Ep 193 Necrotizing Fasciitis: A strange beast

If you were asked to describe necrotizing fasciitis in three words, you might choose: rapid, deadly, and rare. The third of those adjectives may provide some comfort, but the first two are the clear inspiration for this infection’s more lurid nickname: flesh-eating bacteria. In this episode, we get up close and personal with necrotizing fasciitis and its causative agents. We start off by examining step by step how these infections wreak so much havoc and why doctors still struggle with its treatment. Then we take a tour through its grisly history, featuring maritime misadventures and wicked war wounds. We wrap up the story with a look at the global trends in these infections as well as some promising new research. This episode may not be for the faint of heart, but it is for the endlessly curious.

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Episode Transcript

Speaker 1 (00:00):
My name is Maggie, and my story begins nearly two
years ago.

Speaker 2 (00:02):
On New Year's Eve.

Speaker 1 (00:03):
My family went for a short hike in the woods
that morning and then met some friends.

Speaker 2 (00:07):
To go bowling that evening.

Speaker 1 (00:09):
I thought maybe bowling had given me bresidas, as my
elbow felt unusually painful. We went to bed long before
ringing in the New Year, but the pain kept growing.
I really wanted to sleep, so I made an ic
sleeve out of a sock, but that pressure was too much,
so I resorted to an old prescription pain med and
waited impatiently for that to kick in before adding ibuprofento

(00:29):
the mix. Soon after, my husband found me lying on
our bedroom floor as I felt like I might pass out.
He thought this was just my normal response to pain,
because I have passed out in the pass But later
I began vomiting, which I then attributed to taking meds
on an empty stomach.

Speaker 2 (00:45):
By morning, I could not get out of bed. I
was so sick.

Speaker 1 (00:48):
My husband kept trying to get me to stand so
we could go to urgent care, but I couldn't. I
finally felt a short window and we made it downstairs
to the car and headed straight to the YAR instead.
My husband wheeled me in with my bucket, and they
found my blood pressure was considerably low. My normal resting
heart rate of around sixty was elevated to ninety four
beats per minute. I also coincidentally tested positive for COVID,

(01:11):
so the er gave me my own room with full
COVID precautions in place. On the second day, after multiple
bags of ivy fluids that failed to bring up my
blood pressure, they transferred me to the intensive care unit
to treat me for septic shock. It's worth noting that
three to four days prior to all this, I had
visited my general practitioner for a lingering cold or sinus infection,

(01:32):
and I was about three days into a prednizone prescription
to calm down my inflammation. I was feeling good, but
my immune system had clearly seen better days. This whole time,
my arm had a noticeable redness that radiated from my elbow,
and it was.

Speaker 2 (01:45):
Growing by the hour.

Speaker 1 (01:46):
Doctors were tracking the spread with sharpies, and there was
a lot of discussion about whether to operate. My amazing
infectious disease doctor was pushing for this to happen. I
could hear my own voice telling my students how this
can happen to anyone, but I could not believe that
I was now that person. I remember trying to mentally
prepare myself to give permission to amputate my arms should
it become necessary to save my life. As the pain

(02:09):
of redness approached my arm pit and shoulder, they found
a surgeon that agreed to perform a debreedment of my arm.

Speaker 2 (02:15):
They opened me up with four long.

Speaker 1 (02:17):
Incisions that averaged three to four inches apiece, and after
surgery they were wide open with all my deep tissues
on full display. My dad was sent a picture and
he passed out behind the wheel just thinking about it.
He survived, his car did not, And it's pretty clear
where I get my vasovagal response. My left arm had

(02:37):
undergone so many blood draws and ivs that I developed
a painful clot, forcing doctors to put in a central
line to continue my meds. I was on at least
three different antibiotics, and now I had to worry about
the risk of a new infection going straight to my heart,
as any catheter comes with the risk of infection. My
most unpleasant memories, though, were the nights I insisted my
family go home to sleep at night to stay strong

(02:59):
and healthy. But many nights I cried myself to sleep,
terrified I could not turn in my bed, and the
morphine drip gave me startling dreams that would waken me.
It was one of those nights I sent an email
to the Errands asking them to save me a spot
for when I beat this infection. I had made the
mistake of reading the dire statistics for my condition online,
and I was not about.

Speaker 2 (03:18):
To leave my six year old son or my husband behind.

Speaker 1 (03:21):
In the end, I had three surgeries, including another where
they placed a wound back on my elbow and another
to insert a wound drain and staple my arm closed.
I was in the hospital for nearly nine days. I
went in with suspected versidas, but the list of itises
kept growing. I had cellulitis, toxic shock, sepsis, septic shock,

(03:43):
and necrotizing fasciitis. The culture confirmed the infection was caused
by group A strip. I was sent home with ivy
penicillin through a pickline in my left arm while the
wound drain hung from my right arm. I felt a
bit like Pinocchio with so many strings but I was
grateful to be home.

Speaker 2 (03:59):
I was very fortunate throughout all of this to have
such great support.

Speaker 1 (04:02):
I'm grateful to my husband and my sisters, my care team,
and all the friends and family who supported us through
the scary time.

Speaker 2 (04:08):
We felt so loved and we hoped to never have
to experience love in this way again.

Speaker 3 (04:58):
Oh my gosh, that is I mean, it's so it's terrifying, terrified.
Oh oh, we're really glad that you're okay, and we
appreciate you so much for being willing to share your story,
that scary, scary story.

Speaker 4 (05:14):
Yeah, yeah, thank you, thank you so much.

Speaker 3 (05:17):
Yeah. Hi, I'm Aaron Welsh.

Speaker 4 (05:19):
And I'm Erin aman Updyke.

Speaker 3 (05:21):
And this is this podcast will Kill You.

Speaker 5 (05:23):
And today we're talking tissue death because we're covering necritizing
fasci itis.

Speaker 3 (05:30):
We've covered as I was doing the history much of
this in other capacities. I mean, this is a strange
beast of a thing, right, Like enough said, Okay.

Speaker 5 (05:43):
Said, I agree, because we're talking like multiple bacterial species
or groups.

Speaker 3 (05:52):
But there are so many questions that I have, and
so I really just want to like go straight to things.
So let's just get through the rest this business quickly.

Speaker 4 (06:01):
Yeah sounds good. First, it's quarantin any.

Speaker 3 (06:04):
Time it is it is. What are we drinking this week?
We're drinking hit the gas Aaron. It was gas made like.

Speaker 5 (06:14):
It's one of those where you have to explain it,
but it works on so many levels once you do.
Gas means group a strap, but it also means gas
as in air bubbles, which you might see on imaging
if you have an advertizing soft tissue infection and anyways.

Speaker 3 (06:34):
In keeping in line with the gas air bubbles, of course,
our drink is a well our plusy berita this week
is a club soda plus BlackBerry syrup plus lemon juice.
There you go. We did it, guys, we did it.
We'll post it on our website. We're going to try

(06:54):
to plus definitely social media. We will be posting it there,
so make sure you're following us. We're also on YouTube,
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(07:18):
of our episodes, music by Bloodmobile and some more goodies.
So check it out.

Speaker 4 (07:24):
This podcast will kill you dot Com? Great?

Speaker 3 (07:27):
Great shall we? We shall?

Speaker 4 (07:29):
Okay right after this break.

Speaker 5 (07:45):
In some ways, Aaron, I think of necrotizing fasci itis
as like an old friend of the pod.

