The Parasites Tryanosomes

Categories: Disease

Trypanosomes are unicellular parasites. They come from the genus Trypanosoma, the family Trypanosomatidae, and the order Kinetoplastida. They cause diseases in animals and humans in Africa. They are blood parasites that go into the vertebrate, the tissue fluid, and the blood. Trypanosomes use their flagellum and the undulating membrane to move through the blood and tissue fluid. The way the trypanosome moves can determine what species the parasite is. Trypanosomes reproduce through binary fission to create two daughter cells. First the kinetoplast divides, then the paranasal body develops.

The nucleus divides, and the rest of the trypanosome body recreates all the structures that are in the cytoplasm.

Finally, the entire body divides (“African Animal Trypanosomes”). The basic morphology of trypanosomes is a parasite that is single celled. The trypanosomes does everything a unicellular organism does, including respiration, excretion, reproduction, and digestion. It has protoplasm and is suspended in cytoplasm. The biggest part of the cell is the nucleus, which controls the cell and helps with reproduction.

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It contains deoxyribonucleic acid. The cytoplasm can also have small granules. Trypanosomes adapt to their environment, from moving and living in the blood or lymph fluid of the host. Trypanosomes are streamlined, tapered at both ends, and elongated. The outer layer of the cytoplasm is flexible but durable, which allows the trypanosome to move freely. There is also a flagellum and a undulating membrane, which is a thin tissue that runs along the outer part of the flagellum and the length of the body.

The trypanosomes have well defined bodies that differ in size depending on the kind of species.

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It has kinetoplast, which helps with metabolism, reproduction, and is important for the cyclical transmission through the tsetse flies. Some morphological characteristics are the different shape of the body and the average length of the trypanosome (“African Animal Trypanosomes”).There are also differential morphology. Trypanosomes are different in size, shape, and appearance. Scientists study the different individual trypanosomes to identify them, reveal more possible species, and discover if there are mixed infections. To identify the different trypanosomes, scientists look at the presence or absence of trypanosomes of different appearance, the size, the presence or absence of a flagellum, the position and size of the kinetoplast, the shape of the parasite, the posterior end of the parasite, and the development stage of the undulating membrane (“African Animal Trypanosomes”).

Trypanosomes have four different stages of its development: trypomastigotes, epimastigotes, promastigotes, and amastigotes. During the trypomastigote stage, the kinetoplast is posterior and the flagellum forms a long undulating membrane. In the epimastigote stage, the kinetoplast is anterior and the flagellum forms a short undulating membrane. The promastigote has a kinetoplast, a short flagellum, but no prominent undulating membrane. Finally, the amastigotes have kinetoplast but no prominent flagellum or undulating membrane (“Trypanosoma”). The pathophysiology of trypanosomes is that a fly injects the trypanosome into the bloodstream, and they multiple by binary fission. Then, they spread through the bloodstream. A group of the trypanosomes avoid the immune destruction by changing in the variant surface glycoprotein and then multiply. Later, the trypanosomes go to the fluid of the organs and eventually the central nervous system. This continues when the tsetse fly bites an infected animal or person (Pearson).

The ecology of trypanosomes are their vectors and the host of the species. Trypanosoma brucei are commonly carried by the tsetse fly, which can be mainly found in Central and Western Africa. The tsetse flies have migrated in masses over the past forty years, causing an increase in the number of cases. The ecological role of trypanosomes are that they are parasites carried by the tsetse fly (“Trypansoma”). For genetics, the major surface antigens of Trypanosoma brucei are procyclin at the procyclic stage and the variant surface glycoprotein at the bloodstream stage. The differences in the variant surface glycoprotein prevent trypanosomes from being affected by the antibody response of its host. This happens through not having DNA arrangement in the different telomeric variant surface glycoprotein genera expression sites or through having DNA rearrangement telomeric variant surface glycoprotein gene expression site. The genes of procyclin and variant surface glycoprotein are from polycistronic transcription units. “Although the promoters of these units are both active at the two main stages of the parasite life cycle, stage-specific controls operating at the level of RNA elongation and processing lead to strictly differential expression of the end products of the two units” (Pays).

