Speaker 1: My name is Alex Trio and I am an assistant
Speaker 1: professor at Gettysburg College. I'm an professor of animal behavior
Speaker 1: and tropical biology. I got diagnosed with denge in the
Speaker 1: summer of twenty and sixty. I do a lot of
Speaker 1: field work and I work in Panama Dismissed On and
Speaker 1: Tropical Research Institute, and our work is to set up
Speaker 1: speakers and playbacks that have frog calls to attract predators
Speaker 1: and parasites of these frog So we attract bats and
Speaker 1: we attract these very small midges, and so most of
Speaker 1: our work during the summer at least is in the field,
Speaker 1: all across different field sites in Pana. I was doing
Speaker 1: this work with some of my students in twenty sixty.
Speaker 1: I first started feeling very tired, but I thought that
Speaker 1: it was just because I wasn't sleeping well, because you know,
Speaker 1: I had a young baby and I was working at
Speaker 1: me And one of the days I was so tired
Speaker 1: that my husband recalled me just like kind of collapsing
Speaker 1: on the on the trail going to one of the
Speaker 1: sites where we had our speakers, and he noticed that
Speaker 1: I just felt, well, you know, one of those days
Speaker 1: where I just am tired, and we kind of let
Speaker 1: that go, and then a couple of days later, I
Speaker 1: started feeling much more sick. I got a very small fever.
Speaker 1: I don't really get fevers, and I think that that
Speaker 1: was one of the reasons why it took me so
Speaker 1: long to realize I had them, or I had something
Speaker 1: else than a cold. I was in an actual moment
Speaker 1: where I was really stressed out because not only that
Speaker 1: they had to finish old or they need to do
Speaker 1: all the field work. I had to leave a lot
Speaker 1: of things set up during the field work for my
Speaker 1: students because I was traveling to a conference, and so
Speaker 1: I wasn't really hoping and or expecting and or wanting
Speaker 1: to be sick. I was just you know, trying really
Speaker 1: hard to power through. My cold still went on on
Speaker 1: the plane, and I remember arriving to the US and
Speaker 1: I had to walk to my next gate, and I
Speaker 1: just remember like sitting, you know, on the floor next
Speaker 1: to the chairs and just being like calling my husband
Speaker 1: and saying, I just don't know if I can make
Speaker 1: it to the gate to the connection, like I'm that tired.
Speaker 1: So at this point, what I was feeling mostly was
Speaker 1: extreme my lace like super super tired, and what I
Speaker 1: had was like really strong joint pain. I remember very
Speaker 1: little about the conference. My talk was second or the
Speaker 1: third day of the conference, so I just worked really
Speaker 1: hard and the day I gave my talk. That day
Speaker 1: I started with the fevers. After I finished the talk,
Speaker 1: I came back to my room and I passed out
Speaker 1: for like almost twenty four hours. I was fine, but
Speaker 1: I was in like a lot of pain. When I
Speaker 1: came back, I got this horrible headaches. It just feels
Speaker 1: that you have pressure on top of your nose and
Speaker 1: on the sides of your head like like but the
Speaker 1: pressure is from the inside. It is like if someone's
Speaker 1: like put a hand inside your brain and trying to
Speaker 1: pull it from the inside. That's kind of what it
Speaker 1: feels like. But on the second day of this really
Speaker 1: terrible headaches, we just I just said, we have to go.
Speaker 1: I something has to stop. I don't know what it is,
Speaker 1: but we're going to the emergency room because like I
Speaker 1: want to literally like pull my brain out. The doctor
Speaker 1: saw me and he at first said, oh, it must
Speaker 1: be a really bad sineside as infection, and I was like,
Speaker 1: I have signed as infections before and this is not
Speaker 1: it there's something else that's beaker. And it was actually
Speaker 1: my husband who was like, we're not leaving this place
Speaker 1: until you test for the like you have to test for.
Speaker 1: And so they went ahead and they tested, and then
Speaker 1: we were waiting at the waiting room. So I just
Speaker 1: remember being asleep and then wake up and then the
Speaker 1: doctor being there and said like, yes, you know, you
Speaker 1: were tested positive for denge And I just remember both
Speaker 1: Michael and I actually being happy about it because we
Speaker 1: finally figured out there was like a reason why. I
Speaker 1: was like, I was like, Okay, now we know what
Speaker 1: to do, right, Like we have a diagnosis and we
Speaker 1: know what to do about it, but I mean, there's
Speaker 1: not much you can do, right. I slowly started like
Speaker 1: getting a little bit better. I was weak and tired
Speaker 1: and feeling my laise for like at least two months
Speaker 1: after that. A lot of people thought that I probably
Speaker 1: had it from working in Gamboa in the forest, but
Speaker 1: I do remember about ten days a week to ten
Speaker 1: days before I started feeling sick. I was actually with
Speaker 1: a friend of mine, you guys know here we were
Speaker 1: sitting at a at a restaurant outside in the city
Speaker 1: of Panama. So I honest I think that I got
Speaker 1: it in the city. And so from then on, I
Speaker 1: told my student and I we all like whenever we
Speaker 1: never were, like nobody were skirts or shorts or or
Speaker 1: shorts leaves. We all like get lungs leaves and pants
Speaker 1: and shoes every time we go to town because we're like
Speaker 1: a little bit nervous about that. So yeah, so no
Speaker 1: more skirts in the city.
Speaker 2: You just heard from doctor Alex Trio, who was nice
Speaker 2: enough to share her experiences with dangay with us, and
Speaker 2: if you want to learn more about the awesome research
Speaker 2: that she does, you can check out her website at
Speaker 2: www dot Alextrio dot com. That's a l e X
Speaker 2: t r I l l O and you can also
Speaker 2: follow her on Twitter at t R I l l
Speaker 2: O underscore PA. Thanks again, Alex. Hi.
Speaker 3: I'm erin Welsh and I'm erin omen Updake and.
Speaker 2: This is this podcast will kill you.
Speaker 3: Yeah. Today we're talking about do you say dangy or dangay?
Speaker 2: I think I say both.
Speaker 3: I think we've done this before, right, we have discussed this.
Speaker 3: We have discussed this and we didn't come to a conclusion.
Speaker 2: Yeah, well I'll say dangy, you say dangay perfect.
Speaker 3: That sounds excellent. Okay, great, cover all our faces.
Speaker 2: We can irritate everyone that.
Speaker 3: Way, exactly our favorite thing to do.
Speaker 2: Yes, So, as you might have guessed, we are talking
Speaker 2: about or Dan Gay today, which is a very fascinating
Speaker 2: mosquito born virus. Yes, and it is actually an episode
Speaker 2: or a topic that we have covered once before. We have,
Speaker 2: although only a few of you may have heard it.
Speaker 3: Yeah, So in October we got invited shout out Nick
Speaker 3: Kaiser to University of Florida to give a little talk
Speaker 3: and we talked about Dan Gay, so we technically have
Speaker 3: heard each other talk about Dan Gay before. However, I
Speaker 3: don't remember anything you said, Erin, because I was really
Speaker 3: nervous during this talk, so I was like not actually
Speaker 3: paying attention.
Speaker 2: Well, thank you and same. Also my memory is terrible,
Speaker 2: so but it'll be great.
Speaker 3: I'll still learn new things.
Speaker 2: Apologies to anyone who was in the audience in Florida,
Speaker 2: because if you remember anything, then some of this or
Speaker 2: all of this will be a repeat, but add a
Speaker 2: little bit more to kind of fill in the edges.
Speaker 3: We definitely have some new things and some answers to
Speaker 3: some questions that people asked during that event. Ooh, stay tuned.
Speaker 3: Well is it Quarantini?
Speaker 4: Da?
Speaker 2: I think it is.
Speaker 3: I think it is too.
Speaker 2: What are we drinking this week?
Speaker 3: We're drinking the bone Breaker?
Speaker 2: M what's in the bone Breaker?
Speaker 3: It is mes call. Preferably you could use tequila if
Speaker 3: it's all you've got, passion fruit simple syrup. Oh yeah,
Speaker 3: pin juice, pineapple juice, and you rim it with taheen,
Speaker 3: which is one of our little favorite things.
Speaker 2: It is and it's really refreshing and delicious, so tasty
Speaker 2: and hopefully won't make your bones feel like they're breaking,
Speaker 2: let's hope not just your head the next day. If
Speaker 2: you have too many, don't do that, just have one.
Speaker 2: We will post the recipe for the alcoholic Quarantini and
Speaker 2: the non alcoholic plusy Berta on our website and also
Speaker 2: so on our social media which you can follow us
Speaker 2: at This podcast will Kill You on Instagram and TPWKY
Speaker 2: on Twitter, and you can also find us on Facebook.
Speaker 3: Yeah, any other business that we should discuss erin?
Speaker 2: I don't think so.
Speaker 3: I don't think so either. Should we jump right into
Speaker 3: this episode?
Speaker 2: Let's do it.
Speaker 3: Dangay virus. You already know a lot about it, it's
Speaker 3: a virus. This is a flava virus, so that's in
Speaker 3: the same group of viruses as yellow fever, West Nile Zeka,
Speaker 3: a bunch of different encephalitis viruses, etc. Okay, there are
Speaker 3: five zero types, so that means five different strains of
Speaker 3: this virus. It used to only be four, but in
Speaker 3: twenty thirteen they announced a new one. Ooh, and so
Speaker 3: this means that if you get infected with one strain
Speaker 3: of dngay, you're not protected against the other strains of dngay. Right,
Speaker 3: and as we'll talk about later, it's actually a lot worse. Yeah, spoilers.