Speaker 3 (07:50):
Yeah, I think that's fair to say, thank you.

Speaker 4 (07:52):
I'm glad you.

Speaker 5 (07:53):
I'm glad you agree, because we have covered so many
of the major causes of necrotizing fasciitis classically, the primary
agent that we think of within necrotizing fasciadis infection is
a beta heat meltic streptococcie called strap piogenies aka group
A strap aka the cause of scarlet fever, among many

(08:14):
other things.

Speaker 3 (08:15):
Which we have done exactly We've done that. We've also done.

Speaker 5 (08:19):
Yeah, we've also done toxic shock very recently, which necrotizing
fasciitis often leads to a toxic shock syndrome. Necrotizing fasciidis
also can often lead to sepsis, which we've also covered.

Speaker 3 (08:35):
I mean, I think this just goes to show if
I may be a little not like philosophical, but I
guess like historical. You know, back when germ theory was
the newest thing of the day, and it was suddenly
like every disease is one germ, right, like each disease
has one germ kind of a thing. And this disrupts
that paradigm on which I find so interesting because are

(09:00):
the way that we approach this podcast is very much
one disease, one thing.

Speaker 4 (09:07):
Well, and it's interesting too, and we've talked about this.

Speaker 5 (09:09):
I wish I could remember on what episode it was,
because you have both, right, you have sometimes like one
pathogen that can cause so many different types of disease,
like with MRSA, like with streptococcus, but then you also
have one disease or one clinical syndrome like necrotizing fasciitis,
that can be caused by so many different pathogens because

(09:31):
it isn't just group A strip no no. Necrotizing fasciitis.
Infections can also be caused by another good friend of
the pod, Staphlococcus aureus, including MRSA or methicillin resistant Staph oureus.
It can also be caused by clusterdium species by Vibrio vulnificus,
which we haven't yet covered.

Speaker 4 (09:50):
And we should we should.

Speaker 5 (09:52):
Vibrio is a marine or aquatic bacterium that can cause
a neckritizing infection, especially after injuries, so like you get
you know, nicked while you're fishing, or a fish scale
kind of scratches you, or you just go swimming when
you have a bug bite or a scratch. Anyways, but
there also are a whole bunch of necrotizing fasci idis

(10:14):
infections that are actually polymicrobial, and these can include both
gram negative and gram positive bacterium so friends like E.
Coli or Clipsiella in addition to all of the things
that we've already described. So whatever the organism in question,
what is necrotizing fasci i itis you mean? Yeah, I've
said the words so many times now. It is a

(10:37):
severe bacterial infection that starts in the skin usually and
spreads down deep through the layers, through the dermis, through
the subcutaneous fat, and into a layer called the fascia.
And I want to spend a moment to talk about
our fascia. Okay, great, We have a lot of different

(10:59):
types of fashia in our bodies. It is basically a
part of our connective tissue network. Our fascia layers give
support to various structures in our body, so just underneath
our if you think, I'm using my finger as an example,
So if you think of looking at the palm of
your hand, the top of your finger being your skin,

(11:21):
You've got your epidermis and dermis, and then you have
a layer. Then you've got your subcutaneous tissue like under
your first knuckle, okay, and then just under that you're
going to have a layer like under your second knuckle
here of superficial fascia and then a layer of deep
fascia and then muscle.

Speaker 3 (11:39):
What's the purposes of superficial and deep fascia.

Speaker 5 (11:42):
They're all there to support our structure. So the superficial
fascia is like the underlayer underneath our skin. The deep
fascia is what surrounds our muscles, So all of our
muscles are covered in their own layer of fascia. Our
organs inside of our body also have their own versions
of fascia, and then our body cavi these have their
own layer of fascia as well, our abdominal wall and

(12:04):
our thoracic cavity. So we've got layers upon layers upon
layers of fascia.

Speaker 3 (12:08):
What's fascia made of?

Speaker 5 (12:10):
Mostly collagen. Oh okay, Yeah, it's mostly collagen. And when
you look at it, it usually looks like a kind
of white, kind of filamentous.

Speaker 4 (12:19):
Sort of structure, almost like I don't know a.

Speaker 3 (12:23):
Good example, like angel hair, spaghetti.

Speaker 4 (12:28):
No, it's more like like.

Speaker 5 (12:30):
Insulation and your wall quite the inside of an orange peel,
because it's stringier than that, like.

Speaker 3 (12:39):
Like fungal growth in the last of us.

Speaker 5 (12:42):
Yeah, except imagine it being quite firm, you know, like
like really tough spider web.

Speaker 4 (12:48):
Okay, like you know those.

Speaker 5 (12:49):
Like cellulose shades that you sometimes can have on your
cover your window where like the sun can't get in
but you can still kind of see out or whatever,
or the sun can get in but they can't like that. Okay,
not quite opaque. And anyways, that was a struggle. I
probably should have thought of it before I started talking.

Speaker 3 (13:07):
Had a really fun time guessing guessing things that I
have no idea what the actual image of it.

Speaker 5 (13:13):
Is, especially based on my hand motions, which are entirely unhelpful. Anyways,
So we're talking about a bacterial infection that spreads down
into this layer, and which layer of fashion just depends
on how far the infection goes. But as this infection spreads,
what makes it a necrotizing infection is that the bacteria

(13:33):
start to produce various toxins, which one which type. It's
all going to depend on what the pathogen is, because
there can be so many, but many of the types,
and sometimes it's not even toxic. Media is more just
like this overwhelming bacterial infection. But in any case, whether
it's toxin mediated or just from so many bacteria, we
see a lot of inflammatory damage, including in the blood

(13:57):
vessels of our tissues that ends up leading to blood
clots so called microthrombi, and that caused death necrosis of
the tissue itself. Now, the term necrotizing fasciitis, that's what
we're using in this. It's not an incorrect term, but
what we have come to learn is that there are

(14:19):
a lot of other kinds of necrotizing soft tissue infections.
So an umbrella term that's often used now is NSTI
necrotizing soft tissue infections. Some of them get their own name,
Like if it's only in the skin and subcutaneous fat,
you can have a necrotizing cellulitis and that would be
less deep, not all the way down to the fascia.

(14:40):
If it's all the way to the muscle or primarily
in the muscle, this might start from a muscle injury
rather than like a skin damage. You can get a
piomocitis or a myonecrosis. Myonecrosis is what we see with
gas ganggreen, which is caused by a type of clustered
am species. Yes, but these are not all mutually exclusive.

(15:01):
But the reason that neckartizing fasci itis itself kind of
I think holds a lot of esteem. I don't know
if esteem is the right word, but that is like
the one that we think of when we think of
a necrotizing soft tissue. Infection is in part because it's
the most common, and the reason that it's most common
is because the fascia has some components to it that

(15:22):
make it particularly vulnerable to infection. First of all, the
blood supply to our fascia is not nearly as robust
as the blood supply to our skin, to our subcutaneous
tissue and to our muscle. It is just there for support,
I see, and so it doesn't need usually as robust
of a blood supply. It's not a muscle that's contracting,

(15:42):
it's not our skin that's constantly regenerating. It's just there
as like a you know, shingles on the outside of
your house. That's a bad example. It's a sport structures,
but it's not as support structure at all.

Speaker 4 (15:54):
That's your skin.

