Speaker 1: On the seventh of September, my boy took her from
Speaker 1: the pasture a little before sunset and harnessed her. While
Speaker 1: standing at the door, I observed she slavered freely and
Speaker 1: was stupid and downcast in her appearance. I observed that
Speaker 1: she was loath to go faster than the walk, and,
Speaker 1: although repeatedly urged forward by the whip, would shortly resume
Speaker 1: the walk. Once or twice, on ascending a hill she
Speaker 1: stopped for a second as if fatigued or in pain,
Speaker 1: and several times in descending small pitches she appeared in
Speaker 1: great danger of falling from the very bungling manner of
Speaker 1: using her fore feet. I continued my ride without discovering
Speaker 1: anything farther till the latter part of the evening, except
Speaker 1: that whenever the whip was applied, a distinct interval was
Speaker 1: obvious between the time I struck her and the time
Speaker 1: she perceived the blow. When she did perceive it, the
Speaker 1: effect was greater than expected, for she started off as
Speaker 1: if surprise had been added to the usual effects of
Speaker 1: the lash. On my return home in the latter part
Speaker 1: of the evening, I experienced great difficulty in keeping her
Speaker 1: in the road on account of an obstinate and constant
Speaker 1: tendency to the left that required strong effort to counteract.
Speaker 1: She could scarcely be urged out of a walk, and
Speaker 1: it was perfectly evident that she was laboring under some
Speaker 1: alarming disease. I now made a careful examination and found
Speaker 1: the whole surface of the body cold and tremulous, countenance
Speaker 1: dull and listless, a leaning and stepping to the left,
Speaker 1: with so much appearance of general weakness as to induce
Speaker 1: the fear that she would fall in the harness. With
Speaker 1: much ado, I got her home, which was then but
Speaker 1: a short distance. She, however, grew worse very fast, and
Speaker 1: when she arrived home, did not recognize her own stable.
Speaker 1: She was now well rubbed and a gallon of blood
Speaker 1: taken from the neck. While this was doing, and afterwards
Speaker 1: she often kicked violently with her left foot. About eleven
Speaker 1: p m. I was called from home and did not
Speaker 1: return until the next day, about two pm. When she
Speaker 1: was down and incapable of rising. She was left in
Speaker 1: care of a farrier, who had her blood again and
Speaker 1: given her several cathartic medicines without effect. She lay stretched
Speaker 1: out upon the floor with her head drawn back and
Speaker 1: the muscles of the neck, abdomen and limbs frequently convulsed.
Speaker 1: At short intervals. She would revive or attempt to get up,
Speaker 1: but could only get upon her hind feet, for her
Speaker 1: fore legs appeared to be completely paralyzed. She would, however,
Speaker 1: make a powerful exertion to rise forwards and throw herself
Speaker 1: several feet ahead, without regard to anything that might be
Speaker 1: in her way. No material alteration took place till next morning,
Speaker 1: except gradual diminution of strength and exertion. In the morning,
Speaker 1: she commenced moving her legs backwards and forwards, was generally
Speaker 1: convulsed and apparently in greatest distress. This state of things
Speaker 1: continued till nine am when she expired. Oh, I know,
Speaker 1: it's really sad. Also, that was about a.
Speaker 2: Horse, that was Yeah, it wasn't.
Speaker 1: It wasn't obviously clear right the firsthand.
Speaker 2: But that was about a horse like taking her from
Speaker 2: the pasture. Yeah, we four feet four feet.
Speaker 1: So that was an account of the eighteen thirty one
Speaker 1: Eastern equine encephalitis outbreak in Massachusetts, written by Gardner M. Peck,
Speaker 1: and it was from a nineteen fifty seven article titled
Speaker 1: in an Epizootic of Equine and Cephalomyelitis by RP.
Speaker 2: Hanson.
Speaker 1: Hi, I'm Aaron.
Speaker 2: Welsh and I'm Erin omen Updyke.
Speaker 1: And this is this podcast will kill you.
Speaker 2: And they were talking about triple.
Speaker 1: A triple A Eastern equine encephalitis.
Speaker 2: Yes, that's very exciting.
Speaker 1: It is so we actually this is similar to our
Speaker 1: Dangay episode. We have done this already in person at
Speaker 1: the University of Michigan.
Speaker 2: Whoop whoop.
Speaker 1: Yeah.
Speaker 2: Uh.
Speaker 1: But just like Dangay, I've forgotten everything.
Speaker 2: I don't remember. I didn't even remember Erin like my
Speaker 2: own part of this. So when I went back to
Speaker 2: my notes, I was like, oh, this is depressing.
Speaker 1: Oh yeah it is. And I yeah, I didn't remember
Speaker 1: any part of a mind, which definitely means I remember
Speaker 1: zero part of yours.
Speaker 2: Oh no, I don't know the history of this, like
Speaker 2: in the slightest.
Speaker 1: So I feel like it's kind of alarming how hotly
Speaker 1: we forget. Yes, but that was but it was super
Speaker 1: fun to be in Michigan and we really liked hanging
Speaker 1: out with Laura, So we wanted to give Laura and
Speaker 1: that group a huge shout out to having us and
Speaker 1: inviting us.
Speaker 2: That was so fun. That was when we did like
Speaker 2: actual chemistry. Remember that.
Speaker 1: Oh my gosh, it was like such an action packed
Speaker 1: fun day.
Speaker 2: It really was.
Speaker 1: We enjoyed meeting everyone and talking to everyone, and yes.
Speaker 2: It was super fun. It was great.
Speaker 1: Is so cute?
Speaker 2: Yeah, I know, I wish we got more time there. Yeah,
Speaker 2: maybe someday in the future we can go back. Yeah,
Speaker 2: someday someday. All right, to be business to attend to, Aaron.
Speaker 1: I mean, we could just do the usual suspects one
Speaker 1: more time. So we've got alcohol free episodes. You can
Speaker 1: find them on this podcast will Kill You dot com
Speaker 1: under the episodes tab. And we also have two things
Speaker 1: related to books. One is a Goodreads list, so we
Speaker 1: have a link to that on our website under the
Speaker 1: books tab. And we also have an affiliate page on
Speaker 1: bookshop dot org that is an online bookseller that works
Speaker 1: with independent bookstores.
Speaker 2: All right, now for the most important business of all,
Speaker 2: it's quarantiny time.
Speaker 1: It's quarantiney time.
Speaker 2: What are we drinking today, Aaron?
Speaker 1: We are drinking the Triple E Shot.
Speaker 2: That's it's a straightforward name.
Speaker 1: Yeah, I know, I feel like I think at the
Speaker 1: time we were like, oh, we'll come up with a
Speaker 1: better one when the episode comes out, and then here
Speaker 1: our creative juicies have just been dried up. I think
Speaker 1: we're used up.
Speaker 2: I don't know both maybe, Well, what's in the triple
Speaker 2: E shot?
Speaker 1: The triple E shot has three things, of course, a
Speaker 1: half an ounce of coffee tequila okay, delicious even on
Speaker 1: its own, A half an ounce of hazel nut liqueur,
Speaker 1: and a half an ounce of half and half fab
Speaker 1: It's it's delicious, it's simple, it's easy.
Speaker 2: There you go, all right, fabulous. Anything else that we
Speaker 2: should cover or should we just jump straight into this
Speaker 2: depressing episode?
Speaker 1: I mean, I think it's just let's just do it, Aaron,
Speaker 1: Let's just let's just.
Speaker 2: Dive right in. It's actually it's going to be very interesting. Okay.
Speaker 1: Well, I'm excited to relearn everything that I've forgotten.
Speaker 2: Yeah, me too.
Speaker 1: Right, well, we will start doing that right after this break.
Speaker 2: Eastern equine encephalitis aka triple E aka also sometimes called
Speaker 2: sleeping sickness, but not to be confused with African sleeping
Speaker 2: sickness or trepanasamiasis okay.
Speaker 1: Or encephalitis lethargica, because I think at the time it
Speaker 1: was also confused with that disease for at least the
Speaker 1: early years.
Speaker 2: Fascinating. Huh yeah, all right, well, this.
Speaker 3: Is not that.
Speaker 2: Eastern equine encephalitis is a viral infection. It is an
Speaker 2: alpha virus, which I don't believe that we've covered any
Speaker 2: alpha viruses thus far in this series. Triple E virus.
