This Podcast Will Kill You - Ep 15 MRSA: Make Resistance Susceptible Again

Episode Date: December 11, 2018

We've gotten pretty graphic on this podcast before, but this episode takes it to a whole new level. The omnipresent Staphylococcus aureus is a bacterium that wears many faces. Often that face is harmless, but Staph has the power to invade and infect nearly every organ of the body, leaving destruction (and a lot of pus) in its wake. While Staphylococcus aureus has been wreaking havoc on humans since well before the discovery of antibiotics, Methicillin-resistant Staph aureus (MRSA) has risen to terrifying prominence as resistance becomes the new norm. If any disease could make you run out (or stay in) and wash your hands, it’s this one. As always, you can find all of our sources at thispodcastwillkillyou.com/episodes.  See omnystudio.com/listener for privacy information.

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Intuit Enterprise Suite. All your data in one place with built-in AI for real-time insights. Learn more at intuit.com slash ERP. Warning. For the squeamish, this is about to get graphic. Inside Tony Love's fingers, they found pockets of pus the size of nickels. There was one in the center of his hand.

It was the size of a golf ball. Orthopedic surgeons probe Tony's hips and shoulders with a long, wide-bore needle, looking for infection trapped behind the joints' cartilaginous sheaths. His left knee, the one he couldn't bend, was rigid and swollen. When they slid the needle in, pus pushed out under pressure, forcing back the base of the syringe. They got out enough to fill a baseball. One of the orthopedic surgeons sliced into Tony's left thigh

and eased apart the muscles. There was pus underneath them, creamy and dull. There was too much to evacuate through the small incision they had cut, so they kept cutting. looking for the end of the pocket. They laid his thigh open from his knee almost to his hip joint. Wherever they cut, they found a dense deposit of pus wrapped around the bone. They used a tool like a dentist jet to work it free,

rinsing the cavity between bone and muscle with high-pressure water and sucking the slurry away. The abscess was so deep that they could not trust they had cleaned out all the infection, and so they left the gash open. They wrapped it in dressings that would let the mess drain and rolled him back to the ICU. I'm Aaron Welsh. And I'm Aaron Alman Updike.

And you're listening to This podcast will kill you. Yep. Yeah, yikes. That's like pretty gnarly even for our standards. Oh, absolutely. Wow. So that was a little excerpt adapted from Superbun. by Marin McKenna.

Shout out, Marin McKenna. Making it grow. Oh, my gosh. So it's part of Tony Love's story, who was a 13-year-old boy from Chicago, who in 2007 became infected with a deadly strain of Staphylococcus, orius,

the star of our show today. Yeah. And this strain was not only metacillin-resistant, but also slightly resistant to vancomycin, which is the last resort antibiotic. We're going to get all into that, so just wait. So as you may have guessed, this week we are covering Staphylococcus aureus, specifically Mercer.

Mercer. What is Mercer? So Merza is mephacillin-resistant Staphylococcus aureus. Okay. We'll get into all of that, but first there's a really important business we need to take care of. Yeah. And what is that again? It's what we're drinking.

Oh, this week is a real doozy, I must say. Yeah, it's pretty. We've outdone ourselves gross wise. far as quarantines go for us. Like we've, we've tried some things. Yeah. And this time is...

The visual is striking. We encourage you to make this. Please do. And then please post pictures of it. Please do. So we are calling it. It's hard to say without laughing. Fruit of the wound.

Fruit of the wound, ladies and gentlemen. So it is a gorgeous licking cocktail. It's truly something spectacular. Basically a gin fizz with... A nice big old scoop of vanilla ice cream on top. Yeah, so that it slowly oozes down into the blood cavity. And make sure you top it with a cluster of grapes. Mm-hmm.

Okay, I guess we should move past what we're drinking. Yeah. And I want to know what is Staphoreas. Yeah. Let's talk about it. Okay, so the first thing to know about Mercer, which is its colloquial name, I suppose, is it's kind of a weird one for us because most of the time when we cover a disease on this show, we're covering something pretty specific, right?

Tuberculosis is transmitted in a certain way. It causes a certain set of symptoms, blah, blah, blah. Right. And this is the epidemic and this is the whatever. Right. So Merza is a little bit different because it's kind of a specific form of a specific pathogen that can cause so many different diseases, as we'll see. So, Mercia, we already said it stands for metacillin-resistant, staphylococcus, orius. So what is Staphoreus? That's the first question that we have to answer. Am I right? You're totally right. I know. So Staphoreus is a gram-positive coxye, which means it's a bacteria that's shaped like a ball.

Okay. Weirdly, usually I can say, you know, this bacteria is transmitted in this way, like fecal oral orl or respiratory droplets, right? These are things that people who have been listening, you know these terms and you're familiar with them, right? But I'm not going to say any of those things right now. Because the thing about staff is it's absolutely everywhere. It just exists. So it's probably on your skin. It's in your nose. It's on your food. It's in your butt. We're talking staff aureus, not necessarily Mercer.

Right. Stafforeas. So I'm going to focus on staff orius for the whole first part of this biology section, just so we can get a feeling for what bug we're talking about. And that would include both strains that are resistant like Mercer, but also ones that are completely susceptible to all antibiotics. Yes, exactly. Just staphoreous. Stafforius, yeah.

