Speaker 1: Soon after my attention had been directed to the liver
Speaker 1: and its associated structures, I found in the blood of
Speaker 1: the portal vein a number of long white helmets, which,
Speaker 1: with the naked eye I considered to be nematodes, but
Speaker 1: soon recognized as something new. A look into the microscope
Speaker 1: revealed a splendid dystomum with a flat body and a
Speaker 1: spiral tail at least ten times as long as the body.
Speaker 1: I have not yet reported the new stages of my
Speaker 1: portal vein worm. It did not, as I had expected,
Speaker 1: develop into an old wives tail, but into something more wonderful,
Speaker 1: a treematode with divided sex. I performed an autopsy on
Speaker 1: a boy who died of meningitis. Upon opening the urinary bladder,
Speaker 1: we found lentil to pea size soft, spongy excrescences. When
Speaker 1: I cut through the largest of the excrescences, a white
Speaker 1: thread adhered to the knife. Examining it more closely, I
Speaker 1: recognized our dystomum hematobium. I searched the depth of the
Speaker 1: incision and pulled out several more the areas of the
Speaker 1: bladder mucosa, where the earliest stages of the tumors appeared
Speaker 1: were covered with viscous, clear mucus containing large numbers of
Speaker 1: dystomum hematobium eggs singly or in clumps. When I showed
Speaker 1: Doctor Lautner the dystomum hematobium found in the bladder, he
Speaker 1: remarked that he too had seen the eggs while studying
Speaker 1: the pathologic changes of the bladder, but had not been
Speaker 1: able to explain them. He and doctor Greisinger encouraged me
Speaker 1: to examine the pathologic changes of the bladder, which were
Speaker 1: so similar to those found in dysenteric degenerations of the intestine.
Speaker 1: Further investigations in this country, which I shall continue zealously,
Speaker 1: as well as those being carried out in Europe, investigations
Speaker 1: to which I invite my colleagues, will have to decide
Speaker 1: whether Dystomum hematobium stands in the same relation to dysentery
Speaker 1: as a Kears scabii does to the itch. All right, then,
Speaker 1: So that was from excerpts from letters from Theodore Billar's
Speaker 1: to his supervisor von Siebold while conducting research in Egypt,
Speaker 1: and this was essentially the discovery of Schista's soma hematopium.
Speaker 2: The subject of today's.
Speaker 1: Episode one of the subjects just a semiasis in jen Hi.
Speaker 2: I'm erin Welsh and I'm erin Oman Updyke and this.
Speaker 1: Is this podcast will kill you. Yeah, welcome to just
Speaker 1: a Semiasis.
Speaker 3: Just a semiasis my first true love of disease.
Speaker 1: I like the qualifier there, not just well. Yeah, I'm
Speaker 1: excited too. I mean, we love a good multi host parasite. Yeah,
Speaker 1: fascinating the ecologies there. It typically has some long history.
Speaker 2: You know, I can't wait.
Speaker 3: To hear the history because I know nothing about it.
Speaker 1: Oh man, this I'm I'm very excited about this. This
Speaker 1: is like a full rich history. I didn't have to
Speaker 1: like color in the edges with some other.
Speaker 2: External historic et cetera.
Speaker 1: Hey, now, no, that was great, not true. Okay, so
Speaker 1: what are we drinking this week?
Speaker 2: We're drinking just a fluke.
Speaker 1: Because also shist ames are known as flukes.
Speaker 2: Flukes. Yeah, it's a type of platform.
Speaker 1: Yeah, and in justin luke is pomegranate juice, vodka, club soda, mint,
Speaker 1: simple syrup, maybe a little bit of lime juice, and
Speaker 1: then you garnish with some pomegranate seeds if we can
Speaker 1: find them from the store.
Speaker 3: And as always, will post the full recipe for this
Speaker 3: quarantini as well as our non alcoholic plusy burrita on
Speaker 3: our social media and our website, so you can check
Speaker 3: it out there.
Speaker 2: Yeah.
Speaker 1: Now let's dive into schisto.
Speaker 3: After this quick break. So shst a semiasis also called
Speaker 3: bill harcia. Yeah, because of as you mentioned from our
Speaker 3: first hand account, the person who discovered.
Speaker 1: It, Theodore bill Ars.
Speaker 2: Can we call him Teddy? Do you think you went
Speaker 2: by Teddy?
Speaker 1: I have no way of knowing. There probably is Google actually.
Speaker 2: But Teddy bill Ars. That's a cute name.
Speaker 1: I like it. I like the name Teddy.
Speaker 3: So shst a semiasis aka bill harcia. It's caused by
Speaker 3: a worm. We haven't done a ton of worms, so
Speaker 3: this is exciting. It's a flatworm, and specifically one that's
Speaker 3: called a fluke. That's like the type of worm that
Speaker 3: it is.
Speaker 1: Why is it called a fluke?
Speaker 3: You know?
Speaker 2: That's a good question that I don't know. Okay, I
Speaker 2: feel like that's a history question.
Speaker 1: Oh dang it, how dare you?
Speaker 3: So? There are a number of different species of shist
Speaker 3: as ome that infect humans. The three most common are
Speaker 3: Schistosoma Mansoni japonicum and Hematobium. There are a few other
Speaker 3: species as well that are less common, and they all
Speaker 3: have the same basic life cycle and overriding general pathways
Speaker 3: by which they travel through the human body and cause disease,
Speaker 3: but they do cause slightly different diseases, especially between Schistosoma,
Speaker 3: Mansoni Japonicum and Hematobium.
Speaker 2: It's kind of like the special one.
Speaker 3: So what we're gonna do is talk about the general
Speaker 3: life cycle and pathway first as a group, like all
Speaker 3: the shistosomes, and then we'll talk about the symptoms. We'll
Speaker 3: talk specifically about the differences between them.
Speaker 2: Does that sound good?
Speaker 1: Sounds great? Also, I just looked up fluke etomology, Oh
Speaker 1: tell me, and apparently it means it's like the old
Speaker 1: English word flock means flatfish, and so the worms were
Speaker 1: called that because they resembled.
Speaker 2: Flat flat fish little flounders. I can see that. Cool.
Speaker 3: Thanks Aaron, answering your own question. All right, So, like
Speaker 3: we mentioned briefly, one of the reasons that Aaron and
Speaker 3: I get excited about a parasite like this is that
Speaker 3: it has a very complex life cycle and transmission cycle.
Speaker 2: So it goes a little something like this.
Speaker 3: I'm I'm simplifying this a little bit, but this is
Speaker 3: the general overview.
Speaker 2: Okay.
Speaker 3: So we'll start with the eggs, because you have to
Speaker 3: start somewhere in a cycle. So the eggs are present
Speaker 3: in the environment, and they hatch in fresh water.
Speaker 2: Okay.
Speaker 3: And out of these eggs hatch these little mirrorciitia is
Speaker 3: what they're called, but we'll call them baby shisto.
Speaker 2: Okay, okay.
Speaker 3: So baby shisto have all these little still around their
Speaker 3: edges which act like swimmers so that they can swim
Speaker 3: through their environment. Aaron I wrote, they swim their way
Speaker 3: into a crab.
Speaker 2: Why did I write crab? What that is incorrect? That
Speaker 2: is incorrect is one percent incorrect. I can't believe I
Speaker 2: wrote crab. How funny.
Speaker 3: So with these little swimmers, they swim their way through
Speaker 3: fresh water into a snail.
Speaker 2: Okay.
Speaker 3: And it depends on what species of schistosome what species
Speaker 3: of snail they go into, but they all make their
Speaker 3: way into snails, and inside these snails, the baby shistos
Speaker 3: begin to multiply asexually.
Speaker 1: When you say, so, that's really interesting, it is, that's
Speaker 1: really wild. I started to talk as you were finishing
Speaker 1: that sentence. Also, how do they get into the snail.
Speaker 1: Do they penetrate the snails?
Speaker 2: Yep, little fleshy body parts.
Speaker 1: Yeah, okay, but they so they replicate a sexually, which
Speaker 1: is wild considering in the first hand account we learn.
Speaker 2: That will get there.
Speaker 1: Okay, don't you worry.
Speaker 3: These are just these are baby shistos. Okay, baby through
Speaker 3: life stage by live stage. So the baby shistos swam
Speaker 3: their way into a snail. They begin to replicate asexually,
Speaker 3: so multiply and multiply, and then they change into what
Speaker 3: are called sir Carrie a mm hmm.
Speaker 2: And these are.
Speaker 3: Kind of like a kid shisto. Okay, kiddo shistos. They
Speaker 3: look kind of like sperms. Okay okay, not quite like
Speaker 3: a sperm, but sperm esque. They have like a head
Speaker 3: and a tail that they use for swimming. So these
Speaker 3: kiddo shistos, spermy looking things, swim burrow their way back
Speaker 3: out of the snail and are released again into fresh water,
Speaker 3: and then they use that to swim around through fresh water.
Speaker 1: How over how many days or how long do they
Speaker 1: replicate in the stale?
Speaker 3: I knew you were gonna ask that question, so let
Speaker 3: me tell you. The eggs they can live in the
Speaker 3: environment for up to seven days, and then once the
Speaker 3: baby shistos make it into the snail, it takes four
Speaker 3: to six weeks before they start shedding the kiddo shistos.
Speaker 2: The cir carrier. It's a long time, it is.
Speaker 3: And now these cir carrier can live in the environment
Speaker 3: for up to seventy two hours, so they're swimming around time.
Speaker 2: That's a short time.
Speaker 3: They're swimming around in fresh water. And now here you come,
Speaker 3: as a human mammal walking around for a nice walk
Speaker 3: through these fresh water ponds or whatever. You're obviously barefoot
Speaker 3: because you wouldn't want to get your shoes wet. And
Speaker 3: these little kiddo shistos see you, swim right up and
Speaker 3: burrow their way through your.
Speaker 2: Skin and into your foot. Okay, okay, all right, okay.
Speaker 3: So now these little spermy circaria have wormed their way
Speaker 3: into your body, okay, and then they're going to change
Speaker 3: yet again. That spermy tail is going to fall off
Speaker 3: and they are going to start to swim in your
Speaker 3: body a mammal body and make their way into your bloodstream.
Speaker 3: So now you can think of them kind of as teenagers.
Speaker 3: These are called schistosomula at this point. Okay, so they're
Speaker 3: like the sperm without the tail, just the little head part. Okay, Okay,
Speaker 3: So inside of you, they make their way, as many
Speaker 3: parasites do, into your bloodstream, either directly through your little
Speaker 3: capillaries or through your lymphatic system.
