Team:CongoDRC-Bel Campus/Project

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You are provided with this team page template with which to start the iGEM season.  You may choose to personalize it to fit your team but keep the same "look." Or you may choose to take your team wiki to a different level and design your own wiki.  You can find some examples <a href="https://2008.igem.org/Help:Template/Examples">HERE</a>.
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|align="center"|[[Team:CongoDRC-Bel_Campus | Team Example]]
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!align="center"|[[Team:CongoDRC-Bel_Campus|Home]]
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!align="center"|[[Team:CongoDRC-Bel_Campus/Team|Team]]
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!align="center"|[https://igem.org/Team.cgi?year=2010&team_name=CongoDRC-Bel_Campus Official Team Profile]
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!align="center"|[[Team:CongoDRC-Bel_Campus/Project|Project]]
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!align="center"|[[Team:CongoDRC-Bel_Campus/Modeling|Modeling]]
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ABSRTACT
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NB. We have two differents approaches for this project: modelling transmission and engineered mycobacterial vaccine.
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<title>Bel Campus</title>
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</head>
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1.TRANSMISSION
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<img src="https://static.igem.org/mediawiki/2011/d/d1/Header_main.gif" width="971" height="50" /><br />
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<div id="tabs">
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  <ul>
 +
    <li><a href="https://2011.igem.org/Team:CongoDRC-Bel_Campus"><span>Home</span></a></li>
 +
    <li><a href="https://2011.igem.org/Team:CongoDRC-Bel_Campus/Team"><span>Team</span></a></li>
 +
    <li><a href="https://2011.igem.org/Team:CongoDRC-Bel_Campus/Project"><span>Project</span></a></li>
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    <li><a href="https://2011.igem.org/Team:CongoDRC-Bel_Campus/Modeling"><span>Modeling</span></a></li>
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    <li><a href="https://2011.igem.org/Team:CongoDRC-Bel_Campus/Notebook"><span>Notebook</span></a></li>
 +
    <li><a href="https://2011.igem.org/Team:CongoDRC-Bel_Campus/Safety"><span>Safety</span></a></li>
 +
    <li><a href="https://2011.igem.org/Team:CongoDRC-Bel_Campus/Attributions"><span>Attributions</span></a></li>
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    <li><a href="https://2011.igem.org/Team:CongoDRC-Bel_Campus/Gallery"><span>Gallery</span></a></li>
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      Buruli Ulcer (BU) is a debilitating disease that mainly affects the skin but which can also affect the bone. The causative agent is called Mycobacterium ulcerans, which although different, belongs to the same family of organisms that cause leprosy and tuberculosis. This affection is one of the most common mycobacterial diseases in human health. Several cases of BU have been identified in at least 26 countries in the African Region since the early 1940s.  However, in recent years, an increasing number of cases have been recorded in nearly all Western Africa countries, along the Gulf of Guinea. The causative agent is Mycobacterium ulcerans. For it to cause disease, it must either be transmitted from one infected individual directly to another    (e.g.; direct contact) or through the environment (e.g.; via an intermediate host) to a susceptible host. It must also have the capability of surviving and multiplying in either the environment or the host or in both.
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  </ul>
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Generally, the reservoir of infection is not exactly known but is believed to be either the sick individual or the environment, especially marshy soil and vegetation along slow-flowing streams and rivers, or perhaps an intermediate host that thrives in such environment conditions. The latent period for infection to progress to disease in the susceptible host is also not well known. The mode of transmission is not entirely known.
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  <img src="https://static.igem.org/mediawiki/igem.org/a/ac/Linez.png" align="left" />
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Recent evidence suggests that certain aquatic insects (aquatic bug) belonging to the genus Naucoris and Diplonychus may be involved in the transmission of the infection. The causative agent is commonly introduced into the skin (from surface contamination) through traumatic breaches in the skin (irrespective of size).
+
</div>
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However, it is not well understood whether infection can occur directly through the intact skin, after an insect bite, or by direct person –to-person contact.
+
-
    One interesting hypothesis concerns the possibility of transmission by some aquatic species. Nevertheless, this bacteria it’s environmental, the simple hypothesis is the direct transmission of M.ulcerans by contaminated water. To identify the more probable way of transmission of M.ulcerans in environment, we rely on data and mathematical modeling transmission of M.ulcerans. Using Synthetic biology approaches we managed to build two different epidemiological models taken account of these two ways of possible transmission. The first model concerns the “environmental” transmission by contact with mycobacteria, through contaminated water. The second epidemiological model concerns the transmission of mycobacterium by ecological “networks”. The parameters of these two epidemiological models will be estimated from data of field with the more probable mode of transmission.
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2.VACCINE.
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<table width="970" border="0" cellspacing="0" bordercolor="#128BE9" bgcolor="#F4F7FB">
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  <div ></div>
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M. ulcerans causing by B.U. This infection can be treated with multi drugs regime (rifampicin and streptomycin) but this is often associated with induced antibiotic resistance and does not protect individuals from re-infection
+
  <tr>
-
Vaccination against M. ulcerans can therefore be aviable alternator to control this wide spread infection. 
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    <td width="942" rowspan="2" bgcolor="#F4F7FB"><div style="font:normal; font-size:24px; color:#333333;">&nbsp;&nbsp;Our Project overview</div></td>
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However, developing an effective vaccine against M. ulcerans has presented a challenge because M. ulcérans or its components, which have frequently been used as parts of vaccines, are modified by mycobacterium such that they avoid host defense mechanism using synthetic biology approaches, we managed to assemble functional ‘’immunobrick’’ into a designer vaccine with a goal to activate both innate and acquired immune response to M. ulcerans.  
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    <td width="8" bgcolor="#F4F7FB">&nbsp;</td>
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We propose developing two forms of such designers’ vaccines.
+
    <td width="14" rowspan="2" bgcolor="#F4F7FB"><h2>&nbsp;&nbsp;</h2></td>
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-One will be based on modifying M. ulcerans component such that it can now recognize by the immune system.
+
  </tr>
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-The other relied upon linking M. ulcerans component to certain molecule of the innate immune response (so called Toll like receptor) to activate and guide M. ulcerans proteins to relevant compartments within the immune cell causing optimal innate and acquired immune response.
+
  <tr>
-
An effective vaccine against M. ulcérans is not available, although it will be a durable solution.
+
    <td width="8" bgcolor="#F4F7FB">&nbsp;</td>
-
M. ulcerans avoids the immune surveillance by modifying several of this components including LAM (lipoarabinoman) ,SL1(sulfolipide 1)  mycolactone to avoid detection by several Toll Like Receptor.  
+
  </tr>
-
The goal of our project was to prepare a modular designer vaccine using the principal of synthetic immunology. An effective vaccine was to trigger activation of adaptive immunity, against microbial proteins (mycolactone), polysaccharides or lipids metabolites (PDM: phtiocerol dimycocerosate, PGL: phenolglycolipide, SL1: sulfolipide 1, GPL: glycopeptidolipide) as well as innate immunity, with which is usually achieved by addition of adjuvant of whole microbes. We prepared a set of ‘immunobricks’ with the defined functions in activation of the immunosystem and can be combined to active a desired response.
+
  <tr>
-
In the first approach, we want to modify the components M.ulcerans wall (LAM, SL1, PGL, PDM, and GPL) to be able to active TLR 2 making it visible to the immune system.
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    <td height="70" colspan="2" background="https://static.igem.org/mediawiki/igem.org/b/b6/Projectst.png" bgcolor="#F4F7FB" style="background-repeat:no-repeat;"><div class="menu_nav">
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  <ul>
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    <li><a href="#pd"><span>1. Project details</span></a></li>
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    <li><a href="#part1"><span>1.1. Part 1</span></a></li>
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'''
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    <li><a href="#experiments"><span>1.2. The experiments</span></a></li>
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    <li><a href="#part2"><span>1.3. Part 2</span></a></li>
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== Project Details==
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    <li><a href="#result"><span>2. Result</span></a></li>
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    </ul>
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WHY THIS CHOICE?
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</div>      <br /></td>
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'''BURULI ULCER'''
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    <td rowspan="2" bgcolor="#F4F7FB"><br /></td>
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  </tr>
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1. INTRODUCTION:
+
 