Speaker 2: It's an RNA virus. It is round in shape, so
Speaker 2: it's very kind of adorable when you look at it
Speaker 2: under scanning electron microscopes. There are four major lineages of
Speaker 2: this virus, so four major strains. But group one, which
Speaker 2: is the one that's most common in North America, is
Speaker 2: also the most virulent and the most common cause of
Speaker 2: disease in humans. So that's the one that we'll focus
Speaker 2: on just because that's the one that makes people sick. Okay,
Speaker 2: uh huh, all right. So I'm not going to talk
Speaker 2: a lot about the evolutionary history or the ecological cycle
Speaker 2: of this virus, because you're.
Speaker 1: Going to do that right erin, I hope, so excellent.
Speaker 2: But I will say, because we have to understand how
Speaker 2: this virus is transmitted. Trips E. That's what I wrote
Speaker 2: down is the name for it.
Speaker 1: That's not going to be confusing at all.
Speaker 2: Triply virus, it's mostly a bird virus, okay, So it
Speaker 2: circulates enzootically among a number of different bird species, but
Speaker 2: it can cause both epizootics, So that is an epidemic
Speaker 2: in animals when it jumps from bird populations into for example,
Speaker 2: horse populations equine populations, hence the name. And it can
Speaker 2: also cause zoonotic outbreaks in humans if it jumps from
Speaker 2: birds into humans. Okay, all right, So among birds, it's
Speaker 2: primarily transmitted by mosquitos in the genus Cula seta, but
Speaker 2: it can be transmitted by a number of different genera
Speaker 2: of mosquitoes, including eighties mosquitoes and others.
Speaker 1: Okay, there's an asterisk to that statement that I'll go into.
Speaker 2: Oh I can't wait to hear about it. I want
Speaker 2: to know.
Speaker 1: Okay, do you know right now?
Speaker 2: Yeah? Kind of.
Speaker 1: So basically they call these other mosquito species the bridge vectors.
Speaker 1: Uh huh, okay, So, jumping a little bit into the
Speaker 1: ecology side of things, Quelo seta, which is the genus well,
Speaker 1: Kulo seta melanera, which is the main species that seems
Speaker 1: to perpetuate this infection cycle in like, you know, birds,
Speaker 1: they are not mammal biers or human biers, like very
Speaker 1: very little, and so researchers are like, well, it might
Speaker 1: be that there's either they occasionally bite humans and that's
Speaker 1: how these things happen, or it's bridge vectors. But in
Speaker 1: one study that looked at the like viral load of
Speaker 1: other species of mosquito, some of the the proposed bridge
Speaker 1: vector species, none of them had viral loads that were
Speaker 1: high enough to actually cause infection. Fascinating, So it might
Speaker 1: be that you can detect the virus because that mosquito
Speaker 1: fed on an infected bird, but the virus might not
Speaker 1: be able to replicate within that mosquito. But there's still
Speaker 1: a lot of like question mark, question mark, question mark, right,
Speaker 1: this sort of thing. So it's like that aspect of
Speaker 1: the ecology is pretty not very well clarified yet in
Speaker 1: terms of like the contributions of this mosquito species versus
Speaker 1: this mosquito species species, and also geographically because that can
Speaker 1: play a huge role.
Speaker 2: So then it's like unclear exactly which mosquitoes might be
Speaker 2: infecting humans.
Speaker 1: Right, So basically, I think the takeaway that I got
Speaker 1: from that article was that if even if you detect
Speaker 1: this virus in a mosquito, it doesn't necessarily mean that
Speaker 1: it's going to be infected and able to transmit.
Speaker 2: Right, because these viruses have to be able to replicate
Speaker 2: within the mosquito and then leave the mosquito's gut and
Speaker 2: travel to their salivary glands and then be there in
Speaker 2: high enough concentration that when the mosquito bites its next host,
Speaker 2: it's injecting enough virus to actually get that host sick.
Speaker 2: So there, these are very complicated cycles within the mosquito.
Speaker 2: So it makes sense that not every mosquito is going
Speaker 2: to be able to transmit every virus, right. So, right,
Speaker 2: even if you can detect it just when you smush
Speaker 2: that mosquito, like, yeah, you found some virus, but where
Speaker 2: was that virus within the mosquito and how much of
Speaker 2: it was there? Cool? How interesting? All right, So we've
Speaker 2: covered now that this is a disease transmitted by mosquitoes.
Speaker 2: Will ignore the details of which mosquito it is for now,
Speaker 2: So let's talk about how this virus makes you sick
Speaker 2: once it gets inside you. Okay, So, like many arboviral diseases,
Speaker 2: so virus is transmitted by arthropods like mosquitoes. When a
Speaker 2: mosquito bites you, the first place that it spits that
Speaker 2: virus is kind of towards your lymphatic system, right, so
Speaker 2: it's kind of right under your skin. They don't spit
Speaker 2: it necessarily directly into your bloodstream, but they spit it
Speaker 2: under your skin, and that virus goes into your lymphatic system.
Speaker 2: From there, it travels to you lymph nodes, and in
Speaker 2: the case of eastern equine and stephalitis virus, it infects
Speaker 2: our white blood cells. Okay, so those are the cells
Speaker 2: that it goes into, and that's where it replicates. Remember
Speaker 2: that viruses have to replicate inside of our cells. They
Speaker 2: don't replicate on their own. So it turns out that
Speaker 2: triple E replicates inside of our white blood cells. White
Speaker 2: blood cells can travel pretty much anywhere in our body,
Speaker 2: including crossing the blood brain barrier and making it into
Speaker 2: our nervous system. All right, so let's go through kind
Speaker 2: of how this makes you sick. This is a bit
Speaker 2: of a spoiler, but this is a horrible, horrible disease.
Speaker 1: Okay, So that much I do remember, yes, from Michigan, if.
Speaker 2: You if you had like a magic eight ball, and
Speaker 2: you shook it, it would say, outlook not so good? Yeah, okay.
Speaker 2: One of the questions that I like to try and
Speaker 2: answer when we look at a disease that causes such
Speaker 2: terrible outcomes is how does it do that? We are
Speaker 2: usually very good at fighting off infections, So how can
Speaker 2: this virus kind of beat our own immune system?
Speaker 3: Right? Like?
Speaker 2: How can it make us so very sick? M okay?
Speaker 3: So.
Speaker 2: The other reason that it's important to understand how this
Speaker 2: virus makes us so sick is because, in theory, if
Speaker 2: we can understand how it makes us so sick, we
Speaker 2: could maybe try and do something about it, right, We
Speaker 2: can try and counteract that. Okay. So I found a
Speaker 2: few different studies that tried to shed some light on
Speaker 2: exactly how this virus makes us so sick. One of
Speaker 2: the important things is that this virus is very good
Speaker 2: at evating our immune system. Specifically, it seems to do
Speaker 2: a very good job of inhibiting one of our major
Speaker 2: responses to viral infections, and that is something called interferon.
Speaker 2: Talked about in like the hepatitis episode. Probably I don't remember,
Speaker 2: but anyways, Interferon is a protein that we make that
Speaker 2: helps to stimulate our immune response specifically to target and
Speaker 2: kill viruses and virallly infected cells.
Speaker 1: Gotcha.
Speaker 2: So Triple E, like many other viruses and a lot
Speaker 2: of arboviruses, specifically targets and shuts down the production of interferon,
Speaker 2: it seems like in us. And what's really interesting is
Speaker 2: that there have been some other studies I found that
Speaker 2: compared the effectiveness of interferon on actually killing virus infected cells.
Speaker 2: So like, even if you gave someone a bunch of interferon, like,
Speaker 2: if that's the problem the virus is blocking this production,
Speaker 2: give them interfer on. This virus actually like inhibits the
Speaker 2: action of interferon.
Speaker 1: That's wild.
Speaker 2: And here's where it gets even cooler. This is why
Speaker 2: I get excited about this. Remember I said, there are
Speaker 2: many different strains of this virus, like at least four,
Speaker 2: and it's only the North American strain that tends to
Speaker 2: be the most virulent and cause infection in humans. So
Speaker 2: this one study compared North American strains to South American strains,
Speaker 2: and what they found was that across the board, all
Speaker 2: cells infected with Triple E viruses North American or South
Speaker 2: American had very low levels of interferon so they blocked
Speaker 2: the production of interferon. But on top of that, the
Speaker 2: North American strains were the ones that were also resistant
Speaker 2: to the effects of interferon. Ah, So, like, no matter
Speaker 2: how much interferre on you had in your body, it
Speaker 2: was going to be lower within triple E infection than
Speaker 2: with other viral infections. But the interfere on that you
Speaker 2: do have works to kill that South American virus but
Speaker 2: not the North American strains.
