tag:theconversation.com,2011:/us/topics/biofilm-6204/articles
Biofilm – The Conversation
2024-03-12T12:36:08Z
tag:theconversation.com,2011:article/225040
2024-03-12T12:36:08Z
2024-03-12T12:36:08Z
TikTok claims ‘tongue scrapers’ can cure bad breath – here’s what the evidence actually says
<figure><img src="https://images.theconversation.com/files/580951/original/file-20240311-24-oankia.jpg?ixlib=rb-1.1.0&rect=57%2C9%2C6438%2C4269&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">Many people use tongue scrapers to remove the 'biofilm' from their tongue.</span> <span class="attribution"><a class="source" href="https://www.shutterstock.com/image-photo/close-girl-cleaning-her-tongue-scraper-666254164">Andrey_Popov/ Shutterstock</a></span></figcaption></figure><p>Most of us know how important it is to brush and floss if we want a healthy smile. But some people on TikTok are suggesting that this isn’t enough – and that if you really want good oral health, you need to use a “tongue scraper”.</p>
<p>Tongue scraping has long been part of <a href="https://www.sciencedirect.com/science/article/abs/pii/S0002817716304536">daily hygiene routines</a> in many parts of the world. It involves running a hard instrument across the tongue to remove bacterial build-up and debris. Tongue scrapers come in all shapes and sizes – with some people even using their toothbrush. They remove the white coating (which contains bacteria) that builds up on the back of some people’s tongues.</p>
<p>Videos on social media of people advocating for the use of tongue scrapers have amassed millions of views. Many proponents claim the practice banishes bad breath. But while there’s some evidence to back these claims, the practise could also come with risks.</p>
<p>Everyone has communities of bacteria, fungi and even viruses living inside their mouth. This is known as your <a href="https://www.sciencedirect.com/science/article/abs/pii/S019643991300041X?casa_token=59XPqoC2RXIAAAAA:Go0cyqIFg99BAsdgZCuvOfd2P5D2xLEQpHYe5SBHk5tfSgLN4R0ji1oOWpk80PcYo5oTmowhGGA">oral microbiome</a>. These bacteria can stick to the surface of your tongue and teeth and build up in layers (known as a biofilm). Plaque is one example of a biofilm. </p>
<p>Poor oral health can lead to a build-up of biofilms containing certain bacterial species which cause dental decay (cavities), gum disease and bad breath. For example, a build-up of the bacteria <em>Streptococcus mutans</em> is associated with cavities, while a build-up of <a href="https://aao-hnsfjournals.onlinelibrary.wiley.com/doi/10.1016/j.otohns.2005.09.036">volatile sulphur compound producing bacteria</a> (VSCs) on the tongue and gums can cause bad breath. <a href="https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0155592">Diets high in sugar</a> and low in fibre can also contribute to the build-up of VSCs.</p>
<p>For most, brushing your teeth twice daily (for two minutes each time) and using floss or interdental brushes to clean between teeth will be enough to remove the build-up of these biofilms. These techniques are also <a href="https://www.gov.uk/government/publications/delivering-better-oral-health-an-evidence-based-toolkit-for-prevention/chapter-8-oral-hygiene#oral-hygiene-principles-for-oral-health">very effective</a> for preventing tooth decay and gum disease. </p>
<p>But there’s less evidence showing whether these techniques are also effective for preventing tongue biofilms and bad breath.</p>
<h2>Tongue scraping</h2>
<p>A couple of reviews have shown that <a href="https://www.cochranelibrary.com/cdsr/doi/10.1002/14651858.CD005519.pub2/full">tongue scrapers</a> can reduce the release of VSCs produced by the bacterial species found in the tongue’s biofilm. Tongue scrapers are also shown to be superior to a toothbrush for <a href="https://onlinelibrary.wiley.com/doi/10.1111/j.1601-5037.2010.00479.x">reducing bad breath</a>.</p>
<p>So, based on the limited evidence out there, it does seem that regularly using a tongue scraper may help remove biofilms and improve bad breath. However, these reviews did find that the benefits of tongue scraping were shortlived and needed to be done using a specific technique to be effective.</p>
<p>Scraping your tongue once or twice a day for around <a href="https://onlinelibrary.wiley.com/doi/10.1111/j.1601-5037.2010.00479.x">15-30 seconds is adequate</a>. You also need to ensure you get far enough back on the tongue (where VSC-producing bacteria live), <a href="https://www.mdpi.com/1660-4601/19/1/108">scrape back to front</a> and keep up your regular tooth-brushing routine for the practise to be effective.</p>
<p>There are other caveats when it comes to tongue scraping. Bad breath isn’t only caused by VSCs. It can also be caused by cavities, <a href="https://www.nhs.uk/conditions/tonsillitis/">tonsillitis</a> and even <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2948765/">stomach problems</a> (such as acid reflux). In these instances, tongue scraping will do little to solve bad breath. </p>
<figure class="align-center ">
<img alt="A father and his young son brush their teeth." src="https://images.theconversation.com/files/580954/original/file-20240311-30-169fj.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/580954/original/file-20240311-30-169fj.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=400&fit=crop&dpr=1 600w, https://images.theconversation.com/files/580954/original/file-20240311-30-169fj.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=400&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/580954/original/file-20240311-30-169fj.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=400&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/580954/original/file-20240311-30-169fj.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/580954/original/file-20240311-30-169fj.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/580954/original/file-20240311-30-169fj.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=503&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
<figcaption>
<span class="caption">Brushing and flossing are still the best ways to look after your oral health.</span>
<span class="attribution"><a class="source" href="https://www.shutterstock.com/image-photo/father-son-brushing-teeth-bathroom-50754166">sirtravelalot/ Shutterstock</a></span>
</figcaption>
</figure>
<p>And despite their bad press, we actually need certain bacteria for good health. For example, <a href="https://journals.sagepub.com/doi/10.1177/00220345221080982">nitrate-reducing bacterial species</a> living on the tongue <a href="https://eurjmedres.biomedcentral.com/articles/10.1186/s40001-023-01413-y">convert nitrate</a> from the foods we eat (such as green leafy vegetables) to nitrite. This mechanism is important, since we swallow the nitrite that’s produced. The nitrite is then converted in the gut to nitric oxide, which <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6147587/">relaxes our blood vessels</a> and keeps blood pressure lower.</p>
<p><a href="https://www.frontiersin.org/articles/10.3389/fcimb.2019.00039/full">One study</a> has suggested that tongue scraping may actually enrich the amount of nitrate-reducing bacteria on the tongue. However, this study was only conducted using a sample of 27 people, the majority of whom were dental hygiene students. It will be important for further research to be done with more participants to better determine both the potential benefits and harms of tongue scraping.</p>
<h2>Should I use a tongue scraper?</h2>
<p>A qualified dentist would find it difficult to strongly advocate the use of tongue scrapers, due to the limited evidence supporting their use. It’s also likely that the benefits and downsides of using a tongue scraper would differ for each person. A check-up would probably be necessary before a dentist could advise – especially so they can ensure a white tongue coating isn’t due to another more serious condition, such as oral thrush or oral cancer.</p>
<p>Not everyone gets a <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7004167/">tongue biofilm</a>, either. Only <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7004167">around 10% of the people</a> develop a thick tongue coating. For these people, removing this thick layer can help counter bad breath. </p>
<p>For others, a thick tongue biofilm may only happen at certain times – for example, during <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8417575/">periods of illness</a>, stress, with <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7004167/">hormone changes</a>, or if they change their diet. So for them, a tongue scraper may only be occasionally beneficial. </p>
<p>If there’s no white coating present at all, there doesn’t seem to be much point using a tongue scraper. <a href="https://www.cochranelibrary.com/cdsr/doi/10.1002/14651858.CD005519.pub3/full">Good oral hygiene</a> will probably be enough to fix bad breath – and aggressive tongue scraping may actually risk making your tongue bleed. We also don’t yet fully know how tongue scraping will affect good bacteria on you tongue. </p>
<p>Anecdotal TikTok videos should not drive your healthcare decisions (especially if those videos haven’t been fact-checked). But in this case, TikTok may be highlighting an area where we need to do more research to better help peoples’ oral health. Producing strong evidence that tongue scrapers really do work (or don’t work), through good quality clinical studies, could lead to a change in UK guidelines in the future. </p>
<p>But until we know more, keep brushing your teeth twice daily for two minutes with a fluoride toothpaste and clean between your teeth with floss. Scrape your tongue, or clean your tongue with a toothbrush, with care, if you must.</p><img src="https://counter.theconversation.com/content/225040/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Zoe Brookes does not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.</span></em></p>
‘Tongue scraping’ has long been a part of daily hygiene routines in parts of Europe, India, South America and Africa.
Zoe Brookes, Associate Professor of Dental Education and Research, University of Plymouth
Licensed as Creative Commons – attribution, no derivatives.
tag:theconversation.com,2011:article/204656
2023-05-26T12:27:10Z
2023-05-26T12:27:10Z
Drilling down on treatment-resistant fungi with molecular machines
<figure><img src="https://images.theconversation.com/files/523869/original/file-20230502-26-xj4lbv.jpg?ixlib=rb-1.1.0&rect=19%2C12%2C2098%2C1387&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">Newly developed molecular drills may be able to fight treatment-resistant fungal infections like *Candida auris*.</span> <span class="attribution"><a class="source" href="https://www.gettyimages.com/detail/photo/candida-auris-fungi-emerging-multidrug-resistant-royalty-free-image/1028379354?phrase=Candida%20auris%20fungi%2C%20emerging%20multidrug%20resistant%20fungus">Dr_Microbe/iStock via Getty Images</a></span></figcaption></figure><p>Fungi are present on the skin of around 70% of the population, without causing harm or benefit. Some fungal infections, like athlete’s foot, are minor. Others, like <em>Candida albicans</em>, can be deadly – especially for individuals with <a href="https://doi.org/10.1038/s41577-022-00826-w">weakened immune systems</a>. </p>
<p><a href="https://doi.org/10.1086/322685">Fungal infections are on the rise</a> because of an aging population and an increased prevalence of chronic diseases. At the same time, fungi are becoming <a href="https://doi.org/10.1038/s41579-022-00720-1">more resistant to treatment</a>. As a result, fungal infections could soon become a serious public health threat.</p>
<p>In 2022, the World Health Organization released its first-ever “<a href="https://www.who.int/publications/i/item/9789240060241">Fungal Priority Pathogen List</a>,” calling for improved surveillance, public health interventions and the development of new antifungal drugs. </p>
<p>We are an <a href="https://www.jmtour.com/">interdisciplinary team</a> of <a href="https://scholar.google.com/citations?user=7g-Vv80AAAAJ&hl=en&oi=sra">chemists</a> and <a href="https://scholar.google.com/citations?user=adrn7L0AAAAJ&hl=en">biologists</a> charting a new path to tackle drug-resistant infections. We are using tiny nanoscale drills that combat harmful pathogens at the molecular level. As the traditional antimicrobial research pipeline struggles, our approach has the potential to rejuvenate the fight against these stubborn infections.</p>
<h2>Molecular machines as alternative antifungals</h2>
<p>While doctors urgently need new antifungal drugs, <a href="https://doi.org/10.1101/cshperspect.a019703">developing them is challenging</a>. First, it is difficult to develop drugs that selectively kill fungi without harming human cells because of their <a href="https://doi.org/10.2174/1389557516666160118112103">many similarities</a>.</p>
<p>Second, fungi can <a href="https://www.cdc.gov/fungal/antifungal-resistance.html">rapidly develop resistance to multiple antifungal drugs at once</a> when medications are misused or overused. As such, developing antifungal drugs is much less rewarding for drug companies than developing medications for chronic conditions like diabetes and hypertension that require long-term use.</p>
<p>One solution to this problem could lie in a <a href="https://www.nobelprize.org/prizes/chemistry/2016/summary/">Nobel Prize-winning technology</a>: molecular machines.</p>
<p>Molecular machines are synthetic compounds that rapidly rotate their components at about 3 million times per second when exposed to light. Doctors can use a light-tipped probe to activate these molecular machines to treat internal infections, or a lamp for skin infections. The light starts the machines spinning, and that rotational motion pushes them to drill through and puncture the cell’s membranes and organelles, which results in cell death. </p>
<p>Our group first used <a href="https://doi.org/10.1038/nature23657">this technology to kill cancer cells</a> in 2017. To target the right cells, molecular machines can be linked to specific peptides that bind only to the desired cells, allowing, for instance, the <a href="https://doi.org/10.1038/nature23657">targeting of specific cancer types</a>. Since then, we have used these molecules to <a href="https://doi.org/10.1126/sciadv.abm2055">kill bacteria</a>, <a href="https://doi.org/10.1021/acsami.9b22595">destroy tissue</a> and <a href="https://doi.org/10.1101/2022.11.04.515191">stimulate muscle contraction</a>. These properties make molecular machines an <a href="https://doi.org/10.1002/advs.202205781">enticing candidate technology</a> to address the growing fungal threat.</p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/526327/original/file-20230515-14468-odbqrr.png?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="A diagram showing the structure of a molecular machine as gray lines connected in the shape of several hexagons" src="https://images.theconversation.com/files/526327/original/file-20230515-14468-odbqrr.png?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/526327/original/file-20230515-14468-odbqrr.png?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=581&fit=crop&dpr=1 600w, https://images.theconversation.com/files/526327/original/file-20230515-14468-odbqrr.png?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=581&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/526327/original/file-20230515-14468-odbqrr.png?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=581&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/526327/original/file-20230515-14468-odbqrr.png?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=730&fit=crop&dpr=1 754w, https://images.theconversation.com/files/526327/original/file-20230515-14468-odbqrr.png?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=730&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/526327/original/file-20230515-14468-odbqrr.png?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=730&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
<figcaption>
<span class="caption">The 3D structure of a molecular machine. The molecular machine consists of rotor (top) and stator (bottom) portions connected by a central axle. Following light activation, molecular machines rotate rapidly, drilling into fungal cells.</span>
<span class="attribution"><span class="source">Tour Lab, Rice University</span></span>
</figcaption>
</figure>
<h2>Testing antifungal molecular machines</h2>
<p>Researchers first tested the ability of light-activated molecular machines to kill fungi in <em><a href="https://www.ncbi.nlm.nih.gov/books/NBK560624/">Candida albicans</a></em>. This yeastlike fungus can cause <a href="https://doi.org/10.1155/2013/204237">life-threatening infections</a> in immunocompromised people. Compared with conventional drugs, molecular machines killed <em>C. albicans</em> much faster.</p>
<p>Subsequent studies found that molecular machines could also kill other fungi, including molds like <em><a href="https://www.ncbi.nlm.nih.gov/books/NBK482464/">Aspergillus fumigatus</a></em> and species of dermatophytes, the types of fungi that cause skin, scalp and nail infections. Molecular machines even eliminated <a href="https://doi.org/10.3389/fmed.2018.00028">fungal biofilms</a>, which are slimy, antimicrobial-resistant communities of microorganisms that stick together on surfaces and commonly cause medical device-associated infections. </p>
<p>Unlike <a href="https://www.ncbi.nlm.nih.gov/books/NBK538168/">conventional antifungals</a>, which target the fungal cell membrane or cell wall, molecular machines localize to the fungal mitochondria. Often referred to as the “<a href="https://www.ncbi.nlm.nih.gov/books/NBK9896/">powerhouses of the cell</a>,” mitochondria produce energy to power other cellular activities. When activated with visible light, molecular machines destroy the fungal mitochondria. Once the fungal cell’s mitochondria stop working, the cell loses its energy supply and dies. </p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/524506/original/file-20230504-19-347m02.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="Two black-and-white electron microscopy images of a fungal cell. The left image shows a large, round, healthy cell, while the cell on the right is shrunken following treatment with light-activated molecular machines." src="https://images.theconversation.com/files/524506/original/file-20230504-19-347m02.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/524506/original/file-20230504-19-347m02.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=360&fit=crop&dpr=1 600w, https://images.theconversation.com/files/524506/original/file-20230504-19-347m02.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=360&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/524506/original/file-20230504-19-347m02.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=360&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/524506/original/file-20230504-19-347m02.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=452&fit=crop&dpr=1 754w, https://images.theconversation.com/files/524506/original/file-20230504-19-347m02.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=452&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/524506/original/file-20230504-19-347m02.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=452&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
<figcaption>
<span class="caption"><em>Candida albicans</em> before and after being exposed to light-activated molecular machines. Molecular machines puncture <em>C. albicans</em>‘ cell wall and intracellular organelles, eventually killing the fungal cell.</span>
<span class="attribution"><span class="source">Matthew Meyer/Rice University.</span></span>
</figcaption>
</figure>
<p>At the same time, molecular machines also <a href="https://doi.org/10.4155/fmc-2016-0050">disrupt the tiny pumps</a> that remove antifungal agents from the cell, thus preventing the cell from fighting back. Because these molecular machines act by a mechanical instead of a chemical mechanism, fungi are unlikely to develop defenses against this treatment.</p>
<p>In lab experiments, combining light-activated molecular machines with conventional antifungal drugs also reduced the amount of fungi in <em>C. albicans</em>-infected worms and in pig nails infected with <em>Trichophyton rubrum</em>, the most common cause of <a href="https://www.ncbi.nlm.nih.gov/books/NBK8301/">athlete’s foot</a>.</p>
<h2>New frontiers for fighting fungal infections</h2>
<p>These results suggest that combining molecular machines with conventional antifungals can improve existing therapies and provide new options for treating resistant fungal strains. This strategy could also help reduce the side effects of traditional antifungals, such as gastrointestinal upset and skin reactions. </p>
<p>Fungal infection rates will likely continue to rise. As such, the need for new treatments will only become more urgent. Climate change is already causing <a href="https://doi.org/10.1371/journal.ppat.1009503">new human pathogenic fungi</a> to emerge and spread, including <a href="https://www.ncbi.nlm.nih.gov/books/NBK563297/"><em>Candida auris</em></a>. <em>C. auris</em> is often resistant to treatment and spread rapidly in health care facilities <a href="https://doi.org/10.1111/myc.13471">during the COVID-19 pandemic</a>. <a href="https://www.cdc.gov/media/releases/2023/p0320-cauris.html">According to the Centers for Disease Control and Prevention</a>, strained health care systems, overuse of immunosuppressants and misuse of antibiotics have all been implicated in <a href="https://theconversation.com/how-do-candida-auris-and-other-fungi-develop-drug-resistance-a-microbiologist-explains-203495">outbreaks of <em>C. auris</em></a>.</p>
<p>In the future, researchers could use <a href="https://doi.org/10.1038/s41586-023-05905-z">artificial intelligence</a> to create better antifungal molecular machines. By using AI to predict how different molecular machines will interact with fungi and human cells, we can develop safer and more effective antifungal molecules that specifically kill fungi without harming healthy cells.</p>
<p>Antifungal molecular machines are still in the early stages of development and are not yet available for routine clinical use. However, continuing research gives hope that these machines could one day provide better treatments for fungal infections and other infectious diseases.</p><img src="https://counter.theconversation.com/content/204656/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Ana L. Santos receives funding from the European Union's Horizon 2020 research and innovation programme under the Marie Skłodowska-Curie grant agreement No. 843116.</span></em></p><p class="fine-print"><em><span>Jacob Beckham receives funding from the National Science Foundation Graduate Research Fellowship Program. </span></em></p><p class="fine-print"><em><span>James M. Tour receives funding from the Discovery Institute and the Robert A. Welch Foundation (C-2017-20190330). Rice University owns intellectual property on the use of electromagnetic (light) activation of molecular machines for the killing of cells. This intellectual property has been licensed to a company in which James M. Tour is a stockholder, although he is not an officer or director of that company.</span></em></p>
Fungal infections can be among the hardest to treat, and since the pandemic began they’ve become only more common. To prevent future antifungal resistance, scientists have developed tiny molecular drills.