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+
 
-
Buruli Ulcer (BU) is a debilitating disease that mainly affects the skin but which can also affect the bone.  The causative agent is called Mycobacterium ulcerans, which although different, belongs to the same family of organisms that cause leprosy and tuberculosis.  This affection is one of the most common mycobacterial diseases in human health.  Several cases of BU have been identified in at least 26 countries in the African Region since the early 1940s.  However, in recent years, an increasing number of cases have been recorded in nearly all Western Africa countries, along the Gulf of Guinea.  The disease is currently known to be endemic there in the following countries: Benin, Ivory Coast, Ghana, Guinea, Liberia, Nigeria, Sierra Leone and Togo (see Africa map).
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  <tr>
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    <td rowspan="2" bgcolor="#F9F9F9">
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2. HISTORICAL OVERVIEW:
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      <table width="100%" border="0" cellpadding="0" cellspacing="0" bordercolor="#F4F7FB" bgcolor="#F4F7FB">
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In 1897, Sir Robert Cook described large ulcers in Uganda, which were almost certainly caused by M. ulcerans.  It was, however, not until 1940 in Bairnsdale, Australia, when Mac Cullum, first described the causative agent of this disease, after discovering the acid-fast-bacill (AFB) in a biopsy specimen from a leg ulcer in a young child. In 1948, he published the first clinical description of this new mycobacterial infection.  Between 1923 and 1935, a missionary physician working in the North-eastern area of Democratic Republic of Congo (Zaire) observed undermined skin ulcers that were rich in AFB.
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          <td width="21%" rowspan="2"><div style="color:#666666; margin-left:20px; margin-right:20px; font:normal 24px/1.5em Arial, Helvetica, sans-serif;">ABSRTACT</div></td>
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          <td width="79%"><div style="color:#666666; font:normal 16px/1.5em Arial, Helvetica, sans-serif;">Zoom text here</div></td>
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3. THE CAUSETIVE AGENTS:
+
        </tr>
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The causative agent is Mycobacterium ulcerans. For it to cause disease, it must either be transmitted from one infected individual directly to another (e.g.; direct contact) or through the environment (e.g.; via an intermediate host) to a susceptible host. It must also have the capability of surviving and multiplying in either the environment or the host or in both.
+
        <tr>
-
Generally, the reservoir of infection is not exactly known but is believed to be either the sick individual or the environment, especially marshy soil and vegetation along slow-flowing streams and rivers, or perhaps an intermediate host that thrives in such environment conditions. The latent period for infection to progress to disease in the susceptible host is also not well known.
+
          <td><div id="slider" class="slider">
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  <div class="knob"></div>
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[[File:Jacinth plant.jpg]]
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</div></td>
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[[File:Mollusc.jpg]]
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        </tr>
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      </table>
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 +
      <div id="fontSize" class="divani"><p>NB. We have two differents approaches for this project: modelling transmission and engineered mycobacterial vaccine. </p>
 +
      <p><b>1.TRANSMISSION </b><br />
 +
      <br />
 +
      Generally, the reservoir of infection is not exactly known but is  believed to be either the sick individual or the environment,  especially marshy soil and vegetation along slow-flowing streams and  rivers, or perhaps an intermediate host that thrives in such  environment conditions. The latent period for infection to progress to  disease in the susceptible host is also not well known. The mode of  transmission is not entirely known.  Recent evidence suggests that certain aquatic insects (aquatic bug)  belonging to the genus Naucoris and Diplonychus may be involved in the  transmission of the infection. The causative agent is commonly  introduced into the skin (from surface contamination) through traumatic  breaches in the skin (irrespective of size). However, it is not well  understood whether infection can occur directly through the intact  skin, after an insect bite, or by direct person –to-person contact. </p>
 +
<p><br />
 +
              One interesting hypothesis concerns the possibility of transmission by some aquatic species. Nevertheless, this bacteria it’s environmental, the simple hypothesis is the direct transmission of M.ulcerans by contaminated water. To identify the more probable way of transmission of M.ulcerans in environment, we rely on data and mathematical modeling transmission of M.ulcerans. Using Synthetic biology approaches we managed to build two different epidemiological models taken account of these two ways of possible transmission. The first model concerns the “environmental” transmission by contact with mycobacteria, through contaminated water. The second epidemiological model concerns the transmission of mycobacterium by ecological “networks”. The parameters of these two epidemiological models will be estimated from data of field with the more probable mode of transmission.</p>  <br />
 +
        <br />
 +
     