Speaker 2: First.
Speaker 3: Then they're going to travel. This is where it gets
Speaker 3: really fun. It's already fun because how complicated is this.
Speaker 3: They travel through your venous system, and remember your veins
Speaker 3: are what carried the deoxygenated blood back to your heart, right,
Speaker 3: so they're going to travel through your veins to the
Speaker 3: right side of your heart. The right side of your
Speaker 3: heart is going to pump these teenage schistos out into
Speaker 3: your lungs, where they can then cross the capillaries and
Speaker 3: travel to the arterials, which go back to the left
Speaker 3: side of your heart, and then your heart can pump
Speaker 3: them out yet again to the rest of your body.
Speaker 3: And where they go from there is actually they make
Speaker 3: their way from your heart.
Speaker 2: To your liver.
Speaker 3: Okay, this is a very complicated route. Okay, they've entered
Speaker 3: your foot, they travel through your bloodstream, make their way
Speaker 3: to your lungs in order to get to your heart.
Speaker 3: In order to get to your liver.
Speaker 1: Okay, So it's kind of like it almost follows the
Speaker 1: root of the hookworm up until the liver part.
Speaker 3: Yeah, exactly, yes, or no, it's before the liver part
Speaker 3: to the lungs.
Speaker 2: Yeah, to the lungs.
Speaker 3: So yeah, hookworms also make it to your lungs, but
Speaker 3: then they make you cough and then you swallow them
Speaker 3: to get into your intestine.
Speaker 2: So these guys go a different way. In your lungs.
Speaker 3: They stay in your blood stream, so they're basically just
Speaker 3: riding your blood flow all the way to your liver.
Speaker 3: The that's their target destination for now, Okay. Then in
Speaker 3: your liver, and this is all all the different species
Speaker 3: of schistosoma do this, okay, Okay, They make their way
Speaker 3: to your liver, and then they're going to in your
Speaker 3: Like your liver has so much blood flow, lots of veins,
Speaker 3: lots of arteries all in there, and so in your liver,
Speaker 3: they're gonna leave the arterial system yet again and make
Speaker 3: make their way back into the veins in your liver,
Speaker 3: and that is where they're going to mature into full
Speaker 3: fledged adult sistosomes. And like you mentioned in the first hand, account,
Speaker 3: they now have male and female shistos Okay. I don't
Speaker 3: know whether you could identify them previously, but at this
Speaker 3: point as adults, there are male schistosomes and female schistosomes.
Speaker 3: And then just like on Love Island, UK.
Speaker 2: Yes, they're going to coupull up okay and sleep in
Speaker 2: the same bed together. Just kidding.
Speaker 3: What happens is the female schistosome literally wedges into a
Speaker 3: canal in the male sistosome called a gaynacophoral canal, and
Speaker 3: then as a pair, they traveled together to their final destination.
Speaker 1: Okay.
Speaker 3: For Schistosoma Mansoni and Japanicum, this final destination is the
Speaker 3: venus plexus around your intestines, the mesenteric veins. For schistosoma hematobium,
Speaker 3: it's the venus plexus around your bladder.
Speaker 1: Huh.
Speaker 2: Okay, I don't know why. Okay, I can see on
Speaker 2: your face you're about to ask me that I was. Yeah.
Speaker 3: It's a very interesting question as to why these like
Speaker 3: most species of shistosoma tend to go to the veins
Speaker 3: around your intestines, but hematobium goes to your bladder.
Speaker 2: It's a really interesting question that I don't know the
Speaker 2: answer to.
Speaker 3: But that is where they go, and then they live
Speaker 3: their lives as adult schistosomes where the female just lays
Speaker 3: eggs and eggs and eggs and eggs, so many eggs.
Speaker 3: And then what has to happen for them to complete
Speaker 3: their life cycle is these eggs have to make their
Speaker 3: way out of your body. So the way that they
Speaker 3: do that if they're in the veins around your intestine
Speaker 3: is those eggs will burrow through those veins into your
Speaker 3: intestine and you poop them out. If they're in your bladder,
Speaker 3: they have to borrow their way all the way through
Speaker 3: your bladder, which is a really thick organ like it
Speaker 3: has a thick wall, cool into your bladder and then
Speaker 3: you pee them out.
Speaker 1: Okay, okay, is there ever any recoupling?
Speaker 3: Recoupling Aaron I practiced for like ten minutes last night
Speaker 3: how to say couple up, and I think I still
Speaker 3: did a terrible job of it.
Speaker 1: Do you mean you watched ten episodes of violence?
Speaker 3: I literally sat with Brett saying the words couple up,
Speaker 3: like for ten solid minutes, trying to get a good accent.
Speaker 1: Anyways, time well spent.
Speaker 2: Mm hmm. So that's the life cycle of schistosama.
Speaker 3: Cool.
Speaker 1: Cool.
Speaker 2: They can live in your body, these adult worms.
Speaker 3: You haven't asked me, but let me tell you, for
Speaker 3: three to ten.
Speaker 1: Years in your That's impressive.
Speaker 3: Just layand eggs, laying eggs, lant eggs.
Speaker 1: Okay, that also makes it very difficult to get rid
Speaker 1: of environmental.
Speaker 3: Do you want to know what the theoretical reproductive potential
Speaker 3: of one schistosome pair is? Six hundred billion sistosomes? Oh,
Speaker 3: because not only are the adults living in you shedding
Speaker 3: for years, but one single Mirricidium that infects a snail
Speaker 3: can shed thousands of circaria every day for months. They
Speaker 3: live in the snail for months.
Speaker 1: That is incredible.
Speaker 3: I know whoa yep, Yeah, it's incredible, and it does
Speaker 3: it makes control of this very very difficult. Okay, so
Speaker 3: let's talk about the path of physiology of how this
Speaker 3: this We know how it moves through your body, but
Speaker 3: how does it actually cause symptoms? How does it actually
Speaker 3: make you sick? What's really important to keep in mind
Speaker 3: about shi just a semiasis is that the symptoms that
Speaker 3: we see from this disease are not from the worms themselves.
Speaker 3: They're from the eggs, and they're also not even necessarily
Speaker 3: from the eggs doing what eggs are supposed to do,
Speaker 3: which is leave your body through your poop or pee.
Speaker 3: But the symptoms are caused by what happens when the
Speaker 3: eggs don't leave your body.
Speaker 2: Really, yes, the fact that the.
Speaker 3: Eggs have to cross through, so they have to leave
Speaker 3: your veins. Right, they're living in the veins around your
Speaker 3: intestines or around your bladder. They have to penetrate through
Speaker 3: your vein walls and either into your bowels or your bladder.
Speaker 3: So you can imagine that this causes inflammation.
Speaker 2: Right.
Speaker 3: They have to make holes in your veins and your
Speaker 3: bowel or bladder wall to make their way into the
Speaker 3: lumen of these organs. So in the case of the
Speaker 3: bowels in your intestines, what can happen is they can
Speaker 3: leave essentially little holes behind, so you can get micro tears,
Speaker 3: micro perforations, you can get intestinal bleeding. Anytime you damage
Speaker 3: the wall of the intestine, you can mess up its
Speaker 3: absorptive capacity, so you can have malabsorption, which means diarrhea
Speaker 3: and also potentially malnutrition because of this, because you have
Speaker 3: bleeding from these little ulcerations, you can end up with anemia,
Speaker 3: especially in children. Who are already prone to anemia. Yeah, okay,
Speaker 3: so that's in the intestine. In the bladder, what can
Speaker 3: happen really commonly is that the bladder wall is very thick,
Speaker 3: so and this can happen in the bowels as well,
Speaker 3: but especially in the bladder because of how thick it is,
Speaker 3: the eggs don't always penetrate all the way through, so
Speaker 3: they can get stuck in the wall of the bladder.
Speaker 3: And what happens when the eggs get stuck in the
Speaker 3: wall of your tissue, essentially, is it causes a massive
Speaker 3: inflammatory response in your body, and your body tries to
Speaker 3: wall off this egg. Like your body recognizes this egg
Speaker 3: doesn't belong here, I'm going to wall it off, and
Speaker 3: it forms what's called a granuloma, which is basically inflammatory
Speaker 3: cells and tissue and debris walling off this egg. It's
Speaker 3: the same thing that we saw in tuberculosis. It happens
Speaker 3: in your lungs. Yeah, so that happens as well in
Speaker 3: shs a semiasis, and in the bladder wall. This can
Speaker 3: cause chronic inflammation. So one of the hallmark symptoms is
Speaker 3: bleeding in your p so huematuria, and that's from actual
Speaker 3: penetration through but also from this chronic inflammation that happens
Speaker 3: in the wall of your bladder. And then the other
Speaker 3: thing that can happen is that if you think about
Speaker 3: which direction blood flow in your veins, blood is flowing
Speaker 3: away from most of your organs in your veins, right,
Speaker 3: So the blood in the veins around your intestines is
Speaker 3: not flowing into the intestine. It's flowing away from the intestine.
Speaker 3: But the eggs are trying to get into the intestine,
Speaker 3: so they're swimming against the current.
Speaker 2: They don't all make it, so.
Speaker 3: Some of them get swept up backwards, and where they
Speaker 3: go is the liver because that's where those veins drain to. Oh,
Speaker 3: the liver, that's where they came from, right, yeah, So
Speaker 3: then they can get lodged in the liver and also
Speaker 3: the spleen because a lot of blood flow drains into
Speaker 3: the spleen as well. So then you have the same
Speaker 3: thing happening that happened in the wall of the bladder,
Speaker 3: these granulomas forming this intense inflammation in the liver and
Speaker 3: the spleen. So this can cause hippatosplenomegaly, so that means
Speaker 3: enlargement of the liver and the spleen.
Speaker 1: Wait, we just talked about this and I said it
Speaker 1: was a great word.
Speaker 2: Yeah you did.
Speaker 1: Which episode?
Speaker 2: Oh, let's see in is it hepsy? No, because hepsy
Speaker 2: doesn't cause spleen? Dangae dangay. It was okay, yeah, dangay.
Speaker 1: Cool.
Speaker 3: Yeah, so fun So connections yep. So it can cause hepatosplinamagally.
Speaker 3: It can also cause what we did talk about with
Speaker 3: hepatitis C, which is fibrosis of the liver. Especially now,
Speaker 3: anytime that you have veins being clogged, like we talked
Speaker 3: about in the hepsy episode, you can have portal hypertension,
Speaker 3: so the veins are being clogged, so the pressure is
Speaker 3: building up on the back end. So you can see
Speaker 3: all the same symptoms that you see with other chronic
Speaker 3: liver disease, like acide's fluid being filled up in your belly.
