Trypanosoma cruzi

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Trypanosoma cruzi
Trypanosoma cruzi in a blood smear.jpg
Trypanosoma cruzi in human blood Giemsa stain. They are typically seen as a C-shape and have a more pronounced kinetoplast compared to other species.
Scientific classification OOjs UI icon edit-ltr.svg
Domain: Eukaryota
Phylum: Euglenozoa
Class: Kinetoplastea
Order: Trypanosomatida
Family: Trypanosomatidae
Genus: Trypanosoma
Species:
T. cruzi
Binomial name
Trypanosoma cruzi
Chagas, 1909 [1] [2] [3]

Trypanosoma cruzi is a species of parasitic euglenoids. 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 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 and then bites. Penetration of the infected faeces is further facilitated by the scratching of the bite area by the human or animal host.

Contents

Etymology

The specific name "cruzi" is an honor to Brazilian scientist Oswaldo Cruz, who taught discoverer Carlos Chagas. [4]

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, 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, 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. [5] [6] [7] 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). [8] [9] 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. [10] 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. [11] 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. [11]

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. [12]

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. [13]

Acute cases are treated with nifurtimox and benznidazole, but no effective therapy for chronic cases is currently known.[ citation needed ]

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. [14]

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. [15]

Myocardial biochemical response

Subcellular findings in murine studies with induced T. cruzi infection revealed that the chronic state is associated with the persistent elevation of phosphorylated (activated) extracellular-signal-regulated kinase (ERK), AP-1, and NF-κB. Also, the mitotic regulator for G1 progression, cyclin D1 was found to be activated. Although there was no increase in any isoform of ERK, there was an increased concentration of phosphorylated ERK in mice infected with T. cruzi. It was found that within seven days the concentration of AP-1 was significantly higher in T. cruzi–infected mice when compared to the control. Elevated levels of NF-κB have also been found in myocardial tissue, with the highest concentrations being found in the vasculature. It was indicated through Western blot that cyclin D1 was upregulated from day 1 to day 60 post-infection. It was also indicated through immunohistochemical analysis that the areas that produced the most cyclin D1 were the vasculature and interstitial regions of the heart. [16]

Rhythm abnormalities

Conduction abnormalities are also associated with T. cruzi. At the base of these conduction abnormalities is a depopulation of parasympathetic neuronal endings on the heart. Without proper parasympathetic innervations, one could expect to find not only chronotropic but also inotropic abnormalities. It is true that all inflammatory and non-inflammatory heart disease may display forms of parasympathetic denervation; this denervation presents in a descriptive fashion in Chagas’ disease. It has also been indicated that the loss of parasympathetic innervations can lead to sudden death due to a severe cardiac failure that occurs during the acute stage of infection. [17]

Another conduction abnormality presented with chronic Chagas’ disease is a change in ventricular repolarization, which is represented on an electrocardiogram as the T-wave. This change in repolarization inhibits the heart from relaxing and properly entering diastole. Changes in the ventricular repolarization in Chagas’ disease are likely due to myocardial ischemia. This ischemia can also lead to fibrillation. This sign is usually observed in chronic Chagas’ disease and is considered a minor electromyocardiopathy. [18]

Epicardial lesions

Villous plaque is characterized by exophytic epicardial thickening, meaning that the growth occurs at the border of the epicardium and not the center of mass. Unlike milk spots and chagasic rosary, inflammatory cells and vasculature are present in villous plaque. Since villous plaque contains inflammatory cells it is reasonable to suspect that these lesions are more recently formed than milk spots or chagasic rosary. [19]

Motility

When mammalian cells are present, trypomastigotes move in a sub diffusive fashion in short periods of time, but under control conditions their motion is diffusive.

