https://microbewiki.kenyon.edu/index.php?title=African_Sleeping_Sickness:_Trypanosome_Invasion_Mechanism&feed=atom&action=historyAfrican Sleeping Sickness: Trypanosome Invasion Mechanism - Revision history2024-03-28T11:23:38ZRevision history for this page on the wikiMediaWiki 1.39.6https://microbewiki.kenyon.edu/index.php?title=African_Sleeping_Sickness:_Trypanosome_Invasion_Mechanism&diff=135962&oldid=prevLensmeyer1: /* Entry and Attack */2018-05-11T17:41:19Z<p><span dir="auto"><span class="autocomment">Entry and Attack</span></span></p>
<table style="background-color: #fff; color: #202122;" data-mw="interface">
<col class="diff-marker" />
<col class="diff-content" />
<col class="diff-marker" />
<col class="diff-content" />
<tr class="diff-title" lang="en">
<td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">← Older revision</td>
<td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">Revision as of 17:41, 11 May 2018</td>
</tr><tr><td colspan="2" class="diff-lineno" id="mw-diff-left-l57">Line 57:</td>
<td colspan="2" class="diff-lineno">Line 57:</td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div><br></div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div><br></div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>[[Image:nan_306_f3.jpg|thumb|400px|right|Fig. 7 - The average number of parasites found within human brain matter with each increasing day post-infection. A substantial amount are shown to be found in the extra-vascular corpus callosum by day 45. This is when the symptoms of coma and death would arise within the victim. [[#References|[13]]] ]]</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>[[Image:nan_306_f3.jpg|thumb|400px|right|Fig. 7 - The average number of parasites found within human brain matter with each increasing day post-infection. A substantial amount are shown to be found in the extra-vascular corpus callosum by day 45. This is when the symptoms of coma and death would arise within the victim. [[#References|[13]]] ]]</div></td></tr>
<tr><td class="diff-marker" data-marker="−"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div>The ultimate goal of the microbe <i>T. brucei</i> is to reach the brain through a variety of flowing parts of the body such as the bloodstream and spinal fluid. The cell’s traveling process to inhabit brain matter takes around fifty days. Research done by neuroscience faculty at the Karolinska Institute in Stockholm, Sweden studied mice to understand at what points the trypanosoma cell became fully immersed into the brain tissue of the host. [[#References|[13]]] By the twelfth day of the study, researchers found the microbe within the blood capillaries of the brain, with only the occasional parasite found living outside of the vessel walls (Fig. 7). At day forty-two, the experimenters began to see trypanosoma frequently throughout the parenchyma (Fig. 7). The amount of cells within this location had only increased by day fifty of the study. Once within the parenchyma, the cells were most often found within the white matter of the brain, opposed to the cerebral cortex. [[#References|[13]]] The white matter is the deeper tissue parts of the brain. This part of the brain is described to be primarily composed of the axons of neurons, which function to send electrical signals from one neuron to the next <ref>https://medlineplus.gov/ency/article/002344.htm “White Matter of the Brain: MedlinePlus Medical Encyclopedia.” <i>MedlinePlus,</i> U.S. National Library of Medicine</ref> It only took an additional five days for these parasitic microbes to move from the white matter to the septal nuclei, confined primarily to the brain parenchyma. It was noted that an remarkable abundance of the found cells were surrounding very large vessels of these nuclei. <ref>https://onlinelibrary.wiley.com/doi/full/10.1046/j.0305-1846.2001.00306.x Mulenga, C., et al. “Trypanosoma Brucei Brucei Crosses the Blood–Brain Barrier While Tight Junction Proteins Are Preserved in a Rat Chronic Disease Model.” <i>Neuropathology and Applied Neurobiology,</i> Wiley/Blackwell (10.1111), 21 Dec. 2001</ref><br></div></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div>The ultimate goal of the microbe <i>T. brucei</i> is to reach the brain through a variety of flowing parts of the body such as the bloodstream and spinal fluid. The cell’s traveling process to inhabit brain matter takes around fifty days. Research done by neuroscience faculty at the Karolinska Institute in Stockholm, Sweden studied mice to understand at what points the trypanosoma cell became fully immersed into the brain tissue of the host. [[#References|[13]]] By the twelfth day of the study, researchers found the microbe within the blood capillaries of the brain, with only the occasional parasite found living outside of the vessel walls (Fig. 7). At day forty-two, the experimenters began to see trypanosoma frequently throughout the parenchyma (Fig. 7). The amount of cells within this location had only increased by day fifty of the study. Once within the parenchyma, the cells were most often found within the white matter of the brain, opposed to the cerebral cortex. [[#References|[13]]] The white matter is the deeper tissue parts of the brain. This part of the brain is described to be primarily composed of the axons of neurons, which function to send electrical signals from one neuron to the next <ref>https://medlineplus.gov/ency/article/002344.htm “White Matter of the Brain: MedlinePlus Medical Encyclopedia.” <i>MedlinePlus,</i> U.S. National Library of Medicine</ref> <ins style="font-weight: bold; text-decoration: none;">The function of the axons gives the disease reason to attack them; The disease is able to produce its devastating affects because of it hijacks the neurons, specifically the electrical output potion of neurons: the axons. </ins>It only took an additional five days for these parasitic microbes to move from the white matter to the septal nuclei, confined primarily to the brain parenchyma. It was noted that an remarkable abundance of the found cells were surrounding very large vessels of these nuclei. <ref>https://onlinelibrary.wiley.com/doi/full/10.1046/j.0305-1846.2001.00306.x Mulenga, C., et al. “Trypanosoma Brucei Brucei Crosses the Blood–Brain Barrier While Tight Junction Proteins Are Preserved in a Rat Chronic Disease Model.” <i>Neuropathology and Applied Neurobiology,</i> Wiley/Blackwell (10.1111), 21 Dec. 2001</ref><br></div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div><br></div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div><br></div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>The largest research question surrounding the inoculation of brain tissue with <i>T. brucei</i> has to do with how this large cell can pass the blood brain barrier, otherwise known as the main filtering system between the brain and capillaries. The blood brain barrier (BBB) is extremely selective in what it allows to pass towards the brain. This structure is one within the human body that has the most security, yet continuously is deceived and allows <i>T. brucei</i> to pass leading to fatality. There are a great variety of theories on how this exchange occurs, but one appears to be more likely than the rest. Using a model system, brain microvascular endothelial cells (BMECs), experimenters found that the passage of the microbe likely has something to do with calcium channels. <ref>https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1570376/ Nikolskaia, O. V. “Blood-Brain Barrier Traversal by African Trypanosomes Requires Calcium Signaling Induced by Parasite Cysteine Protease.” <i>Journal of Clinical Investigation,</i> vol. 116, no. 10, 2006</ref> With the presence of the trypanosome microbe, the BMECs increased greatly in their oscillatory Ca<sup>2+</sup> levels. [[#References|[14]]] This indicated the possibility that these microbes can alter the integrity of the monolayers within the BBB. These clear increases can be dictated by either a living <i>T. Brucei</i> cell or by their secretions. These cells depend largely on the presence of cysteine protease in relationship with the barrier in order to control its permeability. These complexes likely are the structures that recruit these internal calcium ions. The effectiveness of passing by the microbe has been related to the strength of their cysteine