Speaker 1: My name is Daisy Hernandez and I'm an associate professor
Speaker 1: at Miami University in Ohio. And I'm also the author
Speaker 1: of a book about Shaga's disease called The Kissing Bug,
Speaker 1: A true story of an insect, a family, and a
Speaker 1: nation's neglect of a deadly disease. I first learned about
Speaker 1: Shaga's disease when I was about five years old. My
Speaker 1: auntie was diagnosed with Shagas in New York City actually,
Speaker 1: and she was from Colombia where around the time that
Speaker 1: she was twenty nine, she started to get really seriously
Speaker 1: sick and the doctors in Colombia were able to do
Speaker 1: some exploratory surgery, which is how they found out that
Speaker 1: her large intestine was under some kind of attack. They
Speaker 1: actually did not diagnose her with Shaga's disease. It was
Speaker 1: in New York City that that happened. And my auntie
Speaker 1: was very lucky that she was diagnosed and she was
Speaker 1: able to to receive some interventionist kind of treatment at
Speaker 1: that point. But you know, she had chronic Shagas disease
Speaker 1: for the next almost three decades of her life, and
Speaker 1: so she well, I was growing up, she was in
Speaker 1: and out of hospitals over the years, and sometimes she
Speaker 1: was in the hospital for one night or two nights,
Speaker 1: and some years she was in the hospital for a
Speaker 1: month or two. The parasite ended up not only affecting
Speaker 1: her large intestine but also her esophagures. She had multiple
Speaker 1: surgeries during these years, and I grew up thinking that
Speaker 1: Shaga's disease was a very rare or unusual illness. I
Speaker 1: thought my Auntie had just been extremely unlucky. And it
Speaker 1: was not until twenty ten when she became very very
Speaker 1: ill and actually died from this disease. That was the
Speaker 1: point at which I started asking questions about Shaga's disease.
Speaker 1: I think because I had grown up without knowing anyone
Speaker 1: else who had this disease except my Auntie, I thought
Speaker 1: it was rare, and I was really surprised to find
Speaker 1: out that there were that there are an estimated three
Speaker 1: hundred thousand people in the United States who have Shaga's disease,
Speaker 1: and they're like my Auntie's. They're immigrants from South America,
Speaker 1: Central America, and Mexico. And that number was very shocking
Speaker 1: to me, and it made me wonder who these families were.
Speaker 1: And that's how I ended up starting my book actually
Speaker 1: was that I wanted to meet other LATINX families in
Speaker 1: the United States to find out what their experiences with
Speaker 1: Shaga's disease were like, and what obstacles they were facing,
Speaker 1: and just how they were navigating the medical system in
Speaker 1: this country, given that, as far as I knew, was
Speaker 1: a very neglected disease, and something that I discovered while
Speaker 1: working on the book that I did not know know
Speaker 1: about when I was a child was the issue of
Speaker 1: congenital Shaga's disease. I met an incredible woman in the DC,
Speaker 1: Maryland area named Janet, who is from South America and
Speaker 1: her second son was born here in the United States
Speaker 1: with congenital shagus She herself knew about the disease. Similar
Speaker 1: to me, she thought that it was an affliction of Actually,
Speaker 1: in her case, she thought it was the elderly because
Speaker 1: she knew her father had Shaga's disease. She knew her
Speaker 1: older sister had Shaga's disease. She comes from a part
Speaker 1: of South America where the disease is pretty common, but she,
Speaker 1: even though it's common, she did not know about congenital
Speaker 1: Shagas disease and her son was born already having cardiac
Speaker 1: complications due to the disease. I'm happy to share that
Speaker 1: the baby is now gosh now five or six years old,
Speaker 1: and is very much is doing well. But he was
Speaker 1: a very unusual case. He ended up being only the
Speaker 1: second documented case of congenital Shagas disease in the United States,
Speaker 1: and he was unusual just in that he showed symptoms.
Speaker 1: Her situation, though, also really touched me because she herself
Speaker 1: did not have health insurance. She was not working, she
Speaker 1: had a toddler and a new baby, and she was
Speaker 1: home and her husband worked in construction, and she did
Speaker 1: qualify for the Affordable Care Act or for Obamacare, but
Speaker 1: she had not signed up for it, and it's an
Speaker 1: additional expense that the family would have to bear, and
Speaker 1: so she really struggled to actually find a medical provider
Speaker 1: who could diagnose her, who could work with her. It
Speaker 1: was a series of obstacles that I kept hearing over
Speaker 1: the years that I worked on this book, while I
Speaker 1: was talking to both families and medical providers. Is this
Speaker 1: constellation of obstacles not having health insurance, not being fluent
Speaker 1: in English, sometimes being fluent in English, but really struggling
Speaker 1: to advocate for yourself with a medical provider who doesn't
Speaker 1: know about the disease and doesn't understand or isn't being proactive.
Speaker 1: And also something else which came up often, which is
Speaker 1: that you know, if patients aren't experiencing symptoms, they have
Speaker 1: so many other things that feel more urgent and are
Speaker 1: more urgent in some ways in their lives. Like in
Speaker 1: Janet's case, she was, you know, very concerned about her
Speaker 1: child's welfare before her own. She was concerned obviously about
Speaker 1: her family's financial life. She herself has a legal residency,
Speaker 1: but was trying to learn English to work towards citizenship.
Speaker 1: Other families that I interviewed, you know what felt more
Speaker 1: urgent in their lives were the immigration status of different
Speaker 1: family members and job security always comes up, and so
Speaker 1: it's easy it becomes easy to actually ignore or Shaga's
Speaker 1: disease in a way because they're not having symptoms and
Speaker 1: it's not the most pressing concern in their lives. Although
Speaker 1: I knew about this disease from a very young age,
Speaker 1: there was a kind of stigma in my family around it.
Speaker 1: My auntie never wanted anyone to know about this.
Speaker 2: Disease, that she had it.
Speaker 1: She was really afraid, I think, as an immigrant, to
Speaker 1: be rejected in some way by her coworkers, by this country,
Speaker 1: by you know. Just she wanted so much, I think,
Speaker 1: to be the perfect immigrant turned citizen, and in so
Speaker 1: many ways she was. She got her teaching degree, she
Speaker 1: taught Spanish in a public school system in New Jersey.
Speaker 1: She got her master's degree as well. She traveled, she
Speaker 1: married an incredible man. She had such a wonderful life
Speaker 1: in so many ways, and she didn't want to have
Speaker 1: this disease and felt like it tarnished I think when
Speaker 1: I was growing up, I thought it was very normal
Speaker 1: that we did not talk about Shaga's disease. We did
Speaker 1: not tell anyone that my Auntie hadd We did not
Speaker 1: mention it. It definitely felt like something that we were
Speaker 1: supposed to have shame around. And now I look back
Speaker 1: on that was so much sadness because it was just
Speaker 1: a lack of information for my own family. It was
Speaker 1: a lack of information of course, in the healthcare community
Speaker 1: in the United States. The one sadness that I have
Speaker 1: is that I do wish my auntie had lived so
Speaker 1: that I could tell her a lot of what I
Speaker 1: learned about the disease, you know, even the difficult parts
Speaker 1: of this, you know, even the learning about congenital shaugus,
Speaker 1: Like I wish I could have told her that. I
Speaker 1: wish that I could have told her more about just
Speaker 1: all these you know, species of this insect, of the
Speaker 1: triotomine insect. I wish I could have told her about that.
Speaker 1: Even though she hated insects, she would not have wanted
Speaker 1: to probably hear that much detail. But I do wish,
Speaker 1: and I do have sadness that I could have told her,
Speaker 1: because I think that ultimately she died knowing very little
Speaker 1: about her disease. And so for me, part of working
Speaker 1: on the on the book was also a desire that
Speaker 1: people who have shagas and their families have a chance
Speaker 1: to know what they're really facing, you know, and and
Speaker 1: so that you know, no one else should have to
Speaker 1: die without knowing about their own disease and what's happening
Speaker 1: to their bodies.
Speaker 3: Thank you so much, Daisy for taking the time to
Speaker 3: come on the podcast and chat with us. We really
Speaker 3: appreciate it.
Speaker 2: Yeah, thank you. Hi. I'm erin Welsh and I'm erin
Speaker 2: Allman Updike and this.
Speaker 3: Is this podcast Will Kill You.
Speaker 2: And today we're talking about shaugust disease shawgust disease. I okay, listen, erin,
Speaker 2: how do you feel right now? I'm feeling a lot
Speaker 2: of different feelings, like I'm just I'm full of feelings. Okay, okay, listeners.
Speaker 2: You probably don't know this, but I technically did my
Speaker 2: PhD research on shaugust disease technically technically. Yeah, So it
Speaker 2: feels like I feel like I'm just gonna feel like
Speaker 2: I didn't do a good job on this no matter what,
Speaker 2: Like I just don't know enough.
Speaker 3: I mean, well, first of all, you do, you literally
Speaker 3: have a PhD in different aspects of shaugas disease. Yeah,
Speaker 3: And secondly, you know we are It's like we say
Speaker 3: every episode we are not experts.
Speaker 2: No, we're not.
Speaker 3: And this is a really big one to cover, like
Speaker 3: it massive.
Speaker 2: It is, it's so it's so big. I'm excited about it.
Speaker 2: But it's gonna be big.
Speaker 3: Yeah. But also, Aarin, you're gonna do a great job.
Speaker 3: I know what you always do.
Speaker 2: Oh, Aaron, You're so nice. I'm serious, I think before
Speaker 2: we really get into it, though, it's definitely quarantin any time.
Speaker 3: It is it is. What are we drinking this week?
Speaker 2: We're drinking the Kiss good Night.
Speaker 3: And it's It's called this because shaugas disease is transmitted
Speaker 3: by what are commonly called, or one of the names
Speaker 3: for them are is kissing bugs. And what they do
Speaker 3: is they feed on you and animals, mostly while you're sleeping,
Speaker 3: and they suck your blood and that's how you get
Speaker 3: shagas disease.
Speaker 2: It sure is so aarin. What's in a kiss goodnight?
Speaker 3: In the kiss goodnight is tequila, of course, canalope mm hmm,
Speaker 3: agave syrup, lime and orange liqueur.
Speaker 2: Yum. Yeah, that sounds fantastic. We'll post the full recipe
Speaker 2: for that quarantine as well as our non alcoholic plusy
Speaker 2: berta on our website This podcast will Kill You dot
Speaker 2: com and all of our social media channels.
Speaker 3: Yeah other business, let's see. You can check out our
Speaker 3: website This podcast will Kill You dot com. It's got
Speaker 3: lots of great stuff, like transcripts, like the sources for
Speaker 3: all of our past episodes. It's got links to do music,
Speaker 3: to merge, to our Patreon, to our bookshop dot org
Speaker 3: affiliate account, to goodreads list, and so on. Definitely check
Speaker 3: out our website, And also remember that you can listen
Speaker 3: to this episode and all of our past and future
Speaker 3: episodes on Amazon Music, Apple, Stitcher, or wherever you get
Speaker 3: your podcasts.
Speaker 2: Before we get into this episode, speaking of the fact
Speaker 2: that we are not experts, I have a correction to make.
Speaker 2: Bartonella was an episode that came out a few episodes ago.
Speaker 2: Now I want to hugely thank multiple listeners that have
Speaker 2: reached out to help us solve the mystery of cat
Speaker 2: scratch disease that we were postulating about during that episode.
Speaker 2: In that episode, we were trying to figure out how
Speaker 2: bartonella makes it from a cat's blood onto their claws
Speaker 2: or their teeth and then into our bloodstream after a
Speaker 2: bite or a scratch. Okay, multiple people have written in
Speaker 2: It turns out, unsurprisingly when you really think about it,
Speaker 2: it is largely flea feces that are to blame. So
Speaker 2: infected flea feces or in some cases, just infected cat's
Speaker 2: blood itself, can contaminate a cat's claws during grooming, which
Speaker 2: then can introduce the bacteria via a scratch into our
Speaker 2: skin or a bite wound. Fe flee flea feces can
Speaker 2: contaminate a bite wound, et cetera.
Speaker 3: So mystery solved, Darren, flea feces say that three times fast.
Speaker 2: I can't. I couldn't even say it one.
Speaker 3: I also learned with the people who sent in those corrections,
Speaker 3: which was very helpful. Thank you that it's called flea dirt.
Speaker 2: Two.
Speaker 3: I blee dirt, flee dirt.
Speaker 2: I like it.
Speaker 3: It's easier to say than flea feces. Yeah, but it's
Speaker 3: also I know either way.
Speaker 2: Again, but thank you so much. Honestly, like we are
Speaker 2: not experts, so we know ever get everything one thousand
Speaker 2: percent right, So thank you. I appreciate getting to learn
Speaker 2: from you.
Speaker 3: Yeah, okay, okay with that, should we get started.