Ana L. Santos, Postdoctoral Fellow in Microbiology, Rice University
Jacob Beckham, Graduate Student in Chemistry, Rice University
James Tour, Professor of Chemistry, Rice University
Licensed as Creative Commons – attribution, no derivatives.
tag:theconversation.com,2011:article/203495
2023-05-03T12:10:09Z
2023-05-03T12:10:09Z
How do ‘Candida auris’ and other fungi develop drug resistance? A microbiologist explains
<figure><img src="https://images.theconversation.com/files/523473/original/file-20230428-18-9slhum.jpg?ixlib=rb-1.1.0&rect=0%2C0%2C2073%2C1368&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">Candidiasis is a severe fungal infection that can spread easily in medical facilities.</span> <span class="attribution"><a class="source" href="https://flic.kr/p/8ysD2e">Atlas of Pulmonary Pathology/Flickr</a>, <a class="license" href="http://creativecommons.org/licenses/by-sa/4.0/">CC BY-SA</a></span></figcaption></figure><p>One of the scariest things you can be told when at a doctor’s office is “You have an antimicrobial-resistant infection.” That means the bacteria or fungus making you sick can’t be easily killed with common antibiotics or antifungals, making treatment more challenging. You might have to take a combination of drugs for weeks to overcome the infection, which could result in more severe side effects.</p>
<p>Unfortunately, this diagnosis is <a href="https://www.who.int/publications/i/item/9789240062702">becoming more common around the world</a>.</p>
<p>The yeast <em><a href="https://doi.org/10.1128/jcm.01588-17">Candida auris</a></em> has recently emerged as a potentially dangerous fungal infection for hospital patients and nursing home residents. First <a href="https://doi.org/10.3947%2Fic.2022.0008">discovered in the late 2000s</a>, <em>Candida auris</em> has very quickly become a <a href="https://doi.org/10.3390/microorganisms9040807">major health challenge</a> due to its ease of spread and ability to resist common antifungal drugs.</p>
<p>How did this fungus become so strong, and what can researchers and physicians do to combat it? </p>
<p><a href="https://scholar.google.com/citations?user=U69z9VsAAAAJ&hl=en&oi=ao">I am a microbiologist</a> researching new ways to kill fungi. <em>Candida auris</em> and other fungi use three common cellular tricks to overcome treatments. Luckily, exciting new research hints at ways we can still fight this fungus.</p>
<figure>
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<figcaption><span class="caption">Drug-resistant <em>Candida auris</em> infections are on the rise in the U.S. and around the world.</span></figcaption>
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<h2>Targeting the sensitive parts of fungal cells</h2>
<p>Fungal cells contain a structure called a <a href="https://doi.org/10.1128/microbiolspec.funk-0035-2016">cell wall</a> that helps maintain their shape and protects them from the environment. Fungal cell walls are constructed in part from several different types of polysaccharides, which are long strings of sugar molecules linked together. </p>
<p>Two polysaccharides found in almost all fungal cell walls are <a href="https://doi.org/10.1016/j.mib.2010.05.002">chitin</a> and <a href="https://doi.org/10.1016/j.tcsw.2019.100022">beta-glucan</a>. The fungal cell wall is an attractive target for drugs because human cells do not have a cell wall, so drugs that block chitin and beta-glucan production will have fewer side effects. </p>
<p>Some of the most common drugs used to treat fungal infections are called <a href="https://doi.org/10.4103%2F0253-7613.62396">echinocandins</a>. These drugs stop fungal cells from making beta-glucan, which significantly weakens their cell wall. This means the fungal cell can’t maintain its shape well. While the fungus is struggling to grow or is breaking apart, your immune system has a much better chance of fighting off the infection. </p>
<h2>How fungi become drug resistant</h2>
<p>Unfortunately, some strains of <em>Candida auris</em> are resistant to echinocandin treatment. But how does the fungus actually do it? For decades, scientists have been studying how fungi overcome drugs designed to weaken or kill them. In the case of echinocandins, <em>Candida auris</em> commonly uses three tricks to beat these treatments: <a href="https://doi.org/10.1128/AAC.00238-18">hide</a>, <a href="https://doi.org/10.1101%2Fcshperspect.a019752">build</a> and <a href="https://doi.org/10.3389/fmicb.2019.02573">change</a>. </p>
<p>The first trick is to hide in a complex mixture of sugars, proteins, DNA and cells <a href="https://doi.org/10.1128/msphere.00458-19">called a biofilm</a>. Made with irregular 3D structures, biofilms have lots of places for cells to hide. Drugs aren’t good at penetrating biofilms, so they can’t access and kill cells deep inside. Biofilms are especially problematic when they <a href="https://doi.org/10.3390/antibiotics4010001">grow on</a> <a href="https://doi.org/10.2147/ijn.s353071">medical equipment</a> like ventilators or catheters. Once free of a biofilm, cells that have gained the ability to resist the drugs a patient was taking become more dangerous.</p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/523471/original/file-20230428-26-n4nxfs.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="Microscopy image of two types of Candida attaching to each other" src="https://images.theconversation.com/files/523471/original/file-20230428-26-n4nxfs.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/523471/original/file-20230428-26-n4nxfs.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=300&fit=crop&dpr=1 600w, https://images.theconversation.com/files/523471/original/file-20230428-26-n4nxfs.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=300&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/523471/original/file-20230428-26-n4nxfs.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=300&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/523471/original/file-20230428-26-n4nxfs.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=377&fit=crop&dpr=1 754w, https://images.theconversation.com/files/523471/original/file-20230428-26-n4nxfs.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=377&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/523471/original/file-20230428-26-n4nxfs.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=377&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
<figcaption>
<span class="caption">This image shows <em>Candida albicans</em> (red) producing branching filaments that allow it to attach to <em>Candida glabrata</em> (green), forming biofilms. Both of these species can cause infections in people.</span>
<span class="attribution"><a class="source" href="https://flic.kr/p/HE7JbY">Edgerton Lab, State University of New York at Buffalo/Flickr</a>, <a class="license" href="http://creativecommons.org/licenses/by-nc/4.0/">CC BY-NC</a></span>
</figcaption>
</figure>
<p>The second trick fungi use to evade treatment is to build cell walls differently. Fungal cells treated with echinocandins can’t make beta-glucan. So instead, they start to <a href="https://doi.org/10.3109/13693786.2011.577104">make more chitin</a>, another important polysaccharide in the fungal cell wall. Echinocandins are unable to stop chitin production, so the fungus is still able to build a strong cell wall and avoid being killed. While there are some drugs that can <a href="https://doi.org/10.3390/jof6040261">stop chitin production</a>, none are currently approved for use in people. </p>
<p>The third trick fungi rely on is to <a href="https://doi.org/10.3389/fmicb.2019.02788">change the shape of the</a> <a href="https://doi.org/10.1093/cid/civ791">beta-glucan production enzyme</a> so echinocandins cannot block it. These mutations allow beta-glucan production to continue even in the presence of the drug. It is not surprising that <em>Candida</em> uses this trick to resist antifungal drugs since it is <a href="https://doi.org/10.1111%2Fnyas.12831">very effective</a> at keeping the cells alive. </p>
<h2>New tactics to fight fungi</h2>
<p>What can be done to treat echinocandin-resistant fungal infections? Thankfully, scientists and physicians are researching new ways to kill <em>Candida auris</em> and similar fungi. </p>
<p>The first approach is to find new drugs. For example, there are two drugs in development, <a href="https://doi.org/10.3390/antibiotics9050227">rezafungin</a> and <a href="https://doi.org/10.4155%2Ffmc-2018-0465">ibrexafungerp</a>, that appear to be able to stop beta-glucan production even in fungi resistant to echinocandins. </p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/523474/original/file-20230428-14-z7579n.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="Microscopy image of budding yeast cells" src="https://images.theconversation.com/files/523474/original/file-20230428-14-z7579n.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/523474/original/file-20230428-14-z7579n.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=450&fit=crop&dpr=1 600w, https://images.theconversation.com/files/523474/original/file-20230428-14-z7579n.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=450&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/523474/original/file-20230428-14-z7579n.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=450&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/523474/original/file-20230428-14-z7579n.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=566&fit=crop&dpr=1 754w, https://images.theconversation.com/files/523474/original/file-20230428-14-z7579n.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=566&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/523474/original/file-20230428-14-z7579n.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=566&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
<figcaption>
<span class="caption">This microscopy image shows budding yeast cells.</span>
<span class="attribution"><a class="source" href="https://www.gettyimages.com/detail/photo/budding-yeast-cell-in-gram-stain-royalty-free-image/1464904014">toeytoey2530/iStock via Getty Images Plus</a></span>
</figcaption>
</figure>
<p>A complementary approach my research group is exploring is whether a class of enzymes called <a href="https://doi.org/10.1007/s11274-016-2068-6">glycoside hydrolases</a> might also be able to combat drug-resistant fungi. Some of these enzymes actively destroy the fungal cell wall, breaking apart both beta-glucan and chitin at the same time, which could potentially help prevent fungi from surviving on medical equipment or on hospital surfaces.</p>
<p>My lab’s work on discovering enzymes that strongly degrade fungal cell walls is part of a new strategy to combat antifungal resistance that uses a combination of approaches to kill fungi. But the end goal of this research is the same: having a physician tell you, “You’ve got a fungal infection, but we have a good treatment for it now.”</p><img src="https://counter.theconversation.com/content/203495/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Jeffrey Gardner receives funding from the National Science Foundation (NSF) and the National Institutes of Health (NIH).</span></em></p>
Multidrug-resistant fungal infections are an emerging global health threat. Figuring out how fungi evade treatments offers new avenues to counter resistance.
Jeffrey Gardner, Associate Professor of Biological Sciences, University of Maryland, Baltimore County
Licensed as Creative Commons – attribution, no derivatives.
tag:theconversation.com,2011:article/200226
2023-04-11T12:04:46Z
2023-04-11T12:04:46Z
Looming behind antibiotic resistance is another bacterial threat – antibiotic tolerance
<figure><img src="https://images.theconversation.com/files/519955/original/file-20230407-28-ddggzn.jpg?ixlib=rb-1.1.0&rect=0%2C3%2C2309%2C1292&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">Tolerant bacteria are dormant until an antibiotic threat has passed, then reemerge to conduct business as usual.</span> <span class="attribution"><a class="source" href="https://www.gettyimages.com/detail/photo/pseudomonas-aeruginosa-bacterium-illustration-royalty-free-image/1201441647">Christoph Burgstedt/Science Photo Library via Getty Images</a></span></figcaption></figure><p>Have you ever had a nasty infection that just won’t seem to go away? Or a runny nose that keeps coming back? You may have been dealing with a bacterium that is tolerant of, though not yet resistant to, antibiotics. </p>
<p>Antibiotic resistance is a huge problem, contributing to <a href="https://doi.org/10.1016/S0140-6736(21)02724-0">nearly 1.27 million deaths worldwide in 2019</a>. But antibiotic tolerance is a covert threat that researchers have only recently begun to explore. </p>
<p><a href="https://doi.org/10.1371/journal.ppat.1008892">Antibiotic tolerance</a> happens when a bacterium manages to survive for a long time after being exposed to an antibiotic. While <a href="https://doi.org/10.1128/microbiolspec.VMBF-0016-2015">antibiotic-resistant</a> bacteria flourish even in the presence of an antibiotic, tolerant bacteria often exist in a dormant state, neither growing nor dying but putting up with the antibiotic until they can “reawaken” once the stress is gone. Tolerance has been <a href="https://www.doi.org/10.1126/science.aaj2191">linked to the spread of antibiotic resistance</a>.</p>
<p>I am a <a href="https://doerr.wicmb.cornell.edu/current-lab-members/">microbiologist</a> who studies antibiotic tolerance, and I seek to uncover what triggers tolerant bacteria to enter a protective dormant slumber. By understanding why bacteria have the ability to become tolerant, researchers hope to develop ways to avoid the spread of this ability. The exact mechanism that sets tolerance apart from resistance has been unclear. But one possible answer may reside in a process that has been overlooked for decades: how bacteria <a href="https://doi.org/10.3389/fmicb.2020.577564">create their energy</a>.</p>
<h2>Cholera and antibiotic tolerance</h2>
<p>Many antibiotics are designed to <a href="https://doi.org/10.1039/C6MD00585C">break through the bacteria’s outer defenses</a> like a cannonball through a stone fortress. Resistant bacteria are immune to the cannonball because they can either destroy it before it damages their outer wall or change their own walls to be able to withstand the impact. </p>
<p>Tolerant bacteria can remove their wall entirely and avoid damage altogether. No wall, no target for the cannonball to smash. If the threat goes away before too long, the bacterium can rebuild its wall to protect it from other environmental dangers and resume normal functions. However, it is still unknown how bacteria know the antibiotic threat is gone, and what exactly triggers their reawakening. </p>
<p>My colleagues and I at the <a href="https://doerr.wicmb.cornell.edu/">Dörr Lab at Cornell University</a> are trying to understand processes of activation and reawakening in the tolerant bacteria responsible for cholera, <em>Vibrio cholerae</em>. <em>Vibrio</em> is <a href="https://doi.org/10.3389/fitd.2021.691604">rapidly evolving resistance</a> against various types of antibiotics, and doctors are concerned. As of 2010, <em>Vibrio</em> is already <a href="https://doi.org/10.1016/j.vaccine.2019.06.031">resistant to 36 different antibiotics</a>, and this number is expected to continue rising.</p>
<p>To study how <em>Vibrio</em> develops resistance, we chose a strain that is tolerant to a class of antibiotics <a href="https://doi.org/10.3389/fpubh.2016.00231">called beta-lactams</a>. Beta-lactams are the cannonball sent to destroy the bacteria’s fortress, and <em>Vibrio</em> adapts by activating two genes that temporarily remove its cell wall. I witnessed this phenomenon using a microscope. After removing its cell wall, the bacteria activate even more genes that morph it into fragile globs that can survive the effects of the antibiotic. Once the antibiotic is removed or degraded, <em>Vibrio</em> returns to its normal rod shape and continues to grow. </p>
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<figcaption><span class="caption">Normally rod-shaped <em>Vibrio cholerae</em> remove their cell walls and turn into globs in the presence of penicillin, enabling them to survive longer.</span></figcaption>
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<figcaption><span class="caption"><em>Vibrio cholerae</em> revert back to their rod-shaped structure once the antibiotic threat is removed.</span></figcaption>
</figure>
<p>In people, this process of tolerance is seen when a doctor prescribes an antibiotic, typically doxycycline, to a patient infected with cholera. The antibiotic temporarily seems to stop the infection. But then the symptoms start back up again because the antibiotics never fully cleared the bacteria in the first place.</p>
<p>The ability to revert back to normal and grow after the antibiotic is gone is the key to tolerant survival. Exposing <em>Vibrio</em> to an antibiotic for a long enough time would eventually kill it. But a standard course of antibiotics often isn’t long enough to get rid of all the bacteria even in their fragile state.</p>
<p>However, taking a medicine for a prolonged period can harm healthy bacteria and cells, causing further discomfort and illness. Additionally, <a href="https://doi.org/10.3389/fcimb.2020.572912">misuse and extended exposure</a> to antibiotics can increase the chances of other bacteria residing in the body becoming resistant.</p>
<h2>Other bacteria developing tolerance</h2>
<p><em>Vibrio</em> isn’t the only species to exhibit tolerance. In fact, researchers have recently identified many infectious bacteria that have developed tolerance. A bacteria family called <a href="https://doi.org/10.1371/journal.pbio.1001928">Enterobacteriaceae</a>, which include major food-borne disease pathogens <a href="https://doi.org/10.1371/journal.pbio.1001928"><em>Salmonella</em></a>, <a href="https://doi.org/10.1128/AAC.01282-08"><em>Shigella</em></a> and <a href="https://doi.org/10.1038/s41598-021-85509-7"><em>E. coli</em></a>, are just a few of the many types of bacteria that are capable of antibiotic tolerance.</p>
<p>As every bacterium is unique, the way one develops tolerance seems to be as well. Some bacteria, like <em>Vibrio</em>, <a href="https://doi.org/10.1128/AAC.00756-19">erase their cell walls</a>. Others can <a href="https://doi.org/10.1038/nchembio.1754">alter their energy sources, increase their ability to move or simply pump out</a> the antibiotic.</p>
<p>I recently found that a <a href="https://doi.org/10.1128/jb.00476-22">bacterium’s metabolism</a>, or the way it breaks down “food” to make energy, may play a significant role in its ability to become tolerant. Different structures within a bacterium, including its outer wall, are made of specific building blocks like proteins. Stopping the bacterium’s ability to craft these pieces weakens its wall, making it more likely to take damage from the outside environment before it can take the wall down.</p>
<h2>Tolerance and resistance are connected</h2>
<p>Although there has been considerable research on how bacteria develop tolerance, a key piece of the puzzle that has been neglected is how tolerance leads to resistance.</p>
<p>In 2016, researchers discovered how to <a href="https://doi.org/10.1038/nmicrobiol.2016.20">make bacteria tolerant in the laboratory</a>. After repeated exposure to different antibiotics, <em>E. coli</em> cells were able to adapt and survive. DNA, the genetic material containing instructions for cell function, is a fragile molecule. When DNA is damaged rapidly by stress, such as antibiotic exposure, the cell’s repair mechanisms tend to mess up and cause mutations that can create resistance and tolerance. Because <em>E. coli</em> is similar to many different types of bacteria, these researchers’ findings revealed that, ironically, essentially any bacteria can develop tolerance if pushed to their limits by the antibiotics meant to kill them. </p>
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<figcaption><span class="caption">Bacteria form large communities in biofilms.</span></figcaption>
</figure>
<p>Another recent key discovery was that the longer bacteria remain tolerant, the more likely they are to <a href="https://doi.org/10.1073/pnas.2209043119">develop mutations leading to resistance</a>. Tolerance allows bacteria to develop a resistance mutation that reduces their chances of being killed during antibiotic treatment. This is especially relevant to bacterial communities often seen in <a href="https://doi.org/10.2147/IDR.S379502">biofilms that tend to coat high-touch surfaces in hospitals</a>. Biofilms are slimy layers of bacteria that ooze a protective jelly that makes antibiotic treatment difficult and DNA sharing between microbes easy. They can induce bacteria to evolve resistance. These conditions are thought to mimic what could be happening during antibiotic-treated infections, in which many bacteria are living next to one another and sharing DNA. </p>
<p>Researchers are calling for more research into antibiotic tolerance with the hope that it will lead to <a href="https://doi.org/10.1128/mBio.02095-19">more robust treatments</a> in both infectious diseases and cancers. And there is reason to be hopeful. In one promising development, a mouse study found that <a href="https://doi.org/10.1126/science.1211037">decreasing tolerance also reduced resistance</a>. </p>
<p>Meanwhile, there are steps everyone can take to aid in the battle against antibiotic tolerance and resistance. You can do this by <a href="https://www.who.int/news-room/fact-sheets/detail/antibiotic-resistance">taking an antibiotic exactly as prescribed</a> by a doctor and finishing the entire bottle. Brief, inconsistent exposure to a medicine primes bacteria to become tolerant and eventually resistant. Smarter use of antibiotics by everyone can stop the evolution of tolerant bacteria.</p><img src="https://counter.theconversation.com/content/200226/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Megan Keller receives funding from the National Science Foundation Graduate Research Fellowship Program and the National Institutes of Health (NSF GRFP #DGE-1650441 and NIH R01-AI143704)</span></em></p>
Antibiotic resistance has contributed to millions of deaths worldwide. Research suggests that any bacteria can develop antibiotic tolerance, and possibly resistance, when pushed to their limits.