proteases. [[#References|[14]]] Currently, the signals and responses that these proteases send have yet to be fully clarified. However, they are very important target locations for antibiotic treatment. [[#References|[14]]]<br></div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>The largest research question surrounding the inoculation of brain tissue with <i>T. brucei</i> has to do with how this large cell can pass the blood brain barrier, otherwise known as the main filtering system between the brain and capillaries. The blood brain barrier (BBB) is extremely selective in what it allows to pass towards the brain. This structure is one within the human body that has the most security, yet continuously is deceived and allows <i>T. brucei</i> to pass leading to fatality. There are a great variety of theories on how this exchange occurs, but one appears to be more likely than the rest. Using a model system, brain microvascular endothelial cells (BMECs), experimenters found that the passage of the microbe likely has something to do with calcium channels. <ref>https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1570376/ Nikolskaia, O. V. “Blood-Brain Barrier Traversal by African Trypanosomes Requires Calcium Signaling Induced by Parasite Cysteine Protease.” <i>Journal of Clinical Investigation,</i> vol. 116, no. 10, 2006</ref> With the presence of the trypanosome microbe, the BMECs increased greatly in their oscillatory Ca<sup>2+</sup> levels. [[#References|[14]]] This indicated the possibility that these microbes can alter the integrity of the monolayers within the BBB. These clear increases can be dictated by either a living <i>T. Brucei</i> cell or by their secretions. These cells depend largely on the presence of cysteine protease in relationship with the barrier in order to control its permeability. These complexes likely are the structures that recruit these internal calcium ions. The effectiveness of passing by the microbe has been related to the strength of their cysteine proteases. [[#References|[14]]] Currently, the signals and responses that these proteases send have yet to be fully clarified. However, they are very important target locations for antibiotic treatment. [[#References|[14]]]<br></div></td></tr>
</table>Lensmeyer1https://microbewiki.kenyon.edu/index.php?title=African_Sleeping_Sickness:_Trypanosome_Invasion_Mechanism&diff=135960&oldid=prevLensmeyer1: /* Entry and Attack */2018-05-11T17:35:32Z<p><span dir="auto"><span class="autocomment">Entry and Attack</span></span></p>
<table style="background-color: #fff; color: #202122;" data-mw="interface">
<col class="diff-marker" />
<col class="diff-content" />
<col class="diff-marker" />
<col class="diff-content" />
<tr class="diff-title" lang="en">
<td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">← Older revision</td>
<td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">Revision as of 17:35, 11 May 2018</td>
</tr><tr><td colspan="2" class="diff-lineno" id="mw-diff-left-l54">Line 54:</td>
<td colspan="2" class="diff-lineno">Line 54:</td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div><b>Attack through the blood and nervous system</b><br></div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div><b>Attack through the blood and nervous system</b><br></div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div><br></div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div><br></div></td></tr>
<tr><td class="diff-marker" data-marker="−"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div>The invasion mechanism of <i>T. <del style="font-weight: bold; text-decoration: none;">Brucei</del></i> has multiple steps or stages. Every step of the invasion affects a different aspect of the human body, ranging from the lymphatic system and blood to the white matter of the brain. Understanding the disease mechanism of this harmful cell will help in expanding the possibilities of its treatment. The initial attack of the microbe occurs within the blood vessels. The cells begin to push themselves through the capillary beds of the host epithelial cells causing deep lesions. [[#References|[9]]] The goal at this point in the life cycle is to relocate within larger, more favorable blood vessels. These would include any blood vessel that leads to larger organ systems such as the spinal cord. After the lesions have persisted for a few days, the lymph nodes of the host begin to drain in attempt to clear the body of infection allowing the microbes to travel through them, infecting the lymphatic system. [[#References|[9]]] This is the point of the life cycle that initiates symptoms such as headache, fever, fatigue, etc. These symptoms are caused by the trypanosoma microbes invading and than consuming the lymphatic system cells. The infection of the lymphatic system causes an identifiable sequelae: The swelling of a lymph node around the trapezius of the host often referred to as “Winterbottom’s sign”. [[#References|[9]]] <br></div></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div>The invasion mechanism of <i>T. <ins style="font-weight: bold; text-decoration: none;">brucei</ins></i> has multiple steps or stages. Every step of the invasion affects a different aspect of the human body, ranging from the lymphatic system and blood to the white matter of the brain. Understanding the disease mechanism of this harmful cell will help in expanding the possibilities of its treatment. The initial attack of the microbe occurs within the blood vessels. The cells begin to push themselves through the capillary beds of the host epithelial cells causing deep lesions. [[#References|[9]]] The goal at this point in the life cycle is to relocate within larger, more favorable blood vessels. These would include any blood vessel that leads to larger organ systems such as the spinal cord. After the lesions have persisted for a few days, the lymph nodes of the host begin to drain in attempt to clear the body of infection allowing the microbes to travel through them, infecting the lymphatic system. [[#References|[9]]] This is the point of the life cycle that initiates symptoms such as headache, fever, fatigue, etc. These symptoms are caused by the trypanosoma microbes invading and than consuming the lymphatic system cells. The infection of the lymphatic system causes an identifiable sequelae: The swelling of a lymph node around the trapezius of the host often referred to as “Winterbottom’s sign”. [[#References|[9]]] <br></div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div><br></div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div><br></div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>[[Image:nan_306_f3.jpg|thumb|400px|right|Fig. 7 - The average number of parasites found within human brain matter with each increasing day post-infection. A substantial amount are shown to be found in the extra-vascular corpus callosum by day 45. This is when the symptoms of coma and death would arise within the victim. [[#References|[13]]] ]]</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>[[Image:nan_306_f3.jpg|thumb|400px|right|Fig. 7 - The average number of parasites found within human brain matter with each increasing day post-infection. A substantial amount are shown to be found in the extra-vascular corpus callosum by day 45. This is when the symptoms of coma and death would arise within the victim. [[#References|[13]]] ]]</div></td></tr>
</table>Lensmeyer1https://microbewiki.kenyon.edu/index.php?title=African_Sleeping_Sickness:_Trypanosome_Invasion_Mechanism&diff=135957&oldid=prevLensmeyer1: /* Cell Structure and Function */2018-05-11T17:32:39Z<p><span dir="auto"><span class="autocomment">Cell Structure and Function</span></span></p>
<table style="background-color: #fff; color: #202122;" data-mw="interface">
<col class="diff-marker" />
<col class="diff-content" />
<col class="diff-marker" />
<col class="diff-content" />
<tr class="diff-title" lang="en">
<td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">← Older revision</td>
<td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">Revision as of 17:32, 11 May 2018</td>
</tr><tr><td colspan="2" class="diff-lineno" id="mw-diff-left-l40">Line 40:</td>
