Speaker 1: My name is Maggie, and my story begins nearly two
Speaker 1: years ago.
Speaker 2: On New Year's Eve.
Speaker 1: My family went for a short hike in the woods
Speaker 1: that morning and then met some friends.
Speaker 2: To go bowling that evening.
Speaker 1: I thought maybe bowling had given me bresidas, as my
Speaker 1: elbow felt unusually painful. We went to bed long before
Speaker 1: ringing in the New Year, but the pain kept growing.
Speaker 1: I really wanted to sleep, so I made an ic
Speaker 1: sleeve out of a sock, but that pressure was too much,
Speaker 1: so I resorted to an old prescription pain med and
Speaker 1: waited impatiently for that to kick in before adding ibuprofento
Speaker 1: the mix. Soon after, my husband found me lying on
Speaker 1: our bedroom floor as I felt like I might pass out.
Speaker 1: He thought this was just my normal response to pain,
Speaker 1: because I have passed out in the pass But later
Speaker 1: I began vomiting, which I then attributed to taking meds
Speaker 1: on an empty stomach.
Speaker 2: By morning, I could not get out of bed. I
Speaker 2: was so sick.
Speaker 1: My husband kept trying to get me to stand so
Speaker 1: we could go to urgent care, but I couldn't. I
Speaker 1: finally felt a short window and we made it downstairs
Speaker 1: to the car and headed straight to the YAR instead.
Speaker 1: My husband wheeled me in with my bucket, and they
Speaker 1: found my blood pressure was considerably low. My normal resting
Speaker 1: heart rate of around sixty was elevated to ninety four
Speaker 1: beats per minute. I also coincidentally tested positive for COVID,
Speaker 1: so the er gave me my own room with full
Speaker 1: COVID precautions in place. On the second day, after multiple
Speaker 1: bags of ivy fluids that failed to bring up my
Speaker 1: blood pressure, they transferred me to the intensive care unit
Speaker 1: to treat me for septic shock. It's worth noting that
Speaker 1: three to four days prior to all this, I had
Speaker 1: visited my general practitioner for a lingering cold or sinus infection,
Speaker 1: and I was about three days into a prednizone prescription
Speaker 1: to calm down my inflammation. I was feeling good, but
Speaker 1: my immune system had clearly seen better days. This whole time,
Speaker 1: my arm had a noticeable redness that radiated from my elbow,
Speaker 1: and it was.
Speaker 2: Growing by the hour.
Speaker 1: Doctors were tracking the spread with sharpies, and there was
Speaker 1: a lot of discussion about whether to operate. My amazing
Speaker 1: infectious disease doctor was pushing for this to happen. I
Speaker 1: could hear my own voice telling my students how this
Speaker 1: can happen to anyone, but I could not believe that
Speaker 1: I was now that person. I remember trying to mentally
Speaker 1: prepare myself to give permission to amputate my arms should
Speaker 1: it become necessary to save my life. As the pain
Speaker 1: of redness approached my arm pit and shoulder, they found
Speaker 1: a surgeon that agreed to perform a debreedment of my arm.
Speaker 2: They opened me up with four long.
Speaker 1: Incisions that averaged three to four inches apiece, and after
Speaker 1: surgery they were wide open with all my deep tissues
Speaker 1: on full display. My dad was sent a picture and
Speaker 1: he passed out behind the wheel just thinking about it.
Speaker 1: He survived, his car did not, And it's pretty clear
Speaker 1: where I get my vasovagal response. My left arm had
Speaker 1: undergone so many blood draws and ivs that I developed
Speaker 1: a painful clot, forcing doctors to put in a central
Speaker 1: line to continue my meds. I was on at least
Speaker 1: three different antibiotics, and now I had to worry about
Speaker 1: the risk of a new infection going straight to my heart,
Speaker 1: as any catheter comes with the risk of infection. My
Speaker 1: most unpleasant memories, though, were the nights I insisted my
Speaker 1: family go home to sleep at night to stay strong
Speaker 1: and healthy. But many nights I cried myself to sleep,
Speaker 1: terrified I could not turn in my bed, and the
Speaker 1: morphine drip gave me startling dreams that would waken me.
Speaker 1: It was one of those nights I sent an email
Speaker 1: to the Errands asking them to save me a spot
Speaker 1: for when I beat this infection. I had made the
Speaker 1: mistake of reading the dire statistics for my condition online,
Speaker 1: and I was not about.
Speaker 2: To leave my six year old son or my husband behind.
Speaker 1: In the end, I had three surgeries, including another where
Speaker 1: they placed a wound back on my elbow and another
Speaker 1: to insert a wound drain and staple my arm closed.
Speaker 1: I was in the hospital for nearly nine days. I
Speaker 1: went in with suspected versidas, but the list of itises
Speaker 1: kept growing. I had cellulitis, toxic shock, sepsis, septic shock,
Speaker 1: and necrotizing fasciitis. The culture confirmed the infection was caused
Speaker 1: by group A strip. I was sent home with ivy
Speaker 1: penicillin through a pickline in my left arm while the
Speaker 1: wound drain hung from my right arm. I felt a
Speaker 1: bit like Pinocchio with so many strings but I was
Speaker 1: grateful to be home.
Speaker 2: I was very fortunate throughout all of this to have
Speaker 2: such great support.
Speaker 1: I'm grateful to my husband and my sisters, my care team,
Speaker 1: and all the friends and family who supported us through
Speaker 1: the scary time.
Speaker 2: We felt so loved and we hoped to never have
Speaker 2: to experience love in this way again.
Speaker 3: Oh my gosh, that is I mean, it's so it's terrifying, terrified.
Speaker 3: Oh oh, we're really glad that you're okay, and we
Speaker 3: appreciate you so much for being willing to share your story,
Speaker 3: that scary, scary story.
Speaker 4: Yeah, yeah, thank you, thank you so much.
Speaker 3: Yeah. Hi, I'm Aaron Welsh.
Speaker 4: And I'm Erin aman Updyke.
Speaker 3: And this is this podcast will Kill You.
Speaker 5: And today we're talking tissue death because we're covering necritizing
Speaker 5: fasci itis.
Speaker 3: We've covered as I was doing the history much of
Speaker 3: this in other capacities. I mean, this is a strange
Speaker 3: beast of a thing, right, Like enough said, Okay.
Speaker 5: Said, I agree, because we're talking like multiple bacterial species
Speaker 5: or groups.
Speaker 3: But there are so many questions that I have, and
Speaker 3: so I really just want to like go straight to things.
Speaker 3: So let's just get through the rest this business quickly.
Speaker 4: Yeah sounds good. First, it's quarantin any.
Speaker 3: Time it is it is. What are we drinking this week?
Speaker 3: We're drinking hit the gas Aaron. It was gas made like.
Speaker 5: It's one of those where you have to explain it,
Speaker 5: but it works on so many levels once you do.
Speaker 5: Gas means group a strap, but it also means gas
Speaker 5: as in air bubbles, which you might see on imaging
Speaker 5: if you have an advertizing soft tissue infection and anyways.
Speaker 3: In keeping in line with the gas air bubbles, of course,
Speaker 3: our drink is a well our plusy berita this week
Speaker 3: is a club soda plus BlackBerry syrup plus lemon juice.
Speaker 3: There you go. We did it, guys, we did it.
Speaker 3: We'll post it on our website. We're going to try
Speaker 3: to plus definitely social media. We will be posting it there,
Speaker 3: so make sure you're following us. We're also on YouTube,
Speaker 3: so make sure you're subscribed and all of that to
Speaker 3: the exactly right media YouTube channel. We have a website
Speaker 3: where you can find all sorts of things like transcripts
Speaker 3: like our submit your first hand account, form, a Goodreads list, bookshop,
Speaker 3: dot org, affiliate page, sources for each and every one
Speaker 3: of our episodes, music by Bloodmobile and some more goodies.
Speaker 3: So check it out.
Speaker 4: This podcast will kill you dot Com? Great?
Speaker 3: Great shall we? We shall?
Speaker 4: Okay right after this break.
Speaker 5: In some ways, Aaron, I think of necrotizing fasci itis
Speaker 5: as like an old friend of the pod.
Speaker 3: Yeah, I think that's fair to say, thank you.
Speaker 4: I'm glad you.
Speaker 5: I'm glad you agree, because we have covered so many
Speaker 5: of the major causes of necrotizing fasciitis classically, the primary
Speaker 5: agent that we think of within necrotizing fasciadis infection is
Speaker 5: a beta heat meltic streptococcie called strap piogenies aka group
Speaker 5: A strap aka the cause of scarlet fever, among many
Speaker 5: other things.