Speaker 3: You can get esophageal varices, so Varico's veins in your esophagus,
Speaker 3: which can cause massive bleeding if they rupture.
Speaker 1: Oh my gosh, yeah.
Speaker 2: Yeah, isn't that Isn't that fascinating?
Speaker 3: It is. So that's kind of like the pathophysiology of
Speaker 3: how and why it causes the disease that it causes.
Speaker 3: It's not the worms themselves, it's the eggs getting lodged
Speaker 3: in places and then our bodies mounting a massive immune
Speaker 3: response to try and wall these eggs off.
Speaker 1: Okay, fascinating.
Speaker 3: Okay, So then let's talk about the actual symptoms. We've
Speaker 3: kind of touched on them, but we'll go through the
Speaker 3: stages of infection. Okay, okay, so super acutely, like hours
Speaker 3: after you get infected, especially the first time you ever
Speaker 3: get infected. You're right, there is symptoms that happen right
Speaker 3: away from the circarria themselves, and that is an itch
Speaker 3: uh huh, where those little spurmes penetrate your body. Okay,
Speaker 3: This is sometimes called swimmers itch.
Speaker 1: It's also really funny to me that you're calling them
Speaker 1: little spurmes because of something that I'll talk about in
Speaker 1: the history section.
Speaker 3: Oh really yeah yeah, So yeah, you can get a rash.
Speaker 3: It's sometimes called swimmer's itch because again this is from
Speaker 3: freshwater ponds and things like that. That is where they live,
Speaker 3: and it'll be blistery, it'll be itchy, but it's generally
Speaker 3: self limited and it kind of goes away over time.
Speaker 3: Right then there is an acute disease that can happen
Speaker 3: in a number of weeks, usually like two to ten
Speaker 3: weeks after infection. It tends to only really happen with
Speaker 3: Schistosoma japonicum infection, but it also can happen in travelers
Speaker 3: who get infected with Sistosoma mansoni and hematobium, But it
Speaker 3: doesn't tend to happen in people who live in areas
Speaker 3: where this disease is endemic with the other two species,
Speaker 3: if that makes.
Speaker 2: Sense, Uh huh okay.
Speaker 3: And so this acute disease essentially is your body mounting
Speaker 3: a hypersensitivity reaction to all the worms swimming through your
Speaker 3: bloodstream and making their way that long travel down to
Speaker 3: the veins of your intestine or your bladder. It's your
Speaker 3: body seeing those worms swimming and mounting a response to it.
Speaker 3: So again, it is the worms, but it's also not
Speaker 3: the worms. It's your body reacting to the worms. And
Speaker 3: so the symptoms that you see are the same kind
Speaker 3: of general inflammatory symptoms that we see with a lot
Speaker 3: of diseases, fever, fatigue, maybe muscle pains, things like that.
Speaker 3: If you were to test someone's blood at this time,
Speaker 3: what you would see is something called eosinophilia, which is
Speaker 3: I think another fun word, fun words. So that means
Speaker 3: an elevation in the number of eosinophils, which is a
Speaker 3: specific type of white blood cell that we have that
Speaker 3: we use to fight off parasitic infections. So it's your
Speaker 3: body going, hey, I know that there is a parasite,
Speaker 3: a worm here in my body, and I'm trying to
Speaker 3: fight it off, which I think is so cool.
Speaker 1: It's very cool because it just shows how important parasites
Speaker 1: have been to us throughout our evolution.
Speaker 2: We have a whole line of blood cells that are
Speaker 2: specifically four parasites.
Speaker 1: Oh, it's so cool. It's very cool.
Speaker 3: And then the other thing that you'd see if you
Speaker 3: took like a chest X ray of someone with this
Speaker 3: acute shisto reaction, you would see patchiness on chest X
Speaker 3: ray and that's likely because of you know, the worms
Speaker 3: have made their way through your lungs and that causes
Speaker 3: some inflammation in your lungs as well.
Speaker 1: Okay, okay, but this is just two to ten weeks.
Speaker 3: This is just two to ten weeks. This is also
Speaker 3: called Katayama fever. Uh huh, pronouncing that right, But that's
Speaker 3: that's what it's called and yeah, that's sort of the
Speaker 3: acute it doesn't it in endemic areas where schistosoma, mansoni
Speaker 3: and hematopium are the primary causes this, This isn't a
Speaker 3: disease you tend to see very often, right, which is
Speaker 3: very interesting. So the majority of problems associated with just
Speaker 3: asmiasis are in fact the chronic infection of course from
Speaker 3: the eggs.
Speaker 2: And so we've kind of.
Speaker 3: Already talked about what those symptoms are, but will kind
Speaker 3: of just go through system by system to talk about
Speaker 3: what you actually see symptom wise. So in your intestine,
Speaker 3: when you have these eggs burrowing their way through into
Speaker 3: your intestine wall, you're going to have symptoms associated with
Speaker 3: intestinal pain, abdominal pain. I mentioned, you can get micro
Speaker 3: ulcerations in your intestinal wall, which can cause bleeding. So
Speaker 3: you can get diarrhea, either bloody or non bloody diarrhea
Speaker 3: in kids especially, this can lead to malnutrition if you
Speaker 3: think about the intestinal wall being damaged, not being able
Speaker 3: to absorb all the nutrients.
Speaker 1: That you need.
Speaker 3: On top of that having diarrhea, you can have malabsorption problems.
Speaker 3: And then yeah, exactly, you can also get anemia, especially
Speaker 3: in children. So that's the intestinal symptoms. When those eggs
Speaker 3: make their way up into your liver, you can have
Speaker 3: all that those hepatic symptoms that we mentioned already, so
Speaker 3: ascide's portal hypertension, liver fibrosis, all of that kind of
Speaker 3: stuff in your urinary tract. Bloody urine hmaturia is kind
Speaker 3: of the hallmark sign of shostosimiasis, especially in children.
Speaker 1: Okay, especially in children.
Speaker 3: Yeah, there's really no like, there's there's no other well
Speaker 3: in endemic areas. If there is a kid with bloody urine, it's.
Speaker 2: Just a samiasis especially Okay.
Speaker 3: What's very interesting is that in adults, chronic infection with
Speaker 3: shistosoma heemotobia that affects the urinary tract is associated with
Speaker 3: an increased risk of bladder.
Speaker 1: Cancer because of the inflammation.
Speaker 3: It's thought, yeah, it's thought that it's because of the inflammation.
Speaker 3: At least one thing I read said it's also possible
Speaker 3: that just the the action of these eggs, like constantly
Speaker 3: going through your walls, can make your bladder more susceptible
Speaker 3: to other carcinogens like poaking and things like that. So
Speaker 3: it's not entirely clear whether it's like but overall. Yeah,
Speaker 3: it's inflammation, right, yeah, right, yeah, And now here's the
Speaker 3: other really important thing about shys asmachematobium. So it's living
Speaker 3: in the veins around your bladder. Your bladder is in
Speaker 3: your pelvis, which means that this can also affect other
Speaker 3: organs in your pelvis, and so this can cause it
Speaker 3: causes what's called genito urinary just a semiasis, So it
Speaker 3: can affect it can affect the prostate, the seminal vesicles,
Speaker 3: so you can see things like hematospermia, so bloody semen.
Speaker 3: It can also result in very substantial cervical lesions. So
Speaker 3: the cervix is the bottom part of your uterus, top
Speaker 3: part of your vagina. This can cause very substantial cervical lesions,
Speaker 3: vaginal lesions. And what's really important is that this type
Speaker 3: of genito urinary just a semiasis is associated with an
Speaker 3: increased risk of HIV infection and transmission. Yes, yeah, because
Speaker 3: of these lesions you have like open wounds, you have
Speaker 3: increased inflammatory cells, and so it's easier for HIV to
Speaker 3: be transmitted. So that's really important.
Speaker 1: I had no idea about these other manifestations of disease
Speaker 1: until I was reading a review paper about the history
Speaker 1: of it, and then it has you know, I got
Speaker 1: scrolled to page ten and it was just like picture
Speaker 1: after picture of eurogenitor. Wow, of eurogenital just a semiasis, and.
Speaker 2: Yeah, yeah, it's terrible, it's horrible.
Speaker 1: It's horrible.
Speaker 3: Now, because this is something that's in your blo blood,
Speaker 3: it can technically also cause disease anywhere that your blood goes,
Speaker 3: which is to say the rest of your whole body
Speaker 3: as well. So these eggs can also end up traveling
Speaker 3: all the way back to your lungs, which can cause
Speaker 3: the same kind of granulumitus changes that we saw in
Speaker 3: everywhere else in the liver, in the bladder, et cetera.
Speaker 3: So that can end up causing what's called pulmonary hypertension.
Speaker 3: So think of the increased pressure in your portal veins
Speaker 3: of your liver. The same thing can happen in your lungs.
Speaker 3: If you have an increase in pressure in your lungs,
Speaker 3: that causes a backup of pressure onto the right side
Speaker 3: of your heart, which can cause right sided heart.
Speaker 2: Failure, which is called core pullman Al.
Speaker 1: Okay, so does worm burden my favorite phrase, relate to
Speaker 1: these symptoms or the increase of you know, risks for
Speaker 1: bladder cancer and HIV.
Speaker 3: Absolutely it does because we are talking about eggs.
Speaker 2: So the more as you.
Speaker 3: Have in your body, the more symptoms that you're going
Speaker 3: to have, and the more inflammation that you're going to have.
Speaker 3: So the more warm pairs that you have, the more
Speaker 3: eggs are going to be releasing.
Speaker 2: Absolutely.
Speaker 1: What is the average worm burden in endemic areas?
Speaker 2: That's such a good question. I don't know. I'm going
Speaker 2: to look it up. Okay, that's a really important question.
Speaker 2: It's high. I know that.
Speaker 3: But the other place that this can also affect is
Speaker 3: your nervous system.
Speaker 1: I was wondering, does it go into your brain?
Speaker 3: Yeah, it can cross your blood brain barrier potentially, these
Speaker 3: eggs because they have enzymes that let them like break
Speaker 3: down barriers. Right, That's how it makes its way into
Speaker 3: your bowels. So it can break its way into your
Speaker 3: central nervous system and cause neuros. Just a semiasis which
Speaker 3: can cause seizures other neurodegenerative type symptoms. Yeah, it's gnarly.
Speaker 3: That's just a semiosis.
Speaker 1: Wow, that's a very complicated story.