Speaker 3 (15:58):
I have a quick question about this infection. So you
talk about it going deep, What is the it goes
deep and wide? Right, Like, Yeah, what does it do
first and in what order and at what rates?

Speaker 5 (16:11):
That is another component of the fascia itself that makes
it so vulnerable to these type of infections because once
an infection gets into that fascial plane, it can spread
along that fascial plane without interacting with any of the
other tissue areas. Oh so once it gets into that fascia,

(16:32):
think of it like a highway. Now it's just on
this freeway, no stops needed, and so little blood supply
that there's not a lot of things coming in to
carry off or to fight that infection. So, yes, it
is something that spreads widely, very quickly, and oftentimes the
first like where that infection first started, it can't. Most

(16:53):
often it starts from something like a scratch on the skin. Yeah,
it can be a small wound it can be a
large wound, it could be a surgical wound. But it
sometimes isn't even like a known wound to the skin.
Sometimes it's damaged to like the muscle itself. Right, you
injure your muscle, you hid it something like that, and
there you have, for some reason bacteria that made it

(17:16):
from your bloodstream into that fascil plane. How you know,
because so many of these bacteria that tend to cause
this infection live on our skin all the time, right,
Like Streptococcus can live Staphylococcus can just live on us.
And so some people every once in a while might
have some bacteria that make their way into our bloodstream

(17:37):
and then our body manages to fight them off. Most
of the time, it's what we call transient bacteremia. Most
of the time you might never know that that happens.
But if that happens and you have an injury and
these bacteria happen to make it into this fascia, they
could potentially establish an infection. And to be honest, we
don't fully understand like why and who on all of that, Okay,

(17:58):
but once it's there, it can very quickly kind of
spread along this fascial plane without necessarily causing more visible damage. Right,
you might not see damage to the skin because it's
mostly tracking along the fascia. And the final thing about
the fascia that can make this particularly vulnerable is that
because I'm talking about like distinct layers of tissue, there's

(18:20):
kind of this what we call a potential space that exists,
like think of it as like between these layers of tissue.

Speaker 3 (18:26):
So what part of what.

Speaker 5 (18:27):
The fashia does is allow for things to slide against themselves, right,
Like it provides support, but it also allows your muscles
to slide against a smooth surface. What that means is
that there is a like theoretical space microscopic though it
may be between these tissue layers. That space can fill
with fluid, and it does in a necrotizing infection, and

(18:50):
that fluid can make it even harder for our body
to respond and clear that infection because our immune cells
have to like wade through a swimming pool of fluid
to try and to this infection.

Speaker 3 (19:02):
Okay, Okay, so somehow bacteria invade the fascia. H The
fascia dies fairly easily because there's once it erodes the
blood supply there's not a lot of redundancy and so
there's no more like you said, highway. So then once
it goes under like along the rest of the fascia,

(19:25):
then the tissue on top of that will just sort
of die.

Speaker 4 (19:30):
It can or it cannot.

Speaker 5 (19:32):
So sometime like eventually this infection will get so overwhelming
that it will continue to invade, So it'll either invade
down into the muscle or it will invade continue going
like back up and out back towards the skin, and
then you'll see more evidence of the damage on the skin.

Speaker 3 (19:48):
Okay, can we talk about the bacteria involved and what
makes them more likely or toxins or the differences between them,
like why why does this happen?

Speaker 5 (19:59):
Yeah, it's it's a great question, and that because that's
a it's a multi part question, right, because it's why
does this happen to certain people? Why does this happen
in certain situations? And why does this happen from certain bacteria?

Speaker 4 (20:12):
Yeah, and that's a lot.

Speaker 5 (20:14):
I don't think I'm gonna have answers for all of
this questions. We know from episodes that we've done on
group A strep in the past, as well as from
Staphylococcus aureus. These are two bacteria that produce a lot
of exotoxins. These toxins produce a really robust and strong

(20:34):
inflammatory response in us, and that inflammation can cause damage.
Vibrio vugnificence. I didn't actually dig deep into it. I
just know that it is quite virulent and I'm not
exactly sure what all of its virillance factors are.

Speaker 4 (20:47):
Just means you need to do a full episode on it.

Speaker 5 (20:49):
And then Clostridium is also like a toxin mediated infection,
So it's again this toxin and an inflammatory response because
of that toxin.

Speaker 3 (20:58):
Are these the same toxins or different toxins? Is the
mechanism of action different of different kinds? Yeah, a ton
of different kinds, And a lot of these infections are
actually polymicrobial. So another big component is that there are
certain risk factors to who is more likely to get
and what scenarios are more likely to get necrotizing infection. Right,

(21:22):
so individual level factors things like diabetes, cirrhosis or other
liver disease, certain compromising conditions, and the elderly are the
most high at risk for a necritizing skin and soft
tissue infection. Things that are environmental, like fishing in waters
that are contaminated with vibrio and having an open wound

(21:45):
is going to environmentally put you at a higher risk. Right,
how is viio transmitted?

Speaker 4 (21:52):
It just gets into your skin through these open wounds.

Speaker 3 (21:54):
Right, But I mean, like where is it coming from
in the environment.

Speaker 4 (21:57):
It lives in the environment. It can thrive in the ocean.

Speaker 5 (22:00):
It's also can get to very high concentrations in filter
feeders like shellfish like oysters. So you also can get
quite a severe GI infection from eating raw oysters and
things because of embrya.

Speaker 3 (22:12):
So it's not like our residence no staph and.

Speaker 5 (22:16):
Okay, correct, Yeah, this one is like specifically environmental, whereas yeah,
most of the rest of these even E Coli, clubziella,
these are things that just live in us and on us.
And so really it's just about the wrong time and
the right port of entry that contribute to someone eventually
getting a necritizing infection. In terms of what it looks like.

(22:41):
The scariest thing, there's a lot of scary things about
neckritizing fasci itis. One of the scariest things is that
at first it is very hard to distinguish from a
totally benign skin infection, So it can look very similar
to things like arisipolis or there's like a few differences,

(23:04):
but at the very beginning, there's not, like there's not
a lot that necessarily distinguishes these early in the course
of infection. And that's where the danger really lies when
it comes to necritizing fasci idis, because the big difference
is that it progresses incredibly rapidly compared to other skin infections,
and by that I mean on a matter of hours

(23:27):
or a couple of days rather than days to weeks
that we might see the progression of a cellulitis turning
into a lymphangitis streaking up your arm or an ariseplus
turning into something that has you know, a lot of
vesicles or blisters or things like that. So you can
imagine the nightmare which I have seen, and it is

(23:47):
truly a nightmare that someone comes into the emergency room
with like a red spot on say their leg, or
maybe even just kind of like a patchy area of
like discoloration or a little bit of swelling. You're going
to touch it or push on it to see if
there's any in duration or sign of an absess and

(24:07):
one of the signs they teach you to look out
for in medical school is called pain out of proportion.
If you touch a necrotizing infection, that person is practically
going to jump off of the table because of how
incredibly painful it is compared to what it looks like.

Speaker 3 (24:22):
Yes, okay.

Speaker 5 (24:24):
The other thing you can sometimes see early in the
course of infection is that you might have swelling like
edema that goes beyond the area of redness or of
like a dark purplish discoloration, So you're like more swollen
than this area that looks like it has an infection
mm hmm. And then the signs that are like more

(24:44):
classically associated with a neckritizing fasci iis tend to be
pretty late stage signs, which means you might have missed
a pretty critical window for intervention. But these are the
things that you see a lot of pictures of online.

