https://microbewiki.kenyon.edu/index.php?title=Clostridium_difficile-associated_disease&feed=atom&action=historyClostridium difficile-associated disease - Revision history2024-03-28T11:27:03ZRevision history for this page on the wikiMediaWiki 1.39.6https://microbewiki.kenyon.edu/index.php?title=Clostridium_difficile-associated_disease&diff=119603&oldid=prevBarichD at 14:24, 11 February 20162016-02-11T14:24:30Z<p></p>
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<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>[[File:Clostridium difficile spore.gif|380px|thumb|right|Scanning electron microscope image of <i>Clostridium difficile</i>. From: Bioquell.com [http://www.bioquell.com/technology/microbiology/clostridium-difficile/]]]</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>[[File:Clostridium difficile spore.gif|380px|thumb|right|Scanning electron microscope image of <i>Clostridium difficile</i>. From: Bioquell.com [http://www.bioquell.com/technology/microbiology/clostridium-difficile/]]]</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>==Etiology/Bacteriology==</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>==Etiology/Bacteriology==</div></td></tr>
</table>BarichDhttps://microbewiki.kenyon.edu/index.php?title=Clostridium_difficile-associated_disease&diff=114901&oldid=prevAmber.M.Hubbard-1: /* Damage Response Framework */2015-07-15T19:45:13Z<p><span dir="auto"><span class="autocomment">Damage Response Framework</span></span></p>
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<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>===Damage Response Framework===</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>===Damage Response Framework===</div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></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><ins style="font-weight: bold; text-decoration: none;">The damage response framework is a theory that measures the interaction between the pathogen and the host. This theory is able to give an explanation as to why the same pathogen can cause different levels of damage depending on the host. The interaction between the two parties can result in damage to the host, benefit to the host, or can have no effect. These levels of damage can then lead to circumstances of symbiosis, colonization, commensalism, latency, and disease.</ins></div></td></tr>
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</table>Amber.M.Hubbard-1https://microbewiki.kenyon.edu/index.php?title=Clostridium_difficile-associated_disease&diff=114893&oldid=prevCassandra.K.Long-1 at 19:29, 15 July 20152015-07-15T19:29:55Z<p></p>
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<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><i>Clostridium difficile</i> are shed in feces, and therefore these bacteria can be transmitted via the fecal-oral route. The spores can survive on almost any surface for months to years which makes the pathogen very difficult to get rid of once established. The spores are resistant to many extreme environments, including high temperatures, ultraviolet light, harsh chemicals, and antibiotics. Health care settings, including patients and workers, are often the reservoirs for <i>C. difficile</i> spores. Community-acquired infections are thought to be transmitted through soil, water, pets, meats, and vegetables.</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><i>Clostridium difficile</i> are shed in feces, and therefore these bacteria can be transmitted via the fecal-oral route. The spores can survive on almost any surface for months to years which makes the pathogen very difficult to get rid of once established. The spores are resistant to many extreme environments, including high temperatures, ultraviolet light, harsh chemicals, and antibiotics. Health care settings, including patients and workers, are often the reservoirs for <i>C. difficile</i> spores. Community-acquired infections are thought to be transmitted through soil, water, pets, meats, and vegetables.</div></td></tr>
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<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><del style="font-weight: bold; text-decoration: none;">[[File:spores.jpeg|400px|thumb|center|Transmission electron microscope image of <i>Clostridium difficile</i>. From: Austincc.edu [http://www.austincc.edu/microbio/2993q/cdiff.htm]]]</del></div></td><td colspan="2" class="diff-side-added"></td></tr>
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<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>===Infectious dose, incubation, and colonization===</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>===Infectious dose, incubation, and colonization===</div></td></tr>