Speaker 2: Super super complicated.
Speaker 1: And a lot of bad manifestations.
Speaker 2: Yeah, it's a really nice disease. Yeah, what the heck, Aaron,
Speaker 2: what the heck?
Speaker 3: Where did this thing come from? How did it get here?
Speaker 3: And why did it take us for forty five minutes
Speaker 3: to talk about?
Speaker 1: Oh? Good god, Well, let's dive into the very long
Speaker 1: history of shisto right after this break awesome. After hearing
Speaker 1: about the biology, I'm even more excited to talk about
Speaker 1: the history because the history has all the fun things.
Speaker 1: It's got mummies, imperialism, a little bit of climate change, phylogenies,
Speaker 1: it's got everything.
Speaker 3: That's everything you could ask for in an episode of TPWKY.
Speaker 1: Right. Okay, so you asked how did we get here?
Speaker 1: But I want to change that question a little bit
Speaker 1: by asking and hopefully answering, how did we get from
Speaker 1: there to hear? But first, what is there? Basically, where
Speaker 1: did shistisomes come from? And how did some of them
Speaker 1: become parasites of humans? So you mentioned that shistisms are
Speaker 1: a super diverse group. There is about one hundred species,
Speaker 1: and the majority of those actually infect birds and don't
Speaker 1: have anything to do with mammals. But of the ones
Speaker 1: that infect mammals, which is around twenty three species, seven
Speaker 1: of those infect humans regularly. With the three that you
Speaker 1: mentioned being the biggest causes of disease, Okay, but the
Speaker 1: rest of them infect like tons of species of mammals
Speaker 1: like rodents, ungulates, et cetera. And some of the ones
Speaker 1: that infect humans vary in their specificity to humans. So,
Speaker 1: for instance, just to so much japonicum, is that how
Speaker 1: you've been saying it, I I don't know. Just to
Speaker 1: so much Japonicum, which has an Asian origin, can infect
Speaker 1: a wide range of mammals, which suggests that maybe only
Speaker 1: recently on an evolutionary timescale, started infecting humans. But others,
Speaker 1: which may have originated in Africa, that's sort of an asterisk.
Speaker 1: We don't really know. I'll talk about it. They seem
Speaker 1: much more human specific and are even associated with human
Speaker 1: behavior that may enhance the possibility of transmission. So like
Speaker 1: peak infectivity coincides with the time of day and the
Speaker 1: time of year that bathing is most frequent in endemic areas.
Speaker 1: Answering the question where did shistisomes come from was a
Speaker 1: little bit more difficult than I expected, because it turns
Speaker 1: out it doesn't seem entirely clear. Did they originate in
Speaker 1: Asia or in Africa? Don't really know, we can definitely
Speaker 1: rule out the America's, Australia, Antarctica. I'm glad you know,
Speaker 1: because there isn't any fossil evidence of schistosomes. Researchers have
Speaker 1: relied on a few other tools to try to trace
Speaker 1: the origins of the mammal infecting schistosomes. So you know,
Speaker 1: you can do the genomic approach where you compare different
Speaker 1: genomes of different species to estimate when they diverged or
Speaker 1: split from one another. And also you could use the
Speaker 1: evolutionary history of snail hosts or mammal hosts to estimate
Speaker 1: a timeline and geography of their history, which is really cool,
Speaker 1: and so for a long time people most people seem
Speaker 1: to believe that an African origin of the parasites was
Speaker 1: the most likely, but recent research puts the origin in
Speaker 1: what is now northern India, and then they suggest that
Speaker 1: from there sistosomes first spread east to central and Eastern
Speaker 1: Asia and then later spread west to Africa, where they
Speaker 1: more recently diversified into the more human specific species just A.
Speaker 1: Soma mansoni and shsto Soma humatobium. That divergence occurred as
Speaker 1: much as four million years ago. Or as recently as
Speaker 1: three hundred thousand years ago, but again it's not entirely clear.
Speaker 2: We don't know.
Speaker 1: Yeah, but what's cool about this evolutionary history of sistosome's
Speaker 1: is that the evolution of a couple of species seems
Speaker 1: to coincide pretty well with human evolution when early humans
Speaker 1: or the ancestors of modern humans started spreading out all
Speaker 1: across the savannah essentially, so regardless of where shistosmes as
Speaker 1: a group originated exactly, there was probably a longer association
Speaker 1: between humans and some of the parasites in Africa, which
Speaker 1: led to the specialization of Shistosoma humanatobium and Shistosoma mansoni
Speaker 1: in Africa, and that's where they tend to be the most.
Speaker 1: That's where you find the highest burdens typically.
Speaker 2: So I was pronouncing that one wrong too, huh which one? Mansoni?
Speaker 1: I don't know. I just said, Manson.
Speaker 2: What did you say, Manson?
Speaker 1: I manson? I I honestly, I mean your guess is
Speaker 1: as good as mine.
Speaker 2: People must hate me, I think.
Speaker 1: No, people must hate our pronunciations. Yeah, Mansona Mansoni, I
Speaker 1: don't know.
Speaker 3: I like Mansoni sounds more better.
Speaker 1: But this is just how I was reading it in
Speaker 1: my head. So yeah, I don't know, are you ready
Speaker 1: to talk? Ancient Egypt always erin, I live for it.
Speaker 1: For hundreds of thousands of years, humans and schistosomes coexisted,
Speaker 1: I guess, in relative peace, or as much relative peace
Speaker 1: as there could be. But that changed when humans began
Speaker 1: to settle in large communities and practice agriculture and domesticate
Speaker 1: animals for livestock. What's one of the things that is
Speaker 1: crucial for humans their livestock and their crops water? Ah huh, Yes, exactly.
Speaker 1: And so when humans settled, they pretty much always chose
Speaker 1: a place where they could reliably get fresh water. Makes sense, Yeah,
Speaker 1: And as the Sahara Desert got drier and drier, humans
Speaker 1: in North Africa began to seek more hospitable lands, and
Speaker 1: the Nile Valley was a pretty ideal place to form
Speaker 1: large sedentary communities. And so around eight thousand years ago
Speaker 1: when we see these earliest settlements, and just a few
Speaker 1: thousand years after that, these communities had developed extensive irrigation
Speaker 1: systems and canals to provide water for crops, which is
Speaker 1: pretty amazing the technology that they developed that was handed
Speaker 1: to them by ancient aliens just kidding. Probably according to
Speaker 1: the History Channel, a lot of people had extensive contact
Speaker 1: with water, probably every day. They used it for swimming,
Speaker 1: for bathing, sailing, fishing, and some trades like brickmaking that
Speaker 1: required a water source. And what else needs water, of course,
Speaker 1: snails and schistosomes, and so these activities, combined with the
Speaker 1: lack of sanitation, perfectly set the stage for the proliferation
Speaker 1: of snails and of course the schistosomes themselves, and we
Speaker 1: see physical evidence for this in mummies from.
Speaker 2: The time mummies mummies.
Speaker 1: The earliest known case of schistosomiasis actually appears in a
Speaker 1: mummy from modern day in northern Syria dating back to
Speaker 1: around four thousand BCE. Wow, which is incredible. But schistosome
Speaker 1: infections in ancient Egyptian mummies follow not that far behind,
Speaker 1: and so the first retrospective diagnosis of a disease in
Speaker 1: human remains thousands of years old happened around nineteen ten,
Speaker 1: and it was a case of shistasimiasis in a three
Speaker 1: thousand year old Egyptian mummy.
Speaker 2: In nineteen ten. In nineteen two sit. Wow.
Speaker 1: Yeah, So that's that's when paleo epidemiology got its start essentially.
Speaker 3: Wow.
Speaker 1: And so paleo epidemiological studies of mummies from the area
Speaker 1: on the border of Sudan and Egypt shows a sixty
Speaker 1: five percent prevalence of Schistoh.
Speaker 2: Right, everyone had it.
Speaker 1: Every everyone had it. Wow, I mean, hearing about the biology,
Speaker 1: I'm like, well, how is that not one hundred percent?
Speaker 3: Yeah, it's true. We can talk about it.
Speaker 1: Actually, ooh, this is a fun episode, okay. Is the
Speaker 1: finding of fossilized snails that are the host species in
Speaker 1: these areas and beyond, like into Mesopotamia and Palestine also
Speaker 1: suggests that the disease was there as well. What about
Speaker 1: any physical evidence in Eastern Asia? Yeah, so shistosome eggs
Speaker 1: of Shistosoma japonicum were found in a preserved corpse in
Speaker 1: China dating to twenty one hundred BCE. So again, very old,
Speaker 1: long time ago. And so we have Yeah, we've got
Speaker 1: this this physical evidence of schistosomes infecting humans going back
Speaker 1: thousands and thousands of years. So what's in the written record. Yeah,
Speaker 1: let's start with ancient Egypt. Okay, So I have to
Speaker 1: because I say ancient Egypt, I have to mention the Yeah,
Speaker 1: so in the ebslavirus, there's a description of a disease
Speaker 1: that I actually mentioned in the hookworm episode called like
Speaker 1: AAA disease like the letter A three times. I don't know.
Speaker 2: Ah uh huh.
Speaker 1: And so Egyptologists for a long time had thought this
Speaker 1: was likely referring to schistosomiasis, since it seemed to have
Speaker 1: something to do with blood and urine, and it's said
Speaker 1: to avoid polluted water to prevent infection.
Speaker 2: That's so amazing.
Speaker 1: Well this this interpretation has been disputed more recently. Okay, okay,
Speaker 1: moving on, okay, So Herodotus observed that Egypt is the
Speaker 1: land where men men straight, which people have taken to
Speaker 1: mean hematuria, which is caused by schistosoma hematobium. Penile sheaths,
Speaker 1: so like protective sheaths for penises.
Speaker 2: Like a condom kind of essentially. Okay.
Speaker 1: These appear in early writings and illustrations in ancient Egypt,
Speaker 1: and people have suggested that they were used as a
Speaker 1: preventative against schisto since it was thought that the disease
Speaker 1: could enter the body through the penis. That's too bad, yeah,
Speaker 1: but this interpretation has also been called called into question. Anyway,
Speaker 1: and finally, The last bit of evidence that has been
Speaker 1: called into question is that circumcision, which is apparently of
Speaker 1: Egyptian origin. I didn't know that.
Speaker 2: I didn't know that either.
Speaker 1: Yeah, that circumcision was advocated as a way to prevent infection,
Speaker 1: possibly of schistosimiasis.
Speaker 2: That's really interesting though.
