https://microbewiki.kenyon.edu/index.php?title=Free_Fatty_Acids_as_antibacterial_agents_against_several_super_pathogens_including_MRSA&feed=atom&action=historyFree Fatty Acids as antibacterial agents against several super pathogens including MRSA - Revision history2024-03-28T15:14:46ZRevision history for this page on the wikiMediaWiki 1.39.6https://microbewiki.kenyon.edu/index.php?title=Free_Fatty_Acids_as_antibacterial_agents_against_several_super_pathogens_including_MRSA&diff=119049&oldid=prevMccannsmithe: /* Bactericidal Effects of Fatty Acids on Methicillin Resistant and Susceptible Staphylococcus aureus */2015-12-15T19:46:08Z<p><span dir="auto"><span class="autocomment">Bactericidal Effects of Fatty Acids on Methicillin Resistant and Susceptible Staphylococcus aureus</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>==Bactericidal Effects of Fatty Acids on Methicillin Resistant and Susceptible <i>Staphylococcus aureus</i>==</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>==Bactericidal Effects of Fatty Acids on Methicillin Resistant and Susceptible <i>Staphylococcus aureus</i>==</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" 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 mechanism of mutation from methicillin sensitive Staphylococcus aureus to methicillin resistant <i>S. aureus</i> (MRSA) is through the acquisition of the gene mecA, which after integration into the chromosome, codes for the penicillin-binding protein 2a, PBP2a. This protein can continue to crosslink peptidoglycan, the component of the cell wall, because it does not bind to methicillin or other beta-lactam antibiotics, making them all useless in treatment of MRSA.[http://www.jci.org/articles/view/18535 [26]] It is important to study many strains of <i>S. aureus</i>, both resistant and not-resistant to typical antibiotic treatments, to be sure that the treatment in question will behave appropriately towards strains with different genetic variation. Of course, it is most important to find treatments against MRSA, as this has the highest current medical demand for a treatment. But eventually, finding compounds (or a combination of compounds) that prevent mutation in all variations of the species would be beneficial to everyone around the globe, and a way to practice preventative medicine, rather than reactive medicine.<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 mechanism of mutation from methicillin sensitive <ins style="font-weight: bold; text-decoration: none;"><i></ins>Staphylococcus aureus<ins style="font-weight: bold; text-decoration: none;"></i> </ins>to methicillin resistant <i>S. aureus</i> (MRSA) is through the acquisition of the gene mecA, which after integration into the chromosome, codes for the penicillin-binding protein 2a, PBP2a. This protein can continue to crosslink peptidoglycan, the component of the cell wall, because it does not bind to methicillin or other beta-lactam antibiotics, making them all useless in treatment of MRSA.[http://www.jci.org/articles/view/18535 [26]] It is important to study many strains of <i>S. aureus</i>, both resistant and not-resistant to typical antibiotic treatments, to be sure that the treatment in question will behave appropriately towards strains with different genetic variation. Of course, it is most important to find treatments against MRSA, as this has the highest current medical demand for a treatment. But eventually, finding compounds (or a combination of compounds) that prevent mutation in all variations of the species would be beneficial to everyone around the globe, and a way to practice preventative medicine, rather than reactive medicine.<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;"><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>Free fatty acids on human skin have been shown to have antibacterial properties against both methicillin susceptible (MSSA) and resistant (MRSA) Staphylococcus aureus. However, in order for the colonization of the bacteria to occur in the first place, the external mechanisms of protection must be nonfunctioning (i.e. the fatty acids living on the skin normally are not working effectively in protection). This could be because of a pre-existing skin disorder such as eczema (which will be addressed later on in this section), or because of mutations in the bacteria that allow it to survive regardless of the presence of the fatty acids. <i>S. aureus</i> possess surface proteins that interact with human serum proteins and human extracellular matrix proteins. A surface protein IsdA that is covalently attached to the bacterium, is needed in order to colonize the human nose. This is only expressed, however, under iron starvation, which is how the bacteria know they are in contact with their host: the skin is a biologically available iron poor environment.[http://europepmc.org/abstract/MED/18005699 [27]]. The presence of this protein makes <i>S. aureus</i> more hydrophilic and negatively charged, complicating the interaction between itself and the hydrophobic fatty acids.</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>Free fatty acids on human skin have been shown to have antibacterial properties against both methicillin susceptible (MSSA) and resistant (MRSA) Staphylococcus aureus. However, in order for the colonization of the bacteria to occur in the first place, the external mechanisms of protection must be nonfunctioning (i.e. the fatty acids living on the skin normally are not working effectively in protection). This could be because of a pre-existing skin disorder such as eczema (which will be addressed later on in this section), or because of mutations in the bacteria that allow it to survive regardless of the presence of the fatty acids. <i>S. aureus</i> possess surface proteins that interact with human serum proteins and human extracellular matrix proteins. A surface protein IsdA that is covalently attached to the bacterium, is needed in order to colonize the human nose. This is only expressed, however, under iron starvation, which is how the bacteria know they are in contact with their host: the skin is a biologically available iron poor environment.[http://europepmc.org/abstract/MED/18005699 [27]]. The presence of this protein makes <i>S. aureus</i> more hydrophilic and negatively charged, complicating the interaction between itself and the hydrophobic fatty acids.</div></td></tr>
