Speaker 1: No one would believe the mischief the rabbits are doing
Speaker 1: unless they could see it. The sheep farmers have not
Speaker 1: tried to clear them, and now many of the runs
Speaker 1: are so bare that there is not grass enough to
Speaker 1: feed the rabbits, let alone the sheep. The consequence is
Speaker 1: that the rabbits are traveling in thousands in search of food.
Speaker 1: Last Friday morning, soon after sunrise, I met a swarm
Speaker 1: coming from the hills. I never saw such a thing before.
Speaker 1: The ground was scarcely to be seen for about a
Speaker 1: mile in length. Five weeks since I could not find
Speaker 1: a rabbit on my land, but since then we have
Speaker 1: killed thousands. When the sun is hot, you can go
Speaker 1: along the fences or any place where it is shady
Speaker 1: and kill hundreds.
Speaker 2: With a stick.
Speaker 1: Today has been cool, but still I several times killed
Speaker 1: two or three at a blow. The paddocks stink with
Speaker 1: the dead ones.
Speaker 3: Immediately prior to the liberation of Mixamatosis, a combination of
Speaker 3: circumstances had led to the build up of rabbits to
Speaker 3: very high levels over much of most of their range,
Speaker 3: and the situation in many areas could only be described
Speaker 3: as desperate. The change has been almost miraculous. The landscape
Speaker 3: in some areas has been virtually transfigured. Hills that had
Speaker 3: been grazed to the soil for decades and whose slopes
Speaker 3: appeared gray and red on the horizon are now clothed
Speaker 3: in grass. The broad margins of the country roads lying
Speaker 3: outside the boundary fences of grazing properties tended to carry
Speaker 3: dense rabbit populations, and as often as not, showed it
Speaker 3: in the poverty of their groundcover. It is now usual
Speaker 3: to see tall grass to the road's edge looking over
Speaker 3: the fences. It is now very rare to see a
Speaker 3: paddock without a dense and healthy pasture.
Speaker 2: Wow, I love it.
Speaker 1: And those two passages just got me so excited for
Speaker 1: this episode.
Speaker 3: It's very interesting to kind of see like very clear
Speaker 3: before and after quotes. Yeah, those those two quotes I
Speaker 3: lifted from a book called The Biological Control of Vertebrate Pests,
Speaker 3: and they are both about the topic of today's episode.
Speaker 3: Make Sematosis. Make Sematosis the Radiohead song. So we're gonna
Speaker 3: talk in this episode all about Tom Yorke and what
Speaker 3: inspired him to write the song mix and Metosis.
Speaker 1: I have no idea what you're talking about.
Speaker 3: Aaron Okay. Miximatosis is actually the topic of today's episode.
Speaker 3: But it's a virus that affects rabbits, and it also
Speaker 3: happens to be the title of a Radiohead song.
Speaker 1: Wow, I definitely did not know that last part.
Speaker 3: I listened to it in prep uh for the recording today.
Speaker 2: Nice, we should try and get the rights.
Speaker 3: You know, Bloodmobile? Can you write us a knockoff? I
Speaker 3: feel like I should introduce myself before we begin. The
Speaker 3: rest of this introduction is always the place. Hi, I'm
Speaker 3: erin Welsh.
Speaker 2: And I'm Aaron Aman Upnike.
Speaker 3: And this is this podcast will kill you.
Speaker 1: Yes, it is welcome if this is your first time here.
Speaker 1: We usually do things in a different order.
Speaker 3: And maybe a little bit more clean and a little
Speaker 3: bit more organized.
Speaker 1: We're just so excited about mix and metosis. And I
Speaker 1: think you were really excited to tell me about Radiohead.
Speaker 3: I really was, I really was.
Speaker 1: Did you know that I wasn't going to know? I
Speaker 1: feel like you did. I.
Speaker 3: I gave it about a fifty five to forty five Okay, okay, yeah.
Speaker 1: But yes, a rabbit viral disease is what we're talking
Speaker 1: about today. It's going to be great, even if you
Speaker 1: think you don't like animal viruses, or you don't like rabbits,
Speaker 1: or you do like rabbits, you're gonna love this episode.
Speaker 3: I think so too. This is like if you just
Speaker 3: clicked on this out of sheer curiosity and you're like, Okay,
Speaker 3: now I'm having my doubts. This is a rabbit disease. Yeah,
Speaker 3: I promise. I think this is one of the most
Speaker 3: interesting and important stories about disease that we have covered
Speaker 3: on this podcast because it covers so many different topics,
Speaker 3: so many different concepts.