Speaker 1: Yeah. So there's a relief like a picture from an
Speaker 1: Egyptian tomb from like twenty four hundred BCE that shows
Speaker 1: someone performing circumcisions with the caption I will do you good.
Speaker 1: But that also has been challenged. Okay, Okay, So basically
Speaker 1: in ancient Egypt, there are a lot of possible references
Speaker 1: to shista simiasis, but nothing that's absolutely accepted across the board. Okay,
Speaker 1: except for the fact that it's in mummies like that
Speaker 1: we know for sure, so you.
Speaker 2: Know it was there, But writing wise, we don't know what.
Speaker 1: They're talking about exactly. Okay, Now on to the Bible. Oh,
Speaker 1: does Jericho ring a bell?
Speaker 2: Like for sure a song about it? Yeah?
Speaker 1: Huh, exactly.
Speaker 2: Yeah.
Speaker 1: So Jericho was an old walled city, like one of
Speaker 1: the oldest in the world, eleven thousand years old maybe.
Speaker 2: Wow.
Speaker 1: In one passage of the Bible, Joshua was ordered to
Speaker 1: kill everyone in the city and then destroy the city itself.
Speaker 1: It ended with him cursing the city with low fertility,
Speaker 1: which was thought to be caused by infected well water.
Speaker 1: And so a lot of people have said that this
Speaker 1: legend or belief for this story could refer to the
Speaker 1: fact that shistosomi humantobium may obstruct fallopian tubes.
Speaker 2: YEP and seminal tubes as well.
Speaker 3: Yeah.
Speaker 1: Yeah, And so the city was abandoned after its destruction
Speaker 1: and then and there's actually archaeological evidence to support its abandonment.
Speaker 1: The curse on the town was removed when Elisha went
Speaker 1: forth onto the spring of the waters and cast the
Speaker 1: salt in there. There shall not be from thence any
Speaker 1: more death and barren land. And so they're saying, oh,
Speaker 1: if you throw the salt in there, you'll kill all
Speaker 1: the snails, and then she will. But also, I feel like,
Speaker 1: if you salt.
Speaker 2: Your drinking water, it's not it's not gonna be good
Speaker 2: for you.
Speaker 1: It'll be good. Yeah, all right, I promise. I'm almost
Speaker 1: done with the ancient section. So we got to move
Speaker 1: on to ancient China though, So you mentioned Katayama disease
Speaker 1: and symptoms resembling this can be found in old Chinese
Speaker 1: medicine writings dating back to around four hundred BCE. So
Speaker 1: that's all I got for that. But basically, all of
Speaker 1: these little bits of evidence here and there suggest that
Speaker 1: schistosomiasis was widespread and probably pretty dang prevalent across much
Speaker 1: of the tropical and subtropical Old World.
Speaker 2: Makes sense.
Speaker 1: The New World seems to have been shisto free until
Speaker 1: the slave trade began in the sixteenth century, when Schistosoma
Speaker 1: mansoni was brought over, and so that species was able
Speaker 1: to establish where indigenous snail hosts could maintain the parasite's
Speaker 1: life cycle, so like Brazil surname Venezuela and some Caribbean islands.
Speaker 1: All right, So now we're caught up on the origins
Speaker 1: of schistosome's and the evidence for human infection and antiquity.
Speaker 1: But when did people discover the parasite like that first
Speaker 1: hand account, Well, there are descriptions of a disease resembling
Speaker 1: some of the manifestations of schistosomiasis in Italy in the
Speaker 1: sixteenth century, but no one really took much note of that,
Speaker 1: and it wasn't really until Napoleon's army invaded Egypt in
Speaker 1: seventeen ninety eight that a French physician with the army
Speaker 1: noted how men in Egypt menstruate and how many of
Speaker 1: the French troops also had blood in their urine and
Speaker 1: pain in their bladder. And then about fifty years later,
Speaker 1: researchers on two separate continents began to take a closer
Speaker 1: look at this disease. In Japan, in eighteen forty seven,
Speaker 1: a researcher named doctor yoshinow Fuji described what he assumed
Speaker 1: was a new disease. So quote, during the past two
Speaker 1: or three years, farmers have had small eruptions on their
Speaker 1: legs when they entered the water to cultivate the rice field.
Speaker 1: The eruptions are unendurably painful and itchy. Cows and horses
Speaker 1: also show the same symptoms. Most of the residents suffer
Speaker 1: from this disease.
Speaker 2: So that's sounds like shisto.
Speaker 1: Sounds like shisto, the acute shisto at least, right. And
Speaker 1: so one of the counties that was heavily affected by
Speaker 1: this disease was Katayama, which is what gave the disease
Speaker 1: its name. In Japan, to indicate a new and with schistosomes.
Speaker 1: It would be decades though, before the parasite causing this
Speaker 1: Katayama disease was discovered in Japan. In eighteen fifty one,
Speaker 1: a guy named Theodore bill Ar's teddy Bet, was working
Speaker 1: as an assistant professor at a hospital in Cairo when
Speaker 1: he observed this trematode in the portal vein of a
Speaker 1: young guy. And so this is what was in the
Speaker 1: first hand account. But he thought that this might have
Speaker 1: something to do with both the bloody urine and also dysentery,
Speaker 1: both of which were common throughout Egypt. And this is
Speaker 1: what actually got the attention of a lot of people,
Speaker 1: his descriptions and his suggestion of a link between those
Speaker 1: diseases and the parasite itself. This is like in eighteen
Speaker 1: fifty one, Yeah, eighteen fifties, and people started trying to
Speaker 1: figure out the transmission cycle of this parasite, but were thwarted,
Speaker 1: partly because Billar's didn't realize that the morphological differences he
Speaker 1: was seeing in the worms were because they were different species,
Speaker 1: and partly because another leading researcher was adamant that there
Speaker 1: was no intermediate host for the parasite.
Speaker 2: Why would you be so adamant about that?
Speaker 1: Part of it was like, I think hookworm and other
Speaker 1: worms that showed Yeah, I know, but he was very
Speaker 1: I had a lot of conviction, which is a dangerous
Speaker 1: thing in science when you close your mind off. During
Speaker 1: the sixty years following Billar's discovery, many researchers tried to
Speaker 1: pick apart the puzzle of this parasite, including its transmission cycle,
Speaker 1: how it entered the body, and the question of how
Speaker 1: many species were actually present infecting humans. And this was
Speaker 1: a pretty feared disease by colonists who had moved to
Speaker 1: affected regions, so British troops stationed in Egypt and the
Speaker 1: early nineteen hundreds were told to wear a con while
Speaker 1: bathing so as not to get infected. It's not going
Speaker 1: to help you.
Speaker 2: I don't do anything, but no.
Speaker 1: Eventually, in nineteen fifteen, a researcher named Robert Leiper showed
Speaker 1: experimentally that snails are the intermediate host of schistosomes, and
Speaker 1: also showed how the adult worms mature in mammals.
Speaker 3: To be fair like, it's amazing that people figured that
Speaker 3: out because it is such a complicated life cycle.
Speaker 1: It's incredibly complicated.
Speaker 3: Like as much as it seems wild to say to
Speaker 3: be adamant that there is no intermediate host, it's also
Speaker 3: wild that they figured out what the intermediate host was
Speaker 3: and just how like they just figured out this complex
Speaker 3: life cycle oh so long ago, Like that's it's really incredible.
Speaker 1: Absolutely. I mean yeah, you'd think, like, why why would
Speaker 1: you look at snail? Like what would lead you to
Speaker 1: look at snails? Yeah, for instance, So yeah, it is,
Speaker 1: it is cool. So then yeah, so nineteen fifteen was
Speaker 1: pretty much when like, okay, we can finally get to
Speaker 1: the nitty gritty of all the different stages of the
Speaker 1: parasite and uh and look, take a closer look at
Speaker 1: the intermediate hosts. Bill Ar's, though, unfortunately, wouldn't live to
Speaker 1: see the life cycle figured out, because he died only
Speaker 1: like eleven years after his discovery of the worms of
Speaker 1: typhoid fever.
Speaker 2: At least it wasn't shisto. I thought it was going
Speaker 2: to be shisto.
Speaker 1: I wonder if he had shisto.
Speaker 2: Probably, Oh that's sad though.
Speaker 1: Oh I have a quick question. Can you get shisto
Speaker 1: from ingesting contaminated water?
Speaker 2: Good question, Not as far as I know.
Speaker 1: Okay, it's just through contact.
Speaker 3: Yeah, okay, yeah, okay, because it wouldn't Yeah yeah, I
Speaker 3: mean I not as far as I know.
Speaker 1: Okay. So bill Ar's work I think is actually pretty
Speaker 1: impressive that he was making a connection between a microscopic
Speaker 1: parasite and disease symptoms before germ theory was really a thing,
Speaker 1: which is pretty cool. And his significant contributions to the
Speaker 1: study of schistosomes is why schistisimiasis was also called belarcia
Speaker 1: or blarsiasis.
Speaker 2: But that's what that's common harder to say, isn't.
Speaker 1: Much harder at least for us. Yeah, and actually it
Speaker 1: is still called bilarcia in many parts of the world.
Speaker 1: But schistosome was proposed first from the Greek words for
Speaker 1: divided and body. But other names of the disease include
Speaker 1: redwater fever, snail fever, and big belly, big belly.
Speaker 2: That's from the asides.
Speaker 1: Yeah. While the debates for the parasites transmission and life
Speaker 1: cycle were going on, the parasites themselves were experiencing a
Speaker 1: huge growth in prevalence, especially in Egypt. Instead of basin
Speaker 1: or surface irrigation during so that's when the land is
Speaker 1: flooded to soak the crops, and that's an old method
Speaker 1: of irrigation and allowed for one crop harvest along the Nile.
Speaker 1: But then perennial irrigation was introduced in Egypt and that
Speaker 1: allowed for water to be flowing year round, which was
Speaker 1: great news for cotton, which became the country's primary export,
Speaker 1: but it also meant tortuous working conditions and a steady
Speaker 1: source of snail and human hosts for schistosomes. Studies looking
Speaker 1: at how this new irrigation method increases to Semias's prevalence
Speaker 1: estimate anywhere from a tenfold increase to a growth from
Speaker 1: one to three percent prevalence to seventy five to eighty
Speaker 1: percent prevalence. So it just like exploded in terms of prevalence.
Speaker 1: Oh yeah, the enormous growth of interest in justtosomes in
Speaker 1: the late eighteen hundreds and through World War Two didn't
Speaker 1: just happen in a vacuum. Wasn't just driven by curiosity
Speaker 1: In the case of shistosomes. The motive to understand the
Speaker 1: disease was essentially imperialism.