</table>Mccannsmithehttps://microbewiki.kenyon.edu/index.php?title=Free_Fatty_Acids_as_antibacterial_agents_against_several_super_pathogens_including_MRSA&diff=119048&oldid=prevMccannsmithe: /* History of Fatty Acids as Antimicrobial Agents */2015-12-15T19:45:14Z<p><span dir="auto"><span class="autocomment">History of Fatty Acids as Antimicrobial Agents</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>In 1972 a research group from Michigan Sate University published extensive data on the effects of several fatty acids on both gram-positive and gram-negative bacteria.[http://www.ncbi.nlm.nih.gov/pmc/articles/PMC444260/] They demonstrated that by increasing the unsaturation of the fatty acids through the addition of cis double bonds, they could make these fatty acids more effective against gram-positive bacteria, but when the carboxylic acid was esterified the compounds lost their antibacterial effect. Strangely, they found that lauric acid, a saturated fatty acid, had the highest bacteriostatic potential towards these gram-positive bacteria of which included Staphylococcus genus, (which includes MRSA). Lauric acid was found to have the highest antimicrobial activity out a pool of saturated fatty acids, but overall, saturated fatty acids had lower activity than those that were unsaturated.[http://www.karger.com/Article/Abstract/69757] Palmitoleic acid, a monoene of human skin, was found to be most active against gram-positive bacteria, although in combination with ethanol, a synergistic effect against gram-negative bacteria (<i>P. aeruginosa, P. acnes, E. coli</i>) was seen.</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>In 1972 a research group from Michigan Sate University published extensive data on the effects of several fatty acids on both gram-positive and gram-negative bacteria.[http://www.ncbi.nlm.nih.gov/pmc/articles/PMC444260/] They demonstrated that by increasing the unsaturation of the fatty acids through the addition of cis double bonds, they could make these fatty acids more effective against gram-positive bacteria, but when the carboxylic acid was esterified the compounds lost their antibacterial effect. Strangely, they found that lauric acid, a saturated fatty acid, had the highest bacteriostatic potential towards these gram-positive bacteria of which included Staphylococcus genus, (which includes MRSA). Lauric acid was found to have the highest antimicrobial activity out a pool of saturated fatty acids, but overall, saturated fatty acids had lower activity than those that were unsaturated.[http://www.karger.com/Article/Abstract/69757] Palmitoleic acid, a monoene of human skin, was found to be most active against gram-positive bacteria, although in combination with ethanol, a synergistic effect against gram-negative bacteria (<i>P. aeruginosa, P. acnes, E. coli</i>) was seen.</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" 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>Staphylococci epidermidis are found in abundance on healthy skin, whereas <i>S. aureus</i> are usually only found on damaged skin, but the reasons for this are unknown. A study in 1985 showed that staphylococci that were coagulase-positive, i.e. <i>S. aureus</i>, on the skin were sensitive to linolenic acid,[http://jmm.microbiologyresearch.org/content/journal/jmm/10.1099/00222615-14-1-41] while other fatty acids were determined to have the same activity against coagulase-positive versus coagulase-negative staphylococci suggesting interference with the enzyme coagulase as a possible mechanism of action. This finding supports the premise that treatment with linolenic acid may be species specific, which is important because preserving <i>Staphylococcus</i> not of the species <i> S. aureus </i> is beneficial to the human system. The researchers even mutated the <i>S. aureus</i>, changing the characteristics of the bacteria in an attempt to mimic rapid evolution associated with resistance, to find a resistant strain towards linoleic acid. They were unsuccessful, suggesting linolenic acid will not cause resistance in bacteria, like other forms of treatment such as antibiotics. They also found that if human skin was covered in linolenic acid prior to the seeding of <i>S. aureus</i>, the bacteria were rapidly killed. However, the same group also found that antibacterial effects of this acid were reversed <i>in vitro</i> when low concentrations of human serum were present. They suggest a potential “detergent” mechanism, possibly the change in the functional group of the acid. This suggests potential problems with internal treatment of bacterial infections with linolenic acid. Another group got similar results with a different fatty acid, lauric acid, where interactions human blood plasma decreased <del style="font-weight: bold; text-decoration: none;">the </del>antimicrobial activity <del style="font-weight: bold; text-decoration: none;">of the fatty acid</del>.[https://www.jstage.jst.go.jp/article/bpb/27/9/27_9_1321/_article] <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>Staphylococci epidermidis are found in abundance on healthy skin, whereas <i>S. aureus</i> are usually only found on damaged skin, but the reasons for this are unknown. A study in 1985 showed that staphylococci that were coagulase-positive, i.e. <i>S. aureus</i>, on the skin were sensitive to linolenic acid,[http://jmm.microbiologyresearch.org/content/journal/jmm/10.1099/00222615-14-1-41] while other fatty acids were determined to have the same activity against coagulase-positive versus coagulase-negative staphylococci suggesting interference with the enzyme coagulase as a possible mechanism of action. This finding supports the premise that treatment with linolenic acid may be species specific, which is important because preserving <i>Staphylococcus</i> not of the species <i> S. aureus </i> is beneficial to the human system. The researchers even mutated the <i>S. aureus</i>, changing the characteristics of the bacteria in an attempt to mimic rapid evolution associated with resistance, to find a resistant strain towards linoleic acid. They were unsuccessful, suggesting linolenic acid will not cause resistance in bacteria, like other forms of treatment such as antibiotics. They also found that if human skin was covered in linolenic acid prior to the seeding of <i>S. aureus</i>, the bacteria were rapidly killed. However, the same group also found that antibacterial effects of this acid were reversed <i>in vitro</i> when low concentrations of human serum were present. They suggest a potential “detergent” mechanism, possibly the change in the functional group of the acid. This suggests potential problems with internal treatment of bacterial infections with linolenic acid. Another group got similar results with a different fatty acid, lauric acid, where interactions <ins style="font-weight: bold; text-decoration: none;">with </ins>human blood plasma decreased <ins style="font-weight: bold; text-decoration: none;">its </ins>antimicrobial activity.[https://www.jstage.jst.go.jp/article/bpb/27/9/27_9_1321/_article] <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;"><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>==Bactericidal Effects of Fatty Acids on Methicillin Resistant and Susceptible <i>Staphylococcus aureus</i>==</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>==Bactericidal Effects of Fatty Acids on Methicillin Resistant and Susceptible <i>Staphylococcus aureus</i>==</div></td></tr>
</table>Mccannsmithehttps://microbewiki.kenyon.edu/index.php?title=Free_Fatty_Acids_as_antibacterial_agents_against_several_super_pathogens_including_MRSA&diff=119047&oldid=prevMccannsmithe: /* History of Fatty Acids as Antimicrobial Agents */2015-12-15T19:43:27Z<p><span dir="auto"><span class="autocomment">History of Fatty Acids as Antimicrobial Agents</span></span></p>
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<td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">Revision as of 19:43, 15 December 2015</td>