 +
      <p><b>2.VACCINE.</b> </p>
 +
      M. ulcerans causing by B.U. This infection can be treated with  multi drugs regime (rifampicin and streptomycin) but this is often  associated with induced antibiotic resistance and does not protect  individuals from re-infection  Vaccination against M. ulcerans can therefore be aviable alternator to  control this wide spread infection. However, developing an effective  vaccine against M. ulcerans has presented a challenge because M.  ulcérans or its components, which have frequently been used as parts of  vaccines, are modified by mycobacterium such that they avoid host  defense mechanism using synthetic biology approaches, we managed to  assemble functional ‘’immunobrick’’ into a designer vaccine with a goal  to activate both innate and acquired immune response to M. ulcerans. We  propose developing two forms of such designers’ vaccines. -One will be  based on modifying M. ulcerans component such that it can now recognize  by the immune system.  -The other relied upon linking M. ulcerans component to certain  molecule of the innate immune response (so called Toll like receptor)  to activate and guide M. ulcerans proteins to relevant compartments  within the immune cell causing optimal innate and acquired immune  response. An effective vaccine against M. ulcérans is not available,  although it will be a durable solution.  M. ulcerans avoids the immune surveillance by modifying several of this  components including LAM (lipoarabinoman) ,SL1(sulfolipide 1)  mycolactone to avoid detection by several Toll Like Receptor. The goal  of our project was to prepare a modular designer vaccine using the  principal of synthetic immunology. An effective vaccine was to trigger  activation of adaptive immunity, against microbial proteins  (mycolactone), polysaccharides or lipids metabolites (PDM: phtiocerol  dimycocerosate, PGL: phenolglycolipide, SL1: sulfolipide 1, GPL:  glycopeptidolipide) as well as innate immunity, with which is usually  achieved by addition of adjuvant of whole microbes. We prepared a set  of ‘immunobricks’ with the defined functions in activation of the  immunosystem and can be combined to active a desired response. In the  first approach, we want to modify the components M.ulcerans wall (LAM,  SL1, PGL, PDM, and GPL) to be able to active TLR 2 making it visible to  the immune system. </p>     
 +
      <p>&nbsp;</p>
 +
      <p>&nbsp;</p>
 +
      <h2><span id="Project_Details"> <a name="pd" id="pd"></a>Project Details</span></h2>
 +
      <p>WHY THIS CHOICE? <strong>BURULI ULCER</strong> </p>
 +
      <p><b>1. INTRODUCTION:</b> </p>
 +
      <pre style="font-size:12px;">Buruli Ulcer (BU) is a debilitating disease that mainly affects the skin but which can also affect the bone.  <br />The causative agent is called Mycobacterium ulcerans, which although different, belongs to the same family of <br />organisms that cause leprosy and tuberculosis.  This affection is one of the most common mycobacterial diseases <br />in human health.  Several cases of BU have been identified in at least 26 countries in the African Region <br />since the early 1940s.  However, in recent years, an increasing number of cases have been recorded in nearly <br />all Western Africa countries, along the Gulf of Guinea.  The disease is currently known to be endemic there in <br />the following countries: Benin, Ivory Coast, Ghana, Guinea, Liberia, Nigeria, Sierra Leone and Togo (see Africa map).  </pre>
 +
      <p align="justify" style="color:#333333; font-family:Arial, Helvetica, sans-serif;"><b>2. HISTORICAL OVERVIEW:</b><br />  In 1897, Sir Robert Cook described large ulcers in Uganda, which were  almost certainly caused by M. ulcerans. It was, however, not until 1940  in Bairnsdale, Australia, when Mac Cullum, first described the  causative agent of this disease, after discovering the acid-fast-bacill  (AFB) in a biopsy specimen from a leg ulcer in a young child. In 1948,  he published the first clinical description of this new mycobacterial  infection. Between 1923 and 1935, a missionary physician working in the  North-eastern area of Democratic Republic of Congo (Zaire) observed  undermined skin ulcers that were rich in AFB. </p>
 +
      <p align="justify" style="color:#333333; font-family:Arial, Helvetica, sans-serif;"><br />
 +
        <b>3. THE CAUSETIVE AGENTS: </b> <br />The causative agent is Mycobacterium ulcerans. For it to cause disease,  it must either be transmitted from one infected individual directly to  another (e.g.; direct contact) or through the environment (e.g.; via an  intermediate host) to a susceptible host. It must also have the  capability of surviving and multiplying in either the environment or  the host or in both.  Generally, the reservoir of infection is not exactly known but is  believed to be either the sick individual or the environment,  especially marshy soil and vegetation along slow-flowing streams and  rivers, or perhaps an intermediate host that thrives in such  environment conditions. The latent period for infection to progress to  disease in the susceptible host is also not well known. <br /><br />
 +
        <img src="
 +
https://static.igem.org/mediawiki/igem.org/f/f1/Image1.jpg" width="892" height="152" /></p>     
 +
      <p align="justify" style="color:#333333; font-family:Arial, Helvetica, sans-serif;"><b>4. MODE OF TRANSMISSION  </b><br />The mode of transmission is not entirely known.  Recent evidence suggests that certain aquatic insects (aquatic bug)  belonging to the genus Naucoris and Diplonychus may be involved in the  transmission of the infection. The causative agent is commonly  introduced into the skin (from surface contamination) through traumatic  breaches in the skin (irrespective of size). However, it is not well  understood whether infection can occur directly through the intact  skin, after an insect bite, or by direct person –to-person contact.  After entering the subcutaneous tissue of the host, Mycobacterium  ulcerans is known to produce a toxin that causes its characteristic  pathology from nodules, edematous lesions to skin ulcerations. </p><br />
 +
      <p><b>5. EPIDEMIOLOGY: </b><br />
 +
      To better design a public health intervention to control this  disease in Africa, it is imperative to understand its epidemiology.  However, this subject is still under intense investigation in several  countries in the region. </p><br />
