tag:blogger.com,1999:blog-18391092996044624202024-03-05T12:36:07.126-05:00The Grad School GrindMy goal is to write about cutting-edge biology and fill my readers in on the latest research, mainly in the realm of infectious diseases.Anonymoushttp://www.blogger.com/profile/05503168250289145242noreply@blogger.comBlogger32125tag:blogger.com,1999:blog-1839109299604462420.post-90217721473959699472018-07-31T09:29:00.000-04:002018-08-02T16:16:48.534-04:00Out of sight, out of mind: The massive hepatitis A outbreak no one is talking aboutSince early 2017, over 4,500 cases of hepatitis A have been reported in outbreaks across 10 states in the United States, a massive increase from the 1,390 cases and 0 outbreaks seen in the entire country in 2015. And the cases keep rolling in. The states reporting outbreaks so far are Arkansas, California, Indiana, Kentucky, Michigan, Missouri, Ohio, Tennessee, Utah, and West Virginia, but additional cases have been reported in other states. Disease has been fairly severe in these outbreaks, leading to a ~60% hospitalization rate, compared to the typical ~30% for hepatitis A, and at least 62 deaths. These outbreaks have mainly plagued the homeless and illicit drug-using populations, which has kept outbreak coverage largely out of the national news. But there have also been reports of cases in people outside these groups, with a growing number of cases among food service workers.<br />
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The disease hepatitis A is caused by the hepatitis A virus (HAV). While "hepatitis" can be caused by several viruses that share similar names, the hepatitis viruses are quite different from each other. HAV is an unenveloped RNA virus from the picornavirus family, the same family as poliovirus and rhinoviruses. Alternatively, hepatitis B virus is an enveloped double-stranded DNA virus from the hepadnavirus family, hepatitis C virus is an enveloped RNA virus from the flavivirus family, and hepatitis E virus is a quasi-enveloped RNA virus currently classified in the hepevirus family (hepatitis D virus is considered a subviral satellite since it cannot replicate without the presence of hepatitis B).<br />
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<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgvwDWekFemt3f6bUiQilx3EMNKPOamkbsAPXIz5E1jy5otFmpLEyHAIoRYxTxFeqf3PNPhA3eNiZIEHY588E0umLgTz39RxF5OCdC9PZu8nFOQaY-IjyNzs6c4-gaw2E8VC8ttYXP0Zzk/s1600/PHIL_2739+%25281%2529.tif" imageanchor="1" style="clear: left; margin-bottom: 1em; margin-left: auto; margin-right: auto;"><img border="0" data-original-height="1068" data-original-width="1214" height="280" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgvwDWekFemt3f6bUiQilx3EMNKPOamkbsAPXIz5E1jy5otFmpLEyHAIoRYxTxFeqf3PNPhA3eNiZIEHY588E0umLgTz39RxF5OCdC9PZu8nFOQaY-IjyNzs6c4-gaw2E8VC8ttYXP0Zzk/s320/PHIL_2739+%25281%2529.tif" width="320" /></a></td></tr>
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A cluster of HAV virions</div>
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<span style="background-color: white; color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 11.88px;">CDC's Public Health Image Library.</span></div>
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<span style="background-color: white; color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 11.88px;">Image # 2739; photo credit: CDC/Betty Partin.</span></div>
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HAV causes acute liver infections, which typically manifest with symptoms such as fatigue, nausea and vomiting, abdominal pain, low-grade fever, and jaundice (yellowing of the skin and whites of the eyes). Symptoms tend to appear 2-4 weeks after exposure to the virus and can last for a couple months. Previous hepatitis A outbreaks in the United States have been associated with eating contaminated food, such as an outbreak caused by imported pomegranate seeds in 2013. However, in the current outbreaks, the virus is being transmitted from person to person through contact with fecal material, leaving people with poor sanitation and hygiene at increased risk.<br />
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A vaccine for HAV exists and is extremely effective at preventing disease. Children are routinely vaccinated around age 1, providing protective immunity against the virus. Unfortunately, the vaccine was not approved for use until 1995, so many adults over the age of 25 have never been vaccinated and remain susceptible to HAV infection. Vaccination <span style="font-family: inherit;">in adults is an option but is only routinely done for high-risk individuals, such as people traveling to countries where hepatitis A is common, caring for an individual with hepatitis A, or using recreational drugs. The vaccine can be given as a prophylactic before exposure or as a treatment post-exposure; as long as a person is vaccinated within 2 weeks of exposure, infection can still be prevented. H</span>owever, mobilization of the vaccine to those at highest risk of infection in these outbreaks has been difficult due to the barriers in access to health care that exist for the homeless and drug-using popula<span style="font-family: inherit;">tions. Additionally, other than the vaccine, there is no real treatment for HAV infection; giving patients rest, fluids, and adequate nutrition is the only course of action. </span><br />
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<span style="font-family: inherit;">While local health agencies and the Centers for Disease Control (CDC) have been working to contain these outbreaks and prevent further spread, vaccine availability and lack of funding have threatened efforts. When the outbreaks began, demand for the vaccine increased dramatically, leading to shortages in the vaccine supply. Fortunately, this issue has since been resolved thanks to vaccine suppliers GlaxoSmithKline and Merck ramping up production. However, the Section 317 Immunization Program from the CDC that has been essential in paying for these vaccines has already experienced funding cuts and may experience more in the coming year. Additionally, many public health officials feel they are not being provided with enough funding to support the other essential componenets of combating viral hepatitis.</span><br />
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<span style="font-family: inherit;">Since the virus is spreading from person-to-person contact in these outbreaks, improved sanitation and hygiene are key to reducing spread. Achieving these goals in the populations at risk has not been an easy task. In California, officials resorted to cleaning their public buses, streets, and even sidewalks with bleach to complement their vaccine distribution campaigns. It is now believed that the outbreak in California is over, giving hope that employing similar strategies could improve outbreak containment in other states. Outside California, the number of cases per day has been trending downwards in some areas, but that trend has not been consistent, and officials warn that there is still a significant threat. Improving sanitation for the over 500,000 Americans experiencing homelessness is an essential measure to end the hepatitis A outbreaks and prevent future infectious disease outbreaks in the United States. In a tough funding climate, this will not be easy to achieve, but state health departments and private non-profits are working vigilantly towards this goal. Until then, wash your hands, wash your hands, and wash your hands to help fight the spread of HAV.</span><br />
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<span style="font-family: inherit;">Latest case report statistics, July 2018</span><br />
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<b><span style="font-family: inherit;">State<o:p></o:p></span></b></div>
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<b><span style="font-family: inherit;">Cases<o:p></o:p></span></b></div>
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<b><span style="font-family: inherit;">Hospitalizations<o:p></o:p></span></b></div>
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<b><span style="font-family: inherit;">Deaths<o:p></o:p></span></b></div>
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<td style="border-top: none; border: solid windowtext 1.0pt; height: 12.55pt; mso-border-alt: solid windowtext .5pt; mso-border-top-alt: solid windowtext .5pt; padding: 0in 5.4pt 0in 5.4pt; width: 89.75pt;" valign="top" width="120"><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;">
<span style="font-family: inherit;">Arkansas<o:p></o:p></span></div>
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<td style="border-bottom: solid windowtext 1.0pt; border-left: none; border-right: solid windowtext 1.0pt; border-top: none; height: 12.55pt; mso-border-alt: solid windowtext .5pt; mso-border-left-alt: solid windowtext .5pt; mso-border-top-alt: solid windowtext .5pt; padding: 0in 5.4pt 0in 5.4pt; width: .75in;" valign="top" width="72"><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;">
<span style="font-family: inherit;">63<o:p></o:p></span></div>
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<td style="border-bottom: solid windowtext 1.0pt; border-left: none; border-right: solid windowtext 1.0pt; border-top: none; height: 12.55pt; mso-border-alt: solid windowtext .5pt; mso-border-left-alt: solid windowtext .5pt; mso-border-top-alt: solid windowtext .5pt; padding: 0in 5.4pt 0in 5.4pt; width: 95.15pt;" valign="top" width="127"><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;">
<span style="font-family: inherit;">Not reported<o:p></o:p></span></div>
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<span style="font-family: inherit;">≥ 1<o:p></o:p></span></div>
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<td style="border-top: none; border: solid windowtext 1.0pt; height: 13.3pt; mso-border-alt: solid windowtext .5pt; mso-border-top-alt: solid windowtext .5pt; padding: 0in 5.4pt 0in 5.4pt; width: 89.75pt;" valign="top" width="120"><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;">
<span style="font-family: inherit;">California<o:p></o:p></span></div>
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<td style="border-bottom: solid windowtext 1.0pt; border-left: none; border-right: solid windowtext 1.0pt; border-top: none; height: 13.3pt; mso-border-alt: solid windowtext .5pt; mso-border-left-alt: solid windowtext .5pt; mso-border-top-alt: solid windowtext .5pt; padding: 0in 5.4pt 0in 5.4pt; width: .75in;" valign="top" width="72"><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;">
<span style="font-family: inherit;">704<o:p></o:p></span></div>
</td>
<td style="border-bottom: solid windowtext 1.0pt; border-left: none; border-right: solid windowtext 1.0pt; border-top: none; height: 13.3pt; mso-border-alt: solid windowtext .5pt; mso-border-left-alt: solid windowtext .5pt; mso-border-top-alt: solid windowtext .5pt; padding: 0in 5.4pt 0in 5.4pt; width: 95.15pt;" valign="top" width="127"><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;">
<span style="font-family: inherit;">461<o:p></o:p></span></div>
</td>
<td style="border-bottom: solid windowtext 1.0pt; border-left: none; border-right: solid windowtext 1.0pt; border-top: none; height: 13.3pt; mso-border-alt: solid windowtext .5pt; mso-border-left-alt: solid windowtext .5pt; mso-border-top-alt: solid windowtext .5pt; padding: 0in 5.4pt 0in 5.4pt; width: .75in;" valign="top" width="72"><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;">
<span style="font-family: inherit;">21<o:p></o:p></span></div>
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<tr style="height: 12.55pt; mso-yfti-irow: 3;">
<td style="border-top: none; border: solid windowtext 1.0pt; height: 12.55pt; mso-border-alt: solid windowtext .5pt; mso-border-top-alt: solid windowtext .5pt; padding: 0in 5.4pt 0in 5.4pt; width: 89.75pt;" valign="top" width="120"><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;">
<span style="font-family: inherit;">Indiana<o:p></o:p></span></div>
</td>
<td style="border-bottom: solid windowtext 1.0pt; border-left: none; border-right: solid windowtext 1.0pt; border-top: none; height: 12.55pt; mso-border-alt: solid windowtext .5pt; mso-border-left-alt: solid windowtext .5pt; mso-border-top-alt: solid windowtext .5pt; padding: 0in 5.4pt 0in 5.4pt; width: .75in;" valign="top" width="72"><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;">
<span style="font-family: inherit;">298<o:p></o:p></span></div>
</td>
<td style="border-bottom: solid windowtext 1.0pt; border-left: none; border-right: solid windowtext 1.0pt; border-top: none; height: 12.55pt; mso-border-alt: solid windowtext .5pt; mso-border-left-alt: solid windowtext .5pt; mso-border-top-alt: solid windowtext .5pt; padding: 0in 5.4pt 0in 5.4pt; width: 95.15pt;" valign="top" width="127"><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;">
<span style="font-family: inherit;">136<o:p></o:p></span></div>
</td>
<td style="border-bottom: solid windowtext 1.0pt; border-left: none; border-right: solid windowtext 1.0pt; border-top: none; height: 12.55pt; mso-border-alt: solid windowtext .5pt; mso-border-left-alt: solid windowtext .5pt; mso-border-top-alt: solid windowtext .5pt; padding: 0in 5.4pt 0in 5.4pt; width: .75in;" valign="top" width="72"><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;">
<span style="font-family: inherit;">1<o:p></o:p></span></div>
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<tr style="height: 13.3pt; mso-yfti-irow: 4;">
<td style="border-top: none; border: solid windowtext 1.0pt; height: 13.3pt; mso-border-alt: solid windowtext .5pt; mso-border-top-alt: solid windowtext .5pt; padding: 0in 5.4pt 0in 5.4pt; width: 89.75pt;" valign="top" width="120"><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;">
<span style="font-family: inherit;">Kentucky<o:p></o:p></span></div>
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<td style="border-bottom: solid windowtext 1.0pt; border-left: none; border-right: solid windowtext 1.0pt; border-top: none; height: 13.3pt; mso-border-alt: solid windowtext .5pt; mso-border-left-alt: solid windowtext .5pt; mso-border-top-alt: solid windowtext .5pt; padding: 0in 5.4pt 0in 5.4pt; width: .75in;" valign="top" width="72"><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;">
<span style="font-family: inherit;">1,221<o:p></o:p></span></div>
</td>
<td style="border-bottom: solid windowtext 1.0pt; border-left: none; border-right: solid windowtext 1.0pt; border-top: none; height: 13.3pt; mso-border-alt: solid windowtext .5pt; mso-border-left-alt: solid windowtext .5pt; mso-border-top-alt: solid windowtext .5pt; padding: 0in 5.4pt 0in 5.4pt; width: 95.15pt;" valign="top" width="127"><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;">
<span style="font-family: inherit;">687<o:p></o:p></span></div>
</td>
<td style="border-bottom: solid windowtext 1.0pt; border-left: none; border-right: solid windowtext 1.0pt; border-top: none; height: 13.3pt; mso-border-alt: solid windowtext .5pt; mso-border-left-alt: solid windowtext .5pt; mso-border-top-alt: solid windowtext .5pt; padding: 0in 5.4pt 0in 5.4pt; width: .75in;" valign="top" width="72"><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;">
<span style="font-family: inherit;">8<o:p></o:p></span></div>
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</tr>
<tr style="height: 12.55pt; mso-yfti-irow: 5;">
<td style="border-top: none; border: solid windowtext 1.0pt; height: 12.55pt; mso-border-alt: solid windowtext .5pt; mso-border-top-alt: solid windowtext .5pt; padding: 0in 5.4pt 0in 5.4pt; width: 89.75pt;" valign="top" width="120"><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;">
<span style="font-family: inherit;">Michigan<o:p></o:p></span></div>
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<td style="border-bottom: solid windowtext 1.0pt; border-left: none; border-right: solid windowtext 1.0pt; border-top: none; height: 12.55pt; mso-border-alt: solid windowtext .5pt; mso-border-left-alt: solid windowtext .5pt; mso-border-top-alt: solid windowtext .5pt; padding: 0in 5.4pt 0in 5.4pt; width: .75in;" valign="top" width="72"><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;">
<span style="font-family: inherit;">865<o:p></o:p></span></div>
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<td style="border-bottom: solid windowtext 1.0pt; border-left: none; border-right: solid windowtext 1.0pt; border-top: none; height: 12.55pt; mso-border-alt: solid windowtext .5pt; mso-border-left-alt: solid windowtext .5pt; mso-border-top-alt: solid windowtext .5pt; padding: 0in 5.4pt 0in 5.4pt; width: 95.15pt;" valign="top" width="127"><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;">
<span style="font-family: inherit;">695<o:p></o:p></span></div>
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<td style="border-bottom: solid windowtext 1.0pt; border-left: none; border-right: solid windowtext 1.0pt; border-top: none; height: 12.55pt; mso-border-alt: solid windowtext .5pt; mso-border-left-alt: solid windowtext .5pt; mso-border-top-alt: solid windowtext .5pt; padding: 0in 5.4pt 0in 5.4pt; width: .75in;" valign="top" width="72"><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;">
27</div>
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<tr style="height: 13.3pt; mso-yfti-irow: 6;">
<td style="border-top: none; border: solid windowtext 1.0pt; height: 13.3pt; mso-border-alt: solid windowtext .5pt; mso-border-top-alt: solid windowtext .5pt; padding: 0in 5.4pt 0in 5.4pt; width: 89.75pt;" valign="top" width="120"><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;">
<span style="font-family: inherit;">Missouri<o:p></o:p></span></div>
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<td style="border-bottom: solid windowtext 1.0pt; border-left: none; border-right: solid windowtext 1.0pt; border-top: none; height: 13.3pt; mso-border-alt: solid windowtext .5pt; mso-border-left-alt: solid windowtext .5pt; mso-border-top-alt: solid windowtext .5pt; padding: 0in 5.4pt 0in 5.4pt; width: .75in;" valign="top" width="72"><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;">
<span style="font-family: inherit;">145<o:p></o:p></span></div>
</td>
<td style="border-bottom: solid windowtext 1.0pt; border-left: none; border-right: solid windowtext 1.0pt; border-top: none; height: 13.3pt; mso-border-alt: solid windowtext .5pt; mso-border-left-alt: solid windowtext .5pt; mso-border-top-alt: solid windowtext .5pt; padding: 0in 5.4pt 0in 5.4pt; width: 95.15pt;" valign="top" width="127"><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;">
<span style="font-family: inherit;">63<o:p></o:p></span></div>