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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>In 1972 a research group from Michigan Sate University published extensive data on the effects of several fatty acids on both gram-positive and gram-negative bacteria.[http://www.ncbi.nlm.nih.gov/pmc/articles/PMC444260/] They demonstrated that by increasing the unsaturation of the fatty acids through the addition of cis double bonds, they could make these fatty acids more effective against gram-positive bacteria, but when the carboxylic acid was esterified the compounds lost their antibacterial effect. Strangely, they found that lauric acid, a saturated fatty acid, had the highest bacteriostatic potential towards these gram-positive bacteria of which included Staphylococcus genus, (which includes MRSA). Lauric acid was found to have the highest antimicrobial activity out a pool of saturated fatty acids, but overall, saturated fatty acids had lower activity than those that were unsaturated.[http://www.karger.com/Article/Abstract/69757] Palmitoleic acid, a monoene of human skin, was found to be most active against gram-positive bacteria, although in combination with ethanol, a synergistic effect against gram-negative bacteria (<i>P. aeruginosa, P. acnes, E. coli</i>) was seen.</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>In 1972 a research group from Michigan Sate University published extensive data on the effects of several fatty acids on both gram-positive and gram-negative bacteria.[http://www.ncbi.nlm.nih.gov/pmc/articles/PMC444260/] They demonstrated that by increasing the unsaturation of the fatty acids through the addition of cis double bonds, they could make these fatty acids more effective against gram-positive bacteria, but when the carboxylic acid was esterified the compounds lost their antibacterial effect. Strangely, they found that lauric acid, a saturated fatty acid, had the highest bacteriostatic potential towards these gram-positive bacteria of which included Staphylococcus genus, (which includes MRSA). Lauric acid was found to have the highest antimicrobial activity out a pool of saturated fatty acids, but overall, saturated fatty acids had lower activity than those that were unsaturated.[http://www.karger.com/Article/Abstract/69757] Palmitoleic acid, a monoene of human skin, was found to be most active against gram-positive bacteria, although in combination with ethanol, a synergistic effect against gram-negative bacteria (<i>P. aeruginosa, P. acnes, E. coli</i>) was seen.</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" 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>Staphylococci epidermidis are found in abundance on healthy skin, whereas <i>S. aureus</i> are usually only found on damaged skin, but the reasons for this are unknown. A study in 1985 showed that staphylococci that were coagulase-positive, i.e. <i>S. aureus</i>, on the skin were sensitive to linolenic acid,[http://jmm.microbiologyresearch.org/content/journal/jmm/10.1099/00222615-14-1-41] while other fatty acids were determined to have the same activity against coagulase-positive versus coagulase-negative staphylococci suggesting interference with the enzyme coagulase as a possible mechanism of action. This finding supports the premise that treatment with linolenic acid may be species specific, which is important because preserving Staphylococcus not of the species <i> S. aureus </i> is beneficial to the human system. The researchers even mutated the <i>S. aureus</i>, changing the characteristics of the bacteria in an attempt to mimic rapid evolution associated with resistance, to find a resistant strain towards linoleic acid. They were unsuccessful, suggesting linolenic acid will not cause resistance in bacteria, like other forms of treatment such as antibiotics. They also found that if human skin was covered in linolenic acid prior to the seeding of <i>S. aureus</i>, the bacteria were rapidly killed. However, the same group also found that antibacterial effects of this acid were reversed <i>in vitro</i> when low concentrations of human serum were present. They suggest a potential “detergent” mechanism, possibly the change in the functional group of the acid. This suggests potential problems with internal treatment of bacterial infections with linolenic acid. Another group got similar results with a different fatty acid, lauric acid, where interactions human blood plasma decreased the antimicrobial activity of the fatty acid.[https://www.jstage.jst.go.jp/article/bpb/27/9/27_9_1321/_article] <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>Staphylococci epidermidis are found in abundance on healthy skin, whereas <i>S. aureus</i> are usually only found on damaged skin, but the reasons for this are unknown. A study in 1985 showed that staphylococci that were coagulase-positive, i.e. <i>S. aureus</i>, on the skin were sensitive to linolenic acid,[http://jmm.microbiologyresearch.org/content/journal/jmm/10.1099/00222615-14-1-41] while other fatty acids were determined to have the same activity against coagulase-positive versus coagulase-negative staphylococci suggesting interference with the enzyme coagulase as a possible mechanism of action. This finding supports the premise that treatment with linolenic acid may be species specific, which is important because preserving <ins style="font-weight: bold; text-decoration: none;"><i></ins>Staphylococcus<ins style="font-weight: bold; text-decoration: none;"></i> </ins>not of the species <i> S. aureus </i> is beneficial to the human system. The researchers even mutated the <i>S. aureus</i>, changing the characteristics of the bacteria in an attempt to mimic rapid evolution associated with resistance, to find a resistant strain towards linoleic acid. They were unsuccessful, suggesting linolenic acid will not cause resistance in bacteria, like other forms of treatment such as antibiotics. They also found that if human skin was covered in linolenic acid prior to the seeding of <i>S. aureus</i>, the bacteria were rapidly killed. However, the same group also found that antibacterial effects of this acid were reversed <i>in vitro</i> when low concentrations of human serum were present. They suggest a potential “detergent” mechanism, possibly the change in the functional group of the acid. This suggests potential problems with internal treatment of bacterial infections with linolenic acid. Another group got similar results with a different fatty acid, lauric acid, where interactions human blood plasma decreased the antimicrobial activity of the fatty acid.[https://www.jstage.jst.go.jp/article/bpb/27/9/27_9_1321/_article] <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;"><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>==Bactericidal Effects of Fatty Acids on Methicillin Resistant and Susceptible <i>Staphylococcus aureus</i>==</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>==Bactericidal Effects of Fatty Acids on Methicillin Resistant and Susceptible <i>Staphylococcus aureus</i>==</div></td></tr>
