What potential disasters keep you up at night? Meteor strikes? Super Volcanos? World War Three? World war Z? Those are all pretty scary and we didn’t even mention climate change but there’s one other immediate terrifying, scientific problem that rises above the rest… Superbugs I’m not talking about giant spiders of Mirkwood or tracker jackers. I’m talking about antibiotic resistant bacteria. Which by the way are everywhere. Antibiotics are pretty incredible. Since the discovery of penicillin they have extended the average human life by about 10 years. A good percentage of the people watching this right now are only alive today because at some point an antibiotic saved their life. But we’re facing a little bit of a crisis. Antibiotics are starting to loose their effectiveness as bacteria continue to outsmart our technology. And I don’t wanna make you too paranoid here, but the consequences could be big. Remember that little thing called the black death – a pandemic that ravaged Europe and Asia in the 1300s, killing about, meh, 25 mln people. That wouldn’t have happened if antibiotics were a thing back then, but if our drugs stop working now, could it happen again? The US Centers for Disease Control estimates that 23,000 American died in 2012 from antibiotic-resistant bacteria. And the World Health Organization says that in 2010 about half a million people were infected with a resistant strain of tuberculosis, a third of whom died. A post-antibiotic era could essentially mean the end of modern medicine and suddenly a simple operation, sinus infection or a scraped knee could once again have the potential to kill. Now, I’m not saying you should be worried about this. Actually, yeah, I’m saying you should be worried about this. When Scottish physician Alexander Fleming got out of bed one September morning in 1928 he had no idea that he was about to change the world. Fleming had seen countless soldiers die from infected wounds and since the 1st World War ended, he’d been working hard to find better antibacterial agents. He was a good guy and a good scientist, but he was also a bit of a slob. So that morning he was straightening a stack of Petri dishes, where he’d been growing a staphylococcus bacteria, when he noticed mold in one of the dishes. Now, his lab was messy enough that that wasn’t that weird, but what caught his eye was that all around the mold the bacteria was dead. He later identified that mold as penicillium notatum. Years of experimentation followed and after enlisting the help of researchers Howard Florey and Ernst Chain the team figured out how to grow and use the fungus to treat bacterial infections. Mass production began during World War II and by D-Day in 1944 all allied soldiers had penicillin, the world’s first antibiotic. For their work Fleming, Florey and Chain were awarded the Nobel Prize. And, for the next 50 years, or so, antibiotics were unbeatable, saving lives left and right. But lately they’ve struggled to perform as well as they used to. Before we talk about exactly what antibiotics are and how they work, you have to understand what they’re up against. Bacteria!!!! Take a look around your room. Everything, your chair, your sandwich, your dog, your body – inside and out – it’s all covered in millions and millions of different single-celled bacteria. They can pretty much survive anywhere. Even in radioactive waste and in the absence of light and oxygen. But unlike viruses, which need a host cell to reproduce and survive, bacteria can thrive everywhere, because they can share their genetic material with each other. This is the key to their evolving resistance to antibiotics. While some bacteria have genes that make them resistant to like heat, so they can live in boiling water, other bacteria may be resistant to penicillin and both kinds can share what they know. We get our genes from our parents and what we’re born with we’re stuck with our whole lives. Bacteria, however, like to do things a little differently. They don’t to use traditional reproduction to pass their genes along. They can use something called horizontal gene transfer to swap genetic information, like you swap Pokemon cards. And one of the best ways bacteria acquire new genes is to loot their neighbors’ body when they degrade and die. This process is known as transformation, although some pathologists have dubbed it “the funeral grab”. It happens when bacteria are in a special physiological state called competence, during which they can scavenge bits of foreign DNA from their environment. So say Bobby bacterium dies and then Benny bacterium creeps up and grabs whatever genes it wants. So if Bobby was resistant to cold and Benny grabbed that gene, now Benny is suddenly cold resistant. And if Bobby was resistant to a certain antibiotic, boom, now Benny is too. Another way bacteria exchange genetic materials is by passing viruses, also known as transduction. Viruses can infect bacteria just like any other organism and because viruses are just bits of RNA or DNA, they can jump into a bacterium, latch onto some genes and then jump to a different bacterium, transferring those genes in the process. So that’s like I caught the flu from you and with it I got your mother’s eyes. The third way bacteria exchange traits is through conjugation, which is kind of like sex. So let’s say Bobby and Benny E. coli are feeling frisky and Bobby builds a gene passing connection over to Benny and when they break apart Benny can now do something that only Bobby could do before. So you see where this is going. A particular strain of bacteria could suddenly become resistant to an antibiotic by catching a virus, robbing a dead friend or by having sex with a live one. And just like the evolution of any other organism the bacteria that acquire the toughest, most resistant traits become more fit, more adaptable to a range of environments, and are thus more likely to survive and thrive. So in a way the superbug phenomenon, that’s going on right now, is kind of like watching