Speaker 3: Which we have done exactly We've done that. We've also done.
Speaker 5: Yeah, we've also done toxic shock very recently, which necrotizing
Speaker 5: fasciitis often leads to a toxic shock syndrome. Necrotizing fasciidis
Speaker 5: also can often lead to sepsis, which we've also covered.
Speaker 3: I mean, I think this just goes to show if
Speaker 3: I may be a little not like philosophical, but I
Speaker 3: guess like historical. You know, back when germ theory was
Speaker 3: the newest thing of the day, and it was suddenly
Speaker 3: like every disease is one germ, right, like each disease
Speaker 3: has one germ kind of a thing. And this disrupts
Speaker 3: that paradigm on which I find so interesting because are
Speaker 3: the way that we approach this podcast is very much
Speaker 3: one disease, one thing.
Speaker 4: Well, and it's interesting too, and we've talked about this.
Speaker 5: I wish I could remember on what episode it was,
Speaker 5: because you have both, right, you have sometimes like one
Speaker 5: pathogen that can cause so many different types of disease,
Speaker 5: like with MRSA, like with streptococcus, but then you also
Speaker 5: have one disease or one clinical syndrome like necrotizing fasciitis,
Speaker 5: that can be caused by so many different pathogens because
Speaker 5: it isn't just group A strip no no. Necrotizing fasciitis.
Speaker 5: Infections can also be caused by another good friend of
Speaker 5: the pod, Staphlococcus aureus, including MRSA or methicillin resistant Staph oureus.
Speaker 5: It can also be caused by clusterdium species by Vibrio vulnificus,
Speaker 5: which we haven't yet covered.
Speaker 4: And we should we should.
Speaker 5: Vibrio is a marine or aquatic bacterium that can cause
Speaker 5: a neckritizing infection, especially after injuries, so like you get
Speaker 5: you know, nicked while you're fishing, or a fish scale
Speaker 5: kind of scratches you, or you just go swimming when
Speaker 5: you have a bug bite or a scratch. Anyways, but
Speaker 5: there also are a whole bunch of necrotizing fasci idis
Speaker 5: infections that are actually polymicrobial, and these can include both
Speaker 5: gram negative and gram positive bacterium so friends like E.
Speaker 5: Coli or Clipsiella in addition to all of the things
Speaker 5: that we've already described. So whatever the organism in question,
Speaker 5: what is necrotizing fasci i itis you mean? Yeah, I've
Speaker 5: said the words so many times now. It is a
Speaker 5: severe bacterial infection that starts in the skin usually and
Speaker 5: spreads down deep through the layers, through the dermis, through
Speaker 5: the subcutaneous fat, and into a layer called the fascia.
Speaker 5: And I want to spend a moment to talk about
Speaker 5: our fascia. Okay, great, We have a lot of different
Speaker 5: types of fashia in our bodies. It is basically a
Speaker 5: part of our connective tissue network. Our fascia layers give
Speaker 5: support to various structures in our body, so just underneath
Speaker 5: our if you think, I'm using my finger as an example,
Speaker 5: So if you think of looking at the palm of
Speaker 5: your hand, the top of your finger being your skin,
Speaker 5: You've got your epidermis and dermis, and then you have
Speaker 5: a layer. Then you've got your subcutaneous tissue like under
Speaker 5: your first knuckle, okay, and then just under that you're
Speaker 5: going to have a layer like under your second knuckle
Speaker 5: here of superficial fascia and then a layer of deep
Speaker 5: fascia and then muscle.
Speaker 3: What's the purposes of superficial and deep fascia.
Speaker 5: They're all there to support our structure. So the superficial
Speaker 5: fascia is like the underlayer underneath our skin. The deep
Speaker 5: fascia is what surrounds our muscles, So all of our
Speaker 5: muscles are covered in their own layer of fascia. Our
Speaker 5: organs inside of our body also have their own versions
Speaker 5: of fascia, and then our body cavi these have their
Speaker 5: own layer of fascia as well, our abdominal wall and
Speaker 5: our thoracic cavity. So we've got layers upon layers upon
Speaker 5: layers of fascia.
Speaker 3: What's fascia made of?
Speaker 5: Mostly collagen. Oh okay, Yeah, it's mostly collagen. And when
Speaker 5: you look at it, it usually looks like a kind
Speaker 5: of white, kind of filamentous.
Speaker 4: Sort of structure, almost like I don't know a.
Speaker 3: Good example, like angel hair, spaghetti.
Speaker 4: No, it's more like like.
Speaker 5: Insulation and your wall quite the inside of an orange peel,
Speaker 5: because it's stringier than that, like.
Speaker 3: Like fungal growth in the last of us.
Speaker 5: Yeah, except imagine it being quite firm, you know, like
Speaker 5: like really tough spider web.
Speaker 4: Okay, like you know those.
Speaker 5: Like cellulose shades that you sometimes can have on your
Speaker 5: cover your window where like the sun can't get in
Speaker 5: but you can still kind of see out or whatever,
Speaker 5: or the sun can get in but they can't like that. Okay,
Speaker 5: not quite opaque. And anyways, that was a struggle. I
Speaker 5: probably should have thought of it before I started talking.
Speaker 3: Had a really fun time guessing guessing things that I
Speaker 3: have no idea what the actual image of it.
Speaker 5: Is, especially based on my hand motions, which are entirely unhelpful. Anyways,
Speaker 5: So we're talking about a bacterial infection that spreads down
Speaker 5: into this layer, and which layer of fashion just depends
Speaker 5: on how far the infection goes. But as this infection spreads,
Speaker 5: what makes it a necrotizing infection is that the bacteria
Speaker 5: start to produce various toxins, which one which type. It's
Speaker 5: all going to depend on what the pathogen is, because
Speaker 5: there can be so many, but many of the types,
Speaker 5: and sometimes it's not even toxic. Media is more just
Speaker 5: like this overwhelming bacterial infection. But in any case, whether
Speaker 5: it's toxin mediated or just from so many bacteria, we
Speaker 5: see a lot of inflammatory damage, including in the blood
Speaker 5: vessels of our tissues that ends up leading to blood
Speaker 5: clots so called microthrombi, and that caused death necrosis of
Speaker 5: the tissue itself. Now, the term necrotizing fasciitis, that's what
Speaker 5: we're using in this. It's not an incorrect term, but
Speaker 5: what we have come to learn is that there are
Speaker 5: a lot of other kinds of necrotizing soft tissue infections.
Speaker 5: So an umbrella term that's often used now is NSTI
Speaker 5: necrotizing soft tissue infections. Some of them get their own name,
Speaker 5: Like if it's only in the skin and subcutaneous fat,
Speaker 5: you can have a necrotizing cellulitis and that would be
Speaker 5: less deep, not all the way down to the fascia.
Speaker 5: If it's all the way to the muscle or primarily
Speaker 5: in the muscle, this might start from a muscle injury
Speaker 5: rather than like a skin damage. You can get a
Speaker 5: piomocitis or a myonecrosis. Myonecrosis is what we see with
Speaker 5: gas ganggreen, which is caused by a type of clustered
Speaker 5: am species. Yes, but these are not all mutually exclusive.
Speaker 5: But the reason that neckartizing fasci itis itself kind of
Speaker 5: I think holds a lot of esteem. I don't know
Speaker 5: if esteem is the right word, but that is like
Speaker 5: the one that we think of when we think of
Speaker 5: a necrotizing soft tissue. Infection is in part because it's
Speaker 5: the most common, and the reason that it's most common
Speaker 5: is because the fascia has some components to it that
Speaker 5: make it particularly vulnerable to infection. First of all, the
Speaker 5: blood supply to our fascia is not nearly as robust
Speaker 5: as the blood supply to our skin, to our subcutaneous
Speaker 5: tissue and to our muscle. It is just there for support,
Speaker 5: I see, and so it doesn't need usually as robust
Speaker 5: of a blood supply. It's not a muscle that's contracting,
Speaker 5: it's not our skin that's constantly regenerating. It's just there
Speaker 5: as like a you know, shingles on the outside of
Speaker 5: your house. That's a bad example. It's a sport structures,
Speaker 5: but it's not as support structure at all.
Speaker 4: That's your skin.
Speaker 3: I have a quick question about this infection. So you
Speaker 3: talk about it going deep, What is the it goes
Speaker 3: deep and wide? Right, Like, Yeah, what does it do
Speaker 3: first and in what order and at what rates?