The bigger umbrella. Big old essay. Okay. So, yeah, it's just, it's everywhere. It's, you know, it's probably statistically on at least one person in this house right now, just living on us. Yeah, 33%. Yeah, there you go. Boom. Way to go. But most of the time, it doesn't matter that it's everywhere. It just hangs out. It's like a mutual, not even a mutualistic. It's just like an organism that lives on you. It doesn't cause you harm. It probably doesn't do much that we know of. It just hangs out and it's fine. It exists as a part of you. But every once in a while, it can cause disease. And honestly, because we try and keep these episodes in an hour, I can't.

can't even talk about all of the different diseases that it can cause because that's just how many diseases Staphylococcusoreus can cause. And so it causes these diseases, like these so many different diseases because it, where it infects or how it infects or? Yeah, both. So I'll go through some of the different things that you can get from staff. And then we'll talk more specifically about both MRSA and probably what most people think of when they think about a staff infection.

Okay. Okay. So, first of all, there's a range of different diseases you can get from staff. You can get pneumonia. If, for example, you get a viral infection in your respiratory tract that then maybe causes some damage and leaves you susceptible, like your immune system becomes compromised, staff aureus that lives in your nose can sort of travel down into your respiratory tract, infect your lungs, and cause pneumonia. Boom. Number one. Number two, it can cause... How long is this list? It's pretty long. It can cause what's called acute endocarditis, which acute just means rapid onset, which in this case also means more serious, doesn't always. It can cause like a rapid onset endocarditis. Endo means inside card means your heart.

cardio, itis is inflammation. So we're talking inflammation on the inside of your heart. Okay, that sounds pretty, pretty dangerous. That's pretty bad. And we're not even talking about whether or not it's susceptible to antibiotics. This is just staphoreous. Grabbing on to your heart valves. No big deal. No big deal. Well, big deal, actually. It's quite big deal. It's quite a big deal. Yeah, so that can happen. It's especially common in IV drug users because staff can live on your skin. So if you inject into your veins through your skin, that bacteria can travel straight to your tricuspid valve and grab hold. It's fun. The tricuspid valve is in your heart, I assume? It's in your heart. Yeah, yeah, yeah, that's in your heart. Right side. It's pretty cool. All right, number three disease. It can also cause

osteomyelitis. Break that down for me. Osteo bone. Okay. Mial. Hmm. I actually don't know about that one. Ignore it. Iis. Inflammation. Bone inflammation. I really want to know when myel is now.

I mean like myel like myelin is sheath. So it must be sheath. I think because I do think it it, it affects like the very first layer of your bone. But it is like a bone infection that it can cause super common in children, probably what your friend Tony. Tony Love. Tony Love. Not actually friends, but you know what I mean. Our first hand account.

Our first hand account. Tony Love most likely had some form of osteomyelitis based on his symptoms. God, sounds terrifying. It is. It's super scary, especially because in like super young kids, you'll just have this like crazy joint pain. And, you know, if you're a parent or whatever, you're like, what could possibly be wrong? Like, you might not have any visible outer.

issues. Like you had a scrape a couple weeks ago that completely healed and now all of a sudden you can barely walk because your knee's infected with sapporious. Kids are scraped all the time. They're rough and tumble. Like you, I can't, I still have gravel embedded in my knee from. I have some in my head. And so to think like, oh, well, that must be the cause of it. Oh, it's crazy. Yeah. It can also cause various forms of arthritis. So if infects your joint rather than your bone directly. Yeah. It's everywhere.

Also, not done. Stafforeas produces several toxins. Right? So each of those could probably, like we could have a whole episode on all the various toxins that Stafforeas produces, but some of them you've probably heard about. So one of them is an exfoliative toxin. Does that sound nice? Yeah.

Exfoliant. Great for your skin? Sure. Nope. It causes like your skin to just sluff off. I don't like the word sluff. Sluff. That's the word I'm going to use. Yeah. It can also cause, have you heard of it, toxic shock syndrome? Oh yeah. Oh yeah. That's staphoreas, Bip. We're not going to get into soup's detail about it because like, again, it could be a whole episode. But it's basically a toxin called, it's called a super antigen because it basically makes your, it's anogen, which is something that your body reacts to and makes antibodies against and it makes your body make so many antibodies like it is like all the antibodies come

to me and so then your body goes crazy and it goes into shock because you just have so much immune system action that your body is like can't just your immune system goes crazy kind of and that is from staph a serious can i ask a stupid question of course what is going on biologically with shock. Oh, I feel like that's a whole, that's a whole episode. I know, but like give me the. So there's a lot of different forms of shock. There's septic shock, which usually is from some kind of bacterial infection.

And then there's also things like cardiogenic shock, hypovalemic shock, shock. All of these basically involve a drastic drop in blood pressure. So that's the underlying mechanism that's going to make you end up dying, is that your blood pressure essentially plummets and then your organs start to fail because they're not getting blood perfusion to your organs. Okay. And then you die. Okay.

Yeah, cool, right? So toxic shock syndrome. Toxic shock syndrome. Wonderful. So shock induced by a toxin. Not done, by the way. Oh, God. There's more.

There's another toxin that it can produce that causes very rapid onset food poisoning. Drink that drink, Aaron, drink that drink. You're probably fine. Oh, God. As the ice cream curdles. It does. It is curdling. But yeah, this food poisoning is like super, super, super rad rapid onset, like within one to eight hours.

Because what's basically happening is if you leave out a plate of, let's say, spam and eggs, because that's a really good example. Or for you Midwesterners, potato salad. Okay? Potato salad, mac salad, anything. Mayanays, meat. Anything that's called salad only because it has mayonnaise added to it. Yeah. Yeah. Truth.

Yeah. Chicken salad. Tuna. Yeah. You leave that out on the counter. It's covered in Staphoreas. It's everywhere. That Staph aureus starts producing a toxin.