Speaker 2: I already have a question about that. I'm going to
Speaker 2: write it down instead of okay.
Speaker 3: A question down and then ask me later. Yeah, okay,
Speaker 3: you don't want to ask it now.
Speaker 2: I mean, because it's kind of jumping ahead to.
Speaker 3: Okay, all right, yeah, okay, ask it later. Okay, Okay.
Speaker 3: So let's talk about how you get infected with danay.
Speaker 3: You already mentioned aaron. This is a mosquito born virus.
Speaker 3: So dangay is transmitted by eighties mosquitos, which we've talked
Speaker 3: about before. Because these little buggers transmit a whole number
Speaker 3: of different diseases, including yellow fever, Zeca et cetera, chicken gunyah,
Speaker 3: which we haven't talked about yet. One thing that's different
Speaker 3: though about dangay than some of these other viruses, although
Speaker 3: not all of them, is that dan gay is pretty
Speaker 3: specifically often a disease of more urban areas, where a
Speaker 3: lot of other viral hemorrhagic fevers tend to be diseases
Speaker 3: of more rural areas. And this is for a couple
Speaker 3: of different reasons. One is that these eighties mosquitoes that
Speaker 3: transmit dangay are very well adapted to urban environments. They
Speaker 3: breed in little, tiny containers of water, and so anytime
Speaker 3: you have like let's say, pots or tires or whatever
Speaker 3: in your yard that could collect water, eighties can breed
Speaker 3: in those small bodies of water. And dangay is a
Speaker 3: human specific disease, so unlike something like yellow fever that
Speaker 3: can spill over from animal populations into human populations, dangay
Speaker 3: is human spita. So where you have large populations of humans,
Speaker 3: you're more likely to get spread of dang gay in
Speaker 3: those areas.
Speaker 2: I forgot about that aspect of yellow fever. Yeah, Like,
Speaker 2: why do you think evolutionarily, there would be a difference
Speaker 2: between the two, you know, like why would dangay be
Speaker 2: so specific to humans and so interesting?
Speaker 3: Yeah, well, I was hoping you would tell me, like
Speaker 3: where dangay came from.
Speaker 2: I mean, I'll tell you that I don't. I won't
Speaker 2: be able to answer this question. Huh.
Speaker 1: Yeah.
Speaker 3: But yeah, there's no like sylvatic wild cycle like there
Speaker 3: is for yellow fever. It's really interesting interesting. So that also,
Speaker 3: I will say, contributes to some of the lack of
Speaker 3: understanding that we have about dangay fever. We don't fully
Speaker 3: understand dangay, and it's because when we have human specific diseases,
Speaker 3: it's often really difficult to find good animal models to
Speaker 3: study these diseases in. So in the case of dangay,
Speaker 3: there are some like modified mice that you can infect
Speaker 3: with dan gay and use. You can do it in
Speaker 3: monkeys in some cases, but we don't have really good
Speaker 3: animal models for studying dan gay.
Speaker 2: Okay.
Speaker 3: The other way that it is possible to get dan gay,
Speaker 3: although this is much more rare than mosquito transmission, is
Speaker 3: vertical transmission, so across the placenta. So it's possible for
Speaker 3: this virus to cross the placenta. So during pregnancy, if
Speaker 3: someone is infected, especially late in the pregnancy, then the
Speaker 3: fetus can potentially get infected as well, and this can
Speaker 3: have pretty bad outcomes once the baby is born. That
Speaker 3: we'll talk about a little bit more later, Okay, But
Speaker 3: it doesn't seem to cause birth defects the way that
Speaker 3: something like zeca virus does, which I think is very interesting. Yeah, huh, Yeah,
Speaker 3: it's not entirely clear if someone gets infected very early
Speaker 3: in their pregnancy, if they might have poor outcomes like
Speaker 3: maybe a miscarriage or something like that. It's not entirely
Speaker 3: clear if that happens if you get infected with dangay
Speaker 3: or in your pregnancy, Okay, but definitely if you get
Speaker 3: infected late, then the fetus can get infected and then
Speaker 3: basically when it's born, it can either have symptoms of
Speaker 3: dangay or it might just have antibodies, like it might
Speaker 3: be born having antibodies against dangae virus.
Speaker 2: Okay, like having already been infected and then.
Speaker 3: And survived the infection. Yeah, yes, Oh, put a pin
Speaker 3: in that. Okay, that oh is the perfect Oh okay,
Speaker 3: So that's how you get transmitted or how you get infected. Rather,
Speaker 3: that's the transmission cycle what basically happens. We've talked about
Speaker 3: a number of mosquito born diseases on this podcast by now,
Speaker 3: so what's important to remember about all mosquito born diseases
Speaker 3: is that there's the cycle of the virus in the
Speaker 3: human and then there's also the cycle of the virus
Speaker 3: in the mosquito mm hm. And so the mosquitoes get
Speaker 3: infected if they bite a person who's actively febrile. For
Speaker 3: the most part, it's all it's possible like a couple
Speaker 3: days before you show symptoms and a couple days after
Speaker 3: you recover. If a mosquito bites a person infected with
Speaker 3: dungay during that time period, then the mosquito sucks up
Speaker 3: a bunch of viral particles. Those will travel through the
Speaker 3: gut of the mosquito, and then they have to make
Speaker 3: it out of the gut and back to the salivary
Speaker 3: glands of the mosquito. Importantly, that whole process in the
Speaker 3: mosquito takes like eight to ten days. Wow, Yeah, it's
Speaker 3: kind of a long time, okay, And that means that
Speaker 3: if you can somehow stop that process in that eight
Speaker 3: to ten day window, then you could block the transmission
Speaker 3: of dengay, right right, So that's really important. We'll talk
Speaker 3: even more about that in the current events section, because.
Speaker 2: That's a lot of people are all these little hints.
Speaker 3: It's all I do. This whole bio section is just
Speaker 3: going to be hints for later.
Speaker 2: Oh my god. Also, I just need to have a
Speaker 2: little point out right now that I remember nothing excellent,
Speaker 2: Like I'm like, okay, yeah, I know that it's a flavivirus,
Speaker 2: I know that this and that, but like that was
Speaker 2: all pervictage.
Speaker 3: I'm so sorry. I think we must have been like
Speaker 3: nervous blackout when we were presenting.
Speaker 2: For sure, I remember nothing of that whole trip there.
Speaker 3: Okay. So then when if that does work properly in
Speaker 3: the mosquito, then you have a bunch of virus in
Speaker 3: the mosquito salivary glands. Then they're going to bite another
Speaker 3: human and spit all of that virus into you essentially,
Speaker 3: and then that virus will go into your usually your
Speaker 3: lymph system, and in the case of Dane virus, it'll
Speaker 3: enter your white blood cells, and that is where the
Speaker 3: virus replicates in human bodies. So then after about four
Speaker 3: to seven days usually after you get infected with this virus,
Speaker 3: that's when you'll start to show symptoms. Okay, cool, Okay,
Speaker 3: so now we know the transmission. We know that it's
Speaker 3: infecting your white blood cells, which, if you don't recall,
Speaker 3: are part of your immune system. So that's really important
Speaker 3: because it's directly sort of targeting your immune cells. Okay,
Speaker 3: so what kind of symptoms do we have if you
Speaker 3: get infected with dangay. If you get infected with dangay
Speaker 3: for the first time, most people will never have any symptoms.
Speaker 3: What's most eighty percent?
Speaker 2: Wow?
Speaker 3: Yeah, so, like eighty percent of people who are infected
Speaker 3: for the first time with dangay have either very very
Speaker 3: mild symptoms or are entirely asymptomatic, which you can imagine
Speaker 3: makes it even more difficult to understand how many people
Speaker 3: really do get infected every year and how to actually
Speaker 3: control this virus. Yeah, if you do get symptoms from
Speaker 3: a primary infection, it generally starts as all of our
Speaker 3: favorite diseases do. With a fever. You'll often get a
Speaker 3: headache and very classically you get severe muscle and joint pain.
Speaker 3: So that's how it got the name breakbone fever, right,
Speaker 3: and the symptoms can actually be broken down into three
Speaker 3: main phases, but the last two phases tend to only
Speaker 3: happen if you're getting infected with dange for the second time. Aha, okay,
Speaker 3: so here are the three main phases. Febrile, critical but
Speaker 3: oh not good, and recovery oh asterisk or death Okay, yeah, okay,
Speaker 3: So the febrile phase that we kind of already started
Speaker 3: talking about. If you get infected for the second time,
Speaker 3: it's much more likely to be symptomatic, and this phase
Speaker 3: will probably start out worse than the first infection. So
Speaker 3: it starts out with a super high fever. We're talking
Speaker 3: over one hundred and four fahrenheit, yes, forty celsius sting. Yeah,
Speaker 3: wait is that right? Yeah, I'm pretty sure it's right.
Speaker 2: That's high.