Parasites increase their mean speed; they explore smaller areas at short time scales and show a preference to be located nearby cells’ periphery. The extent of these changes depends on the cell type. Therefore, T. cruzi trypomastigotes can sense mammalian cells and modify their motility patterns to prepare themselves for infection. [12]

Parasite reorientation

Epimastigotes, which are the culture forms of T. cruzi, swim in the direction of their flagellum, due to tip-to-base symmetrical flagellar beats, that are interrupted by base-to-tip highly asymmetric beats. Switching between both beating modes facilitates parasite reorientation, allowing many movements and trajectories. Epimastigote motility is characterized by alternation of quasi-rectilinear and restricted and complex paths. [12]

Invasion efficiency

The invasion efficiency is positively correlated with the average parasite mean speed, and negatively correlated with the mean square displacement (MSD). Therefore, the motility modifications undergone by the parasites in the presence of mammalian cells may be functionally related to the cell invasion process.

Moreover, different parasite strains infect different tissues with a variable invasion efficiency, due to the high genetic and phenotypic variability found among T. cruzi strains. T. cruzi trypomastigotes are capable of sensing mammalian cells to a different degree, depending on the cell type, and can modify their motility patterns to increase their invasion efficiency. [12]

Virulence chemistry

T. cruzi does not produce prostaglandins itself. Instead Pinge-Filho et al. 1999 finds that the parasite induces mice to overproduce 2-series prostaglandins themselves. [20] These PG2s are immunosuppressive and so aid in immune evasion. [20]

Imipramines are trypanocidal. [20] Doyle & Weinbach 1989 find imipramine and various of its derivatives – 3-Chlorimipramine, 2-Nitroimipramine, and 2-Nitrodesmethylimipramine – are trypanocidal in vitro. [20] They find 2-Nitrodesmethylimipramine is the most effective among them. [20]

Epidemiology

T. cruzi transmission has been documented in the Southwestern U.S., and warming trends may allow vector species to move north. U.S. domestic and wild animals are reservoirs for T. cruzi. Triatomine species in the southern U.S. have taken human blood meals, but because triatomines do not favor typical U.S. housing, risk to the U.S. population is very low. [21]

Chagas' disease's geographical occurrence happens worldwide but high-risk individuals include those who don't have access to proper housing. Its reservoir is in wild animals but its vector is a kissing bug. This is a contagious disease and can be transmitted through a number of ways: congenital transmission, blood transfusion, organ transplantation, consumption of uncooked food that has been contaminated with feces from infected bugs, and accidental laboratory exposure. [ citation needed ]

Over 130 species can transmit this parasite [22]

Six taxonomic subunits are recognised. [23]

Clinical

The incubation period is five to fourteen days after a host comes in contact with feces. Chagas disease undergoes two phases, which are the acute and the chronic phase. The acute phase can last from two weeks to two months but can go unnoticed because symptoms are minor and short-lived. Symptoms of the acute phase include swelling, fever, fatigue, and diarrhea. The chronic phase causes digestive problems, constipation, heart failure, and pain in the abdomen. [ citation needed ]

Diagnostic methods include microscopic examination, serology, or the isolation of the parasite by inoculating blood into a guinea pig, mouse, or rat.[ citation needed ]

No vaccines are available. The most used method for epidemiological management and disease prevention resides within vector control, [24] mainly by the use of insecticides and taking preventative measures such as applying bug repellent on the skin, wearing protective clothing, and staying in higher quality hotels when traveling. Investing in quality housing would be ideal to decrease risk of contracting this disease. [25]

Genetic exchange

Genetic exchange has been identified among field populations of T. cruzi. [26] This process appears to involve genetic recombination as well as a meiotic mechanism. Despite the capability for sexual reproduction, natural populations of T. cruzi exhibit clonal population structures. It appears that frequent sexual reproduction events occur primarily between close relatives resulting in an apparent clonal population structure. [27]

See also

Related Research Articles

<span class="mw-page-title-main">Chagas disease</span> Mammal parasitic disease

Chagas disease, also known as American trypanosomiasis, is a tropical parasitic disease caused by Trypanosoma cruzi. It is spread mostly by insects in the subfamily Triatominae, known as "kissing bugs". The symptoms change over the course of the infection. In the early stage, symptoms are typically either not present or mild, and may include fever, swollen lymph nodes, headaches, or swelling at the site of the bite. After four to eight weeks, untreated individuals enter the chronic phase of disease, which in most cases does not result in further symptoms. Up to 45% of people with chronic infections develop heart disease 10–30 years after the initial illness, which can lead to heart failure. Digestive complications, including an enlarged esophagus or an enlarged colon, may also occur in up to 21% of people, and up to 10% of people may experience nerve damage.

