Can You Guess What’s 11,000 Times Dirtier Than a Toilet Seat?
By Larry Schwartz
America is a gas-guzzling, car-obsessed, open-road nation. Few things appeal to Americans more than a (traffic-free, ideally) leisurely drive to a fun, kick-back-your-heels destination, all the while enjoying the passing scenery. Of course, in order to achieve this bucolic vision of paradise, we need to fuel up the car, and in order to do that, we have to stop at the gas station. A study by Kimberly-Clark in 2015 investigating bacterial hot spots in the workplace fingered gas pumps as one of the unhealthiest things you can handle, and a new survey recently corroborates those findings.
Admittedly, it's probably no great surprise that gas pumps are not exactly pristine. Never mind the chemical contamination that comes from gasoline itself, think about the sheer number of people endlessly grabbing the pump, often after returning from a pit stop at the not-so-hygienic gas station bathroom. You get the idea. Still, the new study gives one pause and suggests a bottle of sanitizer might not be a bad glove compartment staple.
It's not just the number of germs present on gas pump handles, but the quality of those germs. The earlier Kimberly-Clark study, led by University of Arizona microbiologist Charles Gerba, whom colleagues know as "Dr. Germ," found that 71 percent of the pumps were highly contaminated with germs associated with disease.
The new survey, conducted by Busbud, studied samples from three different gas stations, as well as three different charging stations, to see what we may be exposing ourselves to. The sample size is small, but the results mirror the larger earlier study and are eye-opening.
Based on laboratory results from swabs from the sample gas pumps, handles on gas pumps had an average of 2,011,970 colony-forming units (CFUs), or viable bacteria cells, per square inch. Worse, the buttons on the pumps (where you select the grade of gas you want), had 2,617,067 CFUs per square inch.
Mike Mozart / Flickr
To put that in perspective, money, which is considered quite dirty since it changes hands often, has only 5.2 CFUs per square inch. A toilet seat has 172 CFUs per square inch. That makes a gas pump handle about 11,000 times more contaminated than a toilet seat, and a gas pump button 15,000 times more contaminated.
Okay, so there are over 2 million CFUs dancing around on the gas pump. What kind of germs are they? Luckily, about half of them are usually harmless. These are the CFUs known as gram-positive rods. (I say usually because gram-positive rods can sometimes cause some types of infections, but are not considered unusually worrisome.) But those other million or so CFUs are mostly of the gram-positive cocci variety, and these are nasty critters that can cause skin infections, pneumonia and toxic shock syndrome.
Does the type of gas you select safeguard you in any way? It would seem so, to some small degree. The sampling showed that the buttons for regular gas contained 3,255,100 CFUs per square inch, about a third of which were the gram-positive cocci (bad germs), and another third of which were bacilli, another type of bad-guy bacteria linked to food poisoning and infections in newborn babies. The other third were mostly the safer gram-positive rods, with a smattering, about 5 percent, of gram-negative rods. These latter germs are especially worrisome as they are linked to antibiotic resistance as well as meningitis and pneumonia. The premium gas button had about 2,022,034 CFUs per square inch, divided about half gram-positive rods and half yeast (and we all know about yeast infections).
Since a typical visit to the gas station involves pressing the gas grade button as well as lifting the pump handle, that means, for regular gas, exposure to about 5,267,070 CFUs per square inch, and for premium gas about 4,034,004 CFUs per square inch.
Tesla and Volt owners, rejoice! If you own an electric car, and use a charging station, you can breathe a lot easier. The typical car charger has only 7.890 CFUs per square inch.
If you want to minimize your exposure to these germs, use a paper towel to hold the handle and push the button, or keep that hand sanitizer around and wash your hands after filling up.
Reposted with permission from our media associate AlterNet.
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By Jacob L. Steenwyk and Antonis Rokas
From the mythical minotaur to the mule, creatures created from merging two or more distinct organisms – hybrids – have played defining roles in human history and culture. However, not all hybrids are as fantastic as the minotaur or as dependable as the mule; in fact, some of them cause human diseases.
