Speaker 1: Warning for the squeamish, this is about to get graphic.
Speaker 2: Inside Tony Love's fingers they found pockets of puss the
Speaker 2: size of nickels. There was one in the center of
Speaker 2: his hand. It was the size of a golf ball.
Speaker 2: Orthopedic surgeons probed Tony's hips and shoulders with a long,
Speaker 2: wide boarn needle, looking for infection trapped behind the joints
Speaker 2: cartilaginous sheaths. His left knee, the one he couldn't bend,
Speaker 2: was rigid and swollen. When they slid the needle in,
Speaker 2: puss pushed out under pressure, forcing back the base of
Speaker 2: the syringe. They got out enough to fill a baseball.
Speaker 2: One of the orthopedic surgeons sliced into Tony's left thigh
Speaker 2: and eased a part the muscles. There was puss underneath them,
Speaker 2: creamy and dull. There was too much to evacuate through
Speaker 2: the small incision they had cut, so they kept cutting,
Speaker 2: looking for the end of the pocket. They laid his
Speaker 2: thigh open from his knee almost to his hip joint.
Speaker 2: Wherever they cut they found a dense deposit of puss
Speaker 2: wrapped around the bone. They used a tool like a
Speaker 2: dentist jet to work it free, rinsing the cavity between
Speaker 2: bone and muscle with high pressure water and sucking the
Speaker 2: slurry away. The abscess was so deep that they could
Speaker 2: not trust they had cleaned out all the infection, and
Speaker 2: so they left the gash open. They wrapped it in
Speaker 2: dressings that would let the mess drain, and rolled him
Speaker 2: back to the ICU.
Speaker 1: I'm erin Welsh and i'm erin almond updyke.
Speaker 2: And you're listening to this podcast will kill you?
Speaker 3: Yep.
Speaker 2: Yeah, yikes.
Speaker 1: That's like pretty gnarly even for our standards.
Speaker 2: Oh absolutely wow. So that was a little excerpt adapted
Speaker 2: from Superbug by Maren McKenna.
Speaker 3: Shout out Marey McKenna making it grud.
Speaker 2: Oh my gosh. So it's it's part of Tony Love's story,
Speaker 2: who was a thirteen year old boy from Chicago who
Speaker 2: in two thousand and seven became infected with a deadly
Speaker 2: strain of Staphylococcus aureus, the star of our show today. Yeah,
Speaker 2: and this strain was not only methicine resistant, but also
Speaker 2: slightly resistant to vankamisin, which is the last resort antibiotic.
Speaker 2: But we're going to get all into that, so just wait. So,
Speaker 2: as you may have guessed, this week we are covering
Speaker 2: Staphla caucus oreus, specifically MERSA mersa.
Speaker 1: What is mersa so mersa is mephicillin resistant Staphylococcus aureus. Okay,
Speaker 1: we'll get into all of that, but first there's really
Speaker 1: important business we need to take care of that. It's
Speaker 1: what we're drinking.
Speaker 2: This week is a real doozy. I must say. Yeah,
Speaker 2: we've outdone ourselves even as.
Speaker 1: Far as quarantine needs go for us, Like we've we've
Speaker 1: tried some things. Yeah, and this time is.
Speaker 2: The visual is striking. We encourage you to make this
Speaker 2: please do, and then please post pictures of it, please
Speaker 2: do so. We are calling it hard to say without.
Speaker 1: Laughing, Fruit of the wound, Fruit.
Speaker 2: Of the wound, ladies and gentlemen. So it is a
Speaker 2: gorgeous looking cocktail.
Speaker 1: It's truly something spectacular.
Speaker 2: Basically a gin fizz with.
Speaker 1: A nice big old scoop of vanilla ice cream on top.
Speaker 2: Yeah, so that it slowly oozes down into the blood cavity.
Speaker 1: And make sure you top it with a cluster of grapes.
Speaker 2: Okay, I guess we should move past what we're drinking. Yeah,
Speaker 2: and I want to know what is STEPH forrius.
Speaker 3: Yeah, let's talk about it. Okay.
Speaker 1: So the first thing to know about MRSA, which is
Speaker 1: its colloquial name, I suppose, is it's it's kind of
Speaker 1: a weird one for us because most of the time
Speaker 1: when we cover a disease on this show, we're covering
Speaker 1: something pretty specific. Right, Tuberculosis is transmitted in a certain way,
Speaker 1: it causes a certain set of symptoms, blah blah blah.
Speaker 2: Right, and this is the epidemic and this is though
Speaker 2: exactly right.
Speaker 1: So MRSA is a little bit different because it's kind
Speaker 1: of a specific form of a specific pathogen that can
Speaker 1: cause so many different diseases, as we'll see. So MRSA,
Speaker 1: we already said it stands for methicillin resistant Staphyococcus oreus.
Speaker 1: So what is staph oreus? That's the first question that
Speaker 1: we have to answer, am I right, You're totally right,
Speaker 1: I know. So staph aureus is a gram positive coxi,
Speaker 1: which means it's a bacteria that's shaped like a ball.
Speaker 3: Okay, Weirdly, usually.
Speaker 1: I can say, you know, this bacteria is transmitted in
Speaker 1: this way like fecal, oral or respiratory droplets.
Speaker 3: Right.
Speaker 1: These are things that people who have been listening you
Speaker 1: know these terms, and you're familiar with them, right, But
Speaker 1: I'm not going to say any of those things right
Speaker 1: now because the thing about staff is it's absolutely everywhere.
Speaker 3: It just exists.
Speaker 1: So it's probably on your skin, it's in your nose,
Speaker 1: it's on your food, it's in your butt.
Speaker 2: We're talking staff oreas, not necessarily MRSA.
Speaker 1: Right, staff orious. So I'm going to focus on staff
Speaker 1: Orias for the whole first part of this biology section
Speaker 1: just so we can get a feeling for what bug
Speaker 1: we're talking about.
Speaker 2: And that would include both strains that are resistant like MRSA,
Speaker 2: but also ones that are completely susceptible to all antibiotics.
Speaker 4: Yes, exactly, staff orioas staff Orius. Yeah, the bigger, big
Speaker 4: old essay. Okay, So yeah, it's just it's everywhere. It's
Speaker 4: you know, it's probably statistically on at least one person
Speaker 4: in this house right now, just living on us.
Speaker 2: Yeah, thirty three percent.
Speaker 3: Yeah, there you.
Speaker 1: Go, boom, way to go. But most of the time
Speaker 1: it doesn't matter that it's everywhere. It just hangs out.
Speaker 1: It's like a mutual not even a mutualistic It's just
Speaker 1: like an organism that lives on you. It doesn't cause
Speaker 1: you harm. It probably doesn't do much that we know of.
Speaker 1: It just hangs out and it's fine. It exists as
Speaker 1: a part of you. But every once in a while
Speaker 1: it can cause disease. And honestly, because we try and
Speaker 1: keep these episodes in an hour, I can't even talk
Speaker 1: about all of the different diseases that it can cause,
Speaker 1: because that's just how many diseases staphylococcusorius can cause.
Speaker 3: It's so crazy.
Speaker 2: It causes these diseases like these, so many different diseases
Speaker 2: because it where it infects or how it infects or yeah.
Speaker 3: Both.
Speaker 1: So I'll go through some of the different things that
Speaker 1: you can get from staff, and then we'll talk more
Speaker 1: specifically about both MRSA and probably what most people think
Speaker 1: of when they think about a staff infection. Okay, okay,
Speaker 1: So first of all, there's a range of different diseases
Speaker 1: you can get from staff. You can get pneumonia if,
Speaker 1: for example, you get a viral infection in your respiratory
Speaker 1: tract that then maybe causes some damage and leaves you susceptible,
Speaker 1: like your immune system becomes compromised. Staph oureus that lives
Speaker 1: in your nose can sort of travel down into your
Speaker 1: respiratory tract, infect your lungs and cause pneumonia. Boom number one,
Speaker 1: number two. It can cause pretty long. It can cause
Speaker 1: what's called acute endocarditis, which acute just means rapid onset,
Speaker 1: which in this case also means more serious. Doesn't always.