Speaker 1: Wow, that's very interesting.
Speaker 3: I know.
Speaker 2: Okay, so that's how it causes disease and why at
Speaker 2: least part of the reason why it probably causes such
Speaker 2: severe disease. Okay, now let's start to talk about the
Speaker 2: really depressing part, which is the actual symptoms. Okay, the
Speaker 2: one good news I have this is it it's estimated
Speaker 2: that only about four to five percent of human infections
Speaker 2: actually result in symptomatic disease. So, like I'm just about
Speaker 2: to ask that, oh good, I preempted you. Ninety six
Speaker 2: percent of people who get infected with triple E virus
Speaker 2: will never have symptomatic disease. They're going to be just fine. Okay,
Speaker 2: that's the.
Speaker 1: Estimates, But that's I feel like that's a trend that
Speaker 1: we see a lot in rble viral diseases, that there's
Speaker 1: a huge rate of asymptomatic individuals. Yeah, do these people
Speaker 1: have immunity? Do they develop immunity to treat question?
Speaker 2: I did see in several review papers just sort of
Speaker 2: talking about the symptoms in general, that it is thought that, yes,
Speaker 2: when you are exposed to this virus, you develop long
Speaker 2: lasting immunity. Remember that point because it will become very
Speaker 2: interesting when we talk about the vaccine. Yes, okay, but yes,
Speaker 2: it is thought that if you get infected with this virus,
Speaker 2: whether you're symptomatic or not, you do generate long lasting immunity. Okayes,
Speaker 2: that's the thought.
Speaker 1: That's good news.
Speaker 2: It is good news. That's the end of the good news. Okay.
Speaker 2: So let's talk about the symptoms of this virus. It's
Speaker 2: called Eastern equine encephalitis. Encephalitis. We've talked about this before, right,
Speaker 2: This is inflammation in your actual brain. It's not good news.
Speaker 2: So this causes a viral encephalitis. In theory, almost any
Speaker 2: virus could potentially cause an encephalitis if it gets into
Speaker 2: your brain causes infection there. For most viruses, that's a
Speaker 2: very uncommon manifestation, but for some reason, a lot of arboviruses,
Speaker 2: so mosquito born viruses do cause viral encephalitis. And we've
Speaker 2: also talked on this podcast about one of the most
Speaker 2: famous causes of viral encephalitis, that is.
Speaker 1: Rabies. Oh I saw.
Speaker 2: Your face just being completely blank, and I was like,
Speaker 2: don't worry. So rabies is like the most probably famous
Speaker 2: viral encephalitis I think. So let's talk about the characteristic
Speaker 2: symptoms of viral encephalitis. There's three Number one fever. This
Speaker 2: fever tends to be quite high and it tends to
Speaker 2: come on very rapidly. Number two headache because your brain
Speaker 2: is inflamed. Number three altered level of consciousness. Now, that
Speaker 2: doesn't necessarily mean that you will go unconscious, although as
Speaker 2: you'll see, it often leads to that, but it does
Speaker 2: mean that, like overall, you can have fluctuating levels of
Speaker 2: consciousness okay, and kind of awareness. And then, because viral
Speaker 2: encephalitis is a viral infection of your brain, you will
Speaker 2: often have specific neurological symptoms that can be very varied,
Speaker 2: and they tend to depend. The specific symptoms you see
Speaker 2: tend to depend on what part of your brain is
Speaker 2: the most infected. Okay, so let's talk about triple E specifically.
Speaker 2: If you have symptomatic infection with triple E, which again
Speaker 2: it is only four to five percent of people, so
Speaker 2: that's the good news. The symptoms begin with a prodrome,
Speaker 2: which essentially means nonspecific symptoms before the real bad symptoms.
Speaker 2: This is like that fever, maybe headache, maybe even some
Speaker 2: abdom o pain, just very non specific symptoms. And then
Speaker 2: about five days later is when the neurologic symptoms begin.
Speaker 2: And in the case of triple E, this can be
Speaker 2: anything from a mild confusion to maybe some focal weakness,
Speaker 2: like your arm feels weak or your leg feels weak. Okay,
Speaker 2: you might have seizures. Seizures are actually very common in
Speaker 2: triply Okay. You might have peristigias, so like weird tingling
Speaker 2: feelings or just like sort of sensory things that aren't normal.
Speaker 1: Is this just because your brain is inflamed?
Speaker 2: Yes, absolutely, okay, yep. But in the case of triple E,
Speaker 2: once any of these neurologic symptoms tend to start, even
Speaker 2: just sort of confusion and maybe like coming in and
Speaker 2: out of being very aware, you know, like not being
Speaker 2: able to focus, that kind of thing, very rapidly. In
Speaker 2: the case of Tripoli, people progress to coma.
Speaker 1: Okay, what's the timeline of this.
Speaker 2: Like hours to a couple of days.
Speaker 1: Oh wow, yeah.
Speaker 2: So once people develop these neurologic symptoms, after this like
Speaker 2: five day prodrome of kind of feeling cruddy, having a fever,
Speaker 2: having a headache, people deteriorate very, very rapidly, and then
Speaker 2: once they're in a coma. The mortality rate is between
Speaker 2: thirty and forty percent.
Speaker 1: Okay, So what proportion of people go into a coma
Speaker 1: like develop these severe neurological symptoms.
Speaker 2: So almost everyone. So if you become symptomatic, almost certainly
Speaker 2: you're going to go into a coma. Of those that survive,
Speaker 2: about a third of them will have significant neurologic impairment
Speaker 2: permanently as a result of this infection.
Speaker 1: Oh yeah, I have a question. Okay, these unlucky four percent.
Speaker 2: Why such a good question, Aaron, I have no idea,
Speaker 2: and I think part of the reason that so okay,
Speaker 2: some of the literature says children under age fifteen and
Speaker 2: adults over age fifty they are more likely to actually
Speaker 2: get the encephalitis form of triple E. That's the most
Speaker 2: that I've seen in terms of like who is it
Speaker 2: that ends up getting triple E versus just getting infected
Speaker 2: and not showing symptoms. I think we have to remember
Speaker 2: that this is a very very rare infection, so it's
Speaker 2: really hard to understand exactly who is the most at
Speaker 2: risk and why, Like, what is it about the characteristics
Speaker 2: of these people that make them more likely to have
Speaker 2: this neurologic manifestation versus never having symptoms?
Speaker 1: Right, exactly.
Speaker 2: Yeah, So of all the ARBA viral encephalitis viruses in
Speaker 2: the United States, this is by far the worst one, Like, yeah,
Speaker 2: mortality rate is so much higher. It's possibly even worse
Speaker 2: than Japanese encephalitis, although that's more common. That's not in
Speaker 2: the United States, it's in like China and Japan. But
Speaker 2: there's a vaccine for Japanese encephalitis.
Speaker 1: So why isn't there a vaccine then for triple A virus?
Speaker 2: Oh, Aaron, I was going to talk about all of
Speaker 2: this in more detail in the future, in the current events.
Speaker 1: Let's just wait for the future then, Yeah, do you.
Speaker 2: Want me to talk about it now or do you
Speaker 2: want me to talk about it in the future.
Speaker 1: Up to your girl.
Speaker 2: Let's talk about it later because we'll talk in more
Speaker 2: detail about the research that is being done. Okay, But
Speaker 2: one thing that I think is really interesting is, uh,
Speaker 2: although there are small case numbers, there have been a
Speaker 2: few good studies like grouping all of these cases and
Speaker 2: trying to understand like what is affected in the brain
Speaker 2: when you get infected with eastern neck wine encephalitis. And
Speaker 2: it tends to actually be the basal ganglia, which is
Speaker 2: part of the brain we talked about that's affected in Parkinson's.
