Speaker 1: Towards the end of September eighteen twenty seven, a disease
Speaker 1: of a very singular character suddenly made its appearance in
Speaker 1: the island of Saint Thomas and attacked almost every individual
Speaker 1: in the town, which contains a population of about twelve
Speaker 1: thousand souls. The disease appeared so suddenly and spread with
Speaker 1: such rapidity, and the suffering attending it was so great
Speaker 1: that at first it caused universal alarm and was considered
Speaker 1: a sort of plague that would probably ravage the whole country.
Speaker 1: It was soon, however, discovered that although a very painful
Speaker 1: it was by no means a dangerous disease, and that
Speaker 1: if the attack was rapid, the recovery was no less speedy. This,
Speaker 1: at least was the general belief until longer experience showed
Speaker 1: the troublesome nature of the secondary pains that constitute the
Speaker 1: third stage of the disorder. The most usual mode of
Speaker 1: attack was the following. A person in perfect health would
Speaker 1: suddenly feel a stiffness amounting almost to a pain in
Speaker 1: one of his fingers, and frequently his little finger. The
Speaker 1: stiffness increased and was accompanied by an intense degree of pain,
Speaker 1: which spread rapidly over the whole hand and up the
Speaker 1: arm to the shoulder. The fingers of both hands in
Speaker 1: a few hours became swelled, stiff, and painful, preventing all
Speaker 1: attempts at bending the joints. This was followed in a
Speaker 1: short time by restlessness, depression of spirits, and a degree
Speaker 1: of nausea, ending in some cases in vomiting. Then came
Speaker 1: on shivering, succeeded by fever, great heat of skin, intense headache,
Speaker 1: most acute pain in the back, knees, ankles, and in
Speaker 1: short in every joint. But perhaps the most distressing symptom
Speaker 1: of this stage was the intense pain in the eyeballs.
Speaker 1: In every case where the first stage was in any
Speaker 1: degree well marked, patients declared that they had never experienced,
Speaker 1: nor could have conceived, pains equal to what they felt
Speaker 1: in this fever. Not one inch of the body from
Speaker 1: head to foot was exempt from suffering. An efflorescence was
Speaker 1: perceived at this time to begin at the palms of
Speaker 1: the hands and to spread over the whole body. After
Speaker 1: the aberuptive stage, the patient began to recover his spirits
Speaker 1: and his strength, but in many cases a complete want
Speaker 1: of taste remained for some days. Many people did not
Speaker 1: get rid of the pains in the joints for many weeks.
Speaker 1: In general, however, the disease gave a degree of respite
Speaker 1: for three, four and even in some cases six weeks,
Speaker 1: and then attacked the joints with more pain and paralysis
Speaker 1: than at first. I conclude with the hope that I
Speaker 1: have done my duty in endeavoring to record a disease
Speaker 1: attended with so many curious symptoms, as justly to challenge
Speaker 1: the attention of every medical man, and particularly of those
Speaker 1: who are destined to practice in tropical countries. I love
Speaker 1: these old timey descriptions, Aaron so much.
Speaker 2: I love that. So that was excerpted from this paper
Speaker 2: published in eighteen twenty eight by George Steadman. Yeah, titled
Speaker 2: some account of an anomalous disease which raged in the
Speaker 2: Islands of Saint Thomas and Santa Cruz in the West
Speaker 2: Indies during the months of September, October, November, December and
Speaker 2: January eighteen twenty seven to eighteen twenty eight. I guess
Speaker 2: they didn't have character limits and titles back then.
Speaker 1: The most descriptive and specific title.
Speaker 2: Yeah so that. Like that whole paper, which is available
Speaker 2: online is an interesting read. There's so much more detailed there,
Speaker 2: but I just pulled little excerpts that I thought were
Speaker 2: most descriptive of the topic of today's episode, which is
Speaker 2: chicken chicken virus. Hi, I'm erin Welsh.
Speaker 1: And I'm erin Almond Updike.
Speaker 2: And this is this podcast will kill You.
Speaker 1: Welcome to Is this our first mosquito born virus of
Speaker 1: our whole season?
Speaker 2: I think, so? Wow, I can't keep track anymore.
Speaker 1: Eric, I know same. I feel like we've done I mean,
Speaker 1: we've done like some lice and things.
Speaker 2: Yeah, we've done some vectors. Yeah, but yeah, mosquito born virus,
Speaker 2: I think.
Speaker 1: So. I'm excited. It's gonna be a good one.
Speaker 2: It is. I didn't really know anything about chicken gunya
Speaker 2: besides the name before getting into this, and yeah, I'm
Speaker 2: very curious to hear how the biology works. I know.
Speaker 1: I remember in twenty thirteen and twenty fourteen when the
Speaker 1: big outbreaks were happening in the Americas and being like,
Speaker 1: what's gonna happen with chicken gun yet? And then that
Speaker 1: was it. Yeah, And I never really learned much more
Speaker 1: about it, So it was it was fun to get
Speaker 1: to research. Yeah, but first, it's quarantiny time.
Speaker 2: It's quarantin any time. What are we drinking this week?
Speaker 1: We're drinking head, shoulders, knees and toes.
Speaker 2: Yeah, so we are drinking head, shoulders, knees and toes
Speaker 2: because one of the hallmark symptoms of chicken gunya virus,
Speaker 2: as you heard in our first hand account, is joint
Speaker 2: pain and headache.
Speaker 1: Yep, pretty pretty severe, as we'll discuss, very severe.
Speaker 2: Yeah. Yeah, So what is in head shoulders, knees and toes.
Speaker 1: Oh, it's a perfect little fall concoction. You've got some
Speaker 1: apple cider, some orange and some mez call for smokiness.
Speaker 2: Yeah. And also so as a callback to deng Gay,
Speaker 2: our dan Gay episode and our Dangae quarantini which had
Speaker 2: mes call in it. And because you're gonna hear a
Speaker 2: lot about dang Gay, I know there'll be.
Speaker 1: A lot of compare condrass, Dangay, chick Gunya, et cetera.
Speaker 1: So it makes sense, so we called back to it.
Speaker 1: We'll post the full recipe for our quarantine as well
Speaker 1: as our non alcoholic plausive to read it on our website.
Speaker 1: This podcast will tell you dot com and all of
Speaker 1: our social media channels.
Speaker 2: Before we dive into the episode. Of course, like the routine,
Speaker 2: check out our website, et cetera, et cetera. There's a
Speaker 2: lot of stuff there. But also, this is our second
Speaker 2: to last episode of season five. What Yeah, there's just
Speaker 2: one more coming out after this. But don't worry, we
Speaker 2: will be back. We're just gonna take a break and
Speaker 2: not read about disease stuff for a minute.
Speaker 1: I mean, we'll probably still read about disease stuff, but
Speaker 1: like just quietly to ourselves.
Speaker 2: Actually that's true, and then we'll just text each other exactly. Well,
Speaker 2: in any case, we will be back, and so make
Speaker 2: sure you follow us on all of our social media
Speaker 2: accounts so that you know when we are on our
Speaker 2: way back, and if you have suggestions that you really
Speaker 2: want to hear for next season, send them our way.
Speaker 1: Well with that, Aaron, shall we get into chicken gonavirus.
Speaker 1: Let's do it right after this break. Chicken gonavirus is
Speaker 1: an arbovirus, which means a virus transmitted by arthropod vectors.
Speaker 1: And in this case, like we said, mosquitoes, I'm probably
Speaker 1: gonna end up talking about the two main mosquito vectors
Speaker 1: more than anyone bargain for it's gonna be fun.
Speaker 2: I'm so glad because I did a little bit of
Speaker 2: diving into the ecology and I was like, I don't
Speaker 2: know where this goes in the history section. Hopefully erin
Speaker 2: we'll talk about it.
Speaker 1: Well. I found myself thinking so much of Ali and
Speaker 1: Allison in our old lab and being like, I wish
Speaker 1: I could call and be like, can you tell me
Speaker 1: about their ecology? Anyways, So let's get into it, shall we.
Speaker 1: Chicken gunia virus is in the genus alpha virus in
Speaker 1: the family Toga Virida, and these viruses there RNA viruses,
Speaker 1: the majority of which are arboviruses. They are transmitted by
Speaker 1: mosquitoes and other vectors. A few that people may have
Speaker 1: heard of include Ross River virus and Western and Eastern
Speaker 1: equine encephalitis viruses. One thing I thought was interesting about
Speaker 1: alpha viruses in general is that at least one of
Speaker 1: the papers that I was reading was talking about how
Speaker 1: for a lot of alpha viruses, humans and our domestic
Speaker 1: animals are often considered dead end hosts, so we aren't
Speaker 1: necessarily like the evolutionary hosts for these pathogens, which is
Speaker 1: I think very interesting, especially because I'm going to end
Speaker 1: up comparing and contrasting chicken guna virus in this episode,
Speaker 1: because it's compared a lot in the literature to a
Speaker 1: few other arboviruses like dengay zeca virus, yellow fever virus.
Speaker 1: All of those viruses are not in the alpha virus family.
Speaker 1: Those are all flaviaviruses, so a completely different family of viruses,
Speaker 1: some of which are very human specific like yellow fever
Speaker 1: or can cause disease in animals and humans kind of equally.
Speaker 2: That's interesting that humans are considered the dead end host
Speaker 2: for alpha viruses. Is that because of like viroemia and
Speaker 2: mosquitoes not being able to get enough virus or is
Speaker 2: it because mosquitoes aren't biting as much? Yeah?
Speaker 1: I think both from what I could tell. Okay, yeah, yeah,
Speaker 1: But as we'll see, that's not the case chicken gunyam.