Megan Keller, Ph.D. Candidate in Microbiology, Cornell University
Licensed as Creative Commons – attribution, no derivatives.
tag:theconversation.com,2011:article/181824
2022-04-26T18:39:43Z
2022-04-26T18:39:43Z
Disease-causing parasites can hitch a ride on plastics and potentially spread through the sea, new research suggests
<figure><img src="https://images.theconversation.com/files/459606/original/file-20220425-25-tfbr1v.png?ixlib=rb-1.1.0&rect=0%2C0%2C2310%2C1296&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">The sticky biofilms that form on microplastics can harbor disease-causing pathogens and help them spread.</span> <span class="attribution"><a class="source" href="https://www.gettyimages.com/detail/photo/sea-water-contaminated-by-micro-plastic-royalty-free-image/1036767280">Tunatura/iStock via Getty Images Plus</a></span></figcaption></figure><p>Typically when people hear about plastic pollution, they might envision seabirds with bellies full of trash or sea turtles with plastic straws in their noses. However, plastic pollution poses another threat that’s invisible to the eye and has important consequences for both human and animal health.</p>
<p><a href="https://doi.org/10.1016/j.marenvres.2016.05.012">Microplastics</a>, tiny plastic particles present in many cosmetics, can form when larger materials, such as clothing or fishing nets, break down in water. Microplastics are now widespread in the ocean and have been found in fish and shellfish, including <a href="https://doi.org/10.1016/j.envpol.2014.06.010">those that</a> <a href="https://doi.org/10.1016/j.marpolbul.2018.05.047">people eat</a>.</p>
<p>As <a href="https://scholar.google.com/citations?user=v15DbVcAAAAJ&hl=en">researchers</a> <a href="https://shapirolab.vetmed.ucdavis.edu/people/emma-zhang">studying</a> how waterborne pathogens spread, we wanted to better understand what happens when microplastics and disease-causing pathogens end up in the same body of water. In our recent study published in the journal <a href="https://doi.org/10.1038/s41598-022-10485-5">Scientific Reports</a>, we found that pathogens from land can hitch a ride to the beach on microscopic pieces of plastic, providing a new way for germs to concentrate along coastlines and travel to the deep sea.</p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/459605/original/file-20220425-2721-yy4mz1.png?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="Aerial shot of boat floating through plastic pollution on water" src="https://images.theconversation.com/files/459605/original/file-20220425-2721-yy4mz1.png?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/459605/original/file-20220425-2721-yy4mz1.png?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=400&fit=crop&dpr=1 600w, https://images.theconversation.com/files/459605/original/file-20220425-2721-yy4mz1.png?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=400&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/459605/original/file-20220425-2721-yy4mz1.png?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=400&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/459605/original/file-20220425-2721-yy4mz1.png?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/459605/original/file-20220425-2721-yy4mz1.png?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/459605/original/file-20220425-2721-yy4mz1.png?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=503&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
<figcaption>
<span class="caption">Microplastic pollution has negative consequences for human, animal and environmental health.</span>
<span class="attribution"><a class="source" href="https://www.gettyimages.com/detail/photo/plastic-pollution-in-the-ocean-man-cleaning-plastic-royalty-free-image/1301941387">Yunaidi Joepoet/Moment via Getty Images</a></span>
</figcaption>
</figure>
<h2>Investigating how plastics and pathogens interact</h2>
<p>We focused on three parasites that are <a href="https://www.who.int/publications/i/item/9789241563826">common contaminants</a> in marine water and seafoods: the single-celled protozoans <em>Toxoplasma gondii</em> (<em>Toxo</em>), <em>Cryptosporidium</em> (<em>Crypto</em>) and <em>Giardia</em>. These parasites end up in waterways when feces from infected animals, and sometimes people, contaminate the environment.</p>
<p><a href="https://doi.org/10.1146/annurev.publhealth.18.1.135"><em>Crypto</em> and <em>Giardia</em></a> cause gastrointestinal disease that can be deadly in young children and immunocompromised individuals. <a href="https://doi.org/10.1128/cmr.05013-11"><em>Toxo</em></a> can cause lifelong infections in people, and can prove fatal for those with weak immune systems. Infection in <a href="https://www.waterpathogens.org/book/toxoplasma-gondii">pregnant women</a> can also cause miscarriage or blindness and neurological disease in the baby. <em>Toxo</em> also infects a wide range of marine wildlife and kills endangered species, including <a href="https://doi.org/10.7589/0090-3558-39.3.495">southern</a> <a href="https://doi.org/10.1017/s0031182015001377">sea otters</a>, <a href="https://doi.org/10.1016/j.vetpar.2012.11.001">Hector’s dolphins</a> and <a href="https://doi.org/10.3354/dao03047">Hawaiian monk seals</a>.</p>
<p>To test whether these parasites can stick onto plastic surfaces, we first placed microplastic beads and fibers in beakers of seawater in our lab for two weeks. This step was important to induce the formation of a <a href="https://www.livescience.com/57295-biofilms.html">biofilm</a> – a sticky layer of bacteria and gellike substances that coats plastics when they enter fresh or marine waters. Researchers also call this sticky layer an <a href="https://doi.org/10.1126/sciadv.abd1211">eco-corona</a>. We then added the parasites to the test bottles and counted how many became stuck on the microplastics or remained freely floating in the seawater over a seven-day period.</p>
<figure>
<iframe width="440" height="260" src="https://www.youtube.com/embed/pHLP5CZMnL4?wmode=transparent&start=0" frameborder="0" allowfullscreen=""></iframe>
<figcaption><span class="caption">Biofilms are vast communities of microbes that can form on almost any surface, including your teeth.</span></figcaption>
</figure>
<p>We found that significant numbers of parasites were clinging to the microplastic, and these numbers were increasing over time. So many parasites were binding to the sticky biofilms that, gram for gram, plastic had two to three times more parasites than did seawater.</p>
<p>Surprisingly, we found that microfibers (commonly from clothes and fishing nets) harbored a greater number of parasites than did microbeads (commonly found in cosmetics). This result is important, because microfibers are the most common type of microplastic found in <a href="https://doi.org/10.1016/j.marpolbul.2013.12.035">marine waters</a>, on <a href="https://doi.org/10.1016/j.scitotenv.2017.09.100">coastal beaches</a> and even in <a href="https://doi.org/10.1016/j.marpolbul.2018.12.039">seafood</a>.</p>
<h2>Plastics could change ocean disease transmission</h2>
<p>Unlike <a href="https://doi.org/10.1016/j.marenvres.2016.07.004">other pathogens</a> that are commonly found in seawater, the pathogens we focused on are derived from terrestrial animal and human hosts. Their presence in marine environments is entirely due to <a href="https://doi.org/10.1016/j.pt.2004.08.008">fecal waste</a> <a href="https://dx.doi.org/10.1016%2Fj.fawpar.2019.e00049">contamination</a> that ends up in the sea. Our study shows that microplastics could also serve as transport systems for these parasites.</p>
<p>These pathogens <a href="https://doi.org/10.1016/j.pt.2004.08.008">cannot replicate in the sea</a>. Hitching a ride on plastics into marine environments, however, could fundamentally alter how these pathogens move around in marine waters. We believe that microplastics that float along the surface could potentially <a href="https://www.nationalgeographic.com/science/article/microplastics-in-virtually-every-crevice-on-earth">travel long distances</a>, spreading pathogens far from their original sources on land and bringing them to regions they would not otherwise be able to reach.</p>
<p>On the other hand, plastics that sink will concentrate pathogens on the sea bottom, where filter-feeding animals like clams, mussels, oysters, abalone and other shellfish live. A sticky biofilm layer can camouflage synthetic plastics in seawater, and animals that typically eat dead organic material may <a href="https://doi.org/10.1126/sciadv.abd1211">unintentionally ingest them</a>. Future experiments will test whether live oysters placed in tanks with and without plastics end up ingesting more pathogens.</p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/459555/original/file-20220425-14-c1bmzs.png?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="Diagram illustrating how pathogens can associate with biofilms on microplastics and spread through the sea." src="https://images.theconversation.com/files/459555/original/file-20220425-14-c1bmzs.png?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/459555/original/file-20220425-14-c1bmzs.png?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=344&fit=crop&dpr=1 600w, https://images.theconversation.com/files/459555/original/file-20220425-14-c1bmzs.png?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=344&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/459555/original/file-20220425-14-c1bmzs.png?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=344&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/459555/original/file-20220425-14-c1bmzs.png?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=432&fit=crop&dpr=1 754w, https://images.theconversation.com/files/459555/original/file-20220425-14-c1bmzs.png?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=432&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/459555/original/file-20220425-14-c1bmzs.png?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=432&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
<figcaption>
<span class="caption">The biofilms that form on microplastics can help pathogens spread through the sea.</span>
<span class="attribution"><span class="source">Emma Zhang</span>, <a class="license" href="http://creativecommons.org/licenses/by-nc-nd/4.0/">CC BY-NC-ND</a></span>
</figcaption>
</figure>
<h2>A One Health problem</h2>
<p><a href="https://www.cdc.gov/onehealth/basics/index.html">One Health</a> is an approach to research, policy and veterinary and human medicine that emphasizes the close connection of animal, human and environmental health. While it may seem that plastic pollution affects only animals in the ocean, it can ultimately have consequences on human health.</p>
<p>Our project was conducted by a multidisciplinary team of experts, ranging from microplastics researchers and parasitologists to shellfish biologists and epidemiologists. This study highlights the importance of collaboration across human, animal and environmental disciplines to address a challenging problem affecting our shared marine environment.</p>
<p>Our hope is that better understanding how microplastics can move disease-causing pathogens in new ways will encourage others to think twice before reaching for that plastic straw or polyester T-shirt.</p>
<p>[<em>Get fascinating health and science news in your inbox.</em> <a href="https://memberservices.theconversation.com/newsletters/?nl=science&source=inline-science-fascinating">Sign up for The Conversation’s weekly science newsletter</a>.]</p><img src="https://counter.theconversation.com/content/181824/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Karen Shapiro receives funding from the Ocean Protection Council and California Sea Grant program
(Grant #19-0592).</span></em></p><p class="fine-print"><em><span>Emma Zhang received student funding from STAR (Students Training in Advanced Research) Program at UC Davis School fo Veterinary Medicine.</span></em></p>
Normally land-bound pathogens that cause deadly diseases for both humans and animals can cling to microplastics and end up in your seafood.
Karen Shapiro, Associate Professor of Pathology, Microbiology and Immunology, University of California, Davis
Emma Zhang, Veterinary researcher, University of California, Davis
Licensed as Creative Commons – attribution, no derivatives.
tag:theconversation.com,2011:article/115110
2019-04-15T10:54:17Z
2019-04-15T10:54:17Z
A frenemy fungus provides clues about a new deadly one
<figure><img src="https://images.theconversation.com/files/268689/original/file-20190410-2914-1us6jlb.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">The fungus _Candida albicans_ causes candidiasis, or thrush.</span> <span class="attribution"><a class="source" href="https://www.shutterstock.com/image-illustration/3d-illustration-fungi-candida-albicans-which-400086208?src=dmmLdGO2gswZgJLD5Idc6g-1-4">Kateryna Kon/Shutterstock.com</a></span></figcaption></figure><p>It seems like every few years there’s a virus or bacterium that threatens human health in a new way. But a new fungus that is a threat to humans? That doesn’t happen very often. That’s why we in the medical mycology community – the people who study dangerous fungi – are so intrigued and concerned by news reports about a new, deadly fungus called <em>Candida auris</em>.</p>
<p><em>C. auris</em> is believed to have been first identified in 2009 in the ear canal of a patient in <a href="https://doi.org/10.1111/j.1348-0421.2008.00083.x">Japan</a>, but has taken the medical community by surprise with its rapid spread across the globe in the last decade. <em>C. auris</em> has now been detected in about 20 countries and shows no evidence of <a href="https://www.nytimes.com/2019/04/06/health/drug-resistant-candida-auris.html?module=inline">stopping</a>. </p>
<p>What makes this well-traveled fungus fascinating and scary? Unlike other species of <em>Candida</em>, it is known to survive in hospital rooms for prolonged periods of time and is responsible for several outbreaks due to patient-to-patient transmission. The most concerning characteristic of this fungus, however, is its ability to withstand <a href="https://doi.org/10.1093/mmy/myy054">anti-fungal treatment</a>. </p>
<p>We are a team of medical mycologists working at Tufts University and specializing in the study of a different fungus, <em>Candida albicans</em>, and how it affects human health. We have been interested in <em>C. albicans</em> for years because its interactions with humans are so complex: Sometimes it seems friendly and sometimes it is our enemy. The new fungus <em>C. auris</em> seems very mysterious but we believe we can use what we have learned from studying other fungi to deal with this new organism. </p>
<h2>A formidable new adversary</h2>
<p>Fungi are among the most successful, resilient and fascinating groups of organisms on Earth. In fact, the largest organism on Earth is believed to be a <a href="http://www.bbc.com/earth/story/20141114-the-biggest-organism-in-the-world">mushroom</a>. We do not know exactly how long fungi have been around, but it is believed that they might be some of the <a href="https://www.smithsonianmag.com/smart-news/440-million-years-old-fossil-fungus-oldest-land-organism-ever-discovered-180958268/">oldest land dwellers on Earth</a>. </p>
<p>During their existence, fungi have dealt with a multitude of global catastrophes, including five – and perhaps a coming sixth – mass extinctions. In order to survive and thrive during these extreme conditions, fungi have developed amazing strategies which have allowed them to conquer every environment imaginable. Out of the estimated <a href="http://doi.org/10.1101/cshperspect.a019273">1.5 to 5 million</a> fungal species on Earth, about 300 are able to cause disease in humans. In the case of <em>C. auris</em>, we know whom it is related to, but we do not know where it came from or how people acquire it.</p>
<figure class="align-right zoomable">
<a href="https://images.theconversation.com/files/268859/original/file-20190411-44776-1v8h7r1.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="" src="https://images.theconversation.com/files/268859/original/file-20190411-44776-1v8h7r1.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=237&fit=clip" srcset="https://images.theconversation.com/files/268859/original/file-20190411-44776-1v8h7r1.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=400&fit=crop&dpr=1 600w, https://images.theconversation.com/files/268859/original/file-20190411-44776-1v8h7r1.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=400&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/268859/original/file-20190411-44776-1v8h7r1.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=400&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/268859/original/file-20190411-44776-1v8h7r1.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/268859/original/file-20190411-44776-1v8h7r1.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/268859/original/file-20190411-44776-1v8h7r1.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=503&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
<figcaption>
<span class="caption">Fungi are important in the natural environment as well as food and drug production.</span>
<span class="attribution"><a class="source" href="https://www.shutterstock.com/image-photo/penicillium-ascomycetous-fungi-major-importance-natural-747671938?src=Fh67ni9zEuTtVW02o3u5sA-1-4">Rattiya Thongdumhyu/Shutterstock.com</a></span>
</figcaption>
</figure>
<p>Unlike anti-bacterials, the number of types of useful anti-fungal drugs is quite <a href="https://doi.org/10.1038/nrd.2017.46">limited</a>. There are only three main classes, and the chance of discovering new drugs is limited by the fact that fungi are in the group of organisms called eukaryotes, as humans are, which makes it difficult to find a drug that can kill a fungus but not a person. Additionally, anti-fungal resistance has been <a href="https://doi.org/10.1126/science.aap7999">emerging</a> over the past few decades in some fungi that cause disease in humans, but <em>C. auris</em>’ resistance to anti-fungals leaves other resistant fungi in the dust. Some <em>C. auris</em> strains are resistant to all classes of clinically used anti-fungals, which is extremely alarming.</p>
<p><em>C. auris</em> is also able to form <a href="https://wwwnc.cdc.gov/eid/article/23/2/16-1320_article">biofilms</a>, which are microbial communities attached to a surface and protected by a “glue-like” layer. The architecture of the biofilm protects <em>C. auris</em> from anti-fungals and immune system attacks. In the context of health care, microbial biofilms often form on plastics such as catheters, pacemakers and other implanted devices. These biofilms have been well studied for many microbes, but we do not fully understand the importance of biofilms formed by <em>C. auris</em> in the context of human disease.</p>
<p>Where did this new pathogen come from? Why is it highly drug-resistant and able to spread so easily? How does it interact with our body and the other microbes in and on our body? While we don’t know much about <em>C. auris</em> yet, we know quite a bit more about its distant cousin, <em>C. albicans</em>.</p>
<h2>Lessons from <em>C. albicans</em></h2>
<p>The fungus <a href="http://doi.org/10.1128/9781555817176"><em>C. albicans</em></a> was first described by <a href="http://www.hup.harvard.edu/catalog.php?isbn=9780674995260">Hippocrates</a> in 400 B.C. when he was describing oral thrush, a disease characterized by white lesions that form in the oral cavity when there is overgrowth of <em>C. albicans</em>. Since then, <em>C. albicans</em> has become one of the most studied fungi next to <em>Saccharomyces cerevisiae</em>, the baker’s and brewer’s yeast.</p>
<p><em>C. albicans</em> can cause fatal infections in humans, but more commonly this fungus resides in the human body, in the gut or on the skin, as a harmless member of the microbiome, which is the whole collection of microorganisms in and on our bodies. </p>
<p>In a <a href="https://doi.org/10.1016/0003-9969(73)90176-3">study</a> from the 1970s, investigators showed that if you test one-month-old babies for fungi, you find that almost every one of them had acquired a fungus, usually <em>C. albicans</em>. The conclusion was that it is completely normal for a person to have <em>C. albicans</em> in their body. </p>
<p>Yet, if the person develops a weakened immune system, the <em>C. albicans</em> that was already inhabiting their gut could become dangerous by changing its shape to elongated cells known as hyphae. These hyphae are then able to invade and destroy tissue, enter the bloodstream and cause a potentially fatal infection. </p>
<h2>Hope in the time of <em>C. auris</em></h2>
<p>A few years ago, <a href="https://sackler.tufts.edu/facultyResearch/faculty/kumamoto-carol/research">our group</a> started to wonder why this happens. Why is it OK that humans would have a fungus in our bodies that might kill us if conditions changed? Is there anything that the fungus does that might be good? We decided to investigate this question using a mouse model of infection. </p>
<p>We <a href="https://doi.org/10.1080/19490976.2018.1465158">found</a> that mice that carried <em>C. albicans</em> in their guts were protected from lethal doses of the bacterium <em>Clostridioides difficile</em> (<em>C. diff</em>). These findings showed that <em>C. albicans</em> has wide-ranging effects on its human host and in some situations could actually be beneficial. </p>
<p>Many aspects of <em>C. albicans</em> biology have been studied. We have a good understanding of what type of conditions push <em>C. albicans</em> to become a disease-causing organism and form <a href="https://www.annualreviews.org/doi/10.1146/annurev-micro-091014-104330">biofilms</a>. We also have identified some of the tricks that allow it to become drug resistant, such as acquiring mutations in a gene called <a href="https://aac.asm.org/content/46/6/1704"><em>ERG11</em></a>. Interestingly, the <a href="https://academic.oup.com/cid/article/64/2/134/2706620"><em>ERG11</em> gene of <em>C. auris</em></a> has also acquired mutations that contribute to its drug resistance.</p>
<p>So why is it important to consider <em>C. albicans</em> and other related <em>Candida</em> species when we are dealing with <em>C. auris</em>? If we understand some of the complex ways that <em>C. albicans</em> interacts with humans, this knowledge gives us a window to understand how <em>C. auris</em> might cause disease in people. Additionally, the lessons learned from studying <em>C. albicans</em> and other related fungi could help us develop solutions to deal with <em>C. auris</em>. </p>
<p>Know thy enemy, in this case, by understanding its family.</p><img src="https://counter.theconversation.com/content/115110/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Carol A Kumamoto receives funding for research from the National Institutes of Health (AI118898). </span></em></p><p class="fine-print"><em><span>Jesus A. Romo receives funding from the National Institutes of Health (T32AI007329). He is a Postdoctoral Fellow at Tufts University. </span></em></p>
A deadly fungus called Candida auris, is among us and is now detected in more than 20 countries. It is resistant to many anti-fungal drugs. But a familiar fungus may reveal a solution.