Speaker 2: Yeah it is. It is such a good story. Promise
Speaker 2: it is.
Speaker 3: But we have some business to take care of.
Speaker 2: We do.
Speaker 1: It is first quarantiny time.
Speaker 3: It is What are we drinking this week?
Speaker 2: We're drinking Bunny's Bug? Get it.
Speaker 3: Bunny's Bug is a tasty little drink that has hop water.
Speaker 2: Because because bunnies hop.
Speaker 3: I don't know if we needed to explain that, but I.
Speaker 2: Like it though, I like the explanation.
Speaker 3: It has lime juice, it has mescal, it has simple syrup,
Speaker 3: and it has some grapefruit juice.
Speaker 2: Yum delish.
Speaker 1: We'll post the full recipe for that quarantini as well
Speaker 1: as our non alcoholic plusy Berta on our website, This
Speaker 1: podcast will kill You dot com and all of our
Speaker 1: social media channels.
Speaker 3: Oh is it my turn to do the website information now?
Speaker 2: Okay, it is.
Speaker 3: On our website. You can find transcript You can find
Speaker 3: our bookshop dot org affiliate account. You can find our
Speaker 3: good Reads list. You can find links to music by Bloodmobile.
Speaker 3: You can find all of the sources for each one
Speaker 3: of our episodes. You can find links to the promo
Speaker 3: codes that we mentioned in our ads, merch.
Speaker 1: We've got transcripts, We've got.
Speaker 2: Yeah, we got it all.
Speaker 3: That's got to be it.
Speaker 1: Yeah, okay, well then should we you know, let's get
Speaker 1: into it.
Speaker 3: Let's do it. Okay, we've hyped it enough, you think,
Speaker 3: I hope we haven't overhyped it.
Speaker 1: Oh, let's find out.
Speaker 4: Right after this break.
Speaker 1: Fair warning, listeners, I am starting off this biology section
Speaker 1: kind of intentionally withholding.
Speaker 2: Details for later dramatic effect. So let us begin.
Speaker 1: Mixamatosis is a disease caused by the Mixoma virus, which
Speaker 1: is a member of a family we are familiar with
Speaker 1: here on the podcast. It is a pox virus, as
Speaker 1: in smallpox. I don't think we've covered any other pox viruses.
Speaker 1: I was just gonna ask I can't remember. Oops, But anyways, Yeah,
Speaker 1: this is a different genus of poxvirus. This is a
Speaker 1: lay poroxy pox virus, and smallpoxes an orthopox pox virus
Speaker 1: if anyone cares.
Speaker 2: But all of the pox viruses are.
Speaker 1: Double stranded DNA viruses. They have pretty big genomes. And
Speaker 1: the virus itself, if you look at it under a microscope,
Speaker 1: is shaped like a brick, which I just think is
Speaker 1: funny that every single paper described it as.
Speaker 2: A brick shaped virus.
Speaker 4: Interesting it is, huh the poxvirus.
Speaker 1: Mixoma virus replicates in the cytoplasm of cells, and it's
Speaker 1: a really fascinating virus because it has a lot of
Speaker 1: proteins that interact with the host immune response. That become
Speaker 1: really important in terms of how much disease we actually
Speaker 1: see in its various hosts, and Mixoma virus causes disease.
Speaker 2: Only in rabbits.
Speaker 1: It infects a large number of species of rabbits, but
Speaker 1: as far as I can tell, it doesn't cause clinical
Speaker 1: disease in any of the other hosts that it has
Speaker 1: been tested in other than rabbits. And I think one
Speaker 1: species of hair yeah, which are all called lagomorphs. I
Speaker 1: learned so many new words researching this episode. But Mixima virus, interestingly,
Speaker 1: can replicate in vitro like in a petri dish or
Speaker 1: a cell culture bottle, in cells from many many different
Speaker 1: host species, including human cancer cells, which it turns out
Speaker 1: are particularly good at letting mixoma virus in and letting
Speaker 1: it replicate.
Speaker 3: Interesting.
Speaker 1: Very And I'm throwing that little tidbit out there and
Speaker 1: then just gonna leave it to dangle and circle back
Speaker 1: to it at.
Speaker 2: The very end of the episode.
Speaker 3: Okay, I was, I was all poised to ask a question,
Speaker 3: but I can tell you're strange.
Speaker 1: Okay, but today we're talking about rabbits. So this Mixoma
Speaker 1: virus causes the disease known as miximatosis in rabbits and hairs,
Speaker 1: and specifically, it causes the severe disease that we know
Speaker 1: of as miximatosis in the European rabbit Uricdologus cuniculus. If
Speaker 1: I'm saying that right.