</table>Mccannsmithehttps://microbewiki.kenyon.edu/index.php?title=Free_Fatty_Acids_as_antibacterial_agents_against_several_super_pathogens_including_MRSA&diff=119046&oldid=prevMccannsmithe: /* References */2015-12-15T19:39:29Z<p><span dir="auto"><span class="autocomment">References</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;"><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>[1] <del style="font-weight: bold; text-decoration: none;">[</del>http://www.ncbi.nlm.nih.gov/pubmedhealth/PMHT0025827/?figure=1<del style="font-weight: bold; text-decoration: none;">]</del></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>[1] http://www.ncbi.nlm.nih.gov/pubmedhealth/PMHT0025827/?figure=1</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>[2] [http://www.sciencedirect.com/science/article/pii/S1931312807000716 Clarke, S.R., Mohamed, R., Bian, L. et al. The Staphylococcus aureus Surface Protein IsdA Mediates Resistance to Innate Defenses of Human Skin. (2007) Cell Host & Microbe, 1(3): 199-212]</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>[2] [http://www.sciencedirect.com/science/article/pii/S1931312807000716 Clarke, S.R., Mohamed, R., Bian, L. et al. The Staphylococcus aureus Surface Protein IsdA Mediates Resistance to Innate Defenses of Human Skin. (2007) Cell Host & Microbe, 1(3): 199-212]</div></td></tr>
</table>Mccannsmithehttps://microbewiki.kenyon.edu/index.php?title=Free_Fatty_Acids_as_antibacterial_agents_against_several_super_pathogens_including_MRSA&diff=119045&oldid=prevMccannsmithe: /* References */2015-12-15T19:39:13Z<p><span dir="auto"><span class="autocomment">References</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>==References==</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>==References==</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" 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>[1] [<del style="font-weight: bold; text-decoration: none;">https</del>://<del style="font-weight: bold; text-decoration: none;">commons</del>.<del style="font-weight: bold; text-decoration: none;">wikimedia</del>.<del style="font-weight: bold; text-decoration: none;">org</del>/<del style="font-weight: bold; text-decoration: none;">wiki</del>/<del style="font-weight: bold; text-decoration: none;">File%3AHuman_neutrophil_ingesting_MRSA.jpg Wikimedia. NIH.</del>]</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>[1] [<ins style="font-weight: bold; text-decoration: none;">http</ins>://<ins style="font-weight: bold; text-decoration: none;">www</ins>.<ins style="font-weight: bold; text-decoration: none;">ncbi</ins>.<ins style="font-weight: bold; text-decoration: none;">nlm.nih.gov/pubmedhealth</ins>/<ins style="font-weight: bold; text-decoration: none;">PMHT0025827</ins>/<ins style="font-weight: bold; text-decoration: none;">?figure=1</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>[2] [http://www.sciencedirect.com/science/article/pii/S1931312807000716 Clarke, S.R., Mohamed, R., Bian, L. et al. The Staphylococcus aureus Surface Protein IsdA Mediates Resistance to Innate Defenses of Human Skin. (2007) Cell Host & Microbe, 1(3): 199-212]</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>[2] [http://www.sciencedirect.com/science/article/pii/S1931312807000716 Clarke, S.R., Mohamed, R., Bian, L. et al. The Staphylococcus aureus Surface Protein IsdA Mediates Resistance to Innate Defenses of Human Skin. (2007) Cell Host & Microbe, 1(3): 199-212]</div></td></tr>
</table>Mccannsmithehttps://microbewiki.kenyon.edu/index.php?title=Free_Fatty_Acids_as_antibacterial_agents_against_several_super_pathogens_including_MRSA&diff=119044&oldid=prevMccannsmithe: /* An Introduction to Super Pathogens */2015-12-15T19:38:56Z<p><span dir="auto"><span class="autocomment">An Introduction to Super Pathogens</span></span></p>
<table style="background-color: #fff; color: #202122;" data-mw="interface">
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<td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">Revision as of 19:38, 15 December 2015</td>
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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>==An Introduction to Super Pathogens==</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>==An Introduction to Super Pathogens==</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>[[Image:MRSA2.jpg|thumb|300px|left| <b>Figure 1.</b> Scanning electron micrograph of Methicillin-resistant Staphylococcus aureus (MRSA), USA300 strain, being engulfed by a human neutrophil. [http://www.ncbi.nlm.nih.gov/pubmedhealth/PMHT0025827/?figure=1<del style="font-weight: bold; text-decoration: none;">.</del>]]</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>[[Image:MRSA2.jpg|thumb|300px|left| <b>Figure 1.</b> Scanning electron micrograph of Methicillin-resistant Staphylococcus aureus (MRSA), USA300 strain, being engulfed by a human neutrophil. [http://www.ncbi.nlm.nih.gov/pubmedhealth/PMHT0025827/?figure=1<ins style="font-weight: bold; text-decoration: none;">]</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><br>Over the past century, modern science has been overusing and misusing antibiotics, leading to the evolution of many “super pathogens”, or microbes that are resistant to most of the common antibiotics and other methods normally used to treat them. Bacteria and viruses that evade modern treatment through mutation and resistance are health dangers to hospital patients as well as to community members. Free fatty acids are a potential "natural" treatment that can be effective against certain microbes. For example, <i>Staphylococcus aureus</i> a bacterium that colonizes the human nose and skin is susceptible to certain kinds of free fatty acids. This is important because recently, overuse of antibiotics has led to the mutation of this pest bacteria to the super pathogen that is MRSA, Methicillin Resistant <i>Staphylococcus aureus</i> [Figure 1]. MRSA cannot be effectively treated by an entire class of common antibiotics called beta-lactams (which include penicillin and methicillin among others) [http://www.niaid.nih.gov/topics/antimicrobialResistance/Examples/mrsa/]. Even the most potent “last line of defense” antibiotic, vancomycin, is ineffective on some strains of MRSA (VRSA, for vancomycin resistant <i>Staphylococcus aureus</i>)[http://www.sciencedirect.com/science/article/pii/S1473309910702590]. There are many of these pathogens - named super pathogens - that have developed resistance, including <i>Clostridium difficile</i>[http://www.cdc.gov/drugresistance/threat-report-2013/index.html], several <i>Enterococcus</i> species including <i>E. avium</i>[http://www.antimicrobe.org/new/b03.asp], along with many others.</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>Over the past century, modern science has been overusing and misusing antibiotics, leading to the evolution of many “super pathogens”, or microbes that are resistant to most of the common antibiotics and other methods normally used to treat them. Bacteria and viruses that evade modern treatment through mutation and resistance are health dangers to hospital patients as well as to community members. Free fatty acids are a potential "natural" treatment that can be effective against certain microbes. For example, <i>Staphylococcus aureus</i> a bacterium that colonizes the human nose and skin is susceptible to certain kinds of free fatty acids. This is important because recently, overuse of antibiotics has led to the mutation of this pest bacteria to the super pathogen that is MRSA, Methicillin Resistant <i>Staphylococcus aureus</i> [Figure 1]. MRSA cannot be effectively treated by an entire class of common antibiotics called beta-lactams (which include penicillin and methicillin among others) [http://www.niaid.nih.gov/topics/antimicrobialResistance/Examples/mrsa/]. Even the most potent “last line of defense” antibiotic, vancomycin, is ineffective on some strains of MRSA (VRSA, for vancomycin resistant <i>Staphylococcus aureus</i>)[http://www.sciencedirect.com/science/article/pii/S1473309910702590]. There are many of these pathogens - named super pathogens - that have developed resistance, including <i>Clostridium difficile</i>[http://www.cdc.gov/drugresistance/threat-report-2013/index.html], several <i>Enterococcus</i> species including <i>E. avium</i>[http://www.antimicrobe.org/new/b03.asp], along with many others.</div></td></tr>