Speaker 2: I'm so nervous. Okay, let's take a break and then
Speaker 2: get into it. So. Shagus disease Shagus is a severely
Speaker 2: neglected tropical disease, historically very much considered a disease of poverty.
Speaker 2: Like many, if not all, neglected tropical diseases, and like
Speaker 2: you mentioned up top aarin, it's a vector born disease.
Speaker 2: For the most part, it's caused by a protozoan parasite
Speaker 2: called tripanasoma, cruisy or cruise. I take your pick, uh,
Speaker 2: Trypanosoma cruise ie. Tea cruiseye. It's a very cute little parasite.
Speaker 2: It has a little like looks kind of like a
Speaker 2: comma with like wavy flagella. Okay, okay, picture it's cute.
Speaker 2: So Tea cruise I has a shall we say, relatively
Speaker 2: complex life cycle. So we're gonna go through the life
Speaker 2: cycle and then from there we can understand the different
Speaker 2: ways that we as humans can get infected. So we'll
Speaker 2: start the life cycle in the bug, the insect vector
Speaker 2: that transmits it. So Tea cruise ie gets picked up
Speaker 2: during blood feeding by bugs like you mentioned aaron called
Speaker 2: kissing bugs aka triatomines. They have a lot of different
Speaker 2: names in different countries. Kissing bugs are a type of
Speaker 2: what's called true bug in the order amypdura. Okay, already,
Speaker 2: I'm on tangents. These are blood feeding insects. I think
Speaker 2: a lot of people might not know what they look like,
Speaker 2: so let me paint you a visual. They're pretty large bugs.
Speaker 2: The adults are like between three and four centimeters so
Speaker 2: a good inch inch and a half long, and they
Speaker 2: look like they have like a flat oval body with
Speaker 2: a pointy head and a long curved preboscis. That's the
Speaker 2: straw that they use to drink blood. So these are
Speaker 2: big honkin bugs. They're big, right, Like, way bigger than ticks,
Speaker 2: way bigger than mosquitoes, way bigger than most things that
Speaker 2: bite you.
Speaker 3: I would say, like, well, I mean, cockroaches are a
Speaker 3: whole different a whole bunch of different sizes. But yeah,
Speaker 3: like you know about the size of your average cockroach.
Speaker 2: Yeah, like your house, your US house cockroach. Yeah, definitely,
Speaker 2: if not bigger. Now, both males and females drink blood,
Speaker 2: as do all of the nymphal stages. So these are
Speaker 2: bugs that have multiple in star stages and they all
Speaker 2: blood feed. They often have like a nest that they
Speaker 2: stay near, but then the adults can fly, so they
Speaker 2: can fly farther from home base to look for blood meals.
Speaker 3: They have a nest, family nest or individual nest.
Speaker 2: Like little families or even like multi generation little families.
Speaker 2: Just like a lot of bugs will often hang out
Speaker 2: together in like a palm tree or whatever.
Speaker 3: Ooh, that's interesting.
Speaker 2: Yeah, so like a bunch of nymphs a bunch of adults,
Speaker 2: you might find a lot kind of living together. Okay,
Speaker 2: depending on the species. We'll I'll get into that later. Okay.
Speaker 2: So this bug takes a blood meal from someone, picks
Speaker 2: up a whole bunch of parasites. These parasites travel through
Speaker 2: the bugs guts, they differentiate, they replicate, and then when
Speaker 2: that bug gets hungry again and goes to take another
Speaker 2: blood meal, that bug will poop, and in that poop
Speaker 2: or frasts are a whole bunch of parasites, not unlike
Speaker 2: the fleas in Bartonella.
Speaker 3: Hey.
Speaker 2: Yeah, And then these parasites that are now pooped onto
Speaker 2: your skin have to find their way either into that
Speaker 2: bite wound that the bug just made or some other
Speaker 2: mucus membrane like your eye or your mouth, et cetera.
Speaker 2: And from there they make it into our bloodstream. You
Speaker 2: look like you have a questionnairein.
Speaker 3: I do have a question.
Speaker 2: Okay.
Speaker 3: So they're pooping while they're eating, or shortly thereafter or
Speaker 3: shortly after. And so the poop that they have that
Speaker 3: they're pooping out is from the fresh meal or from
Speaker 3: the previous meal.
Speaker 2: Great question, It's from the previous meal.
Speaker 3: Yeah, And how often do they have to feed?
Speaker 2: Great question? Totally varies by species and by life stage,
Speaker 2: so at least once per nymphl stage, and then as adults,
Speaker 2: like the females have to feed every time that they're
Speaker 2: going to make a clutch of eggs. So it kind
Speaker 2: of just depends. Okay, gotcha, Yeah, good questions, Aaron. Okay,
Speaker 2: So now this parasite is inside of us, that made
Speaker 2: it into our bloodstream. Inside of us, these parasites penetrate
Speaker 2: our cells. They actually can penetrate a pretty wide variety
Speaker 2: of cells, and what cells or what tissue type they
Speaker 2: infect can then lead to different symptoms of disease. They replicate,
Speaker 2: they differentiate again inside our cells, they replicate a whole bunch,
Speaker 2: and then they burst out from our cells to travel
Speaker 2: through our bloodstream and either infect another cell and start
Speaker 2: a new replication cycle to just keep going, or in
Speaker 2: the bloodstream they can be picked up by another kissing bug,
Speaker 2: thus completing their life cycle. So that's just like the
Speaker 2: life cycle of tea cruise eye.
Speaker 3: Yeah, I mean it's a complicated one.
Speaker 2: Yeah, it's part one of complication.
Speaker 3: Yeah.
Speaker 2: But what I'm in my very bias opinion. What's also
Speaker 2: very important and interesting about the Shagas disease story is
Speaker 2: how complex the ecology of this disease is I'm biased,
Speaker 2: but I think listeners will agree once I get into it.
Speaker 2: So this is one parasite, right, Tripanosoma cruisy, But it
Speaker 2: has like six different clades within this species. And these
Speaker 2: different clades vary in terms of virulence, so how sick
Speaker 2: they make you and disease manifestations, what tissues there may
Speaker 2: be more likely to infect, or how likely they are
Speaker 2: to cause more chronic disease. And these different clades can
Speaker 2: vary in geography, they can vary by vector. There's a
Speaker 2: lot of variation in these different clades of T. Cruizy.
Speaker 2: Then there's the vector. And I hinted at this already,
Speaker 2: so I said that it's a triatomine a kissing bug,
Speaker 2: but aarin is it just one bug?
Speaker 3: No, Aaron, it's many bugs.
Speaker 2: It is many bugs.
Speaker 3: So it's a lot, Yeah, it is.
Speaker 2: So there's like one hundred and thirty eight. I think
Speaker 2: maybe more species of triatomine everyone could potentially transmit Tripanosoma crusy.
Speaker 2: There's at least three species that are often cited as
Speaker 2: being the most important. One in particular, Triatoma infestins is
Speaker 2: a species that's most closely associated with human dwellings. It
Speaker 2: has adapted to live its entire life cycle within human dwellings,
Speaker 2: so in walls, in roofs, inside of our homes. So
Speaker 2: historically that's been the one considered kind of the biggest deal.
Speaker 2: But there's a lot of other species in a whole
Speaker 2: bunch of different genera of triatomine that are capable of
Speaker 2: and potentially important of Shaugus disease. Spoiler, that was like
Speaker 2: my whole dissertation. So like I could go on and on,
Speaker 2: but I think I can pause there. Okay. Each of
Speaker 2: these species has differences in terms of their ecology, so
Speaker 2: like where they like to live. Do they live in
Speaker 2: palm trees or do they live under rocks, et cetera.
Speaker 2: They have differences in terms of who they like to
Speaker 2: feed on, and like you asked Aaron, how often they feed,
Speaker 2: they have differences in how long they feed for, how
Speaker 2: soon after feeding they take a poop, and where they
Speaker 2: take a poop after feeding. It's really really complicated.
Speaker 3: Yeah, I mean, all of this just kind of serves
Speaker 3: to like underline how difficult this is to control or
Speaker 3: to prevent or to like reduce the numbers of it's
Speaker 3: It's sort of like you have to hit it from
Speaker 3: so many different angles and right.
Speaker 2: Yeah, yeah, and to throw one last angle on their
Speaker 2: erin this isn't a human in specific disease. This is
Speaker 2: a parasite that infects over one hundred and fifty species
Speaker 2: of mammal h all right, So that's the lot that's
Speaker 2: really complicated. So we know that in general, this is
Speaker 2: a group of insects and therefore parasite and disease that
Speaker 2: was typically considered endemic to the New World, so North
Speaker 2: Central and South America and mostly just the southern part
Speaker 2: of North America because it's really restricted to more tropical
Speaker 2: type latitudes. But as we'll see when we talk about
Speaker 2: the clinical picture of disease, which I promise I'm about
Speaker 2: to get to, because of the way that Shaugus disease
Speaker 2: manifests clinically, it is a global disease today. It is
Speaker 2: not limited to South America or even just the Americas.
Speaker 2: So let's talk symptoms in humans. Shagas disease has two forms,
Speaker 2: the acute disease like you get sick shortly after getting infected,
Speaker 2: and then a chronic disease. This parasite can lay dormant
Speaker 2: in our bodies for decades ten twenty thirty years and
Speaker 2: then pop up and cause disease very long down the road.
Speaker 2: So we'll go through those one by one. In the
Speaker 2: acute phase. Honestly, shacus is mostly asymptomatic, and by mostly
Speaker 2: I mean ninety ninety five percent of the time completely asymptomatic.
Speaker 2: So you get bit, you scratch this parasite into your bloodstream,
Speaker 2: and you don't know about it at all. If people
Speaker 2: do have symptoms, so that five to ten percent of
Speaker 2: people that do have symptoms, they're often quite mild and
Speaker 2: consist of something like maybe some fever, maybe inflammation wherever
Speaker 2: the parasites entered. And because it's common for the parasites
Speaker 2: to enter via something like your eye, there's a classic
Speaker 2: sign that's called Romagna's sign, which is when one eye
Speaker 2: whichever i the parasites win in from, gets really swelling
Speaker 2: swelling of your eye and eyelid. But it could be anywhere.
Speaker 2: So let's say it happened on your arm, then maybe
Speaker 2: your arm swells up. Occasionally you might also get some
Speaker 2: hepatosplenomegaly one of our favorite, oh my words. Yeah, so
Speaker 2: that's swelling of your liver and spleen from the parasite
Speaker 2: and inflammation and immune response associated with it, or swelling
Speaker 2: of any various lymph nodes. Potentially it can cause things
Speaker 2: like anemia if it gets more severe, and in very
Speaker 2: rare instances, like I think, usually only one to five
Speaker 2: percent of the time, although one paper I read said
Speaker 2: five to ten percent. It can be a little bit
Speaker 2: more severe, and the specific symptoms depend on which organ
Speaker 2: is infected severely. So if it's the heart, we can
Speaker 2: see things like myocarditis or pericarditis, inflammation of the heart
Speaker 2: muscle or lining very rarely. If it infects the brain,
Speaker 2: you can get me ninjo encephalitis and these kind of
Speaker 2: severe manifestations can be fatal, but that's very rare.
Speaker 3: It can be fatal in the acute phase.
Speaker 2: In the acute phase exactly.
Speaker 3: Yeah, okay, So why is it the enlargement? Why is
Speaker 3: there such inflammation? Like what cells are they attacking?
Speaker 2: Yeah, good question. They they enter into our cells, and
Speaker 2: from what I can tell, it's not very specific. So
Speaker 2: they can enter white blood cells, which is probably why
Speaker 2: we see a lot of hippatosplenomegaly and lymphatinopathy. This is
Speaker 2: where our white blood cells are congregating. But they can
Speaker 2: also enter the lining of your heart. They can enter
Speaker 2: a whole bunch of different tissue types. What makes them
Speaker 2: either decide or just happen to end up somewhere probably
Speaker 2: depends on how much parasite you have, Like how far
Speaker 2: they make it before our immune system kicks in. Probably
Speaker 2: depends on how great of an immune response you have
Speaker 2: to It probably depends on what specific genotype you were
Speaker 2: infected with. There's probably a lot of variables that I
Speaker 2: don't know the full answer to.
Speaker 3: Okay, okay. And then of the so you said ninety
Speaker 3: five percent or asymptomatic, are there any patterns as to why,
Speaker 3: like who the five percent are that become symptomatic?
Speaker 2: It's a good question. I don't know. Okay, Yeah, yeah,
Speaker 2: good question.
Speaker 3: And another question real quick while I have you Yeah, uh, immunity,
Speaker 3: like with re exposure. So you said that your immune
Speaker 3: system can kind of recognize take care of it if
Speaker 3: they If someone gets re exposed, are they immune or
Speaker 3: can they get reinfected?
Speaker 2: Okay, let's let's keep going.
Speaker 3: And I I had a feeling I was I was
Speaker 3: jumping the gun.
Speaker 2: Yeah, okay, So let's then talk about the chronic phase.
Speaker 3: Yep, yep.