Speaker 3: Do you remember the Book'spinicula. No, it was like about
Speaker 3: a vampiric rabbit that sucked the juices out of vegetables.
Speaker 2: I do not. I've never read that book.
Speaker 3: Really, it was like a series of books for kids.
Speaker 3: But I remember, like when I saw the scientific name
Speaker 3: of the European rabbit, I was like, Oh my gosh,
Speaker 3: that's where the that it comes from.
Speaker 1: That's very funny. I have not read those books. I'll
Speaker 1: put them on my Goodreads lists.
Speaker 3: They're wonderful.
Speaker 1: Okay, so let's go over what this disease looks like
Speaker 1: in this European rabbit. So the incubation period tends to
Speaker 1: be about four days and the initial symptoms. I'll kind
Speaker 1: of go over what this progression of disease looks like
Speaker 1: initially after that, about four days after infection, the symptoms
Speaker 1: are generally redness in the eyes, so kind of a
Speaker 1: conjunctival inflammation, and an elevated body temperature. What temperature are
Speaker 1: rabbits bodies normally, you.
Speaker 3: May ask, I would ask, yes, yeah, well I did
Speaker 3: google it.
Speaker 1: It's about one o two to one oh three fahrenheit,
Speaker 1: which is thirty eight point nine to thirty nine point
Speaker 1: four c. So they run a little hot. This virus
Speaker 1: makes them a little hotter. And then following after a
Speaker 1: few more days after initial infection, after these kind of
Speaker 1: red eye symptoms, these secondary lesions appear. They're often called
Speaker 1: cutaneous popular lesions. Basically just little lumps, little skin colored
Speaker 1: lumps on the rabbits that appear kind of throughout their body,
Speaker 1: but most prominently at the bases of their ears. They
Speaker 1: also get swelling in the anogenital region almost universally, and
Speaker 1: then they begin to have discharge, both kind of a
Speaker 1: clear like cirrus discharge as well as a mucopurulent or
Speaker 1: kind of pus filled discharge from the nose and the eyes.
Speaker 1: And then by days eight to ten, these poor little
Speaker 1: rabbits will have a very very swollen face, droopy ears
Speaker 1: because of all the swelling at the base of their ears.
Speaker 1: They'll have severely swollen eyelids and really goopy eyes, goopy
Speaker 1: noses that get so filled with gunk that their tiny
Speaker 1: little nasal passages get clogged, and then all across their body,
Speaker 1: like throughout their body, they'll have these little anywhere from
Speaker 1: a few millimeters to a few centimeters these little skin
Speaker 1: swellings across their body, and their anogenital region will become
Speaker 1: really really swollen, especially the testicles, and then their breathing
Speaker 1: will become more difficult and labored. They'll have this kind
Speaker 1: of stirter, which is that like gasping inhale. And they
Speaker 1: generally die between eight to twelve days following infection.
Speaker 3: And so that's like eight to twelve days after they
Speaker 3: first get exposed, so it's only like a period of four.
Speaker 4: To yeah, four to six days, wow, four.
Speaker 2: To eight days.
Speaker 1: Yeah, it's a very very rapid course of disease. And mixamatosis,
Speaker 1: this disease classically has an almost unbelievably high mortality rate
Speaker 1: in the European rabbit ninety nine point eight to one
Speaker 1: hundred percent mortality. This is along the lines of I
Speaker 1: think just rabies and preons are the only two diseases
Speaker 1: that match this kind of mortality that we've ever covered.
Speaker 3: Yeah, we yeah, that we've covered so far.
Speaker 2: Yeah. Yeah.
Speaker 1: And so the virus, this mixoma virus is present in
Speaker 1: all of those goopy secretions as well as in all
Speaker 1: of those skin lesions, and it's very easily transmitted to
Speaker 1: other rabbits, potentially by direct contact, but mostly by various
Speaker 1: biting arthropod vectors. But even though this is a virus
Speaker 1: that's transmitted by vectors like mosquitoes and lice or fleas,
Speaker 1: and especially in terms of epizootics or these outbreak scenarios.
Speaker 1: It does seem like vectors, especially mosquitoes, are pretty pivotal
Speaker 1: in terms of large scale transmission. Without them, these outbreaks
Speaker 1: don't really spread or don't spread us quickly. Oh yeah,
Speaker 1: but the virus does not rely on mosquitos for its
Speaker 1: life cycle or transmission. It doesn't infect or replicate in
Speaker 1: mosquitoes the way of most, if not, I think all
Speaker 1: of the vector born diseases that we've ever covered on
Speaker 1: this podcast do. What that means is that this vectoral
Speaker 1: transmission is just mechanical, right, which means that the virus
Speaker 1: has to be in very very high tighters in the
Speaker 1: cutaneous lesions, these skin lumps on the rabbits in order
Speaker 1: for the mosquito or the flea to have enough virus
Speaker 1: on its mouth parts to then transmit it to the
Speaker 1: next rabbit.