Speaker 1: So the two major vector species of chicken gunya virus
Speaker 1: are mosquitoes that might be familiar to longtime listeners. They
Speaker 1: are mosquitoes in the genus eighties, particularly eighties albapictus and
Speaker 1: eighties agypdi. These are the same mosquitoes that are responsible
Speaker 1: for the transmission of dannge fever of yellow fever and
Speaker 1: of Zeca virus, among many others. There are a lot
Speaker 1: of other species of eighties mosquitoes that can also transmit
Speaker 1: chicken gunya as well as perhaps some species of Culex
Speaker 1: that have been found to be infected, but predominantly, especially
Speaker 1: for humans, it's Albapictus and Agypti, and that's probably how
Speaker 1: I'll refer to them throughout this episode. And like many
Speaker 1: of our mosquito born viral and other pathogens, this life
Speaker 1: cycle can be a little bit complicated, but it goes
Speaker 1: a little something like this. The mosquito takes the bite
Speaker 1: of an infected blood meal from an animal or a
Speaker 1: human in the case of chicken gunya, the virus has
Speaker 1: to travel through the guts of that mosquito, disseminate through
Speaker 1: the gut wall of the mosquito, travel through the hemolymph,
Speaker 1: and invade the salivary glands where they can replicate. And
Speaker 1: this process for chicken gunya virus within the mosquito takes
Speaker 1: between two and five days to happen. Okay, So what
Speaker 1: that means is that the adult mosquito, after it takes
Speaker 1: its first blood meal, has to live at least two
Speaker 1: to five days to then be infectious to another person.
Speaker 2: I have a question about mosquito longevity.
Speaker 1: Ooh, kyote, so glad Eron has so many fun facts
Speaker 1: about these mosquitoes.
Speaker 2: Yes, okay, excellent. How long on average do the different
Speaker 2: species Albapictus and Egypti live?
Speaker 1: So these mosquitoes take about a week to develop from
Speaker 1: an egg into adult, but once they are adults, they
Speaker 1: can live for four to six weeks okay mm hm,
Speaker 1: which is.
Speaker 2: A lot of very long biting potential.
Speaker 1: It sure is, and it's only female mosquitoes that bite.
Speaker 1: They have to take a blood meal in order to
Speaker 1: make eggs in order to lay a brood, and eighties
Speaker 1: mosquitoes if they are able to take an entire blood meal,
Speaker 1: and there are differences between eighties agypdi and Albapictus in
Speaker 1: terms of like how often they lay eggs and things
Speaker 1: like that, but if they took a whole entire blood meal,
Speaker 1: they might be able to go several days between feedings.
Speaker 1: But what often happens is that they get interrupted really
Speaker 1: frequently during their feedings, so they don't get a whole
Speaker 1: blood meal at once, so they might bite and then bite,
Speaker 1: and then bite and then bite in order to get
Speaker 1: enough blood to be able to make an egg brood.
Speaker 2: So it's not like one blood meal or one feeding
Speaker 2: sash one infected person. It could be five feeding sesshes
Speaker 2: to get your you know, stomach full, and you infect
Speaker 2: five people. So is it there? Yeah, like viral load,
Speaker 2: infectious dose, like you know, does that play a role
Speaker 2: in it as well?
Speaker 1: Great question. I totally don't have answers for you on that,
Speaker 1: Like how many viral particles does a mosquito have in
Speaker 1: their salvary glands and how many are they injecting with
Speaker 1: aged feed? I have no idea, but at least in theory,
Speaker 1: if this mosquito is biting many different hosts, not only
Speaker 1: is that many opportunities to become infected, but it's also
Speaker 1: many opportunities to transmit that pathogen.
Speaker 2: Makes sense and wow, But going back.
Speaker 1: To the timeline of it, so two to five days
Speaker 1: for that process of dissemination through the guts before a
Speaker 1: mosquito becomes infectious. Here we start to compare contrast something
Speaker 1: like chicken gunya with something like dan gay virus. Dingay
Speaker 1: virus takes eight to ten days before it's transmissible in
Speaker 1: the adult mosquito. So all, you have a mosquito that
Speaker 1: doesn't have to live nearly as long before it can
Speaker 1: start infecting other people.
Speaker 2: Interesting, So I guess that would probably play a big
Speaker 2: role in how fast an epidemic or an outbreak happens.
Speaker 1: Sure could mm hmm. All right, So continuing on in
Speaker 1: our life cycle, once that mosquito is infectious, it takes
Speaker 1: another blood meal, and then those viruses are injected from
Speaker 1: the salivary glands into our subcutaneous tissues. Those viruses make
Speaker 1: their way into our bloodstream, they infect a number of
Speaker 1: different cells. They infect our fibroblast cells, they can replicate
Speaker 1: in our skin cells. They make their way into our
Speaker 1: liver and into our joints, where they infect a variety
Speaker 1: of cells. I'm going to pause in the life cycle
Speaker 1: here because i want to talk a little bit more
Speaker 1: about these two species of mosquito, even though we've already
Speaker 1: kind of like dove into some of the fun bits.
Speaker 1: These two species of mosquito, eighties albapictus and eighties agypti.
Speaker 1: We've talked about them a lot because we've done zeca,
Speaker 1: we've done yellow fever, we've done dengey. These mosquitoes are
Speaker 1: particularly good particularly well adapted to rural, urban, and human
Speaker 1: built environments, especially eighties agypti. This is a mosquito that
Speaker 1: like just loves humans and our urban environments. These two
Speaker 1: mosquito species are generally both container breeding mosquitoes, so they
Speaker 1: do really well in things like old tires or that
Speaker 1: pot you forgot about that one pothole in your street
Speaker 1: that absolutely never drains your neighbor's pool that they drained
Speaker 1: three years ago but they never filled it, so there's
Speaker 1: just like an inch of water in there. Also tree
Speaker 1: holes in more like suburban or rural environments, et cetera.
Speaker 1: Any tiny amount of standing water is enough for eighties
Speaker 1: and hype and Albapictus both to be able to breed
Speaker 1: and survive. These two mosquitoes are also very aggressive. They're
Speaker 1: really aggressive biters, especially for humans, like they really like humans,
Speaker 1: and especially eighties Albapictus tend to be more diurnal than
Speaker 1: most mosquito species, so they can primarily bite during the daytime,
Speaker 1: in the mornings and in the evenings, so they're really
Speaker 1: difficult to avoid, and things like bednets that are often
Speaker 1: used to protect against other mosquito species that bite at
Speaker 1: night don't do anything to prevent the bites of eighties
Speaker 1: albapictus and eighties agypty right, And like I said, they
Speaker 1: can complete their entire initial life cycle in as little
Speaker 1: as a week from egg all the way to adult.
Speaker 1: So in times of plenty in terms of rainfall, like
Speaker 1: the rainy season, you have many many broods of mosquitoes
Speaker 1: over and over hatching and going out in search of
Speaker 1: new blood meal. But at the same time, like many
Speaker 1: mosquito species, these eggs can dry out completely and then
Speaker 1: survive until the next rainfall season. That's why they can
Speaker 1: do so well. In these small containers of water that
Speaker 1: might dry out completely, they can just hang on.
Speaker 2: It's amazing and I respect it, but I also hate it.
Speaker 1: I know, I know, I know. So that's just kind
Speaker 1: of some fun facts about eighties agypti and Albapictus. I'll
Speaker 1: probably talk more about them in the current event section
Speaker 1: because they're also really important invasive species worldwide, especially eighties albapictus. Yeah, so,
Speaker 1: and they spread so many different diseases that they're an
Speaker 1: incredibly important source of vector born disease. But if that
Speaker 1: isn't enough, chicken gunya virus can also be spread via
Speaker 1: vertical transmission within the mosquito, meaning it can pass into
Speaker 1: the eggs and result in larvae and therefore adults that
Speaker 1: are already infected.
Speaker 2: It's horrible. It's terrible.
Speaker 1: I didn't I don't know the rate at which this happens,
Speaker 1: but it definitely happens. And just to make it even worse,
Speaker 1: males who become infected at birth. Males do not blood feed,
Speaker 1: so they can't become infected as adults, but they can
Speaker 1: be born infected and can infect females during the mating process.
Speaker 1: So this virus is just really good at spreading through
Speaker 1: these mosquitoes.
Speaker 2: And that's just for eighties Egypti. Right, the vertical transmission.
Speaker 1: I saw it primarily for eighties EGYPTI.
Speaker 2: Okay, Yeah, And like I.
Speaker 1: Said, chicken gunya virus is more than just a human virus.
Speaker 1: So these mosquitoes can become infected by biting a huge
Speaker 1: variety of mammals, including rodents, bats, non human primates, but
Speaker 1: also even birds and reptiles that can become infected and
Speaker 1: harbor chicken gunea virus. I didn't get a sense. And
Speaker 1: I think that because this disease has largely been an
Speaker 1: outbreak disease. The outbreak patterns in humans tend to be
Speaker 1: from human to vector to human transmission, so like humans
Speaker 1: being the primary reservoir, largely because these two species of
Speaker 1: mosquitoes do really like to bite humans. So I didn't
Speaker 1: get a sense of what the natural reservoirs likely are
Speaker 1: across the globe, but it probably varies in different parts
Speaker 1: of the world.
Speaker 2: Yeah, it seems like historically they found it in non
Speaker 2: human primates, and then the more sampling they did, the
Speaker 2: more they found in other species, as as tense often happens.
Speaker 1: Yeah, so all of that is just the virus, the
Speaker 1: mosquitoes and the transmission. Let's get into the disease that
Speaker 1: chicken gunya causes, shall we.
Speaker 2: Let's do it.