Speaker 5: That is another component of the fascia itself that makes
Speaker 5: it so vulnerable to these type of infections because once
Speaker 5: an infection gets into that fascial plane, it can spread
Speaker 5: along that fascial plane without interacting with any of the
Speaker 5: other tissue areas. Oh so once it gets into that fascia,
Speaker 5: think of it like a highway. Now it's just on
Speaker 5: this freeway, no stops needed, and so little blood supply
Speaker 5: that there's not a lot of things coming in to
Speaker 5: carry off or to fight that infection. So, yes, it
Speaker 5: is something that spreads widely, very quickly, and oftentimes the
Speaker 5: first like where that infection first started, it can't. Most
Speaker 5: often it starts from something like a scratch on the skin. Yeah,
Speaker 5: it can be a small wound it can be a
Speaker 5: large wound, it could be a surgical wound. But it
Speaker 5: sometimes isn't even like a known wound to the skin.
Speaker 5: Sometimes it's damaged to like the muscle itself. Right, you
Speaker 5: injure your muscle, you hid it something like that, and
Speaker 5: there you have, for some reason bacteria that made it
Speaker 5: from your bloodstream into that fascil plane. How you know,
Speaker 5: because so many of these bacteria that tend to cause
Speaker 5: this infection live on our skin all the time, right,
Speaker 5: Like Streptococcus can live Staphylococcus can just live on us.
Speaker 5: And so some people every once in a while might
Speaker 5: have some bacteria that make their way into our bloodstream
Speaker 5: and then our body manages to fight them off. Most
Speaker 5: of the time, it's what we call transient bacteremia. Most
Speaker 5: of the time you might never know that that happens.
Speaker 5: But if that happens and you have an injury and
Speaker 5: these bacteria happen to make it into this fascia, they
Speaker 5: could potentially establish an infection. And to be honest, we
Speaker 5: don't fully understand like why and who on all of that, Okay,
Speaker 5: but once it's there, it can very quickly kind of
Speaker 5: spread along this fascial plane without necessarily causing more visible damage. Right,
Speaker 5: you might not see damage to the skin because it's
Speaker 5: mostly tracking along the fascia. And the final thing about
Speaker 5: the fascia that can make this particularly vulnerable is that
Speaker 5: because I'm talking about like distinct layers of tissue, there's
Speaker 5: kind of this what we call a potential space that exists,
Speaker 5: like think of it as like between these layers of tissue.
Speaker 3: So what part of what.
Speaker 5: The fashia does is allow for things to slide against themselves, right,
Speaker 5: Like it provides support, but it also allows your muscles
Speaker 5: to slide against a smooth surface. What that means is
Speaker 5: that there is a like theoretical space microscopic though it
Speaker 5: may be between these tissue layers. That space can fill
Speaker 5: with fluid, and it does in a necrotizing infection, and
Speaker 5: that fluid can make it even harder for our body
Speaker 5: to respond and clear that infection because our immune cells
Speaker 5: have to like wade through a swimming pool of fluid
Speaker 5: to try and to this infection.
Speaker 3: Okay, Okay, so somehow bacteria invade the fascia. H The
Speaker 3: fascia dies fairly easily because there's once it erodes the
Speaker 3: blood supply there's not a lot of redundancy and so
Speaker 3: there's no more like you said, highway. So then once
Speaker 3: it goes under like along the rest of the fascia,
Speaker 3: then the tissue on top of that will just sort
Speaker 3: of die.
Speaker 4: It can or it cannot.
Speaker 5: So sometime like eventually this infection will get so overwhelming
Speaker 5: that it will continue to invade, So it'll either invade
Speaker 5: down into the muscle or it will invade continue going
Speaker 5: like back up and out back towards the skin, and
Speaker 5: then you'll see more evidence of the damage on the skin.
Speaker 3: Okay, can we talk about the bacteria involved and what
Speaker 3: makes them more likely or toxins or the differences between them,
Speaker 3: like why why does this happen?
Speaker 5: Yeah, it's it's a great question, and that because that's
Speaker 5: a it's a multi part question, right, because it's why
Speaker 5: does this happen to certain people? Why does this happen
Speaker 5: in certain situations? And why does this happen from certain bacteria?
Speaker 4: Yeah, and that's a lot.
Speaker 5: I don't think I'm gonna have answers for all of
Speaker 5: this questions. We know from episodes that we've done on
Speaker 5: group A strep in the past, as well as from
Speaker 5: Staphylococcus aureus. These are two bacteria that produce a lot
Speaker 5: of exotoxins. These toxins produce a really robust and strong
Speaker 5: inflammatory response in us, and that inflammation can cause damage.
Speaker 5: Vibrio vugnificence. I didn't actually dig deep into it. I
Speaker 5: just know that it is quite virulent and I'm not
Speaker 5: exactly sure what all of its virillance factors are.
Speaker 4: Just means you need to do a full episode on it.
Speaker 5: And then Clostridium is also like a toxin mediated infection,
Speaker 5: So it's again this toxin and an inflammatory response because
Speaker 5: of that toxin.
Speaker 3: Are these the same toxins or different toxins? Is the
Speaker 3: mechanism of action different of different kinds? Yeah, a ton
Speaker 3: of different kinds, And a lot of these infections are
Speaker 3: actually polymicrobial. So another big component is that there are
Speaker 3: certain risk factors to who is more likely to get
Speaker 3: and what scenarios are more likely to get necrotizing infection. Right,
Speaker 3: so individual level factors things like diabetes, cirrhosis or other
Speaker 3: liver disease, certain compromising conditions, and the elderly are the
Speaker 3: most high at risk for a necritizing skin and soft
Speaker 3: tissue infection. Things that are environmental, like fishing in waters
Speaker 3: that are contaminated with vibrio and having an open wound
Speaker 3: is going to environmentally put you at a higher risk. Right,
Speaker 3: how is viio transmitted?
Speaker 4: It just gets into your skin through these open wounds.
Speaker 3: Right, But I mean, like where is it coming from
Speaker 3: in the environment.
Speaker 4: It lives in the environment. It can thrive in the ocean.
Speaker 5: It's also can get to very high concentrations in filter
Speaker 5: feeders like shellfish like oysters. So you also can get
Speaker 5: quite a severe GI infection from eating raw oysters and
Speaker 5: things because of embrya.
Speaker 3: So it's not like our residence no staph and.
Speaker 5: Okay, correct, Yeah, this one is like specifically environmental, whereas yeah,
Speaker 5: most of the rest of these even E Coli, clubziella,
Speaker 5: these are things that just live in us and on us.
Speaker 5: And so really it's just about the wrong time and
Speaker 5: the right port of entry that contribute to someone eventually
Speaker 5: getting a necritizing infection. In terms of what it looks like.
Speaker 5: The scariest thing, there's a lot of scary things about
Speaker 5: neckritizing fasci itis. One of the scariest things is that
Speaker 5: at first it is very hard to distinguish from a
Speaker 5: totally benign skin infection, So it can look very similar
Speaker 5: to things like arisipolis or there's like a few differences,
Speaker 5: but at the very beginning, there's not, like there's not
Speaker 5: a lot that necessarily distinguishes these early in the course
Speaker 5: of infection. And that's where the danger really lies when
Speaker 5: it comes to necritizing fasci idis, because the big difference
Speaker 5: is that it progresses incredibly rapidly compared to other skin infections,
Speaker 5: and by that I mean on a matter of hours
Speaker 5: or a couple of days rather than days to weeks
Speaker 5: that we might see the progression of a cellulitis turning
Speaker 5: into a lymphangitis streaking up your arm or an ariseplus
Speaker 5: turning into something that has you know, a lot of
Speaker 5: vesicles or blisters or things like that. So you can
Speaker 5: imagine the nightmare which I have seen, and it is
Speaker 5: truly a nightmare that someone comes into the emergency room
Speaker 5: with like a red spot on say their leg, or
Speaker 5: maybe even just kind of like a patchy area of
Speaker 5: like discoloration or a little bit of swelling. You're going
Speaker 5: to touch it or push on it to see if
Speaker 5: there's any in duration or sign of an absess and
Speaker 5: one of the signs they teach you to look out
Speaker 5: for in medical school is called pain out of proportion.
Speaker 5: If you touch a necrotizing infection, that person is practically
Speaker 5: going to jump off of the table because of how
Speaker 5: incredibly painful it is compared to what it looks like.
Speaker 3: Yes, okay.
Speaker 5: The other thing you can sometimes see early in the
Speaker 5: course of infection is that you might have swelling like
Speaker 5: edema that goes beyond the area of redness or of
Speaker 5: like a dark purplish discoloration, So you're like more swollen
Speaker 5: than this area that looks like it has an infection
Speaker 5: mm hmm. And then the signs that are like more
Speaker 5: classically associated with a neckritizing fasci iis tend to be
Speaker 5: pretty late stage signs, which means you might have missed
Speaker 5: a pretty critical window for intervention. But these are the
Speaker 5: things that you see a lot of pictures of online.