And then it just sits there. So then you're like, oh, I forgot. I'll put this back in the fridge. It doesn't matter. The toxins already there. And then you're going to eat that Mac salad because it was so good yesterday. day and then eight hours later you're barfing all over the place and it is preferentially barfing and not diarrhea ink so interesting okay yeah okay so if you ever have food poisoning

barf yeah like super right after you ate something where you were like i probably shouldn't have eaten that oh god i was my rap today you're not barfing yet not yet it's almost been eight hours yeah so that's a lot that is a lot and there's one more this is crazy Isn't it crazy that all of these different things can be caused by the same bacterium? It's bizarre is what it is. It's so, it is so, so interesting to me. But probably the most common thing that people associate with staff infections, I know what I used to associate with staff infections, goes a little something like this.

I saw a bump. Maybe it was on my butt. Maybe it was on my arm. I don't know. I just had a bump. I thought it was a pimple. So I tried to pop it. Or maybe I thought it was a bug bite, but it didn't itch.

So I was like, that's kind of weird. Huh. But it's just like a bug bite. It's fine. It's going to go away. Maybe a spider bite. Maybe definitely a spider bite. But it wasn't.

And then it just didn't go away. And then the next day, it was kind of bigger. And it was kind of like leaking and oozing. And then the next day, my entire butt was covered in a giant bloody pussy absente. Yes. It was just oozing and it was bleeding. Oh, God. This did not happen to me, by the way. I'm saying me, but I'm just saying the royal me. It could have.

It could have. Luckily, it hasn't as much as I'm willing to say, at least. But that's sort of the classic staff infection, and that would be a staff skin infection. Okay. Right? So staff gets into any kind of open wound, super common to happen after. shaving where you get like infected hair follicles. Stop shaving your peeps, peeps.

Seriously. Seriously. And yeah. And so that's kind of the prototypical staff infection. Yeah. That is skin infection. You end up with this open abscessing wound that kind of just doesn't heal and maybe keeps growing or maybe kind of stays the same size but just doesn't heal.

Like you put neosporin on it and it just doesn't go away. So that's super common. And that's Staff Oreus. How crazy it is that staff can infect so much of your body. Yeah. Like so many different parts. Yeah. So one of the questions is how on earth can it actually do that, right?

Like how can it infect your lungs and give you pneumonia but also give you a skin infection? Right. That's weird. It's like the jack of all trades bacteria. Yeah. It really is. So there's a few different ways that it manages to do this. And it mostly just centers around evading your immune system full stop.

Okay. It's just kind of really good at that. So one of the things it does is produce exotoxins, which we already talked about, right, some of the toxin-mediated diseases like toxic shock syndrome and barfing food poisoning, for example. Okay, but it also has another way that it is able to cause disease. and that's by this particular surface protein that it has. It's called Protein A, which is not creative. But it basically is just a protein that is really good at both evading our immune system.

So it's good at hiding from our immune system. And it's really good at invading our epithelial cells. And epithelium are the cells that line basically everything in your body. So your skin is epithelium. But also the inside of your lungs, that's epithelium. The inside of your heart, also epithelium. Your entire GI tract, also epithelium. So this protein allows it to invade those cells very, very easily.

Okay. So this bacterium lives on the surface of a lot of our body. Yes. But it also possesses the key to invade the surface of our body? Yes. That seems highly serious. suss. Right? It is. It's a highly sus. I think I use that perfectly. Perfectly correctly. So can we talk for a second about resistance? Yeah, that's, I think,

what we need to talk about next. Okay. So yeah, so Mursa is a resistant form of this horrible staff bacteria that we've been talking about. So antibiotic resistance in general, just for people, who might not be aware, just means that when you try and give somebody an antibiotic, which normally would help cure an infection of bacteria, it doesn't work. Okay. Mercer happens to be a strain of staph aureus that is resistant to what are called beta-lactam antibiotics, which means like metacillin, penicillin, a bunch of the... Illins?

Cillins, illins, chillins. And the way that it does that, it's basically just changes a protein so that the antibiotic can't bind to it anymore. Okay. That's pretty much it. But I know the question that you want to know is how on Earth can it become resistant? Yeah. Right? Like how does that happen?

I want to talk for like an hour about this. Oh, that sounds like a great idea. Should we maybe do a future episode all about antibiotic resistance? I think we're going to. Or antibiotics? Antibiotics and antibiotic resistance because it is really fascinating the way, like the evolutionary arms race that happens between a bacteria and what you treat it with. Most of the antibiotics that we have actually come from other bacteria or fungi or plants. So these are substances that are produced in nature in order to.

fight off bacterial infections that invade them. So whether it's a bacteria fighting off another bacteria or a fungus trying to fight off a bacterial infection or what have you. And so bacteria are constantly evolving ways to fight off these defenses and then other bacteria and funguses and plants and people are constantly evolving ways to try and fight off those bacteria. but basically what can happen is that once you get a mutation, for example, in the case of MERSA, in this single protein essentially, you can then, you change this protein just enough that this antibiotic can no longer bind. Once that single bacteria has that protein, anytime you give it penicillin or metacillin,

it's going to survive, which means it's going to still hang out in your body. And reproduce. And reproduce. So now that the new colony that's in your body now or in your nose is now all of them are resistant. And even if you have other bacteria, like, let's say you've got like six different kinds of staff living on your body because that's not insane. Staff is everywhere, right? Once you start hitting those staff with an antibiotic, if there's one that happens to

resistant. Bacteria can do something called conjugation, which is kind of like bacteria sex. Yep. Basically, they can give each other the ability to also resist penicillin. And so it can spread both by a single bacterium replicating, but it can also spread from bacterium to bacterium via conjugation. And it's really more, it becomes a numbers game. Yeah, absolutely. You just have so many bacteria reproducing or replicating that one just by probability is going to evolve that mutation. Exactly, right. Or that mutation will emerge and then it will spread in that population. Yeah, yeah, yeah, exactly.