Speaker 3: It's very high. And this fever lasts usually between two
Speaker 3: and seven days. Oh my gosh, I know it's a
Speaker 3: long time. You're very, very sick.
Speaker 2: Does it does it respond to like anti piretics?
Speaker 3: Good question, probably, But it's also often bi phasic. So
Speaker 3: often you'll get a really high fever and then you'll
Speaker 3: start to get better, and then a couple days later
Speaker 3: it'll come back again.
Speaker 2: Does the fever intensity correspond to like circulating virus anything
Speaker 2: like that.
Speaker 3: That's a really good question that I don't fully know
Speaker 3: the answer to. We'll talk a little bit more about
Speaker 3: like viremia, how much virus you have in your body, uh,
Speaker 3: when we talk about some of the more severe symptoms
Speaker 3: of it. But definitely the higher the viral load, the
Speaker 3: more sick you'll probably get, right, and the more likely
Speaker 3: you are to like have symptoms and things like that.
Speaker 2: But is that why the bi phasic, Like, is that
Speaker 2: part of it?
Speaker 1: There?
Speaker 3: Definitely could be. I mean that's usually when we think
Speaker 3: of things like malaria and stuff like that. That's usually
Speaker 3: when you have those biphasic fevers. So it could be that,
Speaker 3: like you get an initial infection and maybe your immune
Speaker 3: system kicks in is able to knock it down a bit,
Speaker 3: but then the viruses just start replicating like crazy, and
Speaker 3: then you get a secondary second wave.
Speaker 2: Interesting. Yeah, And do we know whether the fever is
Speaker 2: a defense mechanism by your bucket, like an immunological response,
Speaker 2: or is it induced by the virus?
Speaker 3: Excellent question. Most of the symptoms of dengee are your
Speaker 3: immune system responding to the virus. Okay, great questions, Aaron as.
Speaker 3: Other symptoms that you'll see are severe headache, and for
Speaker 3: some reason, don't ask me why on this one because
Speaker 3: I won't have an answer. It's often behind like right
Speaker 3: behind your eyes where you get this severe headache. And then,
Speaker 3: like I mentioned already, muscle and joint pain, nausea and
Speaker 3: vomiting are really common, and then a rash can often
Speaker 3: happen after a few days. And the rash unlike other
Speaker 3: viral illnesses that are really common, like or that used
Speaker 3: to be really common, something like measles, where you also
Speaker 3: get a rash, this rash starts on the torso and
Speaker 3: then spreads to the limbs. Okay, so a lot of
Speaker 3: other rashes will start like on the head and go down.
Speaker 3: So where rashes start can kind of help you figure
Speaker 3: out what disease it might be. Isn't that weird?
Speaker 1: Why?
Speaker 3: I don't know? Viruses are just so cool?
Speaker 2: What did we talk about with the rash and the palms?
Speaker 3: Oh uh so ricketsia causes that, and syphilis causes that,
Speaker 3: and then hand foot in mouth disease.
Speaker 2: Yeah, okay, cool, Yeah, see I'm remembering thing.
Speaker 3: Good. So this one starts on the torsos, writes to
Speaker 3: the limbs. But what's really important is that it's often
Speaker 3: really really hard to see this rash. So it's not like,
Speaker 3: you know, this really huge, you know, scary looking rash
Speaker 3: or anything. It's a very light red, pink, kind of
Speaker 3: splotchy rash. So it's not very descriptive. So after those
Speaker 3: few days, a couple days, you know, two to seven
Speaker 3: days of fever, as the fever starts to fade out,
Speaker 3: especially with the secondary infection, dengay can become more severe.
Speaker 3: This is when we get into two different syndromes called
Speaker 3: dengay hemorrhagic fever and dengay shock syndrome. Overall across like
Speaker 3: all dengay infections, these two syndromes happen in less than
Speaker 3: five percent of cases, but the vast majority of those
Speaker 3: are when someone's been infected the second.
Speaker 2: Time, you mean the second time with a different strain.
Speaker 3: With a different strain exactly, okay.
Speaker 2: And so you cannot get sick again from the same strain,
Speaker 2: Do you have lifetime immunity or what's the deal?
Speaker 3: Pretty much, yeah, from that particular strain, Like maybe unless
Speaker 3: you got infected with a really really low viral load
Speaker 3: and you didn't mount a great immune response, then maybe
Speaker 3: you could be reinfected with the same strain. But for
Speaker 3: the most part, in areas where dengay circulates, multiple strains
Speaker 3: circulate at the same time, so you're much more likely
Speaker 3: to get infected with a different strain. And that's when
Speaker 3: you see Dangay hemorrhagic fever or dan gay shock syndrome.
Speaker 3: So what's happening in these two syndromes. Both of them
Speaker 3: are related to capillary leakage. So your capillaries are the
Speaker 3: tiny ends where your arteries and veins come together, right
Speaker 3: where like gas exchange is happening. And so what happens
Speaker 3: is the virus and your immune response to the virus
Speaker 3: both cause damage to these tiny blood vessels and it
Speaker 3: causes them to leak, and that is going to cause
Speaker 3: you to not have enough blood essentially in your blood vessels,
Speaker 3: and then you're going to go into shock and potentially die.
Speaker 3: So whether you have the hemorrhagic form or just the
Speaker 3: dengay shock form kind of just deppends on whether it's
Speaker 3: damage that's somewhere like in your gi tract and then
Speaker 3: causing massive bleeding, or whether it's damage in other areas
Speaker 3: that just cause plasma leakage. So you're not losing blood volume,
Speaker 3: you're losing plasma volume.
Speaker 2: Okay, So the mechanism is the same, it's just the
Speaker 2: end result.
Speaker 3: That's different, ok exactly, And both of these you can
Speaker 3: end up with massive organ dysfunction, eventual death and symptoms.
Speaker 3: While they're different across the board. You can get severe
Speaker 3: abdominal pain, especially if you have GI tract involvement, persistent vomiting.
Speaker 3: If this happens in your lungs, then you can have
Speaker 3: leakage in your lungs, which can make it really hard
Speaker 3: to breathe, so someone might have really rapid breathing, which
Speaker 3: we call tekipnia. You can have bleeding from your gums
Speaker 3: because your mucous membranes, if those are starting to leak,
Speaker 3: that's going to be blood coming out of your gums,
Speaker 3: et cetera, et cetera. This phase, the critical phase, usually
Speaker 3: only lasts a couple of days, like one to two days.
Speaker 2: Only there's only a couple of days of you bleeding
Speaker 2: out your gun and your.
Speaker 3: Gut and yeah, or you going into shock because all
Speaker 3: of the plasma has left your your bloodstream and you
Speaker 3: have no blood for your heart to pump essentially, So
Speaker 3: if you survive, then you'll enter the recovery phase, which
Speaker 3: in theory in itself, actually happens relatively quickly, like your
Speaker 3: blood vessels kind of heal themselves and stop leaking relatively
Speaker 3: quickly within two or three days. But you can imagine
Speaker 3: that this has caused a lot of damage to your
Speaker 3: body overall, so actual recovery, like you feeling better, can
Speaker 3: take weeks at a time.
Speaker 2: Okay, how many people do survive?
Speaker 3: So overall for severe dengae, if you get treatment, the
Speaker 3: overall mortality rate is like one to five percent, But
Speaker 3: once a person goes into shock, if they don't have treatment,
Speaker 3: it's like a twenty five to thirty percent mortality rate.
Speaker 2: But if you do receive treatment, it's mostly supportive care.
Speaker 3: It is entirely supportive care.
Speaker 2: Yeah.
Speaker 3: So it's a lot of like fluid resuscitation to try
Speaker 3: and combat that fluid leakage, So a lot of ivy
Speaker 3: fluids and things like that to keep your blood to
Speaker 3: keep your blood vessels full of fluid. Okay, yeah, and.
Speaker 2: That's pretty successful.
Speaker 3: Yeah, I mean it reduces the mortality rate from twenty
Speaker 3: five percent to one to five percent. So okay, that's
Speaker 3: pretty dang good. Yeah, yeah, okay. So there's a couple
Speaker 3: of things that we need to talk about when we
Speaker 3: talk about these severe forms of dan gay. First is
Speaker 3: that there's a lot of differences in the severity, not
Speaker 3: just based on whether or not it was your first
Speaker 3: or second infection, So comorbidities like if you already have
Speaker 3: a number of comorbidities, say like diabetes, hypertension, maybe immune compromise,
Speaker 3: these things are obviously going to make it more likely
Speaker 3: that you might have a more severe dingay whether or
Speaker 3: not it's your first or second infection. Also, overall vy riemia,
Speaker 3: so how much virus you get exposed to overall is
Speaker 3: also going to help define whether or not you have
Speaker 3: severe dangay or not. The strain of the virus can
Speaker 3: also play a part, So some strains are more likely
Speaker 3: than others. And for some reason, I didn't write down
Speaker 3: which ones those were.
Speaker 2: I think so I think it's number two in at
Speaker 2: least in the Americas, is associated with hemorrhagic.
Speaker 3: That makes sense, sindra or fever. It's gonna guess two
Speaker 3: or three.
Speaker 2: But I have a question that's related to this. This
Speaker 2: is the one I wrote down, Oh, excellent. So dangae
Speaker 2: hemorrhagic fever happens when you get infected with a second
Speaker 2: strain or a different strain than you first were infected with.