Speaker 2: As it often is.
Speaker 1: As it often is, Yeah, tropical medicine as a field
Speaker 1: essentially began so that the tropical regions of the world
Speaker 1: could be made suitable for white people to inhabit and
Speaker 1: invest in empire building essentially, like the search for malaria
Speaker 1: transmission treatment and yellow fever prevention are two perfect examples
Speaker 1: of this that we've talked about on those episodes. Yeah,
Speaker 1: and so there's even a line in a scientific article
Speaker 1: in the British Medical Journal from eighteen ninety seven that says, quote,
Speaker 1: get rid of or avoid these disease germs, and we
Speaker 1: get rid of a principal obstacle to the colonization of
Speaker 1: the tropics by Europeans.
Speaker 2: Wow, just straight up.
Speaker 1: Uh huh, just wow.
Speaker 2: There's so much anger brewing in.
Speaker 1: Me, you know, I think it's Yeah, the good news
Speaker 1: is that today we have a lot of studies of
Speaker 1: neglected tropical diseases that are motivated not by colonization but
Speaker 1: by wanting to make the world a better place, or
Speaker 1: at least that's what the researchers.
Speaker 2: Does that do. Is that why there is no funding
Speaker 2: for it? Though exactly so.
Speaker 1: The researchers who are working on it, they want to
Speaker 1: make the world a better place. The funding agencies don't know. Oh.
Speaker 1: But also random piece of Trivia here. The first graduate
Speaker 1: school of parasitology in the US was established at the
Speaker 1: University of Illinois in nineteen oh nine.
Speaker 2: I didn't know that.
Speaker 1: Yeah, there's no longer a school of graduate school of parasitolic.
Speaker 3: There's not a ton of There's some you know, some
Speaker 3: of us here, but not a lot of people studying
Speaker 3: parasites anymore. It seems like comparatively.
Speaker 1: Comparatively, Yeah, So the Boer War in South Africa, many
Speaker 1: British troops were stationed there and they became infected and
Speaker 1: incapacitated by shisto. And the presence of British troops in
Speaker 1: Egypt during the late eighteen hundreds and early nineteen hundreds,
Speaker 1: these directly led to the discoveries that I talked about.
Speaker 1: This is why people had such a vested interest in
Speaker 1: figuring out what was going on with the parasites life cycle,
Speaker 1: socalism and war imperalism in war. So, increasing efficiency and
Speaker 1: control in the Egypt meant reducing the prevalence of schistosome's,
Speaker 1: but primarily by reducing it in British troops. So, once
Speaker 1: Leper made the link between the snail and the schistosome,
Speaker 1: he proposed that if you control the snail, you control
Speaker 1: the schistosome, and he recommended drying out the canals for
Speaker 1: a bit every year to kill the snails. This method
Speaker 1: of control doesn't actually work all that well, since all
Speaker 1: you would need is a few snails to keep pumping
Speaker 1: out millions of parasites.
Speaker 2: Personnail per day from one like.
Speaker 3: It's yeah, uh huh, Yeah, it's such a harder thing
Speaker 3: to try and do to control the snails.
Speaker 1: Yep, But that was the primary control strategy for decades
Speaker 1: and is still i think a practice in some places.
Speaker 3: I mean, it's still i think an important component of
Speaker 3: everything it is. It's definitely not going to be the
Speaker 3: only thing going to yeah yeah.
Speaker 1: And this aiming just for the snails kind of shows
Speaker 1: again how early tropical medicine was concerned only with the
Speaker 1: parasites or pathogens themselves, without considering how cultural or behavioral
Speaker 1: practices may have an impact on disease transmission. Water filtration
Speaker 1: was also proposed, but this was limited to British troops.
Speaker 1: It could because setting up infrastructure to get clean water
Speaker 1: going everywhere was way too expensive in their minds, So
Speaker 1: let's just focus on the important people and It also
Speaker 1: might have been that the discovery of an effective treatment
Speaker 1: for schistosmiasis discouraged any infrastructural changes to prevent the disease.
Speaker 1: In nineteen eighteen, antimony tart rate so tartar emetic, was
Speaker 1: found to be relatively successful in treating shisto, which is
Speaker 1: around seventy percent cured. But it was also a poison
Speaker 1: so you had to be careful you didn't die, and
Speaker 1: the doses given to infected people were extreme. They also
Speaker 1: had to be given out over a period of like
Speaker 1: thirty days, so you had to return to a clinic
Speaker 1: every few days, and as you can imagine, the proportion
Speaker 1: of people who actually completed the course of treatment pretty
Speaker 1: low because a day of going to the clinic meant
Speaker 1: a day of lost wages and you know, also potential poisoning.
Speaker 1: And that's something that like, so it's still so very
Speaker 1: relevant today in terms of like reducing the barriers for
Speaker 1: treatment or for just healthcare overall. Is like, let's not
Speaker 1: make it a decision between making the money that you
Speaker 1: need to live and you know, having good health anyway,
Speaker 1: So researchers then were like, okay, well, we need an
Speaker 1: easier solution for reducing the parasite, and so that's one
Speaker 1: of the reasons why snail killing continued at such a
Speaker 1: large scale. And you know, the first large scale efforts
Speaker 1: to reduce snails throughout Egypt did seem to offer at
Speaker 1: least a short term reduction in snail populations, and it
Speaker 1: was striking enough that in nineteen thirty nine it was
Speaker 1: declared that just a samiasis could be eliminated from Egypt
Speaker 1: in twenty five years by clearing the canals.
Speaker 3: I'm sorry, this was in wet year nineteen thirty nine,
Speaker 3: twenty five years years.
Speaker 1: That did not happen, not at all. Many of the
Speaker 1: public health directors in these tropical countries that were overseen
Speaker 1: by European imperialist countries, these were aimed towards controlling infectious disease,
Speaker 1: either through infrastructure improvements limited to citizens of whatever European country,
Speaker 1: or through widespread treatment campaigns. But it became obvious that
Speaker 1: neither of these tactics would result in a lasting improvement
Speaker 1: in actual public health. So gradually sanitation campaigns and improved
Speaker 1: living and working conditions were put in place. But this
Speaker 1: wasn't motivated just by like, oh, we want to make
Speaker 1: the world a better place. Again, the ruling countries simply
Speaker 1: realized that a healthy workforce is more efficient and productive,
Speaker 1: and that's where a lot of the effort ended was
Speaker 1: as long as you got them well enough to work,
Speaker 1: then you leave, you drop it all. Often the medical
Speaker 1: officer of like a mine, for instance, was seen as
Speaker 1: almost this missionary savior of the quote savage or uncivilized natives,
Speaker 1: pulling them out of the filth and disease to which
Speaker 1: they had been accustomed. But in reality, the prevalence of
Speaker 1: many of these diseases in tropical countries increased tremendously during
Speaker 1: imperialist rule. Of course, I mean scurvy accounted. I'm getting
Speaker 1: a little bit outside of schisto, but for example, scurvy
Speaker 1: accounted for thirteen and a half percent of all deaths
Speaker 1: in a mine in what is now Zimbabwe in nineteen
Speaker 1: oh eight. Scurvy like which we talked about and which
Speaker 1: you know could have been prevented, tuberculosis, pneumonia, silicosis, and
Speaker 1: of course just to semiasis became huge problems in these minds,
Speaker 1: among other diseases. And it wasn't just that crowded and
Speaker 1: unsanitary conditions promoted the spread of schistosimiasis. It was also
Speaker 1: the nature of the work itself. Sugar plantations and cotton
Speaker 1: growing both meant exposure to contaminated water, and prevalences reached
Speaker 1: above fifty percent in many places, but the link between
Speaker 1: these conditions and disease wasn't really recognized, at least publicly,
Speaker 1: but instead the sentiment was much more that the indigenous
Speaker 1: populations were acting as a disease reservoir, putting the white
Speaker 1: colonists in harm's way. And you can see this come
Speaker 1: through in the way that shistosomiasis is discussed in some
Speaker 1: of the public health reports in South Africa in the
Speaker 1: early nineteen hundreds, schistosimiasis quote seems well under control among Europeans,
Speaker 1: though of course the natives are commonly infected end quote,
Speaker 1: and attacking the disease quote might help to free the
Speaker 1: country of infection and enable us to bathe safely. H
Speaker 1: Throughout the nineteen thirties, the focus on tropical medicine declined
Speaker 1: in the two main empire builders, so Britain and the US,
Speaker 1: But then World War II broke out, which meant that
Speaker 1: those Europeans or American station in the tropical war zones
Speaker 1: would face the scourge of the diseases there. In terms
Speaker 1: of numbers, things like malaria and STIs far outweighed shisto
Speaker 1: infections in American troops. But one campaign in the Philippines
Speaker 1: saw an explosion of shisto cases. Medical researchers kind of
Speaker 1: like leapt on this outbreak and the funding that was
Speaker 1: provided for it to conduct research into shisto, the stages
Speaker 1: of disease like acute versus chronic, and treatment strategies, And
Speaker 1: this came at a pretty key time in the history
Speaker 1: of tropical medicine, which was a few that was almost
Speaker 1: dying around the same time as imperialism was on the
Speaker 1: decline decline. So remember that that nineteen thirty nine prediction
Speaker 1: that schistos mayass could be eradicated within twenty five years. Yeah, well,
Speaker 1: the snail population did seem to be declining, but the
Speaker 1: shisto no. A bunch of kids born after the eradication
Speaker 1: campaign began were screened for the parasite and the prevalence
Speaker 1: of the parasite was found to be sixty three percent,
Speaker 1: incredibly high, and in other more rural villages that number
Speaker 1: was over ninety five percent. Wow, So obviously something was wrong.
Speaker 1: The eradication campaign recognized this and changed their name from
Speaker 1: the Blarzia snail Destruction Section to the Bilarzia snail Control Section.
Speaker 2: Also, snail destruction section is a name.
Speaker 3: Ostractions meeting them like at a bar after work, like, oh,
Speaker 3: what do you do? Oh?
Speaker 2: I just work for the snail destruction section.
Speaker 1: I want that on my business card, mean too, like
Speaker 1: an embroidery on a zipper jacket. Yeah. They the people
Speaker 1: working in these destruction and control sections, They couldn't answer
Speaker 1: how low the infection prevalence had to be in snails
Speaker 1: in order to break the cycle of transmission in humans.
Speaker 1: So how could they even direct the campaign effectively?
Speaker 3: Cannot?