So, yeah, that's pretty much, that's pretty much MERSA in a nutshell. It's not an all bad news game because most Mersa is still. susceptible to another antibiotic called vancomycin. Okay. Okay. So it's not like we've run out completely of treatment options. But yeah, I mean, it's, it is really scary because if you don't identify an infection as a MRSA infection and you start treating it with penicillin or metacillin, it's not going to do anything. And in some cases it might make it worse because now you're going to have, you know, your, your resistant populations spreading that gene to.

susceptible populations within a single individual. So tell me, Erin, how did we get to this horrible, horrible place? Great question. Do you remember the first time that you heard about Mercer? No. I don't remember like the first time, but I feel like when I was in maybe middle school or high school, it started to be talked about a lot. Huh. I think I didn't hear about staff infections until I was in college, and I wanted to go to Morea to do work. And my mom was like, you just got a staff infection from the coral. And I was like, okay.

Wise mothers. No, I remember hearing it probably on like Channel One News or something like that. But I remember all of these scary headlines about locker rooms and gym mats and the pimple that brings death. And I feel like a lot of these headlines focused on individual stories of parents losing a child or someone losing an eye or a leg or something like that. I feel like there was this larger story to it where Mercer seemed to represent dinner shows up every night, whether you're prepared for it or not. And with Blue Apron, you won't need to panic order takeout again. Blue Apron meals are designed by chefs and arrive with pre-portioned ingredients so there's no meal planning and no extra. grocery trip. There, assemble and bake meals, take about five minutes of hands-on prep. Just spread the pre-chopped ingredients on a sheet pan, put it in the oven, and that's it. And if there's truly no time to cook, dish by Blue Apron meals are fully prepared. Just heat them in the oven or microwave,

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com slash this podcast. A failings of modern medicine. It was this wake-up call where suddenly we could no longer rely on the antibiotics that we had taken for granted in some ways over the past 50 or 60 years. It was kind of like we were being sent back in time. Before antibiotics, you could easily die from that scratch on your leg that you got walking through some bushes. A little swelling, a little redness, a little fever, a lot of.

of pus and the next thing you know you could be dead from systemic infection. Yeah. And if you were unfortunate enough to have surgery in pre-antibiotic days, forget it. Like, you're a goner. You're dead, 100%. You're a goner. I don't know how anyone survived surgery. But infection was such an everyday part of life that we don't really have a written history of something like Staph-Oreus the way we do for the other big names and infection. Yeah, that makes sense. So, let's go back to around 1880. I know that you're going to be thrilled with this.

I'm always thrilled. Because you are a Scottish man. Oh, my God. You've been practicing for this. I have been. With an amazing mustache. Brochurch. You can say the one word that you know how to say.

In my Scottish accent. So you are a surgeon and professor at the University of Aberdeen. Aye. And your name, Alexander Ogston. Oh, I'm not even going to try to do that in a Scottish accent. You're welcome, everyone. Yeah, no, I've listened to it. It's pretty bad.

It's awful. It's really bad. Not that I could do better, but. But why? do I keep trying is the question. I don't know. But I will. Continue.

Anyway. Okay. So you happen to be one of the surgeons who got into medicine so that you could help people and improve their lives, which is great. But there's one problem. About half of your patients seem to die after you stitch them back up. Aye. Now, as part of your, quote, med school training, you have been told.

that pus production from the incision site is an essential stage in the healing process. Oh. But something about that doesn't sit right with you. In your search to try to find out how to, quote, do no harm, you come across someone named Joseph Lister. Love him. Right. Joseph had this crazy idea that maybe surgical tools and wounds should be cleaned

after before and after surgery? It's so fun to think of how novel this. I mean, it's not even novel. It was revolutionary. Yeah. It was completely, yeah. But that also, he also thought that maybe a seeping wound wasn't a good thing.

You know? You decide to try out his approach, which was applying carbolic acid to wounds. which had been shown to be pretty dang effective. And it works for you too. Congratulations. Thank you. And you actually become such a fan of the practice

that your students make up a song about it. Do I get to sing it? Yes. Okay. And so the song goes like this? Sing it. The spray. The antiseptic spray. A. O would shower at morning, night, and day. For every sort of scratch where others would.

attach a stinking plaster patch he gave the spray. I think it was sticking plaster pet. Is it stinking? I don't know how I said. It does say sticking. Good enough. Close enough. Good enough.

It probably stunk, if we're being honest. Oh, yeah, absolutely. That was amazing. Thank you. That was a beautiful song. If I do say so myself. This is pretty great. Wonderfully done.

So, yeah. Lister. thinks that the wounds are putrefying because of bad air. He's close. You, on the other hand, are a bit more forward thinking and suspect that it's some kind of infection. So one day you take some pus from an abscess on one of your unfortunate patients and smear it on a microscope slide.

Under the microscope, you see some round clusters of cells that look like grapes. Later, you journal about it. Quote, my delight may be conceived when there were revealed to me beautiful tangles, tufts and chains of round organisms in great numbers, which stood out clear and distinct among the pus cells and debris. I love it. Yeah. The name Staphylococcus is given to the bacteria, staphile from the Greek, meaning

bunch of grapes, and cocus meaning berry. Later, orias is given to the staff species that grows yellowy clusters on a plate. orius from the Latin orum meaning gold. Gorge. There you go. Okay, enough etymology, though. Clearly, you are thrilled about this finding, and you figure that the rest of the medical establishment

would also be pretty pumped. Right? No, they're not. Not at all. They're skeptical and resistant to any challenge to the long-held view that infection was just a natural part of wound healing. Typical.