Speaker 1: So, once a person gets bitten and this mosquito injects
Speaker 1: you full of virus, the incubation period tends to be
Speaker 1: about two to four days. Different papers report slightly different ranges,
Speaker 1: but that's about the average.
Speaker 2: I feel like that's a pretty tight range. It is.
Speaker 1: I mean, it does range from like one to twelve,
Speaker 1: but I think.
Speaker 2: Okay, never mind, I take it back.
Speaker 1: I know, I know, but in general, like most papers
Speaker 1: consensus two to four. Some like to say three to
Speaker 1: seven just to hedge their bets. Okay, but symptom onset
Speaker 1: tends to be abrupt and severe. The first hand account
Speaker 1: that we read was actually a pretty decent description of
Speaker 1: what I'm about to talk about, especially when you consider
Speaker 1: those from the eighteen hundreds. So love that the symptoms
Speaker 1: tend to start with a fever, of course, headache, back pain,
Speaker 1: very very severe joint pain and in potentially any joint ankles, wrist, fingers, hips, knees,
Speaker 1: large joints, small joints, and it does tend to be
Speaker 1: like so severe that it is difficult to bear. And
Speaker 1: people often will have like rigers and be bent over
Speaker 1: and just in an excruciating amount of pain. About fifty
Speaker 1: percent of people ish will also have some kind of
Speaker 1: skin involvement. The most common rash is a very itchy,
Speaker 1: red splotchy kind of what I think of is just
Speaker 1: a very generic viral looking rash, so like little red
Speaker 1: splotches with bumps in the middle, what we call maculo popular.
Speaker 1: And this can be across the chest, the stomach, the back.
Speaker 1: I know the first hand account mentioned the palms, but
Speaker 1: I don't think that we tend to see that very commonly.
Speaker 1: What's interesting is that in children the rash can often
Speaker 1: be quite different, with more of a blistering appearance, like
Speaker 1: very large blisters across the whole skin, or even with petikia,
Speaker 1: which are those tiny little purple spots that mean that
Speaker 1: you're having little, tiny pinpoint bleeds underneath your skin.
Speaker 2: Why is it different? Just immune system stuff?
Speaker 1: Yeah, great question, no clue. And in general, chicken gunya
Speaker 1: fever tends to be considered a self limited condition. Usually
Speaker 1: these symptoms are going to resolve in seven to ten days,
Speaker 1: which is a long time to be this sick. However,
Speaker 1: this incredibly painful arthritis can in some cases persist for
Speaker 1: months or even years afterwards.
Speaker 2: Oh my gosh.
Speaker 1: Yeah, it's horrible. And what's truly awful is that this
Speaker 1: happens in up to thirty to forty percent of people
Speaker 1: who are infected with chicken gunyavirus.
Speaker 2: Wow.
Speaker 1: Huge number. We don't know exactly what causes this chronic
Speaker 1: joint pain, this chronic arthritis, but so far it's not
Speaker 1: thought to be due to chronic infection. Okay, because in general,
Speaker 1: when we've tried to study it, people have not been
Speaker 1: able to isolate virus from the joint fluid of people
Speaker 1: with this chronic arthritis as a result of chicken gunya.
Speaker 1: So it's thought to likely be something that's immune mediated,
Speaker 1: which is something that we see with other rboviral, viral
Speaker 1: and bacterial infections as well, and one of those things
Speaker 1: that we still just don't really understand.
Speaker 2: What causes the acute joint pain.
Speaker 1: Oh great question. Arin to say that we don't really
Speaker 1: understand the path of physiology of chicken gunya virus, I
Speaker 1: think is an understatement and I always say that we
Speaker 1: don't understand things. In small animal studies, we see that
Speaker 1: it's primarily muscular skeletal tissues that are in infected by
Speaker 1: this virus, especially muscles surrounding joints as well as skin fibroblasts.
Speaker 1: Fibroblasts are this like generic cell type that are involved
Speaker 1: in connective tissue formation. And so since this is a
Speaker 1: virus that has to infect our cells in order to replicate,
Speaker 1: these are the cell types, these fibroblasts and these muscle
Speaker 1: cells that they tend to infect and replicate in. There
Speaker 1: is some evidence from these again animal studies, that mice
Speaker 1: who lack T cells, especially certain subsets of T cells,
Speaker 1: have much less severe joint swelling and tissue damage as
Speaker 1: a result of this viral infection. So it's thought that
Speaker 1: perhaps it's at least in part a T cell mediated
Speaker 1: response that causes all of this joint pain and inflammation
Speaker 1: in those spaces, because that's where the virus is actually infecting.
Speaker 2: And that's like the muscle, there's like muscle involvement.
Speaker 1: It can infect muscle cells. It doesn't mean that the
Speaker 1: inflammation will be in the muscles necessarily, but there's also
Speaker 1: often a lot of muscle pain with chaspana as well.
Speaker 2: So this only because we've just covered gout. How does
Speaker 2: how does this joint pain differ from gout joint pain?
Speaker 1: What a fun question. So gout tends to be a
Speaker 1: very one joint at a time or a few joints
Speaker 1: at a time. This is every joint in your body.
Speaker 1: There's similarities in that in both of them, a lot
Speaker 1: of the pain is going to be driven by the inflammation,
Speaker 1: which is driven by our immune response to some kind
Speaker 1: of stressor in this case, we think that it is
Speaker 1: the virus infecting particular cells, fibroblasts, muscle cells, other cells
Speaker 1: near and around our joints that then cause a lot
Speaker 1: of inflammation that then cause a lot of pain. Okay.
Speaker 1: The difference in gout, of course, is that we know
Speaker 1: exactly what those particular drivers are. See our gout episode.
Speaker 2: Interesting.
Speaker 1: But I do think it's important to talk about this
Speaker 1: pain and especially the chronicity that this pain can have.
Speaker 1: This can last for weeks to months to potentially years
Speaker 1: after this acute infection, and it can be debilitating. And
Speaker 1: chicken gunya virus is often portrayed as a much less
Speaker 1: virulent pathogen compared to other arbaviruses like yellow fever or dengay,
Speaker 1: and in a lot of ways it is. In general,
Speaker 1: the estimated case fatality rates for chicken gunya are less
Speaker 1: than one percent. It was thought, especially historically, to be
Speaker 1: very very rare to die from chicken gunya, although with
Speaker 1: more recent outbreaks we have seen an increase in mortality,
Speaker 1: especially in the very old, the very young, or the
Speaker 1: otherwise immunal compromised, so that less than one percent is
Speaker 1: probably an underestimate, but it certainly historically has been much
Speaker 1: less virulent than dangay fever, which if it causes dang
Speaker 1: gay shock syndrome, has a mortality rate of twenty percent
Speaker 1: or more or yellow fever which has a case fatality
Speaker 1: rate between ten and fifty percent, or my marsh. Yeah,
Speaker 1: so when you compare those, then yes, chicken gunya seems
Speaker 1: relatively benign. But months or years of debilitating joint pain
Speaker 1: can cause disability. It can cause inability to work, which
Speaker 1: might mean inability to feature family. So it does have
Speaker 1: really serious consequences. So I want to emphasize that it's
Speaker 1: not a benign illness by any means.
Speaker 2: Yeah, chicking gunya.
Speaker 1: Can also infect people during pregnancy. Of course, you can
Speaker 1: be infected at any point in your life. It doesn't
Speaker 1: seem to cross the placenta and cause fetal infection the
Speaker 1: way that something like zekeavirus does, but it can cause
Speaker 1: neonatal infections if someone is highly vyriemic, like has an
Speaker 1: acute infection at delivery, and those can actually be very
Speaker 1: severe and have resulted in neonatal deaths. Okay, when it
Speaker 1: comes to whether or not you can have an asymptomatic infection,
Speaker 1: which is something that we talk a lot about, especially
Speaker 1: in viral diseases or mosquito born diseases, I don't know
Speaker 1: who to believe in terms of how many asymptomatic cases.
Speaker 1: There are a lot of papers that I read. I
Speaker 1: would say the majority estimate that it's actually very rare
Speaker 1: to have an asymptomatic infection, which is quite different than
Speaker 1: something like dangay or zica.
Speaker 2: Yeah. I think I saw like a CDC cheat sheet
Speaker 2: that was like three and four chicken gunya cases are
Speaker 2: symptomatic and one in four dang gay are symptomatic.
Speaker 1: Yeah, it's estimated that anywhere from like five to twenty
Speaker 1: five percent, But most of the estimates I saw were
Speaker 1: about fifteen percent of people will be asymptomatic, which is
Speaker 1: pretty low. Yeah, but then some of the papers were
Speaker 1: like lots ofbody symptomatic, and I'm like, I don't know,
Speaker 1: but anyways, I think it's low compared to dange, compared
Speaker 1: to zica as far as we can tell.
Speaker 2: So, joint pain is like the hallmark symptom of chicken gunya.
Speaker 2: Are there any other organs that are involved?
Speaker 1: Great question. There doesn't tend to be a ton of
Speaker 1: organ involvement that results in organ damage that we would
Speaker 1: then see on things like lab results or resulting in
Speaker 1: like kidney failure, liver failure, which I think is why
Speaker 1: it's historically been considered a pretty mild disease. It can
Speaker 1: and has, in more recent outbreaks, caused neurologic effects, but
Speaker 1: again tends to do that at a much lower rate
Speaker 1: than something like zica.
Speaker 2: Right, It's something that you would commonly see in huge outbreaks.
Speaker 2: But yeah, yeah, okay, yeah, okay. So let's say that
Speaker 2: there's an outbreak of what suspected to be chicken gunya
Speaker 2: and someone is sick with what is probably chicken gunya.
Speaker 2: What do they do? What happens?
Speaker 1: Great question. So in terms of treatment, it's mostly supportive care.