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<td style="border-bottom: solid windowtext 1.0pt; border-left: none; border-right: solid windowtext 1.0pt; border-top: none; height: 13.3pt; mso-border-alt: solid windowtext .5pt; mso-border-left-alt: solid windowtext .5pt; mso-border-top-alt: solid windowtext .5pt; padding: 0in 5.4pt 0in 5.4pt; width: .75in;" valign="top" width="72"><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;">
<span style="font-family: inherit;">0<o:p></o:p></span></div>
</td>
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<tr style="height: 12.55pt; mso-yfti-irow: 7;">
<td style="border-top: none; border: solid windowtext 1.0pt; height: 12.55pt; mso-border-alt: solid windowtext .5pt; mso-border-top-alt: solid windowtext .5pt; padding: 0in 5.4pt 0in 5.4pt; width: 89.75pt;" valign="top" width="120"><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;">
<span style="font-family: inherit;">Ohio<o:p></o:p></span></div>
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<td style="border-bottom: solid windowtext 1.0pt; border-left: none; border-right: solid windowtext 1.0pt; border-top: none; height: 12.55pt; mso-border-alt: solid windowtext .5pt; mso-border-left-alt: solid windowtext .5pt; mso-border-top-alt: solid windowtext .5pt; padding: 0in 5.4pt 0in 5.4pt; width: .75in;" valign="top" width="72"><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;">
<span style="font-family: inherit;">176<o:p></o:p></span></div>
</td>
<td style="border-bottom: solid windowtext 1.0pt; border-left: none; border-right: solid windowtext 1.0pt; border-top: none; height: 12.55pt; mso-border-alt: solid windowtext .5pt; mso-border-left-alt: solid windowtext .5pt; mso-border-top-alt: solid windowtext .5pt; padding: 0in 5.4pt 0in 5.4pt; width: 95.15pt;" valign="top" width="127"><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;">
<span style="font-family: inherit;">114<o:p></o:p></span></div>
</td>
<td style="border-bottom: solid windowtext 1.0pt; border-left: none; border-right: solid windowtext 1.0pt; border-top: none; height: 12.55pt; mso-border-alt: solid windowtext .5pt; mso-border-left-alt: solid windowtext .5pt; mso-border-top-alt: solid windowtext .5pt; padding: 0in 5.4pt 0in 5.4pt; width: .75in;" valign="top" width="72"><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;">
<span style="font-family: inherit;">0<o:p></o:p></span></div>
</td>
</tr>
<tr style="height: 13.3pt; mso-yfti-irow: 8;">
<td style="border-top: none; border: solid windowtext 1.0pt; height: 13.3pt; mso-border-alt: solid windowtext .5pt; mso-border-top-alt: solid windowtext .5pt; padding: 0in 5.4pt 0in 5.4pt; width: 89.75pt;" valign="top" width="120"><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;">
<span style="font-family: inherit;">Tennessee<o:p></o:p></span></div>
</td>
<td style="border-bottom: solid windowtext 1.0pt; border-left: none; border-right: solid windowtext 1.0pt; border-top: none; height: 13.3pt; mso-border-alt: solid windowtext .5pt; mso-border-left-alt: solid windowtext .5pt; mso-border-top-alt: solid windowtext .5pt; padding: 0in 5.4pt 0in 5.4pt; width: .75in;" valign="top" width="72"><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;">
<span style="font-family: inherit;">113<o:p></o:p></span></div>
</td>
<td style="border-bottom: solid windowtext 1.0pt; border-left: none; border-right: solid windowtext 1.0pt; border-top: none; height: 13.3pt; mso-border-alt: solid windowtext .5pt; mso-border-left-alt: solid windowtext .5pt; mso-border-top-alt: solid windowtext .5pt; padding: 0in 5.4pt 0in 5.4pt; width: 95.15pt;" valign="top" width="127"><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;">
<span style="font-family: inherit;">64<o:p></o:p></span></div>
</td>
<td style="border-bottom: solid windowtext 1.0pt; border-left: none; border-right: solid windowtext 1.0pt; border-top: none; height: 13.3pt; mso-border-alt: solid windowtext .5pt; mso-border-left-alt: solid windowtext .5pt; mso-border-top-alt: solid windowtext .5pt; padding: 0in 5.4pt 0in 5.4pt; width: .75in;" valign="top" width="72"><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;">
<span style="font-family: inherit;">0<o:p></o:p></span></div>
</td>
</tr>
<tr style="height: 12.55pt; mso-yfti-irow: 9;">
<td style="border-top: none; border: solid windowtext 1.0pt; height: 12.55pt; mso-border-alt: solid windowtext .5pt; mso-border-top-alt: solid windowtext .5pt; padding: 0in 5.4pt 0in 5.4pt; width: 89.75pt;" valign="top" width="120"><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;">
<span style="font-family: inherit;">Utah<o:p></o:p></span></div>
</td>
<td style="border-bottom: solid windowtext 1.0pt; border-left: none; border-right: solid windowtext 1.0pt; border-top: none; height: 12.55pt; mso-border-alt: solid windowtext .5pt; mso-border-left-alt: solid windowtext .5pt; mso-border-top-alt: solid windowtext .5pt; padding: 0in 5.4pt 0in 5.4pt; width: .75in;" valign="top" width="72"><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;">
<span style="font-family: inherit;">264<o:p></o:p></span></div>
</td>
<td style="border-bottom: solid windowtext 1.0pt; border-left: none; border-right: solid windowtext 1.0pt; border-top: none; height: 12.55pt; mso-border-alt: solid windowtext .5pt; mso-border-left-alt: solid windowtext .5pt; mso-border-top-alt: solid windowtext .5pt; padding: 0in 5.4pt 0in 5.4pt; width: 95.15pt;" valign="top" width="127"><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;">
<span style="font-family: inherit;">139<o:p></o:p></span></div>
</td>
<td style="border-bottom: solid windowtext 1.0pt; border-left: none; border-right: solid windowtext 1.0pt; border-top: none; height: 12.55pt; mso-border-alt: solid windowtext .5pt; mso-border-left-alt: solid windowtext .5pt; mso-border-top-alt: solid windowtext .5pt; padding: 0in 5.4pt 0in 5.4pt; width: .75in;" valign="top" width="72"><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;">
<span style="font-family: inherit;">≥ 2<o:p></o:p></span></div>
</td>
</tr>
<tr style="height: 13.3pt; mso-yfti-irow: 10;">
<td style="border-top: none; border: solid windowtext 1.0pt; height: 13.3pt; mso-border-alt: solid windowtext .5pt; mso-border-top-alt: solid windowtext .5pt; padding: 0in 5.4pt 0in 5.4pt; width: 89.75pt;" valign="top" width="120"><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;">
<span style="font-family: inherit;">West Virginia<o:p></o:p></span></div>
</td>
<td style="border-bottom: solid windowtext 1.0pt; border-left: none; border-right: solid windowtext 1.0pt; border-top: none; height: 13.3pt; mso-border-alt: solid windowtext .5pt; mso-border-left-alt: solid windowtext .5pt; mso-border-top-alt: solid windowtext .5pt; padding: 0in 5.4pt 0in 5.4pt; width: .75in;" valign="top" width="72"><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;">
<span style="font-family: inherit;">699<o:p></o:p></span></div>
</td>
<td style="border-bottom: solid windowtext 1.0pt; border-left: none; border-right: solid windowtext 1.0pt; border-top: none; height: 13.3pt; mso-border-alt: solid windowtext .5pt; mso-border-left-alt: solid windowtext .5pt; mso-border-top-alt: solid windowtext .5pt; padding: 0in 5.4pt 0in 5.4pt; width: 95.15pt;" valign="top" width="127"><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;">
<span style="font-family: inherit;">428<o:p></o:p></span></div>
</td>
<td style="border-bottom: solid windowtext 1.0pt; border-left: none; border-right: solid windowtext 1.0pt; border-top: none; height: 13.3pt; mso-border-alt: solid windowtext .5pt; mso-border-left-alt: solid windowtext .5pt; mso-border-top-alt: solid windowtext .5pt; padding: 0in 5.4pt 0in 5.4pt; width: .75in;" valign="top" width="72"><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;">
<span style="font-family: inherit;">2<o:p></o:p></span></div>
</td>
</tr>
<tr style="height: 12.55pt; mso-yfti-irow: 11; mso-yfti-lastrow: yes;">
<td style="border-top: none; border: solid windowtext 1.0pt; height: 12.55pt; mso-border-alt: solid windowtext .5pt; mso-border-top-alt: solid windowtext .5pt; padding: 0in 5.4pt 0in 5.4pt; width: 89.75pt;" valign="top" width="120"><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;">
<b><span style="font-family: inherit;">Total<o:p></o:p></span></b></div>
</td>
<td style="border-bottom: solid windowtext 1.0pt; border-left: none; border-right: solid windowtext 1.0pt; border-top: none; height: 12.55pt; mso-border-alt: solid windowtext .5pt; mso-border-left-alt: solid windowtext .5pt; mso-border-top-alt: solid windowtext .5pt; padding: 0in 5.4pt 0in 5.4pt; width: .75in;" valign="top" width="72"><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;">
<b><span style="font-family: inherit;">4,548<o:p></o:p></span></b></div>
</td>
<td style="border-bottom: solid windowtext 1.0pt; border-left: none; border-right: solid windowtext 1.0pt; border-top: none; height: 12.55pt; mso-border-alt: solid windowtext .5pt; mso-border-left-alt: solid windowtext .5pt; mso-border-top-alt: solid windowtext .5pt; padding: 0in 5.4pt 0in 5.4pt; width: 95.15pt;" valign="top" width="127"><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;">
<b><span style="font-family: inherit;">≥ 2,787<o:p></o:p></span></b></div>
</td>
<td style="border-bottom: solid windowtext 1.0pt; border-left: none; border-right: solid windowtext 1.0pt; border-top: none; height: 12.55pt; mso-border-alt: solid windowtext .5pt; mso-border-left-alt: solid windowtext .5pt; mso-border-top-alt: solid windowtext .5pt; padding: 0in 5.4pt 0in 5.4pt; width: .75in;" valign="top" width="72"><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;">
<b><span style="font-family: inherit;">≥ 62<o:p></o:p></span></b></div>
</td>
</tr>
</tbody></table>
<br />Anonymoushttp://www.blogger.com/profile/05503168250289145242noreply@blogger.com0tag:blogger.com,1999:blog-1839109299604462420.post-68765434736655702652018-06-29T11:38:00.002-04:002018-06-29T11:38:20.188-04:00I've got the power: How the potential bioterrorism agent Francisella tularensis manipulates host cells<br />
<div style="margin-bottom: .0001pt; margin: 0in;">
<span style="color: black; font-family: "Arial",sans-serif; font-size: 11.0pt;">In an age of advanced weaponry and
warfare, the risk of bioterrorism is increasingly acute. One potential
bioterrorism agent is the bacterium <i style="mso-bidi-font-style: normal;">Francisella
tularensis, </i>which is responsible for the similarly named disease tularemia.
<i style="mso-bidi-font-style: normal;">F. tularensis </i>is classified as a category
A potential bioterrorism agent, the same classification as anthrax and the
plague. A low number of bacteria are capable of causing disease, which can be
fatal in up to 60% of cases if untreated. Outside the potential threat for
bioterrorism, <i style="mso-bidi-font-style: normal;">F. tularensis </i>infection
also happens naturally. While cases of tularemia in the United States have
largely declined since the 1950s, this is not the case throughout the world,
with multiple outbreaks occurring in Europe in the last 10 years. <o:p></o:p></span></div>
<div style="margin-bottom: .0001pt; margin: 0in;">
<br /></div>
<table cellpadding="0" cellspacing="0" class="tr-caption-container" style="float: left; margin-right: 1em; text-align: left;"><tbody>
<tr><td style="text-align: center;"><a href="https://phil.cdc.gov//PHIL_Images/03182002/00016/PHIL_1903_lores.jpg" imageanchor="1" style="clear: left; margin-bottom: 1em; margin-left: auto; margin-right: auto;"><img border="0" height="256" src="https://phil.cdc.gov//PHIL_Images/03182002/00016/PHIL_1903_lores.jpg" width="320" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;"><i><span style="font-family: Arial, Helvetica, sans-serif; font-size: x-small;">F. tularemia<span style="background-color: white;">.</span></span></i><br />
<span style="background-color: white; font-family: Arial, Helvetica, sans-serif; font-size: x-small;">CDC's Public Health Image Library.</span><br />
<span style="font-family: Arial, Helvetica, sans-serif; font-size: x-small;"><span style="background-color: white;">Image # 1903; photo credit: </span>Larry Stauffer, </span><br />
<span style="font-family: Arial, Helvetica, sans-serif; font-size: x-small;">Oregon State Public Health Laboratory.</span></td></tr>
</tbody></table>
<div style="margin-bottom: .0001pt; margin: 0in;">
<span style="color: black; font-family: "Arial",sans-serif; font-size: 11.0pt;">Disease management and bacterial
elimination can be difficult because <i style="mso-bidi-font-style: normal;">F. tularensis</i> can
survive in over 100 species of mammals, birds, cold-blooded animals, and
arthropods, including rabbits, mice, rats, squirrels, cats, dogs, horses, pigs,
and sheep. To further complicate matters, transmission of <i style="mso-bidi-font-style: normal;">F. tularensis </i>can
occur in several ways, including the consumption of contaminated water or food;
contact with urine, excrement, or blood from infected animals; bites from blood-sucking
arthropods like ticks, flies, and mosquitoes; and inhalation of aerosolized
bacteria. The symptoms of tularemia depend on the route of transmission and can
include a skin ulcer at the site of bacterial entry; swollen glands; sore
throat; and high fever. <i>F</i><i style="mso-bidi-font-style: normal;">. tularensis </i>is
naturally resistant to many antibiotics because it is an intracellular
bacterium that spends most of its life hiding inside a host cell; an antibiotic
must first get into the host cell before it can have any effect on the pathogen.
Aminoglycosides, tetracyclines, and fluoroquinolones have been shown to be
effective, but 5-15% of infections relapse following treatment, and the side
effects from these antibiotics can be unmanageable, limiting their use.<o:p></o:p></span></div>
<div style="margin-bottom: .0001pt; margin: 0in;">
<br /></div>
<div style="margin-bottom: .0001pt; margin: 0in;">
<span style="color: black; font-family: "Arial",sans-serif; font-size: 11.0pt;">Due to the low infectious dose,
high mortality rate, ease of transmission, and difficulty in treatment, natural <i style="mso-bidi-font-style: normal;">F. tularensis </i><span style="mso-bidi-font-style: italic;">infection is a serious threat to public
health, and a weaponized version of the bacteria could be catastrophic. </span>To
counteract these risks, researchers have been studying how <i style="mso-bidi-font-style: normal;">F. tularensis</i> causes infection to identify ways to inhibit or kill
the bacteria. We know that once in the human body, <i style="mso-bidi-font-style: normal;">F. tularensis </i>is
taken up by phagocytic cells, such as macrophages. The job of these phagocytic
cells is to engulf the bacterium into a compartment called a phagosome for
degradation. Typically, this is how the immune system would capture and kill a
pathogen. However, in the case of <i style="mso-bidi-font-style: normal;">F. tularensis, </i>the
bacterium escapes from the phagosome through a process that is not well
understood to begin replicating in the cytosol of the host cell. A recent study
shed a little light on this process and found that <i style="mso-bidi-font-style: normal;">F. tularensis </i><span style="mso-bidi-font-style: italic;">is </span>manipulating the host macrophage
in a unique way.<o:p></o:p></span><o:p></o:p></div>
<div style="margin-bottom: .0001pt; margin: 0in;">
<br /></div>
<table cellpadding="0" cellspacing="0" class="tr-caption-container" style="float: right; text-align: left;"><tbody>
<tr><td style="text-align: center;"><a href="https://phil.cdc.gov//PHIL_Images/8731/8731_lores.jpg" imageanchor="1" style="clear: left; margin-bottom: 1em; margin-left: auto; margin-right: auto;"><img border="0" height="320" src="https://phil.cdc.gov//PHIL_Images/8731/8731_lores.jpg" width="251" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;"><span style="font-family: Arial, Helvetica, sans-serif; font-size: x-small;">Macrophage (right) containing rickettsial microbes.<br />CDC's Public Health Image Library.<br />Image # 8731; photo credit: CDC, Dr. Ed Ewing.</span></td></tr>
</tbody></table>
<div style="margin-bottom: .0001pt; margin: 0in;">
<span style="font-family: Arial, sans-serif;"><span style="font-size: 11pt;">Dr. Forrest Jessop and colleagues
at the National Institute of Allergy and Infectious Disease found that </span></span><i style="color: black; font-family: Arial, sans-serif; font-size: 11pt;">F. tularensis </i><span style="font-family: Arial, sans-serif;"><span style="font-size: 11pt;">alters
the function of the mitochondria in the macrophage. The mitochondria are
essential cellular organelles that are responsible for providing “power” to the
cell, much like a battery provides power to a flashlight. When </span></span><i style="color: black; font-family: Arial, sans-serif; font-size: 11pt;">F. tularensis</i><span style="font-family: Arial, sans-serif;"><span style="font-size: 11pt;"> first
enters the macrophage, it improves the function of the mitochondria, which keeps
the macrophage alive and prevents an inflammatory response from the immune
system. A few hours later, the bacterium reverses these effects and decreases
mitochondrial function, decreasing the macrophage's power</span><span style="font-size: 11pt;"> supply and leading to rapid bacterial replication and oncosis, a
type of cell death that involves the swelling of the cell. This facilitates the
pathogen’s ability to get out of the cell after replicating and move on to a
new host cell.<o:p></o:p></span></span><o:p></o:p></div>
<div style="margin-bottom: .0001pt; margin: 0in;">
<br /></div>
<div style="margin-bottom: .0001pt; margin: 0in;">
<span style="font-family: Arial, sans-serif; font-size: 11pt; line-height: 107%;">The researchers were able to take this new-found
knowledge of the bacteria’s effect on mitochondria a step further and test a
therapeutic treatment in culture. They found that by treating <i style="mso-bidi-font-style: normal;">F. tularensis</i>-infected
macrophages with drugs that protect typical mitochondrial function, they were
able to reduce macrophage cell death and decrease levels of bacterial replication. It
remains to be seen if this type of intervention will work in an animal system,
but this is a promising step in the right direction towards increasing the number
of treatments available for these infections. Since the environmental reservoir
for <i>F. tularensis</i> is so vast, increased awareness of the risks of disease and
research focus are important to stem the outbreaks and prevent future
bioterrorism threats.</span></div>
Anonymoushttp://www.blogger.com/profile/05503168250289145242noreply@blogger.com0tag:blogger.com,1999:blog-1839109299604462420.post-2517127929593672022018-05-31T22:39:00.001-04:002018-05-31T22:40:20.751-04:00Broadly neutralizing antibodies take down bacteria, viruses, and yeast<span style="font-family: inherit;">Antibodies are an important player in the body's immune system. The job of an antibody is to
recognize a very specific feature of a foreign protein, known as an epitope.