Speaker 2: It's also infected in encephalitis lethargica if you remember, yeah, Okay,
Speaker 2: and it also infects like your mid brain and that's
Speaker 2: part of your brain stem. And so it's really interesting
Speaker 2: because you know, when I am looking at this, I
Speaker 2: want to think, like why do we see the symptoms
Speaker 2: that we see. So if you have a virus like
Speaker 2: rabies that infects your brain, it affects a part of
Speaker 2: your brain that changes the way that you behave right
Speaker 2: and your mood. And then we see that in the
Speaker 2: symptoms right where you get angry et cetera. If you
Speaker 2: get a herpes encephalitis, which is actually the most common
Speaker 2: cause of encephalitis viral encephalitis in the US. It infects
Speaker 2: the temporal lobe, which is where your language centers are.
Speaker 2: So your symptoms are like having trouble finding words, which
Speaker 2: is called aphasia. Okay, So for me, I'm like, okay,
Speaker 2: so we know that it infects this part of the brain,
Speaker 2: But how come we don't see these symptoms like maybe
Speaker 2: shakiness like in Parkinson's or these certain types of symptoms.
Speaker 3: Yeah.
Speaker 2: My guess is because it causes lesions in these areas
Speaker 2: like your brain stem, that are so important for generally
Speaker 2: being alive. Then you progress so rapidly and deteriorate so
Speaker 2: quickly that there's no time to have those specific isolated
Speaker 2: neurologic findings right right, So it makes me pressing. Yeah, yeah,
Speaker 2: it makes sense. We can talk quickly about treatment if
Speaker 2: you'd like.
Speaker 1: There isn't any I was gonna say, is it just
Speaker 1: supportive care?
Speaker 2: Yeah, it is. There are no anti virals, even in
Speaker 2: screening studies that have been shown to be effective against
Speaker 2: Tripoli virus. Okay, that's a bummer. I did find a
Speaker 2: few case reports where they've been using iv ig, which
Speaker 2: is intravenous pooled concentrated human immunoglobulin, which is used a
Speaker 2: lot in autoimmune disorders. It's used in the treatment of
Speaker 2: neurologic disorders. Whether or not it works, who knows, because
Speaker 2: I found two case reports that were like, we used
Speaker 2: this and they survived and did great. And then I
Speaker 2: found one that said we used this and they died,
Speaker 2: but that person also had lymphoma, So like, who knows.
Speaker 2: But we have such little data on any of this,
Speaker 2: and it's so difficult to study because we have so
Speaker 2: few cases that we really have no idea if iv
Speaker 2: ig would be actually an effective treatment or not at
Speaker 2: this point.
Speaker 1: But gotcha. But what about with other of the encephalitis viruses.
Speaker 2: Whether we have antivirals, Yeah, good question. I don't know. Yeah, yeah,
Speaker 2: I don't believe we have any for dengay, which can
Speaker 2: cause encephalitis. The more common ones like Saint Louis and
Speaker 2: cephalitis West Nile virus, I honestly don't know. I haven't
Speaker 2: done the research on those yet. Yeah.
Speaker 1: Interesting, But we.
Speaker 2: Will talk in more detail about the vaccine in a bit.
Speaker 2: But first, Aaron, First, what the heck where did this
Speaker 2: thing come from? And why does it invade our brains
Speaker 2: and kill us? So rapidly.
Speaker 1: Oh, I don't know if I can answer the why
Speaker 1: to that. I think we're just sort of a bystander.
Speaker 1: I mean, once again, this is we did not plan this.
Speaker 1: But coincidentally we're talking about two things for which humans
Speaker 1: seem to be a bystander, and for which birds are
Speaker 1: heavily involved, birds killing us. I will answer those, no,
Speaker 1: I will. I will attempt to answer those right after
Speaker 1: this break. Okay, ready, Yes, the year was nineteen thirty three.
Speaker 2: I love it when your sections start like this, Aaron.
Speaker 1: I'll do it each time. I also love the little
Speaker 1: cherry picked things that I have here. I'm like, why, okay,
Speaker 1: well whatever, anyway, lots of bad things were happening in
Speaker 1: nineteen thirty three in the US. The Depression was in
Speaker 1: its worst year. Hitler became German Chancellor. The dust Bowl
Speaker 1: was still raging in the Midwest. In the US, an
Speaker 1: earthquake in California caused massive damage in Long Beach. There
Speaker 1: were four fires in Oregon, and horses were dying by
Speaker 1: the dozens. In pockets of the Northeast, particularly along coastal
Speaker 1: or swampy areas of New Jersey, Delaware, and Maryland. Horses
Speaker 1: started acting strange. They started to walk clumsily, their heads
Speaker 1: were only able to look in one direction, and that
Speaker 1: led to them walking in circles and gradually losing mobility
Speaker 1: before dying. About ninety percent of the one thousand horses
Speaker 1: roughly that were affected by this illness died during this epizootic.
Speaker 2: Wow, yeah, that's a lot. That's bad.
Speaker 1: It's really bad. And because this was nineteen thirty three,
Speaker 1: germ theory and microbiology had advanced enough to the point
Speaker 1: where researchers were kind of like, you know, quickly mobilized
Speaker 1: on the case, taking brain samples from these horses that
Speaker 1: had died and seeing if they could isolate whatever pathogen
Speaker 1: was causing this damage. And they figured out pretty quickly
Speaker 1: that it was a transmissible filterable agent, which is essentially
Speaker 1: code for a virus most of the time, or a preon,
Speaker 1: not case, not a preon. And they discovered that it
Speaker 1: was this transmissible filterable agent because they were able to
Speaker 1: successfully inject it, whatever it was, into guinea pigs who
Speaker 1: also died as a result of the same sort.
Speaker 4: Of symptoms, acting like guinea pigs, and the researchers gave
Speaker 4: this virus a name Eastern equine encephalitis virus Eastern.
Speaker 1: Of course, like the etymology is not very exciting for
Speaker 1: this one Eastern because it was in the Eastern US
Speaker 1: equine to indicate that it was found in horses. As
Speaker 1: you've mentioned, encephalitis for all the reasons that you've mentioned,
Speaker 1: like the least exciting.
Speaker 2: Of all of the most are I think boring?
Speaker 1: Yeah, yep. So, at the time when this virus was
Speaker 1: isolated and named, and many researchers were treating it as
Speaker 1: a new infection that had never been seen before. But
Speaker 1: it didn't take long for people to realize that triple
Speaker 1: E virus had shown up in the northeastern US previously,
Speaker 1: and it only took a few more years to realize
Speaker 1: that this epizootic wasn't an isolated one off, that there
Speaker 1: would actually be another outbreak, even within the same decade.
Speaker 1: In nineteen thirty eight, which is five years after this
Speaker 1: massive outbreak in horses took place, another outbreak of TRIPLEY began,
Speaker 1: but this time it wasn't just in horses. Although horses
Speaker 1: were affected, humans especially children, were showing signs of infection
Speaker 1: and also dying at extremely high rate. So in late
Speaker 1: summer and early fall in Massachusetts, particularly the southeastern part
Speaker 1: of the state, there were thirty four cases in humans
Speaker 1: and twenty five deaths. Oh so, oh man, pretty high
Speaker 1: case fatality rate.
Speaker 2: And that's a lot of cases for just a couple
Speaker 2: of months in one state. Like that's a lot.
Speaker 1: Yeah, And like you said, the handful of people that
Speaker 1: did survive had these long term effects. And so because
Speaker 1: of the severity of the disease and the really like
Speaker 1: horrible side effects in the people who did survive, this
Speaker 1: kind of gained really widespread national attention.
Speaker 2: I imagine too because it was primarily affecting children that.
Speaker 1: That way, m hm, yeah, it was when it kind
Speaker 1: of really became apparent that like children were a very
Speaker 1: high risk group for this. Yeah. And so because of
Speaker 1: the severity of this illness, people were started to put
Speaker 1: in the hours to do research. They started to look
Speaker 1: in the past, asked for old epidemics, and they also
Speaker 1: started looking around them to see whether they could determine
Speaker 1: what the source of this current disease outbreak was. And
Speaker 1: people started noticing some unusual deaths among pigeons and ringed
Speaker 1: neck pheasants in the same places that people were getting sick.
Speaker 1: And then researchers were able to isolate the virus from
Speaker 1: some of these birds, and researchers were suspicious that mosquitoes
Speaker 1: were responsible for transmitting the virus or the transmitsible filterable agent,
Speaker 1: but it would take a little bit of time before
Speaker 1: they could pin down the exact species that seemed to
Speaker 1: be the culprit. And part of the reason is because
Speaker 1: a hurricane washed away all of these mosquito collection sites
Speaker 1: in nineteen thirty eight when they were fear at the
Speaker 1: height of their research.