Speaker 1: It can cause like a rapid onset that endocarditis, ENDO
Speaker 1: means inside card means your heart, like cardio itis is inflammation,
Speaker 1: So we're talking inflammation on the inside of your heart.
Speaker 2: Okay, that sounds pretty pretty dangerous.
Speaker 3: It's pretty bad.
Speaker 1: And we're not even talking about whether or not it's
Speaker 1: susceptible to antibiotics. This is just stapf orous grabbing on
Speaker 1: to your heart valves. No big deal, No big deal,
Speaker 1: Well big deal.
Speaker 3: Actually it's a huge deal. It's quite a big deal. Uh. Yeah,
Speaker 3: So that can happen.
Speaker 1: Uh. It's especially common in IVY drug users because staff
Speaker 1: can live on your skin. So if you inject into
Speaker 1: your veins through your skin, that bacteria can travel straight
Speaker 1: to your tri cuspid valve and grab hold fun.
Speaker 2: Try cuspid valve is in your heart, in your heart.
Speaker 1: Yeah, yeah, that's in your heart right side.
Speaker 3: Pretty cool, all right?
Speaker 1: Number three disease. It can also cause osteo myelitis.
Speaker 2: Break that down for me.
Speaker 1: Osteo bone Okay, Mile, I guess you don't know about
Speaker 1: that one. Ignore it itis inflammation.
Speaker 3: Bone inflammation.
Speaker 2: I really wanted to on Mile too.
Speaker 1: I mean, like Mile, like mayle In is sheath, so
Speaker 1: it must be sheath, I think, because I do think it.
Speaker 1: It affects like the very first layer of your bone.
Speaker 1: But it is like a bone infection that it can cause,
Speaker 1: super common in children. Probably what uh, your friend Tony
Speaker 1: Tony Tony Love not actually friends, but you know what
Speaker 1: I mean, our first hand account, our first Tony Love
Speaker 1: most likely had some form of osteomyelitis based on his symptoms.
Speaker 2: God sounds terrifying. It is.
Speaker 1: It's super scary, especially because in like super young kids,
Speaker 1: you'll just have this like crazy joint pain. And you know,
Speaker 1: if you're a parent or whatever, you're like, what could
Speaker 1: possibly be wrong? Like you might not have any visible
Speaker 1: outer issues, Like you had a scrape a couple of
Speaker 1: weeks ago that completely healed, and now all of a
Speaker 1: sudden you can barely walk because your knees infected with
Speaker 1: staff oreas.
Speaker 2: Kids are scraped all the time, they're rough and tumbled
Speaker 2: like you, I can't. I still have gravel embedded in
Speaker 2: my knees. I have some in my head, and so
Speaker 2: to think like, oh, well that must be the cause
Speaker 2: of it.
Speaker 3: Oh it's crazy.
Speaker 1: Yeah. It can also cause various forms of arthritis. So
Speaker 1: if it infects your joint rather than your bone directly, yeah,
Speaker 1: it's everywhere.
Speaker 3: Also not done.
Speaker 1: Staff Orias produces several toxins, right, so each of those
Speaker 1: could probably like we could have a whole episode on
Speaker 1: all the various toxins that staff Orias produces. But some
Speaker 1: of them you've probably heard about. So one of them
Speaker 1: is an exfoliative toxin. Doesn't that sound nice? It's foliant,
Speaker 1: great for your skin. Sure, Nope, it causes like your
Speaker 1: skin to just sluff off.
Speaker 2: I don't like the word sluff sluf.
Speaker 1: That's the word I'm gonna use. Yeah, it can also
Speaker 1: cause have you heard of it? Toxic shock syndrome? Oh yeah,
Speaker 1: oh yeah, that's staph orious bip. We're not going to
Speaker 1: get into soups detail about it because like, again, it
Speaker 1: could be a whole episode, but it's basically a toxin
Speaker 1: called it's called a super anigen because it basically makes
Speaker 1: your it's an anigen, which is something that that your
Speaker 1: body reacts to and makes antibodies against, and it makes
Speaker 1: your body make so many antibodies, like it is like all.
Speaker 3: The antibodies come to me.
Speaker 1: And so then your body goes crazy and it goes
Speaker 1: into shock because you just have so much immune system
Speaker 1: action that your body is like, can't just your immune
Speaker 1: system goes crazy kind of And that is from staph orious.
Speaker 2: Can I ask a stupid question?
Speaker 3: Of course?
Speaker 2: What is going on biologically with shock?
Speaker 1: I feel like that's a whole. That's a whole, but like,
Speaker 1: give me the So there's a lot of different forms
Speaker 1: of shock. There's septic shock, which usually is from some
Speaker 1: kind of bacterial infection, and then there's also things like
Speaker 1: cardiogenic shock, hypovolemic shop shock. All of these basically involve
Speaker 1: a drastic drop in blood pressure. So that's the underlying
Speaker 1: mechanism that's going to make you end up dying, is
Speaker 1: that your blood pressure essentially plummets, and then your organs
Speaker 1: start to fail because they're not getting blood perfusion to
Speaker 1: your organs, and then you die.
Speaker 3: Okay, yeah, cool, right.
Speaker 2: So toxic shocks and toxic shocks in wonderful.
Speaker 1: So shock induced by a toxin not done, by the way.
Speaker 3: Oh god, there's more.
Speaker 1: There's another toxin that it can produce that causes very
Speaker 1: rapid onset food poisoning. Drink that drink, air, and drink
Speaker 1: that drink. You're probably fine.
Speaker 2: Oh god, as the as the ice cream curdles.
Speaker 3: It does, it is curdling.
Speaker 1: But yeah, this food poisoning is like super super rad
Speaker 1: rapid onset, like within one to eight hours. Because what's
Speaker 1: basically happening is if you leave out a plate of
Speaker 1: let's say, spam and eggs, because that's a really good example,
Speaker 1: or for you Midwesterners, potato salad, okay, potato salad, mac salad,
Speaker 1: anything mayonnaise, meat.
Speaker 2: Anything that's called salad only because it has mayonnaise added
Speaker 2: to it.
Speaker 1: Yeah, yeah, truth, yeah yeah, salad, tuna salad. Yeah, you
Speaker 1: leave that out on the counter. It's covered in staff oreos.
Speaker 1: It's everywhere that staff aureus starts producing a toxin and
Speaker 1: then it just sits there. So then you're like, oh,
Speaker 1: I forgot, I'll put this back in the fridge. It
Speaker 1: doesn't matter. The toxin's already there. And then you're gonna
Speaker 1: eat that mac salad because it was so good yesterday.
Speaker 1: And then eight hours later you're barfing all over the
Speaker 1: place and it is preferentially barfing and not diarrheating.
Speaker 2: So interesting. Okay, yeah, okay, So if you ever have
Speaker 2: food poisoning, barf.
Speaker 1: Yeah, like super right after you ate something where you
Speaker 1: were like, I probably shouldn't have eaten that. Oh god,
Speaker 1: probably it was my wrap.
Speaker 3: Today you're not barfing.
Speaker 2: Yet, not yet. It's almost eight hours.
Speaker 1: Yeah, So that's a lot. That is a lot, and
Speaker 1: there's one more. This is crazy, isn't it crazy that
Speaker 1: all of these different things can be caused by the
Speaker 1: same bacterium.
Speaker 2: It's bizarre, is what it is.