Speaker 2: Are there different combinations of strains that like will lead
Speaker 2: to that being more severe or more likely to occur?
Speaker 3: Maybe that's that's a really it's a good question, like
Speaker 3: if you get infected with one first and then two
Speaker 3: versus two first and then one. Right, Yeah, good question.
Speaker 3: I don't know based on what I've read about, but
Speaker 3: I'm sure there's some EPI studies out there that are
Speaker 3: looking into that or that have looked into it. It's
Speaker 3: a really good question.
Speaker 2: And is there any partial immunity conferred based on like
Speaker 2: yellow fever, if you've been exposed to yellow fever or
Speaker 2: zeka or other flabby viruses.
Speaker 3: I don't think so. I don't think so.
Speaker 1: Yeah.
Speaker 3: I don't think that they're even though they're all flaviviruses,
Speaker 3: I don't think they're similar enough to provide any sort
Speaker 3: of cross immunity or anything like that. Yeah, good questions though,
Speaker 3: So fun Aaron, Okay. And then the other people who
Speaker 3: are more likely to have severe dengey regardless of number
Speaker 3: of infection are children and the elderly, and this is
Speaker 3: for a couple of reasons. Both children and the elderly
Speaker 3: have kind of a lower threshold for capillary leakage to
Speaker 3: begin with, so they're at increased risk for bleeding in general.
Speaker 3: They're like in older people, their capillaries are just kind
Speaker 3: of weak, and in children they're not fully formed, so
Speaker 3: they're more likely to have leakage from that. Bleeding especially
Speaker 3: is more common in older, older adults and things than
Speaker 3: in children. Okay, but we talked briefly about how infants
Speaker 3: can be born with antibodies to dengay. So a group
Speaker 3: that's at very very high risk of severe dan gay
Speaker 3: deng gay hemorrhagic fever or dung gay shock syndrome is
Speaker 3: infants that have maternal antibodies to dengay still circulating. So
Speaker 3: if a mom was infected and then the baby is
Speaker 3: born with those antibodies, if that baby gets infected with
Speaker 3: another strain of dingay, they're at very very high risk
Speaker 3: of going on to develop severe symptoms.
Speaker 2: But how would like if only twenty percent of people
Speaker 2: show signs or know that they've been infected with dangay,
Speaker 2: then how do you know.
Speaker 3: That's the thing.
Speaker 2: How do you know.
Speaker 3: That's scary too, It's really scary. Yeah.
Speaker 2: And there's no screening protocol in any places.
Speaker 3: That are like during pregnancy. Yeah, not that I know of,
Speaker 3: that I know of. Yeah. So then the question becomes,
Speaker 3: why is it that a secondary infection with dengay is
Speaker 3: worse than a first infection? Yeah, that's very bizarre.
Speaker 2: Right, So I can't tell if this is a true
Speaker 2: guess or recovered memory, but is it something like the
Speaker 2: way you know in the nineteen eighteen flu where it's
Speaker 2: like the immune system just goes like super ham good question.
Speaker 3: That's that is one of the hypotheses that was out
Speaker 3: there for a long time, that it's kind of like
Speaker 3: a cytokine response. That was what happened in the nineteen
Speaker 3: eighteen That's what.
Speaker 2: I was looking excited a kind stories Maybe not a
Speaker 2: recovered memory.
Speaker 3: Then, yeah, that's one of the hypotheses that are out there.
Speaker 3: There's a number of different hypotheses there as to what
Speaker 3: exactly is the cause of this secondary severe infection. The
Speaker 3: exact mechanism isn't entirely clear, but the most parsimonious and
Speaker 3: the most well supported hypothesis is called antibody dependent enhancement.
Speaker 3: And I will say the fact that infants who are
Speaker 3: born with antibodies only like to me, that provides really
Speaker 3: good support to this hypothesis. Because the idea is basically this.
Speaker 3: If you have antibodies against let's say dean Gay strain
Speaker 3: number one, these antibodies are similar to the antibodies that
Speaker 3: you would make to dan Gay number two, but they're
Speaker 3: not exactly the same. And so for some reason, these
Speaker 3: antibodies bind to dangay number two virus. Right, And when
Speaker 3: antibodies bind, what they do is they encourage your white
Speaker 3: blood cells to engulf that virus in order to kill it.
Speaker 1: Right.
Speaker 3: That's the point of an antibody. It's like a flag
Speaker 3: that our immune system puts on viruses. So these antibodies
Speaker 3: that you've made to dan Gay one flag dan Gay two,
Speaker 3: but they don't do it perfectly. And for some reason,
Speaker 3: what that does is it causes the virus when it
Speaker 3: gets into the white blood cells, which remember, is where
Speaker 3: Danay wants to be. That's where Dangay replicates. It causes
Speaker 3: a massive amount of replication. So something about the antibodies
Speaker 3: that are a little bit mismatched binding to that virus,
Speaker 3: enhances their ability to replicate and then increases viremia. Ooh right.
Speaker 2: Also, what's really interesting about this is that these strains
Speaker 2: evolved in isolation, because that's how strains evolve, and so
Speaker 2: this is like a recent thing. So it just so
Speaker 2: happens that it turned out to be really really really
Speaker 2: bad for humans.
Speaker 3: Yeah, and really good for the virus if it's increasing viromium, right,
Speaker 3: because the more virus you have circulating, then the more
Speaker 3: likely a mosquito is going to be able to pick
Speaker 3: up that virus and transmit it to the next host.
Speaker 2: That's really fascinating.
Speaker 3: Though, it is, and there's a number of really cool
Speaker 3: papers out there looking into, like, you know, getting more
Speaker 3: detail on or more support for this hypothesis. So that
Speaker 3: is dang gay, that's the biology. That's how it gets
Speaker 3: you sick. That's how it kills you. It's a horrible illness.
Speaker 3: And we'll talk later about how many people it kills
Speaker 3: every year. Aaron, Where did this thing come from? Why
Speaker 3: is it here? And why is it so bad?
Speaker 2: Great questions. Let's take a quick break and then we'll
Speaker 2: begin excellent dungi virus, all of its types probably originated
Speaker 2: in Asia and then kind of exploded out from there,
Speaker 2: And there has been some debate about like whether it
Speaker 2: really originated or diversified in Asia or Africa, but most
Speaker 2: things that I read suggested Asia as the origin.
Speaker 3: Okay, So about.
Speaker 2: Two thousand to four thousand years ago, the Dungy virus,
Speaker 2: which had been hiding out in the jungle, hitched a
Speaker 2: ride in a type of mosquito species that likes to
Speaker 2: hang around human settlements, and these mosquitoes probably transmitted the
Speaker 2: infection to these small human settlements. But then these outbreaks
Speaker 2: were like little bursts, so they would happen infrequently. Everyone
Speaker 2: would get exposed, and then everyone would gain immunity, and
Speaker 2: then dengey would retreat and wouldn't be seen again until
Speaker 2: the number of sceptible people in that settlement would increase
Speaker 2: to a point where an outbreak could happen again. So
Speaker 2: then that kind of like that cycle continued on and
Speaker 2: on until humans started to live in bigger and bigger
Speaker 2: groups and in the distance between these settlements or groups shrink,
Speaker 2: and then things like commerce and migrations led to the
Speaker 2: groups being like more and more connected, and so over
Speaker 2: the course of that time, it was kind of a
Speaker 2: one location, one strain situation. But evolution happens and different
Speaker 2: strains of Dengi start to evolve, and they would also
Speaker 2: make the leap from the silvatic cycle. So I think
Speaker 2: originally dengay did circulate in primates and non human primates.
Speaker 3: It makes sense that it came from non human primates. Yeah,
Speaker 3: just like specified onto humans or whatever.
Speaker 2: Right, And so more and more strains made the leap
Speaker 2: from just the that cycle of monkeys and mosquitoes to
Speaker 2: then this urban cycle or more urban cycle of mosquitos
Speaker 2: and humans. But still, even though more strains evolved, there
Speaker 2: was still this geographical isolation among the strains. So you know,
Speaker 2: one strain would be in this location, one strain would
Speaker 2: be in that location, and there wasn't a whole lot
Speaker 2: of opportunities for overlap. It did, of course happen occasionally,
Speaker 2: but not that often. But it's kind of in a way.
Speaker 2: Having these different strains is really interesting because researchers can
Speaker 2: compare the DNA sequences of these strains and then put
Speaker 2: a timeline on their emergence and where they emerged as well. Okay,
Speaker 2: so this general pattern that I just described, one strain
Speaker 2: per outbreak small outbreaks, very sporadic. This continued for hundreds
Speaker 2: of years, probably thousands of years, and then around the
Speaker 2: sixteenth and seventeenth centuries, the slave trade began, and for
Speaker 2: Dengey in particular, this meant that a the world became flat,
Speaker 2: so the virus could be transmitted or carried all over
Speaker 2: the world by these ships and introduced to new populations
Speaker 2: that were full of susceptible humans. And the other thing
Speaker 2: is that the slave trade also spread the key vector
Speaker 2: mosquito species eighties Agypti. Yeah, because as you mentioned, eighties
Speaker 2: Egypti lives really well, like literally well in urban like
Speaker 2: next to humans, and it doesn't need a whole lot
Speaker 2: to continue its life cycle. Yeah, it's just basically small
Speaker 2: bits of water.