Speaker 2: Just on things on top of things.
Speaker 1: Huh, things on top of things. Okay, So, as I mentioned,
Speaker 1: researchers also realized, hey, this is not and brand new
Speaker 1: disease to humans or to horses. So let's go back
Speaker 1: to eighteen thirty one. Yes, the year was eighteen thirty one,
Speaker 1: just kidding, but just like in nineteen thirty three and
Speaker 1: eighteen thirty one, lots of horses were dying in the Northeast,
Speaker 1: particularly Massachusetts. Not as many as in the nineteen thirty
Speaker 1: three epizootic, but about seventy five horses died in total,
Speaker 1: which you know, thinking about in eighteen thirty one and
Speaker 1: how people you know, used to use horses so much
Speaker 1: more than they did in nineteen thirty three. It would
Speaker 1: have been devastating to the horse's owners and also devastating emotionally.
Speaker 1: But yeah, in terms of like economics and losing a
Speaker 1: horse would have been hugely, hugely devastating, right, And like
Speaker 1: in the nineteen thirty three episolotic the one in eighteen
Speaker 1: thirty one, and horses also occurred in late and had
Speaker 1: a very high mortality rate as well, again close to
Speaker 1: ninety percent. Why is it higher in horses than in humans, Sarin, Uh.
Speaker 2: It's a good question. I've been thinking a lot about
Speaker 2: that ever since you mentioned that, and also you were
Speaker 2: mentioning the like symptoms that you see in horses where
Speaker 2: they have a lot more motor symptoms and like huh
Speaker 2: trouble walking and leaning. Yeah, it's a really good question.
Speaker 2: I don't know enough about veterinary medicine to know, like
Speaker 2: what the differences are in their immune response maybe or what.
Speaker 2: But I wonder if they like have a longer period
Speaker 2: before they deteriorate and that's why you see those motor symptoms,
Speaker 2: as it affects their basal ganglia and things like that.
Speaker 2: But yeah, I don't know, maybe they have this interfere
Speaker 2: on or something to begin with. Maybe they just have
Speaker 2: a different I don't know anything about horse immunology, so
Speaker 2: I have no idea, but it's a really interesting question.
Speaker 1: Interesting interesting. So it's also interesting to contrast the eighteen
Speaker 1: thirty one epizootic and the nineteen thirty three epizootic in
Speaker 1: terms of the response, like the scientific response, because if
Speaker 1: you think about eighteen thirty one, germ theory wasn't really
Speaker 1: a thing yet, and so people were like, we have
Speaker 1: no idea what's causing this, And so some of the
Speaker 1: guesses were like, well, the horses that fed on grass
Speaker 1: were the ones who got sick, so there was maybe
Speaker 1: something in the grass.
Speaker 2: What have another thought? Okay, because it sounded like from
Speaker 2: what you were saying, like twenty five out of thirty
Speaker 2: kids died in Massachusetts. That's a lot higher than today.
Speaker 2: So I wonder if it could too have to do
Speaker 2: with supportive care, like today the mortality rate is thirty percent,
Speaker 2: maybe in humans because we have some supportive care in
Speaker 2: the hospital, whereas you're not going to probably intubate a
Speaker 2: horse and try and keep them alive if they've got
Speaker 2: TRIPI I don't know, just a thought.
Speaker 1: Yeah, I mean that seems definitely possible. Possible, I don't know. Yeah, yeah,
Speaker 1: so like the nineteen thirty eight outbreak was around seventy
Speaker 1: four percent of people.
Speaker 2: Okay, yeah, yeah, so maybe it's just the difference in
Speaker 2: supportive care or something. Yeah, I don't know. Yeah, we're
Speaker 2: guessing here.
Speaker 1: Yeah, we should stand on not so shaky ground.
Speaker 2: Yeah.
Speaker 1: And so part of the reason that one of the
Speaker 1: guesses was, oh, well, the horses that fed on grass
Speaker 1: were the ones who got sick as opposed to like
Speaker 1: hay in the stables, okay, is because what they were
Speaker 1: seeing was that horses that were kept on the pasture
Speaker 1: seemed to be more likely to be sick than the
Speaker 1: ones who stayed in the stable. And so the miasma
Speaker 1: explanation almost kind of worked in this case. But you know,
Speaker 1: let's go to the treatments. So treatments were not helpful
Speaker 1: for horses. Mostly, as you heard in the first hand account,
Speaker 1: it was to drain the horse of a couple of
Speaker 1: gallons of blood.
Speaker 2: The one and only thing I remember from our Michigan day, Aaron,
Speaker 2: was that we had someone in the middle of our presentation,
Speaker 2: Google how money gallons of blood does a horse have?
Speaker 1: Yeah? I loved that. I think that they also googled,
Speaker 1: like several other things for us. Yeah, an auto fact checker.
Speaker 1: But do you remember how many gallons of blood a
Speaker 1: horse has?
Speaker 2: No? Now I'm gonna have to google it for myself.
Speaker 1: Okay, twelve point three. Did you get that from the
Speaker 1: horse dot com?
Speaker 2: I got it, Yeah, the horse dot com. It's gotta
Speaker 2: be a legit website. Right.
Speaker 1: Oh see, now I'm seeing different responses here. Okay, so
Speaker 1: it seems like, I mean, horses aren't coming all different
Speaker 1: shapes and sizes. So if you have a massive horse,
Speaker 1: it could be fifteen gallons fifteen gallons, let's say like
Speaker 1: ten to fifteen gallons.
Speaker 2: Sure, that sounds reasonable.
Speaker 1: So a fifth of your blood.
Speaker 2: That's a lot of blood.
Speaker 1: It's a lot of blood, and it's not going to
Speaker 1: do you any good. Okay. But after this relatively short
Speaker 1: lived epizootic ran its course, it kind of just faded
Speaker 1: from memory because it showed up again in eighteen forty
Speaker 1: seven in horses again and people were like, oh my gosh,
Speaker 1: there's this new disease. It's horrible. It's killing our horses.
Speaker 1: We don't know where it came from.
Speaker 2: So interesting that it fades from memory so quickly.
Speaker 1: I mean, but it's so I think it was so
Speaker 1: localized in eighteen thirty one.
Speaker 2: It didn't happen to the same individual people that second time.
Speaker 1: Maybe right, And I don't think I mean it maybe
Speaker 1: it did happen in the same region, but I also
Speaker 1: don't think that's like, you know, you can't google if
Speaker 1: you're in eighteen forty seven, you can't google horse disease. Yes,
Speaker 1: it's true, So there were probably many other things on
Speaker 1: their minds as well. Okay, so all of this had
Speaker 1: happened before, meaning Triple E outbreaks in humans and in horses,
Speaker 1: But what had taken so long for it to return?
Speaker 1: And since the nineteen thirty three outbreak in horses in
Speaker 1: the nineteen thirty eight outbreak in humans, Triple E virus
Speaker 1: has continued an upward climb in human cases, or at
Speaker 1: least in the frequency of outbreaks, which is, you know,
Speaker 1: a pretty big concern for the people who live in
Speaker 1: these high risk areas, right, Okay, So, but in order
Speaker 1: to answer why it seemingly disappeared for about one hundred years,
Speaker 1: because from eighteen forty seven to nineteen thirty three. There's
Speaker 1: not There doesn't seem to be any outbreaks, or at
Speaker 1: least notable outbreaks that I could find. And so to
Speaker 1: answer why it disappeared and then also why it's on
Speaker 1: the rise now, we have to look back at history.
Speaker 1: But we have to do that through the lens of ecology, which.
Speaker 2: Is our favorite, our favorite.
Speaker 1: All right, So we already talked a little bit about
Speaker 1: the ecology of triple E virus, but let's kind of
Speaker 1: go into it again in a little more detail. Yeah,
Speaker 1: all right, So, first of all, we know about the
Speaker 1: triple virus itself. We don't need to cover that again.
Speaker 1: The mosquito. The mosquito species that's most closely associated with
Speaker 1: triple virus again is Cula seta melanura. And we have
Speaker 1: not talked about this mosquito on any other episodes of
Speaker 1: the podcast before, even though we've done like a fair
Speaker 1: number of mosquito born diseases at this point. And the
Speaker 1: reason for that is kind of what I've already said.