Procyclin and the variant surface glycoprotein have similar characteristics even though the have different expressional roles. They both have a similar gene and make the copy of genetic information by the same type of RNA polymerase. There are eight genes in the variant surface glycoprotein transcription unit, but the purpose of the other genes is unidentified (Pays). Trypanosomes contact with the immune system through the blood and lymph. Trypanosomes operate through antigenic variation, which is a mechanism that changes between the 107 surface proteins to escape the immune response. Five percent of the protein of the trypanosome is made up of the surface variant surface glycoprotein molecules. There are about fifty variant surface glycoprotein genes and over 950 pseudo-variant surface glycoprotein in the genome. All of the variant surface glycoprotein are inactive for transcription except for one.

The active variant surface glycoprotein translates and duplicates to one of twenty variant surface glycoprotein extrusion sites. Each expression site is by a chromosomal telomere. Only one expression site is active, which is located in the nucleus. In the nucleus, it is transcribed by RNA polymerase (Donelson). Lab staining of trypanosomes is usually with a giemsa stain. Blood is collected and sodium citrate or heparin is used to prevent the clotting of blood (“Giemsa Stain”). The slide can be prepared as a thin blood film (see fig. 1), a thick blood film (see fig. 2), or a combination of both (“Trypanosomiasis, African”). There are two main mechanical ways of transmission. The first way is by the insect biting. The insect passes blood from an infected animal to another through its feeding. Because trypanosomes die when the blood dries, the time in between feeding is very important. It can also move by using needles or surgical instruments that have been infected with blood that has trypanosomes.

There are other less common forms of transmission. Ingesting the meat of an animal that has been infected with trypanosomes. Trypanosomes can also transmit from a mother to her offspring by moving through the placenta or through bleeding during birth (“African Animal Trypanosomes”). Different trypanosomes associate with different hosts. Trypanosoma brucei gambiense associates with humans and domestic animals through the tsetse fly, causing African sleeping sickness in West Africa. Trypanosoma brucei rhodesiense affects humans and certain mammals through the tsetse fly, which causes African sleeping sickness in East Africa. Trypanosoma brucei brucei cause trypanosomiasis in Africa and associates with mammals because of the tsetse fly. Trypanosoma congolense associates with domestic animals and cattle through the tsetse fly, causing trypanosomiasis in Africa.

Trypanosoma vivax affects horses by the tsetse fly and causes trypanosomiasis in Africa. Trypanosoma simiae associates with mammals through the tsetse fly, causing trypanosomiasis in Africa (“Trypanosoma”). The life cycle of trypanosomes happen in two phases: one phase happens in the insect and the other happens in the host. At first, the tsetse fly does not have trypanosomes. The fly will acquire the infection when it feeds on a mammal that has the parasite in its blood. The trypanosomes develop and multiply in the digestive system of the fly. Then, the fly remains infected for the rest of its life. When the fly feeds, it breaks into skin. When a small pool of blood is formed, the fly injects its saliva. Then the trypanosomes enters into the animal through the fly’s saliva (“African Animal Trypanosomes”). In the mammal host, the infective trypanosomes grow and multiply at the chancre. When the trypanosomes mature, they are released into the lymph nodes and lymph vessels and into the blood circulation.

The trypanosomes reproduces though binary division. They feed by absorbing the nutrients of the host through its membranes. Oxygen, proteins, fats, and carbohydrates are digested by enzyme systems of the protoplasm of the trypanosomes, and wastes are dispelled in the opposite manner. In the tsetse fly, the trypomastigotes change into epimastigotes, which are long and slender. The epimastigotes grow and multiple until they are fully developed (“African Animal Trypanosomes”). There are two different types of African trypanosomiasis. East African trypanosomiasis is caused by the parasite Trypanosoma brucei rhodesiense. Aching muscles and joints, fever, swollen lymph nodes, severe headaches, irritability, and extreme fatigue are all symptoms of East African trypanosomiasis. A chancre, which is a red sore where the tsetse fly bit into the skin, can also be a sign of this disease.

