Trypanosoma cruzi is a species of parasitic kinetoplastid which causes Chagas disease. Among the protozoa, the trypanosomes characteristically bore tissue in another organism and feed on blood (primarily) and also lymph. This behaviour causes disease or the likelihood of disease that varies with the organism: Chagas disease and sleeping sickness in humans, dourine and surra in horses, and a brucellosis-like disease in cattle. Parasites need a host body and the haematophagous insect triatomine (descriptions "assassin bug", "cone-nose bug", and "kissing bug") is the major vector in accord with a mechanism of infection. The triatomine likes the nests of vertebrate animals for shelter, where it bites and sucks blood for food. Individual triatomines infected with protozoa from other contact with animals transmit trypanosomes when the triatomine deposits its faeces on the host's skin surface while blood feeding. Penetration of the infected faeces is further facilitated by the scratching of the bite area by the human or animal host.
Etymology The specific name "cruzi" is an honor to Brazilian scientist Oswaldo Cruz, who was the teacher of the discoverer: Carlos Chagas.
Life cycle The Trypanosoma cruzi life cycle starts in an animal reservoir, usually mammals, wild or domestic, including humans. A triatomine bug serves as the vector. While taking a blood meal from an infected host, it ingests T. cruzi. In the triatomine bug (the principal species of which in terms of parasite transmission to humans being Triatoma infestans) the parasite goes into the epimastigote stage, making it possible to reproduce. After reproducing through binary fission, the epimastigotes move onto the rectal cell wall of the kissing bug, where they become infectious. Infectious T. cruzi are called metacyclic trypomastigotes. When the triatomine bug subsequently takes a blood meal from a host, it defecates—its waste containing T. cruzi propagation stages. As a result, Trumper and Gorla 1991 find transmission success centers around the triatomine's defecation behaviors. Alternatively, in nature and in most recent cases of epidemiological outbreaks, infection occurs through the oral ingestion of parasites (mainly through a lack of infected food disinfection in the case of human infection). The trypomastigotes are in the feces and are capable of swimming into the host's cells using flagella, a characteristic swimming tail dominant in the Euglenoid class of protists. The trypomastigotes enter the host through the bite wound or by crossing mucous membranes. The host cells contain macromolecules such as laminin, thrombospondin, heparin sulphate, and fibronectin that cover their surface. These macromolecules are essential for adhesion between parasite and host and for the process of host invasion by the parasite. The trypomastigotes must cross a network of proteins that line the exterior of the host cells in order to make contact and invade the host cells. The molecules and proteins on the cytoskeleton of the cell also bind to the surface of the parasite and initiate host invasion.
Life cycle forms of Trypanosoma cruzi
Trypanosoma cruzi exhibits three major morphological forms during its complex life cycle: epimastigote, trypomastigote, and amastigote stages. The epimastigote form develops and multiplies in the midgut of the triatomine vector. It is an elongated, flagellated stage that divides by binary fission. Toward the end of the insect phase, epimastigotes migrate to the hindgut and differentiate into metacyclic trypomastigotes, which are the infective, non-dividing forms excreted with the insect’s feces. After entering the mammalian host through mucous membranes or skin lesions, metacyclic trypomastigotes invade host cells and transform into amastigotes. Amastigotes are intracellular, rounded forms with a short flagellum; they multiply in the cytoplasm by binary fission. Following several replication cycles, they differentiate into cell-derived trypomastigotes (also known as bloodstream trypomastigotes), which are released when the host cell ruptures. These trypomastigotes circulate in the bloodstream and can infect new cells or be ingested by another triatomine, where they revert to epimastigotes, completing the cycle.
Pathophysiology Trypanosomiasis in humans progresses with the development of the trypanosome into a trypomastigote in the blood and into an amastigote in tissues. As the infection progresses, the number of infected cells increases, as well as the number of amastigotes per infected cell (APC). If the average of APC is one or close to one, the infection has just begun. A higher APC means that amastigotes have started to replicate. The acute form of trypanosomiasis is usually unnoticed, although it may manifest itself as a localized swelling at the site of entry. In this form appears elevated parasitism, myocarditis, and changes in the myocardial gene expression. The chronic form may develop 30 to 40 years after infection and affect internal organs (e.g., the heart, the oesophagus, the colon, and the peripheral nervous system). Affected people may die from heart failure and severe heart lesions. Acute cases are treated with nifurtimox and benznidazole, but no effective therapy for chronic cases is currently known.
Cardiac manifestations Researchers of Chagas disease have demonstrated several processes that occur with all cardiomyopathies. The first event is an inflammatory response. Following inflammation, cellular damage occurs. Finally, in the body's attempt to recover from the cellular damage, fibrosis begins in the cardiac tissue. Another cardiomyopathy found in nearly all cases of chronic Chagas disease is thromboembolic syndrome. Thromboembolism describes thrombosis, the formation of a clot, and its main complication is embolism, the carrying of a clot to a distal section of a vessel and causing blockage there. This occurrence contributes to the death of a patient by four means: arrhythmias, stasis secondary to cardiac dilation, mural endocarditis, and cardiac fibrosis. These thrombi also affect other organs such as the brain, spleen and kidney.
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