Speaker 2: So the chronic phase is the phase of disease that's
Speaker 2: more severe. Here's the thing about it. Most people, and
Speaker 2: when I say most, I don't have an exact number,
Speaker 2: but some of the papers I read made it sound
Speaker 2: like almost all people, if untreated during the acute phase,
Speaker 2: will in fact have some level of chronic infection, but
Speaker 2: only about thirty to forty percent of those people will
Speaker 2: actually go on to have any chronic disease as a
Speaker 2: result of this infection. Okay, okay, okay, okay. So for
Speaker 2: those unlucky, thirty to forty percent of people anywhere from
Speaker 2: ten to thirty years after the initial infection, which again
Speaker 2: most of the time is asymptomatic, so you never know
Speaker 2: that you had it. The two most common organs that
Speaker 2: end up getting infected are the heart and the gastintestinal tract,
Speaker 2: and the parasite ends up doing similar things but with
Speaker 2: very different outcomes since it's heart versus GI tract. Okay,
Speaker 2: So in the heart often what happens is this parasite
Speaker 2: and this infection causes an enlargement of the heart. It
Speaker 2: causes what's called a dilated cardiomyopathy, an enlargement of the heart.
Speaker 2: This causes the heart to not be able to conduct
Speaker 2: electrical impulses properly. That's your heart's like one job, right,
Speaker 2: it's to have electrical impulses that all go simultaneously so
Speaker 2: that your heart contracts in one beautiful thump thump with
Speaker 2: enough force to pump blood to the rest of your
Speaker 2: body when it gets dilated, and those electrical impulses can't transmit,
Speaker 2: the heart can't contract in sync or it can't contract
Speaker 2: with enough force or the right timing and synchronization to
Speaker 2: be able to push your blood forward. So there's a
Speaker 2: lot of different ways that this can manifest, anything from
Speaker 2: things like heart block to heart fail two different a arrhythmias,
Speaker 2: just depending on what parts of the heart are the
Speaker 2: most affected and when. But overall, the most common cause
Speaker 2: of death in these individuals is sudden cardiac death because
Speaker 2: your heart is just all of a sudden not able
Speaker 2: to pump properly, and then you die from sudden cardiac death.
Speaker 2: The other organ that's most commonly affected is the GI tract,
Speaker 2: and same as with the heart, shaugust disease tends to
Speaker 2: cause enlargement of either the esophagus or the colon, either
Speaker 2: or usually in the esophagus This leads to dismotility, and specifically,
Speaker 2: it leads to something called a kalaysia, which anyone in
Speaker 2: med school will be like, oh yeah, shaugus disease. A
Speaker 2: kalasia basically means your esophageal sphincter, the one that lets
Speaker 2: your food into your stomach, doesn't it relax properly, and
Speaker 2: your esophagus gets expanded and then it looks like a
Speaker 2: like a bird's beak. So there's a really tight hole
Speaker 2: where it enters the stomach, and then the rest of
Speaker 2: it is really dilated. Does that make sense instead of
Speaker 2: being a nice little tube. And so this leads to
Speaker 2: like not being able to swallow properly, et cetera.
Speaker 3: Oh, that sounds really difficult.
Speaker 2: It's really problematic. It can lead to reflex it can
Speaker 2: lead to weight loss because if you're not able to
Speaker 2: swallow your food, then you're not eating essentially, and a
Speaker 2: similar thing can happen in the colon. Shaugus can lead
Speaker 2: to what's called mega colon, where the entire colon becomes
Speaker 2: dilated and then isn't able to contract properly to move
Speaker 2: your digestive food along. So that leads to constipation, which
Speaker 2: is problematic. But what's even more worrisome is it can
Speaker 2: lead This dilation can lead to twisting of your bowels,
Speaker 2: which is called volvulus, and that can lead to ischemia
Speaker 2: because that twisting can then cut off blood float to
Speaker 2: the organ. Okay, okay, yeah, So it's a problematic disease
Speaker 2: and it's a cause of really really chronic disease problems.
Speaker 3: Right.
Speaker 2: These are like mega colon, the esophageal dismotility, heart failure,
Speaker 2: dilated cardiomyopathy. These are things that happen from a lot
Speaker 2: of other sources. But now this is happening from an
Speaker 2: infectious disease, So what's going on? Okay, yeah, off the bat, Aaron.
Speaker 2: This is a very understudied disease from like every possible angle,
Speaker 2: and that's still true for the pathophysiology. So especially in
Speaker 2: the chronic phase, we still don't know the exact details
Speaker 2: of this pathogenesis, so we don't know exactly what's going on,
Speaker 2: but we know a few things. So we know that
Speaker 2: in the acute phase, the organ damage when it happens
Speaker 2: is due to direct action of the parasite, So it's
Speaker 2: parasites causing damage to the tissue from bursting out of
Speaker 2: our cells that stimulates an inflammatory response, et cetera, et cetera.
Speaker 2: That's the acute phase, so you think probably similar things
Speaker 2: are happening in the chronic phase. We know that you
Speaker 2: asked about who gets chronic disease versus who doesn't. The
Speaker 2: balance of who gets chronic disease versus just who has
Speaker 2: infection without ever having disease from it seems to depend
Speaker 2: a lot on individual balances between our chronic inflammatory response
Speaker 2: and the parasite infection itself. So like, how much is
Speaker 2: our immune system trying really hard to kill off this
Speaker 2: parasite versus just tolerating this parasite and like coexisting with it. Right,
Speaker 2: But Okay, it gets really complicated because in some areas
Speaker 2: where transmission has been reduced significantly, so where control efforts
Speaker 2: have reduced incidents of disease, but of course people are
Speaker 2: still infected, right because it's infection. The development of things
Speaker 2: like cardiomyopathy have actually decreased. There's been a reduction in
Speaker 2: the development of things like heart disease. So it's thought
Speaker 2: that maybe there's also some interaction between recurrent exposure to
Speaker 2: the parasite and increased inflammation.
Speaker 3: Yeah, so it's like every time, like, let's say you
Speaker 3: get infected and then your body never sees this again
Speaker 3: and it's just like, okay, well this is just this
Speaker 3: thing here. Then if you get continually re exposed and
Speaker 3: your immune system keeps waking up and keeps getting like inflammation.
Speaker 4: Right exactly, ok yeah, okay, but it is it does
Speaker 4: seem to be the case that a lot of the
Speaker 4: damage is parasite persistence.
Speaker 2: And that's important because it's not purely an inflammatory or
Speaker 2: purely an immune response. Like the parasite is a really
Speaker 2: big part of it. Does that make sense? And yeah,
Speaker 2: it's important when we talk about things like therapy, vaccines
Speaker 2: like this interplay between parasite and immune response. Like, so
Speaker 2: it's really complicated and we don't know the full answer. Ha.
Speaker 2: I'm gonna throw a little bit more complication in there
Speaker 2: before I hand it off to you Erin. Okay, okay,
Speaker 2: Because it's important to mention that while this is largely
Speaker 2: a vector born disease, vector born transmission is the primary root,
Speaker 2: it is certainly not the only root. Right, So, because
Speaker 2: this is essentially a blood borne pathogen, this is something
Speaker 2: that can also be transmitted via blood transfusion, or organ transplant,
Speaker 2: but of course that's quite rare, and in many places
Speaker 2: blood is screened for Shougust disease. It can also be
Speaker 2: a congenital infection, so during pregnancy it can cross the
Speaker 2: placenta and infect a fetus, which can result from anything
Speaker 2: from spontaneous pregnancy loss to premature birth, to a number
Speaker 2: of different problems in the newborn, or in many cases
Speaker 2: asymptomatic infection. But then life lung infection of the baby.
Speaker 3: Yeah, it's really bad.
Speaker 2: Yeah, and increasingly people are realizing that it's a much
Speaker 2: bigger problem than had ever been thought before, probably just
Speaker 2: because nobody had thought to study it.
Speaker 3: Can I read you a disheartening statistic?
Speaker 2: Oh gosh. Yeah.
Speaker 3: So there was a survey in two thousand and eight
Speaker 3: by the CDC and the American College of Obstetricians and Gynecologists,
Speaker 3: and it there was the question can a pregnant person
Speaker 3: passed he cruisy onto their baby? And so again, these
Speaker 3: are obstricians and gynecologists in the US, and eighty four
Speaker 3: percent of them answered I don't know to that question.
Speaker 2: I'm not surprised about that. I can tell you that
Speaker 2: this absolutely never came up in medical.
Speaker 3: School Yeah, that's that's a huge problem.
Speaker 2: I mean, shagus came up, but not congenital transmission of.
Speaker 3: Right, But that's like such a big problem.
Speaker 2: It's a huge problem. Yeah.
Speaker 3: Oh my gosh, that's frustrating.
Speaker 2: I know that's not the end. Yeah. Shaugus has also,
Speaker 2: though rarely, been associated with oral transmission. Because this parasite
Speaker 2: is found in the feces of bugs, and a lot
Speaker 2: of species of triatomine make their little nests in the
Speaker 2: tops of palm trees. There have been a handful of
Speaker 2: outbreaks of Shauga's disease associated with consumption of things like
Speaker 2: palm fruit juice or other fruits and vegetables that were
Speaker 2: contaminated with the feces of kissing bugs.
Speaker 3: I always see ASAE being called out.
Speaker 2: Yeah, Asie is, like, I think, the most well documented. Yeah.
Speaker 2: Oh that's a lot aaron, And there's not any good
Speaker 2: news in this section because there is treatment, but in general,
Speaker 2: it's really effective only during the acute phase of the disease.
Speaker 2: It's much less effective during the chronic phase. And you
Speaker 2: can imagine it's pretty difficult to catch during the acute phase.
Speaker 3: Yeah, why is it only effective in the acute phase.
Speaker 2: It's a good question, Aaron. Okay, I think if we
Speaker 2: knew that, we might have better drugs.
Speaker 3: Okay, yeah, fair.
Speaker 2: Ah So Aaron, yes, you think you could tell me
Speaker 2: a little bit about this little parasite here, and I
Speaker 2: mean it's got a lot going on.
Speaker 3: It's got a lot going on. Yeah, I'll tell you
Speaker 3: all about its history. Let's take a quick break first.
Speaker 3: I am so excited to talk about the history of
Speaker 3: shagas disease because at each step of the way, from
Speaker 3: its evolutionary origins and prehistory to the research leading to
Speaker 3: its discovery and then a better understanding of disease progression,
Speaker 3: I was surprised at all of these steps by what
Speaker 3: I learned.
Speaker 2: Ooh fun, I really was.
Speaker 3: I mean, granted, I didn't know much about the history
Speaker 3: of shagus going into the episode, but I think it
Speaker 3: does stand out for me as a parasite and a
Speaker 3: disease where things didn't really happen in quite the way
Speaker 3: you might expect, which is definitely something that can be
Speaker 3: said for its biology as well. It's complicated. You're like,
Speaker 3: I don't know what's going on. You can't really predict
Speaker 3: things sometimes, so yeah, yeah, definitely. So like always, let's
Speaker 3: start at the beginning, which is easier said than done.
Speaker 3: Until fairly recently, like maybe within the last ten fifteen
Speaker 3: years or so, the origins of Tripanosoma cruisy seemed like
Speaker 3: fairly cut and dry, or at least like as cut
Speaker 3: and dry as evolutionary origins can be in terms of like,
Speaker 3: you know, stuff, it's always being rewritten. It's fine, that's
Speaker 3: how science works. But there was a general consensus that
Speaker 3: the Tripanosoma cruisi clade originated on the Southern super continent
Speaker 3: made up of South America, Antarctica, and Australia, where they
Speaker 3: evolved in isolation in early terrestrial mammals, and then when
Speaker 3: that super continent broke up around forty million years ago,
Speaker 3: the tea cruisy clade further diversified in South America. And
Speaker 3: so if this were the sequence of events that actually happened,
Speaker 3: we would expect to see a great deal of diversity
Speaker 3: within Tea cruisy in South America, as well as maybe
Speaker 3: some evidence of coevolution between mammalian host and parasite with
Speaker 3: some maybe species specific strains. However, however, however, there's actually
Speaker 3: fairly low diversity of the tea cruisy clade in South
Speaker 3: American mammals like lower than you would expect if it
Speaker 3: had been there for forty million years. And in addition
Speaker 3: to this, members of the tea cruisy clade also have
Speaker 3: been found in African and Australian land mammals. So what's
Speaker 3: going on here? Yeah, Well, it seems most likely that
Speaker 3: tea crusy originated elsewhere, likely in Africa, where the other
Speaker 3: major human tripanisome is most prevalent. So which is T.
Speaker 3: BRUCEI brucy, which is the causative agent of African sleeping sickness.
Speaker 3: We should figure how to pronounce that before we do
Speaker 3: an episode on that, which we.
Speaker 2: Will definitely will.