Speaker 4 (24:56):
These are like.

Speaker 5 (24:57):
Bullet or the really large flow you would filled or
sometimes blood filled blisters. You get a lot of bruising
of the skin, and you get that before you start
to see tissue death like skin death or necrosis of
the skin. If you do imaging, which we often do.
It'll be a seed t scan or an MRI scan.

(25:18):
You might see gas in the tissues, especially tracking along
that fascion plane.

Speaker 3 (25:23):
Where's the gas coming from.

Speaker 5 (25:24):
The gas is coming from the bacteria itself. It's part
of their metabolism.

Speaker 3 (25:28):
Yeah, what I thought.

Speaker 5 (25:29):
You also sometimes can see this without imaging by crepitence
on exam, So that's that like rice crispy feeling and
sound when you press on the skin when it gets
very severe, instead of that pain out of proportion, you
might actually have anesthesia cutaneous anesthesia where you don't even
feel your skin at all because so much of those
nerves have died without treatment. This will progress incredibly rapidly

(25:54):
and will then include fever, hypotension, It can progress to
toxic shit syndrome, it can progress to sepsis and shock
and death. And really one of the hardest parts is
that early diagnosis. The statistics, unfortunately are not great. The
best ones I saw were that about fifty percent of

(26:16):
the time necrotizing soft tissue infections are not diagnosed initially
on an admission in the er. But I've seen other
papers that said like eighty five to one hundred percent.

Speaker 4 (26:24):
Of the time, which it just seems actually bananas.

Speaker 5 (26:27):
But yeah, yeah, it's it's it's a really that's a
really huge problem because the treatment for this is early
surgical intervention, Okay, and by early I mean within twenty
four hours of this diagnosis, and the earlier the better.
So if if oars are set up to be there

(26:49):
in a matter of hours, that person is more likely
to have a better outcome than otherwise. The surgical degreement
can be really extensive. The average number of surge that
somebody needs after a necrotizing fasciitis is.

Speaker 4 (27:02):
Three to four.

Speaker 5 (27:05):
They sometimes require amputation depending on the location and the
extent of that initial infection, and even if they don't
require amputation, they often require such extensive debreedment of all
of that dead tissue to be able to get down
to healthy tissue that you are going to have an

(27:26):
open wound for a very long time in order to
allow healthy tissue to kind of heal back in while
you're on antibiotics to fight off that infection. That may
require packing changes, or it may require what's called a
wound back, which keeps like negative pressure on the wound,
which can be quite painful and cumbersome, and then very
often people need skin graphs or complex reconstructive surgeries to

(27:50):
be able to heal over time. So this is something
that has like a pretty long lasting impact on somebody's
life if they survive.

Speaker 3 (27:59):
Yeah, I know that necrotizing fasciitis. We have fascia all
over our bodies, and so it can happen anywhere. Are
there places that it's more likely to happen?

Speaker 5 (28:12):
Most likely places are the extremities. I think the legs,
lower legs are the most likely, just because that is
where you have so much potential for exposure to like wounds.
Plus they're such a strong association with diabetes, and so
diabetic foot wounds are a place that you can really
easily get a necritizing infection.

Speaker 4 (28:31):
But there are a.

Speaker 5 (28:32):
Few places that have specific names associated with them because
they have like a specific set of syndromes. So Fournier's
ganggreen is a specific name for necrotizing fasciitis of the genitalia. Yeah,
which can be really really horrific. Has a high mortality
rate and just a huge amount of morbidity associated with it.

(28:54):
It's often caused by polymicrobial infections, but sometimes, like some
of them, bacteria that are associated with it are things
like staff aureus e coli. One of the big problems
with a Fournier's ganggreen is because if it extends to
involve like near the anal sphincter or the perineum down

(29:15):
towards the anal sphincter, then you have a really high risk,
especially after surgery, of fecal contamination of the wound. So
it's really hard to keep these wounds from getting like reinfected.
Sometimes it has to go so far, like the surgical
correction has to go so far as to do like
a diverting colostomy just so that those tissues can actually heal.

(29:35):
So this is a major major problem. And then there's
also other areas of your body, like deep space fascia
that you can get infections in. There's one called ludwings angina,
which is an infection of the fascia of like the
submandibular space, and there's a few other like deep neck
space infections that you can get that are a necrotizing
fasci idis.

Speaker 4 (29:54):
Those are very dangerous because they could.

Speaker 5 (29:55):
Potentially involve your airway, so that usually needs emergent surgery
to like decompro us your airway and things like that.
And then of course we talked about vibrio neckfash, which
is a little different than our classic streptococcal neckfash. There's
actually a they classify it into, like type one is
the polymicrobial infections. Type two is Streptococcus or staff oureus.

(30:18):
And there's some people that are like, we should have
a type three for Vibrio plus or minus Clustridium. I
don't know if that's like official yet.

Speaker 2 (30:24):
But.

Speaker 5 (30:26):
And that is what we see in association with marine
life or like marine coastal waters, that kind of a thing.

Speaker 3 (30:33):
Like so subtropical tropical coastal waters.

Speaker 5 (30:37):
Not anymore because of climate change, right, talk more about that.

Speaker 3 (30:40):
I mean the water is warming, yes, yeah, exactly, yes.

Speaker 4 (30:43):
Yes, it likes warm water.

Speaker 5 (30:47):
But yeah, I mean, I don't know aeron if you
have more questions, that's like the main thing that I have.

Speaker 4 (30:52):
I have more on like how we diagnose.

Speaker 5 (30:53):
It in that, but it's probably a little bit boring,
and so tell me if you have more questions. Otherwise,
I want to know what you know about how we
got here.

Speaker 3 (31:02):
I mean, I guess most of my questions now are
probably more epidemiological, like have we gotten better, Where is
this happening? What you know, what advancements are there, potential advancements.
Will AI help us diagnose?

Speaker 5 (31:19):
That's a fun question. Yes, I don't have an answer
to that, but that's a fun question.

Speaker 3 (31:23):
Not that AI is the end all be all, but
I feel like for diagnostic stuff, it is an interesting it.

Speaker 5 (31:28):
Is, especially especially for radiology diagnostics, and that is a
big really like a lot of what research needs to
be done is on how to better diagnose this quickness
right and in the early stages of infection.

Speaker 3 (31:44):
Okay, so maybe that's a question how low can we
get mortality down if you catch it early enough? And
what is that early enough?

Speaker 5 (31:50):
We can get it down at least in the studies
where they have looked at this, which have their own
sets of biases, because they're like, you know, only looking
at the things that they have diagnosed, and you know,
so it's there's nuance there. But at least in the
studies that have looked at this, average mortality is like
twenty five to thirty five percent. And in the studies
that have tried to compare early versus delayed debreedment, early

(32:11):
debreedment can get it down to as low as close
to ten percent. The biggest problem is those are all
in studies where that has been identified, right, And so
the question is like, how do we get better at
identifying those ones that we missed who we sent home
with antibiotics and then they came back and now they
have an acritizing infection. So that's the tricky part, and
we don't have great answers for that necessarily. Right erin, Erin,

(32:38):
I know these bacteria have always been here. Sure, tell
me about the necrotizing infections.

Speaker 4 (32:46):
Oh, do I want to know? I do?

Speaker 3 (32:48):
I think you do?