<td colspan="2" class="diff-lineno">Line 40:</td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>The only known vector for the disease is the tsetse fly. Strangely, this fly initially contracts the microbe from biting infected mammals, either human or animal, who conceal the pathogenic parasite <ref>http://www.who.int/mediacentre/factsheets/fs259/en/ WHO. “Trypanosomiasis, Human African (Sleeping Sickness).” <i>World Health Organization,</i> World Health Organization, 21 Mar. 2017</ref> Once an individual fly gains the pathogenic cell, it modifies itself into a form that can be delivered to human hosts. In order to transform into the correct version of itself, that is the metacyclic form, the cell undergoes a series of developmental cycles including cell division to prepare themselves for infection. At the end of the development within the vector, the cell is not yet pathogenic. Once relocated into the host, the cell modifies into its pathogenic form. The development of this cell has three different chronological forms: the procyclic form, the epimastigote form and the metacyclic form (Fig. 5). The procyclic and epimastigote forms exist for multiplication purposes, whereas the metacyclic form functions as an adaptation period in order to effectively integrate itself within a human host. <ref>https://microbewiki.kenyon.edu/index.php/Trypanosome_Life_Cycle “Trypanosome Life Cycle.” <i>Trypanosome Life Cycle - Microbewiki,</i> 10 Aug. 2010</ref> <br></div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>The only known vector for the disease is the tsetse fly. Strangely, this fly initially contracts the microbe from biting infected mammals, either human or animal, who conceal the pathogenic parasite <ref>http://www.who.int/mediacentre/factsheets/fs259/en/ WHO. “Trypanosomiasis, Human African (Sleeping Sickness).” <i>World Health Organization,</i> World Health Organization, 21 Mar. 2017</ref> Once an individual fly gains the pathogenic cell, it modifies itself into a form that can be delivered to human hosts. In order to transform into the correct version of itself, that is the metacyclic form, the cell undergoes a series of developmental cycles including cell division to prepare themselves for infection. At the end of the development within the vector, the cell is not yet pathogenic. Once relocated into the host, the cell modifies into its pathogenic form. The development of this cell has three different chronological forms: the procyclic form, the epimastigote form and the metacyclic form (Fig. 5). The procyclic and epimastigote forms exist for multiplication purposes, whereas the metacyclic form functions as an adaptation period in order to effectively integrate itself within a human host. <ref>https://microbewiki.kenyon.edu/index.php/Trypanosome_Life_Cycle “Trypanosome Life Cycle.” <i>Trypanosome Life Cycle - Microbewiki,</i> 10 Aug. 2010</ref> <br></div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div><br></div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div><br></div></td></tr>
<tr><td class="diff-marker" data-marker="−"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div>Upon entrance into the insect from ingesting an infected human’s blood, the so called “stumpy” form of <i>T. brucei</i> enters and must adjust itself to survive within the environment of the fly. This initial transformation is composed of a variety of chemical transformations that are not yet fully understood. It is assumed that proteases that exist within the insect’s midgut ignite a response to the new environment. [[#References|[9]]] Beyond this idea, some believe that the microbe posses a cold-shock response that appears as the microbe travels from the warm-blooded human to the exothermic fly. Despite the controversy of this transformation, the “stumpy” form of the trypanosome remodels into the first form, the procyclic form. [[#References|[9]]] This form only lasts a very short period of time before it transforms again. The microbe attaches itself onto the cells within the gut of the fly, a space referred to as the ecto peritrophic space. The connection to the cells within this space allows the form to change into one more suitable for travel. This new form is called the trypomastigote. [[#References|[9]]] The trypomastigote moves rather rapidly up the midgut of the insect and into the salivary glands. By connection to the kinetoplast, the cell enters the second form, epimastigote form. This long form resides and begins replication within the salivary gland cell membranes. The cell must soon divide to form the short epimastigote form. [[#References|[9]]] This form is currently believed to be responsible for the production of the infectious version of the trypanosome. The epimastigote form provides the groundwork for the growth of the metacyclic trypanosomes, which is the first form of the infectious agent seen once translocated into the host. [[#References|[9]]] Figure 5 depicts these many forms, identifying the <del style="font-weight: bold; text-decoration: none;">many </del>changes within the cell's shape (Fig. 5). This cycle through the tsetse fly gut and salivary glands takes a minimum of two weeks. The exact series of changes that causes the differentiation of the cell forms is still under research. However, research up to this point has proven that the relocation of the kinetoplast is vital to the growth of long epimastigote cells.<br></div></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div>Upon entrance into the insect from ingesting an infected human’s blood, the so called “stumpy” form of <i>T. brucei</i> enters and must adjust itself to survive within the environment of the fly. This initial transformation is composed of a variety of chemical transformations that are not yet fully understood. It is assumed that proteases that exist within the insect’s midgut ignite a response to the new environment. [[#References|[9]]] Beyond this idea, some believe that the microbe posses a cold-shock response that appears as the microbe travels from the warm-blooded human to the exothermic fly. Despite the controversy of this transformation, the “stumpy” form of the trypanosome remodels into the first form, the procyclic form. [[#References|[9]]] This form only lasts a very short period of time before it transforms again. The microbe attaches itself onto the cells within the gut of the fly, a space referred to as the ecto peritrophic space. The connection to the cells within this space allows the form to change into one more suitable for travel. This new form is called the trypomastigote. [[#References|[9]]] The trypomastigote moves rather rapidly up the midgut of the insect and into the salivary glands. By connection to the kinetoplast, the cell enters the second form, epimastigote form. This long form resides and begins replication within the salivary gland cell membranes. The cell must soon divide to form the short epimastigote form. [[#References|[9]]] This form is currently believed to be responsible for the production of the infectious version of the trypanosome. The epimastigote form provides the groundwork for the growth of the metacyclic trypanosomes, which is the first form of the infectious agent seen once translocated into the host. [[#References|[9]]] Figure 5 depicts these many forms, identifying the changes <ins style="font-weight: bold; text-decoration: none;">seen </ins>within the cell's shape (Fig. 5). This cycle through the tsetse fly gut and salivary glands takes a minimum of two weeks. The exact series of changes that causes the differentiation of the cell forms is still under research. However, research up to this point has proven that the relocation of the kinetoplast is vital to the growth of long epimastigote cells <ins style="font-weight: bold; text-decoration: none;">and ultimately the production of the infectious agent</ins>.<br></div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div><br></div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div><br></div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>[[Image:Life-cycle-stages-and-the-surface-coat-of-Trypanosoma-bruceiThe-T-brucei-life-cycle.png.jpg|thumb|200px|left|Fig. 6 - The life cycle describing the sturcture of each form of the <i>T. brucei</i> cell on its way to pathogenicity. The “stumpy”, or pathogenic, version of the cell is distinct by its shorter and less-slender shape. The cell no longer needs its lenth for mobility, but instead must be as compact as possible in order to infect. [https://www.researchgate.net/figure/Life-cycle-stages-and-the-surface-coat-of-Trypanosoma-bruceiThe-T-brucei-life-cycle_fig2_6639682].]]</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>[[Image:Life-cycle-stages-and-the-surface-coat-of-Trypanosoma-bruceiThe-T-brucei-life-cycle.png.jpg|thumb|200px|left|Fig. 6 - The life cycle describing the sturcture of each form of the <i>T. brucei</i> cell on its way to pathogenicity. The “stumpy”, or pathogenic, version of the cell is distinct by its shorter and less-slender shape. The cell no longer needs its lenth for mobility, but instead must be as compact as possible in order to infect. [https://www.researchgate.net/figure/Life-cycle-stages-and-the-surface-coat-of-Trypanosoma-bruceiThe-T-brucei-life-cycle_fig2_6639682].]]</div></td></tr>