Speaker 3: Yeah. Yeah, So then it originated in Africa and then
Speaker 3: was brought to South America. And this is where I
Speaker 3: introduced to you the bat seeding hypothesis.
Speaker 2: Bat seeding bat Yeah, okay, okay.
Speaker 3: This idea basically holds that tea cruisy was brought over
Speaker 3: to South America from the Old World, likely the African continent,
Speaker 3: by bats between seven to ten million years ago in
Speaker 3: several different independent colonization events, and this bat seeding hypothesis
Speaker 3: has gotten a good deal of support more recently with
Speaker 3: molecular studies showing that the closest relative to Tea cruisey
Speaker 3: is a South American bat tripanisome that diverged like six
Speaker 3: point five to eight point five million years ago, and
Speaker 3: two other trypanosome species recently described that are related to
Speaker 3: Tea cruisey are found in bats from Mozambique.
Speaker 2: Huh.
Speaker 3: Yeah. And in addition, one genotype of Tea crusy called
Speaker 3: TC bat is only found in yeah, like bats in
Speaker 3: South America.
Speaker 2: I knew about that one.
Speaker 3: Yeah, And that one is closely related to T. Crusy
Speaker 3: TC one, which, like, I'm not going to get into
Speaker 3: all the different genotypes and stuff, but this is I
Speaker 3: think a really interesting part of the story. So TC
Speaker 3: one is mostly associated with a possums and arboreal triatomines. Right, So,
Speaker 3: once these tripanosome infected bats infected with Tea crusey or
Speaker 3: some you know, ancestor of Tea crusy made it to
Speaker 3: South America, they were fed on by blood feeding insects
Speaker 3: triatomines that also took meals from other mammals also living
Speaker 3: in trees or a high right, yeah, like opossums. Yeah,
Speaker 3: And so then those apossums were probably some of the
Speaker 3: first to get infected with T.
Speaker 2: Crusy okay, yeah, yeah, yeah, okay, and.
Speaker 3: The ancientness of this relationship might be reflected in the
Speaker 3: way that the parasite infects those animals. Yeah. I read
Speaker 3: a paper actually, I think it was mentioned in two
Speaker 3: that I read because I was like, for real, this
Speaker 3: is this is wild. And these these papers reported finding
Speaker 3: a mast a goats, which is like.
Speaker 2: The no, I know, I didn't even get into it, Aaron, I.
Speaker 3: Know, it's a it's a part of the life stage
Speaker 3: of TA cruisy intracellular part of the life stage, right,
Speaker 3: thank you. And so they found a mast goats in
Speaker 3: the tissues of opossums, which is totally what you would
Speaker 3: expect of mammals susceptible to the parasite, that's where you
Speaker 3: find them. And then they found epi mastigoats, which are
Speaker 3: found usually only in the insects. Yeah, they found them
Speaker 3: multiplying and differentiating in the opossum's anal glance. What yeah, Okay,
Speaker 3: that I think is fascinating.
Speaker 2: I don't even know how to interpret. Okay.
Speaker 3: So they were able to take those epimastigotes and then
Speaker 3: like complete the infection cycle stop it. Yeah. So opossums
Speaker 3: might be able to transmit Tripanosoma cruzi in their That
Speaker 3: was my interpretation of this, and I think that's what
Speaker 3: it means. What Yeah, And so I know, I know.
Speaker 3: And so this paper, which was written before the bat
Speaker 3: seating hypothesis gained momentum, it suggested that this might have
Speaker 3: been the earliest route of transmission before the triatomines got involved,
Speaker 3: but it might also have evolved after. In any case,
Speaker 3: this mode of transmission where where you know, opossums might
Speaker 3: be able to transmit through their poop or through like
Speaker 3: the anal gland secretions. This might play a role currently
Speaker 3: in semi urban environments or places where the vectors aren't
Speaker 3: quite as present.
Speaker 2: Yeah what Yeah, I.
Speaker 3: My mind was bulown.
Speaker 2: I just feel really glad that I finished my PhD.
Speaker 3: Before you found that paper. Yeah. Yeah, it's uh, it's
Speaker 3: it's really it's really interesting. I will definitely I'll definitely
Speaker 3: put the the paper in the.
Speaker 2: On the website. Would have had my hands on a
Speaker 2: lot more possum poop or something, to be thankful.
Speaker 3: Yeah, it's super interesting. So okay, So, but once Tripanosoma
Speaker 3: cruzy landed in South America and found its way into
Speaker 3: opossums and it. You know, of course, other host of
Speaker 3: mammals followed, and the parasite diversified into its current lineages
Speaker 3: around one to three million years ago, which seems to
Speaker 3: be around the same time that the triatomine vectors diversified.
Speaker 3: And then over the past you know, few million years,
Speaker 3: it just continued to spread across South America up through
Speaker 3: Central America and North America through primarily animal movement. Eggs
Speaker 3: and nymphs, for instance, have been found to be carried
Speaker 3: in bird feathers, which I think is interesting. And then later,
Speaker 3: of course, human movement would have helped to spread things
Speaker 3: along too. All right, By the time that humans arrived
Speaker 3: in South America, which was at least fifteen thousand years ago,
Speaker 3: tripanisomacruzie was present in animals across the continent, although to
Speaker 3: what extent is not quite known, since not all habitats
Speaker 3: might be conducive for the insect vector and whatever susceptible
Speaker 3: mammal species. But here comes the next First we thought
Speaker 3: it was this, then we realized it was that moment.
Speaker 3: It was originally thought that humans first became exposed to
Speaker 3: the parasite after the domestication of like guinea pigs around
Speaker 3: two thousand BCE, along with other animals that would have
Speaker 3: like attracted the bugs and thus the parasite to you know,
Speaker 3: human dwellings, or it was thought that human dwellings built
Speaker 3: later on and particularly after European invasion, would have provided
Speaker 3: you know, excellent homes for the triatomine vectors. And that's
Speaker 3: I mean, those things are probably true in that they
Speaker 3: did increase contact with the bugs, but paleo parasitology came
Speaker 3: along to change the story. The Atta Kama Desert in
Speaker 3: southern Peru and northern Chile is you know, it's a desert,
Speaker 3: so as you would expect, it's extremely arid. There's virtually
Speaker 3: no rainfall, and so when a body is buried, it
Speaker 3: rapidly dehydrates rather than decays or disintegrates, and that has
Speaker 3: left many, many mummified remains in the area, and genetic
Speaker 3: analysis of these mummies has shown not only the presence
Speaker 3: of Tea Cruzy, but there are actually enough samples to
Speaker 3: get prevalence estimates. What yeah, So, one study from two
Speaker 3: thousand and three screened two hundred and eighty three mummies
Speaker 3: for Tea Crusy, with the mummies dating as old as
Speaker 3: nine thousand years and as young as the eighteen hundreds. Wow. Yeah. Overall,
Speaker 3: the prevalence of tea cruzy was forty point six percent. Yeah, yeah, yeah,
Speaker 3: and that well, this is actually fairly steady over time.
Speaker 3: I mean, there are a few dips and a few surges,
Speaker 3: but like, and the sample sizes in some of these
Speaker 3: groups are low and whatever, but that was that's a
Speaker 3: pretty like shockingly high number. I think nearly fifty percent
Speaker 3: of people. Yeah, And the oldest of these mummies infected
Speaker 3: was this nine thousand year old mummy, and that indicated
Speaker 3: that humans in South America were exposed to the parasite
Speaker 3: long before domestication of guinea pigs and construction of European
Speaker 3: style housing or whatever, and that they probably first became
Speaker 3: infected from the sylvatic cycle of the parasite so between
Speaker 3: like the wild animals and the bugs. And that was
Speaker 3: well established by the first human occupation of the area.
Speaker 3: And it's not just in South America, but also in
Speaker 3: Central and North America that we have evidence of prehistoric infection.
Speaker 3: The oldest known case in North America, for instance, is
Speaker 3: a mummy in South Texas from around eleven hundred fifty
Speaker 3: years ago with a mega colon full of feces. Oh wow.
Speaker 3: And analysis of these copper lights, because we love our
Speaker 3: copper lights shows that this person, I think this is
Speaker 3: so fascinating, like you get to see what.
Speaker 2: People ate we're eating.
Speaker 3: Yeah, this person had ingested fish, snakes, bats, white footed mouse,
Speaker 3: pocket gopher, and grasshoppers. And so this led the researchers
Speaker 3: to suggest that the oral root of transmission might have
Speaker 3: played like a stronger role maybe in that area, especially
Speaker 3: if triatomine bugs were directly ingested huh yeah yeah. And
Speaker 3: so evidence of chronic infection in these prehistoric humans, like
Speaker 3: with this mega colon in Texas, has also been found
Speaker 3: in Peru and in Brazil in the forms of mega
Speaker 3: colon or cardiac lesions. So it seems clear that humans
Speaker 3: became infected with tea cruisy basically as soon as they
Speaker 3: arrived in an area where it was circulating in mammals.
Speaker 3: And since that time, the geographic distribution of the parasite,
Speaker 3: the dominant genotype, the transmission route, the vector species responsible.
Speaker 3: All these things likely shifted as human settlement patterns changed,
Speaker 3: as housing construction changed and like the materials, and as
Speaker 3: cultural practices changed, as well, but what didn't change and
Speaker 3: what remains true today is that there continued to be
Speaker 3: opportunities for infection. So the prevalence estimate that I mentioned
Speaker 3: in the mummies from the Atakama Desert is like pretty
Speaker 3: dang high at forty point six percent, and in the
Speaker 3: more recent mummies tested like in the last six hundred
Speaker 3: years or so, it was even higher at over fifty percent.
Speaker 3: So people had to know about this disease, right.
Speaker 5: Like wrong, wrong, yeah, I mean, Shaga's disease has been
Speaker 5: called the most neglected of the neglected tropical diseases.
Speaker 3: And that is due possibly in part to its relative
Speaker 3: clinical invisibility. Right, Just like you talked about, like the
Speaker 3: acute stage. When it is there, it doesn't necessarily have
Speaker 3: superdistinctive signs or symptoms, and it's not often severe, and
Speaker 3: so you just kind of get over it and then
Speaker 3: you forget about it, right, right, And the chronic stage
Speaker 3: can go unnoticed for a very long time, and it
Speaker 3: can then be attributed to other things or just like oh,
Speaker 3: heart failure.
Speaker 2: Right you, Oh, you have all these other risk factors
Speaker 2: for heart failure. You have heart failure. It's it's a
Speaker 2: normal kind of heart failure right right.
Speaker 3: It's not like leshmaniasis with its visible lesions, or river
Speaker 3: blindness with the itching and blindness, or dracunculiasis with like
Speaker 3: the actual word coming out of your foot. And because
Speaker 3: of this relative invisibility, there don't really seem to be
Speaker 3: many historical descriptions of shagas disease prior to its discovery.
Speaker 2: I'm not surprised about that.
Speaker 3: Yeah, the triatomin bugs, on the other hand, do get
Speaker 3: some early mentions. I've talked a lot on this podcast
Speaker 3: about what we can tell from the name of a disease,
Speaker 3: or in this case, like the vector. The name of
Speaker 3: the vector. The name itself can tell us what it
Speaker 3: meant to the people using it, how it was perceived,
Speaker 3: The number in geographic spread of the names can tell
Speaker 3: us how widespread the disease was, and it can help
Speaker 3: trace the history. When did the name first appear, how
Speaker 3: often was it used, did it increase in use, etc.
Speaker 3: In the case of shagas disease, we don't have historical
Speaker 3: descriptions of the disease, but we do have a long
Speaker 3: history and a long current list of names for the
Speaker 3: insect vector. Oh yeah, we have vinshu uka, a Quechua
Speaker 3: word meaning bug that lets itself fall chin chay, and
Speaker 3: many other nicknames that mean things like barber or sucking, blood,
Speaker 3: blood stealer, kissing bug, bug that dislikes the cold, big
Speaker 3: piercing bug, and so on.
Speaker 2: I like bug that dislikes the cold.
Speaker 3: Yeah. In one of the chapters I read, there's like
Speaker 3: a giant table showing these different nicknames and where they
Speaker 3: are used. It's really really cool table. Actually. The most
Speaker 3: famous description of these bugs, though, or at least the
Speaker 3: one that I saw referenced over and over, comes from
Speaker 3: none other than Charles Darwin. What yeah? In eighteen thirty
Speaker 3: five okay, quote the night I experienced an attack, for
Speaker 3: it deserves no lesser name of the vinchuka, a species
Speaker 3: of Rejuvius, the great black bug of the Pampas. It
Speaker 3: is most disgusting to feel soft, wingless insects about an
Speaker 3: inch long crawling over one's body before sucking. They are
Speaker 3: quite thin, but afterwards become round and bloated with blood,
Speaker 3: and in this state they are easily crushed.
Speaker 2: But it's really good. But Darwin, the adults have wings.
Speaker 3: Yeah, I mean, what would he? It wasn't like a
Speaker 3: famous naturalist or anything.