</table>Mccannsmithehttps://microbewiki.kenyon.edu/index.php?title=Free_Fatty_Acids_as_antibacterial_agents_against_several_super_pathogens_including_MRSA&diff=119043&oldid=prevMccannsmithe: /* An Introduction to Super Pathogens */2015-12-15T19:38:10Z<p><span dir="auto"><span class="autocomment">An Introduction to Super Pathogens</span></span></p>
<table style="background-color: #fff; color: #202122;" data-mw="interface">
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<td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">Revision as of 19:38, 15 December 2015</td>
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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>==An Introduction to Super Pathogens==</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>==An Introduction to Super Pathogens==</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>[[Image:MRSA2.jpg|thumb|300px|left| <b>Figure 1.</b> Scanning electron micrograph of Methicillin-resistant Staphylococcus aureus (MRSA), USA300 strain, being engulfed by a human neutrophil. [<del style="font-weight: bold; text-decoration: none;">https</del>://<del style="font-weight: bold; text-decoration: none;">commons</del>.<del style="font-weight: bold; text-decoration: none;">wikimedia</del>.<del style="font-weight: bold; text-decoration: none;">org</del>/<del style="font-weight: bold; text-decoration: none;">wiki</del>/<del style="font-weight: bold; text-decoration: none;">File%3AHuman_neutrophil_ingesting_MRSA.jpg]</del>.]]</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>[[Image:MRSA2.jpg|thumb|300px|left| <b>Figure 1.</b> Scanning electron micrograph of Methicillin-resistant Staphylococcus aureus (MRSA), USA300 strain, being engulfed by a human neutrophil. [<ins style="font-weight: bold; text-decoration: none;">http</ins>://<ins style="font-weight: bold; text-decoration: none;">www</ins>.<ins style="font-weight: bold; text-decoration: none;">ncbi</ins>.<ins style="font-weight: bold; text-decoration: none;">nlm.nih.gov/pubmedhealth</ins>/<ins style="font-weight: bold; text-decoration: none;">PMHT0025827</ins>/<ins style="font-weight: bold; text-decoration: none;">?figure=1</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><br>Over the past century, modern science has been overusing and misusing antibiotics, leading to the evolution of many “super pathogens”, or microbes that are resistant to most of the common antibiotics and other methods normally used to treat them. Bacteria and viruses that evade modern treatment through mutation and resistance are health dangers to hospital patients as well as to community members. Free fatty acids are a potential "natural" treatment that can be effective against certain microbes. For example, <i>Staphylococcus aureus</i> a bacterium that colonizes the human nose and skin is susceptible to certain kinds of free fatty acids. This is important because recently, overuse of antibiotics has led to the mutation of this pest bacteria to the super pathogen that is MRSA, Methicillin Resistant <i>Staphylococcus aureus</i> [Figure 1]. MRSA cannot be effectively treated by an entire class of common antibiotics called beta-lactams (which include penicillin and methicillin among others) [http://www.niaid.nih.gov/topics/antimicrobialResistance/Examples/mrsa/]. Even the most potent “last line of defense” antibiotic, vancomycin, is ineffective on some strains of MRSA (VRSA, for vancomycin resistant <i>Staphylococcus aureus</i>)[http://www.sciencedirect.com/science/article/pii/S1473309910702590]. There are many of these pathogens - named super pathogens - that have developed resistance, including <i>Clostridium difficile</i>[http://www.cdc.gov/drugresistance/threat-report-2013/index.html], several <i>Enterococcus</i> species including <i>E. avium</i>[http://www.antimicrobe.org/new/b03.asp], along with many others.</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>Over the past century, modern science has been overusing and misusing antibiotics, leading to the evolution of many “super pathogens”, or microbes that are resistant to most of the common antibiotics and other methods normally used to treat them. Bacteria and viruses that evade modern treatment through mutation and resistance are health dangers to hospital patients as well as to community members. Free fatty acids are a potential "natural" treatment that can be effective against certain microbes. For example, <i>Staphylococcus aureus</i> a bacterium that colonizes the human nose and skin is susceptible to certain kinds of free fatty acids. This is important because recently, overuse of antibiotics has led to the mutation of this pest bacteria to the super pathogen that is MRSA, Methicillin Resistant <i>Staphylococcus aureus</i> [Figure 1]. MRSA cannot be effectively treated by an entire class of common antibiotics called beta-lactams (which include penicillin and methicillin among others) [http://www.niaid.nih.gov/topics/antimicrobialResistance/Examples/mrsa/]. Even the most potent “last line of defense” antibiotic, vancomycin, is ineffective on some strains of MRSA (VRSA, for vancomycin resistant <i>Staphylococcus aureus</i>)[http://www.sciencedirect.com/science/article/pii/S1473309910702590]. There are many of these pathogens - named super pathogens - that have developed resistance, including <i>Clostridium difficile</i>[http://www.cdc.gov/drugresistance/threat-report-2013/index.html], several <i>Enterococcus</i> species including <i>E. avium</i>[http://www.antimicrobe.org/new/b03.asp], along with many others.</div></td></tr>
</table>Mccannsmithehttps://microbewiki.kenyon.edu/index.php?title=Free_Fatty_Acids_as_antibacterial_agents_against_several_super_pathogens_including_MRSA&diff=118689&oldid=prevMccannsmithe: /* Bactericidal Effects of Fatty Acids on Methicillin Resistant and Susceptible Staphylococcus aureus */2015-12-09T03:25:37Z<p><span dir="auto"><span class="autocomment">Bactericidal Effects of Fatty Acids on Methicillin Resistant and Susceptible Staphylococcus aureus</span></span></p>
<table style="background-color: #fff; color: #202122;" data-mw="interface">