When Looking Through a Microscope Isn’t Close Enough.<p>For the last few years, <a href="http://www.rokaslab.org/" target="_blank">our team at Vanderbilt University</a>, <a href="https://www.researchgate.net/lab/Gustavo-Goldman-Lab" target="_blank">Gustavo Goldman's team at São Paulo University in Brazil</a> and many other collaborators around the world have been collecting samples of fungi from patients infected with different species of <em>Aspergillus</em> molds. One of the species we are particularly interested in is <a href="https://doi.org/10.1006/rwgn.2001.0082" target="_blank"><em>Aspergillus nidulans</em>, a relatively common and generally harmless fungus</a>. Clinical laboratories typically identify the species of <em>Aspergillus</em> causing the infection by examining cultures of the fungi under the microscope. The problem with this approach is that very closely related species of <em>Aspergillus</em> tend to look very similar in their broad morphology or physical appearance when viewing them through a microscope.</p><p>Interested in examining the varying abilities of different <em>A. nidulans</em> strains to cause disease, we decided to analyze their total genetic content, or genomes. What we saw came as a total surprise. We had not collected <em>A. nidulans</em> but <em>Aspergillus latus</em>, a close relative of <em>A. nidulans</em> and, as we were to soon find out, <a href="https://doi.org/10.1016/j.cub.2020.04.071" target="_blank">a hybrid species that evolved through the fusion of the genomes</a> of two other <em>Aspergillus</em> species: <em>Aspergillus spinulosporus</em> and an unknown close relative of <em>Aspergillus quadrilineatus</em>. Thus, we realized not only that these patients harbored infections from an entirely different species than we thought they were, but also that this species was the first ever <em>Aspergillus</em> hybrid known to cause human infections.</p>
Several Different Fungal Hybrids Cause Human Disease.<p>Hybrid fungi that can cause infections in humans are well known to occur in several different lineages of single-celled fungi known as yeasts. Notable examples include multiple different species of <a href="https://doi.org/10.1002/yea.3242" target="_blank">yeast hybrids</a> that cause the human diseases <a href="https://rarediseases.info.nih.gov/diseases/6218/cryptococcosis" target="_blank">cryptococcosis</a> and <a href="https://www.cdc.gov/fungal/diseases/candidiasis/index.html" target="_blank">candidiasis</a>. Although pathogenic yeast hybrids are well known, our discovery that the <em>A. latus</em> pathogen is a hybrid is a first for molds that cause disease in humans.</p>
(Left) Candida yeasts live on parts of the human body. Imbalance of microbes on the body can allow these yeasts, some of which are hybrids, to grow and cause infection. (Right) Cryptococcus yeasts, including ones that are hybrids, can cause life-threatening infections in primarily immunocompromised people. Centers for Disease Control and Prevention<p><a href="https://doi.org/10.1371/journal.ppat.1008315" target="_blank">Why certain <em>Aspergillus</em> species are so deadly</a> while others are harmless remains unknown. This may in part be because <a href="https://doi.org/10.1016/j.fbr.2007.02.007" target="_blank">combinations of traits, rather than individual traits</a>, underlie organisms' ability to cause disease. So why then are hybrids frequently associated with human disease? Hybrids inherit genetic material from both parents, which may result in new combinations of traits. This may make them more similar to one parent in some of their characteristics, reflect both parents in others or may differ from both in the rest. It is precisely this mix and match of traits that hybrids have inherited from their parental species that <a href="https://www.nytimes.com/2010/09/14/science/14creatures.html" target="_blank">facilitates their evolutionary success</a>, including their ability to cause disease.</p>
The Evolutionary Origin of an Aspergillus Hybrid.<p>Multiple evolutionary paths can lead to the emergence of hybrids. One path is through mating, just as the horse and donkey mate to create a mule. Another path is through the merging or fusion of genetic material from cells of different species.</p><p>It is this second path that appears to have been taken by our fungus. <em>A. latus</em> appears to have two of almost everything compared to its parental species: twice the genome size, twice the total number of genes and so on. But unlike other hybrids, which are often sterile like the mule, we found that <em>A. latus</em> is capable of reproducing both asexually and sexually.</p><p>But how distinct were the parents of <em>A. latus</em>? By comparing the parts contributed by each parent in the <em>A. latus</em> genome, we estimate that its parents are approximately 93% genetically similar, which is about as related as we humans are with lemurs. In other words, <em>A. latus</em>, an agent of infectious disease, is the fungal equivalent of a human-lemur hybrid.</p>
How A. Latus Differs From its Parents.<p>Elucidating the identity of closely related fungal pathogens and how they differ from each other in infection-relevant characteristics is a key step toward reducing the burden of fungal disease. For example, we found that <em>A. latus</em> was three times more resistant than <em>A. nidulans</em>, the species it was originally identified as using microscopy-based methods, to one of the most common antifungal drugs, <a href="https://www.drugbank.ca/drugs/DB00520" target="_blank">caspofungin</a>. This result provides a clear example of the potential importance of accurate identification of the <em>Aspergillus</em> pathogen causing an infection.</p><p>We also examined how <em>A. latus</em> and <em>A. nidulans</em> interact with cells from our immune system. We found that immune cells were less efficient at combating <em>A. latus</em> compared to <em>A. nidulans</em>, suggesting the hybrid fungus may be trickier for our immune systems to identify and destroy.</p><p>In the midst of the COVID-19 pandemic, our quest to understand <em>Aspergillus</em> pathogens is becoming more urgent. Growing evidence suggests that <a href="https://doi.org/10.1111/myc.13096" target="_blank">a fraction of COVID-19 patients are also infected with <em>Aspergillus</em>.</a> More worrying is that these <a href="https://doi.org/10.3201/eid2607.201603" target="_blank">secondary <em>Aspergillus</em> infections</a> can worsen the clinical outcomes for those infected with the novel coronavirus. That being said, we stress that little is known about <em>Aspergillus</em> infections in COVID-19 patients due to a lack of systematic testing, and none of the infections identified so far appear to have been caused by hybrids.</p><p>So, when it comes to hybrids, some are fantastic (the minotaur), some are helpful (the mule) and some are dangerous (<em>Aspergillus latus</em>). Understanding more about the biology of <em>Aspergillus latus</em> may help in our understanding of how microbial pathogens arise and how to best prevent and combat their infections.</p>
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