Speaker 2: Right, No, just like you know, minor natural minor.
Speaker 3: Yeah, this is a side gig.
Speaker 2: You know, isn't it? Thought he might have died from
Speaker 2: complications of Shagas disease.
Speaker 3: Oh well well look who's jumping the gun now? Oh
Speaker 3: what can we go? Yeah? So many people have retrospectively
Speaker 3: diagnosed Darwin with Shauga's disease, thinking that he was maybe
Speaker 3: exposed while on the HMS Beagle in like eighteen thirty four,
Speaker 3: eighteen thirty five. And it is true that he did
Speaker 3: become quite sick while in Chile and ended up being
Speaker 3: bed rich for seven weeks, and at the time it
Speaker 3: was thought to be typhoid, but no one else and
Speaker 3: the crew got sick. He eventually recovered, but later in
Speaker 3: his life he complained of palpitations, extreme fatigue, trembling, flatulence,
Speaker 3: and vomiting, and he was diagnosed first with hypochondriasis are
Speaker 3: you which is yeah and like a nervous condition or
Speaker 3: whatever they called it back then, and then later with
Speaker 3: heart failure after experiencing anginal attacks accompanied by extreme exhaustion
Speaker 3: and digestive disturbances that forced him to abandon his work.
Speaker 3: But it also might not have been Shaga's disease, since
Speaker 3: at least some of these health problems that he complained
Speaker 3: about he had before he ever went to South America,
Speaker 3: So I mean it's possible. Who knows. And other descriptions
Speaker 3: of the blood feeding nature of the comes from Augustin Lizaraga,
Speaker 3: a Peruvian farmer who discovered Machu Pichu in the early
Speaker 3: nineteen hundreds before Hiram Bingham stole all the credit. I
Speaker 3: just really wanted to throw that in there, because I
Speaker 3: didn't know that it like Hiram Bingham had stolen all
Speaker 3: the credit from somebody else. But I should have guessed.
Speaker 3: And then there are some earlier descriptions of the bugs,
Speaker 3: and even some that might hint at the disease by conquistadors.
Speaker 3: Although these descriptions I didn't even put in because they're
Speaker 3: pretty hand wavy, Like one of them is like or
Speaker 3: it could be hemorrhoids, and I'm like, okay, well this
Speaker 3: look like kind of different.
Speaker 2: They are pretty different.
Speaker 3: Yeah, yeah, all right, But I jumped around a bit
Speaker 3: in time back in here, so let's get reoriented bod things. Basically,
Speaker 3: by the very early nineteen hundreds, although Shagas disease was
Speaker 3: probably quite prevalent across parts of Central and South America
Speaker 3: and into North America. It seemed to be unknown entirely
Speaker 3: as medical condition.
Speaker 4: Wow.
Speaker 3: But by nineteen twenty one, all of that would change.
Speaker 3: Not only would it become well known across the world
Speaker 3: to infectious disease researchers, but its discoverer became famous in
Speaker 3: his own right, earning both acclaim he was nominated for
Speaker 3: a Nobel Prize twice, as well as criticism.
Speaker 2: Oh okay, Oh this is fun and I didn't know this.
Speaker 3: Yeah, this is a this is a very I think
Speaker 3: this is a very interesting story. And I'll get to why.
Speaker 3: And I hope that your mind will be blown just
Speaker 3: like mine was. Okay. Carlos Shagas was born on July ninth,
Speaker 3: eighteen seventy nine, on a coffee farm in Minas Cherais, Brazil.
Speaker 3: His father and two brothers died while Carlos was still young,
Speaker 3: leaving him to become head of the family. When he
Speaker 3: was old enough for college, his mother urged him to
Speaker 3: become an engineer, but he didn't pass the entrance exams
Speaker 3: and became very depressed until one of his uncles, who
Speaker 3: was a physician, was like hey, you know, why don't
Speaker 3: you try for med school? And so that's what he did.
Speaker 3: And in his time at med school he focused his
Speaker 3: work on malaria, and after graduating in nineteen o three,
Speaker 3: he received an invitation from the man who had become
Speaker 3: his friend and mentor, Oswaldo Cruz oh Yeah, to work
Speaker 3: at the Hygiene and Public Health Office monitoring malaria and
Speaker 3: shagus Like readily took him up on this since he
Speaker 3: needed a steady income in order to support his new
Speaker 3: family like he had just gotten married, just had a kid,
Speaker 3: and when Shaugus began working there, he was not only
Speaker 3: starting his medical career at a unique time, but also
Speaker 3: at a unique place. So around this time, in the
Speaker 3: early nineteen hundreds, theory had been fully embraced, and many
Speaker 3: pathogens and parasites had been described and were continuing to
Speaker 3: be discovered. Tropical medicine as a field was really starting
Speaker 3: to grow as imperialist countries struggled to develop the countries
Speaker 3: that they had laid claim to, with many people dying
Speaker 3: of tropical infectious diseases. And for all its imperialist and
Speaker 3: colonialist beginnings, tropical medicine did mean looking at the whole
Speaker 3: picture of public health, from the life cycle and habitat
Speaker 3: preferences of a vector, to the epidemiological characteristics of a disease,
Speaker 3: to the economic and productivity costs of these infectious diseases.
Speaker 3: It involved combining applied and basic research with an aim
Speaker 3: of prevention and control, not just descriptive knowledge building. Right
Speaker 3: and Oswaldo Cruz and the institute he founded, which was
Speaker 3: later to bear his name, the Oswaldo Cruz Institute, encapsulated
Speaker 3: this and then some. This institute placed the highest importance
Speaker 3: on the combination of research, education and assistance. Like other
Speaker 3: tropical medicine organizations, it integrated applied in basic research to
Speaker 3: solve problems. But unlike the others, Cruz wanted his institute
Speaker 3: to focus not just on the economic benefits of urban
Speaker 3: development for the colonialist countries or like the big companies,
Speaker 3: but also on the improvement of the lives of Brazilians
Speaker 3: of everyone by preventing infectious disease. And Carlos Shagas picked
Speaker 3: up this attitude from his mentor, and it greatly influenced
Speaker 3: his career and the way that he viewed medicine. In
Speaker 3: the words of his son quote, for Shagas, science was
Speaker 3: valid only if it was directed toward the welfare of humanity.
Speaker 3: Those are pretty good words.
Speaker 2: Yeah yeah.
Speaker 3: His first project under Cruz was to implement a malaria
Speaker 3: control strategy, which was pretty successful in reducing the cases
Speaker 3: of malaria and also showing that a lot of transmission
Speaker 3: actually occurred with inoholme rather than outside as was previously thought.
Speaker 3: His clinical background as a physician and his research background
Speaker 3: on vector borne disease it perfectly qualified him for this
Speaker 3: type of work, and soon he was assigned to a new,
Speaker 3: bigger project, a cross country railroad to transport agricultural products,
Speaker 3: the Brazil Central Railroad linking Belo Horizonte to Rio de Janeiro.
Speaker 3: It was under construction, but it kept getting delayed when
Speaker 3: workers fell ill during malaria outbreaks like big bad outbreaks
Speaker 3: in nineteen oh seven, Shagas was called in to stop
Speaker 3: the outbreaks using the method that was most commonly employed
Speaker 3: at the time, combat the vector combat disease. Essentially, he
Speaker 3: was tasked with setting up research stations at the towns
Speaker 3: along the railroad ahead of the construction to identify potential
Speaker 3: malaria hotspots and then get rid of the mosquitoes.
Speaker 2: Okay, cool, And it was at one of.
Speaker 3: These towns Laissance, I hope that's how you say it.
Speaker 3: A small town on the South Francisco River where Shagas
Speaker 3: heard a chief railroad engineer describe a blood sucking insect
Speaker 3: that was infesting the huts in the region and feeding
Speaker 3: on people while they slept. He called the bug the
Speaker 3: barber bug, since barbers were kind of like surgeons at
Speaker 3: the time they did a lot of like cutting and
Speaker 3: whatever they did. And from this tidbit of information, Chagas
Speaker 3: pulled off the reverse triple discovery.
Speaker 2: What a reverse triple discovery?
Speaker 3: Yeah, So we've been doing this podcast a while, which
Speaker 3: means we've gone through a of a lot of disease discoveries. Yeah,
Speaker 3: and it usually goes a little something like this. First,
Speaker 3: a bunch of people get sick and their symptoms are
Speaker 3: described and classified into one illness. Second, researchers began digging
Speaker 3: around for the causative agent after the rise of germ
Speaker 3: theory and begin using that as part of like diagnosis.
Speaker 3: And then third is usually when the root of transmission
Speaker 3: is determined, whether that means like arthropod vector or fecal
Speaker 3: oral or whatever. But what rarely, if ever, happens is
Speaker 3: that sequence in reverse.
Speaker 2: I love this.
Speaker 3: That's fantastic, and that is exactly what Shaugus did, the
Speaker 3: reverse triple discovery. Wow, all right, I got to read
Speaker 3: you a quote, okay from Shagus. Once we heard of
Speaker 3: the bloodsucking habits of this insect, and of its proliferation
Speaker 3: in human dwelling places, we became very interested in knowing
Speaker 3: its exact biology, and above all, in ascertaining if, by
Speaker 3: any chance, it were, as I immediately supposed, a transmitter
Speaker 3: of any parasite of man or of another vertebrate.
Speaker 2: Oh my gracious.
Speaker 3: So he found these bugs, was shown these bugs, and
Speaker 3: then was like, I'm pretty sure these probably because they
Speaker 3: feed on humans, they must transmit a disease.
Speaker 2: Super logical, honestly, Like he'd been working with malaria mosquitoes forever.
Speaker 2: He's like, bro, everything that bites you is gonna get
Speaker 2: you sick somehow, let's be honest, exactly.
Speaker 3: It's like this discovery was the product of his training,
Speaker 3: his like bright mind, but also like the type of
Speaker 3: job that he was doing too, and like the way
Speaker 3: tropical medicine is being practiced. It's definitely like a of
Speaker 3: course it happened this way, but also Oh my gosh,
Speaker 3: it happened this way.
Speaker 4: I know.
Speaker 3: Yeah, that's cool, amazing. So he tested his suspicion of
Speaker 3: this barber bug as a disease vector by dissecting its
Speaker 3: hindgut and examining it under the scope, where he found trypanosomes.
Speaker 3: So he gathered up a bunch more bugs, shipped them
Speaker 3: off to Oswaldo Cruz and asked him to feed them
Speaker 3: on monkeys, and he did. They got sick and shagas
Speaker 3: then later named his parasite Tripanosoma Cruzie after his mentor
Speaker 3: and friend, Oswaldo Cruz.
Speaker 2: You know what's so interesting, Aaron, is like it could
Speaker 2: have gone so differently, uh huh right, Like he could
Speaker 2: have found I don't know, just like he could have
Speaker 2: found something that transmitated a pair a virus that he
Speaker 2: never could have figured out, or something that only infected humans.
Speaker 2: So he tried to feed it on monkeys and it
Speaker 2: didn't work, or like, there are so many ways that
Speaker 2: this could have not gone the way that it went.
Speaker 2: But it was like, here's an obvious parasite that looks
Speaker 2: like not so dissimilar to malaria, which I'm familiar with.
Speaker 2: Let's feed it on a monkey. The monkey kids say, sure,
Speaker 2: it does, because any mammal will like what.
Speaker 3: I I know. I love it. I think it was
Speaker 3: such a like fantastic, fascinating story in the history of medicine.
Speaker 2: I love it.
Speaker 3: It's just so like, it's so unbelievable but also totally believable.
Speaker 2: She's just like, exactly what good way to describe it?
Speaker 2: Unbelievable but totally believable.
Speaker 3: Yeah, and so at this point, yeah, Shagas had identified
Speaker 3: a vector and a parasite that was at least somewhat
Speaker 3: pathogenic to you know, animals or some animals, but he
Speaker 3: still didn't know whether it was a disease of humans.
Speaker 3: And for a couple of years after first discovering the tripanosome,
Speaker 3: he looked for it in animals and humans all over
Speaker 3: and it took him a while, but in nineteen oh
Speaker 3: nine he found it in both, first in a cat
Speaker 3: and after on April fourteenth, which was declared in twenty
Speaker 3: twenty by the WHO as International Shaugust Disease Day. Oh so,
Speaker 3: on this date he found this parasite in a two
Speaker 3: year old girl named Bernice, the first described case of
Speaker 3: what would later be known as Shaugus disease, and Shaga
Speaker 3: disease was named in fact by Oswaldo Cruz. Of course
Speaker 3: it was is that just like really cute. I just
Speaker 3: think that's really nice.
Speaker 2: He's like, I name the parasite after you. Oh cool,
Speaker 2: name the disease after you.