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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:Sapienic_acid_MRSA.png|thumb|300px|left| <b> Figure 3. </b> Transmission electron microscopy showing the morphology of <i>S. aureus</i> after 2 hour killing assay in the absence (A) or presence (B) of 5 µg/ml sapienic acid. The arrows show aberrant septation events. [http://aac.asm.org/content/58/7/3599.full].]]</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:Sapienic_acid_MRSA.png|thumb|300px|left| <b> Figure 3. </b> Transmission electron microscopy showing the morphology of <i>S. aureus</i> after 2 hour killing assay in the absence (A) or presence (B) of 5 µg/ml sapienic acid. The arrows show aberrant septation events. [http://aac.asm.org/content/58/7/3599.full].]]</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" 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 most effective fatty acid against <i>S. aureus</i> colonization was found to be cis-6-Hexadecanoic acid (commonly known as sapienic acid).[http://aac.asm.org/content/58/7/3599.full [28]] This fatty acid was linked to <i>S. aureus</i> when it was found that people with atopic dermatitis (eczema) had higher levels of <i>S. aureus</i> on their skin, corresponding with lower levels of sapienic acid. [http://www.karger.com/Article/Abstract/87018 [29]]. MRSA is a big enough problem for people without skin disorders, but for individuals with atopic dermatitis, recurrent infections often lead to eczema exacerbation. There is currently no standard treatment for prevention of recurrent infections in either this patient group or the total patient group with MRSA. [http://www.sciencedirect.com/science/article/pii/S2213219814001718 [30]]. People with atopic dermatitis are also more likely to be colonized by <i>S. aureus</i>, prompting a closer look at their skin composition compared to those without a skin disorder. A difference in concentration of sapienic acid, a fatty acid usually found in high abundance on human skin in healthy patients, was found between groups. Patients with atopic dermatitis had lower amounts of acid on their skin, which correlated with higher colonization of <i>S. aureus</i>. Most interesting is that this is a reversible problem. [[Image:Carbohydrate_FA.png|thumb|300px|right| <b> Figure 4. </b> Carbohydrate fatty acid derivatives that have antibacterial qualities towards <i>S. aureus</i>, excluding compound 4, which has its hydroxyl group in the wrong orientation. [http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2672.2009.04622.x/epdf].]] <del style="font-weight: bold; text-decoration: none;">When patients with atopic dermatitis were topically </del>treated with sapienic acid, colonization of <i>S. aureus</i> decreased, excitingly suggesting that sapienic acid is a pivotal factor in the skin’s innate immune system against <i>S. aureus</i> specifically.</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 most effective fatty acid against <i>S. aureus</i> colonization was found to be cis-6-Hexadecanoic acid (commonly known as sapienic acid).[http://aac.asm.org/content/58/7/3599.full [28]] This fatty acid was linked to <i>S. aureus</i> when it was found that people with atopic dermatitis (eczema) had higher levels of <i>S. aureus</i> on their skin, corresponding with lower levels of sapienic acid. [http://www.karger.com/Article/Abstract/87018 [29]]. MRSA is a big enough problem for people without skin disorders, but for individuals with atopic dermatitis, recurrent infections often lead to eczema exacerbation. There is currently no standard treatment for prevention of recurrent infections in either this patient group or the total patient group with MRSA. [http://www.sciencedirect.com/science/article/pii/S2213219814001718 [30]]. People with atopic dermatitis are also more likely to be colonized by <i>S. aureus</i>, prompting a closer look at their skin composition compared to those without a skin disorder. A difference in concentration of sapienic acid, a fatty acid usually found in high abundance on human skin in healthy patients, was found between groups. Patients with atopic dermatitis had lower amounts of acid on their skin, which correlated with higher colonization of <i>S. aureus</i>. Most interesting is that this is a reversible problem. <ins style="font-weight: bold; text-decoration: none;">When patients with atopic dermatitis were topically </ins>[[Image:Carbohydrate_FA.png|thumb|300px|right| <b> Figure 4. </b> Carbohydrate fatty acid derivatives that have antibacterial qualities towards <i>S. aureus</i>, excluding compound 4, which has its hydroxyl group in the wrong orientation. [http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2672.2009.04622.x/epdf].]] treated with sapienic acid, colonization of <i>S. aureus</i> decreased, excitingly suggesting that sapienic acid is a pivotal factor in the skin’s innate immune system against <i>S. aureus</i> specifically.</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>The mechanism of sapienic acid on MSSA, was determined to be a multi component mechanism. Sapienic acid leads to the inability of <i>S. aureus</i> to control its internal pH because of a loss of membrane potential. This happens because at low pH, the carboxylic acid is deprotonated and can release a proton into the cytoplasm, increasing the pH. This explains the inhibitory effects of salts on fatty acids. The salts may bind to the fatty acid, rendering it useless, or they may stabilize the membrane of the bacteria. Another proposed mechanism of action is that since the acid increases the membrane fluidity, it may also disrupt membrane processes that lead to the cell division problems seen in Figure 3. A third possible mechanism of action is that the fatty acids disrupt the production of mitochondrial reactive oxygen species by interfering with electron transport.</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 mechanism of sapienic acid on MSSA, was determined to be a multi component mechanism. Sapienic acid leads to the inability of <i>S. aureus</i> to control its internal pH because of a loss of membrane potential. This happens because at low pH, the carboxylic acid is deprotonated and can release a proton into the cytoplasm, increasing the pH. This explains the inhibitory effects of salts on fatty acids. The salts may bind to the fatty acid, rendering it useless, or they may stabilize the membrane of the bacteria. Another proposed mechanism of action is that since the acid increases the membrane fluidity, it may also disrupt membrane processes that lead to the cell division problems seen in Figure 3. A third possible mechanism of action is that the fatty acids disrupt the production of mitochondrial reactive oxygen species by interfering with electron transport.</div></td></tr>