Speaker 1: Cannot. Meanwhile, Egypt was not the only country dealing with
Speaker 1: incredibly high prevalences of schistosimiasis. China faced a similar situation,
Speaker 1: and a mass campaign against the disease was started by
Speaker 1: the Nine Man just A Semias's Subcommittee, which are like
Speaker 1: the best names for these the nine Subcommittee UH. Starting
Speaker 1: in nineteen fifty eight, this set up prevention and treatment
Speaker 1: units across the country, as well as research institutes to
Speaker 1: study the parasite. Treatment regimens were shortened to just a
Speaker 1: few days, but it seems that the majority of the
Speaker 1: campaign's efforts were concentrated in reducing the snail host. Latrines
Speaker 1: were repaired, swamp land drained, snails buried, grass burned, and
Speaker 1: chemicals applied. Within a year or two, several counties were
Speaker 1: announcing that they had eradicated just asimiasis excellent. Mao Zidong
Speaker 1: wrote a poem called Farewell to the God of Plague
Speaker 1: in response to this news, and you can go read
Speaker 1: the poem in a book that I'll mention, but anyway,
Speaker 1: you can probably find it online. Anyway, the campaign against
Speaker 1: just a Semiasis seemed to be incredibly successful, if you
Speaker 1: believe the claims about the progress made. But was shisto
Speaker 1: actually eradicated in these counties. Probably not, but it does
Speaker 1: seem that substantial progress had been made in the prevalence
Speaker 1: of infection. Obviously, you know, I'm sure you'll talk about
Speaker 1: what the prevalence is today. But one of the main problems,
Speaker 1: and maybe something that's affecting the parasite today, is that
Speaker 1: other mammals, especially cattle, were the main source of schistosome
Speaker 1: eggs in the environment. And as far as I read,
Speaker 1: cattle themselves were not a target for treatment. So in
Speaker 1: the decades following World War Two, interest in schistosomias's grew
Speaker 1: for a number of reasons. One was the fear that
Speaker 1: soldiers returning back to the US or Britain would carry
Speaker 1: with them the parasites that could establish in native snail populations.
Speaker 1: Another was the fear of a looming food crisis. If
Speaker 1: enough food was going to be produced globally, people in
Speaker 1: the most productive agricultural regions had to be healthy enough
Speaker 1: to work. But irrigation and dams had only led to
Speaker 1: an increase in schistosomias's prevalence. For example, in Ghana, in
Speaker 1: nineteen sixty five, a lake was created after damning a river.
Speaker 1: Within a year, the snail host of Shistosoma heematobium had appeared,
Speaker 1: and two years after that the prevalence of schistosomiasis was
Speaker 1: fifty percent in the population living around the lake.
Speaker 2: Yeah, damser damns are not great for shisto shisto.
Speaker 1: So so. Another reason for this increased interest was simply
Speaker 1: the increase in cases. In nineteen fifty one, shistasmiasis had
Speaker 1: been declared next in importance to malaria among the world's
Speaker 1: tropical diseases.
Speaker 2: I think it remains.
Speaker 1: I think it does. Yeah, which has been sort of
Speaker 1: contended in terms of is it truly the second most important?
Speaker 2: But I think we'll talk about it.
Speaker 1: Yeah, okay. But the control programs kind of went like this, first,
Speaker 1: kill the snails. Oh, that didn't work. All right, Well,
Speaker 1: let's try treating people. Oh, that didn't work either, because peop,
Speaker 1: we can't afford to miss a ton of work to
Speaker 1: go get a shot. And also side notes, so this is,
Speaker 1: you know, making another connection with the hepatitis C episode.
Speaker 1: These tartar emetic campaigns in Egypt throughout the nineteen fifties
Speaker 1: through the nineteen eighties. These were like huge campaigns to
Speaker 1: get the treatment for sistsymiasis. They tended to reuse needles
Speaker 1: to save money, and this led to a massive spread
Speaker 1: of HEPC, which is only discovered decades later. I think
Speaker 1: even now Egypt has one of the highest prevalences of
Speaker 1: heptitis C.
Speaker 2: Oh wow, perfections.
Speaker 1: Yeah, huh, So, how do we improve the treatments or
Speaker 1: maybe we do a combination of treatment and molluscicides. But
Speaker 1: so far, it doesn't really seem like any of these
Speaker 1: strategies have been super successful. If the hundreds of millions
Speaker 1: of infections today is any indication, I'm sure you'll talk
Speaker 1: about it.
Speaker 3: M hmm.
Speaker 1: Okay, a wrap up now, But I want to say
Speaker 1: that before researching this episode, I hadn't really considered how
Speaker 1: a possible negative consequence of germ theory was that people
Speaker 1: kind of stopped considering the social aspects of diseases. So
Speaker 1: there was a pathogen or a parasite or a vector,
Speaker 1: and so the research concentrated more on understanding or controlling
Speaker 1: or treating those aspects rather than the underlying causes contributing
Speaker 1: to not just one specific disease, but a whole suite
Speaker 1: of them. So like before it was recognized that tuberculosis
Speaker 1: was caused by a bacterium, it was known that like
Speaker 1: crowded conditions and this and that, and so instead of
Speaker 1: focusing on treating the disease itself, let's treat some of
Speaker 1: the underlying issues associated with its spread or establishment. So
Speaker 1: it's kind of that part is I mean, obviously germ
Speaker 1: theory was hugely important, but it is interesting how these
Speaker 1: social aspects were neglected. Building that knowledge of the pathogen
Speaker 1: and parasite biology and treatments is obviously hugely important, but
Speaker 1: it does seem to have come at a cost to
Speaker 1: social medicine. So like how social factors contribute to disease,
Speaker 1: especially for these neglected tropical diseases, And these were researched
Speaker 1: and described by Western scientists through their lens, and the
Speaker 1: vast majority of those doing the research did not have
Speaker 1: any knowledge of local customs, knowledge or beliefs, which may
Speaker 1: have given them not only a more full picture of
Speaker 1: the disease they were studying, but also clues to its control.
Speaker 1: And I'm primarily referring to schistosoma in Africa when talking
Speaker 1: about this, and then later in South America and so
Speaker 1: over the past few decades there has been a push
Speaker 1: towards social medicine and constructing a fuller picture of these
Speaker 1: diseases which are so multifaceted. But the disproportionate disease burden
Speaker 1: around the globe definitely shows that there is still so
Speaker 1: much work to be done, plus the looming specter of
Speaker 1: climate change because I had to sneak it in there. Yeah,
Speaker 1: it means that the distribution and prevalence of shistosomiasis will
Speaker 1: likely change in ways that are going to be difficult
Speaker 1: to predict. Since the African continent has the vast majority
Speaker 1: of schistosomiasis infections and is one of the most vulnerable
Speaker 1: regions for climate change and climate instability, there's a big
Speaker 1: push for predictive modeling for what the disease is going
Speaker 1: to look like. But that's the future and there's still
Speaker 1: a whole lot of work that needs to be done.
Speaker 1: So I'm ready to hear about what's going on with
Speaker 1: shisto in the world today.
Speaker 3: I'm ready to tell you right after this break. So
Speaker 3: it's just a semiasis today. The World Health Organization considers it,
Speaker 3: of course, a neglected tropical disease, which we've talked about
Speaker 3: a number of these in the past. It is estimated
Speaker 3: that globally, nearly eight hundred million people are at.
Speaker 2: Risk of infection. Oh my gosh, Yeah, at risk of infection.
Speaker 3: And it's thought that about two hundred and fifty million
Speaker 3: people are infected worldwide, and about two hundred million of
Speaker 3: these people live in on the African continent. So yeah,
Speaker 3: that's pretty massive. And you asked earlier about worm burden.
Speaker 3: Uh huh, So let's circle back to that. I don't
Speaker 3: know the exact numbers like how many worms do people
Speaker 3: get infected with? But by and large, children have the
Speaker 3: highest worm burdens and are the most affected. And one
Speaker 3: thing that I think is really interesting is that it
Speaker 3: used to be thought that this was entirely behavioral. Kids
Speaker 3: play in the water, they run around, that's how they
Speaker 3: get infected, whereas adults have different behavioral patterns and so
Speaker 3: they are infected at less of a burden. But there's
Speaker 3: more research that shows that there's also likely a strong
Speaker 3: immunological component to this, because you do build up immunity
Speaker 3: slowly over time.
Speaker 2: Interesting, so that, first of all, is.
Speaker 3: Important because we'll talk in a minute about the potential
Speaker 3: for vaccination. If you can't build up immunity to this,
Speaker 3: then there's no point in a vaccine.
Speaker 2: It wouldn't work.
Speaker 3: But we can build immunity to it, it just takes
Speaker 3: a really long time, and we don't know exactly what
Speaker 3: the best targets are necessarily, So it's thought that that's
Speaker 3: part of the reason why we see less of a
Speaker 3: burden and less egg shedding in adults than we do
Speaker 3: in children. The adults who tend to have the highest
Speaker 3: burdens are people who who are frequently exposed to freshwater sources.
Speaker 3: So if you fish for a living, if you work
Speaker 3: in flooded rice patties and things like that for a living,
Speaker 3: occupational exposure is where adults tend to get infected. Right, So, yeah,
Speaker 3: I think that's something important to keep in mind that
Speaker 3: we used to think it was entirely behavioral, but it's
Speaker 3: likely not entirely behavioral. But in addition to just the
Speaker 3: number of people infected, we know that this is a
Speaker 3: chronic disease and it causes these chronic symptoms. And so
Speaker 3: when we look at something like shis a semiasis, one
Speaker 3: of the metrics that people use to estimate the overall
Speaker 3: burden are what we call disability adjusted life years, which
Speaker 3: we've talked about DALIS.
Speaker 2: And trying to.
Speaker 3: Get a hand on the Daly's Forcehossi semiasis is really difficult.
Speaker 3: We don't have really solid numbers on this.
Speaker 2: Surprise surprise why though, I.
Speaker 3: Think because it's kind of hard to estimate how much
Speaker 3: of an effect infection has on people.
Speaker 1: Well, I guess because it's probably not like often there
Speaker 1: are co infections with a lot of other things too,
Speaker 1: absolutely separating those out, Yeah.
Speaker 3: Absolutely, co infection is going to be huge but then
Speaker 3: also like the greater the worm burden is going to
Speaker 3: make a difference on how severe your infection is, So
Speaker 3: like infection severity is going to range how often you
Speaker 3: get reinfected, you know, if you have access to treatment,
Speaker 3: things like that. So it's it's complicated. So estimates kind
Speaker 3: of are all over the place. Twenty sixteen Global Burden
Speaker 3: of Disease estimated that it's about one point nine million
Speaker 3: dallis so disability adjusted life years.