Speaker 4: These are like.
Speaker 5: Bullet or the really large flow you would filled or
Speaker 5: sometimes blood filled blisters. You get a lot of bruising
Speaker 5: of the skin, and you get that before you start
Speaker 5: to see tissue death like skin death or necrosis of
Speaker 5: the skin. If you do imaging, which we often do.
Speaker 5: It'll be a seed t scan or an MRI scan.
Speaker 5: You might see gas in the tissues, especially tracking along
Speaker 5: that fascion plane.
Speaker 3: Where's the gas coming from.
Speaker 5: The gas is coming from the bacteria itself. It's part
Speaker 5: of their metabolism.
Speaker 3: Yeah, what I thought.
Speaker 5: You also sometimes can see this without imaging by crepitence
Speaker 5: on exam, So that's that like rice crispy feeling and
Speaker 5: sound when you press on the skin when it gets
Speaker 5: very severe, instead of that pain out of proportion, you
Speaker 5: might actually have anesthesia cutaneous anesthesia where you don't even
Speaker 5: feel your skin at all because so much of those
Speaker 5: nerves have died without treatment. This will progress incredibly rapidly
Speaker 5: and will then include fever, hypotension, It can progress to
Speaker 5: toxic shit syndrome, it can progress to sepsis and shock
Speaker 5: and death. And really one of the hardest parts is
Speaker 5: that early diagnosis. The statistics, unfortunately are not great. The
Speaker 5: best ones I saw were that about fifty percent of
Speaker 5: the time necrotizing soft tissue infections are not diagnosed initially
Speaker 5: on an admission in the er. But I've seen other
Speaker 5: papers that said like eighty five to one hundred percent.
Speaker 4: Of the time, which it just seems actually bananas.
Speaker 5: But yeah, yeah, it's it's it's a really that's a
Speaker 5: really huge problem because the treatment for this is early
Speaker 5: surgical intervention, Okay, and by early I mean within twenty
Speaker 5: four hours of this diagnosis, and the earlier the better.
Speaker 5: So if if oars are set up to be there
Speaker 5: in a matter of hours, that person is more likely
Speaker 5: to have a better outcome than otherwise. The surgical degreement
Speaker 5: can be really extensive. The average number of surge that
Speaker 5: somebody needs after a necrotizing fasciitis is.
Speaker 4: Three to four.
Speaker 5: They sometimes require amputation depending on the location and the
Speaker 5: extent of that initial infection, and even if they don't
Speaker 5: require amputation, they often require such extensive debreedment of all
Speaker 5: of that dead tissue to be able to get down
Speaker 5: to healthy tissue that you are going to have an
Speaker 5: open wound for a very long time in order to
Speaker 5: allow healthy tissue to kind of heal back in while
Speaker 5: you're on antibiotics to fight off that infection. That may
Speaker 5: require packing changes, or it may require what's called a
Speaker 5: wound back, which keeps like negative pressure on the wound,
Speaker 5: which can be quite painful and cumbersome, and then very
Speaker 5: often people need skin graphs or complex reconstructive surgeries to
Speaker 5: be able to heal over time. So this is something
Speaker 5: that has like a pretty long lasting impact on somebody's
Speaker 5: life if they survive.
Speaker 3: Yeah, I know that necrotizing fasciitis. We have fascia all
Speaker 3: over our bodies, and so it can happen anywhere. Are
Speaker 3: there places that it's more likely to happen?
Speaker 5: Most likely places are the extremities. I think the legs,
Speaker 5: lower legs are the most likely, just because that is
Speaker 5: where you have so much potential for exposure to like wounds.
Speaker 5: Plus they're such a strong association with diabetes, and so
Speaker 5: diabetic foot wounds are a place that you can really
Speaker 5: easily get a necritizing infection.
Speaker 4: But there are a.
Speaker 5: Few places that have specific names associated with them because
Speaker 5: they have like a specific set of syndromes. So Fournier's
Speaker 5: ganggreen is a specific name for necrotizing fasciitis of the genitalia. Yeah,
Speaker 5: which can be really really horrific. Has a high mortality
Speaker 5: rate and just a huge amount of morbidity associated with it.
Speaker 5: It's often caused by polymicrobial infections, but sometimes, like some
Speaker 5: of them, bacteria that are associated with it are things
Speaker 5: like staff aureus e coli. One of the big problems
Speaker 5: with a Fournier's ganggreen is because if it extends to
Speaker 5: involve like near the anal sphincter or the perineum down
Speaker 5: towards the anal sphincter, then you have a really high risk,
Speaker 5: especially after surgery, of fecal contamination of the wound. So
Speaker 5: it's really hard to keep these wounds from getting like reinfected.
Speaker 5: Sometimes it has to go so far, like the surgical
Speaker 5: correction has to go so far as to do like
Speaker 5: a diverting colostomy just so that those tissues can actually heal.
Speaker 5: So this is a major major problem. And then there's
Speaker 5: also other areas of your body, like deep space fascia
Speaker 5: that you can get infections in. There's one called ludwings angina,
Speaker 5: which is an infection of the fascia of like the
Speaker 5: submandibular space, and there's a few other like deep neck
Speaker 5: space infections that you can get that are a necrotizing
Speaker 5: fasci idis.
Speaker 4: Those are very dangerous because they could.
Speaker 5: Potentially involve your airway, so that usually needs emergent surgery
Speaker 5: to like decompro us your airway and things like that.
Speaker 5: And then of course we talked about vibrio neckfash, which
Speaker 5: is a little different than our classic streptococcal neckfash. There's
Speaker 5: actually a they classify it into, like type one is
Speaker 5: the polymicrobial infections. Type two is Streptococcus or staff oureus.
Speaker 5: And there's some people that are like, we should have
Speaker 5: a type three for Vibrio plus or minus Clustridium. I
Speaker 5: don't know if that's like official yet.
Speaker 2: But.
Speaker 5: And that is what we see in association with marine
Speaker 5: life or like marine coastal waters, that kind of a thing.
Speaker 3: Like so subtropical tropical coastal waters.
Speaker 5: Not anymore because of climate change, right, talk more about that.
Speaker 3: I mean the water is warming, yes, yeah, exactly, yes.
Speaker 4: Yes, it likes warm water.
Speaker 5: But yeah, I mean, I don't know aeron if you
Speaker 5: have more questions, that's like the main thing that I have.
Speaker 4: I have more on like how we diagnose.
Speaker 5: It in that, but it's probably a little bit boring,
Speaker 5: and so tell me if you have more questions. Otherwise,
Speaker 5: I want to know what you know about how we
Speaker 5: got here.
Speaker 3: I mean, I guess most of my questions now are
Speaker 3: probably more epidemiological, like have we gotten better, Where is
Speaker 3: this happening? What you know, what advancements are there, potential advancements.
Speaker 3: Will AI help us diagnose?
Speaker 5: That's a fun question. Yes, I don't have an answer
Speaker 5: to that, but that's a fun question.
Speaker 3: Not that AI is the end all be all, but
Speaker 3: I feel like for diagnostic stuff, it is an interesting it.
Speaker 5: Is, especially especially for radiology diagnostics, and that is a
Speaker 5: big really like a lot of what research needs to
Speaker 5: be done is on how to better diagnose this quickness
Speaker 5: right and in the early stages of infection.
Speaker 3: Okay, so maybe that's a question how low can we
Speaker 3: get mortality down if you catch it early enough? And
Speaker 3: what is that early enough?
Speaker 5: We can get it down at least in the studies
Speaker 5: where they have looked at this, which have their own
Speaker 5: sets of biases, because they're like, you know, only looking
Speaker 5: at the things that they have diagnosed, and you know,
Speaker 5: so it's there's nuance there. But at least in the
Speaker 5: studies that have looked at this, average mortality is like
Speaker 5: twenty five to thirty five percent. And in the studies
Speaker 5: that have tried to compare early versus delayed debreedment, early
Speaker 5: debreedment can get it down to as low as close
Speaker 5: to ten percent. The biggest problem is those are all
Speaker 5: in studies where that has been identified, right, And so
Speaker 5: the question is like, how do we get better at
Speaker 5: identifying those ones that we missed who we sent home
Speaker 5: with antibiotics and then they came back and now they
Speaker 5: have an acritizing infection. So that's the tricky part, and
Speaker 5: we don't have great answers for that necessarily. Right erin, Erin,
Speaker 5: I know these bacteria have always been here. Sure, tell
Speaker 5: me about the necrotizing infections.