Speaker 4 (32:49):
I definitely do, I think you do.

Speaker 3 (32:51):
Okay, antibiotic resistant bugs aside, which I know is like

(33:12):
a big thing to put aside. Yeah, there are relatively few,
I would say, bacterial infections that have the power to
transport us back to an era before we had any
tools to fight these germs.

Speaker 5 (33:26):
Right, No, it's I mean necrotizing infections are terrifying, terrifying.

Speaker 3 (33:30):
And what I mean is that even in the most
well equipped hospital, with the most skilled specialized infectious disease docs, surgeons, whatever,
modern medicine is sometimes powerless to stop the ravages of
necrotizing fasciitis. Regardless of the bacterium that's causing it. It
is destructive, it's deadly, it's humbling in the way that

(33:53):
it rejects the hundreds of years of scientific advancements that
we've made in so many areas of medicine.

Speaker 4 (34:00):
YEP.

Speaker 3 (34:01):
I understand why nicknames like quote unquote, galloping gang green
or flesh eating bacteria. I understand why those are frowned
on by the medical community. They're sensationalist, they're stigmatizing, their imprecise,
and they can incite undo fear and panic that this
new deadly disease, like something out of a horror novel,

(34:22):
is about to strike you down and everyone else in
your family or community, because that's not the way that
necrotizing fasciatis works. But I think that those names sensationalists,
though they may be, also convey the genuine fear that
comes with being largely powerless in the face of this
deadly disease. And I think it could also be argued

(34:46):
that they have helped raise awareness of the disease, and
since time is certainly of the essence, that could maybe
have saved lives in the past. But still we're sticking
with necrotizing fasciatis for this episode or soft what is it?
Soft tissue?

Speaker 4 (35:00):
Necrosisizing, negritizing infections.

Speaker 3 (35:03):
Okay, the words are all a jumble. Yes, So I've
got a quote for you, and strap in because this
is the first of many many quotes.

Speaker 4 (35:12):
Okay, can't wait.

Speaker 2 (35:13):
Quote.

Speaker 3 (35:14):
Few entities challenged the surgeon's clinical and operative skills as
intensely as devastating necrotizing soft tissue infections. End quote. Yep,
that statement. Although it was written in an article from
nineteen ninety one Necrotizing Lesions of Soft Tissues or Review
by Patino and Castro, that quote is still as relevant

(35:37):
today as it was thirty four years ago, and in fact,
a paper written eighteen years later in two thousand and
nine reported that over the previous three decades, so from
nineteen seventy nine to two thousand and nine, mortality from
necrotizing fasciitis had not budged, despite better tools and more

(35:59):
knowledge about the condition.

Speaker 4 (36:01):
Yeah, I'm surprised by that.

Speaker 3 (36:03):
Unfortunately, I know I'm not saying this to like terrify
everyone and say let's jump on the catastrophizing train, just
that we're still figuring it out. Modern medicine is still
figuring it out, and we have been working on it
for centuries.

Speaker 4 (36:18):
Yeah, we'll get to later. How rare these are.

Speaker 3 (36:21):
They're quite rare.

Speaker 4 (36:22):
They're quite rare.

Speaker 3 (36:23):
Yes, yep, not historically in certain situations. Yeah. So, when
cases of an unusually virulent strain of group A strap
began popping up in the mid to late eighties, the
question was raised, is this something new? And I don't
know how sincere of a question that was, although I

(36:45):
did read one article that was titled flesh eating bacteria
a new disease or old story? Because a quick review
of the literature shows that the answer is that this
is a very old story. Let's bring out some Hippocrates, right, Yes,
fifth century DCEE, Volume one of Epidemics. Quote. Many were
attacked by the aricipolus all over the body. When the

(37:07):
exciting cause was a trivial accident or a very small wound,
the ariciplus would quickly spread widely in all directions. Flesh, sinews,
and bones fell away in large quantities. The flux which
formed was not like puss, but a different sort of putrefaction,
with a copious and varied flux. Fever was sometimes present

(37:28):
and sometimes absent. There were many deaths. The course of
the disease was the same to whatever part of the
body it spread. Many lost the arm and the entire forearm.
If the malady settled in the sides, there was rotting
either before or behind. In some cases the entire thigh
was bared, or the shin and the entire foot. But

(37:48):
the most dangerous cases of all such cases were when
the pubis and genital organs were attacked. End quote.

Speaker 5 (37:57):
The way that that fluid is described to is called
dishwater fluid because it is like, it's not a pus,
it's not a purulent infection. It's like a very liquity
fluid that's kind of foamy and looks.

Speaker 4 (38:10):
Like that grayish after you've washed dishes.

Speaker 2 (38:14):
Yeah.

Speaker 4 (38:17):
Uh, it's horrific.

Speaker 3 (38:19):
It's horrific.

Speaker 5 (38:19):
Yeah.

Speaker 3 (38:21):
Yeah. And that quote though, like, did that sound to
you like necrotizing fasci idis? I mean absolutely right, Like
definitely yeah. And I think that this brings to light
one of the unique or interesting facets of necrotizing fasci
itis is that finding historical traces of necrotizing fasci idis

(38:43):
in like medical texts requires much less guesswork because its
symptoms and clinical course are so distinctive. It's not like
there's a fever and maybe a rash and some malaise
and maybe a sore throat and like maybe your head hurts.
You know, it's it's it's necrotizing fasciidis. Whether it goes
by necrotizing fasciitis or malignant ulcer, or a gangrenous ulcer,

(39:07):
putrid ulcer, fagiadina, phagidenic ulcer, fajidina gangrenosa, or hospital gangreene,
all of the whether it's called any of those things,
the description will pretty clearly point towards necrotizing fasciidis as
the culprit. And so digging back through the medical literature,
we can find traces of this condition dating back at

(39:29):
least to the late eighteenth century in France, where a
doctor out of hospital for the impoverished described it, and
it was also mentioned in an eighteen oh four book
on nautical medicine, where it was thought to be newly
emergent in the British home seies, quote unquote, mostly appearing
in those who had returned from long cruises in warm regions.

(39:52):
I don't think it was new, but I think, like
you said, it was rare, and so it was like
how widely known was it?

Speaker 4 (39:58):
Anyway?

Speaker 3 (39:59):
So I've go got a quote for you from this
this nautical medicine book quote. In the summer of seventeen
ninety nine, the malignant ulcer made its appearance on board
the Temaare with all the characteristic symptoms in virulence which
marked it in other ships. Every wound, abrasion of the cuticle,
blistered part, scald or burn passed rapidly through the various

(40:23):
stages of inflammation, gangreen and spaceless in a few days,
leaving the bones almost bare from the separation of immense
slufs en oohlarin yep. The ship the Saturn seemed especially
unlucky when it came to this disease. And there was

(40:43):
one case in particular that is truly horrific, like historically horrific.
So while in port, this sailor had contracted gonorrhea, and
it just kept getting worse, like the inflammation kept getting worse,
the everything kept get worse.

Speaker 2 (41:00):
Quote.

Speaker 3 (41:03):
If you're squeamish, you may want to pause here or
skip ahead. Yeah, thirty seconds feet I mean you've tuned
into an episode on acrotizing fasci itis. So like you've
made it this it's a little bit of a yeah, yeah,
here we go. Quote. The symptoms advanced by two hasty
strides to be arrested by any resources of medical skill.