Speaker 1: Wow.
Speaker 3: But there have been some other analyzes that suggested much
Speaker 3: higher estimates. And that's I think if you include the
Speaker 3: fact that there is under nutrition anemia, right, this just.
Speaker 1: Feel like you should because of the mafestations, you absolutely should.
Speaker 3: And so this is where I actually want to touch
Speaker 3: on something that is really important with a disease like
Speaker 3: shist a semiasis and neglected tropical disease, and that is
Speaker 3: this cycle of poverty. Right. I feel like we've talked
Speaker 3: about this in bits and pieces before, but with something
Speaker 3: like shista semiasis, it's really important to touch on just
Speaker 3: how huge of an impact socioeconomics have on this disease,
Speaker 3: and how much of an impact this disease can have
Speaker 3: on socioeconomics. Right, So, a disease like shist a semiasis
Speaker 3: that causes chronic and severe symptoms, especially in children, this
Speaker 3: can cause malnutrition, impaired growth, and compromise cognitive development in children,
Speaker 3: especially when you consider you know, coinfection, generalized under nutrition
Speaker 3: and lack of access to nutrition and things like that.
Speaker 3: On top of this, Okay, then in adults, this illness
Speaker 3: can lead to the reduced ability to work, which can
Speaker 3: have profound impacts on economics, especially because of how widespread
Speaker 3: it is. So on a population level, a disease like
Speaker 3: schistosimiasis takes a huge impact. It has a huge impact
Speaker 3: on a populations and an individual's socioeconomic status. Then when
Speaker 3: you combine that with poor sanitation and poor water quality
Speaker 3: which means opportunity for reinfection and continued exposure which means
Speaker 3: continued disease, you have further reduced productivity, further reducing a
Speaker 3: person's ability to move out of posity feedback and basically
Speaker 3: perpetuating that cycle. It's a feedback loop.
Speaker 1: Yeah, and it's the same thing that that we see
Speaker 1: also with hookworm and with many other geohelmets. Basically many
Speaker 1: other of these intestinal parasites or neglectrotropical diseases. That's like,
Speaker 1: that's part of the one of the hallmarks of.
Speaker 2: A neglected tetropical diseases exactly.
Speaker 3: Especially these ones that are that are chronic like this,
Speaker 3: you know, uh huh, yeah, So it's in that way.
Speaker 3: It's just as miss is, like, we have a huge
Speaker 3: long way to go. The mainstay of control at this
Speaker 3: point is mass drug administration, so treating entire populations of
Speaker 3: people even if you don't know for sure if they're infected.
Speaker 3: So essentially the World Health Organization can go into an
Speaker 3: area and see what proportion of children are symptomatic or
Speaker 3: have for example, hematuria or eggs in their stool, and
Speaker 3: if more than fifty percent of children in an area
Speaker 3: are infected, which is a very high proportion, and everyone
Speaker 3: in that area will be treated. Yeah, and the treatment
Speaker 3: now is there's only one drug really that's approved for use.
Speaker 3: We can talk about the problems with that, but it's
Speaker 3: called prosy quantal or prazy quantal. It's effective, asterisk, it's effective,
Speaker 3: and so you can administer this to entire groups of
Speaker 3: people and you know, essentially wipe out adult worms from
Speaker 3: that population. But there's the asterisk. This drug is only
Speaker 3: effective against adult worms, so it does nothing if the
Speaker 3: worms that are in your body are still in that
Speaker 3: teenage stage marval stage. It does nothing for the eggs
Speaker 3: that are already in your body, right that those are
Speaker 3: the ones that are causing a lot of the symptoms
Speaker 3: that we see. And it does nothing for the environmental
Speaker 3: aspect of it, right, so it does nothing to prevent reinfection.
Speaker 1: How long is this treatment? Is it just a one
Speaker 1: time thing?
Speaker 2: It is.
Speaker 3: It's a one time dose, which is great, pretty effective
Speaker 3: at this point.
Speaker 1: Is there any resistance?
Speaker 3: That's why I said, at this point, ah, so there
Speaker 3: As with any drug, there is certainly concern for drug resistance.
Speaker 3: There isn't at this point a lot of evidence for
Speaker 3: resistance in the field, so it seems to still be
Speaker 3: pretty effective in the field. There is some evidence in
Speaker 3: mouse models, and I think this is really interesting and terrifying.
Speaker 3: There's evidence in mouse models that immature schistosomes, so like
Speaker 3: the teenage versions in your liver that are exposed to praziquantal,
Speaker 3: are more likely to be resistant as adults, and that
Speaker 3: this tends to increase resistance through generations. So like if
Speaker 3: because it doesn't kill those larval stages in mouse models.
Speaker 3: If those larval stages are exposed to this drug as adults,
Speaker 3: they're more likely to be resistant.
Speaker 1: How does that work mechanistically?
Speaker 3: Probably some kind of epigenetics thing. Okay, it's like turning
Speaker 3: on or off genes that they might already have in place.
Speaker 1: That's really interesting.
Speaker 3: Yeah, it's it's only in mouse models, so it's unclear
Speaker 3: whether this is happening in real life.
Speaker 2: There isn't at this point a lot of.
Speaker 3: Evidence for resistance in human populations with this drug.
Speaker 2: It's still an effective drug, okay, good, Yeah, but.
Speaker 3: It also can't be used for like chemoprophylaxis because it
Speaker 3: doesn't do anything for those larval stages. It doesn't prevent
Speaker 3: you from getting infected in any way, and it has
Speaker 3: a really short half life. So it basically is like,
Speaker 3: you take one dose of this drug, it kills the
Speaker 3: adult worms.
Speaker 2: End of story.
Speaker 1: Cool the end, okay, okay, So we.
Speaker 3: Need something better is pretty much the long and short
Speaker 3: of it. Right. So, there's a lot of work being
Speaker 3: done to try and develop a vaccine, in part by
Speaker 3: none other than our good friend Peter Hotez.
Speaker 2: Yeah, Peter, Hotez Doctor Peter Hotez.
Speaker 3: His group in Texas, as well as a number of
Speaker 3: other groups are working on vaccines. There are a number
Speaker 3: of challenges, largely in that we don't sort of develop
Speaker 3: classical immunity to this parasite the way that we do
Speaker 3: to other viruses or bacteria kind of a thing, so
Speaker 3: it's a more difficult target essentially. But basically there's a
Speaker 3: lot of mathematical modeling that show that any vaccine that
Speaker 3: can overall reduce egg output and can last so can
Speaker 3: actually prevent reinfection and prevent egg output from going up again,
Speaker 3: can massively help to interrupt transmission.
Speaker 1: I mean that makes sense, yeah.
Speaker 3: Right, So that's kind of going to be one of
Speaker 3: the main things going forward, is trying to develop a
Speaker 3: vaccine that can do that. There are at least three
Speaker 3: vaccines right now in clinical trials. They are component vaccines,
Speaker 3: so they're made up of specific antigens of Schistosoma mansoni
Speaker 3: or mansoni along with adjuvants. Because one of the big
Speaker 3: things is that because this is a parasite that we
Speaker 3: know can elicit an immune response, it takes a very
Speaker 3: long time, so we have to include adjuvants in these
Speaker 3: vaccines to elicit a stronger immune response so that your
Speaker 3: body can actually then fight off any further infection with
Speaker 3: this parasite.
Speaker 2: Does that make sense?
Speaker 3: Yeah, yeah, So there's a long way to go, but
Speaker 3: there is a lot of really great work being done
Speaker 3: by people to try and develop a vaccine for this,
Speaker 3: which is great.
Speaker 1: That's awesome. Yeah, yeah, cool, it's always I think good
Speaker 1: to hear after a very depressing history section and a
Speaker 1: little bit daunting, not even daunting, but like horrifying numbers
Speaker 1: of people infected around the world, some promising future for
Speaker 1: the disease that we talk about.
Speaker 3: Yeah, and World Health Organization, I will say, has a
Speaker 3: lot of goals in terms of trying to reduce morbidity
Speaker 3: and mortality from shisasmiasis, So they really are trying to
Speaker 3: get prosi quanto, the drug to as many people as possible.
Speaker 3: In twenty eighteen, about forty percent of people who needed
Speaker 3: treatment were actually reached and about sixty two percent of
Speaker 3: children were being treated who needed to get treated. So
Speaker 3: we still have a ways to go there, but again,
Speaker 3: there are people really working hard to try and get
Speaker 3: people access to drugs as well as developed vaccines for this.
Speaker 2: Horrible disease.
Speaker 1: Truly.
Speaker 2: So yeah, that's just asmisis.
Speaker 1: Tropical A good a good turn for tropical medicine. It's
Speaker 1: not changed changed its intent and that's great.
Speaker 2: Yeah, So sources, sources.
Speaker 1: I want to shout out, first of all, a book
Speaker 1: called Belarzia, A History of Imperial Tropical Medicine by John Farley.
Speaker 1: Fantastic book, really thorough, is very very fascinating, great resource.
Speaker 1: And then I also want to shout out a few
Speaker 1: other papers that I read, Where do human just toems
Speaker 1: come From? By Claude Comb's nineteen ninety by DiBella at All,
Speaker 1: twenty eighteen, History of Semiasis and Humans from Egyptian medical
Speaker 1: papyri to molecular biology on mummies, and finally by my
Speaker 1: Mood two thousand and four, A Semiasis from Antiquity to
Speaker 1: the Present. And there I've got a whole bunch more
Speaker 1: that I'll post on the website.
Speaker 3: If you would like a really really comprehensive overview of
Speaker 3: schrissmiasis biology and ecology. There's a great primer in Nature
Speaker 3: Reviews Disease Primers by Donald McManus from twenty eighteen. And
Speaker 3: then I have a number of other review articles and
Speaker 3: papers about the vaccine development. We'll post all of our
Speaker 3: sources on our website, This podcast will Kill You dot
Speaker 3: com under the episodes tab where you can find all
Speaker 3: our sources for this and every single episode we've ever done,
Speaker 3: so check those out.
Speaker 1: Yeah, thank you so much for listening and for letting
Speaker 1: us do this podcast because it's the most fun thing
Speaker 1: and honestly, I can't believe that we get to do it.
Speaker 2: It's so fun.
Speaker 3: And thank you to Bloodmobile for the music in this
Speaker 3: episode and all of our episodes.
Speaker 1: And finally, until next time, wash your hands you feel
Speaker 1: the animals.
Speaker 3: Um um um um