Difference between revisions of "African Sleeping Sickness: Trypanosome Invasion Mechanism"

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==Section==
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==Introduction==
[[Image:PHIL_1181_lores.jpg|thumb|300px|right|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 [http://www.cdc.gov/ CDC].]]
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[[Image:GettyImages-654679151-59636a305f9b583f180e29eb.jpg|thum|300px|right|The insector vector of the trypansome breci microbe, the tsetse fly]]
<br>By [My Name]<br>
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<br>By [Katie Lensmeyer]<br>
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African Sleeping Sickness (<i>Trypanosome brucei gambiense</i>) is a microbial vector driven disease that affects many parts of Africa. The disease takes action by first invading the peripheral nervous system of its host, and soon after passes the blood brain barrier to complete more neurological damage. The result of this infection is fatal to the mammalian host. From initial infection to death of the host system, this microbe needs only a few short months to become fatal. How is it that this disease can invade such secure parts of the human system so quickly? The human immune system seems to be far to advanced to let this microbe produce the effects that it does. Recent research looks deeply into both the spread of the infection through the mammalian host as well as the growth of the microbe within its vector, the tsetse fly.<br>
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The relationship between the tsetse fly and T. Brucei is that of an obligate parasite, meaning the cell needs a host cell in order to function. Once transmitted from the tsetse fly to a mammal, the microbe becomes pathogenic. Unsurprisingly, across the 36 African countries that it is found in, the tsetse fly is known to carry a variety of trypanosomiasis infections. The tsetse fly is immune to all of the trypanosome diseases that they transmit. This protection comes down to their lack of hemolymph within their blood. Their nutrient availability can not provide the microbe with the nourishment needed for the trypanosome cells to replicate into their pathogenic form. The cell does however have a mild effect on its fly host in the way that any normal parasite-host relationship would.<br>
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Phylogenetic reconstruction of this disease has shown that this disease has existed for approximately 300 million years. The microbial coexistence with its insect parasites has existed for equally as long. This ancient coexistence between African mammals and their blood-sucking insect counterparts is assumed to be why most native Animalia are not affected by the disease. This immunity, however, does not stretch to the domesticated animals of the area. Trypanosoma brucei, the form of trypanosomes that causes sleeping sickness, is expected to be a recent development within history of trypanosomes. Most researchers suspect this because Trypanosoma brucei is the only trypanosome microbe that humans are not resistant to. <ref>Steverding, Dietmar. “The History of African Trypanosomiasis.<i>Parasites & Vectors,</i> BioMed Central, 2008</ref><br>
<br><b>Legend/credit:</b> 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 [http://www.cdc.gov/ CDC].
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Sleeping Sickness is a unique microbe that, despite its phylogenetic relatives, is extremely pathogenic to humans and other mammals. What is the disease mechanism to this harmful cell? Research explored here aims to explain the inoculation of the disease within both the host and the parasite, as well as explains how the unique symptoms of the disease are produced within the infected human host.<br>
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==Section 1==
 
==Section 1==

Revision as of 20:24, 6 May 2018

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Introduction

The insector vector of the trypansome breci microbe, the tsetse fly


By [Katie Lensmeyer]

African Sleeping Sickness (Trypanosome brucei gambiense) is a microbial vector driven disease that affects many parts of Africa. The disease takes action by first invading the peripheral nervous system of its host, and soon after passes the blood brain barrier to complete more neurological damage. The result of this infection is fatal to the mammalian host. From initial infection to death of the host system, this microbe needs only a few short months to become fatal. How is it that this disease can invade such secure parts of the human system so quickly? The human immune system seems to be far to advanced to let this microbe produce the effects that it does. Recent research looks deeply into both the spread of the infection through the mammalian host as well as the growth of the microbe within its vector, the tsetse fly.

The relationship between the tsetse fly and T. Brucei is that of an obligate parasite, meaning the cell needs a host cell in order to function. Once transmitted from the tsetse fly to a mammal, the microbe becomes pathogenic. Unsurprisingly, across the 36 African countries that it is found in, the tsetse fly is known to carry a variety of trypanosomiasis infections. The tsetse fly is immune to all of the trypanosome diseases that they transmit. This protection comes down to their lack of hemolymph within their blood. Their nutrient availability can not provide the microbe with the nourishment needed for the trypanosome cells to replicate into their pathogenic form. The cell does however have a mild effect on its fly host in the way that any normal parasite-host relationship would.

Phylogenetic reconstruction of this disease has shown that this disease has existed for approximately 300 million years. The microbial coexistence with its insect parasites has existed for equally as long. This ancient coexistence between African mammals and their blood-sucking insect counterparts is assumed to be why most native Animalia are not affected by the disease. This immunity, however, does not stretch to the domesticated animals of the area. Trypanosoma brucei, the form of trypanosomes that causes sleeping sickness, is expected to be a recent development within history of trypanosomes. Most researchers suspect this because Trypanosoma brucei is the only trypanosome microbe that humans are not resistant to. [1]

Sleeping Sickness is a unique microbe that, despite its phylogenetic relatives, is extremely pathogenic to humans and other mammals. What is the disease mechanism to this harmful cell? Research explored here aims to explain the inoculation of the disease within both the host and the parasite, as well as explains how the unique symptoms of the disease are produced within the infected human host.

Section 1

Include some current research, with at least one figure showing data.

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Section 2

Include some current research, with at least one figure showing data.

Section 3

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Section 4

Conclusion

References

  1. Steverding, Dietmar. “The History of African Trypanosomiasis.” Parasites & Vectors, BioMed Central, 2008



Authored for BIOL 238 Microbiology, taught by Joan Slonczewski, 2018, Kenyon College.