Carol A Kumamoto, Professor of Molecular Biology and Microbiology, Tufts University
Jesus A. Romo, Postdoctoral Fellow in Molecular Biology and Microbiology, Tufts University
Licensed as Creative Commons – attribution, no derivatives.
tag:theconversation.com,2011:article/102698
2018-10-16T10:40:01Z
2018-10-16T10:40:01Z
How scientists are fighting infection-causing biofilms
<figure><img src="https://images.theconversation.com/files/236757/original/file-20180917-158243-7f66pd.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">An artist depiction of a biofilm harboring antibiotic-resistant rod-shaped and spherical bacteria.
</span> <span class="attribution"><a class="source" href="https://www.shutterstock.com/image-illustration/360degree-spherical-panorama-view-inside-biofilm-449656513?src=EossfLJ3eo9oOQb0QrDj7A-1-9">Kateryna Kon/Shutterstock.com</a></span></figcaption></figure><p>The surfaces people interact with every day may seem rather mundane, but at the molecular scale, there is more activity than meets the eye. </p>
<p>Every surface we touch has its own unique chemical properties. It’s because of these properties that some materials stick to surfaces, while others slide off. For a person, a sticky surface may be a minor annoyance, but for a bacterial cell, surface attachment can be a matter of life and death. Bacteria have evolved their own surfaces to be sticky, like Velcro. </p>
<p>When bacteria colonize a surface, they create a community called a biofilm, which can be a source of infection on medical devices or implants. Growing concerns over these infections has led a number of researchers to develop materials to block these sometimes dangerous films.</p>
<p>As biophysical chemists, <a href="https://www.chemistry.msstate.edu/people/faculty/nicholas-fitzkee/">my research group</a> and I are trying to understand the molecular forces that allow biological molecules – like those on bacteria – to attach to surfaces during the earliest phases of biofilm formation. By understanding this early attachment stage, we can reduce the risks that a biofilm will form on implanted medical devices and pose a threat to humans.</p>
<h2>Bacterial colonies</h2>
<p>Biofilms are densely packed <a href="https://theconversation.com/unlocking-the-secrets-of-bacterial-biofilms-to-use-against-them-59148">communities</a> of bacteria or other microorganisms living on a surface. Like a city, growing within a biofilm has certain advantages. For example, it provides structural support, like the floors of a high rise, and microbes can share nutrients. Compared to free-floating bacteria, bacteria in a biofilm are shielded, allowing them to evade our immune system and resist antibiotics. </p>
<p>When biofilms form on medical devices or implants, they can serve as a persistent source of hard-to-treat <a href="http://doi.org/10.1126/science.284.5418.1318">infections</a>. These cost not only <a href="https://dx.doi.org/10.1586%2Ferp.09.53">billions of dollars</a> to treat, but claim <a href="https://doi.org/10.1177%2F003335490712200205">thousands of lives</a> each year in the U.S. alone.</p>
<p>Scientists are trying to understand how biofilms form and how to prevent them. Molecular biologists are working out how bacterial DNA encodes for the <a href="https://iai.asm.org/content/67/10/5427">machinery</a> that allows cells to attach to surfaces and one another. Microbiologists and medicinal chemists are looking for <a href="https://theconversation.com/triclosan-often-maligned-may-have-a-good-side-treating-cystic-fibrosis-infections-98063">drugs</a> that can penetrate and disrupt biofilms. And biophysical chemists like myself are trying to sleuth out the molecular interactions that make these biofilms challenging to prevent.</p>
<figure class="align-center ">
<img alt="" src="https://images.theconversation.com/files/236762/original/file-20180917-158225-tjo9f3.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/236762/original/file-20180917-158225-tjo9f3.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=403&fit=crop&dpr=1 600w, https://images.theconversation.com/files/236762/original/file-20180917-158225-tjo9f3.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=403&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/236762/original/file-20180917-158225-tjo9f3.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=403&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/236762/original/file-20180917-158225-tjo9f3.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=506&fit=crop&dpr=1 754w, https://images.theconversation.com/files/236762/original/file-20180917-158225-tjo9f3.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=506&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/236762/original/file-20180917-158225-tjo9f3.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=506&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
<figcaption>
<span class="caption"><em>Staphylococcus aureus</em> biofilm on the surface of a catheter.</span>
<span class="attribution"><a class="source" href="https://commons.wikimedia.org/wiki/File:Staphylococcus_aureus_biofilm_01.jpg">Rodney M. Donlan, Janice Carr /CDC</a></span>
</figcaption>
</figure>
<h2>Surface complexity</h2>
<p><em>Staphylococcus aureus</em> and <em>S. epidermidis</em> are two bacterial species that normally pose little problem for our bodies. However, when a staphylococcal biofilm forms on the surface of a medical implant like an artificial hip, these cells can cause disease. Staphylococcal biofilms are held together by sugars or <a href="https://iai.asm.org/content/73/10/6868">polysaccharides</a>, <a href="https://doi.org/10.1046/j.1365-2958.1997.4101774.x">proteins</a> and <a href="https://doi.org/10.5301/ijao.5000051">nucleic acids</a>, the molecular building blocks of all living organisms. These components enable the bacterial cells to stick not only to <a href="https://doi.org/10.1073/pnas.1208134110">each other</a>, but also to natural and implanted surfaces in the body – like a heart valve.</p>
<p>The surfaces of medical devices are complex, especially once they have been exposed to the body. <a href="https://doi.org/10.1093/infdis/158.4.693">Human blood proteins</a> rapidly coat the surface of medical implants, altering the character as both the patient and the device age. When a bacterial cell attaches to one of these surfaces, the components of the cell interact with the surface of the medical implant, forming a complex network of interactions. In our research, we are investigating the bacterial surface proteins that are involved in surface attachment. </p>
<figure class="align-center ">
<img alt="" src="https://images.theconversation.com/files/236759/original/file-20180917-158216-thegt0.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/236759/original/file-20180917-158216-thegt0.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=438&fit=crop&dpr=1 600w, https://images.theconversation.com/files/236759/original/file-20180917-158216-thegt0.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=438&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/236759/original/file-20180917-158216-thegt0.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=438&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/236759/original/file-20180917-158216-thegt0.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=551&fit=crop&dpr=1 754w, https://images.theconversation.com/files/236759/original/file-20180917-158216-thegt0.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=551&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/236759/original/file-20180917-158216-thegt0.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=551&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
<figcaption>
<span class="caption">Biofilms pervade all elements of our lives. For example the plaque that forms on your teeth is a biofilm that shelters bacteria. If the plaque isn’t removed, the tissue around the tooth will become inflamed.</span>
<span class="attribution"><a class="source" href="https://www.shutterstock.com/image-vector/dental-plaque-inflammation-healthy-tooth-on-324725045?src=EossfLJ3eo9oOQb0QrDj7A-1-60">Nita_Nita/Shutterstock.com</a></span>
</figcaption>
</figure>
<p>Studying these interactions is challenging. Typically, chemistry experiments are carried out in solution, but biofilm experiments must be done on a surface. Detecting the molecules at the surface is a challenge. That’s because there are fewer of those molecules compared to the overall volume of the material, just as the skin of the tomato is tiny fraction of the mass of the entire tomato.</p>
<h2>Introducing the nanoscale</h2>
<p>To overcome this limitation, we are investigating how proteins present on the bacterial surface interact with <a href="https://doi.org/10.1038/nmat2442">nanoparticle surfaces</a>. Specifically, we are using nanoparticles designed to mimic the surface of medical devices, and we are targeting proteins involved in staphylococcal infections, a major source of hospital related illness. </p>
<p>Nanoparticles have a diameter much smaller than a bacterial cell. But while a typical cell would dwarf a nanoparticle, the nanoparticle is still much bigger than the molecules on the surface of a cell. By using many nanoparticles it is easier to observe how the bacterium and particle interact and observe the bacterial molecules involved in biofilm formation. </p>
<figure class="align-right zoomable">
<a href="https://images.theconversation.com/files/235705/original/file-20180910-123113-1h4kzh8.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="" src="https://images.theconversation.com/files/235705/original/file-20180910-123113-1h4kzh8.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=237&fit=clip" srcset="https://images.theconversation.com/files/235705/original/file-20180910-123113-1h4kzh8.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=401&fit=crop&dpr=1 600w, https://images.theconversation.com/files/235705/original/file-20180910-123113-1h4kzh8.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=401&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/235705/original/file-20180910-123113-1h4kzh8.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=401&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/235705/original/file-20180910-123113-1h4kzh8.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/235705/original/file-20180910-123113-1h4kzh8.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/235705/original/file-20180910-123113-1h4kzh8.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=503&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
<figcaption>
<span class="caption">Randika Perera places a nanoparticle sample into an NMR spectrometer, one of the instruments used to study protein-surface interactions.</span>
<span class="attribution"><span class="source">Sarah Tewolde, MSU Office of Public Affairs</span>, <a class="license" href="http://creativecommons.org/licenses/by-sa/4.0/">CC BY-SA</a></span>
</figcaption>
</figure>
<p>Specifically, we are trying to understand the structure and orientation of proteins on different types of surfaces. While we are not the first or the only group to be interested in this topic, our work has begun to reveal the <a href="http://doi.org/10.1021/jp411543y">molecular details</a> of how proteins interact with nanoparticle surfaces. </p>
<p>We can probe how tightly the bacteria are clinging to a surface – and we can examine how protein molecules <a href="https://doi.org/10.1021/acs.jpcc.6b08469">compete</a> for the same surface. For example, given a collection of bacterial proteins, which of these will ultimately attach to the surface of a medical implant?</p>
<p>As we discover the answers to these questions we will be able to identify the important elements involved in early biofilm formation. This will be useful for scientists attempting to inhibit those interactions <a href="https://doi.org/10.1046/j.1365-2958.2002.02827.x">therapeutically</a>, or those seeking to design new <a href="https://doi.org/10.1016/j.biomaterials.2013.07.089">biofilm-resistant surfaces</a>.</p><img src="https://counter.theconversation.com/content/102698/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Nicholas Fitzkee receives funding from the National Institutes of Health and the National Science Foundation. </span></em></p>
Smooth surfaces often provide nooks and crannies for bacteria to hold onto and create a colony. New research with nanoparticles is revealing the secrets of surfaces that prevent bacterial attachment.
Nicholas Fitzkee, Associate Professor of Chemistry, Mississippi State University
Licensed as Creative Commons – attribution, no derivatives.
tag:theconversation.com,2011:article/98063
2018-07-11T11:15:22Z
2018-07-11T11:15:22Z
Triclosan, often maligned, may have a good side — treating cystic fibrosis infections
<figure><img src="https://images.theconversation.com/files/226366/original/file-20180705-122274-zwsz42.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">Antibiotic-resistant bacteria inside a biofilm.</span> <span class="attribution"><a class="source" href="https://www.shutterstock.com/image-illustration/antibiotic-resistant-bacteria-inside-biofilm-3d-733165693?src=S-PIB9t8jY1oDGnWwDSB3w-1-0">Kateryna Kon/Shutterstock.com</a></span></figcaption></figure><p>Maybe you’ve had the experience of wading in a stream and struggling to keep your balance on the slick rocks, or forgetting to brush your teeth in the morning and feeling a slimy coating in your mouth. These are examples of <a href="http://www.biofilm.montana.edu/biofilm-basics/index.html">bacterial biofilms</a> that are found anywhere a surface is exposed to bacteria in a moist environment.</p>
<p>Besides leading to falls in streams or creating unhealthy teeth, <a href="https://theconversation.com/unlocking-the-secrets-of-bacterial-biofilms-to-use-against-them-59148">biofilms</a> can cause large problems when they infect people. Biofilms, multicellular communities of bacteria that can grow on a surface encased in their own self-produced matrix of slime, <a href="https://www.sciencedirect.com/science/article/pii/B9780128002629000019?via%3Dihub">can block immune cells</a> from engulfing and killing the bacteria or prevent antibodies from binding to their surface. </p>
<p>On top of this, bacteria in a biofilm <a href="http://www.jbc.org/content/291/24/12565.long">resist being killed</a> by antibiotics due to the sticky nature of the matrix and activation of inherent resistant mechanisms, such as slow-growing cells or the ability to pump antibiotics out of the cell. </p>
<p>Biofilms are one of the primary growth modes of bacteria, but all antibiotics currently used clinically were developed against <a href="http://www.mdpi.com/1420-3049/20/4/5286/htm">free-swimming planktonic bacteria</a>. This is why they do not work well against biofilms. </p>
<p><a href="https://msu.edu/%7Ewatersc3/">My laboratory</a> studies how and why bacteria make biofilms, and we develop new therapeutics to target them. Because <a href="https://www.nature.com/articles/s41579-018-0019-y">antibiotic resistance</a> is the most problematic aspect of biofilms during infections, we set out to identify novel molecules that could enhance antibiotic activity against these communities. </p>
<p>We discovered that an antimicrobial that has recently obtained a bad reputation for overuse in many household products could be the secret sauce to kill biofilms.</p>
<h2>The hunt for antibiotic superchargers</h2>
<figure class="align-center ">
<img alt="" src="https://images.theconversation.com/files/226772/original/file-20180709-122277-1xmz7kg.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/226772/original/file-20180709-122277-1xmz7kg.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=472&fit=crop&dpr=1 600w, https://images.theconversation.com/files/226772/original/file-20180709-122277-1xmz7kg.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=472&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/226772/original/file-20180709-122277-1xmz7kg.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=472&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/226772/original/file-20180709-122277-1xmz7kg.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=593&fit=crop&dpr=1 754w, https://images.theconversation.com/files/226772/original/file-20180709-122277-1xmz7kg.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=593&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/226772/original/file-20180709-122277-1xmz7kg.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=593&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
<figcaption>
<span class="caption">Dr. Alessandra Agostinho Hunt measures biofilm formation of <em>Psuedomonas aerugionsa</em> by pipetting in the purple dye crystal violet to stain the microbial structure.</span>
<span class="attribution"><span class="source">Derrick Turner/Michigan State University</span>, <a class="license" href="http://creativecommons.org/licenses/by-sa/4.0/">CC BY-SA</a></span>
</figcaption>
</figure>
<p>To find such compounds, we developed an <a href="https://www.medicinenet.com/script/main/art.asp?articlekey=8412">assay</a> to grow plates of 384 tiny <a href="http://aac.asm.org/content/62/6/e00146-18.long">biofilms</a> of the bacterium <a href="https://www.tandfonline.com/doi/abs/10.1517/14728220903454988?journalCode=iett20"><em>Pseudomonas aeruginosa</em></a>. We did this to screen for molecules that enhance killing by the antibiotic <a href="https://www.rxlist.com/consumer_tobramycin_nebcin/drugs-condition.htm">tobramycin</a>. We chose this bacterium and this antibiotic as our test subjects because they are commonly associated with <a href="https://www.cff.org/Life-With-CF/Daily-Life/Germs-and-Staying-Healthy/What-Are-Germs/Pseudomonas/">cystic fibrosis lung infections</a> and treatment.</p>
<p>People with cystic fibrosis (CF) are at particular risk from <a href="https://www.ncbi.nlm.nih.gov/pubmed/19374653">biofilm-based infections</a>. These infections often become chronic in the lungs of cystic fibrosis patients and are often never cleared, even with aggressive antibiotic therapy.</p>
<p>After we screened 6,080 small molecules in the presence of tobramycin, we found multiple compounds that showed the antibiotic enhancement activity we were searching for. Of particular interest was the antimicrobial <a href="https://www.fda.gov/ForConsumers/ConsumerUpdates/ucm205999.htm">triclosan</a> because it has been widely used in household products like toothpaste, soaps and hand sanitizers for decades, indicating that it had potential to be safely used in CF patients. <a href="https://onlinelibrary.wiley.com/doi/abs/10.1002/jat.1660">Triclosan</a> has also garnered a <a href="https://theconversation.com/why-you-should-dispense-with-antibacterial-soaps-65297">bad reputation</a> due to its overuse, and states like Minnesota have banned it from these products. The <a href="https://theconversation.com/why-you-should-dispense-with-antibacterial-soaps-65297">Food and Drug Administration banned</a> its use from hand soaps in September 2016. This ruling was not based on safety concerns, but rather because the companies that made these products did not demonstrate higher microbial killing when triclosan was added, compared to the base products alone.</p>
<p>Another fact that piqued our interest is that <em>P. aeruginosa</em> is resistant to triclosan. Indeed, treatment with either tobramycin or triclosan alone had very little activity against <em>P. aeruginosa</em> biofilms, but we found that the combination was 100 times more active, killing over 99 percent of the bacteria.</p>
<p>We further studied this combination and found that it worked against <em>P. aeruginosa</em> and other bacterial species that had been isolated from the lungs of CF patients. The combination also significantly enhanced the speed of killing so that at two hours of treatment, virtually all of the biofilm is eradicated. </p>
<p>Our efforts are now focused on pre-clinical development of the <a href="https://www.tobipodhaler.com/index.jsp?usertrack.filter_applied=true&NovaId=2935377102246013691">tobramycin-triclosan combination</a>. For CF, we envision patients will inhale these antimicrobials as a combination therapy, but it could also be used for other applications such as diabetic non-healing wounds. </p>
<p>Although questions about the safety of triclosan have emerged in the mainstream media, there are actually dozens of studies, including in humans, <a href="https://ec.europa.eu/health/ph_risk/committees/04_sccp/docs/sccp_o_166.pdf">concluding that it is well tolerated</a>, summarized in this extensive EU report from 2009. My laboratory completely agrees that triclosan has been significantly overused, and it should be reserved to combat life-threatening infections.</p>
<p>The next steps for development are to initiate safety, efficacy and pharmacological studies. And thus far, our own studies indicate that <a href="http://aac.asm.org/content/early/2018/04/10/AAC.00146-18.full.pdf+html">triclosan is well tolerated</a> when directly administered to the lungs. We hope that in the near future we will have enough data to initiate clinical trials with the FDA to test the activity of this combination in people afflicted with biofilm-based infections.</p>
<p>We think our approach of enhancing biofilm activity with the addition of novel compounds will increase the usefulness of currently used antibiotics. Learning about how these compounds work will also shed light on how bacterial biofilms resist antibiotic therapy.</p><img src="https://counter.theconversation.com/content/98063/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Chris Waters receives funding from the NIH, NSF, Michigan State University, and Hunt for a Cure Foundation to support this research.</span></em></p>
Triclosan, an ingredient in soap and many household cleansers, has gained a bad reputation. A recent study looking for a way to boost an antibiotic, however, found that tricloscan did a great job.