Speaker 1: It's so it is so so interesting to me. But
Speaker 1: probably the most common thing that people associate with staph infections.
Speaker 1: I know what I used to associate with staff infections
Speaker 1: goes a little something like this. I saw a bump.
Speaker 1: Maybe it was on my butt, maybe it was on
Speaker 1: my arm.
Speaker 3: I don't know. I just had a bump.
Speaker 1: I thought it was a pimp, so I tried to
Speaker 1: pop it, or maybe I thought it was a bug bite,
Speaker 1: but it didn't itch. So I was like, that's kind
Speaker 1: of weird, huh. But it's just like a bug bite,
Speaker 1: it's fine, it's gonna go away.
Speaker 2: Maybe a spider bite.
Speaker 1: Maybe definitely a spider bite, but it wasn't. And then
Speaker 1: it just didn't go away. And then the next day
Speaker 1: it was kind of bigger and it was kind of
Speaker 1: like leaking and oozing. And then the next day my
Speaker 1: entire butt was covered in a giant, bloody pussy absss.
Speaker 1: It was just oozing and it was bleeding. Oh God,
Speaker 1: this did not happen to me, by the way I'm
Speaker 1: saying me, but I'm just saying the royal me.
Speaker 2: It could have.
Speaker 3: It could have.
Speaker 1: Luckily it hasn't as much as I'm willing to say
Speaker 1: at least. But that's sort of the classic staph infection,
Speaker 1: and that would be a staff skin infection. Okay, Right,
Speaker 1: So staff gets into any kind of open wound, super
Speaker 1: common to happen after shaving, where you get like infected
Speaker 1: hair follicles.
Speaker 4: Stop shaving your puobes peopes.
Speaker 1: Seriously, seriously seriously. And yeah, and so that's kind of
Speaker 1: the prototypical staph infection.
Speaker 3: YEA, that is skin infection.
Speaker 1: You end up with this open, absessing wound that kind
Speaker 1: of just doesn't heal and maybe keeps growing or maybe
Speaker 1: kind of stays the same size but just doesn't heal.
Speaker 1: Like you put neosporin on it and it just doesn't
Speaker 1: go away. So that's super common, and that's staff areous.
Speaker 1: How crazy it is that staff can infect so much
Speaker 1: of your body? Yeah, right, like so many different parts.
Speaker 1: So one of the questions is how on earth can
Speaker 1: it actually do that?
Speaker 3: Right?
Speaker 1: Like, how can it infect your lungs and give you
Speaker 1: pneumonia but also give you a skin infection? Like that's weird.
Speaker 2: It's like the jack of all trades bacteria.
Speaker 3: Yeah, it really is.
Speaker 1: So there's a few different and it manages to do
Speaker 1: this and it mostly just centers around evading your immune
Speaker 1: system full stop. Okay, it's just kind of really good
Speaker 1: at that. So one of the things it does is
Speaker 1: produce exotoxins, which we already talked about, right, some of
Speaker 1: the toxin mediated diseases like toxic shock syndrome and barfing
Speaker 1: food poisoning for example. Okay, but it also has another
Speaker 1: way that it is able to cause disease, and that's
Speaker 1: by this particular surface protein that it has. It's called
Speaker 1: protein A, which is not creative, but it basically is
Speaker 1: just a protein that is really good at both evading
Speaker 1: our immune system, So it's good at hiding from our
Speaker 1: immune system and it's really good at invading our epithelial cells.
Speaker 1: And epithelium are the cells that line basically everything in
Speaker 1: your body. So your skin is epithelium, but also the
Speaker 1: inside of your lungs that's epithelium, The inside of your
Speaker 1: heart also epithelium. Your entire GI tract also epithelium. So
Speaker 1: this protein allows it to invade those cells very very easily.
Speaker 2: Okay, So this bacterium lives on the surface of a
Speaker 2: lot of our body, Yes, but it also possesses the
Speaker 2: key to invade the surface of our body.
Speaker 3: Yes.
Speaker 2: That seems highly sus right.
Speaker 3: It is. It's a highly sub.
Speaker 2: I think I use that perfectly correctly, perfectly correctly. So
Speaker 2: can we talk for a second about resistance.
Speaker 1: Yeah, that's I think what we need to talk about now. Okay, So, yeah,
Speaker 1: so Mursa is a resistant form of this horrible staff
Speaker 1: bacteria that we've.
Speaker 3: Been talking about.
Speaker 1: So antibiotic resistance in general just for people who might
Speaker 1: not be aware. Just means that when you try and
Speaker 1: give somebody an antibiotic, which normally would help cure an
Speaker 1: infection of bacteria, it doesn't work.
Speaker 2: Okay.
Speaker 1: MRSA happens to be a strain of staff aureus that
Speaker 1: is resistant to what are called beta lactam antibiotics, which
Speaker 1: means like methicillin, penicillin, a bunch of the sillins, silins, ellins, chillins.
Speaker 1: And the way that it does that, it's basically just
Speaker 1: changes a protein so that the antibiotic can't bind.
Speaker 3: To it anymore. Okay, it was pretty much it.
Speaker 1: But I know the question that you want to know
Speaker 1: is how on earth can it become resistant?
Speaker 4: Yeah?
Speaker 1: Right, like, how how does that happen? I want to
Speaker 1: talk for like an hour about this.
Speaker 2: Oh that sounds like a great idea. Should we maybe
Speaker 2: do a future antibiotic?
Speaker 1: I think, yeah, We're going for antibiotics, antibiotics and antibiotic
Speaker 1: resistance because it is really fascinating the way, like the
Speaker 1: evolutionary arms race that happens between a bacteria and what
Speaker 1: you treat it with. Most of the antibiotics that we
Speaker 1: have actually come from other bacteria. Or fungi or plants.
Speaker 1: So these are substances that are produced in nature in
Speaker 1: order to fight off bacterial infections that invade them. So
Speaker 1: whether it's a bacteria fighting off another bacteria, or a
Speaker 1: fungus trying to fight off a bacterial infection.
Speaker 3: Or what have you.
Speaker 1: And so bacteria are constantly evolving ways to fight off
Speaker 1: these defenses, and then other bacteria and funguses and plants
Speaker 1: and people are constantly evolving ways to try and fight
Speaker 1: off those bacteria. But basically what can happen is that
Speaker 1: once you get a mutation, for example, in the case
Speaker 1: of MRSA in this single protein, essentially you can then
Speaker 1: change this protein just enough that this antibiotic can no
Speaker 1: longer bind. Once that single bacteria has that protein, anytime
Speaker 1: you give it penicillin or methicillin, it's gonna survive, which
Speaker 1: means it's gonna still hang out in your body and
Speaker 1: reproduce and reproduce. So now that the new colony that's
Speaker 1: in your body now or in your nose is now
Speaker 1: all of them are resistant. And even if you have
Speaker 1: other bacteria, like let's say you've got like six different
Speaker 1: kinds of staff living on your body, because that's not insane.
Speaker 1: Staff is everywhere, right, Once you start hitting those staff
Speaker 1: with an antibiotic, if there's one that happens to be resistant,
Speaker 1: bacteria can do something called conjugation, which is kind of
Speaker 1: like bacteria sex yep. Basically they can give each other
Speaker 1: the ability to also resist penicillin, and so it can
Speaker 1: spread both by a single bactium replicating, but it can
Speaker 1: also spread from bacterium to bacterium via conjugation.
Speaker 2: And it's really more it becomes a numbers game. Yeah.
Speaker 3: Absolutely, you just have.
Speaker 2: So many bacteria reproducing or replicating that one just by probability, Yeah,
Speaker 2: to evolve that mutation exactly right, or it's going that
Speaker 2: that mutation will emerge and then it will.