Speaker 3: They're very hardy. M h.
Speaker 2: And I think this is fascinating because eighties Agypti is
Speaker 2: it's of African origin, So eighties Agypti is now the
Speaker 2: primary mosquito.
Speaker 3: Yeah, but it wasn't the first if no.
Speaker 2: Eighties Albapicctus was probably.
Speaker 3: Interesting what was originated with eighties Egypti and eighties Albapictus
Speaker 3: are both the like two main vectors, but they talk
Speaker 3: about eighties agypti as the like primary just because of
Speaker 3: I think think it's distribution, and it's a more voracious
Speaker 3: biter as well.
Speaker 2: Apparently it's yeah, it's more efficient at transmitting the virus
Speaker 2: as well. Wow, And so this is this is kind
Speaker 2: of what caused this debate as to the geographical origin
Speaker 2: of dengay, because it would make more sense that like
Speaker 2: this virus and this mosquito species fit so well together
Speaker 2: and work so well together, Yeah, that that would be
Speaker 2: the origin that they would have evolved together as well.
Speaker 2: But it seems that actually albu Pictus is where it
Speaker 2: came from.
Speaker 3: So fascinating.
Speaker 2: I don't know anyway, So eighties a jip dye being
Speaker 2: the super cosmopolitan mosquito species, really helped the distribution of dengay,
Speaker 2: and so probably by the eighteenth century the Dengae virus
Speaker 2: was all over the global tropics, and also its distribution
Speaker 2: could creep northwards during the warmer months, especially in port
Speaker 2: cities thanks to the widespread distribution of eighties a jip dye,
Speaker 2: and even in those more northern or more southern places
Speaker 2: like a little bit outside of the Mosquitos. Year long
Speaker 2: environmental requirements it would just be reintroduced. Yeah, it'd be like, oh,
Speaker 2: it's warm enough in the summer, I'll die off in
Speaker 2: the winter and then be reintroduced. Knowing the evolutionary origins
Speaker 2: of danngae is one thing, But when did humans actually
Speaker 2: first recognize the disease. Yeah, so it's around the late
Speaker 2: eighteenth century, seventeen seventy nine to be exact, that we
Speaker 2: see what is considered to be the first dange pandemic.
Speaker 2: In seventeen seventy nine, there are descriptions of a dnge
Speaker 2: like illness in Java in Egypt, and in the following
Speaker 2: year we see it pop up in Philadelphia. And this
Speaker 2: is actually when it gets its colloquial name breakbone fever,
Speaker 2: which was coined by Benjamin Rush. And he was also
Speaker 2: a physician. And so to give you an idea of
Speaker 2: the scale of this epidemic in Philadelphia, he saw over
Speaker 2: the course of like two months, around one thousand people
Speaker 2: he treated them for DENGI.
Speaker 3: Two months, one thousand people in Philadelia, he alone.
Speaker 2: Yeah, wow, And so yeah, I couldn't find an exact
Speaker 2: estimate of the total number of people likely infected, but
Speaker 2: probably it was pretty high.
Speaker 3: Wait a second, this is the one recovered memory I
Speaker 3: have from the time that we talked about dangay in Florida.
Speaker 3: Benjamin Rush is one of the founding fathers. Yeah, I
Speaker 3: learn that from you, So glad.
Speaker 2: That's see, that's the one bit of trivia next time
Speaker 2: you go to trivia at the Blind Pig.
Speaker 3: Mm hmm. Benjamin Rush, Ben Rush the only one founding fathers.
Speaker 3: Oh God.
Speaker 2: Moving on anyway, So this the epidemic in Philadelphia, from
Speaker 2: Benjamin Rush's description was pretty likely. Dangy okay Egypt and
Speaker 2: Java may have been chicken gunya. There's been a lot
Speaker 2: of recent debate over whether these early descriptions are actually
Speaker 2: chicken gunya virus as opposed to dangae virus, But in
Speaker 2: any case, it seems that Philadelphia was pretty likely and
Speaker 2: that's the earliest more like convinced or most convincing instance.
Speaker 2: There are descriptions of a dangye like disease and a
Speaker 2: Chinese encyclopedia dating back to the year nine nine two.
Speaker 2: Whoa yeah, And in this encyclopedia, this disease is referred
Speaker 2: to as water poison and was known to be associated
Speaker 2: with flying insects that.
Speaker 3: Live into the water.
Speaker 2: So fascinating mosquitoes, and the symptoms of this disease sound
Speaker 2: a lot like dangy. So you've got the fever, rash,
Speaker 2: eye pain, bleeding, sometimes high mortality. And this also lends
Speaker 2: further support to the hypothesis that the virus originated in Asia.
Speaker 2: But anyway, the virus was circulating throughout like much of
Speaker 2: the world during the eighteenth and nineteenth centuries, with an
Speaker 2: estimated eight pandemics each lasting three to seven years from
Speaker 2: seventeen seventy nine to nineteen sixteen.
Speaker 3: Wow.
Speaker 2: Yeah, With a disease that is as old and in
Speaker 2: particularly as wide ranging as dengay, it makes sense that
Speaker 2: it would accumulate a few names over its lifetime.
Speaker 3: Yes, I love the name.
Speaker 2: Yes, I hope that there's another one that you remember,
Speaker 2: because I did a little more digging. Okay, okay. So
Speaker 2: the word dang gay first seems to pop up in
Speaker 2: Spain around eighteen oh one, and researchers think that the
Speaker 2: most likely origin of that was actually from the Swahili
Speaker 2: name for the disease, key dinga pepo, meaning a disease
Speaker 2: characterized by a sudden cramp like seizure caused by an
Speaker 2: evil spirit.
Speaker 3: That sounds familiar okay.
Speaker 2: Yeah, so it was called dinga or denga from the
Speaker 2: early nineteenth century on, but it had a lot of
Speaker 2: other names. We already heard water poison, I've already heard
Speaker 2: breakbone fever, break heart fever.
Speaker 3: Oh yeah, do.
Speaker 2: You remember that one? I do remember that all the
Speaker 2: women that Benjamin Rush treated were crying.
Speaker 3: They were crying women, yeah, yeah, And old Ben was like, well,
Speaker 3: these poor ladies and their heartbreak.
Speaker 2: No one of the supposed patients was like, you should
Speaker 2: call it break heart fever because I'm just broken hearted.
Speaker 2: Oh gracious, scarlatina, rheumatic polka fever, ephemeral fever, and our
Speaker 2: the most baffling one at the time, dandy fever, dandy fever. Yes,
Speaker 2: you remember this.
Speaker 3: We were like, what the heck is a dandy? And
Speaker 3: I was thinking of that character in American Horror story.
Speaker 3: That's who I think of.
Speaker 2: And I still haven't seen that, so I don't.
Speaker 3: Know, well everyone else you know the Circus season, it's
Speaker 3: the guy who's a really horrible person, but he's like
Speaker 3: a dandy. I think he's a dandy. Tell me what's
Speaker 3: a dandy?
Speaker 2: Okay, So I did a little slew thing, which basically
Speaker 2: means that I went to the Wikipedia article for dandy,
Speaker 2: which is pretty lengthy. Actually cool. All right, So, according
Speaker 2: to Wikipedia quote, a dandy historically is a man who
Speaker 2: places particular importance on physical appearance, refined language, and leisurely
Speaker 2: hobbies pursued with the appearance of nonchalance in a cult
Speaker 2: of self like Yankee doodle dandy.
Speaker 3: Yankee doodle dandy. Yeah, a feather pick it. He puts
Speaker 3: a feather in his cap because he's concerned about his appearance.
Speaker 2: He called it macaroni. He wanted to stand out exactly.
Speaker 3: Yeah, yeah, okay, So that's a dandy.
Speaker 2: That's a dandy. I still don't understand this means in
Speaker 2: terms of dandy fever.
Speaker 3: It doesn't make any sense.
Speaker 2: Any hypotheses, send them our way.
Speaker 1: Yep.
Speaker 2: Okay, So that's dangay etymology. And also hopefully a little
Speaker 2: bit more about dandy fever, yeah than we need.
Speaker 3: Still not an answer, still.
Speaker 2: Unanswered, Okay. So anyway, the disease dangay was known by
Speaker 2: at least the late seventeen hundreds, but it would take
Speaker 2: a bit before some of its biological characteristics were discovered.
Speaker 2: So once scientists made the link between mosquitos and yellow fever,
Speaker 2: which was in the late eighteen hundreds. They kind of
Speaker 2: got the feeling that danga was also transmitted by mosquitoes,
Speaker 2: and that took a little bit longer to show, but
Speaker 2: they did show it. Let's have these infected mosquitoes bite
Speaker 2: humans human volunteers quote unquote. And then right after that,
Speaker 2: researchers discovered that dangy was caused by a filterable transmissible agent,
Speaker 2: which back then before microscopy and microbiology advanced, was pretty
Speaker 2: much going met It was a virus. The viruses wouldn't
Speaker 2: be isolated until nineteen forty three. This was during or
Speaker 2: right after the Nagasaki dangaye epidemic of nineteen forty two,
Speaker 2: which had over twenty three thousand reported cases. Wow. And
Speaker 2: so at this time researchers isolated some serum from someone
Speaker 2: who was infected and then they injected it into the
Speaker 2: brains of suckling mice. Oh and it gave them dang
Speaker 2: Okay weird. But the important thing about this was that
Speaker 2: this isolation of this virus allowed researchers to also look
Speaker 2: at the different strains and which strains were causing which outbreaks.