</table>Mccannsmithehttps://microbewiki.kenyon.edu/index.php?title=Free_Fatty_Acids_as_antibacterial_agents_against_several_super_pathogens_including_MRSA&diff=118688&oldid=prevMccannsmithe: /* History of Fatty Acids as Antimicrobial Agents */2015-12-09T03:24:28Z<p><span dir="auto"><span class="autocomment">History of Fatty Acids as Antimicrobial Agents</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>In 1972 a research group from Michigan Sate University published extensive data on the effects of several fatty acids on both gram-positive and gram-negative bacteria.[http://www.ncbi.nlm.nih.gov/pmc/articles/PMC444260/] They demonstrated that by increasing the unsaturation of the fatty acids through the addition of cis double bonds, they could make these fatty acids more effective against gram-positive bacteria, but when the carboxylic acid was esterified the compounds lost their antibacterial effect. Strangely, they found that lauric acid, a saturated fatty acid, had the highest bacteriostatic potential towards these gram-positive bacteria of which included Staphylococcus genus, (which includes MRSA). Lauric acid was found to have the highest antimicrobial activity out a pool of saturated fatty acids, but overall, saturated fatty acids had lower activity than those that were unsaturated.[http://www.karger.com/Article/Abstract/69757] Palmitoleic acid, a monoene of human skin, was found to be most active against gram-positive bacteria, although in combination with ethanol, a synergistic effect against gram-negative bacteria (<i>P. aeruginosa, P. acnes, E. coli</i>) was seen.</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>In 1972 a research group from Michigan Sate University published extensive data on the effects of several fatty acids on both gram-positive and gram-negative bacteria.[http://www.ncbi.nlm.nih.gov/pmc/articles/PMC444260/] They demonstrated that by increasing the unsaturation of the fatty acids through the addition of cis double bonds, they could make these fatty acids more effective against gram-positive bacteria, but when the carboxylic acid was esterified the compounds lost their antibacterial effect. Strangely, they found that lauric acid, a saturated fatty acid, had the highest bacteriostatic potential towards these gram-positive bacteria of which included Staphylococcus genus, (which includes MRSA). Lauric acid was found to have the highest antimicrobial activity out a pool of saturated fatty acids, but overall, saturated fatty acids had lower activity than those that were unsaturated.[http://www.karger.com/Article/Abstract/69757] Palmitoleic acid, a monoene of human skin, was found to be most active against gram-positive bacteria, although in combination with ethanol, a synergistic effect against gram-negative bacteria (<i>P. aeruginosa, P. acnes, E. coli</i>) was seen.</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" 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>Staphylococci epidermidis are found in abundance on healthy skin, whereas <i>S. aureus</i> are usually only found on damaged skin, but the reasons for this are unknown. A study in 1985 showed that staphylococci that were coagulase-positive, i.e. <i>S. aureus</i>, on the skin were sensitive to linolenic acid,[http://jmm.microbiologyresearch.org/content/journal/jmm/10.1099/00222615-14-1-41] while other fatty acids were determined to have the same activity against coagulase-positive versus coagulase-negative staphylococci suggesting interference with the enzyme coagulase as a possible mechanism of action. This finding supports the <del style="font-weight: bold; text-decoration: none;">premis </del>that treatment with linolenic acid may be species specific, which is important because preserving Staphylococcus not of the species <i> S. aureus </i> is beneficial to the human system. The researchers even mutated the <i>S. aureus</i>, changing the characteristics of the bacteria in an attempt to mimic rapid evolution associated with resistance, to find a resistant strain towards linoleic acid. They were unsuccessful, suggesting linolenic acid will not cause resistance in bacteria, like other forms of treatment such as antibiotics. They also found that if human skin was covered in linolenic acid prior to the seeding of <i>S. aureus</i>, the bacteria were rapidly killed. However, the same group also found that antibacterial effects of this acid were reversed <i>in vitro</i> when low concentrations of human serum were present. They suggest a potential “detergent” mechanism, possibly the change in the functional group of the acid. This suggests potential problems with internal treatment of bacterial infections with linolenic acid. Another group got similar results with a different fatty acid, lauric acid, where interactions human blood plasma decreased the antimicrobial activity of the fatty acid.[https://www.jstage.jst.go.jp/article/bpb/27/9/27_9_1321/_article] <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>Staphylococci epidermidis are found in abundance on healthy skin, whereas <i>S. aureus</i> are usually only found on damaged skin, but the reasons for this are unknown. A study in 1985 showed that staphylococci that were coagulase-positive, i.e. <i>S. aureus</i>, on the skin were sensitive to linolenic acid,[http://jmm.microbiologyresearch.org/content/journal/jmm/10.1099/00222615-14-1-41] while other fatty acids were determined to have the same activity against coagulase-positive versus coagulase-negative staphylococci suggesting interference with the enzyme coagulase as a possible mechanism of action. This finding supports the <ins style="font-weight: bold; text-decoration: none;">premise </ins>that treatment with linolenic acid may be species specific, which is important because preserving Staphylococcus not of the species <i> S. aureus </i> is beneficial to the human system. The researchers even mutated the <i>S. aureus</i>, changing the characteristics of the bacteria in an attempt to mimic rapid evolution associated with resistance, to find a resistant strain towards linoleic acid. They were unsuccessful, suggesting linolenic acid will not cause resistance in bacteria, like other forms of treatment such as antibiotics. They also found that if human skin was covered in linolenic acid prior to the seeding of <i>S. aureus</i>, the bacteria were rapidly killed. However, the same group also found that antibacterial effects of this acid were reversed <i>in vitro</i> when low concentrations of human serum were present. They suggest a potential “detergent” mechanism, possibly the change in the functional group of the acid. This suggests potential problems with internal treatment of bacterial infections with linolenic acid. Another group got similar results with a different fatty acid, lauric acid, where interactions human blood plasma decreased the antimicrobial activity of the fatty acid.[https://www.jstage.jst.go.jp/article/bpb/27/9/27_9_1321/_article] <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>==Bactericidal Effects of Fatty Acids on Methicillin Resistant and Susceptible <i>Staphylococcus aureus</i>==</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>==Bactericidal Effects of Fatty Acids on Methicillin Resistant and Susceptible <i>Staphylococcus aureus</i>==</div></td></tr>
</table>Mccannsmithehttps://microbewiki.kenyon.edu/index.php?title=Free_Fatty_Acids_as_antibacterial_agents_against_several_super_pathogens_including_MRSA&diff=118687&oldid=prevMccannsmithe: /* Bactericidal Effects of Fatty Acids on Methicillin Resistant and Susceptible Staphylococcus aureus */2015-12-09T03:23:39Z<p><span dir="auto"><span class="autocomment">Bactericidal Effects of Fatty Acids on Methicillin Resistant and Susceptible Staphylococcus aureus</span></span></p>