Without high levels of epitope specificity, antibodies can often begin to bind to and
attack self-proteins, leading to dangerous autoimmune reactions. By producing
highly specific antibodies, the body can avoid these autoimmune disasters.
However, this high level of specificity also means that antibodies typically
only recognize one specific species or even sub-species of foreign invaders.
Interestingly, a research group recently identified antibodies from healthy
individuals that could recognize multiple subgroups of </span><i style="font-family: inherit;">Klebsiella pneumoniae</i><span style="font-family: inherit;">,
as well as various other bacteria and even some yeasts and viruses. These
“universal antibodies” have sparked a great deal of interest as a potential
treatment option for patients suffering from infections.</span><br />
<div class="MsoNormal">
<div style="margin-bottom: .0001pt; margin: 0in;">
<span style="font-family: inherit;"><br /></span></div>
<div style="margin-bottom: .0001pt; margin: 0in;">
<span style="font-family: inherit;"><i style="mso-bidi-font-style: normal;">K.
pneumoniae </i>is a species of bacteria that is found frequently in the
environment and in people; it is estimated that over 1/3 of the world’s
population is colonized by <i style="mso-bidi-font-style: normal;">K. pneumoniae. </i>In
individuals with a healthy immune system, the level of bacteria is controlled, and illness does not occur. However, in immunocompromised and
already-ill people, the bacteria can cause severe infections. <i style="mso-bidi-font-style: normal;">Klebsiella </i>are
the third leading cause of hospital-acquired infections in the United States,
with alarmingly high mortality rates: <i style="mso-bidi-font-style: normal;">K. pneumoniae </i>pneumonia
can cause mortality in up to 50% of patients, and bloodstream infections can
cause mortality in 20-30%. Equally concerning is the rising level of antibiotic
resistance found in <i style="mso-bidi-font-style: normal;">K. pneumoniae. </i>This
makes them increasingly difficult to treat.<o:p></o:p></span></div>
<div style="margin-bottom: .0001pt; margin: 0in;">
<span style="font-family: inherit;"><br /></span></div>
<span style="font-family: inherit;"><o:p></o:p>
<o:p></o:p>
<o:p></o:p></span><br />
<div style="margin-bottom: .0001pt; margin: 0in;">
<table cellpadding="0" cellspacing="0" class="tr-caption-container" style="float: left; margin-right: 1em; text-align: left;"><tbody>
<tr><td style="text-align: center;"><a href="https://phil.cdc.gov//PHIL_Images/18170/18170_lores.jpg" imageanchor="1" style="clear: left; margin-bottom: 1em; margin-left: auto; margin-right: auto;"><img border="0" height="320" src="https://phil.cdc.gov//PHIL_Images/18170/18170_lores.jpg" width="306" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;"><i>K. pneumoniae </i>(red)<span style="background-color: white; color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 11.88px;">.</span><br />
<span style="background-color: white; color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 11.88px;">CDC's Public Health Image Library.</span><br />
<span style="background-color: white; color: #333333; font-family: "arial" , "tahoma" , "helvetica" , "freesans" , sans-serif; font-size: 11.88px;">Image # 18170; photo credit: NIAID.</span></td></tr>
</tbody></table>
<span style="color: black; font-family: inherit;">The outer membrane of <i style="mso-bidi-font-style: normal;">K. pneumoniae</i>,
and other bacteria,<i style="mso-bidi-font-style: normal;"> </i>is
covered in lipopolysaccharide (LPS) molecules. Because this molecule is exposed
to the external environment, LPS serves as a good target for the immune system
to produce antibodies against. LPS is made up of repeating sugar residues; in
the case of the <i style="mso-bidi-font-style: normal;">K. pneumoniae </i>subgroups
of interest in this research, that sugar is mannose connected by 1-2 or 1-3 linakages. Researchers identified
a number of antibodies from the blood of healthy individuals that were highly efficient at neutralizing <i style="mso-bidi-font-style: normal;">K. pneumoniae </i>bacteria
by binding to these mannose residues. Because mannose is a common surface sugar molecule and the mannose molecule arrangements used by <i>K. pneumoniae </i>are also used by other microbes, these antibodies had a very broad specificity. They bound not only <i>K. pneumoniae, </i>but also other intestinal microbes, HIV virions, and the yeast <i>Saccharomyces cerevisiae</i>. </span><br />
<span style="color: black; font-family: inherit;"><br /></span>
<span style="font-family: inherit;">These antibodies open the possibility for their use as therapeutics. Giving pre-made antibodies to patients has already been established as an effective strategy to treat or prevent a number of infectious diseases, such as rabies, diptheria, tetanus, hepatitis B, and botulism. In the case of these infections, antibodies that are highly specific to the pathogen of interest have been made and used. However, the identification of these broadly neutralizing antibodies opens the door for a new opportunity. Giving a patient "universal" antibodies could help fight a variety of infections without even necessarily identifying the causative agent, which can be difficult and time-consuming in the face of a life-threatening infection. While it is a long process from antibody identification to the approved use of an antibody as a therapy in patients, this discovery provides researchers direction for the path ahead. Therapeutic advances that use alternative strategies to inhibit and kill pathogens are of the utmost importance in the current age of antibiotic resistance. Antibodies, instead of just antibiotics, that can fight disease will be one of the important tools in our arsenal against the ever-evolving microbes.</span></div>
</div>
Anonymoushttp://www.blogger.com/profile/05503168250289145242noreply@blogger.com0tag:blogger.com,1999:blog-1839109299604462420.post-24005326344823231922018-04-30T21:58:00.000-04:002018-04-30T21:59:32.260-04:00The Fast and the Furious...Antibiotic Discovery<span style="font-size: 11pt;">Over 10 million deaths per year. That's the global death toll
experts predict from drug-resistant infections by 2050 without new ways to
combat these microbes. Unlike most disease areas, where new and improved
drugs are being discovered and developed every year, bacterial infections are
still largely treated with classes of antibiotics that were discovered over 50
years ago. Many of these drugs were found by screening microbes that live in
the soil, which has proven to be a successful strategy for obtaining a vast variety
of chemical compounds. However, most microbes in soil cannot be grown in the
lab, leaving large gaps in our ability to study them and identify potential new
antibiotics. Recent advances, however, have helped overcome this problem and lead
to the identification of the first new classes of antibiotics in 30 years.</span><br />
<span style="font-size: 11pt;"><br /></span>
<div style="margin-bottom: .0001pt; margin: 0in;">
<table cellpadding="0" cellspacing="0" class="tr-caption-container" style="float: left; text-align: left;"><tbody>
<tr><td style="text-align: center;"><img height="209" src="https://www.the-scientist.com/images/September2015/Annagraphic1.jpg" style="margin-left: auto; margin-right: auto;" width="320" /></td></tr>
<tr><td class="tr-caption" style="text-align: center;">The iChip culture method. <br />
Al Granberg. https://www.the-scientist.com/<br />
?articles.view/articleNo/44049/title/Cultural-Riches/</td></tr>
</tbody></table>
<span style="font-size: 11pt;">In 2015, a team of scientists at Northeastern University isolated a new antibiotic using an ingenious method for growing soil microbes with the iChip, a device with wells for bacteria that are separated from a natural environment (like soil) by a diffusion membrane with tiny pores that allow the transfer of nutrients without allowing the bacteria to leave the well. Using this method, researchers were able to isolate new chemical compounds from these bacteria and identify teixobactin. Upon further testing, they found that teixobactin was highly effective at killing several types of bacteria in culture, including </span><i style="font-size: 11pt;">Mycobacterium <span style="mso-bidi-font-style: italic;">tuberculosis </span></i><span style="font-size: 11pt;">and methicillin-resistant </span><i style="font-size: 11pt;">Staphylococcus aureus </i><span style="font-size: 11pt;">(MRSA), by interfering with the ability of the bacteria to build cell walls</span><i style="font-size: 11pt;">.</i><span style="font-size: 11pt;"> Teixobactin was also shown to be effective at clearing infections in mice. Although teixobactin itself is difficult to produce, a group at the University of Lincoln, UK, recently synthesized a much easier-to-make version that maintains potency and could be used for commercial production.</span><span style="color: black; font-size: 11.0pt;"></span></div>
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<span style="color: black; font-size: 11.0pt;">In 2017, another new class of antibiotics was discovered at
Rockefeller University using just bioinformatic analysis of DNA extracted from
the environment; this group didn’t even have to grow the bacteria in the lab.
They based their strategy on the knowledge that there is a family of
calcium-dependent antibiotics. By isolating DNA directly from environmental
samples and searching for sequences that featured the known calcium-binding
signature, they could identify genes that potentially encoded new calcium-dependent antibiotics. They then transferred these DNA sequences into
bacteria that can be cultured for further study. The new antibiotic class they
found, the malacidins, also interferes with the ability of bacteria to properly
form cell walls. Malacidins were shown to clear MRSA infections in the cut
wounds of rats. Importantly, even after 3 weeks of exposure to the drug, there
was no sign of resistant bacteria.<o:p></o:p><o:p></o:p>
This finding suggests that the mechanism of action for the malacidins is one
that cannot be circumvented easily by the bacteria, which bodes well for their
use against multidrug-resistant pathogens.</span><span style="color: black; font-size: 13.5pt;"><o:p></o:p></span></div>
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<span style="color: black; font-size: 11.0pt;">A third novel class of antibiotics was just described earlier this
month in the journal <i style="mso-bidi-font-style: normal;">Molecular Cell </i>by
researchers from the University of Illinois at Chicago and the biotech company
Nosopharm. This class, called the odilorhabdins, was isolated from a bacterium
that lives in a symbiotic relationship with a nematode worm in soil. This bacterium secretes a number of compounds that help the nematode colonize and
kill insects and keep the insect carcass from being invaded by other bacteria
or fungi. The odilorhabdins exert their antimicrobial activity by interfering
with bacterial protein production. While several other antibiotics also target this
process, the odilorhabdins bind to a unique site on the bacterial ribosome (the part of the cell responsible for making proteins);
this means that bacteria that are resistant to other antibiotics that interfere
with protein production will not be resistant to the odilorhabdins. When
tested for their ability to kill several pathogenic bacteria in culture, the
odilorhabdins were highly effective. One of the odilorhabdins, NOSO-95179, was
also tested in mice and could significantly reduce <i style="mso-bidi-font-style: normal;">Klebsiella
pneumoniae </i>septicemia and lung infection.</span><br />
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<table cellpadding="0" cellspacing="0" class="tr-caption-container" style="float: right; text-align: left;"><tbody>
<tr><td style="text-align: center;"><img height="168" src="https://phil.cdc.gov//PHIL_Images/18126/18126_lores.jpg" style="margin-left: auto; margin-right: auto;" width="200" /></td></tr>
<tr><td class="tr-caption" style="text-align: center;">MRSA (green) being enveloped<br />
by a white blood cell.<br />
CDC's Public Health Image Library.<br />
Image # 18126; photo credit: NIAID.</td></tr>
</tbody></table>
<span style="color: black; font-size: 11.0pt;">While these new antibiotics are still in the early stages of
development and are at least 6-10 years from being available for use in people,
the rapid identification of multiple new antibiotic classes after a decades-long
“discovery void” provides hope. The new
techniques for culturing soil bacteria, along with bioinformatic approaches
that avoid this step all together, offer new avenues for drug discovery. Additionally, there is ongoing work to re-investigate previously sidelined drug candidates and modify existing antibiotics to improve their efficacy and overcome
resistance. No matter the approach, the road to develop a new antibiotic is long and expensive, making it impossible for academic research labs to go it alone. Luckily, p</span><span style="font-size: 11pt;">harmaceutical companies are beginning to get more involved. In 2016, the Antimicrobial Resistance Industry Alliance presented the “Davos
Declaration” at the World Economic Forum. Nearly 100 companies signed
the declaration, pledging to support the research and development of new </span><span style="font-size: 14.6667px;">antimicrobials</span><span style="font-size: 11pt;"> and improve access to current and future treatments. With this renewed commitment from the pharmaceutical industry, which had largely been turning away from antimicrobial development in recent years, the financing and man-power to produce these new antibiotics might just be available. While nothing short of a strong, concerted effort to deal with drug resistance will allow us to avoid the looming projection of 10 million deaths per year, the current pace of advancement bodes well for our ability to rise to the challenge.</span></div>
Anonymoushttp://www.blogger.com/profile/05503168250289145242noreply@blogger.com0tag:blogger.com,1999:blog-1839109299604462420.post-30080996313650882372018-03-29T17:33:00.000-04:002018-03-29T17:33:48.453-04:00New funding (and new hope) for a Lassa virus vaccine<div class="MsoNormal">
Nearly 2 years ago in 2016, I wrote a post about a deadly virus that was causing a worrying outbreak in Nigeria: <a href="https://thegradschoolgrind.blogspot.com/2016/05/yearly-outbreaks-of-lassa-fever-take.html">the Lassa virus</a>. For the rest of 2016 and 2017, the outbreak lessened in severity, but it was not completely eliminated. Unfortunately, this year has featured a new surge in infections with the virus. In just the first 2 months of 2018, at least 317 people have been infected with Lassa virus, far surpassing the 143 cases confirmed in all of 2017. Additionally, around 20% of those infected in 2018 have died from the infection.<br />
<br />
While the reports from March suggest that the current outbreak is slowing, major hurdles for the containment and management of Lassa fever cases still exist. The disease is carried by multimammate rats, which are difficult to keep out of homes and away from human food, especially as populations in Africa grow and the once-empty fields where the rodents live are developed. The long asymptomatic period at the beginning of infection makes it difficult to diagnose and treat effectively. Even once symptoms do manifest, they tend to be mild and non-specific, with 80% of those infected suffering from mild fever, general malaise, and/or headache. Additionally, the sub-optimal treatments have not improved in recent years, and there is still no vaccine.<br />
<br />
<table cellpadding="0" cellspacing="0" class="tr-caption-container" style="float: left; text-align: left;"><tbody>
<tr><td style="text-align: center;"><a href="https://pixnio.com/free-images/science/microscopy-images/lassa-hemorrhagic-fever-lassa-virus/lassa-virus-virions-adjacent-to-some-cell-debris-the-virus-a-member-of-the-virus-family-arenaviridae-725x534.jpg" imageanchor="1" style="clear: left; margin-bottom: 1em; margin-left: auto; margin-right: auto;"><img alt="lassa, virus, virions, adjacent, cell, debris, virus, member, virus, family, arenaviridae" border="0" height="233" src="https://pixnio.com/free-images/science/microscopy-images/lassa-hemorrhagic-fever-lassa-virus/lassa-virus-virions-adjacent-to-some-cell-debris-the-virus-a-member-of-the-virus-family-arenaviridae-725x534.jpg" width="320" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;">Lassa virus particles. CDC's Public Health Image Library.<br />
Image # 8700; photo credit: C.S. Goldsmith.</td></tr>
</tbody></table>
In an attempt to deal with these issues, the Coalition for Epidemic Preparedness Innovations (CEPI) awarded $37.5 million to Themis Bioscience earlier this month for the development of their Lassa virus vaccine. CEPI was created in the wake of the Ebola epidemic and receives funding from the Wellcome Trust, the Bill & Melinda Gates Foundation, the European Commission, and the governments of Germany, Japan, Norway, Belgium, Canada, and Australia to support the development of vaccines for potential or existing pandemics. While there are many diseases that could fall into this category, the main focus in the next 5 years for the group will be Lassa virus, the Middle East Respiratory Syndrome (MERS) virus, and Nipah virus.<br />
<br />
With the funding from CEPI, Themis plans to move into human trials with their Lassa virus vaccine as early as this year. Following the Ebola crisis, the World Health Organization developed a procedure to fast-track the approval of products for use in public health emergencies. The hope is that these procedures could be used in the context of the Lassa virus outbreak to accelerate the development of the Themis vaccine. To further speed development, the Themis Lassa virus vaccine will be based on the measles vaccine vector previously created by the Institut Pasteur, which has already been used effectively in humans. By inserting Lassa virus proteins into this vector, a new vaccine that will prime the body to respond to a Lassa infection will be created. This strategy opens the door to allow for the rapid creation of additional vaccines, as well.<br />
<br />
The funding from CEPI will support the preclinical and initial clinical development through a phase 2 trial of the Themis Lassa virus vaccine in order to test its safety and efficacy. The ultimate goal is that the funds will allow the production of a vaccine stockpile that will be ready to test in an outbreak, which may be needed sooner rather than later. While the current outbreak appears to be slowing, and the dry season, when the majority of Lassa fever cases in Nigeria have historically occurred, is coming to an end, a report from Sierra Leone has suggested that the incidence of Lassa fever may actually be higher during the rainy season. This leaves uncertainty about the outlook for the current Lassa fever outbreak. But whether the outbreak continues now or goes dormant for the next 10 years, a vaccine will be a vital weapon in the fight against Lassa virus for the future.</div>