(41:23):
The gland of the penis soon dropped off, but the
misery of the patient did not stop there. The whole
body of the penis passed quickly through the stages of
excessive excitement and inflammation to complete gangreen and mortification and
separate it at its very kura. The whole length of
the urethra to the bulb sloughed away, and also the scrotum,

(41:46):
leaving the testes and spermatic vessels barely covered with cellular substance.
He died end quote. Of course, of course he died.
Of course he died.

Speaker 4 (41:58):
How to have to live through all of that?

Speaker 5 (42:01):
I know?

Speaker 4 (42:01):
And then oh my gosh.

Speaker 3 (42:05):
And then literally like the next sentence, the author says,
cases like these have been frequent on board these ships.
And I don't know what these means. Does it mean
like penis is falling off or does it mean like
necrotizing inclignant ulser? Yeah? Right, yeah, okay, there's more. I yeah,

(42:29):
so there's another book published in eighteen eighteen on the
subject called Observations on Phagiadina Gangrenosa by HH Blackadder that
discusses the condition as though it was well known, at
least to military surgeons. So there's a passage from that
book that is basically an echo of the quote that
I read earlier. Quote gangrenous fagidina is one of those

(42:52):
diseases which happily seldom falls under the observation of civil practitioners.
But on the other hand, it is one of the
those which army and navy surgeons, during a time of
active hostilities, are frequently called upon to resist with all
the resources of their art. No disease requires more circumspection
and personal attention on the part of the surgeon, and

(43:15):
when the circumstances in which it occurs, the occasional rapidity
of its progress, the extent of its ravages, and fatal
tendency are considered, it may justly be esteemed one of
the most dreadful diseases to which mankind are subject end quote.
So it's like this, this is the worst, Yeah, this

(43:36):
is it. He also talks about how important it is
to recognize this disease quickly. Quote where there is any
even the smallest reason to dread the occurrence of this
disease too early or too many precautions cannot be taken
with the view of securing its speedy detection.

Speaker 4 (43:54):
End quote.

Speaker 3 (43:57):
I think it's like it's that was from eighteen eighteen,
and so yeah, it's just.

Speaker 5 (44:05):
They knew all the way back then how important it
was to be quick about it. Yeah.

Speaker 4 (44:09):
Yeah, we're still having trouble with that.

Speaker 3 (44:12):
We are, we are, And I mean it's hard, it's hard.
It's hard. I'm also like, this person's not like prophetic
by any means, right, Like I'm cherry picking these quotes.
He also used arsenic to treat it, and he blamed
the weather for when it showed up.

Speaker 4 (44:27):
Yeah, maybe they were all vibryo maybe yeah.

Speaker 3 (44:30):
I mean, but I think the thing that I appreciated
the most about that entire Like I didn't read the
whole book, but in the introduction he one of the
things he says is the author is fully aware of
his defects to kind of like head off anti criticism.
He's like, I'm yeah, I know. I was like, We're
going to start every single episode like that from now on.

Speaker 4 (44:52):
Yep, yep.

Speaker 3 (44:54):
But so throughout the rest of the eighteen hundreds. More
case descriptions followed, often though not always, associated with some
sort of military or nautical endeavor, in which cases it
may have been more contagious rather than the sporadic cases
that are seen in the general public. And once you
saw it, you never forgot it, a surgeon named John

(45:18):
Hennan said in eighteen twenty quote, to those who have
seen it, once a glance at the sore or even
the smell of the ward will immediately discover it. It
can scarcely be confounded with any other disease or any
other species of ulcers.

Speaker 2 (45:34):
End quote.

Speaker 3 (45:37):
Yeah, distinctive. Yeah. Most scholars put the next big event
in the history of necrotizing fasciitis in the aftermath of
the American Civil War, when medical officers such as Joseph Jones,
who was in the Confederate Army, described some of the
horrors that they witnessed. Jones is often credited with providing

(45:58):
the first modern description of necrotizing fasciitis, which he referred
to as hospital gangreen quote. In some cases, the progress
of the disease is rapid and terrible. The edges of
the wound become hardened and inverted. The surface of the
wound rises up into a pulpy, ragged, gray and greenish mass.

(46:19):
When the sloughs are detached, the disease attacks other adjacent
structures from day to day, extending its ravages both in
length and breadth. Most commonly, after the muscles have been exposed,
they continue to be gradually dissected. Their connecting membrane is
completely destroyed, and they are left covered with an offensive,

(46:39):
greasy looking matter. As the disease advances, hemorrhage from small
vessels is a common occurrence, and in the more advanced stages,
some of the large vessels give way and the patient
is frequently destroyed by the consequent hemorrhage. End quote.

Speaker 5 (47:00):
Yeah, yeah, it's a truly I mean, I flesh eating
bacteria is not a term that is like nice to hear,
but it is. I understand how it got that nickname.
Like it is what it feels like, what it looks like,
you know, I.

Speaker 3 (47:19):
Mean that's what it was like Fajadina was eating away
like that. It is a describes what happens. I think
it's also like when it was happening in military hospitals
it's possible that there were like outbreaks where it was
contagious because you had a bunch of Group A strap
in that hospital and horrible sanitize, you know, sanitary conditions,

(47:41):
and so it spread. But like that, I think that
is sort of the what conjures today, that idea of
like flesh eating bacteria is gonna it's gonna spread, it's
going to.

Speaker 4 (47:51):
Be coming for you, and it's not.

Speaker 3 (47:52):
That's not the way that it works.

Speaker 4 (47:54):
Yeah. Yeah.

Speaker 5 (47:54):
Hospital gangreen is also quite a misnomer for today's infections.
It's usually not at all hospit it required.

Speaker 3 (48:01):
Right, definitely, that was like it probably should have been
military hospital gangren. Yeah, and Joseph Jones, this guy, he
was more than qualified to describe this disease. Over twenty
six hundred cases of hospital gangrene had been diagnosed in
soldiers during the American Civil War. Nearly half of them died.

Speaker 4 (48:22):
That's a lot, holy guacamole.

Speaker 3 (48:26):
Yeah, yeah, and those who lived, like the around the
half of those who lived, they recovered, but they did
so at the cost of limbs or multiple limbs, which
had to be amputated. And in a different book, Jones
recalls the first case of hospital gangrene that he observed,
which was in a young man, a volunteer from Florida

(48:48):
who was stabbed in the scrotum, not during battle, but
during a fight at the drinking saloon. No, yeah, I know.
So he was brought to the hospital eight hours after
being stabbed, and he died less than a week later.
I decided to after reading through the full description, I
was like, I'm actually not going to quote all of this.
I'm sparing you the full description and also involves it

(49:12):
another penis sloughing off. But there's a part that really
stuck out to me at the end quote, the patient
retained his senses to within a few moments of death
and was at no point restless, No active pain was suffered,
and the patient appeared to be insensible to his distressing condition.
He expressed no fears of death, did not complain of

(49:34):
the horrid stench, and although fully warned of his true
situation and informed that every hope of life had vanished,
he actually traded for a watch two or three hours
before his death.

Speaker 5 (49:46):
End quote.

Speaker 3 (49:48):
Isn't that heartbreaking?

Speaker 4 (49:50):
Breaking? Absolutely heartbreaking?

Speaker 2 (49:53):
Ugh?

Speaker 5 (49:55):
Yeah.