Speaker 1: Spread in that population. Yeah, yeah, yeah exactly. So yeah,
Speaker 1: that's pretty much. That's pretty much MERSA in a nutshell.
Speaker 1: It's not an all bad news game because most MRSA
Speaker 1: is still susceptible to another antibiotic called vanko mycin.
Speaker 3: Okay, okay, so we it's not.
Speaker 1: Like we've run out completely of treatment options, but yeah,
Speaker 1: I mean that it's it is really scary because if
Speaker 1: you don't identify an infection as a MERSA infection and
Speaker 1: you start treating it with penicillin or methicillin, it's not
Speaker 1: going to do anything, and in some cases it might
Speaker 1: make it worse because now you're going to have, you know,
Speaker 1: your resistant populations spreading that gene to susceptible populations within
Speaker 1: a single individual. So tell me, Aaron, how did we
Speaker 1: get to this horrible, horrible place.
Speaker 2: It's a great question. Do you remember the first time
Speaker 2: that you heard about MRSA.
Speaker 3: No.
Speaker 2: I don't remember like the first time, but I feel
Speaker 2: like when I was in maybe middle school or high school,
Speaker 2: it started to be talked about a lot.
Speaker 3: Huh.
Speaker 1: I think I didn't hear about staff infections until I
Speaker 1: was in college and I wanted to go to Marea
Speaker 1: to do work and my mom was like, ya, just
Speaker 1: gotta staff infaction from my coral And I was like, Okay, why.
Speaker 2: Is mother's No. I remember hearing it, probably on like
Speaker 2: Channel one News or something like that, but I remember
Speaker 2: all of these scary headlines about locker rooms and Jim
Speaker 2: Matts and the pimple that brings death. And I feel
Speaker 2: like a lot of these headlines focused on individual stories
Speaker 2: of parents losing a child or someone losing an eye
Speaker 2: or a leg or something like that. I feel like
Speaker 2: there was this larger story to it where MRSA seemed
Speaker 2: to represent the failings of modern medicine. It was this
Speaker 2: wake up call where suddenly we could no longer rely
Speaker 2: on the antibiotics that we had taken for granted in
Speaker 2: some ways over the past fifty or sixty years. It
Speaker 2: was kind of like we were being sent back in
Speaker 2: time before for antibiotics, you could easily die from that
Speaker 2: scratch on your leg that you got walking through some bushes,
Speaker 2: a little swelling, a little redness, a little fever, a
Speaker 2: lot of pus, and the next thing you know, you
Speaker 2: could be dead from systemic infection.
Speaker 3: Yeah.
Speaker 2: And if you were unfortunate enough to have surgery in
Speaker 2: pre antibiotic days, forget.
Speaker 1: It, like you're gone or dead.
Speaker 2: You're gone or I don't know how anyone survived surgery.
Speaker 2: But infection was such an everyday part of life that
Speaker 2: we don't really have a written history of something like
Speaker 2: staph oreus the way we do for the other big
Speaker 2: names and infection.
Speaker 3: Yeah, that makes sense.
Speaker 2: So let's go back to around eighteen eighty. I know
Speaker 2: that you're gonna be thrilled with this. I'm always thrilled
Speaker 2: because you are a Scottish man. Oh my god, you've
Speaker 2: been practicing for this. I had an amazing mustache church.
Speaker 2: You can say the one word that you know how
Speaker 2: to say in my Scotch accent. So you are a
Speaker 2: surgeon and professor I at the University of Aberdeen. I
Speaker 2: and your name Alexander Augusten.
Speaker 1: I'm not even gonna try to do that in a scent.
Speaker 3: You're welcome everyone.
Speaker 2: Yeah, now I've listened to it. It's pretty bad.
Speaker 1: It's awful.
Speaker 2: It's really bad. Not that I could do better.
Speaker 1: But but why do I keep trying?
Speaker 3: Is the question? But I will continue anyway.
Speaker 2: Okay, So you happen to be one of the surgeons
Speaker 2: who got into medicines that you could help people and
Speaker 2: improve their lives, which is great, But there's one problem.
Speaker 2: About half of your patients seem to die after you
Speaker 2: stitch them back up. I now, as part of your
Speaker 2: quote med school training, you have been told that pus
Speaker 2: production from the incision site is an essential stage in
Speaker 2: the healing process. Oh, but something about that doesn't sit
Speaker 2: right with you. In your search to try to find
Speaker 2: out how to quote do no harm. You come across
Speaker 2: someone named Joseph Lister.
Speaker 3: Love him right.
Speaker 2: Joseph had this crazy idea that maybe surgical tools and
Speaker 2: wounds should be cleaned before and after surgery.
Speaker 1: It's so fun to think of how novel this, I mean,
Speaker 1: it's not even novel.
Speaker 3: It was revolutionary.
Speaker 2: Yeah, it was completely yeah yeah. But that also he
Speaker 2: also thought that maybe a seeping wound wasn't a good thing.
Speaker 2: You know, you decide to try out his approach, which
Speaker 2: was applying carbolic acid to wounds, which had been shown
Speaker 2: to be pretty dang effective. And it works for you too, congratulations.
Speaker 3: Thank you.
Speaker 2: And you actually become such a fan of the practice
Speaker 2: that your students make up a song about it.
Speaker 3: Do I get to sing it?
Speaker 2: Yes?
Speaker 3: Okay?
Speaker 1: And so the song goes like this, sing it the spray,
Speaker 1: the spray, the antiseptic spray. A oh would shower it morning,
Speaker 1: night and day for every sort of scratch where others
Speaker 1: would attach a stinking plaster patchy gave the spray.
Speaker 2: I think it was sticking plaster. Pet Is it stinky?
Speaker 3: I don't know? It does say sticking?
Speaker 2: Good enough enough? Good enough?
Speaker 3: It probably stunk if we're being honest.
Speaker 2: Oh, yeah, absolutely, that was amazing.
Speaker 3: Thank you. That was a beautiful song.
Speaker 1: If I do say so myself, this is pretty great,
Speaker 1: wonderfully done.
Speaker 2: So yeah, lister thinks that the wounds are putrefying because
Speaker 2: of bad air.
Speaker 3: M he's close.
Speaker 2: You, on the other hand, are a bit more forward
Speaker 2: thinking and suspect that it's some kind of infection. So
Speaker 2: one day you take some puss from an abscess on
Speaker 2: one of your unfortunate patients and smear it on a microscope.
Speaker 2: Slide under the microscope, you see some round clusters of
Speaker 2: cells that look like grapes. Later you journal about it. Quote,
Speaker 2: my delight may be conceived when there were revealed to
Speaker 2: me beautiful tangles, tufts and chains of round organisms in
Speaker 2: great numbers, which stood out clear and distinct among the
Speaker 2: pus cells and debris.
Speaker 3: I love it.
Speaker 2: Yeah. The name staphlococcus is given to the bacteria staphile,
Speaker 2: from the Greek meaning bunch of grapes and caucus meaning berry. Later,
Speaker 2: aureus is given to the staff's species that grows yellowy
Speaker 2: clusters on a plate oureous from the Latin orum meaning
Speaker 2: gold gorge. There you go, Okay, enough etymology, though clearly
Speaker 2: you are thrilled about this finding, and you figure that
Speaker 2: the rest of the medical establishment would also be pretty pumped. Right. No,
Speaker 2: they're not not at all. They're skeptical and resistant to
Speaker 2: any challenge to the long held view that infection was
Speaker 2: just a natural part of wound healing typical. So you
Speaker 2: have to perform a public presentation of your research to
Speaker 2: prove that you covered all your bases and went through
Speaker 2: all of the postulates, and finally they accept that you
Speaker 2: might beyondto something and you get all the praise and
Speaker 2: blah blah blah blah. Okay, So at this point, it's
Speaker 2: eighteen eighty one, and microbiology is an exciting new field
Speaker 2: to be in. New bacteria and parasites and viruses are
Speaker 2: constantly being described, and vaccines are in the works and
Speaker 2: being really least and so on. In the first half
Speaker 2: of the twentieth century is also where we see some
Speaker 2: really amazing medical developments that seem like magic for both
Speaker 2: patients and doctors. In nineteen forty one, penicillin, which is
Speaker 2: an episode in its own right, begins to be used
Speaker 2: to treat infections of all kinds. At first just soldiers
Speaker 2: in World War Two, just restricted to them. But a
Speaker 2: few years later it begins to be widely distributed to
Speaker 2: the public and it was viewed as this wonder drug.
