Trypanosoma cruzi: pathogenesis, epidemiology, and recent developments in the potential treatment of Chagas' disease: Difference between revisions

From MicrobeWiki, the student-edited microbiology resource
Line 6: Line 6:
<i>Trypanosoma cruzi</i> is a protozoan parasite that is most frequently transmitted through triatomine bugs. The genome of <i>T. cruzi</i> was fully sequenced in 2005. [[#References|[8]]] Triatomine bugs belong to the Rediviidae family and are colloquially known as “kissing bugs” due to sucking blood near the victim’s face when feeding. [[#References|[4]]] The infection of <i>T. cruzi</i> results in a lifelong condition known as American trypanosomiasis or Chagas disease. Although only a few species are known to cause Chagas disease, over 130 Triatomine bugs species have been identified. [[#References|[6]]] At least eleven species of triatomine bugs are confirmed to be capable of transmitting the <i>T. cruzi</i> parasite. [[#References|[2]]] Of these Triatoma infestans, Rhodnius prolixus, and Triatoma dimidiate result in the highest number of infections. Triatonimes themselves appear to be unaffected by <i>T. cruzi</i> infections. [[#References|[6]]]
<i>Trypanosoma cruzi</i> is a protozoan parasite that is most frequently transmitted through triatomine bugs. The genome of <i>T. cruzi</i> was fully sequenced in 2005. [[#References|[8]]] Triatomine bugs belong to the Rediviidae family and are colloquially known as “kissing bugs” due to sucking blood near the victim’s face when feeding. [[#References|[4]]] The infection of <i>T. cruzi</i> results in a lifelong condition known as American trypanosomiasis or Chagas disease. Although only a few species are known to cause Chagas disease, over 130 Triatomine bugs species have been identified. [[#References|[6]]] At least eleven species of triatomine bugs are confirmed to be capable of transmitting the <i>T. cruzi</i> parasite. [[#References|[2]]] Of these Triatoma infestans, Rhodnius prolixus, and Triatoma dimidiate result in the highest number of infections. Triatonimes themselves appear to be unaffected by <i>T. cruzi</i> infections. [[#References|[6]]]


There is less research and international concern for <i>T. cruzi</i> and Chagas disease than what many scientists believe is required. The World Health Organization (WHO) has categorized Chagas Disease as “one of the world’s 13 most neglected tropical diseases.” [[#References|[6]]] Although the disease and parasite were discovered over a century ago, there remains to be a lack in scientific efforts for better treatment and cures. The human infection of Chagas disease is endemic to Latin America. [[#References|[11]]] Although Chagas disease was once centered in Latin America, it has gradually spread across the world.[[#References|[6]]] Chagas, a Brazillian physician initially identified the disease in 1909.  Later, it was discovered that Chagas disease had afflicted humans at least as early as 9000 years ago when <i>T. cruzi</i> DNA was isolated from human mummies. Some historians believe that Charles Darwin may have suffered from Chagas Disease according to his recorded accounts of coming in contact with triatomine in South America and symptoms later in life. <ref>Rassi, Anis, and José Antonio Marin-Neto. "Chagas disease." The Lancet 375.9723 (2010): 1388-1402.</ref> Since the turn of the century, the incidence rates of Chagas disease has greatly decreased. [[#References|[11]]]
There is less research and international concern for <i>T. cruzi</i> and Chagas disease than what many scientists believe is required. The World Health Organization (WHO) has categorized Chagas Disease as “one of the world’s 13 most neglected tropical diseases.” [[#References|[6]]] Although the disease and parasite were discovered over a century ago, there remains to be a lack in scientific efforts for better treatment and cures. The human infection of Chagas disease is endemic to Latin America. [[#References|[11]]] Although Chagas disease was once centered in Latin America, it has gradually spread across the world.[[#References|[6]]] Chagas, a Brazillian physician initially identified the disease in 1909.  Later, it was discovered that Chagas disease had afflicted humans at least as early as 9000 years ago when <i>T. cruzi</i> DNA was isolated from human mummies. Some historians believe that Charles Darwin may have suffered from Chagas Disease according to his recorded accounts of coming in contact with triatomine in South America and symptoms later in life. [[#References|[6]]] Since the turn of the century, the incidence rates of Chagas disease has greatly decreased. [[#References|[11]]]





Revision as of 18:16, 28 April 2017

Background and Significance

Emigration routes of individuals with Chagas disease. Numbers indicate total infected individuals in various regions. Nature.