</table>Lensmeyer1https://microbewiki.kenyon.edu/index.php?title=African_Sleeping_Sickness:_Trypanosome_Invasion_Mechanism&diff=135956&oldid=prevLensmeyer1: /* What is African Sleeping Sickness? */2018-05-11T17:26:15Z<p><span dir="auto"><span class="autocomment">What is African Sleeping Sickness?</span></span></p>
<table style="background-color: #fff; color: #202122;" data-mw="interface">
<col class="diff-marker" />
<col class="diff-content" />
<col class="diff-marker" />
<col class="diff-content" />
<tr class="diff-title" lang="en">
<td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">← Older revision</td>
<td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">Revision as of 17:26, 11 May 2018</td>
</tr><tr><td colspan="2" class="diff-lineno" id="mw-diff-left-l18">Line 18:</td>
<td colspan="2" class="diff-lineno">Line 18:</td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div><br></div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div><br></div></td></tr>
<tr><td class="diff-marker" data-marker="−"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div>Trypanosomiasis, or better known as African Sleeping Sickness, is an infection of the human nervous system caused by the transmission of a Trypanosome microbe through an insect vector. The disease belongs to the Trypanosome family, with these symptoms especially attributed to the parasite species ''Trypanosoma brucei''. [[#References|[2]]] The disease species is transmitted via the tsetse fly, a large biting fly located primarily in tropical African countries. The areas most at risk for such an infection are those of Sub-Saharan Africa: countries stretching from Mali to Sudan and than south, with only South Africa as an exception [[#References|[8]]]. Throughout history, this disease has been classified as a public health problem seen primarily in these African countries. About 10,000 cases of the disease are reported every year to the World Health organization, but unfortunately it is expected that the majority of cases go unreported and/or undiagnosed<br><ref>https://www.cdc.gov/parasites/sleepingsickness/ “Disease.” <i>Centers for Disease Control and Prevention,</i> Centers for Disease Control and Prevention, 29 Aug. 2012, www.cdc.gov/parasites/sleepingsickness/disease.html. </ref></div></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div>Trypanosomiasis, or better known as African Sleeping Sickness, is an infection of the human nervous system caused by the transmission of a Trypanosome microbe through an insect vector. The disease belongs to the Trypanosome family, with these symptoms especially attributed to the parasite species ''Trypanosoma brucei''. [[#References|[2]]] The disease species is transmitted via the tsetse fly, a large biting fly located primarily in tropical African countries. The areas most at risk for such an infection are those of Sub-Saharan Africa: countries stretching from Mali to Sudan and than south, with only South Africa as an exception <ins style="font-weight: bold; text-decoration: none;">(Fig. 2) </ins>[[#References|[8]]]. Throughout history, this disease has been classified as a public health problem seen primarily in these African countries. About 10,000 cases of the disease are reported every year to the World Health organization, but unfortunately it is expected that the majority of cases go unreported and/or undiagnosed<br><ref>https://www.cdc.gov/parasites/sleepingsickness/ “Disease.” <i>Centers for Disease Control and Prevention,</i> Centers for Disease Control and Prevention, 29 Aug. 2012, www.cdc.gov/parasites/sleepingsickness/disease.html. </ref></div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div><br> </div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div><br> </div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>Because this disease is vector borne, the microbe, <i>Trypanosoma brucei</i>, 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 infected the central nervous system. When the infection has passed through the blood brain barrier and begins to travel within the central nervous system, the cell has reached the second stage [[#References|[4]]]. 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. <ref>Harless, Julie. “Infectious Disease Flashcards.” African Sleeping Sickness, W.W. Norton and Company</ref> Following weeks lead to neurological deterioration ending in coma and soon after death. An untreated case can expect the disease to become fatal within a few months <ref>https://www.cdc.gov/parasites/sleepingsickness/disease.html “Disease.” <i>Centers for Disease Control and Prevention,</i> Centers for Disease Control and Prevention, 29 Aug. 2012</ref><br></div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>Because this disease is vector borne, the microbe, <i>Trypanosoma brucei</i>, 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 infected the central nervous system. When the infection has passed through the blood brain barrier and begins to travel within the central nervous system, the cell has reached the second stage [[#References|[4]]]. 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. <ref>Harless, Julie. “Infectious Disease Flashcards.” African Sleeping Sickness, W.W. Norton and Company</ref> Following weeks lead to neurological deterioration ending in coma and soon after death. An untreated case can expect the disease to become fatal within a few months <ref>https://www.cdc.gov/parasites/sleepingsickness/disease.html “Disease.” <i>Centers for Disease Control and Prevention,</i> Centers for Disease Control and Prevention, 29 Aug. 2012</ref><br></div></td></tr>
</table>Lensmeyer1https://microbewiki.kenyon.edu/index.php?title=African_Sleeping_Sickness:_Trypanosome_Invasion_Mechanism&diff=135951&oldid=prevLensmeyer1: /* Cell Structure and Function */2018-05-11T17:21:13Z<p><span dir="auto"><span class="autocomment">Cell Structure and Function</span></span></p>
<table style="background-color: #fff; color: #202122;" data-mw="interface">
<col class="diff-marker" />
<col class="diff-content" />
<col class="diff-marker" />
<col class="diff-content" />
<tr class="diff-title" lang="en">
<td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">← Older revision</td>
<td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">Revision as of 17:21, 11 May 2018</td>
</tr><tr><td colspan="2" class="diff-lineno" id="mw-diff-left-l28">Line 28:</td>
<td colspan="2" class="diff-lineno">Line 28:</td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div><b>Cell Structure</b><br></div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div><b>Cell Structure</b><br></div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div><br></div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div><br></div></td></tr>