 +
      <p><b>5.1. IN THE WORLD:</b>  <br />Buruli Ulcer is notified in almost 30 countries with tropical and  subtropical climates, including in America, Asia, Oceania and Africa.  But the disease may also occur in some countries where it has not yet  been recognized.  The map below represents almost the countries of each continent:<br />
 +
      <img alt="BU in the world.jpg" src="https://static.igem.org/mediawiki/igem.org/c/ca/World.jpg" width="488" height="280" /> </p><br />
 +
      <p><B>5.2. GEOGRAPHIC DISTRIBUTION IN AFRICAN REGION:</B>  <br />Nevertheless, it is important to briefly describe the current state of  knowledge about the subject in order to understand the challenges that  confront us in combating this mysterious disease.  The current geographic distribution of the disease in African Region is  depicted in Fig.2. To date, 21 Member States (old and new foci) in  Western (9 countries), Central (6 countries), Eastern (4 countries) and  Southern Africa (2 countries) have reported cases (both suspected and  confirmed). Countries in Westen Africa, however, have reported the  highest number of cases (cumulative range of 1,000 to 10,000), with an  endemic pattern in recent years.<br />
 +
      <img alt="BU in africa.jpg" src="https://static.igem.org/mediawiki/igem.org/d/dd/Africa_BU.jpg" width="377" height="282" border="0" /></p>
 +
      <p><br />
 +
        <b>5.3. GEOGRAPHIC DISTRIBUTION IN DEMOCRATIC REPUBLIC OF CONGO  REGION:</b>  <br />The first case of UB in DRC has been reported in 1950. In 2004, the  national investigation has shown that there were some suspected cases  of UB in 6 of 11 regions. Three(3) of these are considerated highest  endemic: Bas congo, Bandundu and Maniema; whereas others (3) are less  endemic ( Equateur, Katanga and Province orientale). </p>
 +
      <img src="https://static.igem.org/mediawiki/igem.org/1/15/Image2.jpg" width="377" height="282" border="0"/>
 +
      <p> <br /><b>5.3.1. AGE AND SEX DISTRIBUTION:</b> <br />In general, the disease can affect  all age groups. However, children under 15 years of age (range of 2-14  years) are predominantly affected. There are no gender defenses in the  distribution of cases among children, although some studies have  reported more females than males among affected adults. This  observation is believed to be caused by differential gender exposure to  the organism in environment rather than differential susceptibility to  infection.<br /> <img src="https://static.igem.org/mediawiki/igem.org/a/ae/Image3.jpg" /></p>
 +
      <p><br />
 +
        <b>5.3.2. DISTRIBUTION OF SITE LESIONS:  </b><br />
 +
        Most ulcers occur on the extremities, as they are generally more  exposed and prone to injury. Lesions on the lower extremities are  almost twice as common as those on the upper extremities. Ulcers on the  head and trunk are less common. Recurrence of disease at the same or  other sites is common, implying that immunity to infection is generally  minimal. </p><br />
 +
      <p><b>5.3.3. MAGNITUDE OF DISEASE:</b>  <br />Until recently, in several countries where the disease has been  reported, it is not considered to be a public health problem, hence the  exact distribution and number of cases are not known. Available data,  mostly obtained through passive case finding in a few communities where  the prevalence has been estimated, show fairly high prevalence rates. </p><br />
 +
      <p><b>5.3.4. ENVIRONMENTAL FACTORS  BU:</b> <br />Generally occurs in warm, humid environments (tropical and  subtropical regions) especially in areas with marshy soil and stagnant  or slow flowing water bodies. Man made topographical modifications such  as damming of rivers and stream, mining activities and deforestation  are believed to create favorable environmental conditions for the  survival of the organism and the disease it causes. The occurrence of  the disease has also been observed to follow some seasonal pattern,  generally increasing during the rainy season and coinciding with  periods of farming activities.<br /><img src="https://static.igem.org/mediawiki/igem.org/d/da/Image4.jpg" /></p><br />
 +
      <p><b>6. PATHOLOGY </b><br />
 +
      <b>6.1. ACTIVE DISEASE </b> <br />The term “active disease” generally refers to ongoing infections.  During the pre-ulcerative stage the disease, the following forms are  the clinically recognizable:  <br /> Papule: usually painless, sometimes itches, not tender, palpable,  intra-dermal lesion   Nodule: usually painless, palpable, firm lesion, 1-2 cm in diameter  situated in the subcutaneous tissue and typically attached to the skin.  The skin around the lesion is usually hypo-pigmented in dark skinned  people.<br /><img src="https://static.igem.org/mediawiki/igem.org/5/52/Image5.jpg" /></p>
 +
      <p> Plaque: usually painless, well delimited, elevated and firm  lesion, more than 2 cm in diameter  <br /> Edema: diffuse, extensive non-pitting, swelling, ill-defined margins,  firm, usually painful with or without color change others affected  skin.  <br /> Ulcerated Stage: A typical Buruli Ulcer is defined as a skin ulcer  characterized by necrotic center, undermined edges and edematous skin.  In the absence of the secondary bacterial infection, the ulcer is  usually painless or minimally painful ; two mains clinical  entities at this stage of disease may be differentiated as follows: </p>
 +
      <p> Small ulcer: an ulcer with a size less  than 2 cm in diameter. <br /><img src="https://static.igem.org/mediawiki/igem.org/f/f6/Image7.jpg" /></p><br />
 +
      <p> Large ulcer : an ulcer with a size greater than 2 cm in diameter <br /><img src="https://static.igem.org/mediawiki/igem.org/0/0b/Image6.jpg" /></p><br />
 +
    <p><b>6.2. INACTIVE DISEASE </b> <br />This refers to healed lesions that have a characteristic, depressed, star-shaped scar. There are three mains clinical entities:  • Scar without sequel  • Scar with sequel ( e.g. contracture deformities, amputation, loss of organs)  • A mixture of the above <br /><img src="https://static.igem.org/mediawiki/igem.org/c/c6/Image8.jpg" /></p></div></td>
 +
    <td width="8" rowspan="4" background="vertical.png" bgcolor="#F4F7FB">&nbsp;</td>
 +
  </tr>
    
