Tsetse Fly Essay

Published: 2021-06-29 02:00:24
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Tsetse FlyAfrican sleeping sickness is an infectious disease of tropical Africa.
This infectious disease is caused by a protozoan organism that exists as a parasite in the blood of a number of vertebrate hosts. There are three variations of the disease that predominate in humans are transmitted by an insect vector: Two types of African sleeping sickness are caused by the following: Trypanosoma rhodesiense and T. gambiense, both transmitted by the bite of the tsetse fly. Trypanosome, which early symptoms include fever, headache, and chills, followed by anaemia and joint pains. Later, the disease attacks the central nervous system, causing drowsiness, lethargy, and, if left untreated, death.
The cycle of this deadly disease starts out with the tsetse fly and usually end in death if untreated. Tsetse flies are classified in the phylum Arthropoda, class insecta, order Diptera, family Trypanosoma. Tsetse flies are unusual insects. The medium to large brown flies are between six to 14mm long, excluding its proboscis (which is the trunk-like process of the head). The wings are folded and scissor-like while at rest and extend a short distance beyond the end of the abdomen.
Other flies have their wings projecting side-ways unlike the tsetse fly, which has overlapping wings. Tsetse flies are confined to Africa. There are 390 different species and four are found in Zambia. They are in the same family as the house and horse flies, they feed extensively on blood be it that of humans or animals. They are parasites that live in the blood or tissue of humans and other vertebrates.
Egg and larval stages develop within the female. The female fly produces only one egg at a time. The larva hatches from the egg and is nourished during the growing period inside the body of the parent. When the larva is full-grown, it is deposited on the ground, and it becomes a pupa. She gives birth every 9 to 10 days.
Tsetse flies mate only once, but that mating provides enough sperm to fertilize the female throughout her 90 to 100 day lifespan. Female tsetses produce at most nine larvae and therefore have one of the lowest reproduction rates in the insect world. The single-celled trypanosomes that cause sleeping sickness spend their time cycling between humans and tsetse flies. They linger in the gut of the fly, absorbing amino acids and other molecules that the fly gets by biting mammals. After about ten days the trypanosomes move into the fly’s salivary glands.
The larva of the tsetse fly develops inside the body of the mother until it is ready to pupate in the soil. A number of the 21 species can transmit to humans the trypanosomes that cause the Gambian and Rhodesian forms of African sleeping sickness. The tsetse fly also carries the trypanosomes that cause nagana and other diseases of wild and domestic animals. Clearing the brush that the flies inhabit helps to get rid of them; DDT has also been used to exterminate them. The vast majority of human infections result from inoculation with the trypanosome by tsetse flies as they suck human blood. The flies become infected while feeding on the blood of people or other mammals that are already infected with the parasite.
The flies usually cannot infect people or animals until the germs have lived in their bodies several days and have passed through the stomach to their salivary glands. Then, for at least 96 days, the flies can transmit the parasites to anyone they bite. During this time the trypanosomes multiply by binary division in the midgut of the fly, then migrate to the salivary glands, and pass out of the fly’s proboscis in droplets of saliva during the fly’s bloodsucking. To prepare for their new home, the parasites cloak themselves in a coat made of millions of copies of a single sugary molecule.
Our immune cells fashion antibodies that correspond to this molecule’s shape, and the antibodies enable the immune system to kill the parasite in huge numbers. But some individual trypanosomes take evasive action. They shut down the genes they use to build their coat and turn on a new set in their place. They can then build a new surface molecule, one similar enough to the old one to do the job but which no longer matches the antibodies. Now invisible, the parasite thrives while the immune system starts a new eradication campaign from scratch. But trypanosomes have hundreds of coat-coding genes that they hold in reserve, and they can easily continue to slip away from the body’ s attack.
After this saliva has been lying in the humans for about one to two weeks, the trypanosomes are then found in large numbers in the circulating blood of the victim. The disease starts to take on noticeable symptoms, the lymph nodes and spleen are invaded first, and they become swollen, soft, and tender. The lymph nodes at the back of the neck become enlarged (known as Winterbottom’s sign) this is a common sign of the disease. Irregular fever and delayed sensation to pain are also characteristic symptoms at this stage. After these symptoms appear the trypanosomes proceed to invade the brain and spinal cord.
This results in neurological symptoms including severe headache, mental dullness and apathy, a weary shuffling gait, tremors, spastic or flaccid paralysis, chorea, and a profound sleepiness that develops during a meal or when the patient is standing or walking. These symptoms are followed by increasing emaciation, coma, and death. The tsetse fly has a deadly bite that causes African sleeping sickness. The disease causes the body and mind to break down until if it is left untreated death is inevitable. Word count 1085Bibliographyhttp://www. britannica.
com/seo/s/sleeping-sickness/The Columbia Encyclopedia, Fifth Edition, 01-01-1993Kinley, David H. , III, Aerial assault on the tsetse fly: researchers have found a way to eradicate thedisease-carrying tsetse fly from Zanzibar. Vol. 40, Environment, 09-01-1998, pp 14(7). Sandra J. Glover, Tsetse fly.
, World Book Encyclopedia, 01-01-2000Zimmer, Carl, A sleeping storm. (Sleeping sickness in Africa). Vol. 19, Discover Magazine, 08-01-1998, pp 86(9).

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