<tr><td class="diff-marker" data-marker="−"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div>Trypanosoma cells are small (approximately 50um) and heterotrophic, meaning they require complex carbon molecules as means of consumption. The shape of the cell itself is long and oval with curved edges and a strong flagellum projecting off of the back end of the cell (Fig. 4). The cell holds its structure through the presence of a structured cytoskeleton. [[#References|[7]]] <del style="font-weight: bold; text-decoration: none;">Through </del>the <del style="font-weight: bold; text-decoration: none;">presence of </del>many microtubules dictating <del style="font-weight: bold; text-decoration: none;">its </del>form, this cytoskeleton provides definite locations for cell organelles such as the nucleus, kinetoplast, and flagellum throughout the cell. Much of these important organelles live within the posterior end of the cell (end opposite of the the flagella).<ref>[http://jcs.biologists.org/content/118/2/283 Matthews, Keith R. “The Developmental Cell Biology of Trypanosoma Brucei.” <i>Journal of Cell Science,</i> The Company of Biologists Ltd, 15 Jan. 2005, jcs.biologists.org/content/118/2/283.</ref>This end is much wider and as such offers more space for the organelles to fit. <br></div></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div>Trypanosoma cells are small (approximately 50um) and heterotrophic, meaning they require complex carbon molecules as means of consumption. The shape of the cell itself is long and oval with curved edges and a strong flagellum projecting off of the back end of the cell (Fig. 4). The cell holds its structure through the presence of a structured cytoskeleton. [[#References|[7]]] <ins style="font-weight: bold; text-decoration: none;">Because of </ins>the many microtubules <ins style="font-weight: bold; text-decoration: none;">within its structure </ins>dictating <ins style="font-weight: bold; text-decoration: none;">the overall </ins>form, this cytoskeleton provides definite locations for cell organelles such as the nucleus, kinetoplast, and flagellum throughout the cell. Much of these important organelles live within the posterior end of the cell (end opposite of the the flagella).<ref>[http://jcs.biologists.org/content/118/2/283 Matthews, Keith R. “The Developmental Cell Biology of Trypanosoma Brucei.” <i>Journal of Cell Science,</i> The Company of Biologists Ltd, 15 Jan. 2005, jcs.biologists.org/content/118/2/283.</ref>This end is much wider and as such offers more space for the organelles to fit. <br></div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div><br></div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div><br></div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>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. [[#References|[7]]] The function and purpose of this identifiable trait to the flagellum has not yet been fully uncovered. However, this trait has not evolved at all through the phylum’s history, indicating its importance to the cell’s survival.<ref>https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4675581/ Maharana, B. R., et al. “An Overview on Kinetoplastid Paraflagellar Rod.” <i>Journal of Parasitic Diseases</i>, vol. 39, no. 4, 2014, pp. 589–595.</ref> Similarities with members of the cells order, Kinetoplastida, exist as well. The Trypanosome 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 the cell's form once translocated into its human host.</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>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. [[#References|[7]]] The function and purpose of this identifiable trait to the flagellum has not yet been fully uncovered. However, this trait has not evolved at all through the phylum’s history, indicating its importance to the cell’s survival.<ref>https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4675581/ Maharana, B. R., et al. “An Overview on Kinetoplastid Paraflagellar Rod.” <i>Journal of Parasitic Diseases</i>, vol. 39, no. 4, 2014, pp. 589–595.</ref> Similarities with members of the cells order, Kinetoplastida, exist as well. The Trypanosome 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 the cell's form once translocated into its human host.</div></td></tr>
</table>Lensmeyer1https://microbewiki.kenyon.edu/index.php?title=African_Sleeping_Sickness:_Trypanosome_Invasion_Mechanism&diff=135949&oldid=prevLensmeyer1: /* Cell Structure and Function */2018-05-11T17:19:35Z<p><span dir="auto"><span class="autocomment">Cell Structure and Function</span></span></p>
<table style="background-color: #fff; color: #202122;" data-mw="interface">
<col class="diff-marker" />
<col class="diff-content" />
<col class="diff-marker" />
<col class="diff-content" />
<tr class="diff-title" lang="en">
<td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">← Older revision</td>
<td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">Revision as of 17:19, 11 May 2018</td>
</tr><tr><td colspan="2" class="diff-lineno" id="mw-diff-left-l28">Line 28:</td>
<td colspan="2" class="diff-lineno">Line 28:</td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div><b>Cell Structure</b><br></div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div><b>Cell Structure</b><br></div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div><br></div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div><br></div></td></tr>
<tr><td class="diff-marker" data-marker="−"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div>Trypanosoma cells are small (approximately 50um) and heterotrophic, meaning they require complex carbon molecules as means of consumption. The shape of the cell itself is long and oval with curved edges and a strong flagellum projecting off of the back end of the cell. The cell holds its structure through the presence of a structured cytoskeleton. [[#References|[7]]] Through the presence of many microtubules dictating its form, this cytoskeleton provides definite locations for cell organelles such as the nucleus, kinetoplast, and flagellum throughout the cell. Much of these important organelles live within the posterior end of the cell (end opposite of the the flagella).<ref>[http://jcs.biologists.org/content/118/2/283 Matthews, Keith R. “The Developmental Cell Biology of Trypanosoma Brucei.” <i>Journal of Cell Science,</i> The Company of Biologists Ltd, 15 Jan. 2005, jcs.biologists.org/content/118/2/283.</ref>This end is much wider and as such offers more space for the organelles to fit. <br></div></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div>Trypanosoma cells are small (approximately 50um) and heterotrophic, meaning they require complex carbon molecules as means of consumption. The shape of the cell itself is long and oval with curved edges and a strong flagellum projecting off of the back end of the cell <ins style="font-weight: bold; text-decoration: none;">(Fig. 4)</ins>. The cell holds its structure through the presence of a structured cytoskeleton. [[#References|[7]]] Through the presence of many microtubules dictating its form, this cytoskeleton provides definite locations for cell organelles such as the nucleus, kinetoplast, and flagellum throughout the cell. Much of these important organelles live within the posterior end of the cell (end opposite of the the flagella).<ref>[http://jcs.biologists.org/content/118/2/283 Matthews, Keith R. “The Developmental Cell Biology of Trypanosoma Brucei.” <i>Journal of Cell Science,</i> The Company of Biologists Ltd, 15 Jan. 2005, jcs.biologists.org/content/118/2/283.</ref>This end is much wider and as such offers more space for the organelles to fit. <br></div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div><br></div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div><br></div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>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. [[#References|[7]]] The function and purpose of this identifiable trait to the flagellum has not yet been fully uncovered. However, this trait has not evolved at all through the phylum’s history, indicating its importance to the cell’s survival.<ref>https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4675581/ Maharana, B. R., et al. “An Overview on Kinetoplastid Paraflagellar Rod.” <i>Journal of Parasitic Diseases</i>, vol. 39, no. 4, 2014, pp. 589–595.</ref> Similarities with members of the cells order, Kinetoplastida, exist as well. The Trypanosome 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 the cell's form once translocated into its human host.</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>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. [[#References|[7]]] The function and purpose of this identifiable trait to the flagellum has not yet been fully uncovered. However, this trait has not evolved at all through the phylum’s history, indicating its importance to the cell’s survival.<ref>https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4675581/ Maharana, B. R., et al. “An Overview on Kinetoplastid Paraflagellar Rod.” <i>Journal of Parasitic Diseases</i>, vol. 39, no. 4, 2014, pp. 589–595.</ref> Similarities with members of the cells order, Kinetoplastida, exist as well. The Trypanosome 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 the cell's form once translocated into its human host.</div></td></tr>