Speaker 1: This is not a human biter, and so it's not
Speaker 1: really associated with many human diseases like Danngey, yellow fever, Zeka, etcetera.
Speaker 1: Some of the ones that we've covered and so we
Speaker 1: haven't really had much of a reason to talk about
Speaker 1: it before. Yeah, but this mosquito isn't really even a
Speaker 1: mammal biter at all. Like I said, it feeds on birds.
Speaker 1: And so this mosquito species can be found over a
Speaker 1: pretty wide range geographically, so from like the southeastern provinces
Speaker 1: of Canada, throughout the eastern US and some southern states
Speaker 1: along the Gulf. They require fresh water, wooded swamps or
Speaker 1: Sphagnum bogs with little water filled hollows in fallen trees
Speaker 1: in order to lay eggs for the larvae to develop.
Speaker 1: Interesting trees and water right typically standing water or at
Speaker 1: least water at like the soil level. And after the
Speaker 1: larva develop these little nooks and crannies, adult mosquitoes then
Speaker 1: happily emerge to feed on whatever birds are around, and
Speaker 1: those birds tend to be water dwelling birds, although not
Speaker 1: one hundred percent of the time. There was a study
Speaker 1: in Massachusetts that examined the blood meals of mosquitoes. Of
Speaker 1: these mosquitoes both inside and outside of a swamp, and
Speaker 1: in both times, nearly ninety nine percent of blood meals
Speaker 1: were from a bird host. Okay, so it's like a
Speaker 1: very specific feeding patterns, very very specific.
Speaker 2: Yeah.
Speaker 1: So then the virus basically continues in this natural cycle,
Speaker 1: so in birds in mosquitoes, and birds and mosquitoes, So
Speaker 1: from year to year, it's not really entirely clear how
Speaker 1: it overwinters. It either overwinters in birds, although that seems
Speaker 1: less likely because birds do recover from infection or they die.
Speaker 1: There are like some birds, some birds don't seem to
Speaker 1: be affected at all, and some birds die within a
Speaker 1: few days of being infected, at least experimentally, So.
Speaker 2: It's a lot like West Nile.
Speaker 1: I feel like, right, there's very varying susceptibility among abi
Speaker 1: and host birds. Okay, yeah, and some birds contribute more
Speaker 1: than to the viral prevalence. Yeah, but yeah, humans, horses, pigs,
Speaker 1: so I don't think I don't think you mentioned pigs,
Speaker 1: but pigs have also been shown to be infected with
Speaker 1: triple A virus. These are all dead and hosts, as
Speaker 1: we talked about, so they don't contribute to the circulation
Speaker 1: of the virus in the environment. So like, basically what
Speaker 1: that means is that if a mosquito, let's say that
Speaker 1: a horse got infected with the virus, and then a
Speaker 1: mosquito that was uninfected bit that horse, it probably wouldn't
Speaker 1: get enough virus to be able to replicate in that mosquito,
Speaker 1: And then it would also take the appropriate mosquito species
Speaker 1: to bite that horse, which tends to be unlikely given
Speaker 1: the low biting frequency outside of birds. Right, Okay, so
Speaker 1: how on earth do humans or horses or pigs ever
Speaker 1: get infected? And it turns out the answer is not
Speaker 1: that straightforward, as I mentioned earlier, because the disagreement on
Speaker 1: whether these bridge vector species actually contribute to infection. Okay,
Speaker 1: but first let's talk about sort of this year to
Speaker 1: year variation in outbreaks, because some years we see a
Speaker 1: big increase in case some years we see none at all,
Speaker 1: And because this is so rare, it's kind of we
Speaker 1: don't have good enough data to kind of make clear
Speaker 1: cut answers on this. But what it seems to be
Speaker 1: is that it comes down to, you know, mosquito ecology.
Speaker 1: So mosquitoes, because they live outside, are super dependent on
Speaker 1: environmental conditions and the weather. So let's say that there
Speaker 1: was like a super rainy season last year and a
Speaker 1: hot and humid and early summer this year, and that
Speaker 1: could mean, you know, higher warm water for these mosquitoes
Speaker 1: to lay their eggs in the little nooks and crannies
Speaker 1: of the trees and then develop more quickly. And then
Speaker 1: the viral replication itself also depends on external temperature, and
Speaker 1: so that could mean, you know, so let's say last
Speaker 1: year twenty nineteen was rainy and hot in some of
Speaker 1: these more you know, swampy or boggy areas, then maybe
Speaker 1: this year we would have a higher cases of triple
Speaker 1: A virus. And then geographically, the variation has a lot
Speaker 1: to do with these larger weather or climate patterns and
Speaker 1: also just how much mosquito habitat there is for this
Speaker 1: particular mosquito. All right, but let's look at some of
Speaker 1: these larger overall trends in the frequency of outbreaks, so
Speaker 1: like more on this larger time time scale. Okay, okay,
Speaker 1: So remember people get infected by the bite of mosquito,
Speaker 1: whether it's Keela seta melenura or this bridge vector species.
Speaker 1: But in either case, those mosquitoes have to be infected
Speaker 1: by a bird, and these birds tend to live in
Speaker 1: these boggy, swampy areas. And so you think, as a
Speaker 1: human you'd have to be pretty close to those in
Speaker 1: order to get infected, right, all right, So let's talk
Speaker 1: about the history of swamps and bogs in the northeast,
Speaker 1: particularly Massachusetts. And I'm using Massachusetts as a case study
Speaker 1: because that's where triple E cases have been the highest
Speaker 1: and the outbreaks that seemed to impact the most. All right,
Speaker 1: So during the two hundred year pero from around sixteen
Speaker 1: fifty to eighteen fifty, European settlers essentially stripped the land
Speaker 1: of forest and wetlands. They used pines for masts on ships.
Speaker 1: These cedar swamps were destroyed to make shingles, posts, barrels.
Speaker 1: Other forests were used for lumber, firewood, and charcoal, or
Speaker 1: they were cleared entirely to make room for agricultural fields.
Speaker 1: And by the mid eighteen hundreds, deforestation was at its
Speaker 1: peak in Massachusetts and the countryside was like naked It
Speaker 1: was nothing left. Henry David Threaux, who wrote Walden, said
Speaker 1: about conquered Massachusetts around this time, of the primitive wood woodland,
Speaker 1: which was woodland when the town was settled, I know none,
Speaker 1: and so as you can guess, this massive deforestation caused
Speaker 1: enormous cascading ecological effects and especially relevant to triple E
Speaker 1: bird numbers and species richness declined, and Kulasata melanura also
Speaker 1: lost the swampy habitat that it needed to survive, and
Speaker 1: starting in the second half of the eighteen hundreds, reforestation
Speaker 1: picked back up because people were like, uh, we can't
Speaker 1: continue to over exploit the land because there's nothing left,
Speaker 1: like we have really you know, put ourselves in a
Speaker 1: very bad situation by doing this already. And also people
Speaker 1: were started to abandon these unproductive farms to move to cities.
Speaker 1: So it sort of both the conscious decision of we
Speaker 1: need to reforest and also just sort of it happened
Speaker 1: naturally as people stopped using the wood for farms and whatnot.
Speaker 1: And so this meant that forest cover increased greatly throughout
Speaker 1: the early twentieth century, with wetland restoration lagging a bit
Speaker 1: behind deciduous forests. But ultimately what this meant was more
Speaker 1: habitat for birds and mosquitoes and thus triple A virus,
Speaker 1: and several researchers point towards this large scale landscape change
Speaker 1: as being a cause of the reappearance of the virus
Speaker 1: in the nineteen thirties and why it has stuck around
Speaker 1: ever since then. But before you take up your chainsaws
Speaker 1: to reclearcut the forest of New England and drain the
Speaker 1: swamps and bogs, consider please that it's not the mere
Speaker 1: existence of these habitats that leads to these triple the outbreaks.
Speaker 1: But really it's sort of the way that we develop
Speaker 1: suburban communities, especially the residential ones with these areas. And
Speaker 1: so these a lot of these suburban neighborhoods tend to
Speaker 1: creep into and on the borders of these wetlands, and
Speaker 1: so that's where you have this Like once you do that,
Speaker 1: once you get closer to that, that means that you're
Speaker 1: just more likely to come into contact with these infected
Speaker 1: mosquito species. And also, wetland conservation is hugely important for
Speaker 1: flood pre protection and healthy water supply, and they provide
Speaker 1: these amazing habitats for diverse and unique communities of plants
Speaker 1: and animals. And so by the time this episode comes out,
Speaker 1: it will have been roughly a week after Earth Day.