By [Sriya Chadalavada]


Trypanosoma cruzi is a protozoan parasite that is most frequently transmitted through triatomine bugs. The genome of T. cruzi was fully sequenced in 2005. [8] Triatomine bugs belong to the Rediviidae family and are colloquially known as “kissing bugs” due to sucking blood near the victim’s face when feeding. [4] The infection of T. cruzi results in a lifelong condition known as American trypanosomiasis or Chagas disease. Although only a few species are known to cause Chagas disease, over 130 Triatomine bugs species have been identified. [6] At least eleven species of triatomine bugs are confirmed to be capable of transmitting the T. cruzi parasite. [2] Of these Triatoma infestans, Rhodnius prolixus, and Triatoma dimidiate result in the highest number of infections. Triatonimes themselves appear to be unaffected by T. cruzi infections. [6]

There is less research and international concern for T. cruzi and Chagas disease than what many scientists believe is required. The World Health Organization (WHO) has categorized Chagas Disease as “one of the world’s 13 most neglected tropical diseases.” [6] Although the disease and parasite were discovered over a century ago, there remains to be a lack in scientific efforts for better treatment and cures. The human infection of Chagas disease is endemic to Latin America. [11] Although Chagas disease was once centered in Latin America, it has gradually spread across the world.[6] Chagas, a Brazillian physician initially identified the disease in 1909. Later, it was discovered that Chagas disease had afflicted humans at least as early as 9000 years ago when T. cruzi DNA was isolated from human mummies. Some historians believe that Charles Darwin may have suffered from Chagas Disease according to his recorded accounts of coming in contact with triatomine in South America and symptoms later in life. [6] Since the turn of the century, the incidence rates of Chagas disease has greatly decreased. [11]


Humans are typically bitten when asleep. As the face is often left uncovered, most bites occur in this area. Prior to feeding, kissing bugs extend mouthparts from underneath their body. It is then used to feed on blood. [12] Feeding can continue for up to a few minutes. If interrupted when feeding, kissing bugs may leave a cluster of bites. Defecating during feeding is common. [4] Chagas disease spreads to humans when the fecal matter of T. cruzi enters the bloodstream through a break in the skin. Very rarely, it can also be transmitted if consumed with food or drink. [2][6]


T. cruzi is a hemoflagellate, meaning it can live in the bloodstream and has flagella. T. cruzi has a life cycle with three stages: epimastigotes, trypomastigotes, and amastigotes. Replication occurs at the epimastigotic stage, typically in the midgut of kissing bugs. They then become trypomastigotes. This process differentiates the stage from when T. cruzi is nonpathogenic to becoming pathogenic. They are non-replicative. When the insect defecates, the parasite is also released and has the ability to enter the bloodstream and infect a mammalian host. Once inside cells, the T. cruzi begin transforming to amastigotes, the principal form of the parasite in vertebrate hosts. [4] T. cruzi replicate through binary fission. [13]While other mammalian tryposomes divide in the bloodstream, T. cruzi can only replicate in cells. [21] Following replication for multiple generations, they then become trypomastigotes before leaving infected cells for new cells. They then alternate between these last two stages as they enter and leave cells. [14]


There has been research on additional physiological, biochemical, and pathological variations between these forms. As epimastigotes transform to trypomastigotes, there are notable changes to multiple organelles, primarily within the mitochondria and glycosomes. During this stage of differentiation, the parasite was also found to accumulate significantly more lipids to use as its primary energy reserve. [17] Epimastigotes exhibit lower negative surface charges than trypomastigotes. This was found to be due to the presence of increased sialic acid on the surface of the trypomastigotic form. [19]The epimastigotic form of T. cruzi fixes CO2 as facultative anaerobe and produces succinate during glucose metabolism. It is believed that either PEP carboxykinase or malic enzyme is responsible for CO2 fixation. [23]













Double brackets: [[
Filename: Trypanosoma_Cruzi.jpeg
Thumbnail status: |thumb|
Pixel size: |300px|
Placement on page: |right|
Legend/credit: Electron micrograph of the Ebola Zaire virus. This was the first photo ever taken of the virus, on 10/13/1976. By Dr. F.A. Murphy, now at U.C. Davis, then at the CDC.
Closed double brackets: ]]

Other examples:
Bold
Italic
Subscript: H2O
Superscript: Fe3+

Epidemiology

Pathogenesis

Treatment

References


1. de Andrade, Ana Lucia S. Sgambatti, et al. "Randomised trial of efficacy of benznidazole in treatment of early Trypanosoma cruzi infection." The Lancet 348.9039 (1996): 1407-1413.