</table>Lensmeyer1https://microbewiki.kenyon.edu/index.php?title=African_Sleeping_Sickness:_Trypanosome_Invasion_Mechanism&diff=135946&oldid=prevLensmeyer1: /* Cell Structure and Function */2018-05-11T17:11:47Z<p><span dir="auto"><span class="autocomment">Cell Structure and Function</span></span></p>
<table style="background-color: #fff; color: #202122;" data-mw="interface">
<col class="diff-marker" />
<col class="diff-content" />
<col class="diff-marker" />
<col class="diff-content" />
<tr class="diff-title" lang="en">
<td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">← Older revision</td>
<td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">Revision as of 17:11, 11 May 2018</td>
</tr><tr><td colspan="2" class="diff-lineno" id="mw-diff-left-l33">Line 33:</td>
<td colspan="2" class="diff-lineno">Line 33:</td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div><ref>https://microbewiki.kenyon.edu/index.php/Trypanosoma “Disease.” “Trypanosoma.” <i>Trypanosoma - Microbewiki,</i> 7 Aug. 2010</ref> <br></div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div><ref>https://microbewiki.kenyon.edu/index.php/Trypanosoma “Disease.” “Trypanosoma.” <i>Trypanosoma - Microbewiki,</i> 7 Aug. 2010</ref> <br></div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div><br> </div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div><br> </div></td></tr>
<tr><td class="diff-marker" data-marker="−"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div>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. [[#References|[7]]] These VSGs express one of ~1500 surface glycoprotein genes. The majority of these VSG genes function silenty. They recombine to form many different patterns that ultimately <del style="font-weight: bold; text-decoration: none;">create a </del>coat for the outisde of the cell membrane, making the cell undistinguishable by host antibodies. The gene pattern used to express these proteins changes with every 100th replication cycle to ensure the infections longevity. [[#References|[7]]] Upon detection, the host immune system will begin launching a complementary 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 membrane coat has developed and is thereby undetectable. This characteristic is why patients with trypanosomiasis often experience symptoms of the disease followed by a period of latency. [[#References|[7]]] 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 life cycle: when the cell is developing within the saliva of the vector and when traveling through the infected bloodstream. <br></div></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div>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. [[#References|[7]]] These VSGs express one of ~1500 surface glycoprotein genes. The majority of these VSG genes function silenty. They recombine to form many different patterns that ultimately <ins style="font-weight: bold; text-decoration: none;">construct an unknown </ins>coat for the outisde of the cell membrane, making the cell undistinguishable by host antibodies. The gene pattern used to express these proteins changes with every 100th replication cycle to ensure the infections longevity. [[#References|[7]]] <ins style="font-weight: bold; text-decoration: none;">The number of genes and gene combinations is so plentiful to ensure the continued protection of the cell from the human immune system. </ins>Upon <ins style="font-weight: bold; text-decoration: none;">initial </ins>detection <ins style="font-weight: bold; text-decoration: none;">of the cell</ins>, the host immune system will begin launching a complementary protection response against trypanosoma. The change in <ins style="font-weight: bold; text-decoration: none;">the </ins>transcription of the glycoprotein genes ensures that this complementary immune response is ineffective against the pathogen because the new VSG membrane coat has developed and is thereby undetectable. This characteristic is why patients with trypanosomiasis often experience symptoms of the disease followed by a period of latency. [[#References|[7]]] 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 life cycle: when the cell is developing within the saliva of the vector and when traveling through the infected bloodstream. <br></div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div><br></div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div><br></div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div><b>Inoculation Within the Insect Vector</b> <br></div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div><b>Inoculation Within the Insect Vector</b> <br></div></td></tr>
</table>Lensmeyer1https://microbewiki.kenyon.edu/index.php?title=African_Sleeping_Sickness:_Trypanosome_Invasion_Mechanism&diff=135945&oldid=prevLensmeyer1: /* Entry and Attack */2018-05-11T17:07:21Z<p><span dir="auto"><span class="autocomment">Entry and Attack</span></span></p>
<table style="background-color: #fff; color: #202122;" data-mw="interface">
<col class="diff-marker" />
<col class="diff-content" />
<col class="diff-marker" />
<col class="diff-content" />
<tr class="diff-title" lang="en">
<td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">← Older revision</td>
<td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">Revision as of 17:07, 11 May 2018</td>
</tr><tr><td colspan="2" class="diff-lineno" id="mw-diff-left-l54">Line 54:</td>
<td colspan="2" class="diff-lineno">Line 54:</td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div><b>Attack through the blood and nervous system</b><br></div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div><b>Attack through the blood and nervous system</b><br></div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div><br></div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div><br></div></td></tr>
<tr><td class="diff-marker" data-marker="−"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div>The <del style="font-weight: bold; text-decoration: none;">initial attack </del>of <i>T. Brucei</i> occurs within the blood vessels. The cells begin to push themselves through the capillary beds of the host epithelial cells causing deep lesions. [[#References|[9]]] The goal at this point in the life cycle is to relocate within larger, more favorable blood vessels. These would include any blood vessel that leads to larger organ systems such as the spinal cord. After the lesions have persisted for a few days, the lymph nodes of the host begin to drain in attempt to clear the body of infection allowing the microbes to travel through them, infecting the lymphatic system. [[#References|[9]]] This is the point of the life cycle that initiates symptoms such as headache, fever, fatigue, etc. These symptoms are caused by the trypanosoma microbes invading and than consuming the lymphatic system cells. The infection of the lymphatic system causes an identifiable sequelae: The swelling of a lymph node around the trapezius of the host often referred to as “Winterbottom’s sign”. [[#References|[9]]] <br></div></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div>The <ins style="font-weight: bold; text-decoration: none;">invasion mechanism </ins>of <i>T. Brucei</i> <ins style="font-weight: bold; text-decoration: none;">has multiple steps or stages. Every step of the invasion affects a different aspect of the human body, ranging from the lymphatic system and blood to the white matter of the brain. Understanding the disease mechanism of this harmful cell will help in expanding the possibilities of its treatment. The initial attack of the microbe </ins>occurs within the blood vessels. The cells begin to push themselves through the capillary beds of the host epithelial cells causing deep lesions. [[#References|[9]]] The goal at this point in the life cycle is to relocate within larger, more favorable blood vessels. These would include any blood vessel that leads to larger organ systems such as the spinal cord. After the lesions have persisted for a few days, the lymph nodes of the host begin to drain in attempt to clear the body of infection allowing the microbes to travel through them, infecting the lymphatic system. [[#References|[9]]] This is the point of the life cycle that initiates symptoms such as headache, fever, fatigue, etc. These symptoms are caused by the trypanosoma microbes invading and than consuming the lymphatic system cells. The infection of the lymphatic system causes an identifiable sequelae: The swelling of a lymph node around the trapezius of the host often referred to as “Winterbottom’s sign”. [[#References|[9]]] <br></div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div><br></div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div><br></div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>[[Image:nan_306_f3.jpg|thumb|400px|right|Fig. 7 - The average number of parasites found within human brain matter with each increasing day post-infection. A substantial amount are shown to be found in the extra-vascular corpus callosum by day 45. This is when the symptoms of coma and death would arise within the victim. [[#References|[13]]] ]]</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>[[Image:nan_306_f3.jpg|thumb|400px|right|Fig. 7 - The average number of parasites found within human brain matter with each increasing day post-infection. A substantial amount are shown to be found in the extra-vascular corpus callosum by day 45. This is when the symptoms of coma and death would arise within the victim. [[#References|[13]]] ]]</div></td></tr>