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<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>Though most patients with <i>C. difficile</i> can recover without specific therapy, symptoms may be particularly debilitating and drawn out. The elderly are much more susceptible to severe infection, and the mortality rate in this demographic is estimated to be as high as 25%. The disease’s mortality and morbidity seems to have increased in severity in the last decade. The CDC has reported that enteritis deaths more than doubled from 1997 to 2007 in the United States, increasing to 17,000 from about 7,000, and C difficile was associated with 14,500 of these deaths, up from 2,700 in 1999 [[#References|[5]]]. A particularly virulent strain has been traced to several outbreaks in North America, known as the NAP1/027 strain. It shows increased production of toxins A and B, antibiotic resistance, and the production of a binary toxin whose role is not yet clear, but is thought to increase the virulence of the A and B toxins.</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>Though most patients with <i>C. difficile</i> can recover without specific therapy, symptoms may be particularly debilitating and drawn out. The elderly are much more susceptible to severe infection, and the mortality rate in this demographic is estimated to be as high as 25%. The disease’s mortality and morbidity seems to have increased in severity in the last decade. The CDC has reported that enteritis deaths more than doubled from 1997 to 2007 in the United States, increasing to 17,000 from about 7,000, and C difficile was associated with 14,500 of these deaths, up from 2,700 in 1999 [[#References|[5]]]. A particularly virulent strain has been traced to several outbreaks in North America, known as the NAP1/027 strain. It shows increased production of toxins A and B, antibiotic resistance, and the production of a binary toxin whose role is not yet clear, but is thought to increase the virulence of the A and B toxins.</div></td></tr>
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</table>Cassandra.K.Long-1https://microbewiki.kenyon.edu/index.php?title=Clostridium_difficile-associated_disease&diff=114891&oldid=prevCassandra.K.Long-1 at 19:29, 15 July 20152015-07-15T19:29:06Z<p></p>
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<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:OULOGOBIANCO.JPEG|thumb|230px|left|University of Oklahoma Study Abroad Microbiology in Arezzo, Italy[http://cas.ou.edu/study-abroad/]]]</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:OULOGOBIANCO.JPEG|thumb|230px|left|University of Oklahoma Study Abroad Microbiology in Arezzo, Italy[http://cas.ou.edu/study-abroad/]]]</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>[[File:Clostridium difficile spore.gif|<del style="font-weight: bold; text-decoration: none;">400px</del>|thumb|right|Scanning electron microscope image of <i>Clostridium difficile</i>. From: Bioquell.com [http://www.bioquell.com/technology/microbiology/clostridium-difficile/]]]</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>[[File:Clostridium difficile spore.gif|<ins style="font-weight: bold; text-decoration: none;">380px</ins>|thumb|right|Scanning electron microscope image of <i>Clostridium difficile</i>. From: Bioquell.com [http://www.bioquell.com/technology/microbiology/clostridium-difficile/]]]</div></td></tr>
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</table>Cassandra.K.Long-1https://microbewiki.kenyon.edu/index.php?title=Clostridium_difficile-associated_disease&diff=114888&oldid=prevCassandra.K.Long-1 at 19:28, 15 July 20152015-07-15T19:28:01Z<p></p>
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<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" 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>Created by Laura Boucher, Marrett Hild, and Lillian Flannigan, students of Tyrrell Conway, PhD at the University of Oklahoma</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>Created by Laura Boucher, Marrett Hild, and Lillian Flannigan, students of Tyrrell Conway, PhD at the University of Oklahoma <ins style="font-weight: bold; text-decoration: none;"><br></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;"><div>Edited by Cassandra Long and Amber Hubbard, students of Tyrrell Conway, PhD at the University of Oklahoma</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>Edited by Cassandra Long and Amber Hubbard, students of Tyrrell Conway, PhD at the University of Oklahoma</div></td></tr>
</table>Cassandra.K.Long-1https://microbewiki.kenyon.edu/index.php?title=Clostridium_difficile-associated_disease&diff=114887&oldid=prevCassandra.K.Long-1 at 19:27, 15 July 20152015-07-15T19:27:14Z<p></p>