So you have to perform a public presentation of your research to prove that you covered all your bases and went through all of the postulates. And finally, they accept that you might be on to something and you get all the praise and blah, blah, blah, blah. Okay, so at this point, it's 1881 and microbiology is an exciting new field to be in. New bacteria and parasites and viruses are constantly being described, and vaccines are in the works and being released, and so on. In the first half of the first half of the the 20th century is also where we see some really amazing medical developments that seem like magic for both patients and doctors. In 1941, penicillin, which is an episode in its own right,

begins to be used to treat infections of all kinds. At first, just soldiers in World War II, just restricted to them. But a few years later, it begins to be widely distributed to the public. And it was viewed as this wonder drug, which it really was. In the 40s. 1940, I think four was when it was distributed to the public. That is insanely recent. Yeah. Very recent.

So before penicillin, 80 to 90% of people who had staphoreous bacteremia, infection of the blood, died. 80 to 90%. Jesus. And I don't have exact numbers for the number of people every year because, again, And like I said, it was such this, it was a common thing, but it wasn't, it didn't happen in outbreaks and clusters. And so you didn't write it down. Yeah.

And it also wasn't a single disease, right? It was like people were dying from Staphoreus, but from so many versions of Staphorius. Yeah. Yeah. So it was really hard to keep track of. Yeah. But anyway, after the introduction of penicillin, those deaths due to any version of Staphoreus dropped hugely.

Man. In addition to a lot of other bacterial infections. Penicillin became the default treatment for many infections and was handed out like candy at Halloween. You could get penicillin in the grocery store without a prescription, without any information or instructions on how long you should take the pills, how many each day. Oh, my gosh. Mm-hmm. Mm-hmm. And its early effectiveness led to some hygienic practices falling by the wayside.

Oh, no. So basically now that you could cure these common infections, focus shifted away from prevention and more towards treatment, not consciously necessarily, but just because prevention was no longer as crucial as it once was. Wow. And as you can guess, the overuse and misuse of penicillin, even in these early days, led to resistant strains of staph aureus popping up and spreading almost immediately after penicillin was introduced. Like really almost immediately. Yeah, I mean, even currently, it only takes, like, a matter of months to a couple of years for resistance to develop to new antibiotics. Yeah. It's insane.

It's insane. Within five years of penicillin being introduced, 50% of staphoreous strains that were isolated were resistant. And that number would just continue to climb. Oh, my God. So sitting here now, 70 years later, it's easy to go. Well, yeah, duh. Of course, antibiotic resistance evolved. Look at how you dose people.

Look at how you were irresponsible. I can't believe the lack of foresight. You did everything wrong. Right. But I think it's really worth noting that the threat of resistance had been recognized almost immediately by many people. Really? Oh, yeah. Including Alexander Fleming, who was the dude who discovered the mold that made penicillin.

Wow. So in 1945, in his Nobel Prize, acceptance speech, he said, quote, there is the danger that the ignorant man may easily underdose himself, and by exposing his microbes to non-lethal quantities of the drug, make them resistant. Whoa. Yeah, so right after, like, right after. Like literally right out of the gate. He had already been thinking about this clearly for years. He's like, guys, listen, seriously, I know this is great. No, but we can't mess it up.

And then people are like, yeah, cool, great, great, buy, take your prize, peace. Right. Yeah, so despite this warning, by the mid-1950s, penicillin-resistant staff had become a public health crisis around the globe. In Australia, women who had just given birth were showing back up at the hospital with their severely sick newborn, covered in broken blisters or blue with pneumonia, and the mothers were often sick themselves with open weeping abscesses on their breasts often. Oh, no. Yeah. And the strain of staff causing these infections proved to be both extremely infectious and extremely resistant, not just to penicillin, but to many of the other antibiotics that had been developed at that point. Oh, no. And it didn't take long for these outbreaks to appear in the U.S. And the thousands of cases and dozens of deaths prompted an emergency meeting of the American Medical Association. Something had to give.

better hygienic practices, better drugs, and definitely better record keeping because it wasn't a reportable disease. Yeah. Staff infection was normal. This was something of a rude awakening to hospital physicians everywhere, especially those who had joked that infectious disease doctors would soon be made obsolete by antibiotics. Never. No, really, never.

I'm counting on that for a job, quite honestly. Many hospitals instituted practices and appointed committees specifically to control the spread of this resistant staff orias. Newborns were placed into infected or uninfected rooms based on whether they showed any signs of infection. But it wasn't working. Cases were still on the rise and babies that had no apparent contact with an infected person were still becoming infected. This infection was such a problem for newborns because newborns are so fresh and new. I thought you were going to say so fresh and so clean, clean. So when they're born, their skin and mucous membranes are immediately colonized with bacteria

from their mom's vaginal canal, from breast milk, and from the surfaces they encounter after birth. And this goes towards building the microbiome of this tiny human. But there's still a lot of open territory for other potentially harmful bacteria. to colonize. And this resistant staphoreus strain was so infectious and such a fast grower that it pushed out all the other bacteria and basically became the microbiome. Whoa. So what on earth do you do about a bacterial strain that wipes out all competition instantly and is untreatable by the drugs you have? You come up with new ones, but?

Well. Or you die. There's a third option. Okay. So it does seem pretty hopeless. But one doctor had an idea. So this guy was named Heinz Eichenwald, and he remembered an old practice that was used to get rid of diphtheria infections from carriers of the disease in days before the vaccine. I love this.