Speaker 1: We don't have any particular anti virals. We don't have
Speaker 1: any specific treatments targeted towards chicken gunya virus. Most of
Speaker 1: what you'll see online is tilanol. Huh, that's it, thilanol.
Speaker 1: What's interesting about that is that public health agencies do
Speaker 1: tend to specify thaileanol over any other things like en
Speaker 1: sids like ibuprofen. And the reason for that is because clinically,
Speaker 1: during outbreaks, both because the symptoms can be very nonspecific
Speaker 1: in the acute phase, they can overlap a lot, and
Speaker 1: these two viruses tend to occur in the same areas,
Speaker 1: and chicken gunya virus can be difficult to tell apart,
Speaker 1: and enzids can be very dangerous in Dangay because it
Speaker 1: can lead to bleeding, right, okay, yeah, And so for
Speaker 1: that reason, it's like, if you're not sure, just tie
Speaker 1: it all.
Speaker 2: Yeah, okay, Yeah.
Speaker 1: And like many neglected tropical diseases, we don't have the
Speaker 1: best of diagnostics for chicken gunya either, but they exist,
Speaker 1: you know. Yeah, So that is chicken unya and it's
Speaker 1: biology or what I know about it. So, Aaron, tell
Speaker 1: me where did this virus come from? Why does it
Speaker 1: infect us? Well, tell me about it.
Speaker 2: I don't know if I can answer that second one,
Speaker 2: but I'll certainly try for the first. Right after this break,
Speaker 2: the story of chicken gunya virus, or at least part
Speaker 2: of the story of this virus, will probably sound a
Speaker 2: bit familiar to you, Aaron. It definitely will for you,
Speaker 2: because we have recorded Dangay and Zeca episodes, and you
Speaker 2: just talked about all the similarities. But for our listeners too,
Speaker 2: not just the biology or the transmission or the epidemiology
Speaker 2: of these viruses will sound similar, but also a bit
Speaker 2: of the history. I think, Okay, we'll sound a little
Speaker 2: bit echoes of each other, all mosquito born viruses, all
Speaker 2: on the rise, all recently attracting more attention and generating
Speaker 2: more headlines than historically they used to due to their
Speaker 2: recent geographics, spread into new regions, especially regions like Europe
Speaker 2: and North America, where the disease has changed from being
Speaker 2: an over there disease to a weight it's here now one.
Speaker 2: And with dangay and chicken gunya especially, the similarities extend
Speaker 2: beyond epidemiology and disease ecology and down into the clinical
Speaker 2: side of things, since they can cause a lot of
Speaker 2: the same symptoms, as well as their histories, which, as
Speaker 2: I'll talk about, have blended together and are kind of
Speaker 2: in the process of being rewritten.
Speaker 1: I love it.
Speaker 2: Yeah, But with as many similarities as these diseases share,
Speaker 2: they are also distinct in many ways that play a
Speaker 2: huge role in their transmission, their evolution, and in the
Speaker 2: way that public health efforts are focused. And I'm not
Speaker 2: going to do a thorough compare and contrast between chicken
Speaker 2: gunya and dengay, although I may call on you to
Speaker 2: help me erin some of these and we'll get to
Speaker 2: the section where I'm going to be like, all right,
Speaker 2: let's take a closer look, but I do. In researching
Speaker 2: for this, it struck me that these arboviruses are often
Speaker 2: kind of lumped together and talked about as a single entity.
Speaker 2: And I feel like it's just as important to remember
Speaker 2: what differences among these infections can tell us as it
Speaker 2: is to ask what their similarities can say about these diseases. Yeah,
Speaker 2: and I think that throughout this episode we'll have the
Speaker 2: opportunity to do both. But first things first, Aaron, you asked,
Speaker 2: as you always do, where this virus came from, And
Speaker 2: it's a great question that I'm only going to be
Speaker 2: able to answer in part. Okay, most papers I read
Speaker 2: for this episode, if they mentioned the evolutionary origin of
Speaker 2: chicken gunyavirus at all, it was just to say that
Speaker 2: it wasn't clear when or where this virus emerged. Right,
Speaker 2: of course, one paper gave a not super narrow estimate
Speaker 2: that the ancestor of chicken gunyavirus emerged fairly recently, maybe
Speaker 2: as recently as eighteen fifty or as far back as
Speaker 2: the year six fifty CE. It's like, which, like in
Speaker 2: the scheme of things, is not a big range, but
Speaker 2: it does seem like a big range.
Speaker 1: That's still a big range.
Speaker 2: It's a big range. It's a big range. But there
Speaker 2: was a more recent paper that examined the different lineages
Speaker 2: of the chicken gunyavirus and estimated that the virus emerged
Speaker 2: somewhere in Central or East Africa around three hundred to
Speaker 2: five hundred years ago. Okay, and the East Central South
Speaker 2: African lineage, which I think is the predominant one in
Speaker 2: a lot of places, that appeared around nineteen o three
Speaker 2: and then gave rise to the West African and Asian
Speaker 2: genotypes or lineages in the decades after.
Speaker 1: Wow.
Speaker 2: Yeah, so it's like pretty pretty And the most recent lineage,
Speaker 2: the Indian Ocean lineage, only emerged in the very early
Speaker 2: two thousands.
Speaker 1: I know. I can't wait to talk about it.
Speaker 2: It's so mind blowing, it really is. We'll get into later,
Speaker 2: but long story short, This seems to be a relatively
Speaker 2: new virus whose ancestors infected mosquitoes and non human primates
Speaker 2: and other vertebrates, with occasional spillover into humans from this
Speaker 2: enzootic cycle, and then at some point this virus diverged
Speaker 2: into chicken gunya virus transmitted by eighties mosquitoes and o
Speaker 2: nyang nyang virus. I don't know if that's how you
Speaker 2: pronounce it, but that's transmitted by anophilies mosquitoes. As humans
Speaker 2: began to settle in larger groups and especially began to
Speaker 2: store water, even you didn't even have to store that
Speaker 2: much of it, that provided opportunities for the evolution of
Speaker 2: the more domestic eighties agypdi agypdi mosquito subspecies which hung
Speaker 2: around these settlements, and a loud for human to human
Speaker 2: transmission of chicken gunya. So it's maintained and just humans
Speaker 2: and mosquitoes. And that's in contrast, of course, to the
Speaker 2: spillover into humans from the enzootic cycle when a bridge
Speaker 2: vector species of mosquito, one that feeds on both humans
Speaker 2: and non human primates or other vertebrate reservoirs, bites a
Speaker 2: human and transmits the virus.
Speaker 1: Very much like dangay. Honestly, it is very.
Speaker 2: Much like dangay, I mean, and it's much like a
Speaker 2: lot of other mosquito born viruses or mosquito born infections.
Speaker 2: Like there's this enzolotic cycle that just happens all the
Speaker 2: time in the background, and then it happens to spillover
Speaker 2: into humans and then depending on the circumstances that can
Speaker 2: cause this big outbreak yep. And so these big outbreaks
Speaker 2: would happen from time to time, and it fed initially
Speaker 2: by the spillover, and then it would just sweep through
Speaker 2: the population until most people became immune, and then the
Speaker 2: virus would go quiet for a while. And this is
Speaker 2: essentially how the cycle would have continued for hundreds of
Speaker 2: years until its discovery in nineteen fifty two. In July
Speaker 2: of that year, a seemingly new disease began popping up
Speaker 2: in the Makondai Plateaus region in Tanzania. Within two or
Speaker 2: three weeks of the first case appearing in a village,
Speaker 2: sixty to eighty percent of the population became infected. Whoa,
Speaker 2: with some households reporting a one hundred percent infection rate.
Speaker 1: That is impressively fast and impressively infectious.
Speaker 2: Yes, I honestly I just couldn't get over.
Speaker 1: It well, and I think it so does lend credence
Speaker 1: to this idea that there's not a lot of asymptomatic infections.
Speaker 2: Yes, totally. The disease seemed to come on suddenly, with
Speaker 2: the rapid development of a high fever in these horrible
Speaker 2: joint pains quote. The pain was frightening in its severity,
Speaker 2: completely immobilizing many patients and preventing sleep in the first
Speaker 2: few days of the illness. It was intensified by movement
Speaker 2: and localized in larger joints. In some cases, there was
Speaker 2: also severe backache. Morphia was the only analgesic which was
Speaker 2: found to modify the pain. Yeah. No one in the
Speaker 2: region could remember a similar epidemic ever occurring there, and
Speaker 2: so this disease was given a new name from the
Speaker 2: Macondai dialect chicken gunya, meaning that which bends up or
Speaker 2: I've also seen it as the disease that bends up
Speaker 2: the joints. No one who had the disease got it
Speaker 2: a second time. Wow, And people said you either definitely
Speaker 2: had it or you definitely did not. There was just
Speaker 2: no in between.
Speaker 1: Yeah.
Speaker 2: Researchers immediately suspected that it was mosquito born or at
Speaker 2: least transmitted by some blood sucking arthropod vector, both due
Speaker 2: to its pattern of transmission, its occurrence in the rainy season,
Speaker 2: and its similarity to Dangay fever. In one of these
Speaker 2: papers reporting the initial outbreak, quote, indistinguishable from dengay if
Speaker 2: allowance is made for the inherent variability of that disease,
Speaker 2: because dang gay is like clinically quite sabers. Yeah, studies
Speaker 2: were carried out where researchers collected blood feeding arthropods from
Speaker 2: all around the villages where the outbreak occurred, and sure enough,
Speaker 2: all signs pointed to eighties EGYPDI. Because of the clinical
Speaker 2: similarity to dan gay, people figured that when they found
Speaker 2: the virus, it was just going to be like a
Speaker 2: new subtype or a new strain of the Danae virus.