<span class="mw-page-title-main">African trypanosomiasis</span> Parasitic disease also known as sleeping sickness

African trypanosomiasis, also known as African sleeping sickness or simply sleeping sickness, is an insect-borne parasitic infection of humans and other animals. It is caused by the species Trypanosoma brucei. Humans are infected by two types, Trypanosoma brucei gambiense (TbG) and Trypanosoma brucei rhodesiense (TbR). TbG causes over 92% of reported cases. Both are usually transmitted by the bite of an infected tsetse fly and are most common in rural areas.

<span class="mw-page-title-main">Trypanosomatida</span> Flagellate kinetoplastid excavate order

Trypanosomatida is a group of kinetoplastid unicellular organisms distinguished by having only a single flagellum. The name is derived from the Greek trypano (borer) and soma (body) because of the corkscrew-like motion of some trypanosomatid species. All members are exclusively parasitic, found primarily in insects. A few genera have life-cycles involving a secondary host, which may be a vertebrate, invertebrate or plant. These include several species that cause major diseases in humans. Some trypanosomatida are intracellular parasites, with the important exception of Trypanosoma brucei.

<span class="mw-page-title-main">Trypanosomiasis</span> Medical condition

Trypanosomiasis or trypanosomosis is the name of several diseases in vertebrates caused by parasitic protozoan trypanosomes of the genus Trypanosoma. In humans this includes African trypanosomiasis and Chagas disease. A number of other diseases occur in other animals.

<i>Trypanosoma</i> Genus of parasitic flagellate protist in the Kinetoplastea class

Trypanosoma is a genus of kinetoplastids, a monophyletic group of unicellular parasitic flagellate protozoa. Trypanosoma is part of the phylum Euglenozoa. The name is derived from the Greek trypano- (borer) and soma (body) because of their corkscrew-like motion. Most trypanosomes are heteroxenous and most are transmitted via a vector. The majority of species are transmitted by blood-feeding invertebrates, but there are different mechanisms among the varying species. Trypanosoma equiperdum is spread between horses and other equine species by sexual contact. They are generally found in the intestine of their invertebrate host, but normally occupy the bloodstream or an intracellular environment in the vertebrate host.

<span class="mw-page-title-main">Carlos Chagas</span> Brazilian doctor and scientist (1879–1934)

Carlos Justiniano Ribeiro Chagas, or Carlos Chagas, was a Brazilian sanitary physician, scientist, and microbiologist who worked as a clinician and researcher. Most well known for the discovery of an eponymous protozoal infection called Chagas disease, also called American trypanosomiasis, he also discovered the causative fungi of the pneumocystis pneumonia. He described the two pathogens in 1909, while he was working at the Oswaldo Cruz Institute in Rio de Janeiro, and named the former Trypanosoma cruzi to honour his friend Oswaldo Cruz.

<i>Trypanosoma brucei</i> Species of protozoan parasite

Trypanosoma brucei is a species of parasitic kinetoplastid belonging to the genus Trypanosoma that is present in sub-Saharan Africa. Unlike other protozoan parasites that normally infect blood and tissue cells, it is exclusively extracellular and inhabits the blood plasma and body fluids. It causes deadly vector-borne diseases: African trypanosomiasis or sleeping sickness in humans, and animal trypanosomiasis or nagana in cattle and horses. It is a species complex grouped into three subspecies: T. b. brucei, T. b. gambiense and T. b. rhodesiense. The first is a parasite of non-human mammals and causes nagana, while the latter two are zoonotic infecting both humans and animals and cause African trypanosomiasis.

<i>Trypanosoma evansi</i> Contagious protist

Trypanosoma evansi is a parasitic species of excavate trypanosome in the genus Trypanosoma that is one cause of surra in animals. Discovered by Griffith Evans in 1880 at Dera Ismail Khan, it is the first known trypanosome that causes infection. It is a common parasite in India and Iran and causes acute disease in camels and horses, and chronic disease in cattle and buffalo. In Pakistan, it has been found to be the most prevalent trypanosome species in donkeys. It is now established to infect other mammals, including humans.