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</tr><tr><td colspan="2" class="diff-lineno" id="mw-diff-left-l40">Line 40:</td>
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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>The most effective fatty acid against <i>S. aureus</i> colonization was found to be cis-6-Hexadecanoic acid (commonly known as sapienic acid).[http://aac.asm.org/content/58/7/3599.full [28]] This fatty acid was linked to <i>S. aureus</i> when it was found that people with atopic dermatitis (eczema) had higher levels of <i>S. aureus</i> on their skin, corresponding with lower levels of sapienic acid. [http://www.karger.com/Article/Abstract/87018 [29]]. MRSA is a big enough problem for people without skin disorders, but for individuals with atopic dermatitis, recurrent infections often lead to eczema exacerbation. There is currently no standard treatment for prevention of recurrent infections in either this patient group or the total patient group with MRSA. [http://www.sciencedirect.com/science/article/pii/S2213219814001718 [30]]. People with atopic dermatitis are also more likely to be colonized by <i>S. aureus</i>, prompting a closer look at their skin composition compared to those without a skin disorder. A difference in concentration of sapienic acid, a fatty acid usually found in high abundance on human skin in healthy patients, was found between groups. Patients with atopic dermatitis had lower amounts of acid on their skin, which correlated with higher colonization of <i>S. aureus</i>. Most interesting is that this is a reversible problem. [[Image:Carbohydrate_FA.png|thumb|300px|right| <b> Figure 4. </b> Carbohydrate fatty acid derivatives that have antibacterial qualities towards <i>S. aureus</i>, excluding compound 4, which has its hydroxyl group in the wrong orientation. [http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2672.2009.04622.x/epdf].]] When patients with atopic dermatitis were topically treated with sapienic acid, colonization of <i>S. aureus</i> decreased, excitingly suggesting that sapienic acid is a pivotal factor in the skin’s innate immune system against <i>S. aureus</i> specifically.</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 most effective fatty acid against <i>S. aureus</i> colonization was found to be cis-6-Hexadecanoic acid (commonly known as sapienic acid).[http://aac.asm.org/content/58/7/3599.full [28]] This fatty acid was linked to <i>S. aureus</i> when it was found that people with atopic dermatitis (eczema) had higher levels of <i>S. aureus</i> on their skin, corresponding with lower levels of sapienic acid. [http://www.karger.com/Article/Abstract/87018 [29]]. MRSA is a big enough problem for people without skin disorders, but for individuals with atopic dermatitis, recurrent infections often lead to eczema exacerbation. There is currently no standard treatment for prevention of recurrent infections in either this patient group or the total patient group with MRSA. [http://www.sciencedirect.com/science/article/pii/S2213219814001718 [30]]. People with atopic dermatitis are also more likely to be colonized by <i>S. aureus</i>, prompting a closer look at their skin composition compared to those without a skin disorder. A difference in concentration of sapienic acid, a fatty acid usually found in high abundance on human skin in healthy patients, was found between groups. Patients with atopic dermatitis had lower amounts of acid on their skin, which correlated with higher colonization of <i>S. aureus</i>. Most interesting is that this is a reversible problem. [[Image:Carbohydrate_FA.png|thumb|300px|right| <b> Figure 4. </b> Carbohydrate fatty acid derivatives that have antibacterial qualities towards <i>S. aureus</i>, excluding compound 4, which has its hydroxyl group in the wrong orientation. [http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2672.2009.04622.x/epdf].]] When patients with atopic dermatitis were topically treated with sapienic acid, colonization of <i>S. aureus</i> decreased, excitingly suggesting that sapienic acid is a pivotal factor in the skin’s innate immune system against <i>S. aureus</i> specifically.</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" 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;"><br> </del>The mechanism of sapienic acid on MSSA, was determined to be a multi component mechanism. Sapienic acid leads to the inability of <i>S. aureus</i> to control its internal pH because of a loss of membrane potential. This happens because at low pH, the carboxylic acid is deprotonated and can release a proton into the cytoplasm, increasing the pH. This explains the inhibitory effects of salts on fatty acids. The salts may bind to the fatty acid, rendering it useless, or they may stabilize the membrane of the bacteria. Another proposed mechanism of action is that since the acid increases the membrane fluidity, it may also disrupt membrane processes that lead to the cell division problems seen in Figure 3. A third possible mechanism of action is that the fatty acids disrupt the production of mitochondrial reactive oxygen species by interfering with electron transport.</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 mechanism of sapienic acid on MSSA, was determined to be a multi component mechanism. Sapienic acid leads to the inability of <i>S. aureus</i> to control its internal pH because of a loss of membrane potential. This happens because at low pH, the carboxylic acid is deprotonated and can release a proton into the cytoplasm, increasing the pH. This explains the inhibitory effects of salts on fatty acids. The salts may bind to the fatty acid, rendering it useless, or they may stabilize the membrane of the bacteria. Another proposed mechanism of action is that since the acid increases the membrane fluidity, it may also disrupt membrane processes that lead to the cell division problems seen in Figure 3. A third possible mechanism of action is that the fatty acids disrupt the production of mitochondrial reactive oxygen species by interfering with electron transport.</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>Novel carbohydrate fatty acid derivatives have been recently shown to have antimicrobial effects on several strains of <i>S. aureus</i> and MRSA.[http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2672.2009.04622.x/epdf [31]] The configuration of the hydroxyl group on the carbohydrate (not the fatty acid) part of the molecule determined the activity of the compound [Figure 4]. The mechanism of action of these compounds has to do with the cytoplasmic membrane, as well as other possible sites in the bacterium. <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>Novel carbohydrate fatty acid derivatives have been recently shown to have antimicrobial effects on several strains of <i>S. aureus</i> and MRSA.[http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2672.2009.04622.x/epdf [31]] The configuration of the hydroxyl group on the carbohydrate (not the fatty acid) part of the molecule determined the activity of the compound [Figure 4]. The mechanism of action of these compounds has to do with the cytoplasmic membrane, as well as other possible sites in the bacterium. <br></div></td></tr>
</table>Mccannsmithe