Speaker 3: Which it really was in the forties.
Speaker 2: Nineteen forty I think four was when it was distributed
Speaker 2: to the public.
Speaker 3: That is insanely recent.
Speaker 2: Yeah, very recent. So before penicillin, eighty to ninety percent
Speaker 2: of people who had staph areas bacteremia infection of the
Speaker 2: blood died eighty to ninety percent Jesus see. And I
Speaker 2: don't have exact numbers for the number of people every
Speaker 2: year because again, like I said, it was such this
Speaker 2: it was a common thing, but it wasn't It didn't
Speaker 2: happen in outbreaks and cluschase, and so you didn't write
Speaker 2: it down.
Speaker 3: Yeah.
Speaker 1: And it also wasn't a single disease, right, It was
Speaker 1: like people were dying from staff Orius, but from so
Speaker 1: many versions of staff Orius.
Speaker 2: Yeah, yeah, it was really hard to keep track of.
Speaker 3: Yeah.
Speaker 2: But anyway, after the introduction of penicillin, those deaths due
Speaker 2: to any version of staff Orias dropped hugely. Man In
Speaker 2: addition to a lot of other bacterial infections. Penicillin became
Speaker 2: the default treatment for many infections and was handed out
Speaker 2: like candy at Halloween. You could get penicillin in the
Speaker 2: grocery store without a prescription, without any information or instructions
Speaker 2: on how long you should take the pills, how many
Speaker 2: each day? Oh my gosh. H and its early effectiveness
Speaker 2: led to some hygienic practice is falling by the wayside.
Speaker 3: Oh no.
Speaker 2: So basically, now that you could cure these common infections,
Speaker 2: focus shifted away from prevention and more towards treatment, not
Speaker 2: consciously necessarily, but just because prevention was no longer as
Speaker 2: crucial as it once was.
Speaker 1: Wow.
Speaker 2: And as you can guess, the overuse and misuse of
Speaker 2: penicillin even in these early days led to resistant strains
Speaker 2: of staff areas popping up and spreading almost immediately after
Speaker 2: penicillin was introduced, like really almost immediately.
Speaker 1: Yeah, I mean even currently, it only takes like a
Speaker 1: matter of months to a couple of years for resistance
Speaker 1: to develop to new antibiotics.
Speaker 3: Yeah, it's insane.
Speaker 2: It's insane. Within five years of penicillin being introduced, fifty
Speaker 2: percent of staff oreas strains that were isolated were resistant,
Speaker 2: and that number would just continue to climb.
Speaker 3: Oh my god.
Speaker 2: So sitting here now seventy years later, it's easy to go, well, yeah, duh.
Speaker 2: Of course antibiotic resistance evolved. Look at how you dosed people,
Speaker 2: look at how you were irresponsible. I can't believe the
Speaker 2: lack of.
Speaker 1: Fuer side everything wrong, right.
Speaker 2: But it's I think it's really worth noting that the
Speaker 2: threat of resistance had been recognized almost immediately by many
Speaker 2: people really oh yeah, including Alexander Fleming, who was the
Speaker 2: dude who discovered the mold that made penicillin.
Speaker 3: Wow.
Speaker 2: So in nineteen forty five, in his Nobel Prize acceptance speech,
Speaker 2: he said, quote, there is the danger that the ignorant
Speaker 2: man may easily underdose himself and, by exposing his microbes
Speaker 2: to non lethal quantities of the drug, make them resistant.
Speaker 1: WHOA yeah, so right, like right, literally right out of it.
Speaker 2: He had already been thinking about this clearly for years.
Speaker 1: He's like, guys, listen, seriously, I know this is great noll,
Speaker 1: but we can't mess it up. And then people were like, yeah, cool, wait, great,
Speaker 1: by take your price piece, right. Yeah.
Speaker 2: So, despite this warning, by the mid nineteen fifties, penicillin
Speaker 2: resistance staff had become a public health crisis around the globe.
Speaker 2: In Australia, women who had just given birth were showing
Speaker 2: back up at the hospital with their severely sick newborn,
Speaker 2: covered in broken blisters or blue with pneumonia, and the
Speaker 2: mothers were often sick themselves, with open weeping abscesses on
Speaker 2: their breasts often no yeah, and the strain of staff
Speaker 2: causing these infections proved to be both extremely infectious and
Speaker 2: extremely resistant, not just a penicillin, but to many of
Speaker 2: the other antibiotics that had been developed at that point.
Speaker 1: Oh no.
Speaker 2: And it didn't take long for these outbreaks to appear
Speaker 2: in the US, and the thousands of cases and dozens
Speaker 2: of deaths prompted an emergency meeting of the American Medical Association.
Speaker 2: Something had to give, better hygienic practices, better drugs, and
Speaker 2: definitely better record keeping. It wasn't a reportable disease. Yeah,
Speaker 2: staph infection was normal. This was something of a rude
Speaker 2: awakening to hospital physicians everywhere, especially those who had joked
Speaker 2: that infectious disease doctors would soon be made obsolete by antibiotics.
Speaker 3: Never.
Speaker 2: No, really, never.
Speaker 1: I'm counting on that for a job, quite honest.
Speaker 2: Many hospitals instituted practices and appointed committees specifically to control
Speaker 2: the spread of this resistant Staph aureus. Newborns were placed
Speaker 2: into infected or uninfected rooms based on whether they showed
Speaker 2: any signs of infection. WHOA, but it wasn't working. No
Speaker 2: cases were still on the rise, and babies that had
Speaker 2: no apparent contact with an infected person were still becoming infected.
Speaker 2: This infection was such a problem for newborns because newborns
Speaker 2: are so fresh and new.
Speaker 1: I thought you're going to say, so fresh and so clean, clean.
Speaker 2: Fresh and so clean clean. So when they're born, their
Speaker 2: skin and mucous membranes are immediately colonized by bacteria from
Speaker 2: their mom's vaginal canal, from breast milk, and from the
Speaker 2: surfaces they encounter after birth. And this goes towards building
Speaker 2: the microbiome of this tiny human. But there's still a
Speaker 2: lot of open territory for other potentially harmful bacteria to colonize.
Speaker 2: And this resistant steph Oreus strain was so infectious and
Speaker 2: such a fast grower that it pushed out all the
Speaker 2: other bacteria and basically became the microbiome. Whow So, what
Speaker 2: on earth do you do about a bacterial strain that
Speaker 2: wipes out all competition instantly? And is untreatable by the drugs.
Speaker 1: You have, you come up with new ones, well, or
Speaker 1: you die.
Speaker 2: There's a third option. Okay, so what does seem pretty hopeless?
Speaker 2: But one doctor had an idea. So this guy was
Speaker 2: named Heinz Eichenwald, and he remembered an old practice that
Speaker 2: was used to get rid of diphtheria infections from carriers
Speaker 2: of the disease in days before the vaccine. It was
Speaker 2: called bacterial interference. Yep, you're pretty.
Speaker 3: Thrilled, shaking with excitement.
Speaker 2: So the idea was that you expose these people to
Speaker 2: a different harmless bacterium that's a better competitor than the
Speaker 2: one causing the problem. This new bacterium then takes over
Speaker 2: and pushes out the harmful one, and voila infection. Gone.