Speaker 2: So that was pretty important. So speaking of strains. Up
Speaker 2: to this point, this history is mostly about the history
Speaker 2: of dungay viruses, but not specifically dung gay hamorrhagic fever.
Speaker 2: And that's because that's really its own part of the story.
Speaker 2: So let's go to the nineteen forties for that. So
Speaker 2: I've talked before many times every episode probably about how
Speaker 2: important war is in terms of disease transmission. Oh yeah,
Speaker 2: deung gay and dungay hamorrhagic fever are no exceptions to that.
Speaker 2: During World War Two, especially in the Pacific and Asian
Speaker 2: theaters of war, there was massive destruction of like everything
Speaker 2: the landscape, both natural and urban, was just destroyed, and
Speaker 2: so in urban areas in particular, the infrastructure for supplies
Speaker 2: or draining and plumbing essentially collapsed and people had to
Speaker 2: store water in large containers and a lot of water
Speaker 2: pools would form rather than drain. Mosquito populations grew enormously,
Speaker 2: and they found plenty of hosts as people were also
Speaker 2: on the move both during and following the war, with
Speaker 2: a huge influx into urban centers, and the urban centers
Speaker 2: couldn't keep up with the growth in terms of infrastructure,
Speaker 2: and so you just have like all of a sudden
Speaker 2: these mosquitoes are like, wow, we have plenty of hosts
Speaker 2: here to be able.
Speaker 3: To do our thing, and collapsing infrastructure with plenty of
Speaker 3: places for water to collect and exactly Yep.
Speaker 2: It's sort of like perfect storm of yeah, bad things happening.
Speaker 2: So the other thing is that during the nineteen forties,
Speaker 2: both during the war and after, you have massive movement
Speaker 2: of people, not just like from the rural centers to
Speaker 2: urban centers, you have like movement across the entire world.
Speaker 2: What this turned into was no longer a one strain,
Speaker 2: one city situation. Suddenly there were two or three or
Speaker 2: four dangay virus strains mixing in the same location, and that,
Speaker 2: as we know, is how you get dung gae hamorrhagic fever.
Speaker 2: Of course, this had been described before, but it was
Speaker 2: really sporadic and like the exception. But in the years
Speaker 2: after World War Two there were epidemics of dungae hamorrhagic
Speaker 2: fever of very large scales, and since then they have
Speaker 2: pretty much only correct me if I'm wrong, but only
Speaker 2: increased in frequency and geographic spread and size in many cases. Yeah,
Speaker 2: so we see the first epidemics of dangae hamorrhagic fever
Speaker 2: in Southeast Asia in the nineteen fifties and sixties, starting
Speaker 2: in nineteen fifty three in Manila in the Philippines, and
Speaker 2: then these epidemics At first were sporadic every few years,
Speaker 2: but then they grew in size as trade and urbanization
Speaker 2: and populations increase. Epidemics of donge hamorrhagic fever in the
Speaker 2: Americas lagged a bit behind these epidemics in Southeast Asia,
Speaker 2: popping up only in the late nineteen seventies early nineteen eighties,
Speaker 2: and this delay was possibly due to simple geography, but
Speaker 2: also probably had something to do with the widespread mosquito
Speaker 2: eradication campaigns throughout the Americas in the twentieth century. I
Speaker 2: want to talk a little bit about these campaigns because
Speaker 2: I think they're important not only in understanding like the
Speaker 2: current landscape of mosquito born disease risk across the Americas,
Speaker 2: but also I think it's a really good example of
Speaker 2: why it's so important to work interdisciplinarily and how quickly
Speaker 2: things can be undone.
Speaker 3: Oh yeah, yeah.
Speaker 2: The anti mosquito campaigns in the Americas were initially spurred
Speaker 2: on by a desire to get rid of pest mosquitos
Speaker 2: like it was before the true extent of the disease
Speaker 2: causing capabilities of the mosquitoes known, and so mostly it was.
Speaker 3: Just like, these are annoying.
Speaker 2: These are horribly annoying, and to read some of these
Speaker 2: quotes like I can't really blame them, like it sounds madness. Okay,
Speaker 2: let me here's one. This is from an English settler. Okay,
Speaker 2: they said the noise they make in flying cannot be
Speaker 2: conceived by persons who have only heard nats in England.
Speaker 2: That's one. And a Catholic priest said, the greatest torment
Speaker 2: in comparison with which all the rest would be but sport,
Speaker 2: is the mosquitoes. The cruel persecution of the mosquitoes the
Speaker 2: plague of Egypt, I think was no more cruel. This
Speaker 2: little insect has caused more swearing since the French have
Speaker 2: been in Mississippi than had previously taken place in all
Speaker 2: the world.
Speaker 3: So more swearing in Mississippi than in all the world.
Speaker 2: Yeah, what a strange sentence.
Speaker 3: That is a really weird sentence.
Speaker 2: But it does seem that mosquitoes were like unheard of,
Speaker 2: super annoying. Yeah, and they did drive people out of towns,
Speaker 2: they slowed tourism and they reduced property values, and so people,
Speaker 2: particularly landowners, wanted something to be done. Even though it
Speaker 2: started out as this like let's get rid of nuisance
Speaker 2: mosquito's angle, it soon took on public health you know
Speaker 2: motivations as well, once the links between yellow fever and
Speaker 2: mosquitos and dangae and mosquitos and malaria mosquitos, once those
Speaker 2: were all uncovered, and also once in the yellow Fever
Speaker 2: episode we talked about the elimination of mosquitoes and reduction
Speaker 2: in yellow fever in the predominantly white Panama Canal zone exactly.
Speaker 2: So that kind of was like, oh, it can be done,
Speaker 2: so maybe we should, you know, try it. And it
Speaker 2: started in New Jersey, of all places, New Jersey, New Jersey,
Speaker 2: they were one of the most vocal about the mosquito problem,
Speaker 2: and so that's where this began. Basically, the first strategy
Speaker 2: of this campaign was to essentially use oil as they
Speaker 2: did in Panama, to dump it in mosquito breeding grounds
Speaker 2: like standing water, and then this would be like a
Speaker 2: larvacide and whatever. But it's really bad for you know,
Speaker 2: the environment treatment dump oil in. So a bunch of
Speaker 2: fish dyed, a bunch of other animals use like any
Speaker 2: aquatic animals. Plants also dyed.
Speaker 3: They use castor oil.
Speaker 2: Just kidding crow back two weeks ago. And also only
Speaker 2: a subset of mosquitoes were affected by the oil. And
Speaker 2: so they were like, we need another solution. The fishermen
Speaker 2: were like, this can't. We are not standing for this.
Speaker 2: So they were like, let's drain these marshes and swamps
Speaker 2: and wetlands.
Speaker 3: Great, great plans, great plan.
Speaker 2: And they were like, well, no matter that there are
Speaker 2: hundreds of thousands of acres of this, Let's do it anyway.
Speaker 2: And they did run into some problems. One was just
Speaker 2: the sheer size of the project that they were trying
Speaker 2: to undertake, one was funding, and the other was that
Speaker 2: not everyone wanted to have their land be drained. So
Speaker 2: then there were laws put in place, starting a New Jersey.
Speaker 2: Then California followed suit, saying that any standing water is
Speaker 2: a public nuisance and the person would either be fined
Speaker 2: or agree to comply to have their land be drained.
Speaker 2: Mosquito engineering is what it was called. By the nineteen twenties,
Speaker 2: anti mosquito campaigns were pretty much set up across the
Speaker 2: US with one exception being Florida. Like Florida seemed to
Speaker 2: be strangely resistant.
Speaker 3: They love their mosquitos down there. It's always mosquito season,
Speaker 3: as we learned, as we learned when we were there.
Speaker 2: But mosquito control cost money, and it wasn't exactly promising
Speaker 2: results because it would be like, oh, yeah, New Jersey
Speaker 2: was doing great, and then there would be heavy rains
Speaker 2: one year and all their work would be undone shocking
Speaker 2: and everything else died.
Speaker 3: So yeah.
Speaker 2: But then some unexpected and unasked for good pr for
Speaker 2: the anti mosquito campaigns came to Florida in nineteen twenty
Speaker 2: one in the form of a dangae outbreak about five
Speaker 2: hundred diagnosed cases and hundreds more that one unreported. And
Speaker 2: then the following year, as there's a massive dangae epidemic
Speaker 2: across the southeast in like Texas, Georgia, Florida, two hundred
Speaker 2: thousand people infected. Whoa yeah, wow in nineteen twenty two.
Speaker 4: Wow.
Speaker 2: So then people were got behind these anti mosquito campaigns
Speaker 2: pretty quickly after that. So I think it's important to
Speaker 2: point out that this blanket hatred for mosquitoes and full
Speaker 2: steam ahead approach wasn't necessarily unanimous among the people in charge.