Speaker 2: But analysis of serum samples collected showed that it seemed
Speaker 2: to be a new kind of virus, not a Danae virus,
Speaker 2: And so it got to keep the name that it
Speaker 2: got during this first outbreak, Chicken Gunya. And maybe it's
Speaker 2: because we've done so many episodes where the story goes
Speaker 2: something like the disease was first recognized into ancient times
Speaker 2: and people wrote about them for hundreds of years, but
Speaker 2: no one knew what caused it or how it was
Speaker 2: transmitted until recently. But I just think it's so amazing
Speaker 2: that within a few years of its first appearance, we
Speaker 2: had a name, we had a clinical picture. We had
Speaker 2: a vector and a causative agent for this new disease. Yeah,
Speaker 2: I mean, and it shows how far we'd come by
Speaker 2: the nineteen fifties in terms of microbiology. If you cast
Speaker 2: your mind back to our Dangaye episode, you may remember
Speaker 2: that the first epidemics of dangay were described in the
Speaker 2: late seventeen hundreds, and it took another one hundred years
Speaker 2: and then some before it was linked to mosquitoes, and
Speaker 2: decades after that before the virus was identified and like classified.
Speaker 2: And here we are with chicken gunya, learning all that
Speaker 2: and more about this brand new disease in just a
Speaker 2: few years. It's amazing, or is it now?
Speaker 1: It is?
Speaker 2: But maybe things aren't as simple as I presented them.
Speaker 1: Well, Aaron, I'm just I'm waiting for you to drop
Speaker 1: the other shoe, because I know that our first hand
Speaker 1: account was from the eighteen hundred So.
Speaker 2: Yeah, yes, on that. Yeah, So maybe chicken unya isn't
Speaker 2: as brand new as we thought it was. Maybe nineteen
Speaker 2: fifty two was not the year of chicken unya first
Speaker 2: being discovered. Maybe some of those historical outbreaks of dangay
Speaker 2: weren't caused by the dange virus after all, but rather
Speaker 2: the chicken gunya virus. Of course, that doesn't take away
Speaker 2: from how like incredible it is to have built that
Speaker 2: knowledge about the seemingly new disease so quickly. Yeah, totally,
Speaker 2: But I did want to take some time to revisit
Speaker 2: the early history of dangay and see if maybe what
Speaker 2: people thought was dangay was actually chicken gunya. And this
Speaker 2: isn't something that I like came up with on my own.
Speaker 2: There are lots of papers that have been looking into
Speaker 2: this possibility for you know, decades, and they've come up
Speaker 2: with some pretty convincing evidence. All right. So a nineteen
Speaker 2: seventy one paper by Donald Carey titled Chicken Gunya and
Speaker 2: Dngay a Case of Mistaken Identity takes a closer look
Speaker 2: at many so called dengae epidemics since the eighteenth century
Speaker 2: and uses clinical descriptions from eyewitnesses to see whether it
Speaker 2: seems more in line with dengae or chicken gunya. Because
Speaker 2: although the two diseases do bear many similarities and can
Speaker 2: be quite varied in terms of symptom presentation, there do
Speaker 2: seem to be some distinguishing features between the two, like
Speaker 2: one of them is this lingering long, lingering joint pain
Speaker 2: in chicken gunya and also just the fact that dengey
Speaker 2: has a much higher mortality rate, And so these differences
Speaker 2: would be a lot more easily seen in outbreaks and
Speaker 2: epidemics when you can look at a whole bunch of
Speaker 2: people and see patterns emerge, rather than looking at two
Speaker 2: people side by side that like, both have kind of
Speaker 2: a rash, both have headache, joint paine and fever.
Speaker 1: Yeah, live in an area with eighties Egyptian eighties albapictus,
Speaker 1: And Yeah, I'm really excited for this, Aaron, because I
Speaker 1: do think it's really important. Many of the clinical papers
Speaker 1: written recently talk a lot about how difficult it is
Speaker 1: to distinguish chicken gunya and dangay, say in the moment
Speaker 1: during a chicken gunya outbreak or a dan gay outbreak,
Speaker 1: when you don't know which one is at play, or
Speaker 1: if both are happening simultaneously, which can absolutely happen. Yeah,
Speaker 1: So it is really interesting to be able to take
Speaker 1: a step back and look at things historically, because there
Speaker 1: are patterns that emerge when you're able to look not
Speaker 1: at an individual person but at a population yep.
Speaker 2: Oh, that just actually made me wonder though, is there
Speaker 2: any in places where both the viruses co occur? Is
Speaker 2: there competition between them within mosquitoes?
Speaker 1: Oh, my gosh, erin such a good question. There is
Speaker 1: some evidence in one of the papers that I read that,
Speaker 1: especially in eighties I think it's an eighties albu pictus
Speaker 1: that some of the mutations that I know you'll talk
Speaker 1: about actually might facilitate coinfection with danng gay and chicken gunya.
Speaker 2: It's terrified.
Speaker 1: It's terrifying.
Speaker 2: That is really terrifying.
Speaker 1: Yeah, but anyways, sorry, anyways.
Speaker 2: No, no, that's fascinating, okay. But the other thing about
Speaker 2: looking historically at dang gay and chicken gunya is that
Speaker 2: eighties agypdi achieved a global distribution since the sixteen hundreds
Speaker 2: or so, and that greatly expanded the range of dengay
Speaker 2: and yellow fever. So it seems pretty plausible that chicken gunya,
Speaker 2: which does the same transmission cycle more or less, could
Speaker 2: have been another virus carried by these mosquitoes. Yeah. In
Speaker 2: seventeen seventy nine, there was an outbreak of something called
Speaker 2: knuckle quarts or knuckle joint fever. In present day Karta,
Speaker 2: and the description written by David Bylon does suggest who
Speaker 2: was witness at the time does suggest Chicken Gunya. Quote.
Speaker 2: I noticed a gnawing pain in my right hand and
Speaker 2: in the joints of the hand and arm, which gradually increased,
Speaker 2: extending to the shoulder and then over my whole body,
Speaker 2: so that at nine o'clock that evening I was in
Speaker 2: bed with a high fever. I had a restless and
Speaker 2: sleepless night, suffering severe pains over the entire body, especially
Speaker 2: in the legs and arms, and in the joints. This
Speaker 2: is a brief notice concerning a very well known disease, which, however,
Speaker 2: in the memory of man here in Batavia, has never
Speaker 2: reached an epidemic, and which has therefore seemed wondrous to
Speaker 2: the inhabitants. Around this time, an outbreak of a similar
Speaker 2: disease was happening in Cairo. This one known as quote
Speaker 2: the knee trouble. It threw all the people into a fever.
Speaker 2: Its first attack lasted for three days, after which the
Speaker 2: illness increased or diminished, acording to the disposition of the individual.
Speaker 2: It was accompanied by pain in the joints, knees, and
Speaker 2: extremities as well as inability to move, and often with
Speaker 2: swelling of the fingers. The after pains lasted more than
Speaker 2: a month. The onset was sudden, the body being broken
Speaker 2: by it, and the head and knees taken hold of.
Speaker 2: So the descriptions of this disease painted this excruciatingly painful picture,
Speaker 2: but not really a deadly one. And that was something
Speaker 2: that's in sharp contrast to what Benjamin Rush saw during
Speaker 2: a seventeen eighty epidemic in Philadelphia of a disease that
Speaker 2: he nicknamed breakbone fever. This is often considered to be
Speaker 2: the first description of Danngay fever. And I actually had
Speaker 2: this passage in my day notes, and I don't think
Speaker 2: I read it in the episode, so I'm just going
Speaker 2: to read you a snippet of it here. And also,
Speaker 2: this is like a very full of quotation section, but
Speaker 2: I feel like it's important because we're going through historical outbreaks. Okay. Quote.
Speaker 2: The fever generally came on with rigor, but seldom with
Speaker 2: a regular chili fit. When the fever did not terminate
Speaker 2: on the third or fourth day, it frequently ran onto
Speaker 2: the eleventh, fourteenth, and even twentieth days. In some cases,
Speaker 2: the discharge of a few spoonsful of blood from the
Speaker 2: nose accompanied a solution of the fever, while in others
Speaker 2: a profuse hemorrhage from the nose, mouth, and bowels on
Speaker 2: the tenth and eleventh days preceded a fatal issue of
Speaker 2: the disease. The pains which accompanied this fever were exquisitely
Speaker 2: severe in the head, back, and limbs. The disease was
Speaker 2: sometimes believed to be a rheumatism, but its more general
Speaker 2: name among all classes of people was the breakbone fever.
Speaker 2: Russia's description, which also mentions a rash and burning in
Speaker 2: the palms of the hands and soles of the feet,
Speaker 2: it does have some echoes of chicken gunya like are
Speaker 2: There are lots of similarities between these descriptions that I've
Speaker 2: read so far, But it's also much deadlier, Like he's
Speaker 2: talking about hemorrhaging, he's talking about people dying and how
Speaker 2: often it happens, And that didn't seem to happen in
Speaker 2: the descriptions at least from the seventeen seventy nine Jakarta epidemic,
Speaker 2: as well as the series of outbreaks of a similar
Speaker 2: disease that occurred in India. And the West Indies in
Speaker 2: the eighteen twenties, which, like in Jakarta, had a super
Speaker 2: high attack rate but a low mortality rate. In eighteen
Speaker 2: twenty four to eighteen twenty five, an epidemic of Kiddinga
Speaker 2: peppo began in East Africa and spread to India, where
Speaker 2: it caused huge outbreaks, with one contemporary observer estimating that
Speaker 2: ninety five percent of the population of one region was affected. Wow. Yeah,
Speaker 2: And although this has historically been chalked up to denge,
Speaker 2: more recently it's been suggested to have been chicken gunya.