It was called bacterial interference. Yep, you're pretty thrilled. I'm shaking with excitement. So the idea was that you expose these people to a different, harmless bacterium that's a better competitor than the one causing the problem. This new bacterium then takes over and pushes out the harmful one, and voila, infection gone. I love it. Clean, classy. It's really innovative.

Yeah. And very much in line with some technologies and treatments that are becoming popular nowadays, which is why I spent so much time. talking about this. But also, what year is this again? This is in the late 1950s. Okay, wow. So this is like still super early on. Like even antibiotics are pretty brand new. Yeah. Well, and I think it's really fascinating that bacterial interference was developed in like 19, the early 1900s, like 19-teens, I think, before the diphtheria vaccine was invented in 1920. Cool. So, So, yeah, it seems very forward thinking, which is, yeah, very cool. People stopped using bacterial interference in the 1920s when the diphtheria vaccine was released.

But Eichenwald hadn't forgotten about it, fortunately. So he set out to find a strain of staff that was more infectious than the drug-resistant staff strain, but not harmful. And once he found it, he set to exposing these newborns to the new strain. It was a pretty revolutionary idea for the time, but people were desperate to try anything. Yeah. Lives had been really ruined by this persistent infection showing up. Children who were infected weren't allowed to go to school. At least one couple had divorced.

Whoa. Over it, yeah. But Eich and Wald strain worked. The deadly infection was eliminated. It was miraculous. Wow. And for the next few years, it was used occasionally to treat, stubborn infections.

That's pretty cool. Yeah. But bacterial interference once again slipped out of practice in the late 1950s when a new antibiotic was released. Here we are, 1959. Well into the history of Staphoreas, and I haven't yet introduced you to who is in many ways the star of the show. Methicillin.

Methacillin-resistant Staph-Oreus. The new antibiotic that I just mentioned was. metacillin, and when it was released, it was advertised as, quote, effective against all resistance to falcocci. Resistance unlikely to development. Oh, dear. Within a year of its release, resistance to metacillin had already been found. And by the 1970s, Mercer was widespread in hospitals in the UK and making its way to the rest of the world. And cases weren't appearing as one-offs. It was more like a wave of infection. It would start. start off slowly with just a few people infected, and then it would rapidly jump across hospital

units, affecting the most vulnerable patients, like those just out of surgery or with severe burns. Deaths from Mercer were becoming more common, and the periods between Mercer outbreaks were becoming shorter and shorter. And while Mercer may have popped up a bit later in the U.S. and in some parts of the globe, it made up for lost time. In 1975, in U.S. hospitals, 2.4% of strains were metacillin resistant. Oof. In 1991, 38%.

Oh. And jumping ahead of it in 2003, 64.4% in ICUs, intensive care units. Of just like when they swab, like the, the equipment that's in there or... It's, yeah, I think it's like of all isolates from hospitals.

Okay, yeah. Mercer was becoming the new norm. and its spread and persistence was helped along by the hospital setting itself. In a hospital, nurses and doctors are constantly on the move, between rooms, between floors, different units. And while hygienic practices like hand washing and isolation work to a certain degree, Mercer is also carried really easily on the surfaces that we don't really think about as much. Like your nose. Well, yeah, a doctor's coat.

Yeah. The pen that a nurse or a doctor carries from really. room to room. Ties, bra. Ties. Ties are found to be like one of the most, like, germ-ridden. They're very controversial right now in medicine. Well, it's funny. Even bed curtains were found to be ridden with staff. Mercer. So these people were unknowingly spreading the infection around the hospital, between hospitals, and so on. And because hospitals are filled with people in poor health, vulnerable to infection, the bacteria found easy marks. thousands of people every year suffered MRSA infections that they had picked up at a hospital or nursing home, and many died.

And I don't use the word suffered lightly, because for many people, this was at least a life-altering and often a life-ruining infection. Recurrent MRSA infections are really common, and you can go from seemingly healthy one day and on death's door in what seems like a matter of hours without a whole lot of warning. or a whole lot of like, oh, obvious risk factors, whatever. So I do want to mention that several countries such as Denmark, the Netherlands, some Nordic countries, enforced really strict hygienic practices that greatly reduced MRSA infection incidents compared to other parts of the world, including the U.S. Yeah, so they were like very... And we're going to nip this thing in the butt. Wash your hands, no, we're serious.

Yeah, really. And it really reduced, yeah, disease incidents. But in the other places, MERSA infections in hospitals became so frequent that it was basically second nature to look for signs of infection and jump on treatment right away, often relying on vancomycin, which is the antibiotic that Mersa was still susceptible to, which sometimes worked and sometimes didn't. Yep. But being in a hospital meant that you were simultaneously in the work.

place you could be because Mercer was everywhere, but also the best place for rapid diagnosis and treatment. Because Mercer was a hospital infection, right? Right? Right? Yeah. I mean, yeah, sure. For a while, it was. Until it started popping up in the 1980s in a few people here and there who had no history of being in a hospital or nursing home or similar setting. But when these people showed up at the ER with an extremely painful pimple or rash or something else, Mercer wasn't at the top of the list of possible causes. And so people were often misdiagnosed and sent home without the immediate medical care and abscess cleaning that they needed. And it took a while for Mercer to be recognized as something that you could pick up outside a hospital setting. But eventually