Speaker 3 (49:57):
And so to round out this discussion of historic and
negritizing fasciatis, and especially as it applies to the genitals.
I have to mention Fournier and the gangreen that bears
his name. So in his work he was a quote
unquote venereologist, so he studied sexually transmitted infections, and in
eighteen eighty three he described five patients with necrotizing fasciitis

(50:19):
in their genitals and paraneal region. I wasn't sure why
this got a separate name, like why is this But
unless it's just that's where it happens more frequently, Like why, Yes, that's.

Speaker 4 (50:32):
What we call it when it's there.

Speaker 3 (50:33):
Okay, So it's just sort of like almost like a
historical relic in that way.

Speaker 4 (50:37):
Yeah, as far as I know.

Speaker 5 (50:38):
I mean the same thing with like Ludwing's angina is
in a specific location, so it's like to describe the
location of where of where it is, but it is
an ecritizing fasci idis of the fashion of that area.

Speaker 3 (50:49):
Right, So, until germ theory was fully established, people really
did not know where hospital gangreen came from or how
to treat it. Like Jones thought it was the crowded
conditions and poor ventilation in the hospitals. Another surgeon pinned
it on scurvy and nutritional status. There's the guy who

(51:10):
thought it was about weather, Thomas Trotter, who was the
author of the eighteen oh four book on Nautical Medicine.
He pointed out over and over again to alcohol, Like
every case that he described, he was like, and this
person drank this cheap alcohol, and this person drank this
cheap alcohol. Once people were able to identify the causative
bacteria in the wounds, that didn't necessarily clear things up right, Like,

(51:32):
we're still at a disadvantage because it was also turning
out to be multiple different microbes just a mix of
them sometimes. And interest in the condition, though I found
this fascinating, seemed to fall in the late eighteen hundreds
early nineteen hundreds. It was like kind of like this

(51:53):
was a big deal, Rear treatises about it, and then
it was kind of like eh. And there was a
physician who wrote in nineteen oh eight that quote hospital
gangreen so called has been in years past the terror
of military surgeons and camp hospitals. It has almost completely
disappeared from observation and is now practically never seen end quote.

Speaker 2 (52:15):
Isn't that interesting?

Speaker 5 (52:17):
Yeah?

Speaker 4 (52:17):
Why what changed? I?

Speaker 5 (52:18):
Don't know.

Speaker 3 (52:19):
So there is a thought. Do you remember when we
talked about Strap last and we talked about this sudden
decrease in and I'm wondering whether it's in scarlet pathogen shift.

Speaker 5 (52:32):
Yeah, so all of a sudden, we have ones that whatever,
whatever toxins they're making, are not the ones that are
more likely to cause an acritizing infection. Maybe that's super interesting.

Speaker 3 (52:40):
Yeah, So it could be that.

Speaker 4 (52:42):
I don't I should have looked specifically at that, but
I didn't.

Speaker 3 (52:45):
There was a paper that mentioned a little bit of that,
and there was also another paper that looked at genomes
of the group a Strap today and sort of any
sort of shifts in that as well. And I didn't
get into the nitty gritty of it, but like, it
does seem like there could be, like the biology is
there for these types of shifts.

Speaker 4 (53:05):
It's a plausible explanation, it is.

Speaker 3 (53:07):
Yeah, yeah, yeah, but yeah, that whole Oh it's never
it's a disease of the past. I was a little
bit of a premature celebration. The disease continued to pop
up both in times of war, like in World War One,
and in the general public just in other times like
the outbreak that involved at least twenty cases in China,

(53:28):
which was reported on by a physician named Frank Melanie
in nineteen twenty four. And so this actually his description
marks the first twentieth century description of the disease where
he also linked it to particular organisms group.

Speaker 4 (53:42):
A strap, namely ok okay.

Speaker 3 (53:45):
And then in nineteen fifty one Hospital Ganggreen malignant ulcer
phaegiadina gangrenosa, whatever else it was called, it was rebranded
as necrotizing fasciitis. And this was a name chosen by
physician Ben Wilson because fascial necrosis is the most consistent
manifestation of the disease end quote. And in this landmark

(54:08):
paper he went through what was known about the course
of disease, causes, treatment outcomes in epidemiology, you know, essentially
boiling down to rare but not unheard of. Time is
of the essence case fatality rate is lower than in
past decades thanks to early recognition, surgery and antibiotics. Yeah,
and so while the condition was known in medical circles

(54:31):
rare though it was I think again as we talked
about memorable, rare but memorable. It was known from at
least the mid twentieth century. It escaped public attention until
around the nineteen nineties. And this is I would say
largely that's a generalization, but that's around the nineties is
when a series of cases received a ton of media attention.

(54:54):
There was one outbreak, in particular in a place I'm
going to say this wrong, Gloucestershire, involving at least seven individuals,
and it led to headlines that were like, hospitals get
warning on killer bug, mystery bug kills, three more flesh
eating bug kills, young mother, I watched killer bug eat

(55:15):
my body, you know, things like super sensationalist headlines, right,
and so.

Speaker 4 (55:20):
The monsters inside me kind of thing.

Speaker 3 (55:22):
Yes, even though that is partially where I got the
interest in parasitology. Yeah, but this also it seemed not
like shared exposure but more like coincidence that these people
were getting accortizing fasciitis. Interesting, but any factual reporting of
that or exploration of that nuance it got drowned out

(55:43):
by these sensationalists headlines and fear mongering. But like I
pointed out at the top, there might have been the
positive effect of improving recognition, you know, just like knowing
what it is and that it exists right right, and
sure enough. It was interesting to see that following this reporting,
countries around the world began to also report, like release

(56:06):
reports on necortizing fasci idis at higher rates than previously
seen in cases often following like a surgical procedure. And
so this might have helped people, whether in the community
or physicians, recognize some early warning signs in themselves or
their patients. But there's also a cost, of course, to
this type of reporting. It contributes to the stigma that

(56:28):
many people who were covering from necortizing fasci idis face.
You know, the way that we talk about disease, even
legitimately scary ones like necrotizing fasci idis. It really does matter.
But yeah, that's all I have for the history of
neck fash. So, Aaron, why don't you tell us what's
happening with this condition today?

Speaker 5 (56:50):
All right?

Speaker 4 (56:50):
I'd love to.

Speaker 5 (57:24):
Today, thankfully. Necrotizing soft tissue infections, including neckritizing fascia idis,
are relatively rare. However, we don't have great numbers on them.
So group A strep infections like invasive group based strap infections,
which includes necritizing fasci itis, but also includes other types

(57:46):
of infections those are reportable in the US, so we
know that their rate tends to be aboutzero point four
per one hundred thousand in the US. But group A
strap only accounts for a proportion of neckritizing fasciaitis or
neckrotizing soft tissue infections more generally, and what proportion I
don't know. I from what I can tell, the scientific

(58:09):
community at large, the medical community doesn't necessarily have a
great handle on that. What's very interesting is that I
read one paper which I'll link to out of China
that was quite recent that looked at in their hospital
system just in one small part of China, and they
had hardly any group base strip in that particular population. Huh,
So I think it really varies location to location. Maybe

(58:31):
it does vary based on, you know, what stereotypes are
most prevalent, what toxins are being produced, et cetera. But
across the board papers that tried to estimate the incidents
of just necrotizing fasciitis, regardless of the type or the
causative agent. In the US, it's estimated at like eight
to ten cases per one hundred thousand individuals, and it