Anonymoushttp://www.blogger.com/profile/05503168250289145242noreply@blogger.com0tag:blogger.com,1999:blog-1839109299604462420.post-16899492830396099842018-03-05T11:22:00.001-05:002018-03-05T11:22:33.216-05:00Good reason for my writing gapI must apologize for my extended absence from writing these posts. But I promise I had good reason! Since my last post at the end of August, I've completed my dissertation and graduated with my PhD, hunted for a job, gotten a job, moved, and started that new job. But now I'm back and ready to provide you all with more exciting biology posts. Enjoy!Anonymoushttp://www.blogger.com/profile/05503168250289145242noreply@blogger.com0tag:blogger.com,1999:blog-1839109299604462420.post-53443861824769977332018-03-05T11:22:00.000-05:002018-03-05T11:24:00.348-05:00Flu vaccination: Arm yourself against the anti-vax arguement<div class="MsoNormal" style="background-color: white; color: #222222; font-family: arial, sans-serif; font-size: 12.8px;">
The flu vaccine. Always a hot topic, especially in years when the vaccine has poor efficacy as it does this year. At times like this, the anti-vax community can gain leverage. <span style="font-size: 12.8px;">So let's take a look at some of the top arguments used in the anti-vax movement and see if we can shed some light on the controversy.</span></div>
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<b>The flu vaccine makes you sick.</b><br />
People will often say that they got the flu because of the flu shot. This is actually not possible. The flu shot is made with an inactivated, DEAD form of the virus that cannot replicate and transmit. While there can be side effects from the shot that make you feel "sick," this is not the flu. <span style="font-size: 12.8px;">Additionally, the flu vaccine stimulates your immune system, which actually strengthens your ability to fight infections and avoid getting "sick." It is important to note, though, that getting the flu vaccine does not mean you are immediately protected. It typically takes about two weeks to gain the full advantage from the vaccine. People who were already exposed to the virus before receiving the vaccine or who are exposed shortly after vaccination will not be protected.</span><br />
<table cellpadding="0" cellspacing="0" class="tr-caption-container" style="float: right; margin-left: 1em; text-align: right;"><tbody>
<tr><td style="text-align: center;"><a href="https://media.npr.org/assets/img/2015/11/23/flu-shot-1_custom-bba61b7baacd2dec4ec7969b3d5920a9de0255cc-s900-c85.jpg" imageanchor="1" style="clear: right; margin-bottom: 1em; margin-left: auto; margin-right: auto;"><img alt="Image result for flu vaccine" border="0" height="132" src="https://media.npr.org/assets/img/2015/11/23/flu-shot-1_custom-bba61b7baacd2dec4ec7969b3d5920a9de0255cc-s900-c85.jpg" width="200" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;">Brian Snyder/Reuters/Landov</td></tr>
</tbody></table>
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<b>The flu vaccine contains mercury that will poison you.</b><br />
Flu shots that come from a multi-dose vial do typically contain thimerosal, an ethylmercury-based preservative to prevent any bacteria or fungus from contaminating the vaccine. Flu shots that come in prefilled syringes and the nasal flu vaccine do NOT contain this preservative (with the exception of the Fluvirin prefilled syringes from Seqiris, which contain trace amounts of thimerosal). It is important to note the distinction between ethylmercury (found in thimerosal) and methylmercury. Methylmercury is the form of mercury found in foods, like seafood, that is associated with neurological complications. While <i>in vitro</i> studies (in cell culture systems and not in the body) have found little difference between the effects of methyl- and ethylmercury, the story is quite different <i>in vivo </i>(in actual living creatures). Ethylmercury is cleared from the bloodstream significantly more quickly than methylmercury, minimizing the exposure of the body to mercury. Ethylmercury is also compartmentalized by the body more successfully than methylmercury, further limiting exposure. Some may argue that based on the <i>in vitro</i> evidence, ethylmercury is unsafe, but the <i>in vivo</i> data and years of studies have shown that this is not the case. But, if you still want to avoid mercury all together, you can get a prefilled syringe version of the flu shot that contains no thimerosal.<br />
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<b>The flu vaccine causes the virus to mutate, becoming more virulent.</b></div>
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This is a popular argument used in the anti-vax community. While that is always a theoretical possibility, there is currently no scientific evidence that this is happening. The influenza virus has an extremely rapid mutation rate, whether you put selective pressure on it or not, so it’s going to be mutating all the time regardless of what we as humans do. This is just the nature of the virus’s replication; the enzyme it uses to replicate its genome makes a lot of mistakes, and the virus is perfectly happy to continue on with those mistakes (aka mutations).<br />
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The idea that vaccines create more virulent viruses is typically based on the fact that the use of antibiotics can lead to more pathogenic bacteria, which has been observed. But the vaccine works very differently from an antibiotic. In the case of bacteria, they directly come in contact with and are affected by the antibiotic, which gives bacteria that can survive while in contact a direct advantage. In the case of the vaccine, since it is priming an individual’s immune system and not directly contacting the virus, there is no such direct advantage to the virus. Even if the influenza virus you encounter is different from the vaccine strain, your immune system will be primed and you will have a better chance of successfully clearing the virus. While it is theoretically possible that by vaccinating, you remove the predominant influenza strains, leaving an opening in the environment for a “resistant” strain to fill, most of the highly virulent and dangerous strains have emerged in parts of the world where vaccination rates are very low, so this doesn’t seem to be happening.<u></u><u></u></div>
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<div class="MsoNormal" style="background-color: white; color: #222222; font-family: arial, sans-serif; font-size: 12.8px;">
<b>Vaccination causes super strains of the flu virus to emerge that are immune to our vaccines. </b><br />
<table cellpadding="0" cellspacing="0" class="tr-caption-container" style="float: left; text-align: left;"><tbody>
<tr><td style="text-align: center;"><a href="https://carrington.edu/wp-content/uploads/2015/02/flu-vaccine-770x392.png" imageanchor="1" style="clear: left; margin-bottom: 1em; margin-left: auto; margin-right: auto;"><img alt="Image result for flu vaccine" border="0" height="162" src="https://carrington.edu/wp-content/uploads/2015/02/flu-vaccine-770x392.png" style="font-size: 12.8px;" width="320" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;">Influenza virus. Carrington College</td></tr>
</tbody></table>
People often further argue that our lack of vaccine effectiveness in recent years comes from the emergence of “super” strains of the virus that are “immune” to our vaccines. But the research suggests otherwise. Vaccinemakers use a less-than-ideal system for choosing the vaccine strains that relies on a test using ferrets exposed to the virus. This can lead to incorrect selection and a poor vaccine. Also, improved diagnostic techniques make it more likely for us to capture influenza infection than ever before, so people who would have been diagnosed with some unknown viral disease (and therefore considered “protected”) in the past are now being properly diagnosed as influenza patients. And we are learning that our vaccine production system making the vaccine in eggs leads to its own set of mutations in the vaccine strain that often dampen protection in people. A lot of groups are working to improve the vaccine production pipeline and find alternative ways that don’t involve growing the vaccine in eggs, so that will likely be the way of the future in 5-10 years.<br />
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<b>Vaccines cause autism.</b><br />
This claim is not unique to the flu vaccine and has been spouted at the forefront of the anti-vax community ever since 1998, when Andrew Wakefield and colleagues published a study looking at 12 children that claimed there was a link between the measles-mumps-rubella vaccine and autism. What people in the anti-vax community typically fail to realize is that since that article was published, it has been retracted (the authors themselves admitted their conclusions were inaccurate), Wakefield and colleagues have been found guilty of ethical violations and fraud, and Wakefield has been removed from the UK medical registry. They hand-picked the patients for their study and falsified data to ensure that they would conclude there was a link between vaccines and autism. Additionally, they had received funding from lawyers who had been hired by parents to bring lawsuits against vaccine companies. Since the Wakefield study, many large-scale studies have been performed to see if their initial findings could be confirmed in spite of the ethical issues with the study, but no corroborating evidence has been found. The link between vaccination and autism is based on fabricated data and has no true scientific merit.<br />
<br />
<br />
<span style="font-size: 12.8px;">In spite of the potentially poor efficacy, healthcare providers will still push for vaccination. Any protection is better than none, especially if you are in contact with the populations at high-risk of dying from infection, i.e. the elderly, babies, and immuno-compromised individuals. The more people who are protected (even if the protection is sub-optimal), the less likely it is for the virus to come in contact with these highly susceptible individuals, and healthcare providers rely on this to keep patients safe. T</span><span style="font-size: 12.8px;">he bottom line is we may have a sub-optimal vaccine, but a lot of people are actively working on that, any protection is still better than none, and there is no evidence that getting the vaccine has any negative impacts on the pool of viruses we are exposed to. So please do not be discouraged, and use your new flu vaccine knowledge to help educate others!</span></div>
Anonymoushttp://www.blogger.com/profile/05503168250289145242noreply@blogger.com0tag:blogger.com,1999:blog-1839109299604462420.post-38293645903776437362017-08-31T20:30:00.000-04:002017-08-31T20:30:57.530-04:00The mosquito microbiome: An ally in the fight against diseaseThe annoying buzz of pesky little mosquitoes. At this time of year, the sound can be heard in backyards all around the world. Due to emerging threats like Zika and Dengue virus, people are becoming more and more familiar with the harm these little devils can cause. While vaccines and treatments for many mosquito-borne illnesses remain elusive, some researchers are placing new hope in other micro-organisms who may be able to play a role in preventing these dangerous diseases.<br />
<br />
Previous work focused on malaria and its vector, the anopheline mosquitoes, has implicated micro-organisms, such as bacteria or fungi, within the mosquito to have an effect on the mosquito's ability to transmit the disease. Numerous studies in both <i>Anopheles stephensi </i>and <i>Anopheles gambiae </i>have shown that microbes in their midguts can influence the malarial parasite's ability to develop and transmit to new hosts. This is also not a new concept in the <i>Aedes </i>mosquitoes, the vectors for many of the mosquito-borne viruses. Wolbachia bacteria have been successfully introduced multiple times into these mosquitoes to prevent infection in the past.<br />
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Most previous studies have focused on introducing microbes to adult mosquitoes. In the field, this naturally presents challenges with application as adult mosquitoes are constantly migrating from place to place. However, recent work highlights that similar strategies could be used on mosquito larvae to influence their ability to transmit disease as adults. Larvae are much more targetable, due to the relative ease of identifying larval development sites.<br />
<br />
In the latest study of the mosquito microbiota and its effects on vectorial capacity (the ability of a vector, like the mosquito, to transmit a particular disease), researchers found that differences in bacterial colonization of larvae could have an effect on the adult mosquito's traits. This means that by changing the bacteria larvae are exposed to, you could influence their ability to transmit disease as adults.<br />
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While there are many environmental concerns that will need to be addressed before a strategy altering the bacterial make-up of mosquito breeding sites, this new study and the growing body of work focusing on the mosquito microbiome's effects on vectorial capacity offer hope for new strategies to control disease spread. Perhaps some day we will be able to add a simple pellet of bacteria to a pool of water with mosquito larvae and prevent all the subsequent adults from transmitting disease. This may seem like a far-fetched dream today, but with continued research, it could one day be a reality.Anonymoushttp://www.blogger.com/profile/05503168250289145242noreply@blogger.com0tag:blogger.com,1999:blog-1839109299604462420.post-82083477812194525122017-07-31T20:02:00.000-04:002017-08-07T21:11:26.022-04:00New diagnostic method may help fight antibiotic resistanceCoughing, sneezing, runny nose, wheezing; respiratory tract infections are extremely common, with the average American adult enduring two to four each year. Typically, the symptoms last for seven to ten days while you struggle through, and then you get better. If you go to a doctor with these symptoms, they will likely prescribe you a broad-range antibiotic. This may sound fine, but there is a big issue with that: not all respiratory tract infections are caused by a bacterial infection. Over-use of antibiotics has been leading to increased antibiotic resistance for decades. The only way to prevent the over-prescribing of antibiotics for these respiratory tract infections is to determine the cause of each infection. Unfortunately, current technologies for diagnosing these infections are not fast and specific enough to allow timely and proper diagnosis. New technology has emerged that may help with the diagnosis and cut down on the over-use of antibiotics.<br />
<br />
When exposed to different pathogens, the body's immune system responds in different ways. A virus, for example, causes cells to react in a different way than a bacterium. The cells of the immune system that can be found in the blood can be profiled to understand what type of infection they are fighting. This has been done by studying the messenger RNAs (mRNAs), also known as transcripts, found within monocytes, a specific subset of immune cells. mRNAs lead to the proteins being made by a cell and often play key roles in regulating the activation of pathways involved in an immune response. A recent study identified ten different mRNAs that could be used to determine if the body was responding to a bacterial or a viral respiratory tract infection. A more recent study further validated these ten mRNAs by confirming their use in 94 hospitalized adults with respiratory tract infections and identified even more mRNAs that could differentiate a bacterial infection from a viral infection. This allows for more appropriate use of antibiotics in these patients and avoids the potential over-use of antibiotics that threatens their effectiveness.<br />
<br />
As more and more antibiotic-resistant infections emerge, it is becoming more important than ever to safeguard our potent antibiotics by only using them when necessary. When antibiotics are used, they kill off whatever bacteria are susceptible to their effects, leaving behind only those that are resistant. This helps select for antibiotic-resistant bacteria within a population. The over-use of antibiotics has sped this natural selection process, allowing for the rapid development of resistance even to the newest antibiotics. Using technologies such as this transcript profiling of immune cells will help slow the selection process by ensuring antibiotics are only introduced when they can be of help, allowing our antibiotics to maintain their usefulness longer before resistance develops.<br />
<br />
The technology to profile transcripts of immune cells in the blood has the opportunity for application far beyond the identification of bacterial versus viral respiratory infection. Individual pathogens themselves can produce unique immune profiles that could one day be categorized using similar methods. With the standard diagnostics of the past, it is nearly impossible to diagnose a bacterial or viral infection unless the bacteria can be cultured or the virus can be isolated. Knowing the unique transcript profile induced by a pathogen could someday allow for molecular diagnosis of a number of pathogens without the need to culture the bacteria or isolate the virus, allowing for an even more significant reduction in antibiotic over-use. This would also provide more rapid diagnosis; transcript analysis could be performed in a matter of hours, while the diagnostics of the past frequently require days. With emerging technologies, these goals become even more achievable every day, and we may soon see a time when antibiotics are only used for infections confirmed to be caused by a susceptible bacteria.Anonymoushttp://www.blogger.com/profile/05503168250289145242noreply@blogger.com0tag:blogger.com,1999:blog-1839109299604462420.post-38465441216719586482017-06-29T19:23:00.002-04:002017-06-29T19:23:43.754-04:00More vaccination victories needed in the meningitis fight<div class="MsoNormal">
Vaccinations have been proven time and time again to prevent
disease and improve health outcomes. All around the world, vaccines have been
deployed to deal with illnesses as common as the flu and as deadly as Ebola. Meningitis
is another disease for which vaccination has become a major priority. The
“kissing disease,” at it is sometimes called, has made a number of appearances
on college campuses across the United States. While incidence in the U.S.