Speaker 4: Oh, do I want to know? I do?
Speaker 3: I think you do?
Speaker 4: I definitely do, I think you do.
Speaker 3: Okay, antibiotic resistant bugs aside, which I know is like
Speaker 3: a big thing to put aside. Yeah, there are relatively few,
Speaker 3: I would say, bacterial infections that have the power to
Speaker 3: transport us back to an era before we had any
Speaker 3: tools to fight these germs.
Speaker 5: Right, No, it's I mean necrotizing infections are terrifying, terrifying.
Speaker 3: And what I mean is that even in the most
Speaker 3: well equipped hospital, with the most skilled specialized infectious disease docs, surgeons, whatever,
Speaker 3: modern medicine is sometimes powerless to stop the ravages of
Speaker 3: necrotizing fasciitis. Regardless of the bacterium that's causing it. It
Speaker 3: is destructive, it's deadly, it's humbling in the way that
Speaker 3: it rejects the hundreds of years of scientific advancements that
Speaker 3: we've made in so many areas of medicine.
Speaker 4: YEP.
Speaker 3: I understand why nicknames like quote unquote, galloping gang green
Speaker 3: or flesh eating bacteria. I understand why those are frowned
Speaker 3: on by the medical community. They're sensationalist, they're stigmatizing, their imprecise,
Speaker 3: and they can incite undo fear and panic that this
Speaker 3: new deadly disease, like something out of a horror novel,
Speaker 3: is about to strike you down and everyone else in
Speaker 3: your family or community, because that's not the way that
Speaker 3: necrotizing fasciatis works. But I think that those names sensationalists,
Speaker 3: though they may be, also convey the genuine fear that
Speaker 3: comes with being largely powerless in the face of this
Speaker 3: deadly disease. And I think it could also be argued
Speaker 3: that they have helped raise awareness of the disease, and
Speaker 3: since time is certainly of the essence, that could maybe
Speaker 3: have saved lives in the past. But still we're sticking
Speaker 3: with necrotizing fasciatis for this episode or soft what is it?
Speaker 3: Soft tissue?
Speaker 4: Necrosisizing, negritizing infections.
Speaker 3: Okay, the words are all a jumble. Yes, So I've
Speaker 3: got a quote for you, and strap in because this
Speaker 3: is the first of many many quotes.
Speaker 4: Okay, can't wait.
Speaker 2: Quote.
Speaker 3: Few entities challenged the surgeon's clinical and operative skills as
Speaker 3: intensely as devastating necrotizing soft tissue infections. End quote. Yep,
Speaker 3: that statement. Although it was written in an article from
Speaker 3: nineteen ninety one Necrotizing Lesions of Soft Tissues or Review
Speaker 3: by Patino and Castro, that quote is still as relevant
Speaker 3: today as it was thirty four years ago, and in fact,
Speaker 3: a paper written eighteen years later in two thousand and
Speaker 3: nine reported that over the previous three decades, so from
Speaker 3: nineteen seventy nine to two thousand and nine, mortality from
Speaker 3: necrotizing fasciitis had not budged, despite better tools and more
Speaker 3: knowledge about the condition.
Speaker 4: Yeah, I'm surprised by that.
Speaker 3: Unfortunately, I know I'm not saying this to like terrify
Speaker 3: everyone and say let's jump on the catastrophizing train, just
Speaker 3: that we're still figuring it out. Modern medicine is still
Speaker 3: figuring it out, and we have been working on it
Speaker 3: for centuries.
Speaker 4: Yeah, we'll get to later. How rare these are.
Speaker 3: They're quite rare.
Speaker 4: They're quite rare.
Speaker 3: Yes, yep, not historically in certain situations. Yeah. So, when
Speaker 3: cases of an unusually virulent strain of group A strap
Speaker 3: began popping up in the mid to late eighties, the
Speaker 3: question was raised, is this something new? And I don't
Speaker 3: know how sincere of a question that was, although I
Speaker 3: did read one article that was titled flesh eating bacteria
Speaker 3: a new disease or old story? Because a quick review
Speaker 3: of the literature shows that the answer is that this
Speaker 3: is a very old story. Let's bring out some Hippocrates, right, Yes,
Speaker 3: fifth century DCEE, Volume one of Epidemics. Quote. Many were
Speaker 3: attacked by the aricipolus all over the body. When the
Speaker 3: exciting cause was a trivial accident or a very small wound,
Speaker 3: the ariciplus would quickly spread widely in all directions. Flesh, sinews,
Speaker 3: and bones fell away in large quantities. The flux which
Speaker 3: formed was not like puss, but a different sort of putrefaction,
Speaker 3: with a copious and varied flux. Fever was sometimes present
Speaker 3: and sometimes absent. There were many deaths. The course of
Speaker 3: the disease was the same to whatever part of the
Speaker 3: body it spread. Many lost the arm and the entire forearm.
Speaker 3: If the malady settled in the sides, there was rotting
Speaker 3: either before or behind. In some cases the entire thigh
Speaker 3: was bared, or the shin and the entire foot. But
Speaker 3: the most dangerous cases of all such cases were when
Speaker 3: the pubis and genital organs were attacked. End quote.
Speaker 5: The way that that fluid is described to is called
Speaker 5: dishwater fluid because it is like, it's not a pus,
Speaker 5: it's not a purulent infection. It's like a very liquity
Speaker 5: fluid that's kind of foamy and looks.
Speaker 4: Like that grayish after you've washed dishes.
Speaker 2: Yeah.
Speaker 4: Uh, it's horrific.
Speaker 3: It's horrific.
Speaker 5: Yeah.
Speaker 3: Yeah. And that quote though, like, did that sound to
Speaker 3: you like necrotizing fasci idis? I mean absolutely right, Like
Speaker 3: definitely yeah. And I think that this brings to light
Speaker 3: one of the unique or interesting facets of necrotizing fasci
Speaker 3: itis is that finding historical traces of necrotizing fasci idis
Speaker 3: in like medical texts requires much less guesswork because its
Speaker 3: symptoms and clinical course are so distinctive. It's not like
Speaker 3: there's a fever and maybe a rash and some malaise
Speaker 3: and maybe a sore throat and like maybe your head hurts.
Speaker 3: You know, it's it's it's necrotizing fasciidis. Whether it goes
Speaker 3: by necrotizing fasciitis or malignant ulcer, or a gangrenous ulcer,
Speaker 3: putrid ulcer, fagiadina, phagidenic ulcer, fajidina gangrenosa, or hospital gangreene,
Speaker 3: all of the whether it's called any of those things,
Speaker 3: the description will pretty clearly point towards necrotizing fasciidis as
Speaker 3: the culprit. And so digging back through the medical literature,
Speaker 3: we can find traces of this condition dating back at
Speaker 3: least to the late eighteenth century in France, where a
Speaker 3: doctor out of hospital for the impoverished described it, and
Speaker 3: it was also mentioned in an eighteen oh four book
Speaker 3: on nautical medicine, where it was thought to be newly
Speaker 3: emergent in the British home seies, quote unquote, mostly appearing
Speaker 3: in those who had returned from long cruises in warm regions.
Speaker 3: I don't think it was new, but I think, like
Speaker 3: you said, it was rare, and so it was like
Speaker 3: how widely known was it?
Speaker 4: Anyway?
Speaker 3: So I've go got a quote for you from this
Speaker 3: this nautical medicine book quote. In the summer of seventeen
Speaker 3: ninety nine, the malignant ulcer made its appearance on board
Speaker 3: the Temaare with all the characteristic symptoms in virulence which
Speaker 3: marked it in other ships. Every wound, abrasion of the cuticle,
Speaker 3: blistered part, scald or burn passed rapidly through the various
Speaker 3: stages of inflammation, gangreen and spaceless in a few days,
Speaker 3: leaving the bones almost bare from the separation of immense
Speaker 3: slufs en oohlarin yep. The ship the Saturn seemed especially
Speaker 3: unlucky when it came to this disease. And there was
Speaker 3: one case in particular that is truly horrific, like historically horrific.
Speaker 3: So while in port, this sailor had contracted gonorrhea, and
Speaker 3: it just kept getting worse, like the inflammation kept getting worse,
Speaker 3: the everything kept get worse.
Speaker 2: Quote.
Speaker 3: If you're squeamish, you may want to pause here or
Speaker 3: skip ahead. Yeah, thirty seconds feet I mean you've tuned
Speaker 3: into an episode on acrotizing fasci itis. So like you've
Speaker 3: made it this it's a little bit of a yeah, yeah,
Speaker 3: here we go. Quote. The symptoms advanced by two hasty
Speaker 3: strides to be arrested by any resources of medical skill.