Speaker 1: Oh cool, Earth is April twenty second, tomorrow, a couple
Speaker 1: days from now, a couple days from now and Earth Day,
Speaker 1: it'll be the fiftieth anniversary of Earth Day.
Speaker 2: How exciting.
Speaker 1: Wow, Happy late Earth Day everyone, So let's just keep
Speaker 1: that spirit going.
Speaker 2: Yes, we are certainly not anti wetland. No, no, no
Speaker 2: pro forest pro wetland over here.
Speaker 1: I think it's I think it's just a really interesting
Speaker 1: example of how large scale landscape change can influence disease transmission,
Speaker 1: particularly zoonotic diseases.
Speaker 2: Yeah, definitely.
Speaker 1: So from these outbreaks on nineteen thirties to the last
Speaker 1: decade or so, we've seen sporadic human cases here and there,
Speaker 1: largely restricted to the northeastern US, but we have seen
Speaker 1: more horse outbreaks. But since that time we've seen both
Speaker 1: an increase in the frequency of cases and in their
Speaker 1: geographic distribution. And because this is a vector born disease,
Speaker 1: teasing apart, the cause of this re emergency is tricky
Speaker 1: because it depends on so many factors. So, like I
Speaker 1: talked about increased rainfall one year, re establishment of wetlands,
Speaker 1: or development of human dwellings in close proximity to these
Speaker 1: wetland areas, or any sort of habitat where a quela
Speaker 1: seta melinura likes to lay its eggs, So many things
Speaker 1: can play a role in this, and although this is
Speaker 1: a rare disease, it can be extremely deadly and that
Speaker 1: can lead to a fear response, sometimes out of proportion
Speaker 1: to the actual risk. A lot of controversy surrounds the
Speaker 1: control measures that are often used to try to prevent infections,
Speaker 1: and there are these questions like should there be widespread
Speaker 1: aerial spraying with insecticides or is that just asking for
Speaker 1: another ecological disaster? Is public education effective or is it
Speaker 1: even enough? Are we in for a bad year of
Speaker 1: triple A virus? Aaron, what do you think? Where do
Speaker 1: we stand with tripoli today?
Speaker 2: Oh, let's talk about it right after this break. So
Speaker 2: TRIPLEI is unsurprisingly a nationally notifiable disease, right because it's
Speaker 2: pretty devastating. So let's talk about how many cases we
Speaker 2: tend to see in the US per year. From two
Speaker 2: thousand and nine to twenty eighteen, so about the last
Speaker 2: ten y, on average, there were seven cases per year,
Speaker 2: and that ranged from three in two thousand and nine
Speaker 2: to fifteen in twenty twelve. Okay, okay, So like pretty
Speaker 2: rare and like not a huge amount of variation year
Speaker 2: to year from two thousand and nine to twenty eighteen. Now,
Speaker 2: in total. I will say that entire period there was
Speaker 2: only seventy two cases in total.
Speaker 1: Could you extrapolate upwards and say, if that's four percent,
Speaker 1: then there were X number of people who were likely
Speaker 1: exposed to the virus?
Speaker 2: Sure, let's do that.
Speaker 1: Is that Is that a reasonable extrapolation?
Speaker 2: That's a good question theoretically? Why not? If we think
Speaker 2: that ninety six percent of people are asymptomatic, then yeah,
Speaker 2: if there were seventy two known cases that were reported,
Speaker 2: then how many cases is that total over that time period?
Speaker 2: I actually have no idea how you do that math?
Speaker 1: Seventy six over ax equals four over one hundred and
Speaker 1: then find the.
Speaker 3: X seventy two terms one hundred divided by four eighteen
Speaker 3: hundred cases over about ten years.
Speaker 1: Still pretty low prevalence.
Speaker 2: Pretty low? Yeah, absolutely, Now that was two thousand and
Speaker 2: nine to twenty eighteen. What about twenty nineteen. There's a
Speaker 2: reason that we did this as a live episode in Michigan,
Speaker 2: and that is that twenty nineteen was far and away
Speaker 2: the worst year of Triple E in a very long time.
Speaker 2: As of December seventeenth, twenty nineteen, there were a total
Speaker 2: of thirty eight confirmed cases of triple e in the
Speaker 2: United States, including fifteen deaths. Wow, yep, that is more
Speaker 2: than twice the maximum of the last ten years.
Speaker 1: That's very okay, why great question.
Speaker 2: I don't know. I mean, it likely was a lot
Speaker 2: of what you said, right, like a bad year for
Speaker 2: rainfall the year before or something like that. But what's
Speaker 2: interesting is that these cases happened in number of different areas.
Speaker 2: It wasn't just all in one spot. The two states'
Speaker 2: most hardest hit last year were Massachusetts and Michigan. So
Speaker 2: in Massachusetts there were twelve confirmed human cases and ten
Speaker 2: confirmed deaths. Now, there was also a large increase in
Speaker 2: the number of animal cases last year as well. There
Speaker 2: were in Michigan forty eight cases of tripoli and animals
Speaker 2: last year. So yeah, it's a good question. I don't
Speaker 2: think that we have a full handle on exactly how
Speaker 2: to predict which years are going to be the worst.
Speaker 2: Like Fauci said in that article, right, he wasn't the
Speaker 2: first author, but it was Moran's at all. Come on,
Speaker 2: Born at all said in that article, we need to
Speaker 2: do better research to be able to answer those types
Speaker 2: of questions, right, We need to have a better handle
Speaker 2: on what are the factors that contribute to whether or
Speaker 2: not we're going to have a bad year. Right now,
Speaker 2: the only good news about this is that, so you
Speaker 2: kind of mentioned where this tends to be a disease
Speaker 2: that's common, right, It's on the East Coast, a lot
Speaker 2: of it in the Northeast, but also along the East
Speaker 2: Coast and the Gulf Coast as well as the Great
Speaker 2: Lakes region.
Speaker 1: Right.
Speaker 2: So the other states that had reported cases last year
Speaker 2: include Alabama, Connecticut, Georgia, Indiana, New Jersey, North Carolina, Rhode Island,
Speaker 2: and Tennessee.
Speaker 1: What's the good news in.
Speaker 2: This most most of those areas have like a mosquito season, gotcha, Okay,
Speaker 2: So at least it's over for now effectively, right, although
Speaker 2: now it's springtime, so welcome back.
Speaker 1: Yep.
Speaker 2: Yeah, So that's that's the only good news is like,
Speaker 2: at least it's over for now, we can hope that
Speaker 2: this year is going to be better.
Speaker 1: And that's the other thing too, is that it seems
Speaker 1: to be based on when these cases happen, It does
Speaker 1: seem to be like in a very narrow time window
Speaker 1: throughout the year, particularly in the northern in the more
Speaker 1: northern places where mosquito season is so concentrated.
Speaker 2: Yep, which makes sense.
Speaker 1: You can sort of heighten your vigilance during that time,
Speaker 1: I guess.
Speaker 2: So that's where we stand in terms of the number
Speaker 2: of cases of tripoli. You asked about a vaccine.
Speaker 1: Because there's one for horses.
Speaker 2: There is one for horses. It is a whole killed
Speaker 2: virus vaccine. It's not great even for horses, so from
Speaker 2: what I have gathered. For some reason, and this is
Speaker 2: very interesting considering that we believe that if you are
Speaker 2: infected with tripolei virus, you do mount a good immune
Speaker 2: response and are then prevented from getting infected again. But
Speaker 2: for some reason, the vaccine that we've tried to develop
Speaker 2: for humans, and that we even have for horses and
Speaker 2: other animals, it doesn't generate a very good immune response
Speaker 2: and the immunity that it provides is not very long lasting. Huh,
Speaker 2: even in horses. Yeah, so I'm not sure. Like the
Speaker 2: schedule for if you have a horse, how often you
Speaker 2: have to give that horse boosters? It might be something
Speaker 2: like I have to give my dog the rabies shot
Speaker 2: like every year or something like that, So it might
Speaker 2: be the same for horses.
Speaker 1: Yeah, they do do boosters.