Speaker 3: Yeah, I think it's nice. So Shagus wrote in his
Speaker 3: famous nineteen oh nine publication that Bernice had a swollen
Speaker 3: liver and spleen. Have had a splinomega mate. Oh my god,
Speaker 3: I can't say it. I had a spleen o'megaie and
Speaker 3: swollen lymph nodes. She was febrile, she was anemic, she
Speaker 3: had edema, and also he found circulating trepanosoma cruisie. In
Speaker 3: this public of the acute form of the disease, he
Speaker 3: also described the morphology of the tripanosome, as well as
Speaker 3: its life cycle and its intermediate and definitive hosts. He
Speaker 3: described his attempts to culture the tripanosome. He described the
Speaker 3: course of infection, and so on and Over the next
Speaker 3: couple of years, he continued to work on the disease,
Speaker 3: looking for it in more people in autopsies and better
Speaker 3: characterizing the acute stage of the disease as well as
Speaker 3: looking at chronic infection and long term consequences.
Speaker 2: He just like decided to do that or just like
Speaker 2: because of doing autopsies.
Speaker 3: Was like I think probably doing the autopsies kind of
Speaker 3: like led him along. And then he got a researcher
Speaker 3: involved named Gaspar Viana, who was especially crucial in investigating
Speaker 3: some of the cardiac impacts specifically. But it is to
Speaker 3: me it's really impressive that Shagas was like I found
Speaker 3: the acute stage and then was like, there's something about
Speaker 3: I wonder if there's a chronic stage to this.
Speaker 2: Yeah, Yeah, Like I wanna keep going on this.
Speaker 3: Yeah. And after this, this publication was released in nineteen eleven,
Speaker 3: you know, which was more thorough about the parasite itself
Speaker 3: and the disease progression. It was like immediate success and
Speaker 3: attention for Carlos Shagas. Other researchers throughout South and Central
Speaker 3: America began looking for and sometimes finding the tripanosome in
Speaker 3: their areas, and shagus himself was awarded the Shouden Prize,
Speaker 3: which was given out only every four years for the
Speaker 3: best work in parasitology and tropical medicine in the world. Wow.
Speaker 3: But all this success and acclaim came with an ample
Speaker 3: supply of haters, as it usually does.
Speaker 2: Uh huh.
Speaker 3: German microbiologist Rudolph Krauss took great issue with Chagas's claim
Speaker 3: that the disease was prevalent all across South America. Kraus,
Speaker 3: who was working in Argentina, had looked but had been
Speaker 3: unable to find any tripanosomes in any of the areas
Speaker 3: that he looked, and attacks also came from members of
Speaker 3: the Brazilian National Academy of Medicine, who undermined his research
Speaker 3: and tried to discredit him. It's disappointing, I know why,
Speaker 3: well why and so I was thinking about like he
Speaker 3: got in some ways so lucky, right, like you were saying, yeah,
Speaker 3: there is always like with new discoveries, there is always resistance,
Speaker 3: Like there does have to be the sort of like
Speaker 3: ping ponging of like, well, wait a second, we need
Speaker 3: to introduce some healthy skepticism into this. And so maybe
Speaker 3: their attacks were way more personal than they needed to be.
Speaker 3: But I do think at the time, you know, part
Speaker 3: of their skepticism or or hesitance might have been reasonable,
Speaker 3: considering also the fact that Shagus didn't get it all
Speaker 3: right in his first go but I mean, whoever does.
Speaker 3: But you know, he first thought was the bite of
Speaker 3: the bug that transmitted the parasite. You know, sorry, reasonable,
Speaker 3: It's very reasonable. And then the French parasitologist Alexander Brimpt
Speaker 3: soon realized it was through the feces of tritomines. And
Speaker 3: but the other big thing, the big mistake or false
Speaker 3: association that Shagus made, was that he incorrectly associated the
Speaker 3: disease with goiters, which were really prevalent all across Brazil,
Speaker 3: Goiter's being caused by an iodine deficiency, and so other
Speaker 3: researchers were finding people with goiters but without tripanisamiasis. Without it,
Speaker 3: couldn't find the tripanosomes. And so they were like, we're not, like,
Speaker 3: you're seeing something that we're not seeing. And I feel
Speaker 3: like the reverse story where those detractors, those haters like
Speaker 3: have been right in other histories of disease, where they're like,
Speaker 3: you're not seeing what you're seeing, it must be something else.
Speaker 3: So anyway, it's just it's the way history is written now.
Speaker 3: And so some of these haters might have simply been
Speaker 3: jealous of his quick rise to fame and his ample success,
Speaker 3: but some may not have wanted to recognize that someone
Speaker 3: not from North America or Europe had made such a monumental.
Speaker 2: Discovery that was gonna be my guess.
Speaker 3: Yeah. So, like I said earlier, Shagus was nominated twice
Speaker 3: two times for the Nobel Prize, and in the second
Speaker 3: time he was nominated it was nineteen twenty one. The
Speaker 3: Nobel Prize wasn't awarded to any scientist that year, and
Speaker 3: there was no evaluation. There's no record of evaluation of
Speaker 3: his nomination or like his research or whatever by the committee.
Speaker 3: What So it's a little fishy.
Speaker 2: Yeah.
Speaker 3: Apparently there's like some drama in those early years about
Speaker 3: who got the awards and whatever, which is unsurprising. Yeah,
Speaker 3: But as a result of all this negative press, Shaugas
Speaker 3: disease was like all but forgotten about for a short
Speaker 3: period of time, like a few years, until physician Salvador
Speaker 3: Masa from Argentina began researching the disease. His studies across Argentina,
Speaker 3: which were conducted in the late nineteen twenties, found hundreds
Speaker 3: of cases of Shaugas disease where Kraus had found none. Yeap, okay, Yeah,
Speaker 3: I think in one of the publications Shagus like kind
Speaker 3: of hinted about like, oh, well, you might not really
Speaker 3: have the right technique for scope, you know, microscopy or whatever,
Speaker 3: and Matsa was the first to suggest that the taypanosome
Speaker 3: could be transmitted through blood transfusions, which were slowly improving
Speaker 3: and becoming more accessible in like, you know, thirties and forties.
Speaker 3: Maza's work showing widespread prevalence again kicked things off for
Speaker 3: Shaugust disease research as more and more researchers became aware
Speaker 3: that it was this tip of the Iceberg type of situation.
Speaker 3: Increasing development, deforestation, and urbanization throughout the mid twentieth century
Speaker 3: led to both this increase in disease prevalence as well
Speaker 3: as the construction of hospitals where the chronic manifestations of
Speaker 3: the disease and congenital transmission could be more easily studied,
Speaker 3: especially as technology improved to actually see what was going
Speaker 3: on inside, like with your heart and with mega colon
Speaker 3: and so on. Chagas's son, Evandro followed somewhat in his
Speaker 3: father's footsteps and played a big role in uncovering the
Speaker 3: widespread and hidden nature of the disease and the little
Speaker 3: girl Bear Nice Chaugus's first Shagus patient was found again
Speaker 3: at the age of fifty three, still with circulating trepanosomes,
Speaker 3: but no sign of disease. Oh good, Yeah, yeah, she
Speaker 3: died I think at the age of seventy or seventy eight,
Speaker 3: maybe with I think seventy eight, with no relation to
Speaker 3: Shaga's disease.
Speaker 2: Like that's that's pretty good for being born in the
Speaker 2: early nineteen hundreds.
Speaker 3: M h yeah, nineteen oh seven. Shagus himself became a
Speaker 3: huge figure in the history of Brazilian public health as
Speaker 3: the director of the Oswaldo Cruz Institute for seventeen years
Speaker 3: and the head of pandemic influenza campaigns, the head of
Speaker 3: the Department of Health in Brazil. He discovered numaicistis pneumonia
Speaker 3: and created a nursing school. He did a ton of
Speaker 3: work in his like relatively short life. I think he
Speaker 3: died in his fifties. Oh my gosh. Oswaldo Cruz died
Speaker 3: at forty four of kidney disease.
Speaker 2: Oh gracious.
Speaker 3: Yeah.
Speaker 2: There's also a journal named after the institute.
Speaker 3: Oh yeah, I got a lot of I've read a
Speaker 3: lot of papers from that journal. I was like, I
Speaker 3: know you as an institute and a journal, not as
Speaker 3: a human being. It's fun to learn about you. Nice
Speaker 3: to meet you. But not all Shaugus disease researchers were
Speaker 3: like Shaugus. Not all of them cared about the well
Speaker 3: being of the people that they studied. For example, in
Speaker 3: an instance of medicalized torture in Texas, a researcher named
Speaker 3: Ardzruni Pakshanian crushed some kissing bugs and smeared them into
Speaker 3: the eye of a black man in his twenties who
Speaker 3: was likely a patient at Austin State Hospital formerly known
Speaker 3: as the Texas State Lunatic Asylum, just to study the
Speaker 3: progression of disease and how long this person would remain
Speaker 3: with like circulating parasites.
Speaker 2: What.
Speaker 3: Yeah, so the symptoms of the person did show symptoms
Speaker 3: of disease, and eventually they recovered and were declared tripanosome free.
Speaker 3: But yeah, the study continues to be cited. What I know,
Speaker 3: Carlos Shagas recognized all the way back in nineteen oh
Speaker 3: nine the public health relevance of American tripanisamiasis, but it
Speaker 3: wasn't until the nineteen eighties that countrywide surveys were conducted
Speaker 3: using standardized protocols and a reliable estimate of the number
Speaker 3: of people infected and at risk could be even estimated,
Speaker 3: and those numbers were often shocking. I'm not going to
Speaker 3: go through all of them, but you know, I'll throw
Speaker 3: a few out there. So from like twenty percent in
Speaker 3: Bolivia to twenty percent of rural Chile and up to
Speaker 3: fifty percent in parts of rural Venezuela, Shagas's was a
Speaker 3: much bigger problem than I think anyone had any idea about.
Speaker 2: I feel like that's still true.
Speaker 3: Yeah, definitely. And around the same time, the HIV AIDS
Speaker 3: pandemic revealed that tripanosoma cruzie could be reactivated in a
Speaker 3: compromise people and proved to be a huge complication there.
Speaker 3: And this growing awareness of the enormous problem that shagas
Speaker 3: disease poses did help lower the incidents of disease in
Speaker 3: some places, such as through like the Southern Cone Initiative
Speaker 3: and other pushes for eradication and control, and the existence
Speaker 3: of the somewhat effective drug that's used I think it's
Speaker 3: benz ny dazzlely close to it, which was introduced in
Speaker 3: nineteen sixty six. These things also helped, but we're still
Speaker 3: a long way off. Yeah, but exactly how far off
Speaker 3: are we? Aaron?
Speaker 2: Oh, what a good question. Let's get into it right
Speaker 2: after this break. It's interesting, Aaron, because despite just how
Speaker 2: when you think about it, just how inefficient the transmission
Speaker 2: cycle really is in terms of trying to get the
Speaker 2: poop of this bug somewhere near a bite wound, the
Speaker 2: overall ecology of this disease is so complex, with so
Speaker 2: many different wildlife and domestic mammal species involved, and in humans,
Speaker 2: the infection can persist for so long that this is
Speaker 2: not only a very difficult disease to control, but estimates
Speaker 2: of incidents and prevalence are also very difficult. Right, But
Speaker 2: we'll do our best here.
Speaker 3: Yeah.
Speaker 2: Estimates of incidents the number of new infections annually range
Speaker 2: from zero point one percent to four percent of the
Speaker 2: population in endemic regions, so largely in Central and South America.
Speaker 3: Wow.
Speaker 2: Yeah, which is pretty high in and of itself.
Speaker 3: Right, I mean if every year four percent of people
Speaker 3: are getting infected.
Speaker 2: Yeah, yeah, But in a lot of places, shaugus isn't
Speaker 2: even like a reportable disease everywhere that it's endemic, and
Speaker 2: it's often only diagnosed in the chronic phase, and a
Speaker 2: lot of places don't have like registries, so all of
Speaker 2: these are really just estimates. When we look globally, it's
Speaker 2: estimated that between six and seven million people worldwide are
Speaker 2: living with Shaugus disease currently. And what I don't know,
Speaker 2: because I see your face thinking, HM, is does that
Speaker 2: mean six to seven people living with some amount of
Speaker 2: illness from shaugust disease or six to seven million people
Speaker 2: living with tripanosomacrusie in their bloodstream? Right? And I imagine
Speaker 2: because that number is from the World Health Organization, that
Speaker 2: that means people with some amount of disease. Okay, okay,
Speaker 2: But what's worse than that number? Sixty seven million people,
Speaker 2: which is probably an underestimate. That's pretty bad already m hm.
Speaker 2: But it's estimated that only one to two percent of
Speaker 2: those people living with shaugust disease have access to treatment.
Speaker 3: I was gonna ask A, what is the treatment for
Speaker 3: chronic disease? And B how much does it cost?
Speaker 2: So once you get to chronic disease, what you're dealing
Speaker 2: with is whatever your disease manifestation is. So if you
Speaker 2: have heart failure from shaugust disease. You're treating someone for
Speaker 2: heart failure. You're not treating them for shaugust disease, right, right.