Speaker 1: I love it, clean, classy.
Speaker 2: It's really innovative. Yeah, and very much in line with
Speaker 2: some technologies and treatments that are becoming popular nowadays, which
Speaker 2: is why I spent so much time talking about this.
Speaker 3: And also what year is this again?
Speaker 2: This is in the late nineteen fifty.
Speaker 1: Okay, wow, so this is like still super early on,
Speaker 1: like even antibiotics are pretty brand new.
Speaker 3: Yeah.
Speaker 2: Well, and I think it's really fascinating that bacterial interference
Speaker 2: was developed in like nineteen the early nineteen hundreds, like
Speaker 2: nineteen teen. Wow, I think before the dip theory of
Speaker 2: vaccine was invented in nineteen twenty.
Speaker 3: Cool.
Speaker 2: So yeah, it's just very it seems very forward thinking. Yes, yeah,
Speaker 2: very cool. People stopped using bacterial interference in the nineteen
Speaker 2: twenties when the dip theory of vaccine was released, but
Speaker 2: Eichenwald hadn't forgotten about it, fortunately, So he set out
Speaker 2: to find a strain of staff that was more infectious
Speaker 2: than the drug resistant staff strain but not harmful, and
Speaker 2: once he found it, he set to exposing these newborns
Speaker 2: to the new strain. It was a pretty revolutionary idea
Speaker 2: for the time, but people were desperate to try anything. Yeah.
Speaker 2: Lives had been really ruined by this persistent infection showing up.
Speaker 2: Children who were infected weren't allowed to go to school.
Speaker 2: At least one couple had divorced whoa over it. Yeah,
Speaker 2: But eichenwald strain worked. The deadly infection was eliminated. It
Speaker 2: was miraculous.
Speaker 3: Wow.
Speaker 2: And for the next few years it was used occasionally
Speaker 2: to treat stubborn infections.
Speaker 3: That's pretty cool.
Speaker 2: Yeah, But bacterial interference once again slipped out of practice
Speaker 2: in the late nineteen fifties when a new antibiotic was released.
Speaker 2: Here we are nineteen fifty nine, well into the history
Speaker 2: of staff orias, and I haven't yet introduced you to
Speaker 2: who was, in many ways the star of the show,
Speaker 2: methicillin methicillin resistance staff orias. The new antibiotic that I
Speaker 2: just mentioned was methicillin, and when it was released it
Speaker 2: was advertised as quote effective against all resistant staffholcocky resistance
Speaker 2: unlikely to develop.
Speaker 3: It, oh dear.
Speaker 2: Within a year of its release, resistance to methicilline had
Speaker 2: already been found, and by the nineteen seventies, MRSA was
Speaker 2: widespread in hospitals in the UK and making its way
Speaker 2: to the rest of the world, and cases weren't appearing
Speaker 2: as one offs. It was more like a wave of infection.
Speaker 2: It would start off slowly with just a few people infected,
Speaker 2: and then it would rapidly jump across hospital units, affecting
Speaker 2: the most vulnerable patients, like those just out of surgery
Speaker 2: or with severe burns. Deaths from MRSA were becoming more common,
Speaker 2: and the periods between MRSA outbreaks were becoming shorter and shorter,
Speaker 2: and while MRSA may have popped up a bit later
Speaker 2: in the US and in some parts of the globe,
Speaker 2: it made up for lost time. In nineteen seventy five
Speaker 2: in US hospitals, two point four percent of strains were
Speaker 2: methicine resistant, in nineteen ninety one thirty eight percent, and
Speaker 2: jumping ahead of it in two thousand and three, sixty
Speaker 2: four point four percent in ICs intensive care units.
Speaker 1: Of just like when they swabbed, like the equipment that's
Speaker 1: in there.
Speaker 2: Or it's yeah, I think it's like of all isolates
Speaker 2: from laboratory isolets, from hospitals. Yeah, MRSA was becoming the
Speaker 2: new norm, and it's spread and persistence was helped along
Speaker 2: by the hospital setting itself. In a hospital, nurses and
Speaker 2: doctors are constantly on the move between rooms, between floors,
Speaker 2: different units, and while hygienic practices like hand washing and
Speaker 2: isolation work to a certain degree, MRSA is also carried
Speaker 2: really easily on the surfaces that we don't really think
Speaker 2: about as much, like your nose, well, yeah, a doctor's coat, Yeah,
Speaker 2: the pen that a nurse or a doctor carries from
Speaker 2: room to room ties, brought ties ties are found to
Speaker 2: be like one of the most like they're very ridden.
Speaker 1: They're very controversial right now in medicine.
Speaker 2: Well, it's funny. Even bed curtains were found to be
Speaker 2: ridden with staff MRSA. So these people were unknowingly spreading
Speaker 2: the infection around the hospital, between hospitals and so on.
Speaker 2: And because hospitals are filled with people in poor health
Speaker 2: vulnerable to infection, the bacteria found easy marks. Thousands of
Speaker 2: people every year suffered MRSA infections that they had picked
Speaker 2: up at a hospital or nursing home, and many died.
Speaker 2: And I don't use the words suffered lightly because for
Speaker 2: many people this was at least a life altering and
Speaker 2: often a life ruining infection. Recurrent MRSA infections are really common,
Speaker 2: and you can go from seemingly healthy one day and
Speaker 2: on death's door in what seems like a matter of
Speaker 2: hours without a whole lot of warning or a whole
Speaker 2: lot of like whoh obvious for risk factors whatever. So
Speaker 2: I do want to mention that several countries such as Denmark,
Speaker 2: the Netherlands, some Nordic countries in force really strict hygienic
Speaker 2: practices that greatly reduced MRSA infection incidents compared to other
Speaker 2: parts of the world, including the US. Yeah, so they
Speaker 2: were like very.
Speaker 1: And we're gonna this thing in the butt, wash your hands,
Speaker 1: no worse serious.
Speaker 2: Yeah, really's and it really reduced, yeah, disease incidents. But
Speaker 2: in the other places, MRSA infections and hospitals became so
Speaker 2: frequent that it was basically second nature to look for
Speaker 2: signs of infection and jump on treatment right away, often
Speaker 2: relying on vankamycin, which is the antibiotic that MRSA was
Speaker 2: still susceptible to, which sometimes worked and sometimes didn't. Yeah,
Speaker 2: but being in a hospital meant that you were simultaneously
Speaker 2: in the worst place you could be because MRSA was everywhere,
Speaker 2: but also the best place for rapid diagnosis and treatment,
Speaker 2: because MURSA was a hospital infection.
Speaker 3: Right right, right right, Yeah, I mean.
Speaker 2: Yeah, sure, for a while, it was until it started
Speaker 2: popping up in the nineteen eighties in a few people
Speaker 2: here and there who had no history of being in
Speaker 2: a hospital or nursing home or similar setting. But when
Speaker 2: these people showed up at the er with an extremely
Speaker 2: painful pimple or rash or something, else, MRSA wasn't at
Speaker 2: the top of the list of possible causes, and so
Speaker 2: people were often misdiagnosed and sent home without the immediate
Speaker 2: medical care and abscess cleaning that they needed. And it
Speaker 2: took a while for MRSA to be recognized as something
Speaker 2: that you could pick up outside a hospital setting, but
Speaker 2: eventually MRSA infections became grouped into either hospital acquired MURSA
Speaker 2: or community acquired MRSA, and these labels existed not just
Speaker 2: for patient history, but also because the strains were noticeably different.
Speaker 2: Hospital strains were all very similar to one another and
Speaker 2: were resistant to many different antibiotics. Community strains, on the
Speaker 2: other hand, tended to be much more diverse, resistant to
Speaker 2: only a couple antibiotics, but extremely virulent and infectious.