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<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>==Prevention==</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>==Prevention==</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>Prevention with good hygiene habits will go a long way to protect against opportunistic pathogens like C. difficile. The main focus with C. difficile specifically should be on more conscientious antibiotic use, as broad spectrum antibiotics make patients susceptible in the first place. Restricting antibiotic use should lower the incidence of the disease and hopefully slow its growing virulence. When dealing with CDAD patients in a hospital setting, isolation of the sick, proper hand washing techniques, protective gowns and gloves, and cleaning with sodium hypochlorite are all important and effective ways to prevent outbreaks in healthcare settings. Work on a vaccine has begun, which appears to be promising, but is still far from market availability.</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>Prevention with good hygiene habits will go a long way to protect against opportunistic pathogens like <ins style="font-weight: bold; text-decoration: none;"><i></ins>C. difficile<ins style="font-weight: bold; text-decoration: none;"></i></ins>. The main focus with <ins style="font-weight: bold; text-decoration: none;"><i></ins>C. difficile<ins style="font-weight: bold; text-decoration: none;"></i> </ins>specifically should be on more conscientious antibiotic use, as broad spectrum antibiotics make patients susceptible in the first place. Restricting antibiotic use should lower the incidence of the disease and hopefully slow its growing virulence. When dealing with CDAD patients in a hospital setting, isolation of the sick, proper hand washing techniques, protective gowns and gloves, and cleaning with sodium hypochlorite are all important and effective ways to prevent outbreaks in healthcare settings. Work on a vaccine has begun, which appears to be promising, but is still far from market availability.</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>==Host Immune Response==</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>==Host Immune Response==</div></td></tr>
</table>Cassandra.K.Long-1https://microbewiki.kenyon.edu/index.php?title=Clostridium_difficile-associated_disease&diff=114880&oldid=prevAmber.M.Hubbard-1: /* Pathogenesis */2015-07-15T19:19:20Z<p><span dir="auto"><span class="autocomment">Pathogenesis</span></span></p>
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<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>===Virulence factors===</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>===Virulence factors===</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><i>C. difficile</i> expresses two toxins, toxin A (TcdA) and toxin B (TcdB), which are two of the largest bacterial toxins known (review). They are part of the Large Clostridial Toxin family, in which the toxins glucosylate small GTPases in the cytosol of targeted cells. Both toxins disrupt the actin cytoskeleton of fibroblasts and prevent cells from being able to regulate actin polymerization. Toxin A produces a florid inflammatory response, while B has no enterotoxin activity, but instead is a potent cytotoxin. In fact, toxin B is 10 times more potent than A in causing damage in colonic epithelial cells, which points to toxin B as the primary virulence factor. The primary virulence factor for this bacteria has been disputed. It was previously thought to be toxin A, but recent evidence points towards toxin B.</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><i>C. difficile</i> expresses two toxins, toxin A (TcdA) and toxin B (TcdB), which are two of the largest bacterial toxins known (review). They are part of the Large Clostridial Toxin family, in which the toxins glucosylate small GTPases in the cytosol of targeted cells. Both toxins disrupt the actin cytoskeleton of fibroblasts and prevent cells from being able to regulate actin polymerization. Toxin A produces a florid inflammatory response, while B has no enterotoxin activity, but instead is a potent cytotoxin. In fact, toxin B is 10 times more potent than A in causing damage in colonic epithelial cells, which points to toxin B as the primary virulence factor. The primary virulence factor for this bacteria has been disputed. It was previously thought to be toxin A, but recent evidence points towards toxin B.</div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></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><ins style="font-weight: bold; text-decoration: none;"></ins></div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></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><ins style="font-weight: bold; text-decoration: none;">===Damage Response Framework===</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>==Clinical features==</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>==Clinical features==</div></td></tr>
</table>Amber.M.Hubbard-1https://microbewiki.kenyon.edu/index.php?title=Clostridium_difficile-associated_disease&diff=114877&oldid=prevCassandra.K.Long-1 at 19:17, 15 July 20152015-07-15T19:17:04Z<p></p>