    
-
[[File:picture of Naucoris cimicoides.jpg]]          
+
  <tr>
-
[[File:Shematic cut  of aquatic bug Naucoris cimicoides
+
    <td bgcolor="#F4F7FB"><br />
-
.jpg]]
+
    <br /></td></tr>
-
 
+
  <tr>
-
4. MODE OF TRANSMISSION
+
    <td bgcolor="#FFFFFF"><h2><span id="Project_Details"> <a name="part1" id="part1"></a>1.1. Part 1</span></h2></td>
-
The mode of transmission is not entirely known.
+
    <td bgcolor="#F4F7FB">&nbsp;</td>
-
Recent evidence suggests that certain aquatic insects (aquatic bug) belonging to the genus Naucoris and Diplonychus may be involved in the transmission of the infection. The causative agent is commonly introduced into the skin (from surface contamination) through traumatic breaches in the skin (irrespective of size).
+
   </tr>
-
However, it is not well understood whether infection can occur directly through the intact skin, after an insect bite, or by direct person –to-person contact. After entering the subcutaneous tissue of the host, Mycobacterium ulcerans is known to produce a toxin that causes its characteristic pathology from nodules, edematous lesions to skin ulcerations.   
+
  <tr>
-
                                                         
+
    <td bgcolor="#F4F7FB"><h2><a name="experiments" id="experiments"></a>1.2. The Experiments</h2></td>
-
5. EPIDEMIOLOGY:
+
    <td bgcolor="#F4F7FB">&nbsp;</td>
-
 
+
  </tr>
-
To better design a public health intervention to control this disease in Africa, it is imperative to understand its epidemiology. However, this subject is still under intense investigation in several countries in the region.
+
  <tr>
-
 
+
    <td bgcolor="#F4F7FB"><h2><a name="part2" id="part2"></a>1.3. Part 2</h2></td>
-
5.1.   IN THE WORLD:
+
    <td width="8" bgcolor="#F4F7FB">&nbsp;</td>
-
Buruli Ulcer is notified in almost 30 countries with tropical and subtropical climates, including in America, Asia, Oceania and Africa. But the disease may also occur in some countries where it has not yet been recognized.
+
    <td bgcolor="#F4F7FB">&nbsp;</td>
-
The map below represents almost the countries of each continent:
+
  </tr>
-
[[File: BU in the world.jpg]] 
+
  <tr>
-
 