Speaker 3: The gland of the penis soon dropped off, but the
Speaker 3: misery of the patient did not stop there. The whole
Speaker 3: body of the penis passed quickly through the stages of
Speaker 3: excessive excitement and inflammation to complete gangreen and mortification and
Speaker 3: separate it at its very kura. The whole length of
Speaker 3: the urethra to the bulb sloughed away, and also the scrotum,
Speaker 3: leaving the testes and spermatic vessels barely covered with cellular substance.
Speaker 3: He died end quote. Of course, of course he died.
Speaker 3: Of course he died.
Speaker 4: How to have to live through all of that?
Speaker 5: I know?
Speaker 4: And then oh my gosh.
Speaker 3: And then literally like the next sentence, the author says,
Speaker 3: cases like these have been frequent on board these ships.
Speaker 3: And I don't know what these means. Does it mean
Speaker 3: like penis is falling off or does it mean like
Speaker 3: necrotizing inclignant ulser? Yeah? Right, yeah, okay, there's more. I yeah,
Speaker 3: so there's another book published in eighteen eighteen on the
Speaker 3: subject called Observations on Phagiadina Gangrenosa by HH Blackadder that
Speaker 3: discusses the condition as though it was well known, at
Speaker 3: least to military surgeons. So there's a passage from that
Speaker 3: book that is basically an echo of the quote that
Speaker 3: I read earlier. Quote gangrenous fagidina is one of those
Speaker 3: diseases which happily seldom falls under the observation of civil practitioners.
Speaker 3: But on the other hand, it is one of the
Speaker 3: those which army and navy surgeons, during a time of
Speaker 3: active hostilities, are frequently called upon to resist with all
Speaker 3: the resources of their art. No disease requires more circumspection
Speaker 3: and personal attention on the part of the surgeon, and
Speaker 3: when the circumstances in which it occurs, the occasional rapidity
Speaker 3: of its progress, the extent of its ravages, and fatal
Speaker 3: tendency are considered, it may justly be esteemed one of
Speaker 3: the most dreadful diseases to which mankind are subject end quote.
Speaker 3: So it's like this, this is the worst, Yeah, this
Speaker 3: is it. He also talks about how important it is
Speaker 3: to recognize this disease quickly. Quote where there is any
Speaker 3: even the smallest reason to dread the occurrence of this
Speaker 3: disease too early or too many precautions cannot be taken
Speaker 3: with the view of securing its speedy detection.
Speaker 4: End quote.
Speaker 3: I think it's like it's that was from eighteen eighteen,
Speaker 3: and so yeah, it's just.
Speaker 5: They knew all the way back then how important it
Speaker 5: was to be quick about it. Yeah.
Speaker 4: Yeah, we're still having trouble with that.
Speaker 3: We are, we are, And I mean it's hard, it's hard.
Speaker 3: It's hard. I'm also like, this person's not like prophetic
Speaker 3: by any means, right, Like I'm cherry picking these quotes.
Speaker 3: He also used arsenic to treat it, and he blamed
Speaker 3: the weather for when it showed up.
Speaker 4: Yeah, maybe they were all vibryo maybe yeah.
Speaker 3: I mean, but I think the thing that I appreciated
Speaker 3: the most about that entire Like I didn't read the
Speaker 3: whole book, but in the introduction he one of the
Speaker 3: things he says is the author is fully aware of
Speaker 3: his defects to kind of like head off anti criticism.
Speaker 3: He's like, I'm yeah, I know. I was like, We're
Speaker 3: going to start every single episode like that from now on.
Speaker 4: Yep, yep.
Speaker 3: But so throughout the rest of the eighteen hundreds. More
Speaker 3: case descriptions followed, often though not always, associated with some
Speaker 3: sort of military or nautical endeavor, in which cases it
Speaker 3: may have been more contagious rather than the sporadic cases
Speaker 3: that are seen in the general public. And once you
Speaker 3: saw it, you never forgot it, a surgeon named John
Speaker 3: Hennan said in eighteen twenty quote, to those who have
Speaker 3: seen it, once a glance at the sore or even
Speaker 3: the smell of the ward will immediately discover it. It
Speaker 3: can scarcely be confounded with any other disease or any
Speaker 3: other species of ulcers.
Speaker 2: End quote.
Speaker 3: Yeah, distinctive. Yeah. Most scholars put the next big event
Speaker 3: in the history of necrotizing fasciitis in the aftermath of
Speaker 3: the American Civil War, when medical officers such as Joseph Jones,
Speaker 3: who was in the Confederate Army, described some of the
Speaker 3: horrors that they witnessed. Jones is often credited with providing
Speaker 3: the first modern description of necrotizing fasciitis, which he referred
Speaker 3: to as hospital gangreen quote. In some cases, the progress
Speaker 3: of the disease is rapid and terrible. The edges of
Speaker 3: the wound become hardened and inverted. The surface of the
Speaker 3: wound rises up into a pulpy, ragged, gray and greenish mass.
Speaker 3: When the sloughs are detached, the disease attacks other adjacent
Speaker 3: structures from day to day, extending its ravages both in
Speaker 3: length and breadth. Most commonly, after the muscles have been exposed,
Speaker 3: they continue to be gradually dissected. Their connecting membrane is
Speaker 3: completely destroyed, and they are left covered with an offensive,
Speaker 3: greasy looking matter. As the disease advances, hemorrhage from small
Speaker 3: vessels is a common occurrence, and in the more advanced stages,
Speaker 3: some of the large vessels give way and the patient
Speaker 3: is frequently destroyed by the consequent hemorrhage. End quote.
Speaker 5: Yeah, yeah, it's a truly I mean, I flesh eating
Speaker 5: bacteria is not a term that is like nice to hear,
Speaker 5: but it is. I understand how it got that nickname.
Speaker 5: Like it is what it feels like, what it looks like,
Speaker 5: you know, I.
Speaker 3: Mean that's what it was like Fajadina was eating away
Speaker 3: like that. It is a describes what happens. I think
Speaker 3: it's also like when it was happening in military hospitals
Speaker 3: it's possible that there were like outbreaks where it was
Speaker 3: contagious because you had a bunch of Group A strap
Speaker 3: in that hospital and horrible sanitize, you know, sanitary conditions,
Speaker 3: and so it spread. But like that, I think that
Speaker 3: is sort of the what conjures today, that idea of
Speaker 3: like flesh eating bacteria is gonna it's gonna spread, it's
Speaker 3: going to.
Speaker 4: Be coming for you, and it's not.
Speaker 3: That's not the way that it works.
Speaker 4: Yeah. Yeah.
Speaker 5: Hospital gangreen is also quite a misnomer for today's infections.
Speaker 5: It's usually not at all hospit it required.
Speaker 3: Right, definitely, that was like it probably should have been
Speaker 3: military hospital gangren. Yeah, and Joseph Jones, this guy, he
Speaker 3: was more than qualified to describe this disease. Over twenty
Speaker 3: six hundred cases of hospital gangrene had been diagnosed in
Speaker 3: soldiers during the American Civil War. Nearly half of them died.
Speaker 4: That's a lot, holy guacamole.
Speaker 3: Yeah, yeah, and those who lived, like the around the
Speaker 3: half of those who lived, they recovered, but they did
Speaker 3: so at the cost of limbs or multiple limbs, which
Speaker 3: had to be amputated. And in a different book, Jones
Speaker 3: recalls the first case of hospital gangrene that he observed,
Speaker 3: which was in a young man, a volunteer from Florida
Speaker 3: who was stabbed in the scrotum, not during battle, but
Speaker 3: during a fight at the drinking saloon. No, yeah, I know.
Speaker 3: So he was brought to the hospital eight hours after
Speaker 3: being stabbed, and he died less than a week later.
Speaker 3: I decided to after reading through the full description, I
Speaker 3: was like, I'm actually not going to quote all of this.
Speaker 3: I'm sparing you the full description and also involves it
Speaker 3: another penis sloughing off. But there's a part that really
Speaker 3: stuck out to me at the end quote, the patient
Speaker 3: retained his senses to within a few moments of death
Speaker 3: and was at no point restless, No active pain was suffered,
Speaker 3: and the patient appeared to be insensible to his distressing condition.
Speaker 3: He expressed no fears of death, did not complain of
Speaker 3: the horrid stench, and although fully warned of his true
Speaker 3: situation and informed that every hope of life had vanished,
Speaker 3: he actually traded for a watch two or three hours
Speaker 3: before his death.
Speaker 5: End quote.
Speaker 3: Isn't that heartbreaking?