Speaker 2: And that's in large part due to the emphasis on
Speaker 2: the sudden onset an extremely fast onset and lingering joint
Speaker 2: pain quote a protracted debility and long continued pains and
Speaker 2: the ankles and dull aching in the joints of the
Speaker 2: fingers and toes for many weeks after the cessation of
Speaker 2: the fever. The outbreak, which also had high prevalence and
Speaker 2: low mortality, that occurred in the West Indies a few
Speaker 2: years later, around eighteen twenty seven, eighteen twenty eight. So
Speaker 2: that was a description from our first hand account, and
Speaker 2: that's what led to the nickname Dandy fever.
Speaker 1: So yea, what I remember talking about that? Uh huh
Speaker 1: oh my gosh, how interesting.
Speaker 2: Isn't that fascinating? So he even says, he even writes
Speaker 2: in that description like this is not a deadly disease.
Speaker 2: This is not known to be deadly. And it's so
Speaker 2: funny because I definitely like baited you by being like, Aaron,
Speaker 2: does that sound like chicken gunya? Is this a good
Speaker 2: first hand account? Accurate?
Speaker 1: I love it?
Speaker 2: Yeah. So, so some researchers, you know, over the past
Speaker 2: few decades have started to think, like, hey, well, wait
Speaker 2: a second, was that actually dangay right, or was that
Speaker 2: actually caused by dangay virus? I should say?
Speaker 1: Yeah, Well, it's interesting too to think about danay potentially
Speaker 1: infecting a new population who has never been exposed versus
Speaker 1: ademic dan gay because if anyone remembers back to our
Speaker 1: dangay fever episode, initial infections tend to be much more mild.
Speaker 1: So if you have an entirely immune population, all of
Speaker 1: that is going to be primary infection and it's not
Speaker 1: until the second time that people are exposed that you
Speaker 1: have dang gay shocked, dang gae hemorrhagic fever, and severe infections. So,
Speaker 1: especially in an initial infection and in that acute phase.
Speaker 1: I do think that chicken gunya and dan gay can
Speaker 1: be very hard to tell apart for sure.
Speaker 2: Yeah, But what I think is interesting is that people
Speaker 2: made a distinction. Doctors who wrote about these diseases during
Speaker 2: the eighteen hundreds made a distinction between dengey and Benjamin
Speaker 2: Rush's breakbone fever. So Steadman, who wrote the article where
Speaker 2: we drew the first hand account from huh, he brings
Speaker 2: up this point in that article quote, some of the
Speaker 2: physicians here seem to consider this fever the same as
Speaker 2: that described by doctor Rush under the name of the
Speaker 2: breakbone fever or the billious remittant fever. I think that
Speaker 2: the diseases, though somewhat alike in a few symptoms, are
Speaker 2: essentially different. Four circumstances chiefly distinguished the fever that I
Speaker 2: have described. First the suddenness and peculiarity in its mode
Speaker 2: of attack. Secondly, the well marked distinction between different stages. Thirdly,
Speaker 2: the peculiar eruption. Fourthly, the peculiar nature and duration of
Speaker 2: the after pains. So dangay and breakbone fever were not
Speaker 2: always used synonymously, and in fact, for many doctors for
Speaker 2: a time, they seemed to be written about as similar
Speaker 2: but distinct diseases, with breakbone fever being this more deadly
Speaker 2: and debilitating disease and one that you could become reinfected
Speaker 2: with or like you could be susceptible to multiple attacks.
Speaker 2: It's like how it was talked about and what they
Speaker 2: call dangay was milder except for the long period of
Speaker 2: lingering joint pain, and it was a one time only disease.
Speaker 1: That's very interesting.
Speaker 2: Erin, isn't it interesting?
Speaker 1: Yeah? And I don't remember it at all from our
Speaker 1: dang Gay episode.
Speaker 2: No, don't I think that, Like there were a few,
Speaker 2: like I think I made a throwaway comment that was
Speaker 2: something like and some people think this could have been
Speaker 2: chicken gunyahs. But then yeah, with this, it was like
Speaker 2: there's there's a lot more because I think.
Speaker 1: That's so interesting that like people made this distinction. But
Speaker 1: in making that distinction, what were they calling dn gay
Speaker 1: versus what were they calling something different? And what was
Speaker 1: chicken gunya versus? What was you know, new introductions of
Speaker 1: dangay or first outbreaks of danay?
Speaker 2: Totally?
Speaker 1: Ah, how fun isn't it?
Speaker 2: Isn't it? It's so interesting? To think about. And yeah,
Speaker 2: So throughout the rest of the eighteen hundreds, more and
Speaker 2: more outbreaks of what was called dangay or what was
Speaker 2: called breakbone fever. These were described across the tropics and subtropics,
Speaker 2: and some observant writers would note the clinical differences between
Speaker 2: the two, but sometimes they would use the terms interchangeably.
Speaker 2: So how did the two become one? How did breakbone
Speaker 2: fever and dangay become absolutely the same thing?
Speaker 1: Yeah?
Speaker 2: How did we forget about these differences? And honestly, it
Speaker 2: seems to me like it comes down to just a coincidence.
Speaker 2: So yeah, like I said, a lot of physicians that
Speaker 2: wrote about these epidemics did distinguish between dang gay and
Speaker 2: breakbone fever, but by the eighteen hundreds, because they're such
Speaker 2: similar diseases, dang gay became increasingly used to describe both.
Speaker 2: After eighties, e jypdi was identified as the vector for
Speaker 2: yellow fever, researchers became interested in seeing whether dang gay
Speaker 2: was also transmitted by mosquitoes. And I feel like I'm
Speaker 2: not doing a very good job of this, but like,
Speaker 2: when I'm talking about dangay and these historic outbreaks, I
Speaker 2: really should be putting quotes around dan gay, so like
Speaker 2: what they were calling kay, right, And so when these
Speaker 2: researchers decided, like, hey, okay, let's see if we can
Speaker 2: link mosquitoes to this, there was an outbreak of quote
Speaker 2: dangay that was going on in Lebanon, in Australia and
Speaker 2: in the Philippines. And these outbreaks provided the perfect opportunity
Speaker 2: to test this out, this mosquito hypothesis using human quote
Speaker 2: unquote volunteers. Researchers successfully demonstrated that the disease was caused
Speaker 2: by a virus and transmitted that virus from sick people
Speaker 2: to healthy people through the bite of an infected eighties Egypti.
Speaker 2: But it just so happens that the virus that was
Speaker 2: endemic in these study sites in this outbreak of quote
Speaker 2: dangay was not the chicken guna virus, but the dangae virus.
Speaker 2: And so it was assumed that this and all preceding
Speaker 2: historical epidemics that were went under the name dangay were
Speaker 2: caused by this virus alone. And the reason I say coincidence,
Speaker 2: maybe that's like not really the right, We're just a
Speaker 2: matter of like happenstance, I guess is because if these
Speaker 2: researchers had instead been working on an outbreak of quote
Speaker 2: dengay that was actually caused by chicken gunya virus, right,
Speaker 2: dangay would mean something different than it does today. It
Speaker 2: would mean that chicken gunya virus or what we call
Speaker 2: the chicken gunya virus and the virus that we called
Speaker 2: dangay today would probably have a different name.
Speaker 1: How fascinating, Aaron, Isn't that neat? So at the end
Speaker 1: of it, we still can't actually distinguish a lot of
Speaker 1: those early descriptions of course of quote dengay and chicken gunya.
Speaker 2: I mean we can try, like, but no, that's that's
Speaker 2: definitely something that I think is a key takeaway. Yeah, right, Like,
Speaker 2: this was a very long winded way of me saying
Speaker 2: that chicken gunya has probably been around longer than since
Speaker 2: the nineteen fifties and that it probably caused some historical
Speaker 2: outbreaks attributed to dangay. But I wanted to kind of
Speaker 2: dig a little bit deeper because I think it's a
Speaker 2: fascinating example of how the history of a disease is
Speaker 2: constantly evolving. Yeah, whether through the discovery of old texts
Speaker 2: that you know, put it in a new place, or
Speaker 2: bring it back even farther, or through molecular tools tracing
Speaker 2: the actual evolution of a pathogen or a vector, or
Speaker 2: because modern events add to the story. The history of
Speaker 2: chicken gunya that somebody tells in ten years probably isn't
Speaker 2: going to sound the same as this one, the one
Speaker 2: that you know we're telling now. And the second reason
Speaker 2: is that I think this highlights both the benefits of
Speaker 2: using historical descriptions of disease, because they allow you to
Speaker 2: retrace the steps of its spread and how our understanding grew,
Speaker 2: but it also highlights the drawbacks. It certainly seems likely
Speaker 2: that chicken gunya has been more widely distributed for longer
Speaker 2: than we initially thought, given some of these historical descriptions
Speaker 2: being like pretty on the money about chicken gunya, and
Speaker 2: also the fact that its vector eighties a jip die
Speaker 2: or one of its vectors was present in a lot
Speaker 2: of these places, which would have made transmission feasible possible.