Trypanosoma suis is a species of excavate trypanosome in the genus Trypanosoma that causes one form of the surra disease in animals. It infects pigs. It does not infect humans.

<span class="mw-page-title-main">Animal trypanosomiasis</span> Parasitic disease of vertebrates

Animal trypanosomiasis, also known as nagana and nagana pest, or sleeping sickness, is a disease of vertebrates. The disease is caused by trypanosomes of several species in the genus Trypanosoma such as T. brucei. T. vivax causes nagana mainly in West Africa, although it has spread to South America. The trypanosomes infect the blood of the vertebrate host, causing fever, weakness, and lethargy, which lead to weight loss and anemia; in some animals the disease is fatal unless treated. The trypanosomes are transmitted by tsetse flies.

<i>Panstrongylus geniculatus</i> Species of true bug

Panstrogylus geniculatus is a blood-sucking sylvatic insect noted as a putative vector of minor importance in the transmission of Trypanosoma cruzi to humans; this is a parasite, which causes Chagas disease. The insect is described as sylvatic; subsisting primarily in humid forests, and is also known to inhabit vertebrate nesting places such as those of the armadillo, and is also involved in enzootic transmission of T. cruzi to those species. It has wide distribution throughout 16 Latin American countries.

<i>Rhodnius prolixus</i> Kissing bug, vector of Chagas disease

Rhodnius prolixus is the principal triatomine vector of the Chagas parasite due to both its sylvatic and domestic populations in northern South America as well as to its exclusively domestic populations in Central America. It has a wide range of ecotopes, mainly savanna and foothills with an altitude of between 500 and 1,500 metres above sea level and temperatures of 16 to 28 °C. Sylvatic R. prolixus, as virtually all Rhodnius spp., is primarily associated with palm tree habitats and has a wide range of hosts including birds, rodents, marsupials, sloths, and reptiles.

<span class="mw-page-title-main">Disease vector</span> Agent that carries and transmits an infectious pathogen into another living organism

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<span class="mw-page-title-main">Protozoan infection</span> Parasitic disease caused by a protozoan

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Trypanosoma rangeli is a species of hemoflagellate excavate parasites of the genus Trypanosoma. Although infecting a variety of mammalian species in a wide geographical area in Central and South America, this parasite is considered non-pathogenic to these hosts. T. rangeli is transmitted by bite of infected triatomine bugs of the Reduviidae family, commonly known as barbeiro, winchuka(vinchuca), chinche, pito ou chupão.

Cruzipain is a cysteine protease expressed by Trypanosoma cruzi.

<i>Triatoma sanguisuga</i> Species of true bug

Triatoma sanguisuga, also known as the Eastern Bloodsucking Conenose, is an insect of the Triatominae subfamily, known as kissing bugs.

<i>Trypanosoma lewisi</i> Species of parasitic protozoan

Trypanosoma lewisi is a globally distributed parasite of Rattus species and other rodents such as mice, and of kangaroo rats in America. Among these host species were two endemic species of rats: Rattus macleari and Rattus nativitatis. Both are now believed to be extinct. It is not very clear whether or not the same parasite infected both species. However, both parasites are very similar. The northern rat flea acts as the vector for the parasite, harboring the epimastigote stage in its midgut. The trypomastigote is the stage that is present in the main host, the rodent. The epimastigote form attaches itself to the rectum of the insect using its flagella to burrow through the rectal walls. The parasites also appear in the flea's feces. Ingestion of either the flea or its feces during grooming infects the host rodent with the parasites. T. lewisi is normally non-pathogenic but is known to have produced fatal infections in rats.

<i>Triatoma gerstaeckeri</i> Species of true bug

Triatoma gerstaeckeri is an assassin bug in the genus Triatoma. It is an important vector of Trypanosoma cruzi, the causative agent of Chagas disease. The range of T. gerstaeckeri is from the south-western United States to north-eastern Mexico. T. gerstaeckeri goes through three stages during its paurometabolous life cycle: egg, nymphal instars and adult.

