Trypanosoma Brucei Gambiense: Difference between revisions
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==Genome Structure== | ==Genome Structure== | ||
The linear shaped unicellular parasite can range from 15- | The linear shaped unicellular parasite can range from 15-30μm long and 1.5-3.5μm in width. With a content genome of 26-megabases, 9068 predicted genes, ~900 pseudogenes and ~1700 <i>T. brucei</i> specific genes. That also contains 11 mega base-size chromosomes. | ||
The chromosomes in the DNA are organized as a supercoiled network that spans to about 50 maxicircle DNA molecules. Allowing the maxicircle in the DNA to encode up to about a dozen mitochondrial proteins. | The chromosomes in the DNA are organized as a supercoiled network that spans to about 50 maxicircle DNA molecules. Allowing the maxicircle in the DNA to encode up to about a dozen mitochondrial proteins. | ||
Latest revision as of 01:27, 13 December 2023
Classification
Eukaryota; Euglenozoa; Kinetoplastida; Trypanosomatida; Trypanosomatidae
Species
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NCBI: [1] |
Trypanosoma Brucei gambiense
Description and Significance
The genome T. Brucei gambiense is enriched in structural complexity. It is decorated with a flagellum emerging from the posterior end of its basal body. Its elongated body maintains a verbform spindle shape with tapering ends.
Trypanosoma Brucei gambienses' growth is stimulated in the blood of an intermediate host: tsetse fly's midgut, proventriculus, foregut, and salivary glands. But what defines this pathogenesis is the threat of its complex flagella and flagellar motility within mammalian hosts, and the parasitic development in the tsetse fly vector. Although the true depth of contribution of its flagella is unknown, due to its vast complexity.
Genome Structure
The linear shaped unicellular parasite can range from 15-30μm long and 1.5-3.5μm in width. With a content genome of 26-megabases, 9068 predicted genes, ~900 pseudogenes and ~1700 T. brucei specific genes. That also contains 11 mega base-size chromosomes.
The chromosomes in the DNA are organized as a supercoiled network that spans to about 50 maxicircle DNA molecules. Allowing the maxicircle in the DNA to encode up to about a dozen mitochondrial proteins.
Cell Structure, Metabolism and Life Cycle
Similar to the microorganisms that fall within the Trypanosoma family, T. Brucei gambiense shares the common tapered ends and the attachment of the long flagellum on its side.
Through a glycolysis metabolic pathway T. brucei gambiense is able to gain its proper nutrients. Converting glucose into pyruvate, that if exposed to aerobic conditions will breakdown to acetyl coenzyme and carbon dioxide. It is able to do this through the process of the TCA cycle and its reducing equivalents: NADH, FADH2, and GTP.
For energy production of carbon sources T. brucei gambiense will use ATP as an intracellular energy source. ATP is induced via catabolic nutrients of carbon, carbohydrates, fatty acids, and amino acids.
Ecology and Pathogenesis
T. b. gambiense has remained prevalent in Central and Western parts of sub-Saharan Africa. Feeding in areas that have grown largely dependent on fishing, agriculture, animal husbandry, or hunting as a means of survival. Often relying on the mutual relationship of excreted-secreted proteins that include the macrophage arginase. This genome has introduced the production of other disease in livestock: nagana, surra, mal de caderas, and dourine.
T. b. gambiense is transmitted to humans through the bite of the tsetse fly. The fly obtains the parasite from an infected human or animal and then transmits it. The life cycle of the pathogen involves a stage spent in the blood or other tissues in the vertebrate host and a stage in the gut of an invertebrate. The invertebrates that allows for the pathogen to flourish are humans, primates, and ungulates-cattle.
If ever infected a patient can have symptoms that can sometimes go unnoticed due to them being a silent carrier of the virus. Usually when the infected fly bites a human or animal it will first target the central nervous system. This will cause the dysregulation of the hosts' immune system, mental deterioration, sleep disruption, speech problems, irritably, coma, or even death.
References
Swierczewski B, & John H (2011) Trypanosoma Brucei Gambiense- an Overview. Science Direct. https://www.sciencedirect.com/topics/immunology-and-microbiology/trypanosoma-brucei-gambiense
Ralston K, Kabututu Z, Melehani J, Oberholzer M, Hill K (2009) The Trypanosoma brucei Flagellum: Moving Parasites in New Directions. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3821760/
Ooi Pheng C, & Bastin P (2013) More than meets the eye: understanding Trypanosoma brucei morphology in tsetse. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3826061/
Smith T, Bringaud F, Nolan D, Figueiredo L (2017) Metabolic reprogramming during the Trypanosoma brucei life cycle. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5461901/
Author
Page authored by Jamie Montalban Petatan, student of Prof. Bradley Tolar at UNC Wilmington.