+
    <td bgcolor="#F4F7FB"><h2><a name="part3" id="part3"></a>2. Result</h2></td>
-
5.2. GEOGRAPHIC DISTRIBUTION IN AFRICAN REGION:
+
    <td bgcolor="#F4F7FB">&nbsp;</td>
-
Nevertheless, it is important to briefly describe the current state of knowledge about the subject in order to understand the challenges that confront us in combating this mysterious disease.
+
    <td bgcolor="#F4F7FB">&nbsp;</td>
-
The current geographic distribution of the disease in African Region is depicted in Fig.2.  To date, 21 Member States (old and new foci) in Western (9 countries), Central (6 countries), Eastern (4 countries) and Southern Africa (2 countries) have reported cases (both suspected and confirmed). Countries in Westen Africa, however, have reported the highest number of cases (cumulative range of 1,000 to 10,000), with an endemic pattern in recent years.
+
  </tr>
-
[[File:BU in africa.jpg]]
+
  <tr>
-
+
    <td bgcolor="#F4F7FB">&nbsp;</td>
-
 
+
    <td bgcolor="#F4F7FB">&nbsp;</td>
-
5.3. GEOGRAPHIC DISTRIBUTION IN DEMOCRATIC REPUBLIC OF CONGO REGION
+
    <td bgcolor="#F4F7FB">&nbsp;</td>
-
The first case of UB in DRC has been reported in 1950. In 2004, the national investigation has shown that there were some suspected cases of UB in 6 of 11 regions. Three(3) of these are considerated highest endemic: Bas congo, Bandundu and Maniema; whereas others (3) are less endemic ( Equateur, Katanga and Province orientale).
+
  </tr>
-
[[File:BU in DRC in 2004 and 2008.jpg]]
+
   <tr>
-
+
    <td bgcolor="#F4F7FB"><h2>We are sponsored by</h2></td>
-
5.3.1. AGE AND SEX DISTRIBUTION:
+
    <td bgcolor="#F4F7FB">&nbsp;</td>
-
In general, the disease can affect all age groups. However, children under 15 years of age (range of 2-14 years) are predominantly affected. There are no gender defenses in the distribution of cases among children, although some studies have reported more females than males among affected adults. This observation is believed to be caused by differential gender exposure to the organism in environment rather than differential susceptibility to infection.
+
    <td bgcolor="#F4F7FB">&nbsp;</td>
-
[[File:A seven  and eight year old girls infected.jpg]]
+
  </tr>
-
 
+
   <tr>
-
 
+
    <td>&nbsp;</td>
-
5.3.2. DISTRIBUTION OF SITE LESIONS:
+
    <td bgcolor="#F4F7FB">&nbsp;</td>
-
Most ulcers occur on the extremities, as they are generally more exposed and prone to injury.  Lesions on the lower extremities are almost twice as common as those on the upper extremities. Ulcers on the head and trunk are less common. Recurrence of disease at the same or other sites is common, implying that immunity to infection is generally minimal. 
+
    <td bgcolor="#F4F7FB">&nbsp;</td>
-
[[File:Eight year old girl with her right limbs strongly affected
+
  </tr>
-
.jpg]]
+
</table>
-
 
+
</body>
-
5.3.3. MAGNITUDE OF DISEASE
+
</html>
-
Until recently, in several countries where the disease has been reported, it is not considered to be a public health problem, hence the exact distribution and number of cases are not known. Available data, mostly obtained through passive case finding in a few communities where the prevalence has been estimated, show fairly high prevalence rates.
+
-
 
+
-
5.3.4. ENVIRONMENTAL FACTORS
+
-
BU generally occurs in warm, humid environments (tropical and subtropical regions) especially in areas with marshy soil and stagnant or slow flowing water bodies. Man made topographical modifications such as damming of rivers and stream, mining activities and deforestation are believed to create favorable environmental conditions for the survival of the organism and the disease it causes. The occurrence of the disease has also been observed to follow some seasonal pattern, generally increasing during the rainy season and coinciding with periods of farming activities.
+
-
[[File:Ngulu and Maindombe rivers.jpg]]
+
-
 
+
-
6. PATHOLOGY
+
-
 
+
-
6.1. ACTIVE DISEASE
+
-
The term “active disease” generally refers to ongoing infections.
+
-
During the pre-ulcerative stage the disease, the following forms are the clinically recognizable:
+
-
 Papule: usually painless, sometimes itches, not tender, palpable, intra-dermal lesion
+
-
 Nodule: usually painless, palpable, firm lesion, 1-2 cm in diameter situated in the subcutaneous tissue and typically attached to the skin. The skin around the lesion is usually hypo-pigmented in dark skinned people.  
+
-
[[File:Nodule.jpg]]
+
-
 
+
-
 Plaque: usually painless, well delimited, elevated and firm lesion, more than 2 cm in diameter
+
-
 Edema: diffuse, extensive non-pitting, swelling, ill-defined margins, firm, usually painful with or without color change others affected skin.
+
-
 Ulcerated Stage: A typical Buruli Ulcer is defined as a skin ulcer characterized by necrotic center, undermined edges and edematous skin. In the absence of the secondary bacterial infection, the ulcer is usually painless or minimally painful ; two mains clinical entities at this stage of disease may be differentiated as follows:
+
-
 
+
-
 Small ulcer: an ulcer with a size less  than 2 cm in diameter.
+
-
[[File:Small ulcer.jpg]]
+
-
 
+
-
 Large ulcer : an ulcer with a size greater than 2 cm in diameter
+
-
[[File:large ulcers.jpg]]    
+
-
 
+
-
6.2. INACTIVE DISEASE
+
-
This refers to healed lesions that have a characteristic, depressed, star-shaped scar. There are three mains clinical entities:
+
-
• Scar without sequel
+
-
• Scar with sequel ( e.g. contracture deformities, amputation, loss of organs)
+
-
• A mixture of the above
+
-
[[File:Inactive disease.jpg]]    
+
-
 
+
-
 
+
-
 
+
-
 
+
-
 
+
-
=== Part 2 ===
+
-
 
+
-
 
+
-
 
+
-
 
+
-
 
+
-
=== The Experiments ===
+
-
 
+
-
 
+
-
 
+
-
 
+
-
=== Part 3 ===
+
-
 
+
-
== Results ==
+

Latest revision as of 13:03, 1 August 2011

Bel Campus

  Our Project overview
 

  

 


ABSRTACT
Zoom text here

NB. We have two differents approaches for this project: modelling transmission and engineered mycobacterial vaccine.