Speaker 2: But we can't know for sure. We can't know whether
Speaker 2: the author of an account was highlighting an unusual case
Speaker 2: or a typical one, whether they were interested in a
Speaker 2: certain set of symptoms, so they played those up while
Speaker 2: ignoring others, whether there was some reason that they were
Speaker 2: like invested in making a difference between dangay and breakbone
Speaker 2: fever and really like highlighting those differences. These are also
Speaker 2: similar viruses with a substantial overlap in disease symptoms and
Speaker 2: geographic range, And it's possible that one outbreak of dangay
Speaker 2: was actually caused by dangae virus while another was caused
Speaker 2: by chicken gunya virus. Maybe another was caused by yang
Speaker 2: yong virus or a different virus entirely. But in any case,
Speaker 2: these historical accounts aren't just useful for historians, but like
Speaker 2: you talked about, Aaron, also for modern day researchers looking
Speaker 2: for clues into a disease's ecology and epidemiology. What do
Speaker 2: we see on a big scale, What are the things
Speaker 2: that stand out historically and why? But speaking of modern
Speaker 2: day researchers, let's head back to the twentieth century to
Speaker 2: see what happened with chicken gunya once it was formally
Speaker 2: identified in the nineteen fifties. So as you might expect,
Speaker 2: having a name, a vector, and a virus made it
Speaker 2: easier for people to recognize subsequent outbreaks which occurred throughout
Speaker 2: the nineteen sixties and beyond in Sub Saharan Africa. Chicken
Speaker 2: gunya was first detected outside of Africa in nineteen fifty
Speaker 2: eight in Thailand, and over the next few years the
Speaker 2: virus continued. It spread throughout Asia into Cambodia and India,
Speaker 2: although it was probably not its first rodeo there. Yes,
Speaker 2: antibodies against chicken gunya were found in serum collected from
Speaker 2: people in India in the early nineteen fifties. And you
Speaker 2: already heard this whole spiel that I just gave about
Speaker 2: mistaken identity between chicken gunya and danngaey. But what was
Speaker 2: happening in the nineteen fifties, the nineteen sixties into the
Speaker 2: nineteen seventies is that the scale of these epidemics seemed
Speaker 2: to be growing, with one epidemic in Chennai, India in
Speaker 2: nineteen sixty four causing over four hundred thousand cases. But
Speaker 2: chicken unyon didn't maintain this huge growth because after the
Speaker 2: nineteen seventies things seemed to like cool down a bit,
Speaker 2: possibly thanks to a high rate of immunity from previous epidemics.
Speaker 2: It seems like unclear but researchers have pointed to a
Speaker 2: possible cyclical nature of chicken gunya outbreaks, which I think
Speaker 2: is interesting. But then in two thousand and four, everything
Speaker 2: changed yep, or rather an amino acid in the virus changed.
Speaker 2: So it's been hypothesized and I think pretty well supported
Speaker 2: from experimental research that this change of this amino acid
Speaker 2: resulted in this viral lineage of the chicken gunya virus
Speaker 2: being able to be more easily transmitted by eighties Albalpictus,
Speaker 2: a mosquito species that previous to this had not really
Speaker 2: been implicated as a major vector. It was like eighties
Speaker 2: A Jypti for the urban human to human cycle, and
Speaker 2: then other eighties species for the enzootic cycle. But now
Speaker 2: suddenly there's this new Albapictus species in play. And the
Speaker 2: result of that was that chicken gunya exploded in two
Speaker 2: thousand and four from eastern Kenya into islands in the
Speaker 2: Indian Ocean, involving hundreds of thousands of peapleople and attack
Speaker 2: rates as high as thirty five percent or even sixty
Speaker 2: three percent I saw on one island. Over the next years,
Speaker 2: chicken gunya grew to be a major public health problem,
Speaker 2: causing massive outbreaks in South and Southeast Asia involving millions
Speaker 2: of people, where for the first time these neurological and
Speaker 2: other complications of the infection were observed. And with eighties
Speaker 2: Albapictus now as this major vector, its potential for global
Speaker 2: spread grew tremendously because Albopictus also extends further than eighties
Speaker 2: Egypti into temperate regions. It's a great urban mosquito that
Speaker 2: overwinters really well. Like you talked about Aaron loves feeding
Speaker 2: on humans, has these desiccation resistant eggs. I mean, we're
Speaker 2: up against quite a lot in terms of chicken gunya control,
Speaker 2: and I do have a little asterisk there in terms
Speaker 2: of like genotype by genotype interactions between Albalpictus and the virus,
Speaker 2: so like some combo don't do as well as others.
Speaker 2: But I mean it's complicated but still ye, And it
Speaker 2: gets even more complicated when you add urbanization and climate
Speaker 2: change to the mix, as you have to do when
Speaker 2: you talk about disease or vector born diseases. But yeah,
Speaker 2: I mean this is kind of like a rapid wrap up.
Speaker 2: But I think that what I took away from this
Speaker 2: is that we have a lot to learn about the
Speaker 2: future of chicken gunya, and it seems quite daunting, but
Speaker 2: I think looking at the past, and even like the
Speaker 2: very recent past, chicken gunya can serve as yet another
Speaker 2: lesson along with dange, along with SIKA, along with other arboviruses,
Speaker 2: on just how easily mosquito born viruses or other pathogens
Speaker 2: can reach global distributions. But also it's an important reminder
Speaker 2: that we have to consider their individual ecologies and pathology
Speaker 2: in predicting future risk, like for instance, dangae's multiple circulating
Speaker 2: serotypes or chicken Gunya's increased transmission via albul pictus. It's
Speaker 2: all very messy and it's all very complicated, but it's
Speaker 2: so important with that. Aaron, can you tell me what's
Speaker 2: going on with chicken gunya today?
Speaker 1: I can't wait to right after this break. Unsurprisingly, Aaron, let.
Speaker 2: Me guess we don't have good numbers.
Speaker 1: We don't. Yeah, it's hard to get a sense of
Speaker 1: global numbers. But what's interesting and different about the reason
Speaker 1: why for chicken gunya than anything else that we've covered
Speaker 1: is that chicken gunya really only tends to be reported
Speaker 1: in outbreaks. Everything about chicken gunya is there was an
Speaker 1: outbreak this year, There was an outbreak in this area,
Speaker 1: and an outbreak and outbreak and outbreak. It's like, when
Speaker 1: do we just start saying it's everywhere and these are
Speaker 1: just the cases that are happening.
Speaker 2: Well, that's a that's a question.
Speaker 1: Though I know it's a real question. I don't have
Speaker 1: an answer to it. It's like a genuine sounded like
Speaker 1: a sarcastic question, So genuine question.
Speaker 2: No, I'm I'm yeah, I'm very curious and like because
Speaker 2: it does seem like chicken Gunya could have like more
Speaker 2: of a propensity to pop up in outbreaks.
Speaker 1: Right because it does, spoiler, provide pretty long lasting immunity,
Speaker 1: and so as it races through a population causes a
Speaker 1: huge outbreak, then everyone has been exposed and now there's
Speaker 1: no more susceptible people in that particular population, and you
Speaker 1: have to wait for new people to be born or
Speaker 1: to move in, or for that virus to move to
Speaker 1: the town next door. So let's talk a little bit
Speaker 1: about the numbers that we do have and that we
Speaker 1: have seen and what chicken Gunya has been doing globally,
Speaker 1: shall we, Like you mentioned Aaron starting in two thousand
Speaker 1: and four, an outbreak in Kenya spread throughout the Indian
Speaker 1: Ocean and persisted for several years. This kind of one
Speaker 1: big outbreak. It spread to Lari, Union Island, where more
Speaker 1: than a third of the entire population became infected. It
Speaker 1: spread to India, where cases reached more than one point
Speaker 1: five million people by two thousand and six. By two
Speaker 1: thousand and seven, it continued. It's spread and octophenous one
Speaker 1: of my favorite words.
Speaker 2: Oh me too.
Speaker 1: Basically, local transmission was reported in Europe for the first time,
Speaker 1: possibly ever, with several hundred cases reported in two thousand
Speaker 1: and seven.
Speaker 2: Thank you Alba pictish.
Speaker 1: Yeah, that's what I was just going to say, is
Speaker 1: that much of those outbreaks in the early two thousands
Speaker 1: were due to spread by albapictus. And so the strain
Speaker 1: that we saw of this virus was this strain that
Speaker 1: had these particular mutations that made it more able to
Speaker 1: be transmitted by eighties Alba pictus, which is the predominant
Speaker 1: vector in a lot of these parts of the globe.
Speaker 1: So that's fascinating, and it was terrifying, right, this was
Speaker 1: millions of people being infected in the early two thousands.
Speaker 1: By twenty thirteen. If we jump ahead, twenty thirteen is
Speaker 1: when we see chicking gunya spread to the Americas for
Speaker 1: the first time. In twenty thirteen, it was across Caribbean islands,
Speaker 1: where cases reached tens of thousands in a matter of months,
Speaker 1: and then rapidly spread to the South American, Central American
Speaker 1: North American continent, with twenty fourteen having over one million
Speaker 1: suspected cases reported to the Pan American Health Organization. Now,
Speaker 1: these cases, these strains do not have that albapictus gene
Speaker 1: and are spread primarily by eighties Egypti. So we've got
Speaker 1: them both all over the world.
Speaker 2: Well, and how difficult would it be for the one
Speaker 2: that doesn't have the eighties albapictus ability to gain.
Speaker 1: It, to gain it exactly, I mean it's already done
Speaker 1: it once.
Speaker 2: Right, or the one that does have it to continue.
Speaker 1: Its spread a thousand percent Aaron, Yes, And that's kind
Speaker 1: of the concern at this point. In a lot of
Speaker 1: parts of South America, chickiing gunya is now considered endemic,
Speaker 1: and yet still we mostly see reports of outbreaks. I
Speaker 1: tried to get a sense of scale globally, just like
Speaker 1: averages and I did find one paper that was looking
Speaker 1: at both chicken gunya and zeca virus, but trying to
Speaker 1: estimate the disability adjusted life years, which we've talked about
Speaker 1: on this podcast. These are imperfect measures, but they are
Speaker 1: one way to get a sense of the impact and
Speaker 1: burden of disease, and I think, in the case of
Speaker 1: chicken gunya, a really good way to do it, because
Speaker 1: we're not necessarily going to see a lot of death
Speaker 1: or mortality from chicken gunya, but we are going to
Speaker 1: see a lot of years of healthy life lost as
Speaker 1: the result of this disease, and that's what the disability
Speaker 1: adjusted life years are measuring. So in the case of
Speaker 1: chicken gunya, these researchers estimated a global annual burden looking
Speaker 1: at data from twenty ten to twenty nineteen of one
Speaker 1: hundred and six thousand disability adjusted life years.