Speaker 2: It's easy to look back and assume that's the case,
Speaker 2: because this is what actually did happen. There was a
Speaker 2: lot of you know, let's kill all the mosquitoes, But
Speaker 2: there were dissenting voices early on. So there are people
Speaker 2: who worked directly in the mosquito control business were suspicious
Speaker 2: that these poisonous gases were also toxic to fish and birds,
Speaker 2: and others saw right through some of the efforts as
Speaker 2: a money making scheme for real estate developers. But because
Speaker 2: there was more money to be made in complete mosquito
Speaker 2: eradication than in an ecologically balanced approach, these dissenting voices
Speaker 2: were drowned.
Speaker 3: Out, yeah, in the swamps that they drained exactly.
Speaker 2: The nineteen thirties saw even a larger expansion in mosquito
Speaker 2: control efforts at the US scale, and then the following
Speaker 2: decade PAHO of Pan American Health Organization got involved and
Speaker 2: their campaign was to eliminate eighties Egypti across the Americas.
Speaker 3: So how'd that work out for them?
Speaker 4: Well?
Speaker 2: Great, actually for a very short time. Okay, all right, Yeah,
Speaker 2: So in general, these projects were developed or carried out
Speaker 2: by engineers, not ecologists, and so that led to some
Speaker 2: major problem. In some of these marshy areas, there was
Speaker 2: diverse habitat rich with plant and animal life. A few
Speaker 2: years later was just destruction.
Speaker 3: Yeah.
Speaker 2: And this led to a pretty big rift actually between
Speaker 2: mosquito control advocates and conservationists, even though it seems like
Speaker 2: they should both be on the same side of things.
Speaker 2: But this rift would only grow larger because in the
Speaker 2: nineteen forties, a new pesticide called die chlorod phenal trichloroethane DDT,
Speaker 2: you got it, and that was found to be an
Speaker 2: extremely cheap and really effective way to control or kill
Speaker 2: both adult mosquito populations and larvae.
Speaker 3: And like everything else, it's great.
Speaker 2: Just kill everything, just kill everything. And it was great
Speaker 2: also because it persisted in the environment. You just needed
Speaker 2: one treatment and then you can kill everything for years
Speaker 2: to come and just for decades and decades.
Speaker 3: No potential downside to this whatsoever.
Speaker 2: Nope. And so the nineteen forties, fifties, sixties all saw
Speaker 2: a widespread use of DDT. It also saw the emergence
Speaker 2: of DDT resistance, shocking, and it also saw the widespread
Speaker 2: destruction and population declines in a host of other animals,
Speaker 2: and so in nineteen sixty two is sort of when
Speaker 2: things started to turn against the tide of mosquito campaigns.
Speaker 2: Rachel Carson's book Silent Spring was published, and in effect
Speaker 2: that was the birth of the modern environmentalist movement. First
Speaker 2: Earth Day was celebrated in nineteen seventy and by nineteen
Speaker 2: seventy two DDT was banned in the US. And around
Speaker 2: this time also is when PAHO kind of stopped or
Speaker 2: slowed its efforts for mosquito elimination campaigns. And a lot
Speaker 2: of that was just a loss, like a stop, loss
Speaker 2: of funding. Another was that they no longer felt it
Speaker 2: was necessary because yellow fever and dengay was no longer
Speaker 2: an issue in so many of the places. Eighties of
Speaker 2: JYPDI was successfully eliminated in Mexico, Guatemala, Belize, Honduras, El Salvador, Nicaragua,
Speaker 2: Costa Rica, Panama, Columbia, Ecuador, Peru, Chile, Bolivia, Paraguay, Argentina, Uruguay, Brazil,
Speaker 2: the Cayman Islands, and Bermuda. Wow, it was eliminated. That's
Speaker 2: not of countries, not everywhere. It wasn't successful everywhere, right,
Speaker 2: but a lot of them. But when these campaigns stopped,
Speaker 2: within a few years, all the mosquitoes came back. As
Speaker 2: you might expect, this is when and this is when
Speaker 2: you see the first cases of denge hamorrhagic fever in
Speaker 2: the late nineteen seventies. Within a couple decades after that,
Speaker 2: the levels of mosquitos that we have in all of
Speaker 2: those places are at pre eradication levels, like before any
Speaker 2: of these campaigns ever got started.
Speaker 3: Wow, man, mosquito are hardy little bugs, tell you what.
Speaker 2: Yeah, so we're back to where we started essentially, Yeah,
Speaker 2: and or actually in worse situation.
Speaker 3: Right because now it's everywhere.
Speaker 2: Now it's everywhere. The first decade of the twenty first
Speaker 2: century saw huge increases in dang gae incidents in the Americas,
Speaker 2: including two Pan American epidemics with over a million reported cases,
Speaker 2: as well as local transmission within different places. I found
Speaker 2: an article that said, there are five major reasons for
Speaker 2: dengaye's emergence as a public health problem.
Speaker 3: Excellent.
Speaker 2: One unprecedented global population growth okay. Two uncontrolled urbanization and
Speaker 2: all that goes with it, including substandard water treatments. So
Speaker 2: we're in waste management, infrastructure, et cetera. Three lack of
Speaker 2: effective mosquito control in places where the disease is endemic,
Speaker 2: four increased air travel, and five decay in public health infrastructure,
Speaker 2: meaning that there was more of a focus on p
Speaker 2: demic response rather than prevention. Mm So, Aarin, now that
Speaker 2: Dengey is around us everywhere at all times, well not
Speaker 2: here in Chicago in the middle of January, how worried
Speaker 2: should we be? Tell us about the vaccine, tell us
Speaker 2: about the latest epidemics. What's going on?
Speaker 3: All right, let's talk all about it. We'll take one
Speaker 3: quick break first, Aaron.
Speaker 2: It's not good news cool.
Speaker 3: Worldwide denay is I don't know if you would say endemic,
Speaker 3: but certainly circulates in over one hundred countries. Okay, we don't,
Speaker 3: as per usual, have a good handle on how many
Speaker 3: cases there actually are every year. However, do you want
Speaker 3: to hear some terrifying estimates. A modeling study in twenty
Speaker 3: thirteen that was published in Nature, which we'll link on
Speaker 3: our website, estimated and this is now the estimates that
Speaker 3: like who has on their website, et cetera. It's a
Speaker 3: pretty I mean, a good modeling study. They estimated three
Speaker 3: hundred and ninety million dan gay virus infections per year.
Speaker 3: What of which that's three hundred and ninety million infections. Remember,
Speaker 3: the vast majority are asymptomatic, so it's estimated that ninety
Speaker 3: six million of those will manifest clinically at some level
Speaker 3: of severity.
Speaker 5: So yeah, hold on, okay, this is every year, every year.
Speaker 2: But how are there even that many susceptible people?
Speaker 3: Another study estimated that three point nine billion people are
Speaker 3: at risk of infection with dengey.
Speaker 5: That's that's half of the world, yep, exactly, But how
Speaker 5: how does that like?
Speaker 2: Mathematically?
Speaker 3: Every year we need all be how many people are
Speaker 3: born every year?
Speaker 1: Hey?
Speaker 2: Google, how many people are born every year?
Speaker 4: Here's some information from the web that might possibly help.
Speaker 2: On the website the Guardian dot com, they say they are,
Speaker 2: on average about two hundred and fifty.
Speaker 3: Babies born every minute, more than one hundred and thirty
Speaker 3: million in a year.
Speaker 4: To find out more, look.
Speaker 5: For the link in your Google Home or Google Assistant.
Speaker 2: Apt There you go, one hundred and thirty million babies
Speaker 2: born every year.
Speaker 3: Okay, so then at over at a certain point, everyone
Speaker 3: is going to be infected with danay is what that means?
Speaker 2: Yeah, it's only a matter of time.
Speaker 3: It's only a matter of time. Fascinating. Wow, way to
Speaker 3: go Google. Okay, now here's where it gets even more interesting.
Speaker 3: Like you kind of mentioned the number of dangay cases
Speaker 3: has been increasing. Now, you know, we have to balance
Speaker 3: the fact that we're getting better at you know, it's
Speaker 3: being reported more often, et cetera, et cetera. But there's
Speaker 3: no doubt that dengay is growing in its number of cases.
Speaker 3: It's not just because we're reporting it more often. But
Speaker 3: for example, between twenty ten and twenty sixteen, the number
Speaker 3: of cases reported to WHO increased from less than half
Speaker 3: a million to three point three million in only six years.
Speaker 3: What right, And that's just what's reported, you know, So
Speaker 3: that's a lot less than what is actually what it's
Speaker 3: estimated that people are actually infected.
Speaker 2: So is it pretty easy to get screened for dengay?
Speaker 2: Like is the test expensive or is it like fast?
Speaker 3: So that's one of the limitations in dengay research is
Speaker 3: that we don't have perfect screening methods it. You can
Speaker 3: screen for it, you use zero prevalence tests, so you'll
Speaker 3: look for antibodies to dengay just like we do for
Speaker 3: a lot of other diseases. It's usually I think a
Speaker 3: PCR test, So those aren't super cheap, but they're not
Speaker 3: you know, super expensive or very cost prohibitive or anything.
Speaker 3: But it is a limitation that we don't have, you know,
Speaker 3: screening everywhere. Not every clinic is going to be able
Speaker 3: to test for dengay. So in twenty seventeen and eighteen,
Speaker 3: cases were actually down. It was looking good for dengay,
Speaker 3: like there were fewer cases than the past few years.