Speaker 1: WHOA interesting, Yeah, logical?
Speaker 3: Actually, yeah, exactly.
Speaker 2: And so by the early two thousands, which is when
Speaker 2: I was in high school, a large proportion of all
Speaker 2: MRSA cases were community acquired an Epidemiologists had traced the
Speaker 2: source of many community outbreaks to places where staff thrives, warm, moist,
Speaker 2: full of people, So places like gyms and locker rooms. Right, so,
Speaker 2: young athletes showing up to the hospital complaining of a
Speaker 2: sore ankle and within a few hours lying on operating
Speaker 2: table while a surgeon scrapes away infected tissue and washing
Speaker 2: puss off leg bones. You know those kinds of places.
Speaker 2: That's what happened. Once this pattern of MRSA showing up
Speaker 2: in athletes was a parent, many schools and gyms and
Speaker 2: professional athletic organizations took steps to prevent infection. No more
Speaker 2: sharing towels or razors grows and both counts. Anyway, who
Speaker 2: shares razors? Nast I don't know, but apparently it was
Speaker 2: a problem.
Speaker 3: Groad.
Speaker 2: Don't do it. If you do it, no judge, but don't.
Speaker 3: Do it, judge, I'm judging.
Speaker 2: Also regularly cleaning surfaces, but with antibacterial soap, hand washing
Speaker 2: soap available, you know, just basic hygiene stuff. And this
Speaker 2: really did help decrease cases of MRSA in these places.
Speaker 2: But the thing is is that not all school districts
Speaker 2: or gym facilities or other high risk places like prisons
Speaker 2: can afford to maintain these practices, and so we see
Speaker 2: again these health disparities arise, which are then reinforced by
Speaker 2: the fact that poorer people are at higher risk for infection,
Speaker 2: so they have to spend more money and treatment, which
Speaker 2: in the US is often very expensive, and then the
Speaker 2: cycle just sort of continues. It's this positive feedback loop.
Speaker 2: For a while, the distinction between hospital acquired and community
Speaker 2: acquired MRSA was very important for treatment and for predicting
Speaker 2: the severity of the infection and where it might go.
Speaker 2: And doctors and researchers began to worry about the rise
Speaker 2: in community acquired mercy cases, not just because it caused deadly,
Speaker 2: horrific infections that were difficult to treat, but also because
Speaker 2: they were worried about what would happen if, to quote
Speaker 2: the Spice girls to become one. So if hospital acquired
Speaker 2: MRSA and community acquired MRSA met and exchanged genes, and
Speaker 2: so if the hospital strain transferred some of the super
Speaker 2: resistance to the community strain, or if the community strain
Speaker 2: kicked over a few genes for toxin production, Yeah, yeah, problematic,
Speaker 2: very well, as you can probably guess. It was just
Speaker 2: a matter of time. Yep, two did indeed become one,
Speaker 2: and a distinction between a hospital or community acquired became
Speaker 2: less important, Rather worrying about whether we can actually treat
Speaker 2: This thing became the primary focus because a few cases
Speaker 2: of MRSA earned a new name VISA or versa. Uh,
Speaker 2: and those mean either vancom ion intermediate or vancom icein
Speaker 2: resistant staphorus, basically distinguishing between the different levels of resistance
Speaker 2: for this level of staphoras against vancomycin, which had been
Speaker 2: used as the last resort antibiotics.
Speaker 1: Right, So whether like using vancomycin could kill it at
Speaker 1: all or whether you just have to intermediate would be
Speaker 1: you'd have to use like a really high dose of
Speaker 1: vancom issin.
Speaker 2: Right, And because MRSA is still treatable with antibiotics, yeah,
Speaker 2: we mostly, but VERSA and VISA no. So yeah, these
Speaker 2: these infections were truly terrifyingly untreatable. Staph areas had come
Speaker 2: full circle so earlier. When I was researching this episode,
Speaker 2: I kept telling you that this is probably the first
Speaker 2: time that I have been genuinely freaked out by one
Speaker 2: of these infections. Yeah, and there's definitely plenty to be
Speaker 2: scared about with these other diseases that we've talked about,
Speaker 2: but there's something different about this one. I don't know
Speaker 2: what it is exactly.
Speaker 1: It's everywhere I think that's what it is.
Speaker 2: I think a part of it is that I think
Speaker 2: a big part was Maren mckennon's really eloquent descriptions of
Speaker 2: like puss filled cavities and oozing sutures and like horrible,
Speaker 2: very tragic stories in people's lives being hugely impacted. But
Speaker 2: also that, yeah, staff is everywhere. Yeah, and so far
Speaker 2: our medical relationship with it has gone in one direction
Speaker 2: that we're running just to keep up. We've maybe had
Speaker 2: one foot ahead for the briefest amount of time.
Speaker 3: Right, and then it catches right up with us.
Speaker 2: Yeah. Yeah. But so the question is now what comes after?
Speaker 2: How do we fight MSA or VISA or VERSA without antibiotics?
Speaker 2: And so that is where I'll hand it off to you.
Speaker 1: Yeah, Unfortunately I don't have great news. Cool, So just
Speaker 1: let's talk about the news that I have.
Speaker 2: All right.
Speaker 1: So, the CDC has this monitoring program. It's active in
Speaker 1: a few different states California, Georgia, Minnesota, New York, and Tennessee.
Speaker 1: Not the entirety of those states, but several counties in
Speaker 1: each of those states. That basically means that they are
Speaker 1: actively surveilling about fourteen and a half million people and
Speaker 1: they haven't compiled all the numbers from the last couple
Speaker 1: of years, So the most recent numbers that you can
Speaker 1: get are from twenty fifteen, and they're not extrapolated out
Speaker 1: to the whole US. But I did the math for
Speaker 1: you because I'm a.
Speaker 2: Math You had math model in your dissertation.
Speaker 1: Yeah, yeah, yeah, yeah, I did math. So in twenty fifteen,
Speaker 1: which is the most recent numbers, I could find in
Speaker 1: those fourteen and a half million people that they actively surveiled,
Speaker 1: there were two thousand, six hundred cases. So I heard
Speaker 1: that and I was like, well, Marshall's not even a
Speaker 1: big chill out, guys, everyone relaxed.
Speaker 3: It seems like a lot of cases.
Speaker 1: And then there were only three hundred and thirty two
Speaker 1: deaths in that population. I mean, like on the scheme
Speaker 1: of things, right, I was like, that's not so bad.
Speaker 1: Then I was like, also, I'm heartless, and yeah, like
Speaker 1: maybe maybe I have lost my humanity. But I wanted
Speaker 1: more numbers because that made me feel like I was
Speaker 1: a bad person for thinking that wasn't a lot of people.
Speaker 1: So if you extrapolate out those numbers, if we assume
Speaker 1: that that population that they're surveilling is representative of the
Speaker 1: whole country, which is kind of the point of surveillance.
Speaker 3: So let's hope they did a good job.
Speaker 1: Then that would mean that in the US in twenty fifteen,
Speaker 1: there were over fifty three thousand MERSA infections, forty two
Speaker 1: thousand of those would be high hospital acquired and eleven
Speaker 1: one thousand community acquired. Wow, and over sixty six hundred deaths.
Speaker 3: Yeah, I mean, and those numbers do match.
Speaker 1: Yeah, those numbers that I just calculated on my own
Speaker 1: are similar and in line with what the CDC's estimates
Speaker 1: from twenty fourteen were, which were a total of sixty
Speaker 1: one thousand cases and nine thousand deaths. But overall, about
Speaker 1: one in three people are carriers of some form of
Speaker 1: staff areas, like they're just walking around with staff growing
Speaker 1: on them. And it's estimated that about two in every
Speaker 1: one hundred people, so two percent of the global population
Speaker 1: are carriers for some kind of.