remains quite low, at 0.3-4 cases per 100,000 persons, incidence can be as high
as 1 case per 100 persons in the “meningitis belt” of Africa, where epidemics
occur with regularity. <o:p></o:p></div>
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<table cellpadding="0" cellspacing="0" class="tr-caption-container" style="float: left; margin-right: 1em; text-align: left;"><tbody>
<tr><td style="text-align: center;"><a href="https://microbewiki.kenyon.edu/images/thumb/3/30/NMeningitidis.jpg/400px-NMeningitidis.jpg" imageanchor="1" style="clear: left; margin-bottom: 1em; margin-left: auto; margin-right: auto;"><img alt="Image result for neisseria meningitidis" border="0" height="300" src="https://microbewiki.kenyon.edu/images/thumb/3/30/NMeningitidis.jpg/400px-NMeningitidis.jpg" width="400" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;"><i>Neisseria meningitidis</i>, the bacterium responsible for meningitis.<br />Image from Bioquell.com</td></tr>
</tbody></table>
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Infection with the bacterium <i>Neisseria meningitidis</i>, the major cause of meningitis, often goes
unnoticed. The bacteria take up residence within the nasal cavity, where they can
stay without causing disease in a carrier individual. However, in approximately
1-5% of people exposed to the bacteria, invasive disease occurs, and the
bacteria enter the bloodstream, leading to life-threatening disease.<o:p></o:p></div>
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Symptoms of meningitis typically begin almost immediately,
just one day after infection, and include flu-like symptoms of fever, headache,
and stiffness. Because the bacteria enter the bloodstream, any organ or tissue
can become infected and impaired. Despite years of research, mortality rates
continue to range from 10-15%, even in developed countries, with rates above
20% in the developing world. Even for those who survive the invasive disease
stage, meningitis causes lasting impairments in 19% of patients, with
neurological disabilities, seizures, hearing or visual loss, and cognitive
impairment being classical manifestations. The rapidity of disease progression,
along with the high mortality rate, make meningitis a prime disease target for
vaccination.<o:p></o:p></div>
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The first vaccines against meningitis were developed in the
1970s. Unfortunately, these early vaccines lacked the ability to maintain
long-lasting immunity against the bacteria. In the late 1990s, alterations were
made in the vaccine components, allowing for the elicitation of an
immunological memory response that would be effective to protect young children
into their adult years and would even help reduce the rates of carriage of the
bacteria in the nasal cavity. While this was great news for the prevention of
meningitis, challenges still remained. The bacteria that cause disease can
belong to any of 6 different serogroups, meaning that immunity to one serogroup
will not necessarily provide protection from another. This requires
differential targeting of all 6 serogroups to truly prevent disease.<o:p></o:p></div>
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<table cellpadding="0" cellspacing="0" class="tr-caption-container" style="float: right; margin-left: 1em; text-align: right;"><tbody>
<tr><td style="text-align: center;"><a href="https://upload.wikimedia.org/wikipedia/en/5/54/Meningitis_vaccine_project_logo.jpg" imageanchor="1" style="clear: right; margin-bottom: 1em; margin-left: auto; margin-right: auto;"><img alt="Image result for meningitis vaccine" border="0" height="157" src="https://upload.wikimedia.org/wikipedia/en/5/54/Meningitis_vaccine_project_logo.jpg" width="200" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;">Image from the Meningitis Vaccine Project</td></tr>
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Researchers have addressed this challenge by producing different
vaccines for use in specific parts of the world where each serogroup is
problematic. In the meningitis belt of Africa, for example, serogroup A has
historically been the cause of epidemics. To wipe out these epidemics, a mass
vaccination campaign was begun in 2010; the Meningitis Vaccine Project produced
and provided vaccines against <i>N.
meningitidis </i>serogroup A for over 217 million people in 17 different
countries. Thanks to these vaccines, epidemics linked to the serogroup A
bacteria have been eliminated.<o:p></o:p></div>
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Unfortunately, when one serogroup is removed, a niche opens
up for another. Just last month, the CDC announced that a small epidemic in
Liberia had been caused by the <i>N.
meningitidis </i>serogroup C bacteria. Nigeria and Niger have also reported
outbreaks of this serogroup. Luckily, in the case of Liberia, the country’s
response time was extremely rapid. Thanks to the health system improvements
made during the Ebola outbreak, Liberia now has a robust case detection and
monitoring system. Other countries in the area, however, are not nearly as
advanced and could suffer a severe epidemic if serogroup C moves in with force.
<o:p></o:p></div>
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Great strides have been made in the fight against meningitis
outbreaks. However, the complexity of the group of bacteria responsible for the
disease leaves a number of challenges in place that must be overcome. The ideal
solution would be the introduction of a vaccine that combined pieces from each
bacteria serogroup to produce an immune response in patients that would protect
from all six serogroups at the same time. While some quadrivalent vaccines
already exist, which provide protection against four of the six serogroups,
these vaccines have only been recommended for use in the U.S. for adolescents
entering college. Protection from this vaccine only lasts 2-5 years in adults,
making it less than ideal for deployment in rural areas where boosting is not a
viable option, such as Africa. Advances in vaccine technology may help improve
the longevity of protection, making multivalent vaccination a more robust
solution to the meningitis problem. Until then, rapid case detection and
monitoring capabilities, such as those displayed in Liberia, will be the key to
keeping meningitis epidemics in check as they arise. Between vaccine and
monitoring advances, meningitis epidemics may one day become a thing of the
past. <o:p></o:p></div>
Anonymoushttp://www.blogger.com/profile/05503168250289145242noreply@blogger.com0tag:blogger.com,1999:blog-1839109299604462420.post-56758046414491668652017-05-21T22:22:00.000-04:002017-05-21T22:22:02.345-04:00The Stressed-out MicrobiomeStress. It's something we encounter every day. People teach workshops and write books on how to deal with it. We spend countless hours and dollars trying to avoid it. But it's still there. Stress is as much a constant in our world today as the air around us. We all know that stress can have negative impacts on mental well-being, but we are just beginning to realize the effects stress can have on other bodily systems, and the effect these systems can have on our ability to deal with stress. Recent research has shown that the microbiome can be significantly affected by and play a major role in our response to stress.<br />
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The microbiome is the group of microbes (bacteria, fungi, archaea, etc.) that colonize a particular area of the body. The gut microbiome has been a population of intense research for quite a few years now. With increasing technology, we've begun to learn more and more about this population. We know that at homeostasis, each person has a specific microbial population that makes up their gut microbiome. This helps keep us healthy, keeping our digestive system running smoothly and ensuring successful processing of the food we eat. But in times of disease or stress, the microbiome in the gut can change dramatically, causing symptoms from loss of appetite to ulcers.<br />
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How exactly does stress change what's living in your intestines? It's all because of the gut-brain communications. This is achieved through neural projection pathways, neuroendocrine signaling, and entero-endocrine signaling, among other pathways. Your body uses messaging through the neurons and small chemical messengers in the form of endocrine signals to communicate over long distances, such as from the brain to the gut. In return, the gut uses the same mechanisms to send feedback to the brain. The microbes in the gut, however, can also produce chemical messages that get sent to the brain. When your body experiences stress, different chemical signals are sent to the gut; this can, in turn, cause some microbes to die and allow other microbes to take their place. The change in the composition of microbes can then change the chemical signals sent back to the brain. In this way, there is an intimate connection between the signalling input from the brain and the feedback the brain receives. These signals are essential to support mood, higher cognitive function, and behavior.<br />
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Work in animal models has highlighted the influence of stress on the gut microbiome and the subsequent influence of the microbiome on behaviors. For example, when mice are raised in a germ-free environment (no microbiome), the mice show reduced anxiety-like behaviors as compared to mice that are not raised in a germ-free environment. It has also been shown that the microbiome of the mice has an influence on the development of the amygdala, a region of the brain that plays a vital role in controlling behavioral and physiological responses to stress stimuli. The germ-free mice showed increased amygdala volume, suggesting an increased ability to handle stress. Additional studies have found that early-life stress can change an animal's microbiome for the rest of its life and that microbiome transplantation from depressed rats to healthy rats can lead to anxiety-like behaviors in the healthy rats.<br />
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All the interest in the microbiome and stress has led to new insights for the treatment of stress-related behaviors through microbiome alteration. Allowing colonization with particular species of bacteria, for example <i>Lactoacillus helveticus </i>and <i>Bifdobacterium longum </i>in both rats and humans, has been shown to reduce psychological distress. Additionally, treatment with oligosaccharides, such as fructo-oligosaccharide or galacto-oligosaccharide in mice, can have anti-depressant effects by allowing different populations of microbes to thrive on these nutrient sources.<br />
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While the microbiome still holds many mysteries, we are beginning to understand just how important its functions are in our every day lives. So the next time you're feeling stressed out, you might want to check in with your microbes and see how they're feeling. They may play a critical role in getting you through this stress and on with your life without allowing long-term health complications, like depression, anxiety disorders, or inflammatory bowel disease, to develop. The best ways to keep a healthy microbiome are to eat a healthy diet, with emphasis on fibers that support the development of beneficial bacteria, take probiotics, stay physically active, and avoid antibiotics whenever possible. Or, simply change your lifestyle to reduce your stress level. However it is achieved, a healthy microbiome can be a great advantage in the years ahead.Anonymoushttp://www.blogger.com/profile/05503168250289145242noreply@blogger.com0tag:blogger.com,1999:blog-1839109299604462420.post-17684419995749379322017-04-23T23:18:00.000-04:002017-04-23T23:19:15.993-04:00Introverts, Assemble!On Saturday, April 22, the March for Science took place at locations across the United States and the world. I had the good fortune to attend the flagship march in Washington, D.C. From talks and music on the main stage to teach-in tents across the Washington Monument lawn to the march itself, the day was quite an experience for me. I don't normally write personal blog posts, but it seems appropriate for this month to do just that.<br />
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<a href="https://scontent-ord1-1.xx.fbcdn.net/v/t1.0-9/18034151_10154294850940836_7964991187324720203_n.jpg?oh=2a8cdf2e698081839e205a48a1e117c9&oe=59804CBD" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img alt="Image may contain: 5 people, people smiling, people standing and outdoor" border="0" height="400" src="https://scontent-ord1-1.xx.fbcdn.net/v/t1.0-9/18034151_10154294850940836_7964991187324720203_n.jpg?oh=2a8cdf2e698081839e205a48a1e117c9&oe=59804CBD" width="225" /></a>I attended the march with a few fellow biomedical science PhD students and an engineer. I know many of my other biomedical science friends were there as well. But this march wasn't just about biomedical scientists. It was about geologists and mathematicians and chemists and botanists. It was about our past and the present and the world we want to leave behind. It was about coming together from all scientific fields, from competing labs and engineering firms, from all over the globe. It was about making the facts known and showing the world that science has always held and will always hold great value for our society. </div>
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I was amazed by the diversity of the people there. Not only were people diverse in interest, background, and occupation, but they were also diverse in ways you don't typically expect in the sciences. There were young children and senior citizens and everything in between. There were long-time career scientists and Nobel laureates and undergraduates just starting out. There were Christians and Muslims and atheists and agnostics. There were Republicans and Democrats and Independents. Men and women from all walks of life were gathered together to advocate scientific awareness.<br />
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While the message at times turned political, the overwhelming push from the people was for bipartisan, wholehearted support for the sciences. Acceptance of "alternative facts" and statements without data cannot continue to suppress the great advances being made every day in science and technology. Some emphasized the dangers of budget cuts to the National Institutes of Health and other scientific agencies, while others focused on the frightening state at the Environmental Protection Agency. Still others expressed concern for the uninformed American public and policy makers and the great number of sources of unreliable and untrue "scientific" information that create a mistrust of science.</div>
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As the march itself progressed from the Washington Monument to the Capitol Building, signs of all shapes, sizes, and recyclable materials braved the steadily increasing rain. Many gave a nod to the fact that it was Earth Day and featured images of Mother Earth, saying, "I'm with her." Others cleverly incorporated elements from the periodic table to spell out their messages. Still others pointed out how truly desperate the situation of science in America must be with phrases like, "It's so bad even the introverts are here." "Science not silence" and "Make America Smart Again" were other common sentiments. Neil deGrasse Tyson was frequently cited for his quote, "The good thing about science is that it's true whether or not you believe in it." Though many signs suffered from the elements, the spirit of their creators remained undeterred as we progressed along Constitution Avenue. Cheers and chanting were frequent throughout the crowd, as was reflective discussion among the participants.</div>
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The march was, in my opinion, a smashing success. It was a giant nerd convention with the outreach capabilities to include anyone and everyone. The breadth of scientific topics and passions highlighted throughout the event was mind-blowing. We often get so focused on our narrow sliver of the scientific community that it's easy to forget about the incredible power of all of us united. It was truly humbling to see the incredible amount of support for the sciences that exists in our country. We can only hope that the policies of the government will reflect that support moving forward. Recognition of the importance of science will not only lead to funding assurance to support vital research, but it will also ensure that we continue to make the technological advances to improve the health and lives of everyone across the globe. Science saves lives, and science paves the future.</div>
Anonymoushttp://www.blogger.com/profile/05503168250289145242noreply@blogger.com0tag:blogger.com,1999:blog-1839109299604462420.post-89787072521258227592017-03-31T12:43:00.000-04:002017-03-31T12:43:05.688-04:00Mobile phones can make the difference for infectious disease management<div class="MsoNormal">
Imagine going to the doctor for an HIV test in sub-Saharan
Africa. You will likely have to travel a long distance to get to a clinic and,
once you arrive, the HIV test will require specimens to be sent to a central
testing laboratory for the actual test to be performed. You will then have to
wait for the results to be delivered to the clinic and travel back to get the
diagnosis. In Zambia, it takes approximately 92 days for this process to be
completed. When you are an HIV-positive mother waiting to find out if your
newborn child needs anti-retroviral therapy, each of those 92 days can be the
difference between life and death for your baby.</div>
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New work from Dr. William Moss of the Johns Hopkins Bloomberg School of Public Health and his group focuses on finding ways to
shorten the 92-day wait for HIV test results. Capitalizing on the increasing
amount of technology available in rural Zambia, Moss and colleagues conducted a
study using text messaging to deliver the HIV test results directly to mothers
or to the rural health clinics from the central testing lab. They found that by sending a text message to the mother directly,
they could reduce the time from sample collection to receipt of diagnosis to
just 18 days. Unfortunately, the use of mobile phones is still not widespread;
only 30% of mothers in the study had ever used a mobile phone. Luckily, the
local clinics do have mobile phones, so using text messaging to deliver results
to the clinic can still decrease the time to diagnosis to 36 days. By cutting
56 days off the wait for the diagnosis, the HIV-positive children will receive
anti-retroviral therapy nearly 2 months earlier. Reducing the time to treatment
for HIV-positive children has been shown to significantly reduce the
HIV-associated morbidity and mortality, vastly improving their quality of life.<o:p></o:p></div>
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This is not the first time mobile phone technology has been
used in Africa to impact health care. As the number of cell phones throughout
the area has increased, some clinics have chosen to provide expectant mothers
with a mobile phone so that they can get expedited access to an experienced
midwife or healthcare professional. In other areas across the continent, SMS services have been used to target pregnant women and new mothers to ensure early detection of life-threatening emergencies and adherence to treatment regimens for pathogen clearance. These methods and Moss’s study highlight
the same conclusion: increased access to mobile phones throughout the area can have
major positive impacts on health care. Funding and infrastructure for such
technological advances remains a major issue hindering progress.</div>
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As noted by Moss in his recent <i>BMC
Pediatrics </i>paper, implementation of the mobile phone messaging system for
test result delivery was by no means trivial. It required the hiring and
training of new staff members, along with the purchase of the study’s mobile
phone and “talk time” for the phone. However, with the right funding and
infrastructure, the spread of technology throughout Africa has the potential to
have significant and widespread impacts on healthcare. Studies such as the one
by Moss and colleagues highlight the great potential of available technology.