</table>Lensmeyer1https://microbewiki.kenyon.edu/index.php?title=African_Sleeping_Sickness:_Trypanosome_Invasion_Mechanism&diff=135564&oldid=prevLensmeyer1: /* Cell Structure and Function */2018-05-08T15:19:04Z<p><span dir="auto"><span class="autocomment">Cell Structure and Function</span></span></p>
<table style="background-color: #fff; color: #202122;" data-mw="interface">
<col class="diff-marker" />
<col class="diff-content" />
<col class="diff-marker" />
<col class="diff-content" />
<tr class="diff-title" lang="en">
<td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">← Older revision</td>
<td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">Revision as of 15:19, 8 May 2018</td>
</tr><tr><td colspan="2" class="diff-lineno" id="mw-diff-left-l45">Line 45:</td>
<td colspan="2" class="diff-lineno">Line 45:</td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div><b>Final Transformation Within the Host System</b><br></div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div><b>Final Transformation Within the Host System</b><br></div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div><br></div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div><br></div></td></tr>
<tr><td class="diff-marker" data-marker="−"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div>The trypanosome cell type that is transmitted from the tsetse fly to its mammalian host is metacyclic. [[#References|[9]]] Once this happens, an extensive series of chemical signals occurs to change this metacyclic form into the known and pathogenic cell that induces the symptoms of sleeping sickness. When bitten, the microbe is immediately relocated into the bloodstream of the affected host. This is when the metacyclic form transforms into bloodstream trypomastigotes, otherwise known as the slender form of the trypanosome cell. The cell than enters a phase of exponential growth via binary fission. [[#References|[10]]] The human environment is very different from that of the fly’s salivary glands. This series of reproduction serves to adjust the microbe to their new living conditions. After reproduction, the cells transform for the final time into what is called the stumpy version. These cells are now stable and cannot divide in daughter cells anymore. They relocate themselves into an array of bodily fluids such as the lymph nodes or the spinal fluid. Once in these locations, the cell’s main goal is to access the central nervous system (CNS) to bring forth the symptoms we attribute to African Sleeping Sickness<ref>https://www.ncbi.nlm.nih.gov/pubmed/2348830 Hamm, B, et al. “Differentiation of Trypanosoma Brucei Bloodstream Trypomastigotes from Long Slender to Short Stumpy-like Forms in Axenic Culture.” <i>Molecular and Biochemical Parasitology.,</i> U.S. National Library of Medicine, Apr. 1990</ref></div></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div>The trypanosome cell type that is transmitted from the tsetse fly to its mammalian host is metacyclic. [[#References|[9]]] Once this happens, an extensive series of chemical signals occurs to change this metacyclic form into the known and pathogenic cell that induces the symptoms of sleeping sickness. When bitten, the microbe is immediately relocated into the bloodstream of the affected host. This is when the metacyclic form transforms into bloodstream trypomastigotes, otherwise known as the slender form of the trypanosome cell. The cell than enters a phase of exponential growth via binary fission. [[#References|[10]]] The human environment is very different from that of the fly’s salivary glands. This series of reproduction serves to adjust the microbe to their new living conditions. After reproduction, the cells transform for the final time into what is called the stumpy version. These cells are now stable and cannot divide in daughter cells anymore. They relocate themselves into an array of bodily fluids such as the lymph nodes or the spinal fluid. Once in these locations, the cell’s main goal is to access the central nervous system (CNS) to bring forth the symptoms we attribute to African Sleeping Sickness<ins style="font-weight: bold; text-decoration: none;">.</ins><ref>https://www.ncbi.nlm.nih.gov/pubmed/2348830 Hamm, B, et al. “Differentiation of Trypanosoma Brucei Bloodstream Trypomastigotes from Long Slender to Short Stumpy-like Forms in Axenic Culture.” <i>Molecular and Biochemical Parasitology.,</i> U.S. National Library of Medicine, Apr. 1990</ref> <ins style="font-weight: bold; text-decoration: none;">Figure 6 shows the drastic change seen between the metacyclic cell form (first invading cell form) and the "stumpy" form (pathogenic form). The cell is no longer long and slender and lacks its flagellum. The cell's purpose is not to be motile anymore, but instead to be compact in order to pass the BBB and invade brain tissue.</ins></div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>==Entry and Attack==</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>==Entry and Attack==</div></td></tr>
</table>Lensmeyer1https://microbewiki.kenyon.edu/index.php?title=African_Sleeping_Sickness:_Trypanosome_Invasion_Mechanism&diff=135563&oldid=prevLensmeyer1: /* Cell Structure and Function */2018-05-08T15:09:02Z<p><span dir="auto"><span class="autocomment">Cell Structure and Function</span></span></p>
<table style="background-color: #fff; color: #202122;" data-mw="interface">
<col class="diff-marker" />
<col class="diff-content" />
<col class="diff-marker" />
<col class="diff-content" />
<tr class="diff-title" lang="en">
<td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">← Older revision</td>
<td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">Revision as of 15:09, 8 May 2018</td>
</tr><tr><td colspan="2" class="diff-lineno" id="mw-diff-left-l38">Line 38:</td>
<td colspan="2" class="diff-lineno">Line 38:</td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>[[Image:Pathogens-06-00029-g001.jpg|thumb|400px|right|Fig. 5 - The life cycle and cell shape of <i>trypanosoma brucei gambiense</i> within the tsetse fly vector[http://www.mdpi.com/2076-0817/6/3/29].]]</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>[[Image:Pathogens-06-00029-g001.jpg|thumb|400px|right|Fig. 5 - The life cycle and cell shape of <i>trypanosoma brucei gambiense</i> within the tsetse fly vector[http://www.mdpi.com/2076-0817/6/3/29].]]</div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div><br></div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div><br></div></td></tr>