Speaker 4: Breaking? Absolutely heartbreaking?
Speaker 2: Ugh?
Speaker 5: Yeah.
Speaker 3: And so to round out this discussion of historic and
Speaker 3: negritizing fasciatis, and especially as it applies to the genitals.
Speaker 3: I have to mention Fournier and the gangreen that bears
Speaker 3: his name. So in his work he was a quote
Speaker 3: unquote venereologist, so he studied sexually transmitted infections, and in
Speaker 3: eighteen eighty three he described five patients with necrotizing fasciitis
Speaker 3: in their genitals and paraneal region. I wasn't sure why
Speaker 3: this got a separate name, like why is this But
Speaker 3: unless it's just that's where it happens more frequently, Like why, Yes, that's.
Speaker 4: What we call it when it's there.
Speaker 3: Okay, So it's just sort of like almost like a
Speaker 3: historical relic in that way.
Speaker 4: Yeah, as far as I know.
Speaker 5: I mean the same thing with like Ludwing's angina is
Speaker 5: in a specific location, so it's like to describe the
Speaker 5: location of where of where it is, but it is
Speaker 5: an ecritizing fasci idis of the fashion of that area.
Speaker 3: Right, So, until germ theory was fully established, people really
Speaker 3: did not know where hospital gangreen came from or how
Speaker 3: to treat it. Like Jones thought it was the crowded
Speaker 3: conditions and poor ventilation in the hospitals. Another surgeon pinned
Speaker 3: it on scurvy and nutritional status. There's the guy who
Speaker 3: thought it was about weather, Thomas Trotter, who was the
Speaker 3: author of the eighteen oh four book on Nautical Medicine.
Speaker 3: He pointed out over and over again to alcohol, Like
Speaker 3: every case that he described, he was like, and this
Speaker 3: person drank this cheap alcohol, and this person drank this
Speaker 3: cheap alcohol. Once people were able to identify the causative
Speaker 3: bacteria in the wounds, that didn't necessarily clear things up right, Like,
Speaker 3: we're still at a disadvantage because it was also turning
Speaker 3: out to be multiple different microbes just a mix of
Speaker 3: them sometimes. And interest in the condition, though I found
Speaker 3: this fascinating, seemed to fall in the late eighteen hundreds
Speaker 3: early nineteen hundreds. It was like kind of like this
Speaker 3: was a big deal, Rear treatises about it, and then
Speaker 3: it was kind of like eh. And there was a
Speaker 3: physician who wrote in nineteen oh eight that quote hospital
Speaker 3: gangreen so called has been in years past the terror
Speaker 3: of military surgeons and camp hospitals. It has almost completely
Speaker 3: disappeared from observation and is now practically never seen end quote.
Speaker 2: Isn't that interesting?
Speaker 5: Yeah?
Speaker 4: Why what changed? I?
Speaker 5: Don't know.
Speaker 3: So there is a thought. Do you remember when we
Speaker 3: talked about Strap last and we talked about this sudden
Speaker 3: decrease in and I'm wondering whether it's in scarlet pathogen shift.
Speaker 5: Yeah, so all of a sudden, we have ones that whatever,
Speaker 5: whatever toxins they're making, are not the ones that are
Speaker 5: more likely to cause an acritizing infection. Maybe that's super interesting.
Speaker 3: Yeah, So it could be that.
Speaker 4: I don't I should have looked specifically at that, but
Speaker 4: I didn't.
Speaker 3: There was a paper that mentioned a little bit of that,
Speaker 3: and there was also another paper that looked at genomes
Speaker 3: of the group a Strap today and sort of any
Speaker 3: sort of shifts in that as well. And I didn't
Speaker 3: get into the nitty gritty of it, but like, it
Speaker 3: does seem like there could be, like the biology is
Speaker 3: there for these types of shifts.
Speaker 4: It's a plausible explanation, it is.
Speaker 3: Yeah, yeah, yeah, but yeah, that whole Oh it's never
Speaker 3: it's a disease of the past. I was a little
Speaker 3: bit of a premature celebration. The disease continued to pop
Speaker 3: up both in times of war, like in World War One,
Speaker 3: and in the general public just in other times like
Speaker 3: the outbreak that involved at least twenty cases in China,
Speaker 3: which was reported on by a physician named Frank Melanie
Speaker 3: in nineteen twenty four. And so this actually his description
Speaker 3: marks the first twentieth century description of the disease where
Speaker 3: he also linked it to particular organisms group.
Speaker 4: A strap, namely ok okay.
Speaker 3: And then in nineteen fifty one Hospital Ganggreen malignant ulcer
Speaker 3: phaegiadina gangrenosa, whatever else it was called, it was rebranded
Speaker 3: as necrotizing fasciitis. And this was a name chosen by
Speaker 3: physician Ben Wilson because fascial necrosis is the most consistent
Speaker 3: manifestation of the disease end quote. And in this landmark
Speaker 3: paper he went through what was known about the course
Speaker 3: of disease, causes, treatment outcomes in epidemiology, you know, essentially
Speaker 3: boiling down to rare but not unheard of. Time is
Speaker 3: of the essence case fatality rate is lower than in
Speaker 3: past decades thanks to early recognition, surgery and antibiotics. Yeah,
Speaker 3: and so while the condition was known in medical circles
Speaker 3: rare though it was I think again as we talked
Speaker 3: about memorable, rare but memorable. It was known from at
Speaker 3: least the mid twentieth century. It escaped public attention until
Speaker 3: around the nineteen nineties. And this is I would say
Speaker 3: largely that's a generalization, but that's around the nineties is
Speaker 3: when a series of cases received a ton of media attention.
Speaker 3: There was one outbreak, in particular in a place I'm
Speaker 3: going to say this wrong, Gloucestershire, involving at least seven individuals,
Speaker 3: and it led to headlines that were like, hospitals get
Speaker 3: warning on killer bug, mystery bug kills, three more flesh
Speaker 3: eating bug kills, young mother, I watched killer bug eat
Speaker 3: my body, you know, things like super sensationalist headlines, right,
Speaker 3: and so.
Speaker 4: The monsters inside me kind of thing.
Speaker 3: Yes, even though that is partially where I got the
Speaker 3: interest in parasitology. Yeah, but this also it seemed not
Speaker 3: like shared exposure but more like coincidence that these people
Speaker 3: were getting accortizing fasciitis. Interesting, but any factual reporting of
Speaker 3: that or exploration of that nuance it got drowned out
Speaker 3: by these sensationalists headlines and fear mongering. But like I
Speaker 3: pointed out at the top, there might have been the
Speaker 3: positive effect of improving recognition, you know, just like knowing
Speaker 3: what it is and that it exists right right, and
Speaker 3: sure enough. It was interesting to see that following this reporting,
Speaker 3: countries around the world began to also report, like release
Speaker 3: reports on necortizing fasci idis at higher rates than previously
Speaker 3: seen in cases often following like a surgical procedure. And
Speaker 3: so this might have helped people, whether in the community
Speaker 3: or physicians, recognize some early warning signs in themselves or
Speaker 3: their patients. But there's also a cost, of course, to
Speaker 3: this type of reporting. It contributes to the stigma that
Speaker 3: many people who were covering from necortizing fasci idis face.
Speaker 3: You know, the way that we talk about disease, even
Speaker 3: legitimately scary ones like necrotizing fasci idis. It really does matter.
Speaker 3: But yeah, that's all I have for the history of
Speaker 3: neck fash. So, Aaron, why don't you tell us what's
Speaker 3: happening with this condition today?
Speaker 5: All right?
Speaker 4: I'd love to.
Speaker 5: Today, thankfully. Necrotizing soft tissue infections, including neckritizing fascia idis,
Speaker 5: are relatively rare. However, we don't have great numbers on them.