Speaker 3: Twenty nineteen not so much, especially in the Americas. So
Speaker 3: PAHO reported over two point seven million cases and over
Speaker 3: twelve hundred deaths between January and October of twenty nineteen.
Speaker 3: Oh yeah, right, that's a lot. That's just so PAHO
Speaker 3: is the Pan American Health organization. That's just the Americas.
Speaker 3: Across the globe. There was also increases kind of across
Speaker 3: the board. So there were outbreaks in twenty nineteen across Australia, Cambodia, China, Malaysia, Philippines, Singapore, Vietnam, Brazil, Colombia, Tanzania, Congo,
Speaker 3: French Polynesia, everywhere. So overall it's estimated that at least
Speaker 3: five hundred thousand people every year are hospitalized with severe dengay,
Speaker 3: and across the globe this has on average about a
Speaker 3: two and a half percent case fatality rate. So that's
Speaker 3: a lot of people dying every year from dengay.
Speaker 2: That is so many people. What's our what are is
Speaker 2: our hope?
Speaker 3: Well, there are a few, there are kind of a numbers.
Speaker 3: Let's end this episode on a positive note for once
Speaker 3: in our lives. So there is a vaccine, and there's
Speaker 3: more than one. There are I think four or five
Speaker 3: vaccines under study like that are undergoing phase three trials,
Speaker 3: and there's one called denga Vaccia that was licensed in
Speaker 3: twenty fifteen, So this is currently you can get this
Speaker 3: vaccine in a number of different countries. It was actually
Speaker 3: approved by the FDA for the US in May of
Speaker 3: twenty nineteen. The only problem, not the only problem. One
Speaker 3: of the problems with this vaccine is that you know,
Speaker 3: when they first did studies on it, it's it's protective
Speaker 3: against all four zero types all four strains of virus,
Speaker 3: which is really important because remember if you get infected
Speaker 3: with a different strain, then you're more likely to have
Speaker 3: dange heemorrhagic fever or danngey shock. Syndrome. So any vaccine
Speaker 3: has to protect against all of the stereotypes of dangay.
Speaker 2: Aren't there five?
Speaker 3: There are, but the newest one. I don't know if
Speaker 3: it's only circulates in really small areas or if we
Speaker 3: just didn't know enough about it. It's not in any
Speaker 3: of these vaccines, but the four are the ones that
Speaker 3: are like really prevalent.
Speaker 2: Okay.
Speaker 3: Yeah, So from initial trials, the overall efficacy of this
Speaker 3: vaccine was around sixty percent for dengay infection overall, but
Speaker 3: eighty percent protective against severe dengay. So that's really good. However,
Speaker 3: when they went back and like over time, did some
Speaker 3: longer term studies, what they realized is that if you
Speaker 3: give this vaccine to people who have never been infected
Speaker 3: with dengay, so who are zero negative when they get
Speaker 3: the vaccine, over time, they're actually more likely to get
Speaker 3: severe dngay infection.
Speaker 2: Okay.
Speaker 3: So what that suggests is that this vaccine isn't providing
Speaker 3: complete immunity against all four strains, Okay, okay. So the
Speaker 3: current recommendation right now is that if countries are going
Speaker 3: to start introducing the dengay vaccine, they should green people
Speaker 3: for previous infection before they give them the vaccine, because
Speaker 3: in people who have been exposed to at least one strain,
Speaker 3: the vaccine is very protective and doesn't increase your risk
Speaker 3: of severe dangay.
Speaker 2: Gotcha?
Speaker 3: Okay? So yeah, so that's kind of the preferred option
Speaker 3: at this point. It's pre vaccination screening, and you only
Speaker 3: give the vaccine to people who have previously been infected
Speaker 3: with dang gay. Here's where I'm going to answer a question.
Speaker 3: Shout out to Kobe from University of South Florida, who,
Speaker 3: first of all, drove all the way from Tampa to
Speaker 3: Gainesville to come and see us talk, which they still
Speaker 3: can't believe that I drove to see us, like that's wow.
Speaker 2: Yeah.
Speaker 3: So he asked an amazing question after the talk that
Speaker 3: I want to make sure I touch on. He asked,
Speaker 3: why is it that if you give some the deng
Speaker 3: gay vaccine after they've been exposed to dengay, why doesn't
Speaker 3: the vaccine cause dan gay hemorrhagic fever or dungay shock
Speaker 3: syndrome in those people?
Speaker 2: I remember this question right.
Speaker 3: It's a really good question, and my thought at the
Speaker 3: time was, well, maybe the vaccines are only component vaccines
Speaker 3: turns out they're not. So the vaccines that are licensed,
Speaker 3: the vaccine that's licensed and most of the ones that
Speaker 3: are in trials are live attenuated vaccines, which means they
Speaker 3: are live virus of the four different erotypes, but the
Speaker 3: viral strains have been grown in the lab until they're
Speaker 3: no longer very virulent, so they don't make us sick.
Speaker 3: All they do is stimulate an immune response. But your
Speaker 3: immune system has a lot to do with the dung
Speaker 3: gay hemorrhagic fever and dan gay shock syndrome like manifestations.
Speaker 3: So why is it that we don't see this in
Speaker 3: the vaccine? And the answer, I think from what I
Speaker 3: can tell, just turns out to be because these strains
Speaker 3: are not virulent, they don't induce that response, but theoretically
Speaker 3: they could. Huh Yeah, isn't that fascinating? That's really interesting,
Speaker 3: So Kobe, that was a really good question.
Speaker 2: Yeah, yeah, huh.
Speaker 3: And there's a couple of cool papers that I found
Speaker 3: looking at like the current status of vaccine research, because again,
Speaker 3: this isn't the only vaccine that's out there. There's other
Speaker 3: vaccines under trials, so we'll post all of those on
Speaker 3: our website as usual. So that's the good news about
Speaker 3: the vaccine. What's really cool about dang gay too, though,
Speaker 3: is there's a ton of research going on in better
Speaker 3: mosquito control, but not the way that we've done it
Speaker 3: in the past. So for Danay, there's a lot of
Speaker 3: research going on in genetically modifying mosquitoes to no longer
Speaker 3: be able to transmit dang gay virus.
Speaker 2: Very cool.
Speaker 3: I absolutely love this. So one of the main strategies
Speaker 3: that people are using is a bacteria called Wolbachia. Oh yeah,
Speaker 3: So mosquitoes in general, like across like tons of different
Speaker 3: species of mosquitoes are naturally infected with a species of
Speaker 3: bacteria called Wolbachia, and in eighties mosquitoes, it turns out
Speaker 3: that infection with Wolbachia reduces the ability of the mosquito
Speaker 3: to transmit danngae and other arboviruses like yellow fever, chicken
Speaker 3: gun yazica, et cetera. So what they've been doing, and
Speaker 3: I'm I don't we don't have time to really get
Speaker 3: into the nitty gritty details of this, but what they're
Speaker 3: basically doing is, you know, engineering Wolbachia to be able
Speaker 3: to be transmitted between mosquitoes so that a whole population
Speaker 3: of mosquitoes could end up infected with this Wolbachia bacteria
Speaker 3: and that can then make it so that that population
Speaker 3: of mosquitoes can't transmit the danngae virus. Isn't that cool?
Speaker 2: That's really cool.
Speaker 3: Yeah, so we'll end this one on a happy note.
Speaker 3: It's not all doom and gloom and hundreds of thousands
Speaker 3: of people dying every year.
Speaker 2: It's just hundreds of millions of people getting infected with dangay.
Speaker 2: That's it.
Speaker 3: That's all, dear okay.
Speaker 2: Sources So I have several and I want to shout
Speaker 2: out a few. One is called the Mosquito Crusades and
Speaker 2: this is a book by Gordon Patterson. And then another
Speaker 2: great source was Dwyane. Was a book by Dwayne Gobbler
Speaker 2: called Dan Dangay Hamorrhagic Fever, and a paper by Dick
Speaker 2: at All the History of dange outbreaks in the Americas.
Speaker 2: And uh yeah, a few more that I'll post on
Speaker 2: the website.
Speaker 3: That paper from Nature twenty thirteen that estimated the global
Speaker 3: distribution and burden of dangay that was the title was
Speaker 3: by Semir bat at All. And there was a also
Speaker 3: very great paper on titled the Pathogenesis of Dangae adwn
Speaker 3: of a New Era in f one thousand research in
Speaker 3: twenty fifteen, and then a number of textbooks and other
Speaker 3: papers that we will post on our website. This podcast
Speaker 3: will kill you dot com cool.
Speaker 2: Well. Thank you to Bloodmobile for providing the music for
Speaker 2: this episode and all of our episodes.
Speaker 3: And thank you all for listening and allowing us to
Speaker 3: make this podcast. And if you were at our Florida show,
Speaker 3: thank you so much for coming to see us.
Speaker 2: Oh my gosh, thank you. It was so most fun.
Speaker 2: And thanks again, of course to doctor Alex Trio for
Speaker 2: providing the first hand account for this episode. We'll post
Speaker 2: her website and her Twitter information in our show notes. Okay, well,
Speaker 2: with that, wash your hands.
Speaker 4: You filed the animals
Speaker 5: Mu