If left untreated, patients can also experience personality changes, progressive confusion, other neurological problems, or even death (“CDC: East African Trypanosomiasis”). West African trypanosomiasis is caused by the parasite Trypanosoma brucei gambiense. A chancre usually develops. A patient can experience swelling of the hands and feet, rashes, fever, itching skin, aching muscles and joints, fatigue, headache, and the swelling of the lymph nodes. If left untreated, a patient can experience weight loss, confusion, feeling the need to sleep during the day and disturbances in sleeping at night, personality changes, partial paralysis, hormonal imbalances, problems with balance and coordination, and eventually death (“CDC: West African Trypanosomiasis”).

Trypanosoma brucei rhodesiense are easily found in blood and the lymph node fluids. Trypanosoma brucei gambiense can only be found through microscopic examination of the lymph nodes; it is usually hard to detect it in the blood. Anyone who is diagnosed with African trypanosomiasis have to have their cerebrospinal fluid examined to see if the parasite has moved into the central nervous system (“CDC: Diagnosis”). African trypanosomiasis occurs in two stages. At first, the parasite goes to the peripheral circulation. The second stage consists of the parasite crossing into the blood-brain barrier; this allows the parasite to invade the central nervous system. The different types of trypanosome infect differently. Trypanosoma brucei rhodesiense progresses fast. A patient will have a sore and develop symptoms within the first and second week of being bit. After a few weeks, the parasite goes into the central nervous system and causes neurological problems. Then, the patient will likely die in a few months from first being bit.

Trypanosoma brucei gambiense presses a lot slower. The symptoms are mild at first. After one or two years, the central nervous system is affected, but it is affected slightly at first. If a patient is untreated, they can live with it for six to seven years, but most die after three years (“CDC: Disease”). There are no known cures for African trypanosomiasis, but there are treatments. The drugs and treatments are different for Trypanosoma brucei rhodesiense and Trypanosoma brucei gambiense, and it also depends on if the parasite has invaded into the central nervous system. Pentamidine is used for the beginning stages of Trypanosoma brucei gambiense. There are other drugs, like nifurtimox, suramin, eflornithine, and melarsoprol, but a patient can only receive these drugs through the Center of Disease Control. After being treated, a patient’s cerebrospinal fluid must be examined every two years to ensure that the disease has not moved into the central nervous system (“CDC: Treatments”).

Even though there are no cures, there are things that can prevent and control African trypanosomiasis. While being in areas that are heavily infested with the tsetse fly, a person should wear long sleeve shirts and clothing with neutral colors because the tsetse fly is attracted to bright colors. Clothing should also be thick so the fly cannot bite through the material. A person should also inspect vehicles before driving because the flies are attracted to the dust and motion of moving vehicles. The use of insect repellent helps prevent the flies from biting. A person should also avoid bushes because the flies stay in bushes to avoid the heat during the day. To control African trypanosomiasis, people must control the tsetse fly vector and reduce the disease reservoir (“CDC: Prevention and Control”). In “The Origins of a New Trypanosoma Brucei Rhodesiense Sleeping Sickness Outbreak in Eastern Uganda,” E.M. Fevre, P.G. Coleman, M. Odiit, J.W. Magona, S.C. Welburn, and M.E.J. Woolhouse discovered the origins of Sleeping sickness in an area that previously was not affected by the disease. They found that in the Soroti Disctrict, there was a large-scale restocking of cattle.