Speaker 2: If you have somebody with megasoft, you're treating them for megaesophagus.
Speaker 2: That's the problem. That's a huge part of the problem, right, right,
Speaker 2: So you have to be able to find people before
Speaker 2: they have heart failure from chuckus And like we've touched
Speaker 2: on though historically this is a disease of poverty and
Speaker 2: of Central and South America and the southern part of
Speaker 2: the United States, we live in a globalized world and
Speaker 2: because of global migration, this is a global disease. And
Speaker 2: like you touched on Aaron, in non endemic areas like
Speaker 2: Europe and much of North America, physician knowledge of the
Speaker 2: disease is seriously lacking, and it's thought that cases are
Speaker 2: underdiagnosed by like ninety five percent is one of the
Speaker 2: estimates that I saw.
Speaker 3: That's horrifying, but not surprising.
Speaker 2: Right, I mean, because it's again, if somebody comes in
Speaker 2: with heart failure, it's not going to be the top
Speaker 2: thing that you think of as someone living in Europe
Speaker 2: or a lot of North America, Like, is this the
Speaker 2: underlying cause of your heart failure. Right, Yeah, if we
Speaker 2: look at economics, and you know, I don't really love
Speaker 2: talking about the economic part of it, but I think
Speaker 2: it's important from a public policy perspective. Shaugu's disease is
Speaker 2: estimated to have a global economic burden of over seven
Speaker 2: billion dollars annually. That's more than rotavirus, that's more than
Speaker 2: cervical cancer, that's more than lime disease, and results in
Speaker 2: an estimated over eight hundred thousand disability adjusted life years annually.
Speaker 3: Okay, Yeah, it's a big, huge, one huge.
Speaker 2: So when it comes to research needs, there's a lot
Speaker 2: of them, right. Like I said, there's a lot of
Speaker 2: parts of this from the ecology to the path of physiology,
Speaker 2: to treatments to vaccines that we just don't have enough
Speaker 2: information on. We also just don't have a great handle
Speaker 2: on prevalence. So there's a lot of room for investigation.
Speaker 2: And luckily there's a lot of incredible people who are
Speaker 2: researching Shagas disease from every single angle. At this point,
Speaker 2: as far as I could tell in my research, there
Speaker 2: aren't any novel therapeutics that have made it very far
Speaker 2: in the research chain. There are a couple of different
Speaker 2: avenues for promising vaccine research, both in preventative vaccines, so
Speaker 2: vaccines to help prevent the disease, as well as therapeutic vaccines,
Speaker 2: which would be something to help prevent the development of
Speaker 2: chronic disease. But as far as I could tell, these
Speaker 2: are all in pretty early stages of development, and one
Speaker 2: of the biggest issues is funding. And then of course
Speaker 2: people are really starting to realize the impact of non
Speaker 2: vector borne transmit roots such as congenital infection and how
Speaker 2: little we know about that. So suffice to say, there's
Speaker 2: a lot of different research needs. Oh yeah. For that reason,
Speaker 2: we wanted to talk to somebody who has done research
Speaker 2: on a lot of different aspects of shaugas disease, from
Speaker 2: trying to better understand the dynamics of shaugus here in
Speaker 2: the US and involves citizen science, which is so cool,
Speaker 2: to really nitty gritty molecular biology to better understand the
Speaker 2: vectors and the pathogen itself and so much more so,
Speaker 2: we wanted to talk to someone about all of these
Speaker 2: lingering questions that we have regarding shaugas, and for that
Speaker 2: we turned to one of our faves, doctor Sarah Hamer.
Speaker 3: All time shaves.
Speaker 6: I'm Sarah Hamer. I'm an associate professor in the College
Speaker 6: of Veterinary Medicine and Biomedical Sciences at Texas A and
Speaker 6: M University, veterinarian, and I lead a research lab on
Speaker 6: the ecology and epidemiology of infectious diseases.
Speaker 3: Awesome, thank you so much for taking the time to
Speaker 3: chat today. I'm super excited to hear more about shagas disease.
Speaker 3: So in this episode, we have so far largely focused
Speaker 3: on the health impacts of shagast disease on humans, but
Speaker 3: many different animal species can also become infected with tripanosomacuruzi,
Speaker 3: including both domestic and wild animals. So what can infection
Speaker 3: with the tripanisome look like in these different animal species?
Speaker 3: And do some animals tend to be more negatively affected
Speaker 3: than others?
Speaker 6: That's a great question. So I think the first issue is,
Speaker 6: you know, this is a generalist parasite that can infect
Speaker 6: virtually any mammal, and it's a generalist vector that will
Speaker 6: happily feed on lots of different animals, you know, domestic, wild,
Speaker 6: So I think it, yeah, it makes sense to try
Speaker 6: to think about, right, how does disease differ you know,
Speaker 6: depending on the host that's infected. Sadly, we don't really
Speaker 6: know about the impact on a lot of different wildlife
Speaker 6: species that are infected because it's hard to come, you know,
Speaker 6: to find them, it's hard to get money to study
Speaker 6: the clinical outcome or to follow them forward over time.
Speaker 6: It's hard to do that in nature. The nice thing is,
Speaker 6: you know, from what we can understand, what we know,
Speaker 6: disease seems to look similar to what it does in humans.
Speaker 6: We know the most about the disease outcome in dogs,
Speaker 6: in non human primates, and in humans, just because that's
Speaker 6: where the most amount of clinical attention has been paid.
Speaker 6: So just we see in infected humans, what we see
Speaker 6: in these infected animals is that there can be a
Speaker 6: subpopulation of infected animals that might not ever develop signs
Speaker 6: of disease. They might remain asymptomatic for life. So that's
Speaker 6: a very good thing. But there is you know, some percentage,
Speaker 6: some unknown percentage of affected animals that will develop disease,
Speaker 6: usually heart disease, and depending on where the parasite affects
Speaker 6: the heart, we might see different you know, outward manifestation
Speaker 6: of the infection. So you know, just like humans, we
Speaker 6: can see inflammation fibrosis of the heart depending on you know,
Speaker 6: exactly where the parasite localizes in the heart. This can
Speaker 6: lead to you know, acute problems. This can lead to
Speaker 6: chronic problems in the animals, especially with fis of heart failure.
Speaker 6: We see sudden death. Often young dogs can die suddenly
Speaker 6: from this infection. We're working now to try to figure out,
Speaker 6: you know, if there's an infected animal, what are some
Speaker 6: ways that we can predict the outcome of infection. Is
Speaker 6: this something we need to be worried about versus is
Speaker 6: this something that the animal will be able to live
Speaker 6: with this infection for life and we don't need to
Speaker 6: be as worried about it.
Speaker 3: Awesome, Yeah, that was really interesting that you might be
Speaker 3: able to try to figure out who is going to
Speaker 3: be able to live with this long term versus those
Speaker 3: that might not be. And so, since some animals can
Speaker 3: act as reservoirs for a tripanosomacruzie, they can of course
Speaker 3: have a big impact on transmission cycle of shaugast disease
Speaker 3: and then the risk of exposure to humans. So let's
Speaker 3: start with the domestic side of things, which domestic animals
Speaker 3: play a role in the infectious cycle, and what does
Speaker 3: that role look like And are there some domestic animals
Speaker 3: that contribute more than others to the risk of exposure
Speaker 3: for humans.
Speaker 6: Yeah, so when we think about domestic animals and chagas disease,
Speaker 6: the main you know, domestic animals that come to mind
Speaker 6: would be our dogs and cats, you know, the most
Speaker 6: commonly owned pats here in the United States and elsewhere,
Speaker 6: and both those species can play roles in sort of
Speaker 6: the ecology and epidemiology of chogga disease. We know most
Speaker 6: about dogs. Canine shogga disease has received far more veterinary
Speaker 6: attention than like feline shogga disease. But what I'd like
Speaker 6: to start by saying is that there's no evidence that
Speaker 6: infected dogs or infected cats pose a direct transmission risk
Speaker 6: to people. So even if you knowingly or unknowingly own
Speaker 6: a dog that's infected, for example, that sort of direct
Speaker 6: risk dog to human transmission hasn't been shown. Instead, the
Speaker 6: role that infected dogs might play is that they could
Speaker 6: potentially infect kissing bugs that feed on them, and then
Speaker 6: those kissing bugs that are around the home could be
Speaker 6: a source of infection to other animals or to people.
Speaker 6: So when we think about, you know, domestic animals and
Speaker 6: their role as a reservoir, by reservoir here, we mean
Speaker 6: that it's an animal that not only gets infected, but
Speaker 6: it gets infected and can kind of sustain that parasite
Speaker 6: in its body and then serve as a source of
Speaker 6: infection to another animal or two in this case, to
Speaker 6: a vector that's feeding on it. And dogs can certainly
Speaker 6: play that role. It's actually really hard to figure that out, though.
Speaker 6: It's not as simple as just figuring out if an
Speaker 6: animal is a reservoir by taking a blood sample and
Speaker 6: doing a molecular test and Yep, the parasite's there, it's
Speaker 6: a reservoir. Instead, the approach that we've used, you know,
Speaker 6: in our research settings at least to define the role
Speaker 6: of dogs as reservoirs is that we can sample their
Speaker 6: blood and then bring that blood to our kissing bug
Speaker 6: insect colony that we have on campus, and then we
Speaker 6: can feed the blood from the dogs to clean insects
Speaker 6: in a very controlled environment. We can monitor those kissing
Speaker 6: bugs for infection to see if they become infected and
Speaker 6: will shed the infection in their feces. We can do
Speaker 6: that days, weeks or even months after they've been fed
Speaker 6: this potentially infectious blood meal. So it's through you know,
Speaker 6: some really neat techniques like that that we can begin
Speaker 6: to define who are the important reservoirs in domestic environments
Speaker 6: or in wild environments, and that you know, helps us
Speaker 6: understand the ecology of this disease better.
Speaker 3: That is fascinating. Oh my gosh, a little colony of
Speaker 3: clean kissing bugs and then feeding them blood. I can't
Speaker 3: that's really cool.
Speaker 6: Yeah, it's a unique resource that we have, for sure.
Speaker 6: That's you know, people have mosquito colonies and tiktol is,
Speaker 6: but this kissing bug colony is pretty unique and has
Speaker 6: definitely opened the doors for research.
Speaker 3: Yeah. Wow, amazing. Wow. So, you know, I want to
Speaker 3: ask you a little bit more about some of the
Speaker 3: research that you do, in particular your incredible citizen science
Speaker 3: or community science projects, and what they have told us
Speaker 3: so far or what they can tell us about the
Speaker 3: landscape of Chagas disease risk in Texas.
Speaker 2: Yeah.
Speaker 6: So, back in twenty thirteen, we started a big community
Speaker 6: science program where we you know, intended to provide a
Speaker 6: lot of good material for the public about kissing bugs
Speaker 6: and about shaga disease. And in return, if members of
Speaker 6: the public happen to see or find kissing bugs in
Speaker 6: their home, you know, on their property and their dog kennels,
Speaker 6: they could safely collect these insects and then submit them
Speaker 6: to our lab for part of our research. So this
Speaker 6: really started, you know, out of desperation because we were
Speaker 6: out doing fieldwork and these insects are really hard to
Speaker 6: try app using standardized traps, you know, manual fieldwork to
Speaker 6: find them can be pretty labor intensive. But we were
Speaker 6: trapping on these Texas ranches and other areas and the
Speaker 6: landowners would tell us, oh, yeah, I've seen those insects before.
Speaker 6: Oh I've you know, I've captured a couple of those.
Speaker 6: I saved them, you know, and they might have them
Speaker 6: in an old pill jar in the freezer. And so
Speaker 6: it was really through that that was the start of
Speaker 6: our community science program. And it's it's definitely a two
Speaker 6: way street. You know, we want to provide a lot
Speaker 6: of good info. We do that through our website, through
Speaker 6: a smartphone app, through printed brochures and outreach seminars that
Speaker 6: we give and then in return. Since twenty thirteen, we've
Speaker 6: received over eight thousand kissing bugs from people in twenty
Speaker 6: seven different states. Then they've submitted these insects to our
Speaker 6: program and we can learn a lot. And basically at
Speaker 6: the state level, this community science program has replicated, you know,
Speaker 6: what's known of the historic distribution of kissing bugs in
Speaker 6: the United States and has provided just a wealth of
Speaker 6: great material for our research program. So from the community
Speaker 6: science program, we've learned that on average, it's just over
Speaker 6: fifty percent infection prevalence of these insects. So of all
Speaker 6: the insects that we've received from community members that have
Speaker 6: submitted them to our program, will we will dissect them,
Speaker 6: take their gut material out, do DNA extractions, and then
Speaker 6: try to figure out if they're infected with the parasite
Speaker 6: or not. And we've found over fifty percent of the
Speaker 6: adult insects are infected with Trapanosoma cruisy, so pretty high
Speaker 6: infection prevalence. And then furthermore, we've learned that there's two
Speaker 6: major genetic variants of the parasite that we find in
Speaker 6: kissing bugs of the United States, and we're kind of
Speaker 6: mapping out those genetic variants and trying now to figure
Speaker 6: out if there's different health consequences when people or animals
Speaker 6: are infected with one type or another. But the most
Speaker 6: exciting thing I think that we've been able to do
Speaker 6: with these community science submitted kissing bugs is what's called
Speaker 6: a blood meal analysis, where we can taken individual insect
Speaker 6: and figure out what has it fed upon, what type
Speaker 6: of blood meal did it get from what species? And
Speaker 6: this is really important for not just understanding the ecology
Speaker 6: of the disease, but trying to open the doors for management,
Speaker 6: because if we can figure out what types of animals
Speaker 6: are important for feeding kissing bugs and maintaining their populations,
Speaker 6: then maybe we can try to manage those species so
Speaker 6: they have less contact with the vector. So just a
Speaker 6: glimpse of some of our data from blood meal analysis
Speaker 6: of these community science kissing bugs, we find, overall about
Speaker 6: half of them have evidence of feeding on a dog.