Speaker 5: So group A strep infections like invasive group based strap infections,
Speaker 5: which includes necritizing fasci itis, but also includes other types
Speaker 5: of infections those are reportable in the US, so we
Speaker 5: know that their rate tends to be aboutzero point four
Speaker 5: per one hundred thousand in the US. But group A
Speaker 5: strap only accounts for a proportion of neckritizing fasciaitis or
Speaker 5: neckrotizing soft tissue infections more generally, and what proportion I
Speaker 5: don't know. I from what I can tell, the scientific
Speaker 5: community at large, the medical community doesn't necessarily have a
Speaker 5: great handle on that. What's very interesting is that I
Speaker 5: read one paper which I'll link to out of China
Speaker 5: that was quite recent that looked at in their hospital
Speaker 5: system just in one small part of China, and they
Speaker 5: had hardly any group base strip in that particular population. Huh,
Speaker 5: So I think it really varies location to location. Maybe
Speaker 5: it does vary based on, you know, what stereotypes are
Speaker 5: most prevalent, what toxins are being produced, et cetera. But
Speaker 5: across the board papers that tried to estimate the incidents
Speaker 5: of just necrotizing fasciitis, regardless of the type or the
Speaker 5: causative agent. In the US, it's estimated at like eight
Speaker 5: to ten cases per one hundred thousand individuals, and it
Speaker 5: really can vary geographically across the globe, from like less
Speaker 5: than one per one hundred thousand in some studies in
Speaker 5: some parts the world, to twenty cases or more per
Speaker 5: one hundred thousand people in other parts. I will say
Speaker 5: that if you dig deep in these papers, some of
Speaker 5: the studies that are reporting those higher end numbers are
Speaker 5: citing how many cases there are per hospital admission, not
Speaker 5: how many cases there are per general population mission. That's
Speaker 5: going to be quite inflated. But in any case, it
Speaker 5: can really range. What unfortunately doesn't have as huge of
Speaker 5: a range is the mortality rate, and that remains quite high.
Speaker 5: Some studies report a mortality rate as high as forty percent,
Speaker 5: and so in particular studies or in particular areas, the
Speaker 5: mortality rate can really be quite high. But on average globally,
Speaker 5: for the last like you mentioned, airing twenty plus something years,
Speaker 5: it really hasn't changed. The mortality rate on average is
Speaker 5: between twenty five and thirty or thirty five percent. It's
Speaker 5: only in the last couple of years that we've seen
Speaker 5: study more often reporting rates closer to twenty percent. So
Speaker 5: we're seeing maybe some suggestion of a bit of a drop. Okay,
Speaker 5: Like I mentioned some of the studies that are just
Speaker 5: looking at treatments, so they're looking at kind of a
Speaker 5: more well defined population. It's not these like larger retrospective
Speaker 5: studies and things like that. But some of these papers
Speaker 5: suggest that we could be reducing mortality rates to ten
Speaker 5: percent with correct identification and access to surgical management.
Speaker 4: But that is still really high. Like a ten percent.
Speaker 5: Mortality rate is terrifying, and that's the lowest that we've
Speaker 5: been able to get it in studies.
Speaker 4: Yikes, I know, and what is scary.
Speaker 5: And I don't want to necessarily be fear mongering about
Speaker 5: this because again, this is still quite a rare disease,
Speaker 5: but it does seem to be increasing in number. Yes,
Speaker 5: So according to analysis that was published I think in
Speaker 5: twenty twenty three from CDC data that went from two
Speaker 5: thousand and three to twenty twenty.
Speaker 4: Okay, there was an increase. Oh I saw this paper.
Speaker 5: Yeah, yeah, there was an increase of like one hundred
Speaker 5: and twenty percent of deaths associated with necrotizing soft tissue infections.
Speaker 5: Despite the fact that we are at least in theory,
Speaker 5: getting better at treatment right or at least not getting
Speaker 5: worse right, So deaths went from eight hundred and twenty
Speaker 5: four in two thousand and three to one thousand, eight
Speaker 5: hundred and forty two in twenty twenty.
Speaker 3: Is there any difference in like diagnostic or reporting or
Speaker 3: anything like that, or is that simply just the number
Speaker 3: of cases.
Speaker 4: It's a really good question.
Speaker 5: As far as I know, there's not any differences in
Speaker 5: you know, reporting or things like that, because there hasn't
Speaker 5: been a change in like what's required to report versus
Speaker 5: what's not. This is all just still like they've gathered
Speaker 5: this data after the fact. It's not necessarily like it's
Speaker 5: not as easily accessible. I would say we are, and
Speaker 5: I don't have necessarily data to back this up, but
Speaker 5: I would hope that we are getting better rather than
Speaker 5: worse at detecting it because of advances in things like
Speaker 5: CT technology. There's a lot of people interested in using
Speaker 5: things like ultrasound to better identify It's still a little
Speaker 5: bit tough right now, but there's certainly a lot of
Speaker 5: and there's also a ton of these different scores that
Speaker 5: people use, like laboratory values to try and say, if
Speaker 5: I'm not really sure, you know, should I call surgery
Speaker 5: or should I not there wasn't anything clear on imaging.
Speaker 5: There's like these scores that you can calculate to try
Speaker 5: and lean you more likely necrotizing versus not. None of
Speaker 5: them are perfect, but there's a lot of interest in
Speaker 5: like how do we better identify this early? And yet
Speaker 5: we're still seeing this increase in depths and without a
Speaker 5: corresponding increase in the mortality rates. And so I do
Speaker 5: think that this is due to an increase in cases
Speaker 5: from everything that I can tell. The other thing that
Speaker 5: we know there is an increase in is cases of
Speaker 5: Vibrio vulnificus, specifically these wound infections. Between nineteen eighty eight
Speaker 5: and twenty eighteen, Vibrio wound infections increased eightfold and also
Speaker 5: shifted northwards substantially. And we think that this is down
Speaker 5: to climate change change. Vibrio has actually, and this was
Speaker 5: a new fact for me, it's been called a microbial
Speaker 5: barometer of climate change because of how well it thrives
Speaker 5: in this warm brackish water and how highly sensitive it
Speaker 5: is to temperature. I've heard that, yeah, yeah, And so
Speaker 5: we when we combine all of this information plus the
Speaker 5: fact that we have an increasingly elderly population who are
Speaker 5: already at risk of necrotizing infections compared to younger populations.
Speaker 5: It's kind of a scary possibility that things could continue
Speaker 5: to increase vibrio and otherwise, but at this point, at
Speaker 5: least it is still rare.
Speaker 4: That's the only goodness.
Speaker 3: Yeah, Yeah, it's not really silver lining.
Speaker 4: Yeah, that's an acrotizing fasciitis sarin.
Speaker 3: Wow. I don't know how to react. I mean, there's
Speaker 3: I know, I it's horrifying.
Speaker 5: It's horrifying, and I it is a truly horrifying disease.
Speaker 5: And I also it's a it's a tough balance to
Speaker 5: not feel like like those headlines that are like I know,
Speaker 5: I know, you know.
Speaker 3: I mean I think, I think you're right, and I
Speaker 3: think it's like it's a hard balance because I think
Speaker 3: it's really important to be vigilant and like what what
Speaker 3: are things? How do we worry without worrying constantly? Like
Speaker 3: how do we worry about the right stuff? I don't
Speaker 3: know the answers to that me neither. Yeah, And I
Speaker 3: don't think the papers that we're about to guide you
Speaker 3: to will have the answers to that either. So, but
Speaker 3: they are great for reading or great transition so it
Speaker 3: I have a bunch I'm going to shout out too.
Speaker 3: In particular, one is by Louden published in nineteen ninety
Speaker 3: four in The Lancet titled Necrotizing Fasciitis Hospital Gangreen and Fhagiadina,
Speaker 3: and then another is by Quirk and Sternbach from nineteen
Speaker 3: ninety six. I was digging the nineties papers for this.
Speaker 3: I think there was a lot of interest, so a
Speaker 3: lot of papers, and this one was titled Joseph Jones
Speaker 3: Infection with Flesh Eating Bacteria from the Journal of Emergency Medicine.
Speaker 5: I had a bunch of papers, a few that I
Speaker 5: particularly enjoyed. I was a twenty seventeen was my year, Aaron,
Speaker 5: because one from Infectious Disease Clinics in North America from
Speaker 5: twenty seventeen was titled Evaluation and Management of Necrotizing soft
Speaker 5: Tissue Infections by Bonnie and Cadri And then another from
Speaker 5: twenty seventeen from the New England Journal of Medicine by
Speaker 5: Stevens and Bryant called Necrotizing seft tissue Infections. I had
Speaker 5: a bunch more, you know, from the last decades.
Speaker 4: You can find them all on our website. This podcast
Speaker 4: with kill you dot Com under the episode stab Yeah.
Speaker 4: Check it out.
Speaker 3: Thank you again, Maggie so much for sharing your story.
Speaker 3: I'm oh horrifying, harrowing.
Speaker 4: Yeah, thank you, thank you so much. We can't say
Speaker 4: it enough.
Speaker 3: Thank you to Bloodmobile for preventing the music for this
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Speaker 5: Thank you to Leanna and Tom and Brent and Pete
Speaker 5: and Jessica and my everyone, everyone that's exactly right.
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Speaker 4: Thank you, thank you, thank you.
Speaker 5: Well.
Speaker 3: Until next time, wash your hands.
Speaker 4: You feel the animals.
Speaker 5: Um um um