Phytomonas is a genus of trypanosomatids that infect plant species. Initially described using existing genera in the family Trypanosomatidae, such as Trypanosoma or Leishmania, the nomenclature of Phytomonas was proposed in 1909 in light of their distinct hosts and morphology. When the term was originally coined, no strict criterion was followed, and the term was adopted by the scientific community to describe flagellate protozoa in plants as a matter of convenience. Members of the taxon are globally distributed and have been discovered in members of over 24 plant families. Of these 24, the two main families that are infected by Phytomonas are Euphorbiaceae and Asclepiadiacae. These protists have been found in hosts between 50° latitude North and South, and thus they can be found on all continents save for Antarctica.

References

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  21. ↑ Stevens, Lori; Dorn, Patricia L.; Hobson, Julia; de la Rua, Nicholas M.; Lucero, David E.; Klotz, John H.; Schmidt, Justin O.; Klotz, Stephen A. (2012). "Vector Blood Meals and Chagas Disease Transmission Potential, United States". Emerging Infectious Diseases. 18 (4): 646–649. doi:10.3201/eid1804.111396. PMC   3309679 . PMID   22469536.
  22. ↑ Monteiro, Fernando Araujo; Weirauch, Christiane; Felix, Márcio; Lazoski, Cristiano; Abad-Franch, Fernando (2018). "Evolution, Systematics, and Biogeography of the Triatominae, Vectors of Chagas Disease". Advances in Parasitology. Vol. 99. pp. 265–344. doi:10.1016/bs.apar.2017.12.002. ISBN   978-0-12-815192-1. PMID   29530308.
  23. ↑ Reis-Cunha, João Luís; Baptista, Rodrigo P.; Rodrigues-Luiz, Gabriela F.; Coqueiro-dos-Santos, Anderson; Valdivia, Hugo O.; de Almeida, Laila Viana; Cardoso, Mariana Santos; D’Ávila, Daniella Alchaar; Dias, Fernando Hugo Cunha; Fujiwara, Ricardo Toshio; Galvão, Lúcia M. C.; Chiari, Egler; Cerqueira, Gustavo Coutinho; Bartholomeu, Daniella C. (13 November 2018). "Whole genome sequencing of Trypanosoma cruzi field isolates reveals extensive genomic variability and complex aneuploidy patterns within TcII DTU". BMC Genomics. 19 (1): 816. doi: 10.1186/s12864-018-5198-4 . PMC   6234542 . PMID   30424726.
  24. ↑ Quinde-Calderón, Leonardo; Rios-Quituizaca, Paulina; Solorzano, Luis; Dumonteil, Eric (2016). "Ten years (2004–2014) of Chagas disease surveillance and vector control in Ecuador: Successes and challenges" (PDF). Tropical Medicine & International Health. 21 (1): 84–92. doi:10.1111/tmi.12620. PMID   26458237. S2CID   25754153.
  25. ↑ "CDC Works 24/7". Centers for Disease Control and Prevention. Retrieved 2016-04-16.
  26. ↑ Messenger LA, Miles MA (2015). "Evidence and importance of genetic exchange among field populations of Trypanosoma cruzi". Acta Trop. 151: 150–5. doi:10.1016/j.actatropica.2015.05.007. PMC   4644990 . PMID   26188331.
  27. ↑ Berry, Alexander S. F.; Salazar-Sánchez, Renzo; Castillo-Neyra, Ricardo; Borrini-Mayorí, Katty; Chipana-Ramos, Claudia; Vargas-Maquera, Melina; Ancca-Juarez, Jenny; Náquira-Velarde, César; Levy, Michael Z.; Brisson, Dustin; Bartholomeu, Daniella Castanheira (20 May 2019). "Sexual reproduction in a natural Trypanosoma cruzi population". PLOS Neglected Tropical Diseases. 13 (5): e0007392. doi: 10.1371/journal.pntd.0007392 . PMC   6544315 . PMID   31107905.
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