This encourages governments and private sector investors to take note and get
involved. Someday soon, nationwide mobile phone messaging systems may become
common place, drastically cutting the time to diagnosis and improving
individual’s access to care and treatment. <o:p></o:p></div>
Anonymoushttp://www.blogger.com/profile/05503168250289145242noreply@blogger.com0tag:blogger.com,1999:blog-1839109299604462420.post-71657506982192530062017-02-15T17:09:00.000-05:002017-02-15T17:09:16.185-05:00Killing two birds with one stone: A new vaccine to fight rabies and MERS-CovIn 2003, the world was faced with a serious biological threat. The severe acute respiratory syndrome (SARS) virus hit the scene in China and quickly spread to 28 countries across the globe. The reason for the rapid and global spread lay in the very nature of the virus' infection. It can be spread by close person-to-person contact through respiratory droplets produced when an infected person sneezes or coughs, and the initial symptoms of disease are very non-specific. This allowed the virus to easily be carried via international travel throughout the world. While the number of cases quickly rose to a total of 8,098 within 6 months, the global response was also rapid. The World Health Organization quickly activated their global alert system and began aiding countries in identifying and quarantining those infected and at risk. Thanks to this global response, SARS was quickly handled. However, this virus showed the world how at-risk we are to respiratory viruses in an age of increasing global travel.<br />
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<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiUmav0CFxt4Rv_FakTu2vXf8bPSIzgpCm6LwcAprG0bSaLMOyQIM2J1FBxhvrQf9-WQG0kVax-5sThwqk2cS_Xu5AHj00mjYfQ_G22XIVSk2yAKo9xEGhh7Qa6k9M9DNhUJIKOJtR00Ss/s1600/nrmicro3143-i1.jpg" imageanchor="1" style="clear: right; float: right; margin-bottom: 1em; margin-left: 1em;"><img border="0" height="183" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiUmav0CFxt4Rv_FakTu2vXf8bPSIzgpCm6LwcAprG0bSaLMOyQIM2J1FBxhvrQf9-WQG0kVax-5sThwqk2cS_Xu5AHj00mjYfQ_G22XIVSk2yAKo9xEGhh7Qa6k9M9DNhUJIKOJtR00Ss/s200/nrmicro3143-i1.jpg" width="200" /></a></div>
Since the 2003 SARS outbreak, scientists have been on the look-out for the SARS virus and other related viruses in an attempt to minimize outbreaks. These viruses are part of a family known as Coronaviridae, specifically the coronavirus sub-section of this family (a typical virion is shown to the right). They are single-stranded, positive sense RNA viruses, which means that as soon as the virus invades a host cell, it can begin making its own proteins and progeny immediately without the need for time for replication or transcription of the genetic material. The coronaviruses that cause respiratory syndromes infect the cells of the lungs, leading to severe and sometimes deadly pneumonia.<br />
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In 2012, a novel coronavirus was identified in Saudi Arabia; it was named the Middle East Respiratory Syndrome Coronavirus (MERS-CoV). It quickly spread to the United Kingdom through travel. While the MERS-CoV has never caused an outbreak as large as that of the SARS virus, it has also not been contained as successfully. MERS-CoV outbreaks have continued to pop up from 2012 to now, with the most recent outbreak update coming just last week from Saudi Arabia. The MERS-CoV outbreaks have caused a total of 1,905 confirmed cases in 27 countries, with 677 deaths. The severe pneumonia caused by MERS-coV is more deadly than that caused by SARS and other coronoviruses, leading to the alarmingly high 37% death rate.<br />
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There are currently no vaccines and no treatments for MERS-CoV. Quarantining those infected and using additional precautions when treating these patients have been the only successful preventative measures to reduce spread. The biggest problem for complete elimination of this virus is that, unlike the SARS virus, the MERS-CoV can also infect an animal that has frequent contact with humans: camels. In many parts of the globe, camels are essential for transportation and play a pivotal role in the economy. Since camels have been shown to be a reservoir for the MERS-CoV, and people in these regions need to continue to have close contact with these animals, the virus has an easy route to re-enter the human population even with the implementation of the same control measures that were so successful with the SARS virus.<br />
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<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhGIFtbHoh0IysEBMKt_99pfs1_P0cPrZVoVYJbutT1NOrvX4IU-ni7_4Cv-OBCSNX6EN1BNBhQ6rRt7ZL4eVEeY5F2Ru3ZFCRWjLVnrtldhBJyfP8eFCRicEuq4yWjcxYsDntsRbYc8Cw/s1600/Camel-transmission.5.png" imageanchor="1" style="clear: left; margin-bottom: 1em; margin-left: auto; margin-right: auto;"><img border="0" height="300" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhGIFtbHoh0IysEBMKt_99pfs1_P0cPrZVoVYJbutT1NOrvX4IU-ni7_4Cv-OBCSNX6EN1BNBhQ6rRt7ZL4eVEeY5F2Ru3ZFCRWjLVnrtldhBJyfP8eFCRicEuq4yWjcxYsDntsRbYc8Cw/s400/Camel-transmission.5.png" width="400" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;"><span style="font-size: xx-small;">The MERS-CoV can be spread from camels to humans in many ways.</span></td></tr>
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Recent work has focused on elimination of virus from the camel population as a course of action to reduce human infections. Starting with a rabies vaccine, which has long been given to animals and is well-tolerated, a group in the United States has shown that immunity to both rabies and MERS-CoV can be achieved in mice. In order to do this, they took a piece of the MERS-CoV spike protein and fused it to the rabies G protein. This allowed a portion of the MERS-CoV to be incorporated into the rabies virus vaccine particles for delivery to the mice. After receiving the immunization, mice were challenged with the MERS-CoV and were found to be protected from infection. The researchers also found high levels of neutralizing antibodies against both MERS-CoV and the rabies virus in the blood of the mice.<br />
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While this vaccine candidate is still in the early stages of development, the successful use of the previously tested and approved rabies vaccine as a backbone may provide a way to shorten the timeline to implementation of the vaccine for animals on a larger scale. This could provide a way to start to eliminate the MERS-CoV reservoir and begin to reduce outbreaks in people across the globe. While other research groups are still searching for human vaccination and treatment strategies that will greatly improve our ability to decrease disease severity and save lives, dealing with this large camel reservoir will be an essential step before disease elimination and eradication can truly be considered.Anonymoushttp://www.blogger.com/profile/05503168250289145242noreply@blogger.com0tag:blogger.com,1999:blog-1839109299604462420.post-1404271585804040672017-01-27T11:18:00.002-05:002017-01-27T11:18:35.197-05:00Measles on The Oregon Trail and now"John has measles." Our journey along <i>The Oregon Trail </i>wraps up with a member of our party falling ill with the measles virus. This leads to the stereotypical measles rash, along with fever and coughing. The mortality rate from measles tends to be low in developed countries, but in places of poverty and food shortages, the mortality rate can be as high as 28%. One of the biggest problems with measles is that it is highly contagious and can be spread through the air. There is also no treatment for this disease, leaving disease prevention as the best strategy for dealing with the measles.<br />
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While the march towards the eradication of measles has been well underway for many years, cases have begun to rise in number again recently. Just this week, an outbreak occurred in Los Angeles County, infecting 20 people so far. A vaccine for measles was developed in the 1960's, leading to a sharp decline in the number of cases in the U.S. almost immediately in the late 1960's. Global efforts to increase vaccination have been funded by the American Red Cross, the United Nations, the Centers for Disease Control, UNICEF, and the World Health Organization. The measles vaccine has also been improved over the years to provide better immunity to those vaccinated, giving us the MMR (measles-mumps-rubella) vaccine of today. Thanks to these efforts, measles deaths worldwide had decreased to just 164,000 in 2008.<br />
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Unfortunately, in 1998 a paper was written by Wakefield, <i>et al</i>. in <i>The Lancet</i>, showing a link between the MMR vaccine and autism. Although this paper was retracted by 10 of the 12 authors in 2004 and completely retracted by <i>The Lancet </i>in 2010, the publicity this paper received raised doubts for many parents about the safety of the vaccine for their children. Many people may still be unaware that in 2011, the authors of the paper were found guilty of deliberate fraud, which they had committed by picking and choosing what data to include in the paper. As a result, Andrew Wakefield, the lead author of the paper, had his United Kingdom medical license revoked. Even with the retraction and the slew of studies that followed, showing repeatedly no link between the vaccine and autism, parents have continued to voice concerns about vaccinating their children.<br />
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For a vaccine to eliminate disease, 100% vaccination is not essential. In vaccination there is a concept known as herd immunity, which has been defined as "the resistance to the spread of a contagious disease within a population that results if a sufficiently high proportion of individuals are immune to the disease." When a high percentage of the population is immune, the virus cannot be introduced or spread well because it will encounter too many hosts that are not susceptible to infection. For herd immunity to work for the measles, generally about 95% of the population needs to be vaccinated and immune. There have long been religious organizations that have opposed vaccination, as well as immunocompromised individuals who were not eligible for vaccination. Even with these small groups of people, high enough vaccination rates were reached to achieve herd immunity in many countries. Unfortunately, the recent increases in the number of parents actively choosing to not vaccinate their children due to fears of autism or other complications and the number of parents who simply do not see the benefit of vaccination and opt out has led to a decrease in the vaccination levels. This has made herd immunity much less effective, allowing cases of measles to increase again.<br />
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While the scientific community has repeatedly performed studies to test the safety of vaccines and found that there is no link between the MMR vaccine and autism, the negative publicity from the Wakefield, <i>et al.</i> paper has severely damaged the reputation of this vaccine. Re-educating the public about the safety and necessity of this, and other, vaccines has become a major priority in the wake of the number of measles outbreaks in Europe and the U.S. in recent years. With no treatment for measles, the MMR vaccine remains the only real hope for protecting the population from this highly contagious, yet preventable, disease.Anonymoushttp://www.blogger.com/profile/05503168250289145242noreply@blogger.com0tag:blogger.com,1999:blog-1839109299604462420.post-55710340690444640252017-01-25T22:21:00.000-05:002017-01-26T16:11:00.306-05:00More diarrheal disease plagues The Oregon Trail"James has died of dysentery." Another common diarrheal disease you likely remember from <i>The Oregon Trail, </i>dysentery is caused by the consumption of contaminated water, like cholera and typhoid. There are actually two different forms of dysentery; one form is caused by <i>Shigella</i> bacteria (also known as shigellosis), and the other is caused by <i>Entamoeba histolytica, </i>an amoebic parasite. <i>E. histolytica </i>causes milder disease, but is more difficult to treat than that caused by the <i>Shigella </i>bacteria. No matter which form of dysentery you have, the symptoms can include anything from mild diarrhea to severe, bloody diarrhea with a fever, cramps, vomiting, and even pain and complications outside the intestines.<br />
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Dysentery has been known as a disease for quite some time, with case reports dating back to the 1200s. In light of the recent presidential inauguration in the United States, it is interesting to note that one of our own U.S. presidents suffered from dysentery on the very day of his inauguration. In the weeks leading up to James Buchanan's inauguration in 1857, he came down with dysentery. He spent the two weeks before March 4, inauguration day, in seclusion in an attempt to be well enough for the ceremony. He even turned down a dinner invitation from the famed Jefferson Davis in a letter in which Buchanan said he was "now living with great caution." Buchanan was well enough by March 4 to be successfully sworn in without incident.<br />
<br />
While dysentery is considered a fairly rare disease in modern times, it is still estimated that there are 170 million cases each year, along with 14,000 deaths. A recent increase of cases in Zimbabwe has caught much public attention. Corruption within the country has led to a suspected misuse of funds within the government. The Movement for Democratic Change party (MDC), which currently holds the presidency and other governmental positions, has been accused of using the country's money to buy cars and fund their 2018 political campaign instead of building infrastructure and dealing with water sanitation issues. Because proper water sanitation is essential for preventing a disease like dysentery, critics of the government believe the members of the MDC are responsible for the current cases of both typhoid and dysentery that have been spreading through Zimbabwe.<br />
<br />
Although dysentery has existed for hundreds of years, our approach to treatment now is not very different from times gone by. Typically, dysentery clears by itself, so the only remedy is to provide a patient with fluids to prevent dehydration. While antibiotics can be prescribed for dysentery caused by <i>Shigella</i>, instances of antibiotic resistance in <i>Shigella </i>have been on the rise since the 1940s, making many classes of drugs ineffective. Recent work has found that probiotics may play a role in helping to reduce disease duration and intensity in <i>Shigella </i>dysentery, but further work will be required before probiotics can be used for patient treatment.. Treatment of amoebic dysentery, on the other hand, is still almost purely reliant on simply relieving the symptoms.<br />
<br />
As has been highlighted in the cases of cholera, typhoid, and dysentery, sanitary drinking water is the key for the prevention of disease. While many countries are focusing efforts on improving water sanitation, it is a long road to improve an entire country's infrastructure enough to provide all residents with clean water. But support for these initiatives continues to pour in from other countries and private foundations alike, keeping alive the hope for a future with clean drinking water for all.Anonymoushttp://www.blogger.com/profile/05503168250289145242noreply@blogger.com0tag:blogger.com,1999:blog-1839109299604462420.post-91999675807361568932016-11-30T15:37:00.000-05:002016-11-30T15:37:02.665-05:00Further down the trail....Mary has died of typhoid"Mary has died of typhoid." Yet another disease you may remember encountering on <i>The Oregon Trail</i> in childhood, typhoid fever, or simply typhoid, is also still a major public health concern today. Affecting an estimated 20.6 million people and causing 223,000 deaths a year, typhoid is caused by the bacterium <i>Salmonella enterica </i>serovar Typhi (S. Typhi). The bacteria is often spread through contaminated water or from person-to-person contact. In places where clean water and sanitation are standard, the disease has been essentially eliminated. But in developing countries, it remains a major threat.<br />
<br />
The most recent outbreak of typhoid occurred just last week in the city of Masvingo, Zimbabwe. Areas where the disease is endemic and can lead to outbreaks include Southeast Asia, Africa, and South America. Travel to and from these areas also allows for the transmission of the bacteria to industrialized nations and can cause local outbreaks. Although there are currently two approved vaccines against S. Typhi, both have drawbacks that prevent them from being used en masse. The protective efficacy of the vaccines is sub-optimal and ranges from 40%-70%, largely dependent upon age and location. Additionally, the protection from the vaccines is short-lived, averaging 2-3 years for one vaccine and 5-7 years for the other. A further complication is that both vaccines need to be stored with refrigeration until they are used. Transport and storage under these conditions are major difficulties in countries where electricity is a supreme luxury.<br />
<br />
Without a reliable vaccine, the major way to fight the disease is through the use of antibiotics. Chloramphenicol, ampicillin, and trimethoprim-sulfamethoxazole, very common antibiotics, have historically been used to stop the infection, and this strategy was highly successful for many years. However, in recent years, a new threat has emerged to thwart these efforts. In the 1970s, cases of S. Typhi that were resistant to these antibiotics began to emerge. We now face the threat of multi-drug resistant S. Typhi, making disease treatment much more difficult.<br />
<br />
In light of the rising drug resistance, many have begun to see wide-spread vaccination as the best strategy to fight typhoid. Others argue that improving water sanitation will have the greatest effect on decreasing disease prevalence. One thing is certain: either strategy will require a large investment of funds to be achieved.<br />
<br />
The Bill & Melinda Gates Foundation is leading the way in the funding arena and has identified the elimination of typhoid as a public health problem by 2035 as a goal. The Gates Foundation recently gave over half a million dollars to Yale University to explore and determine the cost-effectiveness of typhoid vaccination strategies. Additionally, The Gates Foundation gave a $36.9 million grant earlier this month to a collaboration between the Maryland School of Medicine Center for Vaccine Development, the Oxford Vaccine Group, and PATH, a non-profit public health organization, to accelerate the development of a new vaccine to be used in young children. The goal is to develop a vaccine with more long-lasting protection than the two currently available. The Gates Foundation is also providing funds to increase surveillance for typhoid in South Asia and Africa.<br />
<br />
While the Gates Foundation is leading the way to fund the vaccination strategy, other groups are focusing on improving water sanitation. The United States Agency for International Development (USAID) features water and sanitation as one of its main avenues of focus, with sponsored projects underway in large portions of Africa and Southeast Asia. The World Bank has also been sponsoring projects to improve water quality and health throughout the world. Additionally, UNICEF has been a major player in the increased access to clean water that has over the past decade. Many other smaller non-profits have also played a role in this endeavor.<br />
<br />
As both vaccine and water and sanitation improvements occur, our ability to battle this age-old pathogen will increase. Using both strategies simultaneously allows for the most rapid and sustainable progress toward S. Typhi elimination. With the continued investment of groups like the Gates Foundation and USAID, the goal of typhoid elimination as a public health problem by 2035 might just be achievable.Anonymoushttp://www.blogger.com/profile/05503168250289145242noreply@blogger.com0tag:blogger.com,1999:blog-1839109299604462420.post-45132975404385932992016-10-30T20:07:00.001-04:002017-02-16T10:53:24.927-05:00Cholera: Not just a problem on The Oregon Trail"Sally has died of cholera." This was a common problem in the game <i>The Oregon Trail</i> that many people remember from childhood. Tragically, cholera is still a major public health problem in countries around the world today. Cholera is caused by the bacterium <i>Vibrio cholerae, </i>which is shed in fecal matter from an infected individual and is often transmitted via contamination of water sources. In countries with poor sanitation and a lack of clean water, this can lead to significant and deadly outbreaks.<br />