Speaker 2: Yeah, but so that's it's really interesting, right, Like, why
Speaker 2: is it that we can't develop a vaccine that is
Speaker 2: more immunogenic that provides us with a longer lasting immune response.
Speaker 1: Is part of it in the funding and that this
Speaker 1: is a rare disease.
Speaker 2: You put the nail on the head.
Speaker 1: There.
Speaker 2: Is that.
Speaker 1: How that goes, How that goes?
Speaker 2: Yeah, there is no market for a triple E vaccine, right.
Speaker 2: We still don't even have a West Nile vaccine, and
Speaker 2: that causes a lot more infection in humans every year
Speaker 2: than this does. So if you want proof that there's
Speaker 2: really not a market for it, I have found papers
Speaker 2: of people doing research on this. So in two thousand
Speaker 2: and seven, there was a really interesting paper that made
Speaker 2: a hybrid attenuated vaccine. So instead of doing a killed virus,
Speaker 2: they made a hybrid virus out of triple E virus
Speaker 2: and some other virus, don't remember which one, and they
Speaker 2: tested it in mice and they found that it was
Speaker 2: highly immunogenic. That was in two thousand and seven. Nothing else, okay,
Speaker 2: So in theory, in theory, it's possible. I did check
Speaker 2: clinicaltrial dot gov, which again is where you can find
Speaker 2: all the clinical trials that are happening, and there are
Speaker 2: studies for triple E. Two of them were USA mrid
Speaker 2: Us zamord I don't know how you say it. The
Speaker 2: US Army Medical Research Institute of Infectious Diseases. They had
Speaker 2: two vaccine trials that are now concluded. One of them
Speaker 2: had results posted, which are actually very difficult to sort
Speaker 2: through on clinical trials. By the way, overall, it's hard
Speaker 2: to get an estimate on exactly how long lasting the
Speaker 2: immunity was from this virus that they tested, but it
Speaker 2: was somewhere between like twenty eight to seventy percent of
Speaker 2: people depending on the timeframe that you looked at it.
Speaker 2: So like seventy percent of people that they tested had
Speaker 2: an immune response like right after their second booster. But
Speaker 2: then of the people they were able to test out
Speaker 2: a one year follow up, only twenty eight percent of
Speaker 2: them still had high tiders of antibodies. So they mounted
Speaker 2: an immune response, but it wasn't very long lasting, right,
Speaker 2: just like the horse that Yeah, And so that makes
Speaker 2: it even harder to try and get funding for a
Speaker 2: vaccine like this. If you think like this is a
Speaker 2: very very very rare infection and you'd have to get
Speaker 2: a vaccine for it what like every year, Like that's
Speaker 2: very difficult to try and sort of convince funders or
Speaker 2: people to get a vaccine like that, right.
Speaker 1: Right, So then a lot more so it comes down
Speaker 1: a lot more to the prevention and surveillance aspect.
Speaker 2: Absolutely, yeah, yeah, definitely. So yeah, that's where we stand
Speaker 2: with tripoly virus.
Speaker 1: Well, do you know what the predictions are for this year?
Speaker 1: It was identy in places? Was it hot? Let's see,
Speaker 1: they're in early summer. It's snowed in Chicago like two
Speaker 1: days ago, so.
Speaker 2: You know, I've been thinking about that. And it snows
Speaker 2: every April in Illinois. Every April. I go, I can't
Speaker 2: believe that it's snowing, but it does it every April.
Speaker 1: I remember my prom in Kentucky. It snowed. That's wonderable.
Speaker 2: Yeah.
Speaker 1: I got out of the prom and there was snow
Speaker 1: in my car. I was like, I'm in a hot,
Speaker 1: pink sleeveless dress.
Speaker 2: Oh, I can't believe I've never seen pictures of your
Speaker 2: prom dress.
Speaker 1: Now I'm not what you'd expect.
Speaker 2: Oh, I really want to see it now, hot pink sleeveless,
Speaker 2: I love it. Let's see. According to this news article,
Speaker 2: I just found health experts believe TRIPLEI will rise again
Speaker 2: next year. Uh. I guess normally these cycles tend to
Speaker 2: last for two to three years. So you have two
Speaker 2: to three years in a row of bad year and
Speaker 2: it was very wet and rainy in twenty nineteen, so great, great.
Speaker 2: You know, like how with with lime disease and ticks,
Speaker 2: there's like that distinct like the mast and the mice
Speaker 2: and then the deer and then the ticks.
Speaker 1: Right now, there's sequence of events that lead to these
Speaker 1: high outbreaks or these like outbreak years. They're just not
Speaker 1: well known. And I think it's because the outbreaks themselves
Speaker 1: are so small, so small, and so it's sort of
Speaker 1: now we're playing like you know, retrospective detective, trying to
Speaker 1: pick apart the pieces. And that's right challenging because ecology
Speaker 1: is ecology. Things don't happen according to some I don't
Speaker 1: know plan or so hard. Yeah. Yeah, there's so much
Speaker 1: like random noise in the system, and so trying to
Speaker 1: say is this noise or is this a component is
Speaker 1: really challenging, particularly when when you have such a low
Speaker 1: incidence of disease.
Speaker 3: Yeah.
Speaker 2: Well, and if you have so many different hosts, you
Speaker 2: have so many different bird species that can be affected,
Speaker 2: and they're affected so differentially that it also you know,
Speaker 2: that plays a big part of it too. That's really
Speaker 2: difficult to get a handle on. Is easy college here.
Speaker 1: In Yeah, it's, I mean part of it's. It's why
Speaker 1: I love it and also why it can be so frustrating.
Speaker 2: Yeah, okay, well that was fun. Hopefully it wasn't too depressing.
Speaker 2: Oh I don't know.
Speaker 1: See, I don't think I can judge it anymore.
Speaker 2: Okay, sources, sources, All right, So.
Speaker 1: I want to shout out a few. I have a
Speaker 1: bunch of papers that I liked, but a few that
Speaker 1: I leaned more heavily on. One is titled or one
Speaker 1: is my Armstrong at All from twenty thirteen called Eastern
Speaker 1: equineencephalitis virus Old Enemy, New Threat. And then there was
Speaker 1: that a rego at All paper titled Evolutionary patterns of
Speaker 1: Eastern Equine andcephalitis virus and North versus South America. There's
Speaker 1: more to that title, but it's very long, so I'm
Speaker 1: not going to keep going. Oh and then another one
Speaker 1: where I got a lot of the ecological sort of
Speaker 1: timeline of re emergence in Massachusetts is from a paper
Speaker 1: by Comar and Spielman from nineteen ninety four titled Emergence
Speaker 1: of Eastern Encephalitis in Massachusetts Excellent.
Speaker 2: There are a bunch of different papers that I used
Speaker 2: for different parts. We'll post all of these online if
Speaker 2: you'd like. Kind of the most cited source of the
Speaker 2: clinical aspects of Eastern equin encephalitis, there's a paper from
Speaker 2: nineteen ninety seven called Clinical and neuro Radiographic Manifestations of
Speaker 2: Eastern equin Encephalitis. But again, we'll post all of our
Speaker 2: sources from this episode in all of our episodes online
Speaker 2: under the episode's tab. You can find all of our
Speaker 2: sources listed there, as well as links to bookshop dot
Speaker 2: org if you like to purchase the books yep.
Speaker 1: And also, we neglected to say it earlier, but you
Speaker 1: can find the recipe for our quarantiny and our non
Speaker 1: alcoholic La Siberta on our website this podcast will Kill
Speaker 1: You dot com under the quarantinis tab, and we also
Speaker 1: posts on social media, so if you'd like to see them,
Speaker 1: follow us.
Speaker 2: Yep.
Speaker 1: Thank you to Bloodmobile for providing the music for this
Speaker 1: episode in all of our episodes.
Speaker 2: And thank you to you for listening. Hope you enjoyed
Speaker 2: this episode. Yeah, and I hope you always anyone who
Speaker 2: was at the show in Michigan, First of all, thanks
Speaker 2: so much for coming. We had so much fun there.
Speaker 2: And second of all, hope you still learned something new
Speaker 2: from this episode.
Speaker 1: Yeah. Thanks again to everyone at Michigan who, yeah, helped
Speaker 1: us make that trip one of just the most amazing
Speaker 1: days ever. Awesome. All right, Well, until next time, wash
Speaker 1: your hands.
Speaker 3: You filthy animals.
Speaker 1: Ou