(58:53):
really can vary geographically across the globe, from like less
than one per one hundred thousand in some studies in
some parts the world, to twenty cases or more per
one hundred thousand people in other parts. I will say
that if you dig deep in these papers, some of
the studies that are reporting those higher end numbers are
citing how many cases there are per hospital admission, not

(59:16):
how many cases there are per general population mission. That's
going to be quite inflated. But in any case, it
can really range. What unfortunately doesn't have as huge of
a range is the mortality rate, and that remains quite high.
Some studies report a mortality rate as high as forty percent,

(59:38):
and so in particular studies or in particular areas, the
mortality rate can really be quite high. But on average globally,
for the last like you mentioned, airing twenty plus something years,
it really hasn't changed. The mortality rate on average is
between twenty five and thirty or thirty five percent. It's
only in the last couple of years that we've seen

(59:59):
study more often reporting rates closer to twenty percent. So
we're seeing maybe some suggestion of a bit of a drop. Okay,
Like I mentioned some of the studies that are just
looking at treatments, so they're looking at kind of a
more well defined population. It's not these like larger retrospective
studies and things like that. But some of these papers

(01:00:20):
suggest that we could be reducing mortality rates to ten
percent with correct identification and access to surgical management.

Speaker 4 (01:00:28):
But that is still really high. Like a ten percent.

Speaker 5 (01:00:32):
Mortality rate is terrifying, and that's the lowest that we've
been able to get it in studies.

Speaker 4 (01:00:39):
Yikes, I know, and what is scary.

Speaker 5 (01:00:43):
And I don't want to necessarily be fear mongering about
this because again, this is still quite a rare disease,
but it does seem to be increasing in number. Yes,
So according to analysis that was published I think in
twenty twenty three from CDC data that went from two
thousand and three to twenty twenty.

Speaker 4 (01:01:06):
Okay, there was an increase. Oh I saw this paper.

Speaker 5 (01:01:10):
Yeah, yeah, there was an increase of like one hundred
and twenty percent of deaths associated with necrotizing soft tissue infections.
Despite the fact that we are at least in theory,
getting better at treatment right or at least not getting
worse right, So deaths went from eight hundred and twenty

(01:01:30):
four in two thousand and three to one thousand, eight
hundred and forty two in twenty twenty.

Speaker 3 (01:01:35):
Is there any difference in like diagnostic or reporting or
anything like that, or is that simply just the number
of cases.

Speaker 4 (01:01:43):
It's a really good question.

Speaker 5 (01:01:45):
As far as I know, there's not any differences in
you know, reporting or things like that, because there hasn't
been a change in like what's required to report versus
what's not. This is all just still like they've gathered
this data after the fact. It's not necessarily like it's
not as easily accessible. I would say we are, and
I don't have necessarily data to back this up, but

(01:02:07):
I would hope that we are getting better rather than
worse at detecting it because of advances in things like
CT technology. There's a lot of people interested in using
things like ultrasound to better identify It's still a little
bit tough right now, but there's certainly a lot of
and there's also a ton of these different scores that
people use, like laboratory values to try and say, if
I'm not really sure, you know, should I call surgery

(01:02:31):
or should I not there wasn't anything clear on imaging.
There's like these scores that you can calculate to try
and lean you more likely necrotizing versus not. None of
them are perfect, but there's a lot of interest in
like how do we better identify this early? And yet
we're still seeing this increase in depths and without a
corresponding increase in the mortality rates. And so I do
think that this is due to an increase in cases

(01:02:53):
from everything that I can tell. The other thing that
we know there is an increase in is cases of
Vibrio vulnificus, specifically these wound infections. Between nineteen eighty eight
and twenty eighteen, Vibrio wound infections increased eightfold and also
shifted northwards substantially. And we think that this is down

(01:03:16):
to climate change change. Vibrio has actually, and this was
a new fact for me, it's been called a microbial
barometer of climate change because of how well it thrives
in this warm brackish water and how highly sensitive it
is to temperature. I've heard that, yeah, yeah, And so
we when we combine all of this information plus the

(01:03:38):
fact that we have an increasingly elderly population who are
already at risk of necrotizing infections compared to younger populations.
It's kind of a scary possibility that things could continue
to increase vibrio and otherwise, but at this point, at
least it is still rare.

Speaker 4 (01:03:57):
That's the only goodness.

Speaker 3 (01:04:00):
Yeah, Yeah, it's not really silver lining.

Speaker 4 (01:04:03):
Yeah, that's an acrotizing fasciitis sarin.

Speaker 3 (01:04:08):
Wow. I don't know how to react. I mean, there's
I know, I it's horrifying.

Speaker 5 (01:04:20):
It's horrifying, and I it is a truly horrifying disease.
And I also it's a it's a tough balance to
not feel like like those headlines that are like I know,
I know, you know.

Speaker 3 (01:04:31):
I mean I think, I think you're right, and I
think it's like it's a hard balance because I think
it's really important to be vigilant and like what what
are things? How do we worry without worrying constantly? Like
how do we worry about the right stuff? I don't
know the answers to that me neither. Yeah, And I
don't think the papers that we're about to guide you

(01:04:51):
to will have the answers to that either. So, but
they are great for reading or great transition so it
I have a bunch I'm going to shout out too.
In particular, one is by Louden published in nineteen ninety
four in The Lancet titled Necrotizing Fasciitis Hospital Gangreen and Fhagiadina,

(01:05:13):
and then another is by Quirk and Sternbach from nineteen
ninety six. I was digging the nineties papers for this.
I think there was a lot of interest, so a
lot of papers, and this one was titled Joseph Jones
Infection with Flesh Eating Bacteria from the Journal of Emergency Medicine.

Speaker 5 (01:05:30):
I had a bunch of papers, a few that I
particularly enjoyed. I was a twenty seventeen was my year, Aaron,
because one from Infectious Disease Clinics in North America from
twenty seventeen was titled Evaluation and Management of Necrotizing soft
Tissue Infections by Bonnie and Cadri And then another from
twenty seventeen from the New England Journal of Medicine by

(01:05:52):
Stevens and Bryant called Necrotizing seft tissue Infections. I had
a bunch more, you know, from the last decades.

Speaker 4 (01:05:59):
You can find them all on our website. This podcast
with kill you dot Com under the episode stab Yeah.
Check it out.

Speaker 3 (01:06:05):
Thank you again, Maggie so much for sharing your story.
I'm oh horrifying, harrowing.

Speaker 4 (01:06:12):
Yeah, thank you, thank you so much. We can't say
it enough.

Speaker 3 (01:06:15):
Thank you to Bloodmobile for preventing the music for this
episode and all of our episodes.

Speaker 5 (01:06:20):
Thank you to Leanna and Tom and Brent and Pete
and Jessica and my everyone, everyone that's exactly right.

Speaker 2 (01:06:28):
Thank you.

Speaker 3 (01:06:29):
Thank you to everyone, and thank you to our listeners
who are you know, make us or let us make
this podcast. Words are failing me, And to our patrons
whose support truly means the world to us. You are amazing.

Speaker 4 (01:06:43):
Thank you, thank you, thank you.

Speaker 5 (01:06:46):
Well.

Speaker 3 (01:06:46):
Until next time, wash your hands.

Speaker 4 (01:06:48):
You feel the animals.

Speaker 5 (01:07:02):
Um um um