Chris Waters, Associate Professor of Microbiology, Michigan State University
Licensed as Creative Commons – attribution, no derivatives.
tag:theconversation.com,2011:article/97998
2018-06-11T10:09:57Z
2018-06-11T10:09:57Z
The hunt for life on Mars: new findings on rock ‘chimneys’ could hold key to success
<p>The search for life on Mars has taken a step forward with the NASA Curiosity rover’s <a href="http://science.sciencemag.org/content/360/6393/1096">discovery</a> of organic matter on the bottom of what was once a lake. <a href="https://theconversation.com/rover-detects-ancient-organic-material-on-mars-and-it-could-be-trace-of-past-life-97755">It may once</a> have been part of an alien life form or it might have a non-biological origin – either way this carbon would have provided a food source for any organic living thing in the vicinity. </p>
<p>The discovery adds extra intrigue to NASA’s search for extra-terrestrial life forms themselves. When hunting remotely with one car-sized machine, the question is where best to focus your efforts. It makes sense to look for the same types of places we expect to find fossilised microorganisms on Earth. This is complicated by the fact that these fossils are measured in microns – mere millionths of a metre. </p>
<p>The Curiosity rover looks for certain sedimentary rocks deposited near water, as it did for the latest discovery. This is based on the latest geological advice about the best prospects. Yet which rocks to prioritise is still a matter of some debate – and it’s a question that is just as relevant to geologists trying to unlock the secrets of our own ancient world. The Earth’s rocks and fossils are the nearest thing we have to time machines. </p>
<p>For a century or so, geologists focused on a type of rock called a stromatolite – devoting long hours to crawling around in awkward spaces trying to find them. Stromatolites occur mainly in shallow water and are layered on a millimetre scale. Many of them are undoubtedly built by slimy microbial “biofilms”, but to cut a long story short we now appreciate there is more than one way to make a stripy rock – and they don’t all involve microbes. </p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/221981/original/file-20180606-137306-1vsbzhq.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="" src="https://images.theconversation.com/files/221981/original/file-20180606-137306-1vsbzhq.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/221981/original/file-20180606-137306-1vsbzhq.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=420&fit=crop&dpr=1 600w, https://images.theconversation.com/files/221981/original/file-20180606-137306-1vsbzhq.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=420&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/221981/original/file-20180606-137306-1vsbzhq.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=420&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/221981/original/file-20180606-137306-1vsbzhq.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=527&fit=crop&dpr=1 754w, https://images.theconversation.com/files/221981/original/file-20180606-137306-1vsbzhq.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=527&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/221981/original/file-20180606-137306-1vsbzhq.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=527&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
<figcaption>
<span class="caption">Stromatolite city.</span>
<span class="attribution"><a class="source" href="https://www.flickr.com/photos/31856336@N03/6188521133">Mike Beauregard</a>, <a class="license" href="http://creativecommons.org/licenses/by-sa/4.0/">CC BY-SA</a></span>
</figcaption>
</figure>
<p>More recently geologists have become more interested in other types of rocks, including the “<a href="https://www.sciencedirect.com/topics/earth-and-planetary-sciences/black-smoker">black smoker</a>” tube-type deposits formed by hot hydrothermal water being squeezed out of the Earth’s crust in the deep sea. Slightly easier to examine are similar chimney-like formations found in certain alkaline lakes around the world. </p>
<h2>Mono Lake</h2>
<p>One place on Earth where these chimneys occur is Mono Lake in California, a vast and beautiful stretch of water several hundred miles north of Los Angeles on the eastern slope of the Sierra Nevada mountains. In October 2014, our team obtained permission from the California State Parks to examine and sample some of the calcium carbonate chimneys that have formed there.</p>
<p>The rocks, which are frequently between two and three metres tall, are very young in geological terms, usually only tens of thousands of years old. But since first being <a href="https://books.google.co.uk/books/about/Quaternary_History_of_Mono_Valley_Califo.html?id=AE7nAAAAMAAJ&redir_esc=y">described</a> by the famous American geologist Israel Russell in 1889 they have proven an excellent natural laboratory for groups of scientists trying to understand how these structures came about. </p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/221985/original/file-20180606-137295-11ddjcf.png?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="" src="https://images.theconversation.com/files/221985/original/file-20180606-137295-11ddjcf.png?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/221985/original/file-20180606-137295-11ddjcf.png?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=392&fit=crop&dpr=1 600w, https://images.theconversation.com/files/221985/original/file-20180606-137295-11ddjcf.png?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=392&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/221985/original/file-20180606-137295-11ddjcf.png?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=392&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/221985/original/file-20180606-137295-11ddjcf.png?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=493&fit=crop&dpr=1 754w, https://images.theconversation.com/files/221985/original/file-20180606-137295-11ddjcf.png?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=493&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/221985/original/file-20180606-137295-11ddjcf.png?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=493&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
<figcaption>
<span class="caption">Exploration begins.</span>
<span class="attribution"><span class="source">Alexander Brasier</span></span>
</figcaption>
</figure>
<p>Before our visit, geologists were essentially divided about these chimneys. A group we might call “pure geochemists” <a href="https://www.sciencedirect.com/science/article/pii/001670379390339X">proposed</a> they were nothing to do with microbes, but produced by calcium-rich spring waters coming into contact with the alkaline lake, with its abundance of carbonate ions. </p>
<p>A smaller opposing camp <a href="http://archives.datapages.com/data/sepm/journals/v33-37/data/034/034002/0309.htm">agreed</a> it should be possible for these structures to emerge in the way that pure geochemists were suggesting. But they pointed out that, in the few recorded observations of carbonate rocks forming at the lake in the 19th and 20th centuries, some kind of biofilm did appear to have an influence. They also cited other studies that had shown that waterborne microbes called cyanobacteria did produce slimy substances that can accumulate calcium. </p>
<p>We went to Mono Lake to find out who was right. Our six-strong expedition divided into two factions: one looked for chimneys on the lake bottom using a research boat, while the other explored the famous “tufa towers” that rise up from the lake shore. </p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/221983/original/file-20180606-137309-1mr6wj3.png?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="" src="https://images.theconversation.com/files/221983/original/file-20180606-137309-1mr6wj3.png?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/221983/original/file-20180606-137309-1mr6wj3.png?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=378&fit=crop&dpr=1 600w, https://images.theconversation.com/files/221983/original/file-20180606-137309-1mr6wj3.png?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=378&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/221983/original/file-20180606-137309-1mr6wj3.png?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=378&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/221983/original/file-20180606-137309-1mr6wj3.png?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=475&fit=crop&dpr=1 754w, https://images.theconversation.com/files/221983/original/file-20180606-137309-1mr6wj3.png?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=475&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/221983/original/file-20180606-137309-1mr6wj3.png?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=475&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
<figcaption>
<span class="caption">Tufa towers on the shoreline.</span>
<span class="attribution"><span class="source">Alexander Brasier</span></span>
</figcaption>
</figure>
<p>The boat party toiled and cursed the astonishingly salty waters of the lake, while the shore party made steady progress with the invaluable assistance of local state park ranger, Dave Marquart. Their peace was interrupted only by a phone call from the stranded boaters requesting they urgently try to find someone with a four-wheel drive capable of pulling the boat back out of the water – luckily help was at hand. </p>
<p>One of the sites the shore party visited was in Marquart’s own back garden to the north-west of the lake. The rocks there were part of a set of ancient chimneys formed along a small tectonic fault. Their features suggested they had been built by microbes, but we needed to send them to a lab to be sure. </p>
<h2>Microbial ‘threads’</h2>
<p>Using an optical microscope, we were able to see dark thread-like structures entombed in slices of the rock. As we outline in our <a href="https://onlinelibrary.wiley.com/doi/full/10.1111/gbi.12292">new study</a> published in Geobiology, these “threads” are millions of fossilised photosynthesising cyanobacteria that once surrounded waters rising from a spring on the lake floor. </p>
<p>We sent the samples to Australia for further testing to establish whether the microbes played a key role in building the chimneys. This revealed surrounding patches of carbon and nitrogen, which we took to be fossilised cyanobacterial slime. This slime traps calcium and when it breaks down it creates calcium carbonate, entombing any living and dead cells in rock. </p>
<p>We found other ways in which this microbial slime had affected the fabric of the rock: grains of quartz and aluminosilicates that were clearly sand that had got stuck there, too. </p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/221982/original/file-20180606-137315-1fu6owr.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="" src="https://images.theconversation.com/files/221982/original/file-20180606-137315-1fu6owr.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/221982/original/file-20180606-137315-1fu6owr.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=450&fit=crop&dpr=1 600w, https://images.theconversation.com/files/221982/original/file-20180606-137315-1fu6owr.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=450&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/221982/original/file-20180606-137315-1fu6owr.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=450&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/221982/original/file-20180606-137315-1fu6owr.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=566&fit=crop&dpr=1 754w, https://images.theconversation.com/files/221982/original/file-20180606-137315-1fu6owr.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=566&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/221982/original/file-20180606-137315-1fu6owr.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=566&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
<figcaption>
<span class="caption">Thread-like filaments in the Mono Lake rock.</span>
<span class="attribution"><span class="source">Alexander Brasier</span></span>
</figcaption>
</figure>
<p>In short, we found evidence that cyanobacteria formed tubular mats around rising spring water in the ancient Mono Lake – probably producing the majority of the resulting chimneys there, though there may be examples of “pure geochemistry” chimneys as well. This suggests that these rock formations do indeed represent a promising and fairly large target for exploring ancient or extra-terrestrial life. </p>
<p>They have the added advantage that the calcite rocks in question are geologically quite stable. This means the fossils could potentially be preserved for a very long time – easily hundreds of millions, quite plausibly billions of years. </p>
<p>To our knowledge no chimneys have been found on Mars yet, but they are not common on Earth and there is every chance that they have a Martian equivalent. There, and on other planets and moons, we should be looking for areas with conditions as similar as possible to where these chimneys exist on Earth – volcanic rocks where spring waters might once have risen through the bedrock into an alkaline lake. Without any question, NASA’s hunt for suitable rocks on the red planet should make finding them a high priority.</p><img src="https://counter.theconversation.com/content/97998/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>The authors do not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and have disclosed no relevant affiliations beyond their academic appointment.</span></em></p>
Following NASA’s latest discovery of organic matter on the red planet, new findings in a salt lake in California could point to where to look for alien life.
Alexander Brasier, Lecturer in Geology, University of Aberdeen
David Wacey, Australian Research Council Future Fellow, The University of Western Australia
Mike Rogerson, Senior Lecturer in Earth System Science, University of Hull
Licensed as Creative Commons – attribution, no derivatives.
tag:theconversation.com,2011:article/64284
2016-10-19T01:02:27Z
2016-10-19T01:02:27Z
How many genes does it take to make a person?
<figure><img src="https://images.theconversation.com/files/142060/original/image-20161017-12463-1xoaj7s.jpg?ixlib=rb-1.1.0&rect=1161%2C0%2C5604%2C4000&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">Do we contain the most elaborate set of instructions?</span> <span class="attribution"><a class="source" href="http://www.shutterstock.com/pic-481861843.html">Genome image via www.shutterstock.com.</a></span></figcaption></figure><p>We humans like to think of ourselves as on the top of the heap compared to all the other living things on our planet. Life has evolved over three billion years from simple one-celled creatures through to multicellular plants and animals coming in all shapes and sizes and abilities. In addition to growing ecological complexity, over the history of life we’ve also seen the evolution of intelligence, complex societies and technological invention, until we arrive today at people flying around the world at 35,000 feet discussing the in-flight movie.</p>
<p>It’s natural to think of the history of life as progressing <a href="https://www.wired.com/2014/08/where-animals-come-from/">from the simple to the complex</a>, and to expect this to be reflected in increasing gene numbers. We fancy ourselves leading the way with our superior intellect and global domination; the expectation was that since we’re the most complex creature, we’d have the most elaborate set of genes.</p>
<p>This presumption seems logical, but the more researchers figure out about various genomes, the more flawed it seems. About a half-century ago the estimated number of human genes was in the millions. <a href="http://doi.org/10.1186/gb-2010-11-5-206">Today we’re down to about 20,000</a>. We now know, for example, that bananas, with their <a href="http://doi.org/10.1038/nature11241">30,000 genes</a>, have 50 percent more genes than we do. </p>
<p>As researchers devise new ways to count not just the genes an organism has, but also the ones it has that are superfluous, there’s a clear convergence between the number of genes in what we’ve always thought of as the simplest lifeforms – viruses – and the most complex – us. It’s time to rethink the question of how the complexity of an organism is reflected in its genome.</p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/136179/original/image-20160901-30772-1ngr36h.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="" src="https://images.theconversation.com/files/136179/original/image-20160901-30772-1ngr36h.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/136179/original/image-20160901-30772-1ngr36h.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=325&fit=crop&dpr=1 600w, https://images.theconversation.com/files/136179/original/image-20160901-30772-1ngr36h.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=325&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/136179/original/image-20160901-30772-1ngr36h.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=325&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/136179/original/image-20160901-30772-1ngr36h.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=408&fit=crop&dpr=1 754w, https://images.theconversation.com/files/136179/original/image-20160901-30772-1ngr36h.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=408&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/136179/original/image-20160901-30772-1ngr36h.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=408&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
<figcaption>
<span class="caption">The converging estimated number of genes in a person versus a giant virus. Human line shows average estimate with dashed line representing estimated number of genes needed. Numbers shown for viruses are for MS2 (1976), HIV (1985), giant viruses from 2004 and average T4 number in the 1990s.</span>
<span class="attribution"><span class="source">Sean Nee</span>, <a class="license" href="http://creativecommons.org/licenses/by/4.0/">CC BY</a></span>
</figcaption>
</figure>
<h2>Counting up the genes</h2>
<p>We can think of all our genes together as the recipes in a cookbook for us. They’re written in the letters of the bases of DNA – abbreviated as ACGT. The genes provide instructions on how and when to assemble the proteins that you’re made of and that carry out all the functions of life within your body. A <a href="http://doi.org/10.1093/nar/gki615">typical</a> gene requires about 1000 letters. Together with the environment and experience, genes are responsible for what and who we are – so it’s interesting to know how many genes add up to a whole organism. </p>
<p>When we’re talking about numbers of genes, we can display the actual count for viruses, but only the estimates for human beings for an important reason. One <a href="http://doi.org/10.1038/nrg3117">challenge</a> counting genes in <a href="https://youtu.be/bo0QHAS-x8A">eukaryotes</a> – which include us, bananas and yeast like Candida – is that our genes are not lined up like ducks in a row. </p>
<p>Our genetic recipes are arranged as if the cookbook’s pages have all been ripped out and mixed up with three billion other letters, about <a href="http://book.bionumbers.org/how-many-genes-are-in-a-genome/">50 percent</a> of which actually describe inactivated, dead viruses. So in eukaryotes it’s hard to count up the genes that have vital functions and separate them from what’s extraneous.</p>
<figure class="align-right zoomable">
<a href="https://images.theconversation.com/files/142062/original/image-20161017-12443-15i77k1.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="" src="https://images.theconversation.com/files/142062/original/image-20161017-12443-15i77k1.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=237&fit=clip" srcset="https://images.theconversation.com/files/142062/original/image-20161017-12443-15i77k1.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=620&fit=crop&dpr=1 600w, https://images.theconversation.com/files/142062/original/image-20161017-12443-15i77k1.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=620&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/142062/original/image-20161017-12443-15i77k1.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=620&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/142062/original/image-20161017-12443-15i77k1.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=779&fit=crop&dpr=1 754w, https://images.theconversation.com/files/142062/original/image-20161017-12443-15i77k1.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=779&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/142062/original/image-20161017-12443-15i77k1.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=779&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
<figcaption>
<span class="caption">Megavirus has over a thousand genes, Pandoravirus has even more.</span>
<span class="attribution"><a class="source" href="https://commons.wikimedia.org/wiki/File:Megavirus.jpg">Chantal Abergel</a>, <a class="license" href="http://creativecommons.org/licenses/by-sa/4.0/">CC BY-SA</a></span>
</figcaption>
</figure>
<p>In contrast, counting genes in viruses – and bacteria, which can have <a href="http://doi.org/10.1093/gbe/evs117">10,000</a> genes – is relatively easy. This is because the raw material of genes – nucleic acids – is relatively expensive for tiny creatures, so there is strong selection to delete unnecessary sequences. In fact, the real challenge for viruses is discovering them in the first place. It is startling that all <a href="http://doi.org/10.1098/rsos.160235">major virus discoveries</a>, including HIV, have not been made by sequencing at all, but by old methods such as magnifying them visually and looking at their morphology. <a href="http://doi.org/10.5501/wjv.v4.i3.265">Continuing advances</a> in molecular technology have taught us the remarkable <a href="http://doi.org/10.1038/nrmicro1750">diversity of the virosphere</a>, but can only help us count the genes of something we already know exists.</p>
<h2>Flourishing with even fewer</h2>
<p>The number of genes we actually need for a healthy life is probably even lower than the current estimate of 20,000 in our entire genome. One author of a recent study has reasonably extrapolated that the count for essential genes for human beings <a href="http://www.qmul.ac.uk/media/news/items/smd/171926.html">may be much lower</a>. </p>
<p>These researchers looked at thousands of healthy adults, <a href="http://doi.org/10.1126/science.aac8624">looking for naturally occurring “knockouts,”</a> in which the functions of particular genes are absent. All our genes come in two copies – one from each parent. Usually, one active copy can compensate if the other is inactive, and it is difficult to find people with <em>both</em> copies inactivated because inactivated genes are naturally rare. </p>
<p>Knockout genes are fairly easy to study with lab rats, using modern genetic engineering techniques to inactivate both copies of particular genes of our choice, or even remove them altogether, and see what happens. But human studies require populations of people living in communities with 21st century medical technologies and known pedigrees suited to the genetic and statistical analyses required. <a href="https://www.genome.gov/27561444/iceland-study-provides-insights-into-disease-paves-way-for-largescale-genomic-studies/">Icelanders are one useful</a> population, and the British-Pakistani people of this study are another. </p>
<p>This research found over 700 genes which can be knocked out with no obvious health consequences. For instance, one surprising discovery was that the PRDM9 gene – which plays a crucial role in the fertility of mice – can also be knocked out in people with no ill effects.</p>
<p>Extrapolating the analysis beyond the human knockouts study <a href="http://www.independent.co.uk/news/science/human-genome-study-finds-many-genes-have-no-effect-on-human-health-a6914446.html">leads to an estimate</a> that only 3,000 human genes are actually needed to build a healthy human. This is in the same ballpark as the number of genes in “<a href="http://www.giantvirus.org/">giant viruses</a>.” <a href="http://doi.org/10.1038/nature.2013.13410">Pandoravirus</a>, recovered from 30,000-year-old Siberian ice in 2014, is the largest virus known to date and <a href="http://doi.org/10.1073/pnas.1320670111">has 2,500 genes</a>.</p>
<p>So what genes do we need? We don’t even know what a quarter of human genes actually do, and this is advanced <a href="http://doi.org/10.1186/gb-2006-7-7-r57">compared to our knowledge of other species</a>.</p>
<h2>Complexity arises from the very simple</h2>