<br />
Fast-forward from the days of the Oregon Trail to present-day Haiti. The country has suffered multiple tragedies in recent years. In 2010, they were rocked with a devastating earthquake; now, in 2016, they suffered the wrath of Hurricane Matthew. In light of these recent disasters, there have been humanitarian efforts from the United Nations and other relief organizations. Unfortunately, in the wake of the U.N.'s help after the 2010 earthquake, Haiti experienced its first cholera outbreak.<br />
<br />
Before 2010, the small nation of Haiti had not been exposed to cholera. The citizens had not had the disease, and no immunity to the pathogen existed there. The first case of cholera was reported in mid-October 2010 in the region of the country along the Meille River. The disease quickly became rampant, with a hospital 60 miles away from the first case reporting new cases every 3.5 minutes within just 2 days. Since then, the outbreak has affected nearly 800,000 people and caused more than 9,000 deaths according to the official numbers; however, many experts fear the true impact has been far greater due to poor case reporting.<br />
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Flooding and destruction from Hurricane Matthew on October 4, 2016, have done nothing to help the situation. As many Haitians have lost their homes and their sources of fresh water, cholera has been on the rise again. Flooding has led to increases in contaminated waterways, leaving much of the water unsafe for consumption. Within four days of the storm passing through, officials were reporting 62 cases and 13 deaths from cholera.<br />
<br />
The issue of how cholera came to be endemic in Haiti has been a topic of heated debate in the past few years. Many have blamed the U.N.'s Nepalese peacekeeping troops for bringing the bacteria with them into the country following the 2010 earthquake. The U.N. has denied any potential responsibility for the outbreak for years, even in the face of lawsuits from families of those who had died. Others hypothesized that increases in the temperature and salinity of the rivers throughout Haiti had allowed bacteria that may have been living in a dormant state in coastal waters to populate these rivers after the earthquake.<br />
<br />
Scientific evidence, however, has been on the side of those who blame the U.N.'s peacekeeping troops for the introduction of the disease. Genetic analyses by whole genome sequencing of the bacteria found in Haiti in 2010 showed that this strain was highly similar to the strain found in Nepal in 2010. Additional studies using multiple-locus variable number tandem repeat analysis (aka DNA fingerprinting), a technique that looks at the number of times a DNA sequence is repeated at specific loci in the genome, also suggested a match between the Nepalese and Haitian strains.<br />
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On August 18, 2016, after 6 years of denial, the U.N. finally acknowledged that they did play a role in the initial outbreak. Farhan Haq, the deputy spokesman for the U.N. secretary general, said "over the past year, the U.N. has become convinced that it needs to do much more regarding its own involvement in the initial outbreak and the suffering of those affected by cholera...[a] new response will be presented publicly within the next two months."<br />
<br />
The latest chapter in this story comes with the announcement on October 24 that the U.N. is working on a plan to spend about $400 million on cholera in Haiti. Roughly $200 million will be spent on cholera elimination efforts, while the other $200 million will be given directly to families or communities affected by the disease. The full details of the plan are expected to be solidified in the coming weeks. However, questions remain over how the money for this plan will materialize. U.N. member states have already expressed discomfort with paying money to directly compensate victims, as this is not within the purview of the normal development work the U.N. is chartered to perform.<br />
<br />
While the final details of the U.N.'s action plan remain to be worked out, it looks like Haiti will be receiving some much-needed support to aid in their cholera elimination efforts in the near future. As the country rebuilds after Hurricane Matthew, water sanitation will be a major focus for the nation. With financial support and help from the U.N., experts are hopeful that cholera can be eliminated fairly quickly from Haiti. That would serve as a major beacon of hope for a nation that has borne the brunt of tragedies for too long.Anonymoushttp://www.blogger.com/profile/05503168250289145242noreply@blogger.com0tag:blogger.com,1999:blog-1839109299604462420.post-37357143836475920882016-09-30T15:52:00.001-04:002016-10-26T12:19:33.422-04:00The not-so-loving kissing bug<div class="MsoNormal">
As fall approaches and the weather begins to cool from the
stifling heat of summer, we all like to spend a bit more time outside enjoying
the air. Unfortunately, this is the perfect time for insects who like to feed
on our blood and potentially carry disease to come out and join us. Most people think of ticks and mosquitoes
when they think of insects that carry disease, but there is another major
player in the Americas: the Triatominae, also known as the kissing bug. This
little creature can carry a parasite known as <i>Trypanosoma cruzi</i>, which causes Chagas disease.<o:p></o:p></div>
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<br /></div>
<table cellpadding="0" cellspacing="0" class="tr-caption-container" style="float: left; margin-right: 1em; text-align: left;"><tbody>
<tr><td style="text-align: center;"><a href="http://message.snopes.com/critters/graphics/kissingbughead.jpg" imageanchor="1" style="clear: left; margin-bottom: 1em; margin-left: auto; margin-right: auto;"><img alt="Image result for the kissing bug" border="0" src="http://message.snopes.com/critters/graphics/kissingbughead.jpg" height="126" width="200" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;"><span style="font-size: xx-small;">The Triatominae insect, aka the kissing bug, that <br />can carry the <i>Trypanosoma cruzi </i>parasite that<br />causes Chagas disease.<br />Image from Snopes.com</span></td></tr>
</tbody></table>
<div class="MsoNormal">
Chagas disease is a major global health threat, with 70
million people at risk of exposure and approximately 5.7 million people
becoming infected each year. The disease mainly affects Latin America, but
thanks to population flows and increases in vector populations, the disease has
been spreading to the north, with cases reported in the US in Texas, in Canada, and even in Europe. The disease exists in two phases, the acute phase
and the chronic phase. During acute infection, there are large numbers of
parasites in the blood, but symptoms are few and non-specific. There can be
fever, headache, swollen lymph nodes, or even completely asymptomatic cases. As
the disease transitions into the chronic phase, the parasites sequester into
the muscle of the heart and digestive tract. This can result in severe cardiac and digestive disorders, which can last for years after the original infection began. Most dangerously, heart failure can result, causing death.<o:p></o:p></div>
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<br /></div>
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Treatment for Chagas disease remains a major issue. There
are very effective treatments for the acute phase, with almost 100% efficacy,
but these treatments are underutilized. Treatment requires rapid diagnosis of
the disease, which is often difficult due to the non-descript or non-existent
symptoms. Also, the drugs need to be administered over a very long duration, 60-90
days, leading to low follow-through rates for treatment to completion. Unfortunately, there are currently no treatments for the chronic phase. <o:p></o:p></div>
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<br /></div>
<div class="MsoNormal">
Current work being done at the University of Georgia is
working to address one of these problems. They are focused on developing affordable diagnostic tests that can be used anywhere to diagnose Chagas
disease in the acute phase. Their efforts focus on increasing the number of <i>T. cruzi </i>antibodies being detected in
the test in order to allow for a more sensitive test. Not only will the test
help identify people who have the disease, but it will also improve the ability
to monitor how well a person is responding to treatment, hopefully allowing for
decreases in treatment times. <o:p></o:p></div>
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<br /></div>
<div class="MsoNormal">
Beyond the work at the University of Georgia focusing on
improving diagnostics, there has also been a lot of effort into developing new
treatments for Chagas disease. The Drugs for Neglected Diseases Initiative has
chosen Chagas as one of their focus diseases and has been working on new
therapeutics to treat both the acute and chronic phases of disease. Their goal
is to develop an orally administrated treatment that will require less than 30
days of administration by 2020. They have moved into a Phase II proof of
concept study with two different treatment options, with results expected late
this year and early next year.</div>
<br />
<div class="MsoNormal">
While advances are being made in detection and treatment of Chagas in humans, there are also many animals that are threatened by this disease. Chagas disease can also affect both wild and domestic animals, making elimination of the
parasite reservoir impossible. Notably, Chagas disease in dogs is known to be frequently
fatal, causing the same heart failure and cardiac symptoms seen in humans with
chronic Chagas disease. For dogs, there is currently no available treatment for the disease. <o:p></o:p></div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
The best way to deal with Chagas for the time being is the prevent it. Insecticide spraying is encouraged by the World Health Organization and has been shown to decrease the incidence of disease. Also, being able to identify the Triatominae insects when they are seen can help people avoid areas where they could become susceptible to being bitten. These bugs are known to enjoy living in hay, woodpiles, and under porches, so avoiding these areas can help reduce transmission of the parasite. </div>
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<br /></div>
<div class="MsoNormal">
To protect yourself and your furry friends this fall, be sure to be on the lookout for the kissing bug. One kiss from this little love bug may just be your worst first date ever. </div>
Anonymoushttp://www.blogger.com/profile/05503168250289145242noreply@blogger.com0tag:blogger.com,1999:blog-1839109299604462420.post-89097288056857191442016-08-16T15:14:00.000-04:002016-08-17T11:34:40.380-04:00Amanda Elmore and Team USA's victory in the Olympic W8+ is cause for excitement, but the health risks they faced to achieve this feat are notRio de Janeiro. Already well known for its vibrant culture and nightlife, this Brazilian city has also become known for sports this month as they play host to the Games of the 31st Olympiad. Many brand new athletic facilities were created specifically for these games, and Brazil poured a projected $18 billion or more into bringing these games to life. Even more funding was supplied by sponsors, like Coca Cola. Unfortunately, not all sports venues could be made ideal.<br />
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Guanabara Bay and Copacabana Beach off the coast of Rio are the sites of five aquatic events in this year's games: sailing, rowing, canoe sprinting, the triathlon, and marathon swimming. In addition to hosting these great sporting events, these waterways also play host to many unwelcome guests: multi-drug resistant bacteria and viruses of many varieties.<br />
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The Brazilian government has been aware for years that raw sewage has rushed into their waterways from the cities. In their bid to bring the Olympics to Rio, Brazil pledged to put forth $4 billion to deal with their water contamination issues. Unfortunately, due to a "budget crisis" they were only able to invest $170 million before the Games began. The results of this lack of funding may end up having devastating effects on the health of athletes at these games.<br />
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A study published by Renata Cristina Picao's group in Brazil in 2015 looked specifically at the bacterial populations of the water from the beaches surrounding Rio de Janeiro. They studied a total of 18 water samples from different regions along the coastline. Of these isolates, only one had bacteria with susceptibility to imipenem, a common drug used to treat bacterial infections in this area. Resistance rates to other popular drugs were also alarmingly high, with 77.8% of the isolates showing bacteria with resistance to cefotaxime, 50% showing resistance to cefepime, 27.8% showing resistance to gentamicin and amikacin, and 5.6% showing resistance to ciprofloxacin. With drug resistance running rampant in the bacteria that call this water home, being on or, even worse, in this water may pose a significant health threat to athletes.<br />
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Possibly an even larger threat than the bacteria in these waters are the viruses that can also be found. Hepatitis A virus can be found in human waste, and experts speculate that ~60% of Brazilian adults are exposed to the virus. In waters that contain large amounts of human waste, like the ones the athletes will be exposed to, the risk of infection is significant. The CDC recommends that all travelers to Brazil, not just those who will be exposed to the water, receive the Hepatitis A vaccine. With appropriate use of the vaccine, an outbreak of Hepatitis A can likely be prevented, though some have questioned whether or not the vaccine will protect against the local strains of the virus. <br />
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In addition to Hepatitis A virus, water tests have found alarmingly high levels of multiple types of adenovirus, which can cause severe gastrointestinal problems and do not have vaccines. Fernando Spilki, a Brazilian virologist, performed water testing for the Associated Press and found levels of adenovirus from 14 million to 1.7 billion virions per liter of water. To put this in perspective, California officials become concerned about their water quality if the level rises to just 1,000 virions per liter.<br />
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Many may wonder why, with the popularity of these beaches among Brazilians, there has not been a major viral outbreak or an outbreak of multi-drug resistant bacteria in the region already. The answer likely lies in the fact that these native-born and raised Brazilians have been exposed to these bacteria and viruses from a very young age, allowing their bodies to develop a successful immune response to the pathogens. However, the same immunity will not exist for the foreign athletes who will be exposed to these waters.<br />
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In the year leading up to these games, some athletic groups have already trained and raced on these waters. Many documented athletes experiencing illness. The World Junior Rowing Championships were held in Rio in 2015, and the U.S. team documented 13 rowers who suffered gastrointestinal illness following the event. The Australian sailing team has trained on the waters around Rio for the past several months, and they also have had athletes fall ill with gastrointestinal problems.<br />
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Though independent water testing has identified the water as potentially hazardous to health, the International Olympic Committee has maintained that the water is safe enough for the events to be held. The World Health Organization (WHO) has recognized that the water quality is less-than-ideal, and has issued several statements for travelers warning them of the potential for infection if exposure to contaminated water occurs. Additionally, the WHO has recognized that sites in the Guanabarra Bay, where sailing, rowing, and canoe sprinting take place, do not always meet the standards of safety, based on bacterial testing. As a precaution, they recommend that for all bodies of water "all athletes should cover cuts and grazes with waterproof
plasters prior to exposure, try to avoid swallowing the water, wash/shower as soon as possible after
exposure and, as far as possible, minimize their time in the water and avoid going in the water after
heavy rainfall if possible." In events like the triathlon, where the swim portion is upwards of 20 minutes, and the marathon swim, which can take 2 hours or more to complete, minimizing time in the water is not always a viable option.<br />
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In light of the potential health risks, athletes and spectators alike will need to use increased caution regarding the Rio games. Monitoring for illness is going to be critical to prevent severe illnesses from developing. Many have focused on the potential threat of Zika virus at these games, but the threat of the multi-drug resistant bacteria and viruses in the waters should not be forgotten. All can cause significant problems and really ruin the Olympic experience. Perhaps next time the Olympic Committee will be more skeptical of selecting a location with such serious health concerns unless they are willing to chip in some funds to help the country address the situation. Such a gesture would not only have a positive impact on the athletes, but more importantly, it would have a sustained impact on the residents of the host country for years after the conclusion of the Games.<br />
<br />
<br />
--On a side note, I'm so proud of my former teammate Amanda Elmore and the entire U.S. W8+ for dominating and winning gold at Rio!! Boiler Up!Anonymoushttp://www.blogger.com/profile/05503168250289145242noreply@blogger.com0tag:blogger.com,1999:blog-1839109299604462420.post-85684306064023324502016-07-20T10:15:00.000-04:002016-07-20T10:15:56.098-04:00Pitfalls of some big-name institutions to avoidNote: This article describes my observations at particular institutions and is not meant to be a generalization of all places, though certain themes, I'm sure, are wide-spread.<br />
<br />
Many researchers want to work for a big-name institution. They get the best perks, get the most recognition, and can provide the best resources to employees. However, there are often problems at big-name institutions. Egos the size of dinosaurs fill the halls, and the power-hungry dominate the meeting rooms. In this type of culture, success can seem impossible. In this particular piece, I plan to highlight some of issues that arise in this type of environment, told from my own perspective.<br />
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<b>Student entitlement</b><br />
"I got into this institution, so everyone should be working for my success."<br />
Students can come into these types of institutions with a strong feeling of entitlement. They think that getting into a good school means they will automatically succeed; and, if they aren't succeeding, it must clearly be someone else's fault. Often times, these students turn the professors into scapegoats for their failings. "That prof grades unfairly." "This prof is too demanding of students." "My thesis adviser isn't ok with me just working from 10-3 every day." These are just some of the complaints I've heard. It's never, "I should have studied harder," or "I should have put in more time." Some students are willing to take pretty extreme measures to push their agenda, such as raising an official complaint against a faculty member. And even when an impartial committee hears the case and rules in favor of the faculty member, the student may still continue to hold onto their delusional notion that the faculty member is out to get students. Just one student can do serious damage to a faculty member's reputation.<br />
From the point of view of faculty, there are really two ways to respond to this culture. You can either lower your standards to accommodate the students who refuse to rise up, or you can continue to keep the bar high and let them hate you. It may seem like it would be fairly easy to take the high road and deal with being unliked by the students, but there are some serious consequences to consider here. When other faculty chose to lower their standards and you don't, your department starts viewing you as an outsider. You will be the one member of every thesis committee who is saying, "This person shouldn't be graduating yet," and other faculty can view you as difficult. Additionally, students will no longer chose to work in your lab based on the negative comments from older students, making it very difficult and more expensive to get research done (post-docs will soon make more than twice the salary of a typical PhD student in most institutions thanks to new legislation). This can be too high a price to pay for many faculty.<br />