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<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>===Description===</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>===Description===</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><i>Clostridium difficile</i> is a Gram-positive, spore-forming rod that is an obligate anaerobe. It can be found in soil, water, feces, and the human gut. Infections of <i>Clostridium difficile</i> cause pseudomembranous colitis, toxic megacolon, perforations of the colon, sepsis, and, on occasion, death. <i>C. difficile</i> is a normal inhabitant of the gut microbial community of about 1-3% of adults. The pathogenic form of <i>C. difficile</i> is transferred via the fecal-oral route as well as through spore dispersal. <i>Clostridium difficile</i>-associated disease (CDAD) was initially reported approximately 30 years ago. The CDC first recorded infections from a hyper-virulent strain in 2000 along with a marked increase in the number of CDAD infections. <i>C. difficile</i> causes disease by producing the toxins TcdA and TcdB that function to disrupt protein synthesis within the host cell. The toxins are responsible for producing symptoms such as watery diarrhea, fever, loss of appetite, nausea, and severe abdominal pain [[#References|[1]]]. Although <i>C. difficile</i> only causes about 20% of antibiotic associated colitis, standard treatments fail in about 25% of CDAD cases. Patients treated promptly typically recover. However, CDAD is notorious for recurrence after initial antibiotic treatment. 33% of patients with an infection will have a recurrence with 64% of those being within 30 days of the initial infection [[#References|[2]]]. Complications typically develop in about 11% of patients in the first recurrence. This likely promotes the growth of antibiotic resistant strains that are able to perform horizontal gene transfer between recurrences. In about 20% of patients the infection will resolve itself in 2-3 of discontinuing the inciting antibiotic. Most infections that persist are treated with a 10-14 day course of antibiotics like metronidazole, vancomycin, and rehydration therapy. In more serious cases fecal transplants and surgery can be performed. [[#References|[3]]] Patients at risk for developing CDAD include those taking antibiotics (especially broad spectrum), those taking proton pump inhibitors, GI manipulation or surgery, long term stays in hospital or clinical settings, immunocompromising conditions, and old age. The best practices for preventing infection include judicious administration of antibiotics, quarantine, hand hygiene, and the use of EPA-registered disinfectants with a sporicide (especially hypochlorite based disinfectants).</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><i>Clostridium difficile</i> is a Gram-positive, spore-forming rod <ins style="font-weight: bold; text-decoration: none;">(bacillus) </ins>that is an obligate anaerobe. It can be found in soil, water, feces, and the human gut. Infections of <i>Clostridium difficile</i> cause pseudomembranous colitis, toxic megacolon, perforations of the colon, sepsis, and, on occasion, death. <i>C. difficile</i> is a normal inhabitant of the gut microbial community of about 1-3% of adults. The pathogenic form of <i>C. difficile</i> is transferred via the fecal-oral route as well as through spore dispersal. <i>Clostridium difficile</i>-associated disease (CDAD) was initially reported approximately 30 years ago. The CDC first recorded infections from a hyper-virulent strain in 2000 along with a marked increase in the number of CDAD infections. <i>C. difficile</i> causes disease by producing the toxins TcdA and TcdB that function to disrupt protein synthesis within the host cell. The toxins are responsible for producing symptoms such as watery diarrhea, fever, loss of appetite, nausea, and severe abdominal pain [[#References|[1]]]. Although <i>C. difficile</i> only causes about 20% of antibiotic associated colitis, standard treatments fail in about 25% of CDAD cases. Patients treated promptly typically recover. However, CDAD is notorious for recurrence after initial antibiotic treatment. 33% of patients with an infection will have a recurrence with 64% of those being within 30 days of the initial infection [[#References|[2]]]. Complications typically develop in about 11% of patients in the first recurrence. This likely promotes the growth of antibiotic resistant strains that are able to perform horizontal gene transfer between recurrences. In about 20% of patients the infection will resolve itself in 2-3 of discontinuing the inciting antibiotic. Most infections that persist are treated with a 10-14 day course of antibiotics like metronidazole, vancomycin, and rehydration therapy. In more serious cases fecal transplants and surgery can be performed. [[#References|[3]]] Patients at risk for developing CDAD include those taking antibiotics (especially broad spectrum), those taking proton pump inhibitors, GI manipulation or surgery, long term stays in hospital or clinical settings, immunocompromising conditions, and old age. The best practices for preventing infection include judicious administration of antibiotics, quarantine, hand hygiene, and the use of EPA-registered disinfectants with a sporicide (especially hypochlorite based disinfectants).</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>==Pathogenesis==</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>==Pathogenesis==</div></td></tr>