<p>But whether the final number of human genes is 20,000 or 3,000 or something else, the point is that when it comes to understanding complexity, size really does not matter. We’ve known this for a long time in at least two contexts, and are just beginning to understand the third.</p>
<p>Alan Turing, the mathematician and <a href="http://www.slate.com/blogs/browbeat/2014/12/03/the_imitation_game_fact_vs_fiction_how_true_the_new_movie_is_to_alan_turing.html">WWII code breaker</a> established the theory of multicellular development. He studied simple mathematical models, now called “reaction-diffusion” processes, in which a small number of chemicals – just two in Turing’s model – diffuse and react with each other. With simple rules governing their reactions, these models <a href="http://www.brandeis.edu/now/2014/march/turingpnas.html">can reliably generate</a> very complex, yet coherent structures <a href="https://www.youtube.com/watch?v=-RZLO7_Lk5s&feature=youtu.be">that are easily seen</a>. So the biological structures of plants and animals do not require complex programming.</p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/142061/original/image-20161017-12418-1y6gkfe.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="" src="https://images.theconversation.com/files/142061/original/image-20161017-12418-1y6gkfe.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/142061/original/image-20161017-12418-1y6gkfe.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=449&fit=crop&dpr=1 600w, https://images.theconversation.com/files/142061/original/image-20161017-12418-1y6gkfe.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=449&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/142061/original/image-20161017-12418-1y6gkfe.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=449&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/142061/original/image-20161017-12418-1y6gkfe.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=564&fit=crop&dpr=1 754w, https://images.theconversation.com/files/142061/original/image-20161017-12418-1y6gkfe.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=564&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/142061/original/image-20161017-12418-1y6gkfe.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=564&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
<figcaption>
<span class="caption">The simple building blocks of neurons together generate immense complexity.</span>
<span class="attribution"><a class="source" href="https://www.flickr.com/photos/126293865@N04/14953538130">UCI Research/Ardy Rahman</a>, <a class="license" href="http://creativecommons.org/licenses/by-nc/4.0/">CC BY-NC</a></span>
</figcaption>
</figure>
<p>Similarly, it is obvious that the <a href="http://theastronomist.fieldofscience.com/2011/07/cubic-millimeter-of-your-brain.html">100 trillion connections</a> in the human brain, which are what really make us who we are, cannot possibly be genetically programmed individually. The <a href="http://www.wired.com/2014/10/future-of-artificial-intelligence/">recent breakthroughs in artificial intelligence</a> are based on <a href="http://www.extremetech.com/extreme/215170-artificial-neural-networks-are-changing-the-world-what-are-they">neural networks</a>; these are computer models of the brain in which simple elements – corresponding to neurons – establish their own connections through interacting with the world. The <a href="http://www.kurzweilai.net/how-bio-inspired-deep-learning-keeps-winning-competitions">results have been spectacular</a> in applied areas such as handwriting recognition and medical diagnosis, and Google has invited the public to <a href="https://theconversation.com/leurope-de-lintelligence-artificielle-est-en-marche-63609">play games with</a> and <a href="http://www.theatlantic.com/technology/archive/2015/09/robots-hallucinate-dream/403498/">observe the dreams</a> of its AIs.</p>
<h2>Microbes go beyond basic</h2>
<p>So it’s clear that a single cell does not need to be very complicated for large numbers of them to produce very complex outcomes. Hence, it shouldn’t come as a great surprise that human gene numbers may be of the same size as those of single-celled microbes like viruses and bacteria.</p>
<p>What is coming as a surprise is the converse – that tiny microbes can have rich, complex lives. There is a growing field of study – dubbed “<a href="http://www.ncbi.nlm.nih.gov/pubmed/15639629">sociomicrobiology</a>” – that examines the extraordinarily complex social lives of microbes, which stand up in comparison with our own. <a href="http://rsos.royalsocietypublishing.org/content/3/8/160235">My own contributions</a> to these areas concern giving viruses their rightful place in this invisible soap opera.</p>
<p>We have become aware in the last decade that microbes spend over 90 percent of their lives as <a href="https://theconversation.com/unlocking-the-secrets-of-bacterial-biofilms-to-use-against-them-59148">biofilms</a>, which may best be thought of as biological tissue. Indeed, many biofilms have systems of <a href="http://www.sci-news.com/biology/science-bacteria-neurons-human-brain-03373.html">electrical communication</a> between cells, like brain tissue, making them a model for studying brain disorders such as migraine and epilepsy.</p>
<p>Biofilms can also be thought of as “<a href="http://doi.org/10.1128/JB.182.10.2675-2679.2000">cities of microbes</a>,” and the integration of <a href="http://doi.org/10.1016/j.tim.2004.11.007">sociomicrobiology</a> and medical research is <a href="http://doi.org/10.1128/microbiolspec.VMBF-0019-2015">making rapid progress</a> in many areas, such as the treatment of cystic fibrosis. The <a href="http://doi.org/10.1146/annurev.ecolsys.38.091206.095740">social lives of microbes</a> in these cities – complete with cooperation, conflict, truth, lies and even <a href="http://blogs.scientificamerican.com/lab-rat/the-bacteria-that-commit-honourable-suicide/">suicide</a> – is fast becoming the major study area in evolutionary biology in the 21st century.</p>
<p>Just as the biology of humans becomes starkly less outstanding than we had thought, the world of microbes gets far more interesting. And the number of genes doesn’t seem to have anything to do with it.</p><img src="https://counter.theconversation.com/content/64284/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Sean Nee does not work for, consult, own shares in or receive funding from any company or organization that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.</span></em></p>
The answer – fewer than are in a banana – has implications for the study of human health and raises questions about what generates complexity anyway.
Sean Nee, Research Professor of Ecosystem Science and Management, Penn State
Licensed as Creative Commons – attribution, no derivatives.
tag:theconversation.com,2011:article/63353
2016-09-20T10:59:03Z
2016-09-20T10:59:03Z
How poor NHS testing and antibiotic use is creating super-strength cystitis
<figure><img src="https://images.theconversation.com/files/132653/original/image-20160801-17173-ddukai.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">Close-up of antibiotic resistant bacteria.</span> <span class="attribution"><span class="source">Kateryna Kon/Shutterstock</span></span></figcaption></figure><p>Urinary tract infections – also known as cystitis – are extremely common. Around <a href="https://www.auanet.org/education/adult-uti.cfm">150m people are affected worldwide</a> each year and one in every three women is expected to suffer at least one attack before they are 24. </p>
<p>But the real figure could actually be somewhere much higher. This is because the urine dipstick, the standard test for cystitis, has been shown to <a href="http://www.ncbi.nlm.nih.gov/pubmed/20303096">miss at least half of all infections</a>. Alongside this, the standard laboratory culture that’s used to check for bacteria in the urine also <a href="http://www.ncbi.nlm.nih.gov/pubmed/23596238">misses around 50% of all infections</a>. And if this wasn’t bad enough, around 20-30% of patients won’t respond to the “<a href="http://www.ncbi.nlm.nih.gov/pubmed/15846726">guideline treatment</a>” of antibiotics.</p>
<p>A lot of these problems can be attributed to <a href="https://www.nice.org.uk/guidance/qs90">current health guidelines</a>, which are out of date and ineffective. And the use of these “guidelines” alongside an over-reliance on poor testing methods means there is a real risk a person with a genuine urinary tract infection (UTI) will be missed and won’t receive adequate treatment. </p>
<p>This can then lead to long-term recurrent infections – and for some patients a lifetime of constant symptoms – which are made worse by sex, exercise, alcohol, certain food and drink, stress and many other of life’s normal events.</p>
<h2>Peeing problems</h2>
<p>UTIs happen when the urinary tract becomes infected, usually by bacteria. In most cases, this is bacteria from the gut, which is found in faeces – this enters the urinary tract through the urethra, the bit where wee comes out of. </p>
<p>This sounds pretty bad but it has nothing to do with hygiene or cleanliness. Anyone can get a UTI, but they’re particularly common in women, and especially common after sex. This is thought to be because a woman’s urethra is shorter than a man’s, and is closer to their anus. </p>
<p>A typical case of cystitis starts after sex, when a woman finds she needs to wee more than usual, and that going for a wee is difficult – it is slow to start and the stream is reduced. These are the <a href="http://arxiv.org/abs/1501.03537">typical early symptoms of a urine infection</a>.</p>
<figure class="align-right ">
<img alt="" src="https://images.theconversation.com/files/132656/original/image-20160801-17165-19hmfl6.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=237&fit=clip" srcset="https://images.theconversation.com/files/132656/original/image-20160801-17165-19hmfl6.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=902&fit=crop&dpr=1 600w, https://images.theconversation.com/files/132656/original/image-20160801-17165-19hmfl6.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=902&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/132656/original/image-20160801-17165-19hmfl6.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=902&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/132656/original/image-20160801-17165-19hmfl6.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=1134&fit=crop&dpr=1 754w, https://images.theconversation.com/files/132656/original/image-20160801-17165-19hmfl6.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=1134&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/132656/original/image-20160801-17165-19hmfl6.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=1134&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
<figcaption>
<span class="caption">The failing dipstick test.</span>
<span class="attribution"><span class="source">Bork/Shutterstock</span></span>
</figcaption>
</figure>
<p>At this point, lots of people – even doctors – might believe the best advice is to drink plenty of water to “get things going”, but there is no evidence to justify this and it could actually make matters worse. This is because increased fluid intake dilutes the urine of <a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC292547/">natural antibodies</a>, immune chemicals and antibiotics. Plus, the offending microbes are stuck to the bladder cells so they cannot be simply washed away.</p>
<p>As the infection progresses, it can lead to pain and burning when going for a wee and a general feeling of discomfort around the bladder. At this point, most people will go to their doctors and will have their urine tested with a <a href="http://www.bpac.org.nz/BT/2013/June/urine-tests.aspx">dipstick</a> – but given these miss at least half of infections it can hardly be considered a reliable method of testing. </p>
<h2>Ignoring the evidence</h2>
<p>Left untreated, patients often become much worse – leading to return visits to the doctor. Another dipstick test at this point might reveal there is a “trace positive result” so the urine is sent to be “cultured” at the hospital – this identifies if there are any germs in the urine that could cause a urinary tract infection. But, again because a high number of infections are missed, culturing urine is also problematic.</p>
<figure class="align-left ">
<img alt="" src="https://images.theconversation.com/files/132654/original/image-20160801-17165-rb5i1p.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=237&fit=clip" srcset="https://images.theconversation.com/files/132654/original/image-20160801-17165-rb5i1p.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=400&fit=crop&dpr=1 600w, https://images.theconversation.com/files/132654/original/image-20160801-17165-rb5i1p.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=400&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/132654/original/image-20160801-17165-rb5i1p.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=400&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/132654/original/image-20160801-17165-rb5i1p.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/132654/original/image-20160801-17165-rb5i1p.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/132654/original/image-20160801-17165-rb5i1p.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=503&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
<figcaption>
<span class="caption">It’s a myth that cranberry juice can cure bladder infections.</span>
<span class="attribution"><span class="source">Brent Hofacker/Shutterstock</span></span>
</figcaption>
</figure>
<p>A typical treatment would now be three days of an antibiotic – which could lead to the patient feeling partially better but not cured. This happens in about <a href="http://www.ncbi.nlm.nih.gov/pubmed/15846726">20% to 30% of cases</a>, whether prescribed for three days or 14 days – but we still don’t really know why some people respond and others do not.</p>
<p>At this point, because of the limited nature of current testing methods, a urine culture may well be reported as negative and so “diagnostically” speaking the patient is declared free of infection. This is despite the continued presence of pain and tenderness when the bladder is pressed – indicating signs of infection and inflammation. </p>
<p>From here, if not treated properly, the infection might progress to a hospital admission with <a href="http://www.webmd.com/a-to-z-guides/kidney-infections-symptoms-and-treatments">a kidney infection</a>, or ongoing recurrent infections for the rest of a patient’s life. This recurrence happens because early on in the infection the responsible microbes will have organised themselves into what is known as a “<a href="https://theconversation.com/biofilms-the-bacterial-wound-communities-that-protect-themselves-from-attack-42218">biofilm</a>” which are located on the cell surfaces or inside the bladder cells.</p>
<h2>Hard to beat</h2>
<figure class="align-right zoomable">
<a href="https://images.theconversation.com/files/132661/original/image-20160801-17165-1g2f50l.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="" src="https://images.theconversation.com/files/132661/original/image-20160801-17165-1g2f50l.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=237&fit=clip" srcset="https://images.theconversation.com/files/132661/original/image-20160801-17165-1g2f50l.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=600&fit=crop&dpr=1 600w, https://images.theconversation.com/files/132661/original/image-20160801-17165-1g2f50l.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=600&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/132661/original/image-20160801-17165-1g2f50l.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=600&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/132661/original/image-20160801-17165-1g2f50l.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=754&fit=crop&dpr=1 754w, https://images.theconversation.com/files/132661/original/image-20160801-17165-1g2f50l.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=754&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/132661/original/image-20160801-17165-1g2f50l.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=754&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
<figcaption>
<span class="caption">How a biofilm develops.</span>
<span class="attribution"><span class="source">struna/Shutterstock</span></span>
</figcaption>
</figure>
<p>Biofilms are capable of protecting “delinquent microbes” from immune attack, and reduce the effectiveness of antibiotics – which is what happens in these types of bladder infections. </p>
<p>This may mean that a higher, longer dosage is needed. This goes against the current guidelines for treatment, and so is often not available to patients.</p>
<p>All of this demonstrates how we have become too reliant on tests, and imagine wrongly that they can give us clear “yes” or “no” answers to ease our doubts – they cannot. Instead, we should get back to the old clinical bedside skills that were developed years ago. </p>
<p>While I have been working in this field I have come to realise that in many cases, clinicians are using poorly equipped tests because the numerous inspectors, governors, guideline enthusiasts and dogmatists compel them to do so. This must change. We need to start scrutinising these long-held beliefs with healthy scepticism, reviewing approaches to diagnosis and patient care, because lives depend on it.</p><img src="https://counter.theconversation.com/content/63353/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>James Malone-Lee does not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.</span></em></p>
Poor testing methods and antibiotic use by GPs and urologists has left thousands of women with crippling infections.
James Malone-Lee, Professor of Medicine, Whittington Campus, UCL Medical School, UCL
Licensed as Creative Commons – attribution, no derivatives.
tag:theconversation.com,2011:article/63545
2016-08-08T11:20:18Z
2016-08-08T11:20:18Z
The cities of the future could be built by microbes
<figure><img src="https://images.theconversation.com/files/133226/original/image-20160805-484-1gz30uv.jpg?ixlib=rb-1.1.0&rect=15%2C22%2C1479%2C1868&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">Illustration of pressure sensing bacteria in soils from the 'Computational Colloids Project'. </span> <span class="attribution"><span class="source">Carolina Ramirez-Figuroa, Luis Hernan and Martyn Dade-Robertson</span>, <a class="license" href="http://creativecommons.org/licenses/by-sa/4.0/">CC BY-SA</a></span></figcaption></figure><p>You might be disappointed to hear that some intriguing underwater structures <a href="http://www.sciencedirect.com/science/article/pii/S0264817216301611">recently discovered</a> off the Greek island of Zakynthos are not part of the lost city of Atlantis. But the structures, which resemble colonnades of cobble stones and bases of columns, have an equally fascinating origin. They were actually <a href="http://www.scientificamerican.com/article/underwater-lost-city-built-by-microbes/">constructed by microbes</a> gathering around natural vents of methane and forming a natural cement in the otherwise soft sediment.</p>
<p>To some degree, these formations are an accident, sculpted by the interaction of the microorganisms with their physical and chemical environments. But they still point to a complex ability not usually associated with simple single-celled organisms less than 0.0002cm in diameter. So if bacteria can grow their own “cities”, could we use them to grow ours as well?</p>
<p>Bacterial building is actually more common than you might think. If you rub your tongue across the back of your teeth and find a rough spot between the base of the tooth and your gum you should probably go and see a dental hygienist. But you might also contemplate the fact that you have a city growing on your teeth. The rough patch, known more commonly as plaque, <a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2732559/">is a biofilm</a>, a complex structure built by bacteria living in your mouth.</p>
<p>Biofilms are, in effect, <a href="http://www.sciencedirect.com/science/article/pii/S0925857409001128">buildings for bacteria</a>. They provide the bacteria with physical protection and (unfortunately for us) protection from antibiotics. They also enable a <a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2732559">complex communications network</a> between the bacteria that lets them work together, with different groups of cells performing different functions and even helping control the populations.</p>
<figure class="align-center ">
<img alt="" src="https://images.theconversation.com/files/133252/original/image-20160805-466-18g44h3.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/133252/original/image-20160805-466-18g44h3.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=360&fit=crop&dpr=1 600w, https://images.theconversation.com/files/133252/original/image-20160805-466-18g44h3.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=360&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/133252/original/image-20160805-466-18g44h3.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=360&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/133252/original/image-20160805-466-18g44h3.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=452&fit=crop&dpr=1 754w, https://images.theconversation.com/files/133252/original/image-20160805-466-18g44h3.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=452&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/133252/original/image-20160805-466-18g44h3.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=452&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
<figcaption>
<span class="caption">Underwater microbe ‘cities’ off Zakynthos.</span>
<span class="attribution"><span class="source">University of East Anglia</span></span>
</figcaption>
</figure>
<p>Researchers are now experimenting with using the building abilities of bacteria in the human world. For example, we can make <a href="http://www.citg.tudelft.nl/en/research/projects/self-healing-concrete/">self-healing concretes</a> that use bacteria to re-mineralise cracks. It is even possible to create <a href="http://biomason.com">bacteria-based bio-cements</a> using a process similar to that which built the structures found in Zakynthos.</p>
<p>Both systems use a process known as <a href="http://onlinelibrary.wiley.com/doi/10.1111/j.1472-4669.2008.00147.x/abstract">biomineralisation</a>, where bacteria cause mineral crystals to form by changing the chemical composition of their environment. In the case of self-healing concretes and bio-cements, they combine calcium found in their immediate environment with carbon from carbon dioxide in the air. The beauty of the process is that, unlike normal cements and concretes that produce a lot of carbon dioxide, this actually takes carbon out of the atmosphere. </p>
<h2>Under pressure</h2>
<p>Our research takes this idea even further. We want to use the capacity of microorganisms to sense and respond to their environment, as well as add to it with their own structures. For example, imagine if we could lace the ground of a building site with bacteria that react when they feel mechanical pressure by binding the surrounding soil grains. This would mean we could create a self-constructing foundation just by putting the right amount of pressure on the ground, removing the need for costly excavations and reinforced concrete slabs.</p>
<p>Such a system may still be some way into the future but we have started down the path. Through the emerging discipline of <a href="https://theconversation.com/uk/topics/synthetic-biology">synthetic biology</a> we have already been able to identify genes in certain bacteria that activate in response to pressure. We’ve then used genetic engineering to design bacteria <a href="http://www.synbio.construction/2016/07/11/computational-colloids-project-at-seed-2016/">that glow when pressurised</a>. Our next step is to begin to use this pressure-sensing capacity in the bacteria to trigger the the process of biomineralisation and the production of new binding materials including polymers. </p>
<p>The site off Zakynthos may have been an archaeological disappointment but it reveals something about the way we might construct buildings in the future. Imagine visiting the ancient remains of our microbial-built future cities. When the archaeologists assess whether they are natural or artificial they may not be able to tell.</p><img src="https://counter.theconversation.com/content/63545/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Martyn Dade-Robertson receives funding from the Engineering and Physical Sciences Research Council (EPSRC) for the project 'Comutational Colloids'. EPSRC Reference: EP/N005791/1.</span></em></p>
Bacteria can produce their own ‘buildings’ so scientists are genetically engineering them to build ours.