<tr><td class="diff-marker" data-marker="−"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div>The only known vector for the disease is the tsetse fly. Strangely, this fly initially contracts the microbe from biting infected mammals, either human or animal, who conceal the pathogenic parasite <ref>http://www.who.int/mediacentre/factsheets/fs259/en/ WHO. “Trypanosomiasis, Human African (Sleeping Sickness).” <i>World Health Organization,</i> World Health Organization, 21 Mar. 2017</ref> Once an individual fly gains the pathogenic cell, it modifies itself into a form that can be delivered to human hosts. In order to transform into the correct version of itself, that is the metacyclic form, the cell undergoes a series of developmental cycles including cell division to prepare themselves for infection. At the end of the development within the vector, the cell is not yet pathogenic. Once relocated into the host, the cell modifies into its pathogenic form. The development of this cell has three different chronological forms: 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 in order to effectively integrate itself within a human host. <ref>https://microbewiki.kenyon.edu/index.php/Trypanosome_Life_Cycle “Trypanosome Life Cycle.” <i>Trypanosome Life Cycle - Microbewiki,</i> 10 Aug. 2010</ref> <br></div></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div>The only known vector for the disease is the tsetse fly. Strangely, this fly initially contracts the microbe from biting infected mammals, either human or animal, who conceal the pathogenic parasite <ref>http://www.who.int/mediacentre/factsheets/fs259/en/ WHO. “Trypanosomiasis, Human African (Sleeping Sickness).” <i>World Health Organization,</i> World Health Organization, 21 Mar. 2017</ref> Once an individual fly gains the pathogenic cell, it modifies itself into a form that can be delivered to human hosts. In order to transform into the correct version of itself, that is the metacyclic form, the cell undergoes a series of developmental cycles including cell division to prepare themselves for infection. At the end of the development within the vector, the cell is not yet pathogenic. Once relocated into the host, the cell modifies into its pathogenic form. The development of this cell has three different chronological forms: the procyclic form, the epimastigote form and the metacyclic form <ins style="font-weight: bold; text-decoration: none;">(Fig. 5)</ins>. The procyclic and epimastigote forms exist for multiplication purposes, whereas the metacyclic form functions as an adaptation period in order to effectively integrate itself within a human host. <ref>https://microbewiki.kenyon.edu/index.php/Trypanosome_Life_Cycle “Trypanosome Life Cycle.” <i>Trypanosome Life Cycle - Microbewiki,</i> 10 Aug. 2010</ref> <br></div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div><br></div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div><br></div></td></tr>
<tr><td class="diff-marker" data-marker="−"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div>Upon entrance into the insect from ingesting an infected human’s blood, the so called “stumpy” form of <i>T. brucei</i> enters and must adjust itself to survive within the environment of the fly. This initial transformation is composed of a variety of chemical transformations that are not yet fully understood. It is assumed that proteases that exist within the insect’s midgut ignite a response to the new environment. [[#References|[9]]] Beyond this idea, some believe that the microbe posses a cold-shock response that appears as the microbe travels from the warm-blooded human to the exothermic fly. Despite the controversy of this transformation, the “stumpy” form of the trypanosome remodels into the first form, the procyclic form. [[#References|[9]]] This form only lasts a very short period of time before it transforms again. The microbe attaches itself onto the cells within the gut of the fly, a space referred to as the ecto peritrophic space. The connection to the cells within this space allows the form to change into one more suitable for travel. This new form is called the trypomastigote. [[#References|[9]]] The trypomastigote moves rather rapidly up the midgut of the insect and into the salivary glands. By connection to the kinetoplast, the cell enters the second form, epimastigote form. This long form resides and begins replication within the salivary gland cell membranes. The cell must soon divide to form the short epimastigote form. [[#References|[9]]] This form is currently believed to be responsible for the production of the infectious version of the trypanosome. The epimastigote form provides the groundwork for the growth of the metacyclic trypanosomes, which is the first form of the infectious agent seen once translocated into the host. [[#References|[9]]] The exact series of changes that <del style="font-weight: bold; text-decoration: none;">cause this </del>differentiation is still under research. However, research up to this point has proven that the relocation of the kinetoplast is vital to the growth of long epimastigote cells.<br></div></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div>Upon entrance into the insect from ingesting an infected human’s blood, the so called “stumpy” form of <i>T. brucei</i> enters and must adjust itself to survive within the environment of the fly. This initial transformation is composed of a variety of chemical transformations that are not yet fully understood. It is assumed that proteases that exist within the insect’s midgut ignite a response to the new environment. [[#References|[9]]] Beyond this idea, some believe that the microbe posses a cold-shock response that appears as the microbe travels from the warm-blooded human to the exothermic fly. Despite the controversy of this transformation, the “stumpy” form of the trypanosome remodels into the first form, the procyclic form. [[#References|[9]]] This form only lasts a very short period of time before it transforms again. The microbe attaches itself onto the cells within the gut of the fly, a space referred to as the ecto peritrophic space. The connection to the cells within this space allows the form to change into one more suitable for travel. This new form is called the trypomastigote. [[#References|[9]]] The trypomastigote moves rather rapidly up the midgut of the insect and into the salivary glands. By connection to the kinetoplast, the cell enters the second form, epimastigote form. This long form resides and begins replication within the salivary gland cell membranes. The cell must soon divide to form the short epimastigote form. [[#References|[9]]] This form is currently believed to be responsible for the production of the infectious version of the trypanosome. The epimastigote form provides the groundwork for the growth of the metacyclic trypanosomes, which is the first form of the infectious agent seen once translocated into the host. [[#References|[9]]] <ins style="font-weight: bold; text-decoration: none;">Figure 5 depicts these many forms, identifying the many changes within the cell's shape (Fig. 5). This cycle through the tsetse fly gut and salivary glands takes a minimum of two weeks. </ins>The exact series of changes that <ins style="font-weight: bold; text-decoration: none;">causes the </ins>differentiation <ins style="font-weight: bold; text-decoration: none;">of the cell forms </ins>is still under research. However, research up to this point has proven that the relocation of the kinetoplast is vital to the growth of long epimastigote cells.<br></div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div><br></div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div><br></div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>[[Image:Life-cycle-stages-and-the-surface-coat-of-Trypanosoma-bruceiThe-T-brucei-life-cycle.png.jpg|thumb|200px|left|Fig. 6 - The life cycle describing the sturcture of each form of the <i>T. brucei</i> cell on its way to pathogenicity. The “stumpy”, or pathogenic, version of the cell is distinct by its shorter and less-slender shape. The cell no longer needs its lenth for mobility, but instead must be as compact as possible in order to infect. [https://www.researchgate.net/figure/Life-cycle-stages-and-the-surface-coat-of-Trypanosoma-bruceiThe-T-brucei-life-cycle_fig2_6639682].]]</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>[[Image:Life-cycle-stages-and-the-surface-coat-of-Trypanosoma-bruceiThe-T-brucei-life-cycle.png.jpg|thumb|200px|left|Fig. 6 - The life cycle describing the sturcture of each form of the <i>T. brucei</i> cell on its way to pathogenicity. The “stumpy”, or pathogenic, version of the cell is distinct by its shorter and less-slender shape. The cell no longer needs its lenth for mobility, but instead must be as compact as possible in order to infect. [https://www.researchgate.net/figure/Life-cycle-stages-and-the-surface-coat-of-Trypanosoma-bruceiThe-T-brucei-life-cycle_fig2_6639682].]]</div></td></tr>
</table>Lensmeyer1