1.TRANSMISSION

Generally, the reservoir of infection is not exactly known but is believed to be either the sick individual or the environment, especially marshy soil and vegetation along slow-flowing streams and rivers, or perhaps an intermediate host that thrives in such environment conditions. The latent period for infection to progress to disease in the susceptible host is also not well known. The mode of transmission is not entirely known. Recent evidence suggests that certain aquatic insects (aquatic bug) belonging to the genus Naucoris and Diplonychus may be involved in the transmission of the infection. The causative agent is commonly introduced into the skin (from surface contamination) through traumatic breaches in the skin (irrespective of size). However, it is not well understood whether infection can occur directly through the intact skin, after an insect bite, or by direct person –to-person contact.


One interesting hypothesis concerns the possibility of transmission by some aquatic species. Nevertheless, this bacteria it’s environmental, the simple hypothesis is the direct transmission of M.ulcerans by contaminated water. To identify the more probable way of transmission of M.ulcerans in environment, we rely on data and mathematical modeling transmission of M.ulcerans. Using Synthetic biology approaches we managed to build two different epidemiological models taken account of these two ways of possible transmission. The first model concerns the “environmental” transmission by contact with mycobacteria, through contaminated water. The second epidemiological model concerns the transmission of mycobacterium by ecological “networks”. The parameters of these two epidemiological models will be estimated from data of field with the more probable mode of transmission.



2.VACCINE.

M. ulcerans causing by B.U. This infection can be treated with multi drugs regime (rifampicin and streptomycin) but this is often associated with induced antibiotic resistance and does not protect individuals from re-infection Vaccination against M. ulcerans can therefore be aviable alternator to control this wide spread infection. However, developing an effective vaccine against M. ulcerans has presented a challenge because M. ulcérans or its components, which have frequently been used as parts of vaccines, are modified by mycobacterium such that they avoid host defense mechanism using synthetic biology approaches, we managed to assemble functional ‘’immunobrick’’ into a designer vaccine with a goal to activate both innate and acquired immune response to M. ulcerans. We propose developing two forms of such designers’ vaccines. -One will be based on modifying M. ulcerans component such that it can now recognize by the immune system. -The other relied upon linking M. ulcerans component to certain molecule of the innate immune response (so called Toll like receptor) to activate and guide M. ulcerans proteins to relevant compartments within the immune cell causing optimal innate and acquired immune response. An effective vaccine against M. ulcérans is not available, although it will be a durable solution. M. ulcerans avoids the immune surveillance by modifying several of this components including LAM (lipoarabinoman) ,SL1(sulfolipide 1) mycolactone to avoid detection by several Toll Like Receptor. The goal of our project was to prepare a modular designer vaccine using the principal of synthetic immunology. An effective vaccine was to trigger activation of adaptive immunity, against microbial proteins (mycolactone), polysaccharides or lipids metabolites (PDM: phtiocerol dimycocerosate, PGL: phenolglycolipide, SL1: sulfolipide 1, GPL: glycopeptidolipide) as well as innate immunity, with which is usually achieved by addition of adjuvant of whole microbes. We prepared a set of ‘immunobricks’ with the defined functions in activation of the immunosystem and can be combined to active a desired response. In the first approach, we want to modify the components M.ulcerans wall (LAM, SL1, PGL, PDM, and GPL) to be able to active TLR 2 making it visible to the immune system.

 

 

Project Details

WHY THIS CHOICE? BURULI ULCER

1. INTRODUCTION:

Buruli Ulcer (BU) is a debilitating disease that mainly affects the skin but which can also affect the bone.  
The causative agent is called Mycobacterium ulcerans, which although different, belongs to the same family of
organisms that cause leprosy and tuberculosis. This affection is one of the most common mycobacterial diseases
in human health. Several cases of BU have been identified in at least 26 countries in the African Region
since the early 1940s. However, in recent years, an increasing number of cases have been recorded in nearly
all Western Africa countries, along the Gulf of Guinea. The disease is currently known to be endemic there in
the following countries: Benin, Ivory Coast, Ghana, Guinea, Liberia, Nigeria, Sierra Leone and Togo (see Africa map).

2. HISTORICAL OVERVIEW:
In 1897, Sir Robert Cook described large ulcers in Uganda, which were almost certainly caused by M. ulcerans. It was, however, not until 1940 in Bairnsdale, Australia, when Mac Cullum, first described the causative agent of this disease, after discovering the acid-fast-bacill (AFB) in a biopsy specimen from a leg ulcer in a young child. In 1948, he published the first clinical description of this new mycobacterial infection. Between 1923 and 1935, a missionary physician working in the North-eastern area of Democratic Republic of Congo (Zaire) observed undermined skin ulcers that were rich in AFB.