Martyn Dade-Robertson, Reader in Design Computation, Co-director of the Architectural Research Collaborative, Newcastle University
Licensed as Creative Commons – attribution, no derivatives.
tag:theconversation.com,2011:article/59148
2016-06-01T01:00:21Z
2016-06-01T01:00:21Z
Unlocking the secrets of bacterial biofilms – to use against them
<figure><img src="https://images.theconversation.com/files/124356/original/image-20160527-894-iuv5a8.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">It's bacterial biofilms that give the Grand Prismatic Spring its colorful hues.</span> <span class="attribution"><span class="source">Karin Sauer</span>, <a class="license" href="http://creativecommons.org/licenses/by-nd/4.0/">CC BY-ND</a></span></figcaption></figure><p>Standing on a walkway at Yellowstone National Park, I admired the hues of orange, blue and yellow in the sand of the Grand Prismatic Spring. A small sign nearby read “bacterial mats.” Visitors to Yellowstone may have noticed similar signs all over the park, but they’re often overlooked on the way to waterfalls, geysers, hot springs and more.</p>
<p>But these colorful structures at my feet were the reason I had come. Well, I needed a vacation – and what better place then Yellowstone? – but professional curiosity had a lot to do with the destination. I’m a microbiologist, and I had come to see the bacterial mats.</p>
<p>More commonly known as biofilms, these communities of tightly packed bacteria grow in close association with surfaces such as sand and soil. The term “biofilms” suggests a thin, two-dimensional substance, but these communities feature microscopic-scale tower-like structures crisscrossed with water channels, all of which is encased in a protective, self-produced slimy layer. The bacteria within communicate and demonstrate cooperative behavior reminiscent of primitive organs.</p>
<p>As visually stunning as I find these biofilms in nature, these bacterial communities can be detrimental to human health. Scientists like me are investigating how these bacterial biofilms form and behave so we can figure out new ways to manage and control them.</p>
<h2>Biofilms are all around us</h2>
<p>While made up of bacteria that are invisible to the naked eye, biofilms themselves can be much bigger, ranging from less than an inch to several hundred feet in size. Yellowstone is home to the most extensive and most colorful biofilms I’ve ever seen, but these bacterial communities are not unique to the park. Biofilms are found anywhere in nature, visible as <a href="http://genomealberta.ca/blogs/curiosity-about-stromatolites-and-biofilm.aspx">stromatolites</a>, pond scum and the slimy, slippery layer coating rocks and pebbles in streams.</p>
<p>And biofilms are not limited to the environment, either, since bacteria will stick to almost any surface in aqueous conditions and encase themselves with a slime matrix. Indeed, biofilms pose <a href="http://dx.doi.org/10.1080/87559129209540953">numerous problems to human-made materials</a> such as ship hulls, cooling towers, sewage treatment plants, oil refineries, food processing and beverage plants, and household plumbing. You’ve likely seen them yourself while cleaning or doing repairs in your kitchen or bathroom, as a thick and slimy buildup in your drains and pipes. Biofilms can be a real nuisance, <a href="http://www.slideshare.net/mfornalik/intro-to-biofilms-3522031">causing biofouling and corrosion</a>.</p>
<p>The <a href="http://dx.doi.org/10.1126/science.284.5418.1318">ubiquity of biofilms</a> in our surroundings is supported by findings that the majority of bacteria, up to 90 percent, prefer <a href="http://www.ncbi.nlm.nih.gov/pubmed/340020">living in surface-associated biofilm communities</a> rather than as free-floating, individual bacteria (what we call planktonic bacteria).</p>
<p>So why do bacteria <a href="http://dx.doi.org/10.1128/JB.00003-12">tend to form communities</a>? For one thing, there’s strength in numbers. By banding together within their slimy protection, biofilm bacteria can remain in favorable locations or hosts, better withstand nutrient deprivation, stress, dessication and predation. At the same time, they benefit from increased cooperation and exchange of genetic material.</p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/124520/original/image-20160530-7692-10riis.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="" src="https://images.theconversation.com/files/124520/original/image-20160530-7692-10riis.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/124520/original/image-20160530-7692-10riis.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=400&fit=crop&dpr=1 600w, https://images.theconversation.com/files/124520/original/image-20160530-7692-10riis.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=400&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/124520/original/image-20160530-7692-10riis.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=400&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/124520/original/image-20160530-7692-10riis.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/124520/original/image-20160530-7692-10riis.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/124520/original/image-20160530-7692-10riis.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=503&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
<figcaption>
<span class="caption">Scanning electron micrograph of part of a central venous catheter, removed from a patient, that was colonized by a biofilm of rod-shaped bacteria associated with fibrinlike material on the catheter’s surface.</span>
<span class="attribution"><a class="source" href="http://phil.cdc.gov/">Janice Haney Carr</a></span>
</figcaption>
</figure>
<h2>Biofilms can harm human health</h2>
<p>Biofilms have been linked to contamination of <a href="http://dx.doi.org/10.1089/10445490260099700">contact lenses leading to corneal ulcers</a>. They’re associated with <a href="http://dx.doi.org/10.1177/0022034510368644">dental plaque that leads to caries and periodontitis</a>. <a href="http://dx.doi.org/10.1126/science.284.5418.1318">They can infect</a> <a href="http://dx.doi.org/10.1007/978-3-319-09782-4">surgical sites</a>, the urinary tract, chronic and burn wounds and the lungs of cystic fibrosis patients. And they love to <a href="http://dx.doi.org/10.1016/B978-0-323-22805-3.00005-0">colonize medical devices</a> such as catheters, prosthetic joints and heart valves.</p>
<p>According to the National Institutes of Health, more than 65 percent of <a href="http://dx.doi.org/10.1111/2049-632X.12151">chronic inflammatory and infectious diseases</a> are due to biofilms. According to research, biofilm-related infections claim as many lives as heart attack or cancer. And they are costly, with treatment of biofilm-related infections <a href="http://dx.doi.org/10.1002/bit.21838">ranging into the billions</a> annually worldwide.</p>
<p>Why are we not better equipped to treat such bacterial infections? Research by my laboratory and others has demonstrated that when bacteria attach to a surface and grow as biofilms, they undergo a change, as evidenced by the genes they express and the proteins they produce. One of the consequences of this change is that biofilm bacteria become less susceptible to biocides, disinfectants and antibiotics. </p>
<p>Scientists think there are several reasons for this decrease in susceptibility. First, the slimy layer encasing biofilms can make it hard for disinfectants or antimicrobials to even physically reach the bacteria. Also, bacteria living in biofilms experience high stress levels while growing rather slowly, which can render most antibiotics ineffective since they only work on actively growing cells. My favorite theory is that living in a biofilm changes bacteria and their behavior; something about their mix of active genes and proteins just makes them more resilient. Whatever the contributing factors, bacteria growing in a biofilm can be <a href="http://dx.doi.org/10.1128/JB.00765-12">up to 1,000-fold more resistant to antibiotics</a> than the same bacteria grown planktonically.</p>
<p>This profound tolerance to antimicrobial agents – a hallmark of biofilms – is at the root of many persistent infections and renders biofilms extremely difficult to control in medical settings. <a href="http://www.ncbi.nlm.nih.gov/books/NBK84450/">Conventional therapies have proven inadequate</a> in the treatment of many if not most chronic biofilm infections, mainly because they have been geared toward bacteria growing planktonically and not as biofilms.</p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/124591/original/image-20160531-1943-1tkghh6.png?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="" src="https://images.theconversation.com/files/124591/original/image-20160531-1943-1tkghh6.png?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/124591/original/image-20160531-1943-1tkghh6.png?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=264&fit=crop&dpr=1 600w, https://images.theconversation.com/files/124591/original/image-20160531-1943-1tkghh6.png?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=264&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/124591/original/image-20160531-1943-1tkghh6.png?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=264&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/124591/original/image-20160531-1943-1tkghh6.png?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=332&fit=crop&dpr=1 754w, https://images.theconversation.com/files/124591/original/image-20160531-1943-1tkghh6.png?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=332&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/124591/original/image-20160531-1943-1tkghh6.png?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=332&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
<figcaption>
<span class="caption">The formation of surface-associated biofilm communities (A) can be prevented or significantly reduced (B) by interfering with key factors required for their development. Bacterial cells are stained green.</span>
<span class="attribution"><span class="source">Karin Sauer</span>, <a class="license" href="http://creativecommons.org/licenses/by-nd/4.0/">CC BY-ND</a></span>
</figcaption>
</figure>
<h2>New lines of attack against biofilms</h2>
<p>Research suggests a promising new avenue for biofilm control: the manipulation of the biofilm lifestyle. Yes, for bacteria, being in a biofilm is a lifestyle choice.</p>
<p>The biofilm way of life is initiated when a few planktonic bacteria adhere to a surface. Once attached, these bacteria will divide and grow into more complex, three-dimensional structures – the biofilm. If resources become exhausted or the biofilm become too overcrowded, bacteria can escape it, as a means of survival and dissemination.</p>
<p>It’s the two extremes of their lifestyle, the beginning and the end, attachment and escape, that have become major foci of research endeavors looking for ways to defeat biofilms.</p>
<p>When it comes to controlling attachment, much research has focused on the <a href="http://dx.doi.org/10.1111/j.1574-695X.2011.00858.x">development of new surface materials</a> aimed at preventing the formation of biofilms on medical devices in the first place. The idea is to render devices’ surfaces nonsticky, repelling or otherwise toxic for those first pioneering bacteria. If they can’t latch on and get a toehold, no biofilm can eventually form. Surface coatings containing colloidal silver, antibiotics or micro-brushes can render medical devices inhospitable.</p>
<p>Likewise, the hunt is on for new chemical compounds that prevent attachment or induce escape strategies. Researchers are <a href="http://dx.doi.org/10.1128/JB.01214-08">starting to have some success</a>.</p>
<p><a href="http://bingweb.binghamton.edu/%7Eksauer/">My own research</a>, along with that of colleagues at Binghamton University and around the world, has led me down another path. I’ve been trying to understand how bacteria actually make these amazing biofilm structures. What proteins, polymers and factors do they need to coordinate their lifestyle? What have we learned that would let us manipulate this biofilm lifestyle?</p>
<p>It’s unlikely there will be only one effective treatment strategy to defeat biofilms. For one thing, many varieties of bacteria form biofilms, and they all use somewhat different strategies to enable this lifestyle. For instance, while bacteria may coordinate the formation of biofilms via chemical signals, the molecules used by bacteria such as <em>E. coli</em> or <em>S. aureus</em> to do so differ quite dramatically. Likewise with the species-specific sets of proteins required to coordinate the formation of each kind of biofilm. So as we target individual characteristics, some of our tactics work better on one group than another. </p>
<p>But biofilm bacteria also share some common features that we can take advantage of, including their need for communication and coordination. Building a biofilm, escaping from the biofilm or even living in a biofilm requires some sort of coordination among the millions of bacteria that make it up. They can do so by communicating with each other, using a chemical language or proteins. Jamming the bacterial language (although there are many) or interfering with their key factors required for coordination has proven to be a successful strategy to block or modify biofilm formation, at least in laboratory settings and some clinical pilot studies.</p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/124590/original/image-20160531-1943-iim40a.png?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="" src="https://images.theconversation.com/files/124590/original/image-20160531-1943-iim40a.png?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/124590/original/image-20160531-1943-iim40a.png?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=300&fit=crop&dpr=1 600w, https://images.theconversation.com/files/124590/original/image-20160531-1943-iim40a.png?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=300&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/124590/original/image-20160531-1943-iim40a.png?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=300&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/124590/original/image-20160531-1943-iim40a.png?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=377&fit=crop&dpr=1 754w, https://images.theconversation.com/files/124590/original/image-20160531-1943-iim40a.png?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=377&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/124590/original/image-20160531-1943-iim40a.png?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=377&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
<figcaption>
<span class="caption">Biofilms before (A) and after (B) exposure to ‘Escape from the biofilm!’ chemical signal. Note the biofilms in (B) are hollow, appearing like empty shells. Bacterial cells are stained in green.</span>
<span class="attribution"><span class="source">Karin Sauer</span>, <a class="license" href="http://creativecommons.org/licenses/by-nd/4.0/">CC BY-ND</a></span>
</figcaption>
</figure>
<p>Likewise, repurposing the bacterial language has shown promise. For instance, when we co-opt the bacterial language to signal “<a href="http://dx.doi.org/10.1128/JB.01214-08">escape from the biofilm!</a>” we can trick biofilm bacteria into giving up their protective lifestyle and converting to planktonic cells again. The added benefit is the planktonic cells are more susceptible to antibiotics.</p>
<p>Controlling biofilms in the future will likely require a combination of strategies, addressing both attachment and escape, with and without the use of antibiotics and communication blockers, and likely in a manner more or less tailored toward the different bacterial lifestyles.</p><img src="https://counter.theconversation.com/content/59148/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>My research is currently supported by grants from the National Institute of Health and F. Hoffmann-La Roche Ltd.
</span></em></p>
The vast majority of the bacteria that surround us are not free-floating but prefer to band together in cooperative communities called biofilms. How do biofilms form and cooperate?
Karin Sauer, Professor of Biological Sciences, Binghamton University, State University of New York
Licensed as Creative Commons – attribution, no derivatives.
tag:theconversation.com,2011:article/43052
2015-06-12T03:26:29Z
2015-06-12T03:26:29Z
Pasolini, with Willem Dafoe, offers an unconventional biopic – review
<figure><img src="https://images.theconversation.com/files/84487/original/image-20150610-6793-1g4ki.png?ixlib=rb-1.1.0&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">Willem Dafoe brings a magnanimity to the role of the late poet Pier Paolo Pasolini.</span> <span class="attribution"><span class="source">© Capricci Films</span>, <a class="license" href="http://creativecommons.org/licenses/by/4.0/">CC BY</a></span></figcaption></figure><p><a href="http://www.imdb.com/name/nm0001206/">Abel Ferrara</a> made some of the best films of the 1980s. <a href="http://www.imdb.com/title/tt0087247/">Fear City</a> (1984) is a deliriously sleazy depiction of New York City in the aftermath of its bankruptcy scare. <a href="http://www.imdb.com/title/tt0082776/">Ms 45</a> (1981) (aka Angel of Vengeance), following the revenge killing spree
of a deaf mute, twice raped, is one of the more striking exploitation films of the period. </p>
<p>His best-known films, <a href="http://www.imdb.com/title/tt0103759/">Bad Lieutenant</a> (1992) and <a href="http://www.imdb.com/title/tt0099939/">King of New York</a> (1990), are likewise gruelling explorations of the seedy urban underbelly of NYC. </p>
<p>His recent film, <a href="http://www.imdb.com/title/tt3125652/">Pasolini</a> (2014) – an elegiac ode to the controversial Italian poet, essayist and filmmaker, <a href="http://sensesofcinema.com/2002/great-directors/pasolini/">Pier Paolo Pasolini</a> – is based on completely different subject matter, and yet the images and topics haunting his earlier films are still here. </p>
<p>There is the grim, nightmarish quality of the city at night; there is the romantically-fringed main character defined through his work; there is Ferrara’s willingness to challenge the viewer with confronting images. </p>
<p>Pasolini, rather than attempting to retell the life story of its subject, simply presents a day in his life – his last day, leading up to his <a href="http://romethesecondtime.blogspot.com.au/2014/10/pasolini-remembered-ostia-murder-site.html">murder at Ostia</a>. </p>
<p>We follow Pasolini (played by <a href="http://www.imdb.com/name/nm0000353/">Willem Dafoe</a>) from interview to interview, hearing his political views; we look
over his shoulder as he taps away at his typewriter; we sit with him as he has lunch with his mother and friends; we have dinner with him, and then pick up a young male prostitute from the streets of Rome with him. </p>
<p>We shudder with him as he is beaten to death by a gang of homophobic youths. </p>
<p>Pasolini’s Rome is readily transformed into Ferrara’s New York. The city, a major character in the film, appears murky, crepuscular, slightly menacing. Scenes of Dafoe, American accent unchanged, eating spaghetti with a restauranteur, seem
to be straight from a wise guy film. (While making notes I found myself writing “in Italian restaurant” – something of a tautology, given the film’s set in Rome!)</p>
<p>Layered within the chronological “last day” narrative is Ferrara’s envisioning of Pasolini’s words and stories, including his ideas for a grand film to follow the controversial <a href="http://www.imdb.com/title/tt0073650/">Salò, or the 120 Days of Sodom</a> (1975), his final film released a short time after his death, still banned in several countries. </p>
<p>The different levels of narrative weave in and out of each other – Pasolini as subject of Ferrara’s film, Pasolini’s typewritten speech, voiced over the top of Ferrara’s visions; Pasolini’s final film idea, as written in a letter, enacted for the viewer. </p>
<p>This film will probably be of more interest to viewers with some knowledge of <a href="http://www.understandingitaly.com/profile-content/yearsoflead.html">Italian politics in the 1970s</a> – the clashes between the red brigades and the fascists, the autonomistas, and so on – along with Pasolini’s films. Nevertheless, it
is a pleasure listening to Pasolini’s beautiful words, brought to life by Ferrara. As the interviewer says to Pasolini mid-way through the film:</p>
<blockquote>
<p>Your language has the effect of sunlight filtering through the dust. </p>
</blockquote>
<p>In the current age, in which the left seem to be only interested in identity politics, Pasolini’s words are, furthermore, inspiring for their commitment and clarity. </p>
<p>“Also in democracy, the holy game of kings continues,” he taps into his typewriter at one stage. To the interviewer, he declares: </p>
<blockquote>
<p>You and your schools, your television, your complacent newspapers. You are the great preservers of this appalling tradition that is based on the idea of possessing and destroying …</p>
<p>I ask you to look around and see the tragedy […] That there are no more human beings – there are only machines colliding with each other. </p>
</blockquote>
<p>Pasolini’s words are accompanied by elegant, at times beautiful, images. The colours are warm, and the darkness of the film – much of it is steeped in shadow – is sumptuous, inviting rather than alienating. </p>
<p>The film is shot on celluloid rather than digitally, and this seems to add a texture and depth to the images often absent in contemporary cinema. </p>
<p>Willem Dafoe brings a magnanimity to the title role, as well as a fragility, that clearly reflects Ferrara’s admiration of Pasolini. Indeed, Ferrara’s director’s statement, in the press kit accompanying the film, is written as a poem to Pasolini:</p>
<blockquote>
<p>In search of the death of the last poet</p>
<p>only to find the killer inside me</p>
<p>Sharpening his tools of ignorance on the </p>
<p>memories of never forgotten acts of </p>
<p>kindness in words and deeds, </p>
<p>ideas impossible to comprehend. </p>
<p>In a school in Casarsa sit at my teacher’s feet </p>
<p>yearning then hearing the music of the waves </p>
<p>that wash the feet of the messiah on the beach at Idroscalo, </p>
<p>those who weave their spell in silver are forever bound to the lithe body</p>
<p>of Giotto constantly in search of the creation of the winning goal</p>
<p>forever offside forever in the lead of the faithful of which I am one.</p>
</blockquote>
<p>It is as a kind of poem that the film must be seen – open-ended, impressionistic, evocative rather than hermeneutically locked-off.</p>
<p>Ferrara previously attempted to explore the imbrication of art, sexuality and being in <a href="http://www.imdb.com/title/tt0106660/">Dangerous Game</a> (1993), but that film was overly self-indulgent (as films starring Madonna often seem to be). Pasolini is a much more nuanced study of the relationship between art, politics, and social life than Dangerous Game. </p>
<p>This is by no means a conventional biopic – a refreshing change from the usual self-validating, uplifting success-story tripe that dominates the genre, at least in its Hollywood incarnations (<a href="http://www.imdb.com/title/tt0358273/">Walk the Line</a> (2005), <a href="http://www.rottentomatoes.com/m/jobs/">Jobs</a> (2013), etc.). And yet the whole thing comes across, at times, as unfocused, unfinished, perhaps too elliptical. </p>
<p>Given that the infinitely contingent nature of experience is one of the thematic threads of the film, this is probably intentional (but no less dissatisfying for being so). As the protagonist of Pasolini’s film-idea says: </p>
<blockquote>
<p>The end does not exist. Let’s wait. Something will happen.</p>
</blockquote>
<p><br>
<em>Pasolini was shown as part of the Sydney Film Festival. Details <a href="http://tix2.sff.org.au/session_sff.asp?sn=Pasolini&g_cdr=1">here</a>.</em></p><img src="https://counter.theconversation.com/content/43052/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Ari Mattes does not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.</span></em></p>
Rather than attempting to retell the life story of its subject, Pier Paolo Pasolini, this film simply presents a day in his life – his last day, leading up to his murder at Ostia.
