to the the pioneering Brazilian scientist Carlos Chagas. Trypanosoma cruzi occurs in the Americas from the southern United States to southern Argentina, mainly in poor, rural areas of Mexico, Central America, and South America. (Centers for Disease Control Parasites and Health website)  Chronic Chagas disease is a major health problem in many Latin American countries, where the associated burden from this disease is larger than the combined burden of malaria, leprosy, leishmaniasis, filariasis, schistosomiasis, dengue, and the major intestinal nematode infections (Abad-Franch et al. 2009 and references therein).

An infected triatomine assassin bug takes a blood meal and releases trypomastigotes (the characteristic infective developmental stage) in its feces near the site of the bite wound.  Trypomastigotes enter the host through the wound or through intact mucosal membranes, such as the conjunctiva. Inside the host, the trypomastigotes invade cells near the site of inoculation, where they differentiate into intracellular amastigotes (a developmental stage without visible external  flagella or cilia).  The amastigotes multiply by binary fission and differentiate into trypomastigotes, which are then released into the circulation as bloodstream trypomastigotes.  Trypomastigotes infect cells from a variety of tissues and transform into intracellular amastigotes in new infection sites.  Clinical manifestations can result from this infective cycle.  The bloodstream trypomastigotes do not replicate (in contrast to the trypanosomes that cause African Sleeping Sickness).  Replication resumes only when the parasites enter another cell or are ingested by another vector.  The triatomine bug becomes infected by feeding on human or animal blood that contains circulating parasites.  The ingested trypomastigotes transform into epimastigotes in the vector’s midgut.  The parasites multiply and differentiate in the midgut and differentiate into infective metacyclic trypomastigotes in the hindgut. Common triatomine vector species for trypanosomiasis belong to the genera Triatoma, Rhodnius, and Panstrongylus. Trypanosoma cruzi can also be transmitted through blood transfusions, organ transplantation, transplacentally, and in laboratory accidents. (Centers for Disease Control Parasites and Health website)

It has been estimated that there are 15 to 17 million people infected by T. cruzi in Latin America and 90 to 100 million are exposed to infection, although more optimistic estimates have been made more recently. Humans became important hosts of T. cruzi only during the past several centuries, as extensive deforestation for agriculture and livestock rearing led the triatomine vectors to colonize areas surrounding human dwellings and the dwellings themselves. Their adaptations to this new niche included feeding on the blood of humans and domestic animals. The rates of natural infection of triatomines by T. cruzi vary enormously among species and according to how closely associated they are with the parasite reservoirs. For many triatomine vectors, however, no more than 5% are infected. (Coura and Borges-Pereira 2010 and references therein).

Much progress has been made against this disease in recent years. The genome of T. cruzi was published in 2005. In the last 10 to 15 years, T. cruzi transmission to people has been interrupted over vast areas of southern South America, with an estimated 73% reduction in incidence and sharp declines in burden figures (Abad-Franch et al. 2009 and references therein). Transmission of T. cruzi by the main vector, Triatoma infestans, was halted in  in Uruguay in 1997, in Chile in 1999, in Brazil in 2006, and in Guatemala in 2009. Incidence of Chagas disease has dropped from 700,000 new cases per year to 40,000, and the annual number of deaths has fallen from more than 45,000 to 12,500. However, the epidemiology of the disease has become more complex because of multiple vectors and reservoirs and the added effects of geopolitical, economic, and ecological upheavals. In contrast to South America, the pattern of change in Central America is quite homogeneous, with substantial advances in elimination of the main vector there (Rhodnius prolixus). Because of migration patterns, the United States, Canada, Europe, Australia, and Japan are most at risk for imported Chagas disease (the estimated number of cases of T. cruzi infection imported into the U.S.A. in 2006 was between 30,000 and 300,000). In the U.S.A., several southern states have host vectors and reservoirs for T. cruzi, but native cases in humans there remain very rare. (Lescure et al. 2010 and references therein)

Diverse aspects of the biology, ecology, and epidemiology of T. cruzi and its vectors have been reviewed by Abad-Franch et al. 2009, Coura and Borges-Pereira 2010, and Lescure et al. 2010.

Author(s): Shapiro, Leo
Rights holder(s): Shapiro, Leo


Abad-Franch, F., Monteiro F. A., Jaramillo O. N., Gurgel-Gonçalves R., Dias F B S., & Diotaiuti L. (2009).  Ecology, evolution, and the long-term surveillance of vector-borne Chagas disease: A multi-scale appraisal of the tribe Rhodniini (Triatominae). Acta Tropica. 110(2-3), 159 - 177.
Coura, J R., & Borges-Pereira J. (2010).  Chagas disease: 100 years after its discovery. A systemic review☆. Acta Tropica. 115(1-2), 5 - 13.
Lescure, F-X., Le Loup G., Freilij H., Develoux M., Paris L., Brutus L., et al. (2010).  Chagas disease: changes in knowledge and management. The Lancet Infectious Diseases. 10(8), 556 - 570.