Speaker 2: WOW, which is a lot.
Speaker 1: And these estimates were based on case estimate, so combined
Speaker 1: total global cased estimates of anywhere from fifty to three
Speaker 1: hundred and fifty thousand cases per year. And we know
Speaker 1: that again that varies because some years it might be
Speaker 1: more than a million, and some years it might be less.
Speaker 1: So it's pretty major. And again, up to forty percent
Speaker 1: of people infected are going to have chronic or in
Speaker 1: some cases permanent joint pain and potential disability as a
Speaker 1: result of this disease.
Speaker 2: That's such a high proportion, I.
Speaker 1: Know, it's really terrifying. One theme that I think we
Speaker 1: end up touching on a lot in this podcast, and
Speaker 1: you mentioned it aarin, especially in our vector born disease episodes,
Speaker 1: are the potential effects of things like land use change,
Speaker 1: climate change, urbanization and its effects on disease incidents and
Speaker 1: disease prevalence, And especially in the case of a vector
Speaker 1: born disease that is spread by urban human loving mosquitoes
Speaker 1: like chicken gunya, this is a particularly important thing to
Speaker 1: be worried about. Both of these mosquito species are very
Speaker 1: well suited for urban environments, so there are a lot
Speaker 1: of papers that have looked specifically at the effects of
Speaker 1: rapid urbanization on mosquito density and distribution. And the long
Speaker 1: and short of it is that it's terrifying news in
Speaker 1: terms of mosquito born disease, not just chicken gunya, but
Speaker 1: including chicken gunya. Because these papers tend to conclude that
Speaker 1: urbanization across the globe, not localized to one particular part
Speaker 1: of the world, correlates with a higher risk and abundance
Speaker 1: of these eighties mosquitoes. You have an increase in favorable
Speaker 1: breeding grounds. You have higher larval development rates in urban
Speaker 1: areas compared to natural areas. You have potential for greater
Speaker 1: adult survival time. And all of these things mean that
Speaker 1: you have a potential for greater vector competence, that these
Speaker 1: vectors are living longer and therefore transmitting or at least
Speaker 1: having the potential to transmit disease more readily.
Speaker 2: It's not good news.
Speaker 1: It's not good news. And then, of course there's also
Speaker 1: going to be the effects of climate change. Warming temperatures
Speaker 1: might mean shifts in vector distribution and vector habitat. They
Speaker 1: also will mean shifts in rainfall patterns and prevalents, as
Speaker 1: well as an increase in the strength or severity of
Speaker 1: natural disasters, and all of these have the potential to
Speaker 1: at a minimum shift thereby moving into new populations, if
Speaker 1: not also increase mosquito prevalence disease burden across the globe.
Speaker 1: I guess I didn't mean for this to be like
Speaker 1: such a bummer of an ending but I feel like
Speaker 1: that's an important part. Like arboviral diseases like chicken gunya
Speaker 1: have been popping up throughout human history always, they have
Speaker 1: been here with us, and I think that many of
Speaker 1: us probably remember when chicken gunya was making a ton
Speaker 1: of headlines in twenty thirteen and twenty fourteen because we
Speaker 1: had cases in Texas and in Florida, and then it
Speaker 1: went away and we forgot about it, except that it
Speaker 1: didn't go away. And these viruses, these diseases are not
Speaker 1: going away, and it takes a huge effort of like
Speaker 1: multidisciplinary public health work to be able to understand these
Speaker 1: risks and potentially reduce them.
Speaker 2: And it seems like an incredible challenge to do that.
Speaker 2: You're working against so many things. No, I have two questions, Okay,
Speaker 2: they're unrelated, Okay. The first one is about the impact
Speaker 2: of infection with chicken gunya virus in mosquitoes. Does it
Speaker 2: have any sort of negative impact?
Speaker 1: Great question. I didn't see anything on it, so not
Speaker 1: as far as I know, And I would guess if
Speaker 1: it's so easily vertically transmitted, then it's not as likely
Speaker 1: I would think, to have detrimental effects on the mosquitos themselves.
Speaker 2: Follow up related question before I get into my second question,
Speaker 2: Wellbacchia yestion.
Speaker 1: Mark, Yeah, I don't so Wellbaccia For anyone who doesn't remember,
Speaker 1: I think I talked about it in our Dengay episode.
Speaker 1: Sure question Mark, I think it was Dan Gay. Wellbaccia
Speaker 1: is a symbiotic bacteria that live in a lot of
Speaker 1: insects species, including mosquitoes, and there is a lot of
Speaker 1: really interesting research on Wallbaccia and other microbiome bugs that
Speaker 1: live inside of these mosquitos and their potential effects on
Speaker 1: either increasing or decreasing the ability of these mosquitoes to
Speaker 1: spread disease. I don't have a final answer because I
Speaker 1: just didn't have time to dig into it, but there
Speaker 1: does seem to be at least some evidence that some wobakia,
Speaker 1: if introduced two ads mosquitoes, might decrease the transmission of
Speaker 1: chicken gunya.
Speaker 2: So maykay interesting asterisk.
Speaker 1: There's more there. I just didn't read it.
Speaker 2: There's there's potential. I got it, Okay. So now my
Speaker 2: second non related question is vaccine. Yeah, because chicken gunya
Speaker 2: induces a long immunity.
Speaker 1: It does, so there's a lot of theoretical potential for
Speaker 1: a vaccine. There's also a lot of various groups and
Speaker 1: people that have been working on vaccine development. So there
Speaker 1: are at least ten, possibly more, candidate vaccines that are
Speaker 1: all at various stages in clinical trial. There's probably one
Speaker 1: or two in almost every phase one, two, and three.
Speaker 1: Most of them are in pretty early clinical trials. But
Speaker 1: there is a vaccine of almost every flavor. There are
Speaker 1: mRNA vaccine candidates, there's live attenuated vaccine candidates. There are
Speaker 1: measles vector vaccine candidates, and viral particle vaccine candidates. But
Speaker 1: we don't have any that I could tell. We're particularly
Speaker 1: close to licensure at this point. Okay, Yeah, but the
Speaker 1: potential exists, and there's people working on it. I have
Speaker 1: a feeling it's largely down too funding.
Speaker 2: Yeah, as per us as per us.
Speaker 1: So that's chicken good, Yeaharon, Okay, I don't know. Is
Speaker 1: that enough?
Speaker 2: I think so, I mean, there was a lot there's
Speaker 2: I mean, there's also like it's very clear that there
Speaker 2: are limitations and knowledge about chicken.
Speaker 1: Yeah. I can't wait to see what we learn in
Speaker 1: the coming decades, Darren.
Speaker 2: I'm hopefully it'll be a lot h well sources sources
Speaker 2: speaking of learning a lot, I have a ton of
Speaker 2: sources for this episode. I will post them all, but
Speaker 2: I want to shout out too in particular, so one
Speaker 2: by Weaver and Forrester from twenty fifteen was really great
Speaker 2: about sort of the evolutionary history and the history of
Speaker 2: it spread since nineteen fifty two. And then for the
Speaker 2: discussion of dangay versus chicken gunya and all of that,
Speaker 2: there's that paper by Donald Kerrey from nineteen seventy one
Speaker 2: called Chicken Gunya and Dangay a Case of Mistaken identity.
Speaker 1: That one sounds fun. I also had a lot of
Speaker 1: papers for this episode. One of my favorites for the
Speaker 1: biology was a Nature Reviews microbiology paper from twenty ten,
Speaker 1: so a little old that was called the Biology and
Speaker 1: Pathogenesis of Chicken Gunya Vibevirus. And one of my favorites,
Speaker 1: just because I love this topic, was from Plas Neglected
Speaker 1: Tropical Diseases in twenty twenty one, and that was the
Speaker 1: role of urbanization in the spread of eighties mosquitoes and
Speaker 1: the diseases they transmit a systemic review. So I definitely
Speaker 1: have that one too. It's a good one. It's terri fun.
Speaker 2: Yeah.
Speaker 1: We'll post our sources from this episode and every single
Speaker 1: one of our episodes on our website, this podcast will
Speaker 1: kill you dot Com under the episodes tap.
Speaker 2: We certainly will. Thank you so much to Bloodmobile for
Speaker 2: providing the music for this episode and all of our episodes.
Speaker 1: Thank you to exactly Right Network.
Speaker 2: And thank you to you listeners. I hope that you
Speaker 2: enjoyed this first foray into a mosquito born virus. This
Speaker 2: season sounds like a very specific topic now that I
Speaker 2: say it, but it's not.
Speaker 1: I feel like we have done our mosquito born diseases
Speaker 1: in very interesting orders, so totally but yeah, thank you listeners,
Speaker 1: hopefully you enjoyed this. A special shout out to our patrons.
Speaker 1: Thank you so much for your support.
Speaker 2: Absolutely we can't thank you enough.
Speaker 1: And this is our second to last episode as a reminder.
Speaker 1: As a reminder, so make sure you are subscribed to
Speaker 1: our social media and to our podcast wherever you're listening
Speaker 1: so that you don't miss it when next season drops.
Speaker 2: Very well done, erin thanks and until our season finale,
Speaker 2: wash your hands, you filthy animals. Um