natural selection played out in fast-forward, which is cool and scary. But now you have a sense of how high the stakes would be if say a resistant strain of the plague started moving around the globe. But luckily, for the last 70 years, or so, we’ve had antibiotics, also called antimicrobials or antibacterials. And they work by either destroying the bacteria or slowing their growth enough that the human body’s own immune system can finish the job. Basically an antibiotic is a selective poison designed to find, bind and kill bacteria, without damaging their host cells in your body. These drugs usually work by attacking a unique bacterial target, like a particular protein, or a bacterial process, like the way they build a cell wall or metabolise sugar. For example most bacteria build their cell wall using a specific combination of sugars and amino acids, a combination that our cells don’t use. So antibiotics like penicillin block the production of that material, so the bacteria’s wall is weakened and bursts. Other antibiotics may attack bacteria’s metabolic pathways. All cells require folic acid, aka vitamin B9, to function. This vitamin easily passes into human cells, but it can’t enter bacterial cells. So bacteria have to make their own. The sulfa family of antibiotics, made from a sulphur compound, works by disrupting the production of this vitamin, thus inhibiting their growth. And then there’s tetracycline, which combats infection by attacking how bacteria make protein. Tetracycline can get through bacterial membranes and disrupt protein production, enough to inhibit cell growth, while human cells remain safe. But as amazing as antibiotics are, they’ve got a really smart enemy and bacteria have a few effective ways of wriggling out of the crosshair. For one, some bacteria can basically just barf up the antibiotic when it gets inside it’s cell. They use their chemical energy to fuel what are essentially pumps that spit the antibiotics right back out of the cell, before it can do any harm. They may also get kind of sneaky and change the drugs target, so that the antibiotic can’t find what it’s supposed to destroy, because many antibiotics work only in a very specific molecule. If a bacterium can replace that molecule or rearrange it’s structure, that antibiotic can’t do it’s job. Bacteria can also go on the offensive and basically make a weapon that looks for and breaks down antibiotics. For example, some strains can produce enzymes that destroy penicillin by breaking open the compound that’s basically it’s active ingredient. And, of course, once a bacterium has figured out a good resistance it can pass that information along to it’s neighbors, through sex or viruses or pilfering and then it’s on to other human and animal hosts who travel all over the globe by land sea and air. And then it’s “goodbye drugs – hello plague”. So now you might be wondering – well, can’t we just develop new antibiotics? Well, we’ve already gone after bacteria’s most obvious targets. And what’s left are increasingly difficult alternatives. Basically, new classes of antibiotics will be a lot harder to discover and develop. We’re probably not gonna find them in a moldy lunch box. However, researchers at Oregon state university and other institutions around the world are working on a promising new antibacterial agent, called PPMOs. Lab studies have shown, that one type of PPMO has been really effective at controlling some kind of bacteria that I can’t pronounce. Which happens to be responsible for a lot of hospital infections. PPMOs are lab synthesized analogs of DNA or RNA. They target a bacterium’s genes, instead of just disrupting it’s cellular function. Although they haven’t been tested on humans yet, PPMOs may offer a totally different approach to fighting bacterial infections and possibly even other diseases with genetic components. Other researchers are looking at fighting superbugs with viruses. Bacteriophages are viruses that infect and destroy bacteria and spread to other bacteria. These phages are naturally occurring and can be found all over the place, including soil, river water and the human body. Each phage is specific to a particular type of bacteria and needs the proper host to multiply. The more targets it has, the faster the virus spreads and kills, making it especially effective against high concentrations of bacteria or chronic infections. You only need a tiny bit of the virus, which can be administered through a cream or a spray. And, so far, they don’t seem to infect human cells and they haven’t contributed to antibiotic resistance. So even though the risk of superbugs taking over the world is real and scary, we do have some reasons to be hopeful. And, in the meantime, there are some things you can do to help. First, it’s important to understand when you should and shouldn’t use anitbiotics. You don’t wanna gobble them up every time you feel kind of poopy. You might have a virus and antibiotics won’t help that. Antibiotics should be a last resort reserved for serious infections, when other treatments haven’t worked. And if you do need them, make sure you take them exactly as prescribed until the bottle is empty. Stopping early only makes the surviving bacteria stronger. Likewise, never take antibiotics without a prescription. No passing along left-over medication. And of course make sure you wash your hands, use soap, get vaccinated. If you prevent illness, you prevent the need for medications in the first place. The future peoples of earth will thank you. Thank you for watching this SciShow infusion, especially to our Subbable subscribers who keep these episodes coming. If you’d like a little bit of SciShow for yourself, like a SciShow tie or a chocolate bar, you can go to subbable.com to learn more. And if you have any questions or ideas for an episode you’d like to see, you can find us on Facebook and Twitter and as always in the comments below. If you wanna keep getting smarter with us you can go to youtube.com/scishow and subscribe.