3. THE CAUSETIVE AGENTS:
The causative agent is Mycobacterium ulcerans. For it to cause disease, it must either be transmitted from one infected individual directly to another (e.g.; direct contact) or through the environment (e.g.; via an intermediate host) to a susceptible host. It must also have the capability of surviving and multiplying in either the environment or the host or in both. Generally, the reservoir of infection is not exactly known but is believed to be either the sick individual or the environment, especially marshy soil and vegetation along slow-flowing streams and rivers, or perhaps an intermediate host that thrives in such environment conditions. The latent period for infection to progress to disease in the susceptible host is also not well known.

4. MODE OF TRANSMISSION
The mode of transmission is not entirely known. Recent evidence suggests that certain aquatic insects (aquatic bug) belonging to the genus Naucoris and Diplonychus may be involved in the transmission of the infection. The causative agent is commonly introduced into the skin (from surface contamination) through traumatic breaches in the skin (irrespective of size). However, it is not well understood whether infection can occur directly through the intact skin, after an insect bite, or by direct person –to-person contact. After entering the subcutaneous tissue of the host, Mycobacterium ulcerans is known to produce a toxin that causes its characteristic pathology from nodules, edematous lesions to skin ulcerations.


5. EPIDEMIOLOGY:
To better design a public health intervention to control this disease in Africa, it is imperative to understand its epidemiology. However, this subject is still under intense investigation in several countries in the region.


5.1. IN THE WORLD:
Buruli Ulcer is notified in almost 30 countries with tropical and subtropical climates, including in America, Asia, Oceania and Africa. But the disease may also occur in some countries where it has not yet been recognized. The map below represents almost the countries of each continent:
BU in the world.jpg


5.2. GEOGRAPHIC DISTRIBUTION IN AFRICAN REGION:
Nevertheless, it is important to briefly describe the current state of knowledge about the subject in order to understand the challenges that confront us in combating this mysterious disease. The current geographic distribution of the disease in African Region is depicted in Fig.2. To date, 21 Member States (old and new foci) in Western (9 countries), Central (6 countries), Eastern (4 countries) and Southern Africa (2 countries) have reported cases (both suspected and confirmed). Countries in Westen Africa, however, have reported the highest number of cases (cumulative range of 1,000 to 10,000), with an endemic pattern in recent years.
BU in africa.jpg


5.3. GEOGRAPHIC DISTRIBUTION IN DEMOCRATIC REPUBLIC OF CONGO REGION:
The first case of UB in DRC has been reported in 1950. In 2004, the national investigation has shown that there were some suspected cases of UB in 6 of 11 regions. Three(3) of these are considerated highest endemic: Bas congo, Bandundu and Maniema; whereas others (3) are less endemic ( Equateur, Katanga and Province orientale).


5.3.1. AGE AND SEX DISTRIBUTION:
In general, the disease can affect all age groups. However, children under 15 years of age (range of 2-14 years) are predominantly affected. There are no gender defenses in the distribution of cases among children, although some studies have reported more females than males among affected adults. This observation is believed to be caused by differential gender exposure to the organism in environment rather than differential susceptibility to infection.


5.3.2. DISTRIBUTION OF SITE LESIONS:
Most ulcers occur on the extremities, as they are generally more exposed and prone to injury. Lesions on the lower extremities are almost twice as common as those on the upper extremities. Ulcers on the head and trunk are less common. Recurrence of disease at the same or other sites is common, implying that immunity to infection is generally minimal.


5.3.3. MAGNITUDE OF DISEASE:
Until recently, in several countries where the disease has been reported, it is not considered to be a public health problem, hence the exact distribution and number of cases are not known. Available data, mostly obtained through passive case finding in a few communities where the prevalence has been estimated, show fairly high prevalence rates.


5.3.4. ENVIRONMENTAL FACTORS BU:
Generally occurs in warm, humid environments (tropical and subtropical regions) especially in areas with marshy soil and stagnant or slow flowing water bodies. Man made topographical modifications such as damming of rivers and stream, mining activities and deforestation are believed to create favorable environmental conditions for the survival of the organism and the disease it causes. The occurrence of the disease has also been observed to follow some seasonal pattern, generally increasing during the rainy season and coinciding with periods of farming activities.


6. PATHOLOGY
6.1. ACTIVE DISEASE
The term “active disease” generally refers to ongoing infections. During the pre-ulcerative stage the disease, the following forms are the clinically recognizable:
 Papule: usually painless, sometimes itches, not tender, palpable, intra-dermal lesion  Nodule: usually painless, palpable, firm lesion, 1-2 cm in diameter situated in the subcutaneous tissue and typically attached to the skin. The skin around the lesion is usually hypo-pigmented in dark skinned people.

 Plaque: usually painless, well delimited, elevated and firm lesion, more than 2 cm in diameter
 Edema: diffuse, extensive non-pitting, swelling, ill-defined margins, firm, usually painful with or without color change others affected skin.
 Ulcerated Stage: A typical Buruli Ulcer is defined as a skin ulcer characterized by necrotic center, undermined edges and edematous skin. In the absence of the secondary bacterial infection, the ulcer is usually painless or minimally painful ; two mains clinical entities at this stage of disease may be differentiated as follows:

 Small ulcer: an ulcer with a size less than 2 cm in diameter.


 Large ulcer : an ulcer with a size greater than 2 cm in diameter


6.2. INACTIVE DISEASE
This refers to healed lesions that have a characteristic, depressed, star-shaped scar. There are three mains clinical entities: • Scar without sequel • Scar with sequel ( e.g. contracture deformities, amputation, loss of organs) • A mixture of the above

 


1.1. Part 1

 

1.2. The Experiments

 

1.3. Part 2

   

2. Result

   
     

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