What is the lifecycle of T cruzi?

Updated: Apr 26, 2019
  • Author: Louis V Kirchhoff, MD, MPH; Chief Editor: Pranatharthi Haran Chandrasekar, MBBS, MD  more...
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The T cruzi life cycle consists of 3 main developmental forms. Epimastigotes are an extracellular and noninfective form of the parasite found in the midgut of insect vectors, where they multiply by binary fission. As epimastigotes (depicted in the first image below) move to the hindgut, they differentiate into metacyclic trypomastigotes (depicted in the second image below), which are nondividing forms resistant to mammalian complement that have the capacity to infect mammalian cells. They enter local cells through breaks in the skin, mucous membranes, or the conjunctivas and transform into the third morphologic form, amastigotes. Amastigotes multiply intracellularly until the host cell is overwhelmed, at which point they transform into bloodstream trypomastigotes.

Chagas disease (American trypanosomiasis). The try Chagas disease (American trypanosomiasis). The trypomastigote is the infective flagellated form of the parasite found in the blood of the mammalian hosts (blood trypomastigote) and in the hindgut of vectors (metacyclic trypomastigote). Image courtesy of Peter Darben, MD.
Chagas disease (American trypanosomiasis). The epi Chagas disease (American trypanosomiasis). The epimastigote form of Trypanosoma cruzi is the multiplying stage of the parasite that grows in the gut of the insect vector and also in cell-free culture medium as shown here. Image courtesy of Peter Darben, MD.

As the host cells rupture, the trypomastigotes are released into the lymphatics and bloodstream, through which they spread to distant sites and invade new host cells. See image below.

Trypanosoma cruzi trypomastigotes in a mouse blood Trypanosoma cruzi trypomastigotes in a mouse blood smear (Giemsa, x625). Courtesy of Dr. Herbert B Tanowitz, New York, NY.

This process continues asynchronously for the life of the host. Small numbers of trypomastigotes may be ingested in blood meals taken by uninfected triatomines. The trypomastigotes then transform into epimastigotes in the midgut of these insects, thus completing the cycle.

T cruzi can also be transmitted when mammalian hosts ingest infected insects, and this mechanism of transmission may play a major role in maintaining the sylvatic cycle.

Numerous biological, biochemical, and molecular studies have shown that the population of T cruzi is highly diverse. [5, 6, 7] Although T cruzi is a diploid organism in which some genetic exchange may occur in insect vectors, [8] its genetic and phenotypic diversity is thought to result from the clonal multiplication of the epimastigote and amastigote forms. The current consensus is that T cruzi can be divided into 6 discrete taxonomic units (DTUs; TcI through TcVI). The strains in each DTU show variability in geographic, epizootic, epidemiologic, and pathogenic characteristics. [9, 10, 11] Unfortunately, no clear associations have been found between the strain groups and pathogenicity or drug susceptibility. In general, the extensive genetic and, more recently, proteomics data generated so far, including the framework of the DTUs, have not yet led to new tools to reduce transmission, advances in the management of clinical disease, new drugs, or a vaccine. In the area of diagnosis, however, the results of molecular work on T cruzi have led to the development of accurate assays that are used widely to detect T cruzi infection.

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