Ari Mattes, Lecturer in Media Studies, University of Notre Dame Australia
Licensed as Creative Commons – attribution, no derivatives.
tag:theconversation.com,2011:article/42218
2015-05-27T15:18:58Z
2015-05-27T15:18:58Z
Biofilms – the bacterial wound communities that protect themselves from attack
<figure><img src="https://images.theconversation.com/files/83112/original/image-20150527-4840-1wdv2h5.jpg?ixlib=rb-1.1.0&rect=0%2C0%2C1228%2C851&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">Like something straight out of a biofilm.</span> <span class="attribution"><a class="source" href="https://www.flickr.com/photos/pnnl/3659555383/in/photolist-6zobjt-7Q5tpT-zkhED-bP3Jq2-7Q1xwZ-7PXyc5-7Q5pV4-7Q8Gg3-7Q5uVa-dpRRZi-7Q1WJ6-7Q1mPz-7Q8PG7-7Q4BLs-8tCFs4-8xuvZT-5dp5dM-oyWswN-7o15No-buejys-63ECfU-bvSmVY-7Q5vni-7Q5sKV-7Q5qsV-7PGYNQ-7PDTLx-6zshzo-7Ptm4u-7PDXj6-7PDV34-iFEa6-7PDY6Z-7PHdmd-da3BUj-8xxxN1-8xvYe1-rrGsWA-7PDZsV-7PDYJB-8xsWpZ-7Q8FG1-7Q55q9-97NGJk-aDKzxj-7tLeQL-7PGSEN-cjeXBf-7YFdEu-ibWSdA">Pacific Northwest National Laboratory</a>, <a class="license" href="http://creativecommons.org/licenses/by-nc-sa/4.0/">CC BY-NC-SA</a></span></figcaption></figure><p>Wound infections can occur when bacteria from the skin or from the environment are introduced into damaged tissues. Crucially, all wounds are colonised by bacteria but under certain conditions these bacteria can multiply unchecked, growing to reach numbers that <a href="http://www.woundsinternational.com/media/issues/71/files/content_31.pdf">overwhelm the immune system</a>. </p>
<p>Most wound infections can easily be treated with topical antimicrobials, or in more serious cases, by a course of antibiotics. They are also most commonly seen in clinical environments where, for example, infection-causing bacteria are inadvertently introduced into surgical incision sites after surgery. </p>
<p>Despite rigorous cleaning and hygiene regimens, infections are often unavoidable because of the prevalence of bacteria in the environment and as part of normal human flora. </p>
<figure class="align-left ">
<img alt="" src="https://images.theconversation.com/files/83111/original/image-20150527-4820-hsscf6.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=237&fit=clip" srcset="https://images.theconversation.com/files/83111/original/image-20150527-4820-hsscf6.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=377&fit=crop&dpr=1 600w, https://images.theconversation.com/files/83111/original/image-20150527-4820-hsscf6.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=377&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/83111/original/image-20150527-4820-hsscf6.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=377&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/83111/original/image-20150527-4820-hsscf6.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=474&fit=crop&dpr=1 754w, https://images.theconversation.com/files/83111/original/image-20150527-4820-hsscf6.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=474&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/83111/original/image-20150527-4820-hsscf6.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=474&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
<figcaption>
<span class="caption">Ready for my close up: MRSA.</span>
<span class="attribution"><a class="license" href="http://creativecommons.org/licenses/by/4.0/">CC BY</a></span>
</figcaption>
</figure>
<p>When you add in that antibiotic resistant bacteria are rife within clinical environments, this can make these wound infections exceptionally difficult to treat.</p>
<h2>Chronic, inflammed states</h2>
<p>Without successful treatment, bacteria can remain within the wound, creating a non-healing or chronic state. When this occurs the wound becomes “stuck” in an inflammatory stage where damage can happen to the tissues. Any bacteria in the wound will then continue to grow and aggravate it. </p>
<p>Within chronic wounds, these bacteria exist as complex multi-species communities known as biofilms. These are comprised of layers of bacteria which are stuck to human proteins at the wound surface and which form complex, microscopic structures through which nutrients can flow. </p>
<p>Biofilm bacteria also protect themselves by secreting a sugary-layer that covers the entire microbial community which offers additional protection from antibiotic treatment and your immune response. Bacterial biofilms can remain in wounds despite numerous different types of antimicrobial treatment; in fact it is thought that 60% of chronic wounds <a href="http://onlinelibrary.wiley.com/doi/10.1111/j.1524-475X.2007.00321.x/epdf">are associated with</a> these bacterial communities.</p>
<figure class="align-center ">
<img alt="" src="https://images.theconversation.com/files/83115/original/image-20150527-4820-vdnaky.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/83115/original/image-20150527-4820-vdnaky.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=400&fit=crop&dpr=1 600w, https://images.theconversation.com/files/83115/original/image-20150527-4820-vdnaky.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=400&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/83115/original/image-20150527-4820-vdnaky.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=400&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/83115/original/image-20150527-4820-vdnaky.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=502&fit=crop&dpr=1 754w, https://images.theconversation.com/files/83115/original/image-20150527-4820-vdnaky.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=502&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/83115/original/image-20150527-4820-vdnaky.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=502&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
<figcaption>
<span class="caption">PG reconstruction: wound infection.</span>
<span class="attribution"><a class="source" href="https://www.flickr.com/photos/adaduitokla/6241381326/in/photolist-ruQLDX-6eDsUJ-8ZsXiM-avwHdS-avtWGK-6jnHhD-6KafCN-eajdJ5-9rygrM-645r2X-9nF2Sn-9hXdqa-c7Dn2o-Q8BPg-8BxaPZ-4G9o6y-84ynYJ-84ynmb-84ynEj-84viV6-JXZAn-9nNMRh-9vtFUk-6uE1kZ-9o9rYg-pyJBgE-JXZAD-69it3V-5zdNNm-rbCfNH-5zdNDs-bBG2uz-7NH2f8-9evxuJ-oRb6fP-9eDdKe-avwFjJ-avu3TM-avtYQ6-avtXGP-avxqVY-avwEfq-avwDfG-avuLor-avxsub-ebrJfT-6xEsB4-7m7GUV-7Hcoab-7Hcoa3">Ahmad Fuad Morad</a>, <a class="license" href="http://creativecommons.org/licenses/by-sa/4.0/">CC BY-SA</a></span>
</figcaption>
</figure>
<p>It is possible to impair biofilm growth and to disrupt established biofilms in the laboratory <a href="http://onlinelibrary.wiley.com/doi/10.1111/iwj.12175/epdf">using topical antimicrobials</a>. These antimicrobials function in a number of ways. They can act by preventing adhesion of bacteria to a surface – if bacteria cannot bind to a surface in the first place then they cannot colonise and so a biofilm cannot form. Many such antimicrobials act as an anti-biofilm agent as well as killing bacteria. They are often incorporated into wound dressings, and include compounds such as silver, which leach out of the dressing in time, providing an antimicrobial environment at the wound surface to prevent bacterial growth. </p>
<p>Some antimicrobials are effective against established biofilms. These ones must be able to diffuse through the sticky layer around the biofilm and penetrate the deeper layers <a href="http://www.ncbi.nlm.nih.gov/pubmed/24251838">to remove and kill the bacteria residing there</a>.</p>
<figure class="align-center ">
<img alt="" src="https://images.theconversation.com/files/83114/original/image-20150527-4812-12u81kx.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/83114/original/image-20150527-4812-12u81kx.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=415&fit=crop&dpr=1 600w, https://images.theconversation.com/files/83114/original/image-20150527-4812-12u81kx.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=415&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/83114/original/image-20150527-4812-12u81kx.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=415&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/83114/original/image-20150527-4812-12u81kx.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=521&fit=crop&dpr=1 754w, https://images.theconversation.com/files/83114/original/image-20150527-4812-12u81kx.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=521&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/83114/original/image-20150527-4812-12u81kx.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=521&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
<figcaption>
<span class="caption">Biofilm on sand – better than on skin.</span>
<span class="attribution"><a class="source" href="https://www.flickr.com/photos/adonofrio/4482210139/in/photolist-7Q5uVa-buejys-63ECfU-dpRRZi-7Q1WJ6-7Q1mPz-bvSmVY-7Q8PG7-7Q4BLs-7Q5vni-7Q5sKV-7Q5qsV-bP3Jq2-7Q8FG1-7Q55q9-7PGYNQ-97NGJk-7PDTLx-6zshzo-7Ptm4u-7PDXj6-7PDV34-7PDY6Z-7PHdmd-aDKzxj-7tLeQL-da3BUj-8xxxN1-7PGSEN-cjeXBf-8xvYe1-rrGsWA-7YFdEu-7PDZsV-7PDYJB-ibWSdA-8xsWpZ-iFEa6-8xsWmZ-dUSFYA-9XzKMy-7PE1Qe-7PDS94-apirBs-7Q8GXC-6enjRC-dbRASL-oSfy4c-cCsLpJ-9CYZVm">Anthony D'Onofrio</a>, <a class="license" href="http://creativecommons.org/licenses/by/4.0/">CC BY</a></span>
</figcaption>
</figure>
<h2>Antimicrobial polymers</h2>
<p>Medical devices such as catheters often become infected, providing a ready-made “wound” or incision site where bacterial biofilm can grow. Biofilm can grow on the surface of these devices, which can be very problematic. To try to counter these problems, researchers are beginning to develop devices made <a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4159828/pdf/ijms-15-13849.pdf">from antimicrobial polymers</a> that contain antimicrobial compounds within or on their surface, which are slowly released to prevent bacteria from adhering and to kill any bacteria in the vicinity of the device. The types of antimicrobial compounds used in this way are broad-spectrum, meaning that they are effective against a wide range of infectious bacteria making them highly versatile. The use of antimicrobial polymers also means that bacterial numbers are controlled which should prevent an infection occurring.</p>
<p>In an era where antibiotic resistance is increasing and outstripping the rate of antibiotic discovery, the development of antimicrobials is essential to counter these tough bacterial biofilms. Academic institutions are beginning to work closely with pharmaceutical industries to produce effective treatments for wound infection that are broad-acting and non-toxic – and which do not further antibiotic resistance. </p>
<p>While this will remain a significant challenge, the formulation of new antimicrobial and anti-biofilm treatments can not only improve treatment and prevention of infection, they may also help with the recognised threat of antimicrobial resistance.</p><img src="https://counter.theconversation.com/content/42218/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Sarah Maddocks does not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.</span></em></p>
Biofilms have developed to let nutrients in but keep antimicrobials out.
Sarah Maddocks, Lecturer of Microbiology, Cardiff Metropolitan University
Licensed as Creative Commons – attribution, no derivatives.
tag:theconversation.com,2011:article/41046
2015-05-12T04:17:10Z
2015-05-12T04:17:10Z
How technology is being used in the war on ‘smart’ dirt
<figure><img src="https://images.theconversation.com/files/80408/original/image-20150505-8434-1aaghh7.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">Food security is threatened when irrigation systems get worn out by biofouling as a result of smart dirt.</span> <span class="attribution"><span class="source">AAP</span></span></figcaption></figure><p>You might have heard of smart bugs – viruses that have mutated and become resistant to ordinary antibiotics. But there is another, less well-known microscopic substance that is dangerous to human health – <a href="http://link.springer.com/article/10.1007%2FBF00182412#page-1">“smart” dirt</a>. So what is smart dirt and what is being done to protect the world from these potentially toxic germs?</p>
<h2>What is smart dirt?</h2>
<p>Smart dirt is made up of those germs clinging to the surfaces around us that have become resistant to the chemicals normally used to get rid of them.</p>
<p>A massive dose of chemicals could kill these bugs, but this posses a risk to the environment – most are toxic.</p>
<p>The accumulation of surface-adhering micro-organisms such as bacteria and algae is known as <a href="http://rsta.royalsocietypublishing.org/content/roypta/370/1967/2381.full.pdf">biofouling</a>. The available chemical cleaners no longer have an effective impact on almost all areas fundamental to human existence, including the water treatment industry, food industry and energy sectors.</p>
<h2>Human survival is threatened</h2>
<p>Biofouling has become the <a href="http://www.mdpi.com/2077-0375/2/4/804">biggest hindrance</a> to the development of membrane water treatment plants in South Africa and globally. In the water industry, the filters in water treatment plants can become fouled. This decreases the quality of water and increases operation costs.</p>
<p>Food security is <a href="http://link.springer.com/article/10.1007%2Fs00271-013-0406-0#page-1">threatened</a> when irrigation systems get worn out and production lines in industrial settings become plagued by biofouling. </p>
<p>The energy sector, including South Africa’s power utility Eskom, is also <a href="http://www.gewater.com/handbook/cooling_water_systems/ch_26_microbiological.jsp">victim</a> to this plague. Cooling water towers are constantly down due to heavy fouling, which reduces heat exchanger efficiency. The costs of repair run into millions and cooling tower lifetimes are severely shortened.</p>
<figure class="align-center ">
<img alt="" src="https://images.theconversation.com/files/80412/original/image-20150505-8376-1uk35hd.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/80412/original/image-20150505-8376-1uk35hd.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=341&fit=crop&dpr=1 600w, https://images.theconversation.com/files/80412/original/image-20150505-8376-1uk35hd.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=341&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/80412/original/image-20150505-8376-1uk35hd.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=341&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/80412/original/image-20150505-8376-1uk35hd.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=428&fit=crop&dpr=1 754w, https://images.theconversation.com/files/80412/original/image-20150505-8376-1uk35hd.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=428&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/80412/original/image-20150505-8376-1uk35hd.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=428&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
<figcaption>
<span class="caption">Repair costs for cooling towers damaged by biofouling can run into the millions.</span>
<span class="attribution"><span class="source">EPA/Caroline Seidel</span></span>
</figcaption>
</figure>
<h2>Why there is hope</h2>
<p>Fortunately, nature has also provided a solution to smart dirt. Researchers have discovered that on heavily fouled surfaces, the marine red algae <em>delisea pulcra</em> remained untouched by ocean bacteria and barnacles. A closer look revealed that this marine plant contains substances, “furanones”, that repel bacteria and all other forms of microorganisms from their surface. </p>
<p>In a <a href="http://www.ncbi.nlm.nih.gov/pubmed/23261340">research project</a>, these furanones were prepared and tested on laboratory-scale water filters. The furanone-modified water filters not only demonstrated self-cleaning behaviour (bacteria repelling), but also the ability to destroy the bacteria which attempted to stick to the filter surfaces. </p>
<p>And since the furanone compound is chemically bound to the material, there is no risk of it leaking into the environment. </p>
<p><a href="http://www.sciencedirect.com/science/article/pii/S0734975012001851">Research</a> has shown that the secret to this compound’s effectiveness is that the bugs live together in small communities, referred to as biofilms. They are also in constant communication. Their survival and resistance to certain bug-killing measures relies heavily on this communication. </p>
<p>The presence of furanone compounds stops communication between the bugs. As a result, their destruction is inevitable. Without a “community feel”, these bugs cannot colonise surfaces. Without attachment, they cannot survive.</p>
<p>This technology opens a lot of possibilities in the fight against surface biofouling. It can eliminate the use of chemical cleaners, which are dangerous for the environment and lead to antimicrobial resistance. Smart dirt may be ahead, but the war against biofouling has only just begun.</p><img src="https://counter.theconversation.com/content/41046/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Nonjabulo P. Gule receives funding from the Department of Science and Technology (DST), the National Research Foundation (NRF) and Stellenbosch University. She works for Stellenbosch University.</span></em></p>
Smart dirt is made up of those germs clinging to the surfaces around us that have become resistant to the chemicals normally used to get rid of them.
Nonjabulo P. Gule, NRF-DST Research Fellow; Researcher, Department of Chemistry and Polymer Science, Stellenbosch University
Licensed as Creative Commons – attribution, no derivatives.