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<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>===Transmission===</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>===Transmission===</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><i>Clostridium difficile</i> are shed in feces, and therefore these bacteria can be transmitted via the fecal-oral route. The spores can survive on almost any surface for months to years which makes the pathogen very difficult to get rid of once established. The spores are resistant to many extreme environments, including high temperatures, ultraviolet light, harsh chemicals, and antibiotics. Health care settings, including patients and workers, are often the reservoirs for <i>C. difficile</i> spores. Community-acquired infections are thought to be transmitted through soil, water, pets, meats, and vegetables.</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><i>Clostridium difficile</i> are shed in feces, and therefore these bacteria can be transmitted via the fecal-oral route. The spores can survive on almost any surface for months to years which makes the pathogen very difficult to get rid of once established. The spores are resistant to many extreme environments, including high temperatures, ultraviolet light, harsh chemicals, and antibiotics. Health care settings, including patients and workers, are often the reservoirs for <i>C. difficile</i> spores. Community-acquired infections are thought to be transmitted through soil, water, pets, meats, and vegetables.</div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></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><ins style="font-weight: bold; text-decoration: none;"></ins></div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></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><ins style="font-weight: bold; text-decoration: none;">[[File:spores.jpeg|400px|thumb|center|Transmission electron microscope image of <i>Clostridium difficile</i>. From: Austincc.edu [http://www.austincc.edu/microbio/2993q/cdiff.htm]]]</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>===Infectious dose, incubation, and colonization===</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>===Infectious dose, incubation, and colonization===</div></td></tr>
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<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>===Epidemiology===</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>===Epidemiology===</div></td></tr>
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<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>CDAD is most often a hospital-acquired infection that causes an estimated 3 million cases of diarrhea and colitis per year. Some reports state that 28% of patients who were hospitalized tested positive for <i>C. difficile</i>. Its incidence in hospitals has risen from 30-40 per 100,000 in the 1990s to 84 per 100,000 in 2005 [[#References|[4]]], and despite a decrease in other nosocomial infections from 2000-2009, the number of patients with CDAD discharge diagnosis more than doubled from approximately 139,000 to 336,600. In addition to this, the number of primary CDAD diagnoses more than tripled from 33,000 to 111,000. CDAD can be community-acquired, however the incidence of this is much lower than the hospital-acquired infections. The CDC’s Emerging Infections Program associated approximately 94% of CDAD diagnoses with receiving health care. Outside of the United States, the incidence of CDAD has also increased. For example, in one region of Quebec, its incidence quadrupled in 2003 to 92.2 per 100,000 populations.</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>CDAD is most often a <ins style="font-weight: bold; text-decoration: none;">nosocomial (</ins>hospital-acquired<ins style="font-weight: bold; text-decoration: none;">) </ins>infection that causes an estimated 3 million cases of diarrhea and colitis per year. Some reports state that 28% of patients who were hospitalized tested positive for <i>C. difficile</i>. Its incidence in hospitals has risen from 30-40 per 100,000 in the 1990s to 84 per 100,000 in 2005 [[#References|[4]]], and despite a decrease in other nosocomial infections from 2000-2009, the number of patients with CDAD discharge diagnosis more than doubled from approximately 139,000 to 336,600. In addition to this, the number of primary CDAD diagnoses more than tripled from 33,000 to 111,000. CDAD can be community-acquired, however the incidence of this is much lower than the hospital-acquired infections. The CDC’s Emerging Infections Program associated approximately 94% of CDAD diagnoses with receiving health care. Outside of the United States, the incidence of CDAD has also increased. For example, in one region of Quebec, its incidence quadrupled in 2003 to 92.2 per 100,000 populations.</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>====Morbidity and Mortality====</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>====Morbidity and Mortality====</div></td></tr>