Speaker 6: And that makes sense because we know that a lot
Speaker 6: of these bugs submitted by the public are actually found
Speaker 6: in dog kennels or in areas where their dogs sleep.
Speaker 6: A lot of people submitting bugs will report that they
Speaker 6: own multiple dogs, so that makes sense. We also find
Speaker 6: that kissing bugs have fed on cats, chickens, tortoises, a
Speaker 6: lot of it is, you know, just depending on the
Speaker 6: habitat where they're found, whatever the most abundant host is there,
Speaker 6: that's what they're going to feed on. Like you know,
Speaker 6: kissing bugs collected from a chicken coop, they're gonna feed
Speaker 6: on chickens. But we also get some exciting observations like tigers,
Speaker 6: and that was found from some bugs that were submitted
Speaker 6: from the local zoo, so it makes sense that that
Speaker 6: host is available and the bugs will happily feed on it.
Speaker 6: And two of my favorite observations was an elf owl.
Speaker 6: We found evidence of a kissing bug feeding on the
Speaker 6: elf owl, which is the world's tiniest owl. And this
Speaker 6: was a bug that was collected by a community member
Speaker 6: from Big Bend National Park where these elf owls will nest,
Speaker 6: so that was pretty neat. And then a more recent
Speaker 6: one was our results from Bloodmaal and allis was a
Speaker 6: peach face love bird and we thought lovebird, like, this
Speaker 6: isn't a wild species, you know where this insect was
Speaker 6: submitted from. So we wrote back to the submitter and
Speaker 6: we said we're trying to make sense of this, you
Speaker 6: know DNA sequence that we got, and she wrote back
Speaker 6: immediately and said that's my pet lovebird that I have
Speaker 6: in a cage in the house. And so this, you know,
Speaker 6: this technique can really open our eyes for just how
Speaker 6: flexible these kissing bugs can be in what they feed on.
Speaker 6: And this was all enabled by our community science program.
Speaker 3: That is incredible eight thousand first of all, and also
Speaker 3: feeding on a tiger, like, that's so cool. I never
Speaker 3: would have thought. I was like, Okay, what is the
Speaker 3: coolest animal I could think of, Like the most surprising
Speaker 3: animal I could think of in terms of kissing bugs,
Speaker 3: and a tiger definitely is shocking and very cool.
Speaker 6: Yeah, and over time, it's data like this that will
Speaker 6: help researchers piece together not just the feeding patterns of
Speaker 6: the insect, but if we can couple that with what
Speaker 6: animals are infected and what insects are infected, we can
Speaker 6: just piece together these transmission networks. And I think that's
Speaker 6: going to be really exciting for again opening the doors
Speaker 6: for management.
Speaker 3: Yes, absolutely, And so you know, on the note of
Speaker 3: the fact that these kissing bugs feed on so many
Speaker 3: different species of animal, I kind of want to shift
Speaker 3: to now talk about the wildlife, like the sylvadic cycle
Speaker 3: of these bugs, and so you know, humans might not
Speaker 3: have as much contact with wildlife as they do with
Speaker 3: domestic animals, but many wild animals can still increase the
Speaker 3: risk of shaga disease or the prevalence of the typanosome
Speaker 3: in certain areas, which then might impact the risk to humans.
Speaker 3: So which wildlife species are considered the most important reservoirs?
Speaker 3: I know this changes a lot geographically as well, But
Speaker 3: are there some you know, more than others that seem
Speaker 3: to be, you know, play the largest role And you know,
Speaker 3: I also wanted to kind of ask you about how
Speaker 3: things like deforestation and land use change is impacting Shauga
Speaker 3: disease in wildlife and then thus exposure to humans.
Speaker 6: So across the southern United States where kissing bugs are endemic,
Speaker 6: there have been a lot of different you know, infected
Speaker 6: wild animals that have been identified, but in terms of
Speaker 6: the key species that are most likely playing that role
Speaker 6: as reservoirs infecting other kissing bugs and kind of perpetuating
Speaker 6: this transmission cycle in nature, some of the key species
Speaker 6: that have emerged include raccoons, possums, armadillos, wood rats, coyotes,
Speaker 6: to a lesser extent, other rodents or bats. But very
Speaker 6: little research has been done to really rank their importance,
Speaker 6: to figure out what is the exact wild species that's
Speaker 6: the most important reservoir in this area or another area.
Speaker 6: In terms of you know, your question about land use
Speaker 6: change and you know, deforestation or other types of land
Speaker 6: use change that's occurring. You know, of course, we know
Speaker 6: there's some pretty cool and compelling stories from different vector
Speaker 6: born diseases that would say that certain types of deforestation
Speaker 6: might really increase transmission, for example the lime disease system.
Speaker 6: I think it's a little premature to understand exactly how
Speaker 6: deforestation or other land use change is likely to impact
Speaker 6: the ecology of Chogga's disease. These try it means, you know,
Speaker 6: they're not just found in silvadic or natural environments or
Speaker 6: more rural environments. We also regularly find them in urban areas,
Speaker 6: for example, lots of collections from San Antonio, Dallas, Fort Worth,
Speaker 6: some of these major urban cores here in the South.
Speaker 6: So they're flexible in where these different kissing bug species
Speaker 6: can thrive. But certainly, you know, if we have changes
Speaker 6: to the landscape like deforestation, that might make that area
Speaker 6: more or less attractive to the raccoons or the possums.
Speaker 6: Who really can thrive in small forest fragments adjacent to
Speaker 6: human dwellings. And so maybe if we're changing the landscape
Speaker 6: in a way that makes it more attractive to some
Speaker 6: of these medium sized mammals, then we could have even more,
Speaker 6: you know, more of these reservoirs across the landscape that
Speaker 6: could increase transmission risk. But we can imagine scenarios where
Speaker 6: the opposite could be true as well.
Speaker 3: Yeah, it's such a complex system. It's something it's a
Speaker 3: theme that we've hit on so many times during this episode,
Speaker 3: is that there are just so many moving parts that
Speaker 3: play and so it makes sense that, you know, there's
Speaker 3: not a clear path forward or a clear prediction as
Speaker 3: to things like climate change, things like deforestation, land use change,
Speaker 3: and what impact they'll have. So yeah, yeah, So what
Speaker 3: do you see as the biggest challenges in the control
Speaker 3: of this disease.
Speaker 6: Yes, there are two big, grand challenges that come to
Speaker 6: mind when I think about the control of Chagas disease.
Speaker 6: The first is just simply that this is a sylvadic disease,
Speaker 6: and by that we mean it's associated with these vectors
Speaker 6: that are out in nature interacting with a lot of
Speaker 6: different members of the wildlife community. We talked about how
Speaker 6: the insects will happily feed on all different sorts of critters.
Speaker 6: The parasite can effect virtually any mammal species. So it's sylvatic,
Speaker 6: and it involves a lot of players in the transmission cycle.
Speaker 6: So it's not as simple, not that it's simple, but
Speaker 6: you know, when we think of a different vector born disease,
Speaker 6: you know, human malaria, for example, main reservoir would be humans,
Speaker 6: you know, certain mists, dospecies. In comparison, here, we've got
Speaker 6: just dozens of species that need to be considered in
Speaker 6: the management of this disease in nature. So it's sylvadic.
Speaker 6: The second big challenge that comes to mind is just
Speaker 6: this relative lack of awareness, lack of medical awareness, lack
Speaker 6: of veterinary awareness for chagas disease tapanism a cruisie. This
Speaker 6: is neglected from medical attention, it's neglected from research communities,
Speaker 6: and so it's you know, it's typically, especially when we're
Speaker 6: thinking about shagas disease in the United States, it's quick
Speaker 6: to conclude, oh, this is you know, this is a
Speaker 6: problem elsewhere, this is a problem across Latin America. But
Speaker 6: we've got these endemic kissing bugs, and we've got infected
Speaker 6: wildlife and we have spillover transmission to humans and to
Speaker 6: our domestic animals that are causing big problems. But because
Speaker 6: there's not more attention, we're not testing more. So we
Speaker 6: don't have a good understanding of, really, especially from the
Speaker 6: veterinary perspective, how many animals are impacted, what species, you know,
Speaker 6: what are the impacts for their health? And without those
Speaker 6: numbers to show just how many animals are impacted, then
Speaker 6: you know, it's hard to convince big granting agencies to
Speaker 6: put more money towards this problem. And so I think
Speaker 6: the overall lack of awareness is one of the biggest
Speaker 6: challenges for this disease.
Speaker 3: Yeah, absolutely, So on that note, could you mention the
Speaker 3: name of your the app and the community science project
Speaker 3: that you're talking about in case listeners want to get
Speaker 3: involved or want to find out more about the work
Speaker 3: that you're doing.
Speaker 6: Sure, our community science website is kissing bug dot TAMU
Speaker 6: TA MU dot edu and from that website you can
Speaker 6: learn all about kissing bugs, shogga disease, wildlife reservoirs, dog infection,
Speaker 6: and so forth. But importantly, this is also the portal
Speaker 6: from which you can contribute your observations and insects specimens
Speaker 6: to our program. So there's instructions there on how to
Speaker 6: safely collect these insects and submit them to our program,
Speaker 6: and the same would be true. Our app is available
Speaker 6: for Apple and Android from the iTunes Store and Google
Speaker 6: Play and you can download that there and has the
Speaker 6: same capability as the website.
Speaker 2: Thank you so much, doctor Sarah Hammer for talking with us.
Speaker 3: It was absolutely thrilling and enlightening and wonderful and you
Speaker 3: remain a hero to us, a true hero. Should we
Speaker 3: do sources?
Speaker 2: We should do sources.
Speaker 3: Okay, so I'm going to shout out I think I
Speaker 3: have more sources for this than any other episode.
Speaker 2: Wow.
Speaker 3: Yeah, I just couldn't stop. I'm going to shout out
Speaker 3: a few. So the first one is The Kissing Bug,
Speaker 3: a true story of a family, an insect, and a
Speaker 3: nation's neglect of a deadly disease by none other than
Speaker 3: Daisy Hernandez. Go check it out. And a couple articles
Speaker 3: I found super helpful were by after Hyde at All
Speaker 3: from two thousand and four. A nine thousand year old
Speaker 3: record of Shagas disease by Clement at All twenty twenty
Speaker 3: out of Africa, the origins of the protozoan blood parasites
Speaker 3: of the Tripanosoma cruisy clade found in bats from Africa,
Speaker 3: and by stever Ding from twenty fourteen, the history of
Speaker 3: Shauga's disease, and a whole bunch more that'll post.
Speaker 2: I also had probably not as many as you erin,
Speaker 2: but there's a number of really great, kind of comprehensive reviews.
Speaker 2: A couple in the Lands, one in the New England
Speaker 2: Journal of Medicine. There's actually a whole bunch of really
Speaker 2: nice reviews. We'll post a list of all of our
Speaker 2: sources from this episode and every single one of our
Speaker 2: episodes on our website, This podcast will kill You dot Com.
Speaker 3: Thank you again so much, Daisy for taking the time
Speaker 3: to chat with us. We truly appreciate it.
Speaker 2: Yeah, thank you.
Speaker 3: Thanks to Bloodmobile for providing the music for this episode
Speaker 3: and all of our episodes.
Speaker 2: Thank you to the Exactly Right Network, of whom we're
Speaker 2: very proud to be a part, And.
Speaker 3: Thank you to you listeners. We appreciate you so much
Speaker 3: to keep tuning in episode after episode and listening to
Speaker 3: us talk on and on about Yeah, pathogens and parasites
Speaker 3: and metals and genetic diseases and all of the things.
Speaker 2: And a special shout out to our patrons. We love
Speaker 2: you guys.
Speaker 3: Okay, well, until next time, wash your hands, you filthy animals.
Speaker 3: Oh bu.
Speaker 2: Bonba bonbu
Speaker 3: Bbo oba