2. Montgomery, Susan P., et al. "Neglected parasitic infections in the United States: Chagas disease." The American journal of tropical medicine and hygiene 90.5 (2014): 814-818.

3. Bustamante, Dulce M., et al. "Ecological, social and biological risk factors for continued Trypanosoma cruzi transmission by Triatoma dimidiata in Guatemala." PLoS One 9.8 (2014): e104599.

4. Klotz, John H., et al. "“Kissing bugs”: potential disease vectors and cause of anaphylaxis." Clinical Infectious Diseases 50.12 (2010): 1629-1634.

5. History of insecticide resistance of Triatominae vectors, 48, Revista da Sociedade Brasileira de Medicina Tropical, 2015

6. Rassi, Anis, and José Antonio Marin-Neto. "Chagas disease." The Lancet 375.9723 (2010): 1388-1402.

7. Cardoso, Mariana S., João Luís Reis-Cunha, and Daniella C. Bartholomeu. "Evasion of the immune response by Trypanosoma cruzi during acute infection." Frontiers in immunology 6 (2016): 659.

8. El-Sayed, Najib M., et al. "The genome sequence of Trypanosoma cruzi, etiologic agent of Chagas disease." Science 309.5733 (2005): 409-415.

9. Trischmann, Thomas, et al. "Trypanosoma cruzi: role of the immune response in the natural resistance of inbred strains of mice." Experimental parasitology 45.2 (1978): 160- 168.

10. Ibarra-Cerdeña, Carlos N., et al. "Ecology of north american triatominae." Actatropica 110.2 (2009): 178-186.

11. Abad-Franch, Fernando, et al. "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 (2009): 159-177.

12. Schofield, C. J., and Cleber Galvão. "Classification, evolution, and species groups within the Triatominae." Acta tropica 110.2 (2009): 88-100.

13. Combs, Terry P., et al. "The adipocyte as an important target cell for Trypanosoma cruzi infection." Journal of Biological Chemistry 280.25 (2005): 24085-24094.

14. Bonaldo, Myrna Cristina, et al. "Cell-substrate adhesion during Trypanosoma cruzi differentiation." The Journal of cell biology 106.4 (1988): 1349-1358.

15. Cunha-Neto, Edécio, et al. "Autoimmunity in Chagas' disease. Identification of cardiac myosin-B13 Trypanosoma cruzi protein crossreactive T cell clones in heart lesions of a chronic Chagas' cardiomyopathy patient." Journal of Clinical Investigation 98.8 (1996): 1709.

16. Cantey, Paul T., et al. "The United States Trypanosoma cruzi Infection Study: evidence for vector‐borne transmission of the parasite that causes Chagas disease among United States blood donors." Transfusion 52.9 (2012): 1922-1930.

17. Soares, M. J., et al. "A stereological study of the differentiation process inTrypanosoma cruzi." Parasitology research 75.7 (1989): 522-527.

18. De Souza, E. M., et al. "Antiparasitic activity of aromatic diamidines is related to apoptosis-like death in Trypanosoma cruzi." Parasitology 133.01 (2006): 75-79.

19. Souto-Padron, T., et al. "Further studies on the cell surface charge of Trypanosoma cruzi." Acta tropica 41.3 (1984): 215-225.

20. Piñeyro, María Dolores, et al. "Peroxiredoxins from Trypanosoma cruzi: virulence factors and drug targets for treatment of Chagas disease?." Gene 408.1 (2008): 45-50.

21. Culbertson, James T., and Maxwell H. Kolodny. "Acquired immunity in rats against Trypanosoma cruzi." The Journal of Parasitology 24.1 (1938): 83-90.

22. Hauschka, Theodore S. "Sex of host as a factor in Chagas' disease." The Journal of parasitology 33.5 (1947): 399-404.

23. de Flombaum, María A. Cataldi, et al. "CO2-fixing enzymes in Trypanosoma cruzi." Comparative Biochemistry and Physiology Part B: Comparative Biochemistry 58.1 (1977): 67-69.

24. Fragata Filho, Abílio Augusto, Marco Aurélio Dias da Silva, and Elias Boainain. "Ethiological treatment of acute and chronic Chagas' heart disease." Sao Paulo Medical Journal 113.2 (1995): 867-872.




Authored for BIOL 238 Microbiology, taught by Joan Slonczewski, 2017, Kenyon College.