African Sleeping Sickness: Tyrpanosome Invasion Mechanism

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The insect vector of the trypanosome microbe, the tsetse fly. These flies are found in tropical parts of Southern Africa and are the only known vector for African Sleeping Sickness [3].

By Katie Lensmeyer

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African Sleeping Sickness 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 passing the blood brain barrier to damage neurons within the brain leaving fatal results for the infected host. How is it that this disease can invade such secure parts of the human system so quickly? What is the disease mechanism for this harmful microbe?

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What is African Sleeping Sickness?

African Sleeping Sickness affects 30,000 people every year. The disease has been found in 37 African countries, all in the Sub-Saharan areas. [4].

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African Trypanosomiasis, or better known as African Sleeping Sickness, is a parasite driven infection of the human nervous system. The disease is caused by the microbial parasites of the species Trypanosoma brucei and than transmitted through the tsetse fly, found only in rural parts of Africa. Throughout history, this disease has been classified as a public health problem seen primarily in sub-saharan areas of Africa. About 10,000 cases of the disease are reported every year to the World Health organization, but unfortunately it is expected that most cases go unreported and/or undiagnosed.
Because this disease is vector borne, the microbe, trypanosome brucei, enters the human system by ways of the skin. An infected tsetse fly must bite the host, and through this wound the protozoan enters the system. After initial infection, the disease has two stages. The first of these stages is the time in which the parasite is found within the peripheral nervous system, but has not yet made its way into the central nervous system. The second stage begins when the infection has passed the blood brain barrier and resides within the central nervous system. The disease than acts quickly, leaving its host with symptoms of fever, tremors, swollen lymph nodes, sleep disturbances, and speech problems within the first two weeks of infection. Following weeks lead to neurological deterioration ending in coma and soon after death. An untreated case can expect the the disease to become fatal within a few months. [4]

Cell Structure and Function

The trypanosome cell amongst red blood cells.

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Trypanosoma cells are small (approxiamtely 50um) and heterotrophic, meaning they do not generate their own food source. The shape of the cell itself is long and oval with curved edges with a strong flagellum projecting off of the back end of the cell. The cell holds its struture through the presence of a highly polarized microtubule cytoskeleton. This cytoskeleton provides defiinite locations for the cell’s organelles (i.e. the flagellar pocket, flagellum, kinetoplast, mitochondrion and nucleus) within the center and posterior ends of the cell (end opposite of the flagella). [5] This cell expresses traits within its structure that are rather unique. Analogous to what is seen in its phylum Euglenozoa, the cell has a stiffening paraxial rod within its flagellum. Similarities with members of the cells order, Kinetoplastida, exist as well. The Trypansoma cell expresses a large cluster of DNA at the opposite end of the cell from the flagellum. This clump of DNA, otherwise known as the kinetoplast, extends from the cell’s unusually long mitochondrion and functions to determine its form within its human host. [6]

Upon initial entry into the host environment, the microbe finds itself floating within the bloodstream of the mammal in which it infected. This part of the human system is flowing with host defense mechanisms, both innate and adaptive immune responses, ready to attack any intruder. Trypanosoma has evolved to travel through this environment without detection through the presence of variant surface glycoproteins (VSG) that coat its cell wall. These VSG express one of ~1500 surface glycoprotein genes. The gene used to express these proteins changes with every 100th replication cycle to ensure the infections longevity. Upon detection, the host immune system will begin launching a complimentary protection response against trypanosoma. The change in transcription of the glycoprotein genes ensures that this complementary immune response is ineffective against the pathogen because the new VSG have developed and are undetectable. This characteristic is why patients with trypanosomiasis often experience symptoms of the disease followed by a period of latency. The disease has not dissipated but rather evaded the developed defenses of the host cell. These VSG properties are only found at certain times within the cells lifecycle: when the cell is developing within the saliva of the tsetse fly and when traveling through the host's bloodstream.

Inoculation Within the Insect Vector

The only known vector for the disease is the tsetse fly, which can be found all over Sub-Saharan Africa. Strangely, the tsetse fly acquire the trypanosoma microbe from biting infected animals or humans who conceal pathogenic parasites. [7] Once an individual fly gains the pathogenic cell, it modifies itself into a form that can be delivered and infect human hosts. In order to transform into the correct version of itself, the cell undergoes a series of developemental cycles including cell division to prepare themselves for infection. This augmentation within the insect can be sectioned into three different stages: the procyclic form, the epimastigote form and the metacyclic form. The procyclic and epimastigote forms exist for multiplication purposes, whereas the metacyclic form functions as an adaptation period inorder to effectively integrate itself within a human host. [8]

Section 3

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Section 4



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