Mercer infections became grouped into either hospital-acquired Mercer or community-acquired Mercer. And these labels existed not just for patient history, but also because the strains were noticeably different. Hospital strains were all very similar to one another and were resistant to many different antibiotics. Community strains, on the other hand, tended to be much more diverse, resistant to only a couple antibiotics, but extremely virulent and infectious. Whoa, interesting. And logical, actually. Yeah, exactly. And so by the early 2000s, which is when I was in high school, a large proportion of all MERSA cases were community acquired, and epidemiologists had traced the source of many community outbreaks to places where staff thrives. Warm, moist, full of people. So places like gyms and locker rooms, right? So young athletes showing up to the hospital, completely.

planning of a sore ankle and within a few hours lying on operating table while a surgeon scrapes away infected tissue and washing pus-off leg bones. You know, those kinds of places. That's what happened. Once this pattern of Mercer showing up in athletes was apparent, many schools and gyms and professional athletic organizations took steps to prevent infection. No more sharing towels or razors. Gross and both counts anyway. Wait, who shares a razors. NAST. I don't know, but apparently it was a problem. Geroad. Don't do it if you do it.

No judge, but don't do it. Judge, I'm judging. Also, regularly cleaning surfaces with antibacterial soap, hand-washing soap available, you know, just basic hygiene stuff. And this really did help decrease cases of MRSA in these places. But the thing is that not all school districts, or gym facilities or other high-risk places like prisons can afford to maintain these practices. Yeah.

And so we see, again, these health disparities arise, which are then reinforced by the fact that poorer people are at higher risk for infection, so they have to spend more money on treatment, which in the U.S. is often very expensive, and then the cycle just sort of continues. It's this positive feedback loop. For a while, the distinction between hospital acquired and community, acquired Mercer was very important for treatment and for predicting the severity of the infection and where it might go. And doctors and researchers began to worry about the rise in community acquired Mercer cases, not just because it caused deadly horrific infections that were difficult to treat,

but also because they were worried about what would happen if, to quote the Spice Girls, to become one. So if hospital acquired Marce. Mercer and community-acquired Mercer met and exchanged genes. Ooh. If thought, yeah. And so if the hospital strain transferred some of the super resistance to the community strain, or if the community strain kicked over a few genes for toxin production.

Yeah. Yeah. Problematic. Very. Well, as you can probably guess, it was just a matter of time. Yep. Two did indeed become one. And the distinction between hospital or community.

acquired became less important. Rather, worrying about whether we can actually treat this thing became the primary focus. Because a few cases of Mercer earned a new name, Visa or Versa. And those mean either vancomycin intermediate or vancomycin-res, basically distinguishing between the different levels of resistance for this level of Staphoreus against vancomycin, which had been used as the last resort antibiotic. Right. So whether like using vancomycin could kill it at all. Right.

Or whether you just have to, intermediate would be you'd have to use like a really high dose of vancomycin. Right. And because Mercer is still treatable. Right. With antibiotics. Yeah. With mostly vancomycin. But Versa and Visa, no.

So yeah, these infections were truly terrifyingly untreatable. Staph aureus had come full circle. So earlier when I was researching this episode, I kept telling you that this is probably the first time that I have been genuinely freaked out by one of these infections. Yeah. And there's definitely plenty to be scared about with these other diseases that we've talked about. But there's something different about this one. I don't know what it is exactly. It's everywhere.

I think that's what it is. I think a part of it is that. I think a big part was Marin McKenna's really eloquent descriptions of like, Puss-filled cavities and oozing sutures and poor like horrible very tragic stories in people's lives being hugely impacted. But also that's yeah, staff is everywhere. Yeah. And so far our medical relationship with it has gone in one direction. Yep. We're running just to keep up. We've maybe had one foot ahead for the briefest amount of time. Right. And then it catches right up with us. Yeah. Yeah. But. So,

So the question is now, what comes after? How do we fight MRSA or Visa or Versa without antibiotics? And so that is where I'll hand it off to you. Yeah, unfortunately, I don't have great news. Cool. So let's talk about the news that I have. All right. So the CDC has this monitoring program.

It's active in a few different states, California, Georgia, Minnesota, New York, and Tennessee. Not the entirety of those states, but several counties in each of those states. That basically means that they are actively surveilling about 14.5 million people. And they haven't compiled all the numbers from the last couple of years. So the most recent numbers that you can get are from 2015. And they're not extrapolated out to the whole U.S. Okay. But I did the math for you because I'm a mather. You had a math model in your dissertation.

Yeah, yeah, yeah. Yeah, I did math. So in 2015, which is the most recent numbers I could find, in those 14 and a half million people that they actively surveilled, there were 2,600 cases. So I heard that and I was like, well, Marshall's not even a big deal. Chill out, guys. Relax.

I don't know. Seems like a lot of cases. And then there were only 332 deaths in that population. I mean, like, on the scheme of things. Right. I was like, that's not so bad. Then I was like, also, I'm heartless. And, yeah.

Like, maybe I have lost my humanity. But I wanted more numbers because that made me feel like I was a bad person for thinking that wasn't a lot of people. So if you extrapolate out those numbers, if we assume that that population that they're surveilling is representative of the whole country, which is kind of the point of surveillance. So let's hope they did a good job. Then that would mean that in the U.S. in 2015, there were over 53,000 MERSA infections. 42,000 of those would be hospital acquired and 11,000 community acquired. Wow. And over 6,600 deaths.

Yeah, I mean. And those numbers do match. Yeah, those numbers that I just calculated on my own are similar and in line with what the CDC's estimates from 2014 were, which were a total of 61,000 cases and 9,000 deaths. But overall, about one in three people are carriers of some form of staff orius. Like, they're just walking around with staff growing on them. And it's estimated that about two in every 100 people, so 2% of the global population, are carriers for some kind of MRSA. And carriers, meaning they're growing it, they're breathing it, they're licking it, they're touching it onto their doorknobs. But not necessarily.