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<b>Big egos cause big problems</b><br />
A single room can only hold so much ego before it bursts. At top-tier institutions, there can often be the problem of too much ego for one room to hold. This can lead to passive-aggressive shoving matches fought behind closed doors or all-out shouting battles. This is especially problematic, it seems, in the case of older faculty versus younger faculty. Many older faculty feel very secure in their role at the top of the food chain, thanks to their long track record of professorship. When a young faculty member comes in and brings lots of success quickly, alarm bells go off. The older faculty must now assert their dominance to make sure the younger faculty stays below them on the totem pole. This can mean passing people over for promotions they deserve, intentionally withholding departmental grants from a faculty member or their students, or even using your influence to direct good students and post-docs away from a particular lab.<br />
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<b>Money runs the game</b><br />
"You've heard of the golden rule, haven't you? Whoever has the gold makes the rules." Jafar speaks this classic line in Disney's <i>Aladdin</i>, but it holds true in many situations. Grant money runs the scientific environment, and in the current times of funding shortages, this form of the golden rule has never been more accurate. Labs with funding are able to recruit the "best" post-doctoral fellows and students, while poorly funded labs struggle to bring in much talent. This can be a self-perpetuating cycle. Also, oftentimes, well funded labs do not feel the need to collaborate as much, because they can get things done by themselves. This leaves little room for an up-and-coming lab to break into the system.<br />
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<b>Who you know matters...a lot</b><br />
Why is it that the students from the same labs always win certain awards, or certain labs are always able to get their work into that coveted journal? Sometimes it's because the lab is just that good, and produces superior work over and over again. Sometimes, though, it's because of the politics. Science can be a big game of who you know and what alliances you make. Knowing the right people can go a long way towards boosting scientific success, or at least perceived success in the form of awards or papers in good journals. However, this does not always align with the quality of the work, so "working the system" can catapult researchers to the fore-front of attention ahead of some who do good work, but are less well-connected.<br />
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<b>Competition trumps collaboration</b><br />
The hallmark of a successful scientific institution is often its collaborative environment. Unfortunately, some of the top-tier places lack this feeling. With so many high-powered research groups in one place, it's hard not to feel potentially threatened by your neighbor down the hall. This leads to the strategic withholding of information, omission of key details from departmental meetings, and protocol secrecy. The end result: researchers wasting time optimizing protocols someone next door has already optimized, students worrying that their work is going to be constantly scooped, and people not reaching out for help when they need it. This ultimately slows down the scientific process, not to mention wastes valuable financial resources.<br />
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<b>Don't let the door hit you on the way out</b><br />
Since competition can be so strong at top-tier institutions, when a faculty member that others perceive as a potential threat to their research prowess leaves, others may be far too ready to let them go. Each faculty brings unique skills and insights to a department, but many departments are ready to throw away faculty without a second thought if they feel threatened. The collaborative environment that needs to exist in science is especially threatened by this type of attitude.<br />
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<b>Take some advice from Tim McGraw</b><br />
"Don't take for granted the love this life gives you; when you get where you're goin', don't forget turn back around; and help the next one in line; always stay humble and kind."<br />
Tim McGraw's recent song seems to be speaking a message directly to these top-tier institutions with these words. In a world of competition and surrounded by your own successes, it can be difficult to stay humble and kind. But that's exactly what we need in these institutions to maintain the collaborative spirit and culture of science for the sake of science (and not success) that is essential for improvements in the world. So, please, the next time "the work you put in is realized, let yourself feel the pride but always stay humble and kind."Anonymoushttp://www.blogger.com/profile/05503168250289145242noreply@blogger.com0tag:blogger.com,1999:blog-1839109299604462420.post-91058306540873920842016-07-18T12:45:00.000-04:002016-07-18T12:49:12.490-04:00The wonders of the biofilm worldWhat do you moving your arm and a biofilm of bacteria growing have in common? The answer is more than you might think. You moving your arm involves the propagation of an action potential through neurons that connect your brain with your limbs. This action potential is based on the rapid movement of ions into and out of cells, allowing each cell to pass a message on to the cell next to it through these ions. As the charged ions flux in and out of cells, the membrane potential (or chemical voltage) of the cells changes. It turns out that biofilm bacteria can use a similar system in order to communicate.<span style="font-family: inherit; font-size: 12pt; text-indent: 0.5in;"><br /></span>
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<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhnAnKfLrwITFHPQcPvIvEAbii6CtCJJ9djarueyAV9lGjzMCVVudQZI7YR2STI8blV7r-cpaxxEh1513L_hoxcVxJtepcK1wozIIUGfr4hvRK4FwizxHSFRdoWhfdUAC5GBdLzXk2aTcU/s1600/membrane+pot.jpg" imageanchor="1" style="clear: left; margin-bottom: 1em; margin-left: auto; margin-right: auto;"><span style="font-family: inherit;"><img border="0" height="202" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhnAnKfLrwITFHPQcPvIvEAbii6CtCJJ9djarueyAV9lGjzMCVVudQZI7YR2STI8blV7r-cpaxxEh1513L_hoxcVxJtepcK1wozIIUGfr4hvRK4FwizxHSFRdoWhfdUAC5GBdLzXk2aTcU/s320/membrane+pot.jpg" width="320" /></span></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;"><span style="font-family: inherit;">from <i>Anatomy & Physiology </i>by Phil Schatz</span></td></tr>
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Action potentials have long been known as a rapid way to propagate signals over long distances. As ion channels open or close over the course of the action potential, the charged particles flow in and out of the cell in response to their concentration gradients. This is what allows the changes in membrane potential within the cells. But it has only recently been found that Eukaryotes are not the only organisms that can do this.<br />
<br />
Enter Bacillus subtilis, a bacterium often used as a model organism for studying biofilms. A biofilm is a collection of bacteria that adhere to each other and, often, a surface. Biofilms are more resistant to antibiotic treatment than free-living bacteria, and can commonly be formed on medical devices, such as catheters. It has been known for many years that bacteria within a biofilm are able to communicate through a process known as quorum sensing, which involves the release of chemicals by the members of the biofilm to control the population density. Recently, a study found that in addition to quorum sensing, B. subtilis cells can communicate through the creation of and propagation of action potentials, similar to neuronal signaling.<br />
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It was observed that the entirety of the B. subtilis biofilm would undergo metabolic changes in response to glutamate and ammonium nutrient limitation affecting the cells in the center of the biofilm. In order for these widespread metabolic changes to occur, the cells in the interior of the biofilm must communicate with the cells of the periphery. It was found that an active propagation of a potassium ion signal through the use of potassium channels on the cells was responsible for this communication. As the potassium channels on the surface of the bacteria opened, potassium would rush into the cells from the surrounding environment, resulting in membrane depolarization. The membrane depolarization is linked to a decreased ability of the cells to take up glutamate and ammonium, allowing these nutrients to build up and replenish the supply to the interior cells.<br />
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Biofilms are notoriously difficult to treat when they form in patients. As many as 80% of chronic infections are caused by biofilm formation. Persistent staphylococcal infections are often caused by biofilms, as are Pseudomonas aeruginosa lung infections. It is typically the interior cells of the biofilm, which have a more dormant lifestyle, that are most responsible for antibiotic resistance. Learning more about how the biofilms communicate can facilitate improved treatment. If the action potential creation of these bacteria can be inhibited, the cells will be unable to communicate in times of nutrient depletion, leading the cell death at the interior of the biofilm. This could greatly improve the ability to treat these infections, leading to better outcomes for patients. Perhaps some day soon, we will have better tools for treatment to gain ground against these crafty biofilm bacteria. <br />
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Beyond the impact of these findings on patients, it is truly marvelous to see what these relatively simple organisms can accomplish. Bacterial cells are almost 1000 times simpler than mammalian cells when genome sizes are compared, yet they are capable of accomplishing signaling akin to the complexity of neuronal signaling. There seems to be no end to the surprises these timeless organisms have in store for us. Who knows what will come to light next.Anonymoushttp://www.blogger.com/profile/05503168250289145242noreply@blogger.com0tag:blogger.com,1999:blog-1839109299604462420.post-31968066465804966382016-07-01T13:21:00.003-04:002016-07-01T13:21:43.295-04:00Where did June go?Hello world,<br />
I realized last night as I was trying to go to sleep that I was going to fail at getting a June blog post up in time. I've been working on two different pieces, but neither of them felt ready to post. That's why this month (July), I'll be posting three (yes, that's right, THREE) different pieces. Expect to see those in the fourth week of the month. Until then, I am condemned to a life of boxes and packing as my lab and I prepare to move to Florida. See you when this process ends.Anonymoushttp://www.blogger.com/profile/05503168250289145242noreply@blogger.com0tag:blogger.com,1999:blog-1839109299604462420.post-22370557564028612402016-05-31T21:15:00.002-04:002016-05-31T21:16:14.626-04:00Yearly outbreaks of Lassa fever take center stage<div class="MsoNormal">
The multimammate rat <i>Mastomys
natalensis </i>is a common feature of savannas and forests in many portions of
Africa. These pesky rats often infiltrate people’s homes and make themselves
comfortable indoors, feasting on any available food stores. While doing so, they leave behind urine and
fecal matter. This can be the start of a local Lassa fever epidemic.<o:p></o:p></div>
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Lassa virus is a single-stranded RNA virus that is member of
the <i>Arenaviridae</i> family, similar to the
Ebola and Marburg viruses. The virus is vectored by the multimammate rats of
Africa. Lassa virus, named after the town in Nigeria where the first case arose,
is endemic in Sierra Leone, Liberia, Guinea, and Nigeria. However, cases can
also be picked up by travelers and brought back to their home countries. So far
this year, Lassa has been reported in Nigeria (273 cases, 149 deaths), Liberia
(38 cases, 15 deaths), Germany (2 cases, 1 death), Sweden (1 case), Togo (2
cases, 1 death), and Benin (71 cases, 23 deaths). Lassa is frequently transmitted
from the original infected person to healthcare workers, as the disease is not
easy to diagnose and is easily spread through contact with infected blood,
tissue, or secretions. <o:p></o:p></div>
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<div class="MsoNormal">
The symptoms of Lassa fever are non-specific and almost
non-existent in many cases. 80% of those infected will have mild symptoms of
fever, general malaise, and/or headache. In 20% of cases, however, much more
severe symptoms can occur. Hemorrhaging, respiratory distress, swelling, and
vomiting are associated with severe disease. Additionally, Lassa fever can
often lead to various degrees of deafness, which can be permanent; as many as
25% of people who survive the disease will suffer from some form of deafness, even if they only present with mild symptoms.<o:p></o:p></div>
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Treatments for Lassa include antiviral drugs, such as
Ribavirin, which show the highest efficacy when given early. However, Lassa
symptoms do not usually manifest until 1-3 weeks after exposure to the virus,
and diagnosis requires the use of an enzyme-linked immunosorbent serological
assay (ELISA), which is not cheap and often not available in the clinics. The
small Seattle biotech company Kineta recently won a $7.2 million award to
develop a novel antiviral specifically for treating Lassa fever. This could
help overcome the logistic challenges of treatment. In the current outbreak in
Nigeria, for example, health officials have said that logistics support and delayed case
reporting by the states is severely dampening their ability to combat the
threat. <o:p></o:p></div>
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The typical Lassa virus transmission season is beginning to
wind down this year, and WHO believes that the number of cases is on the decline and that the epidemic will end soon. Others, however, are concerned that the WHO and
local governments have not taken the outbreak seriously enough. The outbreak
was not officially announced until January of 2016, while cases had begun to
occur last August. The public in Nigeria has also raised questions as to
whether or not the government has been down-playing the significance of the
outbreak. This year’s outbreak has been far more deadly and widespread than
others in the past. The mortality rate has approached 50% in Nigeria this year,
a massive increase from the more typical 1%. Additionally, Lassa has spread to
more states in Nigeria than have ever seen the disease before.</div>
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<div class="MsoNormal">
Officials have cited increased awareness of disease as a
major reason for the uptick in mortality and spread. In the wake of the Ebola
outbreak, more cases of fever and hemorrhage have been reported to the health system, allowing for
increased diagnosis of Lassa. But beyond the public health aspects at play,
some researchers fear the virus itself may be undergoing changes that are
allowing the increase in spread and making it more deadly than before. Only
time will tell whether it is just increased vigilance or viral mutations that
are the driving forces here. For now, all we know for sure is that sales of rat poison are on the rise as
the countries continue to fight and manage this most recent epidemic.<o:p></o:p></div>
Anonymoushttp://www.blogger.com/profile/05503168250289145242noreply@blogger.com0tag:blogger.com,1999:blog-1839109299604462420.post-60322902899571642432016-04-30T21:02:00.000-04:002016-07-18T12:50:12.275-04:00Yellow fever strikes againYellow fever is an age-old disease that has plagued Africa, Latin America, and, sporadically, portions of Asia for centuries. A recent outbreak of yellow fever erupted in Luanda, Angola in late 2015. It is estimated that since the outbreak began, there have been over 1700 cases and 238 deaths from the disease, though many organizations believe these could be underestimated numbers due to poor reporting. While the global response was quick and yellow fever vaccine was immediately deployed in the area, this outbreak has exposed our true weakness against this disease: our meager vaccine production capabilities. <br /><br />Yellow fever is a disease cause by a virus of the family Flaviviridae, the same family that plays host to Dengue virus, West Nile virus, and the latest superstar, Zika virus. The yellow fever virus is spread between humans through a mosquito vector. Disease spread occurs through three different transmission cycles: the jungle, or sylvatic, cycle, typically spreads disease from a nonhuman primate to other nonhuman primates, with the occasional cross to humans; the urban cycle typically spreads disease from human to human; and the intermediate, or savannah, cycle can involve transmission from both nonhuman primates and humans to other nonhuman primates and humans. Each transmission cycle uses its own mosquito vectors, with Aedes aegypti, also known as the yellow fever mosquito, being responsible for the urban cycle that typically lead to the most severe outbreaks. Once a mosquito takes a blood meal from a human infected with the virus, the virus begins replicating and infecting the cells of the mosquito. Once the infection spreads to the mosquito’s salivary glands, the virus can be passed on to a new human.<br /><br /> Yellow fever virus often leads to mild, or no, disease in humans. Patients may experience fevers, aches, chills, and other flu-like symptoms. However, about 15% of cases can lead to severe disease and bleeding, shock, and organ failure; roughly half of these cases are fatal. We have no cure for yellow fever, so our best defense is a good offense. The yellow fever vaccine is known to be highly efficacious, typically providing lifelong immunity after just one dose. However, there are major problems with yellow fever vaccine production which have led to our current defensive stance against the virus.<br /><br /> The yellow fever vaccine is produced using a very old-fashioned and low-tech procedure introduced 80 years ago that involves passing the virus through chicken embryos to produce attenuated, less-virulent virions. This process can only be done in four facilities throughout the world, two government-run plants in Russia, the vaccine company Sanofi Pasteur’s plant, and the Pasteur Institute. Between these four facilities, it is estimated that 75 million doses of vaccine can be made each year. In the past, this has been enough to deal with the vaccination of children in many areas, but has not been able to cover the catch-up vaccinations of adults who were not vaccinated as children. Since the outbreak in Luanda, nearly 6 million people in that city alone have been vaccinated, but the disease has continued to spread throughout the rest of Angola, depleting the global emergency stockpile of vaccine. With the vaccine in high demand, a United Nations report estimated that they would need 42% more vaccine than was available in the next 3 years. Unfortunately, vaccine production is expected to decline rather than increase in the near future as one of the four plants will be closing for a 5-month renovation.<br /><br /> Many experts worry that the worst case scenario, a spread of yellow fever to Asia, where the disease has not been able to gain a solid foothold in the past, would be catastrophic. With vaccine stores already depleted, we would have no defense against such a spread. There are currently no signs of this being a threat, so we still have time to gain the upper hand. If we can remain on the offensive against this disease and find ways to streamline and increase vaccine production, this global threat could one day become a thing of the past. But such an achievement would require a renewed research effort into yellow fever vaccine production, and increased funding for this endeavor. In a tight funding climate, this can be a difficult feat to achieve, but such an achievement is essential for ensuring the protection of future generations from outbreaks like the one currently happening in Angola.Anonymoushttp://www.blogger.com/profile/05503168250289145242noreply@blogger.com0