Speaker 2: MRSA and carriers meaning they.
Speaker 1: They're growing it, they're breathing it, they're licking it, they're
Speaker 1: touching it onto their door knobs.
Speaker 2: But not necessarily.
Speaker 1: Probably never getting maybe getting infected with it, right if
Speaker 1: they get a cut, and then that MRSA that's on
Speaker 1: their skin gets into them, but maybe they never ever
Speaker 1: ever see an infection from it, but they give it
Speaker 1: to their brother and their cousin, and their neighbor and
Speaker 1: their barista.
Speaker 2: Yeah, the most important people.
Speaker 1: Yeah, And so that that two percent is just in
Speaker 1: the general population. There are some populations where this situation
Speaker 1: is even worse, like hospitals, right, like you said, hospitals
Speaker 1: are just if you're going to get staff in the hospital,
Speaker 1: it's probably gonna be MRSA. But also places like correctional facilities.
Speaker 1: You can imagine that many correctional facilities aren't exactly sanitary places,
Speaker 1: and many inmates in correctional facilities have various situations that
Speaker 1: would make them immunal compromise. So MRSA is described as hyper.
Speaker 3: Endemic does not sound good. It is not good.
Speaker 1: I had never heard that word before, but I can
Speaker 1: guess what it means, and that is like super and
Speaker 1: it's everywhere. It's not even just like, yeah, we have
Speaker 1: this disease. It's like no, it's everywhere. There are some
Speaker 1: estimates that between four and a half to seventeen percent
Speaker 1: of inmates were carriers from MRSA.
Speaker 2: That's crazy.
Speaker 3: It's so high it's insane.
Speaker 1: Yeah, I mean it's at least twice as high as
Speaker 1: the general population, if not like nine times as high.
Speaker 3: Right, you know, it's seen.
Speaker 1: The question now becomes what do we do and how
Speaker 1: do we move forward from this? And I that's a yeah,
Speaker 1: that's why I want to know.
Speaker 3: I don't have a great answer.
Speaker 2: Okay, yeah, okay, okay.
Speaker 1: Yeah, I don't. I don't have a great answer for you.
Speaker 1: I mean, like you can find things that say the
Speaker 1: number of infections is decreasing, you know, and we're doing
Speaker 1: a great job. But I don't know how to believe
Speaker 1: any of it because I don't know where they're even
Speaker 1: getting these numbers from.
Speaker 2: Right.
Speaker 1: But the real issue is with new treatments. Right, we're
Speaker 1: talking about now versa and with the other one called visa. Right,
Speaker 1: vankoycin resistant, oh, visa whatever, it's not, it's bad news, right,
Speaker 1: But anyway you slice it, the fact that we are
Speaker 1: now seeing resistance to vanko mycin is very very bad news.
Speaker 1: And so the thing is, I found an article that
Speaker 1: was that was basically talking about new novel ways to
Speaker 1: find antibiotics. Right, They were using sequencing to find different
Speaker 1: compounds that could then be used as antibiotics. It was
Speaker 1: very cool. I'll link to the paper. There's another group
Speaker 1: out of Brown who's getting a lot of POPSI articles
Speaker 1: right now written about them because they're doing a lot
Speaker 1: of research on all these novel compounds and they've found
Speaker 1: a few that seemed promising. And that's awesome and it's
Speaker 1: necessary and it's great, but it doesn't solve the problem
Speaker 1: that is the fact that these bacteria will inevitably evolve resistance.
Speaker 2: You're playing the same game that we have been playing,
Speaker 2: right that we are losing at. Yeah, and have never
Speaker 2: won it.
Speaker 1: So I was really hoping when I started researching this
Speaker 1: that I was going to find phage therapy and imm
Speaker 1: you know, globulins, And yeah, I found nothing.
Speaker 2: You didn't find any phage therapy.
Speaker 3: I found that it exists, but I found no details
Speaker 3: on what.
Speaker 1: The state of the research actually is.
Speaker 2: Okay, what about bacterial interference.
Speaker 1: I found nothing on bacteria.
Speaker 2: Wow.
Speaker 1: Yeah, So it doesn't mean it's not out there. It
Speaker 1: just means that it's maybe not the first steps that
Speaker 1: people are working on, which is kind of a bummer.
Speaker 1: But also maybe I'm just totally wrong and was looking
Speaker 1: in the wrong places, and someone listening is going to
Speaker 1: tell us that they're working on a new phage and
Speaker 1: bacterial interference and biofilm treatments something, you know, because it
Speaker 1: has to be happening, right, like I would hope, unless
Speaker 1: it's just that there for some reason, there's no money
Speaker 1: in it. But it seems like if we're going to
Speaker 1: put money anywhere, it should be in finding alternatives to
Speaker 1: antibiotics because we're.
Speaker 3: Going to need them for so different many infections.
Speaker 2: It's a good, good place with some money.
Speaker 1: Yeah, but I don't have a great answer. I don't
Speaker 1: have like here's the newest thing and it's going to
Speaker 1: solve all of our problems goop.
Speaker 2: Yeah. So okay, So how scared should we be of MRSA.
Speaker 1: I mean, I don't want to tell you like like
Speaker 1: don't interact with other humans or something.
Speaker 3: Not that level.
Speaker 2: That ship has sailed.
Speaker 3: Yeah, well that's just for different reasons.
Speaker 1: No. I think Merca is a really scary one. I
Speaker 1: think it's maybe up there with maybe maybe not up
Speaker 1: there with flu, but but it's up there.
Speaker 2: Yeah. I feel like they're all scary in there.
Speaker 1: In there, it's a different scary. I think it's not
Speaker 1: as much like we're gonna have this giant outbreak. It's
Speaker 1: more just like this thing already exists everywhere and we're
Speaker 1: kind of running out of options to treat it.
Speaker 2: So yeah, it freaked me out. Don't look up videos.
Speaker 2: Do look up videos? Yep, well.
Speaker 1: Devil Angel, Devil Angel's who.
Speaker 3: But I do. Do you have any sources that you'd
Speaker 3: like to use sites?
Speaker 2: I do, yes. So I got most of my information
Speaker 2: from Superbug by Maren McKenna, which I is where I
Speaker 2: got the first hand account and it's a really great
Speaker 2: overview of the history of drug resistant staff us, not
Speaker 2: just MRSA but in general, and she's an amazing writer
Speaker 2: and so it's very fun to read.
Speaker 1: I don't have any real sources. I'll post a couple
Speaker 1: of articles that we're interesting about MRSA, antibiotics, new antibiotics. Oh,
Speaker 1: we should also say thank you to Bloodmobile for the
Speaker 1: music as always, so thank you for listening. Yeah, oh yeah,
Speaker 1: we love you.
Speaker 2: Thank you so much for listening.
Speaker 1: And if you don't already follow us on all the
Speaker 1: social medi's Facebook, Instagram, Twitter, we're there, post and gross videos.
Speaker 1: Probably a bunch of pimple poppers for this one, No, Lie,
Speaker 1: I will, she won't I will.
Speaker 3: So check the Twitter.
Speaker 2: We have a good Reads book list.
Speaker 1: All of our sources are available on our website, This
Speaker 1: podcast will kill You dot com. You can find every
Speaker 1: single episode with all of our sources listed. We keep
Speaker 1: it legit and that's it.
Speaker 3: Yeah.
Speaker 1: I think really the only thing that we can say
Speaker 1: for this episode.
Speaker 2: Is really, do please wash your hands.
Speaker 1: You're you're filthy animals.
Speaker 3: We're filthy, all of us. Yeah, I'm gonna go wash
Speaker 3: my hands.
Speaker 2: Yeah, let's go do that.