Probably never getting, maybe getting infected with it, right? If they get a cut and then that MRSA that's on their. their skin gets into them. But maybe they never, ever, ever see an infection from it, but they give it to their brother and their cousin and their neighbor and their barista. Yeah. The most important people. Those are my favorite people. Yeah. And so that that 2% is just in the general population. There are some populations where the situation is even worse, like hospitals, right? Like you said hospitals are just, if you're going to get staff in a hospital, it's probably going to be Merza, but also places like correctional facilities. You can imagine that many correctional

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and join me, Jenna, for The Ripple Effect. It's a reminder that you can start a ripple that changes everything. You really can. Listen to the Ripple Effect with Jenna Kim Jones on the IHeartRadio app, Apple Podcasts, or wherever you get your podcast. Correctional facilities have various situations that would make them immunocompromise. Right.

So MERSA is described as hyperendemic. That does not sound good. It is not good. I had never heard that word before, but I can guess what it means. And that is like super, it's everywhere. It's not even just like, yeah, we have this disease. It's like, no, it's everywhere. There are some estimates that,

between four and a half to 17% of inmates were carriers from Mercer. That's crazy. It's so high. It's insane. Yeah. I mean, it's at least twice as high as the general population, if not, like, nine times as high. Right. You know, it's insane.

The question now becomes, what do we do? And how do we move forward from this? And I... That's a... Yeah. That's what I want to know. I don't have a great answer for you. Okay. Okay. Okay.

Yeah. I don't. I don't have a great answer for you. I mean, like, you can find things that say the number of infections is decreasing, you know, and we're doing a great job. But I don't know how to believe any of it because I don't know where they're even getting these numbers from. Right. But the real issue is, with new... treatments, right? We're talking about now Versa and what the other one called? VISA, right? Vancomycin resistant. Oh, visa, whatever. It's not, it's bad news, right? Any way you slice it, the fact that we are now seeing resistance to vancomycin is very, very bad news. And so the thing is I found

an article that was that was basically talking about new novel ways to find antibiotics, right? They were using sequencing to find different compounds that could then be used as antibiotics. It was very cool. I'll link to the paper. There's another group out of Brown who's getting a lot of Popsai articles right now written about them because they're doing a lot of research on all these novel compounds and they've found a few that seem promising. And that's awesome and it's necessary and it's great. But it doesn't solve the problem that is the fact that these back.

Cacteria will inevitably evolve resistance to those antibiotics. You're just playing the same game that we have been playing that we are losing at. Yeah. And have never won it. So I was really hoping when I started researching this that I was going to find phage therapy and immunoglobulins and I found nothing. You didn't find any phage therapy? I found that it exists, but I found no details on what the state of the research actually is. Okay. What about bacterial interference?

I found nothing on bacteria interference. Wow. Wow. Yeah. So it doesn't mean it's not out there. It just means that it's maybe not the first steps that people are working on, which is kind of a bummer. But also, maybe I'm just totally wrong and was looking in the wrong places, and someone listening is going to tell us that they're working on a new phage and bacterial interference. And biofilm treatment. Something, you know, because it has to be happening, right? Like, I would hope, unless it's just that for some reason there's no money in it. But it seems like if we're going to put money anywhere, it should be in finding alternatives to antibiotics

because we're going to need them for so different many infections. Yeah, it's a good place with some money. Yeah. But I don't have a great answer. I don't have like, here's the newest thing and it's going to solve all of our problems, goop. Yeah So Okay

So how How scared should we be of Merza? I mean I don't want to tell you like Like don't interact with other humans or something Like not that level That ship has sailed Yeah well

That's just for different reasons No I think Merca is a really scary one I think it's maybe up there with Maybe not up there with flu but it's up there. Yeah. I feel like they're all scary in there. It's a different scary, I think.

It's not as much like we're going to have this giant outbreak. It's more just like this thing already exists everywhere, and we're kind of running out of options to treat it. Mm-hmm. So. Yeah. It freaked me out. Don't look up videos.

Do look up videos. Yep. Mel. Devil angel. Devil angel. Take one of a who's who. I do. Do you have any sources that you'd like to cite?

I do, yes. So I got most of my information from Superbug by Marin McKenna, which is where I got the first-hand account. And it's a really great overview of the history of drug-resistant staphoreas, not just Marcia, but in general. And she's an amazing writer, and so it's very fun to read. I don't have any real sources. I'll post a couple of articles that were interesting.

interesting about Mercer antibiotics, new antibiotics. Oh, we should also say thank you to Bloodmobile for the music, as always. Thank you for listening. Oh, yeah. We love you. Thank you so much for listening. And if you don't already follow us on all the social needs, Facebook, Instagram, Twitter, we're there. Post and gross videos, probably a bunch of pimple poppers for this one.

No lie. I will. She won't. I will. So check the Twitter. We have a Goodreads book list. All of our sources are available on our website. This podcast will kill you.com.

You can find every single episode with all of our sources listed. We keep it legit. And yeah, I think really the only thing that we can say for this episode is really do. please wash your hands. You're filthy, you animals. We're filthy, all of us. Yeah, yeah. I'm going to go wash my hands.

Yeah, let's go do that. Success starts with your drive, and American Public University is here to fuel it. With affordable tuition and over 200 flexible online programs, APU helps you gain the skills and confidence to move forward. Whether you're changing careers, starting fresh, or pursuing a lifelong passion, Our programs are designed for people who never stop.

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