The domestic cattle can hold Trypanosoma Brucei Rhodesiense, meaning that the cattle could be the origin of the outbreak of the disease. They did a controlled case study to see if the distance from the market to the villages could be a risk factor for the disease. In this case study, they observed the clustering of the cases of the sleeping sickness to see if the outbreak was relevant to the villages that buy from the market. They discovered that more than half of the cattle from the market were in areas that had an outbreak of sleeping sickness. They also discovered that the distance from the market to the village was a significant risk factor for the disease. Villages close to the market had more cases of sleeping sickness. As the outbreak grew, the cases moved further from the market. They concluded that the cattle from the market was infected.

As people bought the cattle, they brought the disease to their villages, and the disease moved from there. To control the disease, public health measures have to control the animal reservoir and make sure that the cattle being sold is not infected (Fevre). In “Silencing Subtelomeric VSGs by Trypanosoma brucei RAP1 at the Insect Stage Involves Chromatin Structure Changes,” the researchers conducted an experiment where they removed Trypanosoma brucei RAP1 in the pro cyclic form cells by the use of an analytical RNA interference approach. They analyzed the changes in the levels of mRNA in the bloodstream expression site and the metacyclic variant surface glycoprotein after the removal of Trypanosoma brucei RAP1.They preformed a micrococcal-nuclease digestion assays and a FAIRE analysis to figure out the effect of the Trypanosoma brucei RAP1 deficiency on the structure of the chromatin. There was a derepression of metacyclic variant surface glycoproteins in the procyclic form stages and the bloodstream form when there was a deficiency of Trypanosoma brucei RAP1 because of the RNA interference.

Depending on the Trypanosoma brucei RAP1, there is a silence in the bloodstream expression site linked variant surface glycoproteins in procyclic form cells and in the bloodstream form cells. The elimination of Trypanosoma brucei RAP1 causes the chromatin structure to loosen in pro cyclic form calls but not in bloodstream form cells. This shows that there are different mechanisms used during the silencing of Trypanosoma brucei RAP1 that affect the chromatin structure’s modulation in pro cyclic form cells. Their experiments showed that Trypanosoma brucei RAP1 is an important variant surface glycoprotein silencer. They also found that Trypanosoma brucei RAP1 regulates the structure of the chromatin in the loci within the genes in the insect (Pandya). Trypanosomes are unicellular parasites that cause African Trypanosomiasis, otherwise known as sleeping sickness. This disease travels by the tsetse fly because the trypanosome lives part of their live in the fly until the fly bites a human or animal and passes the trypanosomes through the site of contact. Trypanosomes are parasites found in the bloodstream, spinal fluid, and lymph of humans and animals and affect the central nervous system causing neurological problems.

Works Cited

  1. Donelson, John. The Biochemistry of Antigenic Variation in African Trypanosomes. University of Iowa. n.d. Web. 4 Feb 2016.
  2. Fevre, E.; Coleman, P.; Odiit, M.; Magona, J.; Welburn, S.; Woolhouse, M. “The Origins of a New Trypanosoma Brucei Rhodesiense Sleeping Sickness Outbreak in Eastern Uganda” The Lancet. 25 Aug 2001: Pg. 625-628. Web. P
  3. andya, U.; Sandhu, R.; & Li, B. “Silencing Subtelomeric VSGs by Trypanosoma brucei RAP1 at the Insect Stage Involves Chromatin Structure Changes.” Epigenetics & Chromatin. 18 March 2013: Web
  4. Pays, E. “Genetics of Antigenic Variation in African Trypanosomes.” Research in Microbiology. 1 991: pg 731-735. Web.
  5. Pearson, Richard D. African Trypanosomiasis. Merck Manual, n.d. Web. 17 Feb 2016.
  6. African Animal Trypanosomes. FAO Corporate Document Repository, n.d. Web. 31 Jan 2016.
  7. CDC: Diagnosis. Centers for Disease Control and Prevention, 29 Aug 2012. Web. 29 Jan 2016.
  8. CDC: Disease. Centers for Disease Control and Prevention, 29 Aug 2012. Web. 29 Jan 2016.

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The Parasites Tryanosomes. (2021, Sep 29). Retrieved from

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