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<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" 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>Created by Laura Boucher, Marrett Hild, and Lillian Flannigan, students of Tyrrell Conway at the University of Oklahoma</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>Created by Laura Boucher, Marrett Hild, and Lillian Flannigan, students of Tyrrell Conway<ins style="font-weight: bold; text-decoration: none;">, PhD at the University of Oklahoma</ins></div></td></tr>
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</table>Cassandra.K.Long-1https://microbewiki.kenyon.edu/index.php?title=Clostridium_difficile-associated_disease&diff=92016&oldid=prevBarichD at 19:58, 28 August 20132013-08-28T19:58:15Z<p></p>
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<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>{{Curated}}</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>{{Curated}}</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:OULOGOBIANCO.JPEG|thumb|230px|left|University of Oklahoma Study Abroad Microbiology in Arezzo, Italy[http://cas.ou.edu/study-abroad/]]]</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:OULOGOBIANCO.JPEG|thumb|230px|left|University of Oklahoma Study Abroad Microbiology in Arezzo, Italy[http://cas.ou.edu/study-abroad/]]]</div></td></tr>
</table>BarichDhttps://microbewiki.kenyon.edu/index.php?title=Clostridium_difficile-associated_disease&diff=91758&oldid=prevJennifer.E.Gallup-1: /* Host Immune Response */2013-07-25T16:44:48Z<p><span dir="auto"><span class="autocomment">Host Immune Response</span></span></p>
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<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>==Host Immune Response==</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>==Host Immune Response==</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 pathophysiology of <i>C. difficile</i> is directly related to the host immune response to CDI. <i>C. difficile</i> colonizes in the lumen of the small intestine where it can lie dormant by means of sporulation, or it produces enterotoxins TcdA and TcdB<del style="font-weight: bold; text-decoration: none;">, </del>eliciting an inflammatory immune response. Toxin A attracts polymorphonuclear cells (PMNs) or neutrophils to the site of infection via cytokines from epithelial host cells. This influx of leukocytes as a function of the immune response increases vascular permeability, allowing TcdA and TcdB to cross the mucosal membrane. TcdB degrades colonic epithelial cells. Accumulations of leukocytes form a pseudomembrane on the lining of the colon (pseudomembranous colitis).<br><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 pathophysiology of <i>C. difficile</i> is directly related to the host immune response to CDI. <i>C. difficile</i> colonizes in the lumen of the small intestine where it can lie dormant by means of sporulation, or it produces enterotoxins TcdA and TcdB eliciting an inflammatory immune response. Toxin A attracts polymorphonuclear cells (PMNs) or neutrophils to the site of infection via cytokines from epithelial host cells. This influx of leukocytes as a function of the immune response increases vascular permeability, allowing TcdA and TcdB to cross the mucosal membrane. TcdB degrades colonic epithelial cells. Accumulations of leukocytes form a pseudomembrane on the lining of the colon (pseudomembranous colitis).<br><br></div></td></tr>
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<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>Current research suggests that upon exposure to <i>C. difficile</i>, humans develop an adaptive immunity to TcdA and TcdB. It is estimated that approximately 60% of healthy adults exhibit IgG and IgA antibodies against C. difficile toxins. Studies suggest that adaptive immunity can begin in childhood from environmental exposure to <i>C. difficile</i>, and possibly non-toxigenic clostridial species [[#References|[13,14]]]. Studies show that immunoglobulin A (IgA) antibody inhibits TcdA binding to epithelial cells in the colon [[#References|[12]]]. Moreover, higher levels of IgA and IgG anti-toxins were found in asymptomatic patients, as well as those who displayed minor symptoms of CDAD [[#References|[13,14]]].</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>Current research suggests that upon exposure to <i>C. difficile</i>, humans develop an adaptive immunity to TcdA and TcdB. It is estimated that approximately 60% of healthy adults exhibit IgG and IgA antibodies against C. difficile toxins. Studies suggest that adaptive immunity can begin in childhood from environmental exposure to <i>C. difficile</i>, and possibly non-toxigenic clostridial species [[#References|[13,14]]]. Studies show that immunoglobulin A (IgA) antibody inhibits TcdA binding to epithelial cells in the colon [[#References|[12]]]. Moreover, higher levels of IgA and IgG anti-toxins were found in asymptomatic patients, as well as those who displayed minor symptoms of CDAD [[#References|[13,14]]].</div></td></tr>
</table>Jennifer.E.Gallup-1