Speaker 2: Yeah.
Speaker 3: Do you know what the infectious doses like in rabbits?
Speaker 2: Yeah?
Speaker 1: I don't know exactly, but I do know that it
Speaker 1: seems like critical levels in the skin tissue are like
Speaker 1: ten to the seventh viral particles per gram of rabbit tissue,
Speaker 1: So that's like a little over ten million or so
Speaker 1: viral particles per gram, so really really high tighters are
Speaker 1: necessary for this to be efficiently transmitted.
Speaker 3: Okay, yeah, and I'm assuming also that the mosquito has
Speaker 3: to bite one of the lesions or like pick up
Speaker 3: and where the gunk.
Speaker 1: Is exactly yes, And that is why it's thought that
Speaker 1: especially those base of the ear swellings might be very
Speaker 1: important for viral transmission, because that's a commonplace for mosquitoes
Speaker 1: and other vectors to bite the rabbits. So, now, anyone
Speaker 1: who's listening who knows the story of mix andmatosis knows
Speaker 1: that that description that I just gave of this horrifying
Speaker 1: lethal disease of the European rabbit is not the whole story.
Speaker 1: So let me dive a little bit deeper. So, first off,
Speaker 1: Mixoma virus is still and was first a virus of
Speaker 1: a different rabbit species, entirely many different rabbit species, specifically
Speaker 1: the Silvie Lagis species rabbits endemic to South and North
Speaker 1: America and in the Americas.
Speaker 2: In these species of rabbits.
Speaker 1: Mixoma virus causes an entirely different disease, if you can
Speaker 1: even call it a disease, really, in American rabbits of
Speaker 1: the genus silvie lagis mixomavirus causes a single skin lump,
Speaker 1: a single mixoma and that's it.
Speaker 2: That's it, that's what it causes.
Speaker 1: At the sight of inoculation, you get one big cutaneous
Speaker 1: lump and that's it. So right off the bat here,
Speaker 1: this virus.
Speaker 2: Is getting interesting.
Speaker 1: Because we see this huge variation in disease between host
Speaker 1: species in terms of the pathogenicity of this same virus.
Speaker 2: So that's the first part of this story.
Speaker 1: But number two is what I know You're going to
Speaker 1: talk a lot more about aarin in the history section,
Speaker 1: but that is that Mixoma virus is virulence in the
Speaker 1: European rabbit dramatically changed over time, so this incredibly lethal
Speaker 1: version is not the only one which exists. And Okay,
Speaker 1: I don't want to step on your toes too much
Speaker 1: because I think that hearing this story in its entirety
Speaker 1: for the first time for most of our listeners is
Speaker 1: going to be so good. So at this point, let
Speaker 1: me ask you Erin, do you have any other questions
Speaker 1: about the transmission or details that you want to know
Speaker 1: about the path of physiology of this virus.
Speaker 3: Yes, okay, okay, So in the europe rabbit and these
Speaker 3: American rabbits, does the virus sort of enter in the
Speaker 3: same way and go through its normal replication cycle and
Speaker 3: move to the different parts of the skin or ears
Speaker 3: or whatever the body to replicate and cause lesions in
Speaker 3: the same way over the same time period. Where do
Speaker 3: the differences start to jump in?
Speaker 2: Great question?
Speaker 1: Okay, So this mixamma virus when it gets inoculated under
Speaker 1: the skin, either from a mosquito probe or a little
Speaker 1: flea mouth or a needle in a lab, the virus
Speaker 1: first infects the rabbits skin cells, their epidermal cells, or
Speaker 1: their dermal cells, and it quickly rises to pretty high
Speaker 1: tighters in those skin cells, in those lumps that appear.
Speaker 1: And then in addition to infecting the epidermal and dermal cells,
Speaker 1: this virus will go on to infect dendritic cells, which
Speaker 1: I think we've touched on a number of times on
Speaker 1: this podcast. But these are white blood cells that hang
Speaker 1: out in our skin and from there spread to our
Speaker 1: lymphatic system, and their goal is to present to other
Speaker 1: white blood cells these viral particles so that we can
Speaker 1: start to mount an immune response. But what happens with
Speaker 1: mixomavirus is it begins to replicate in these dendritic cells,
Speaker 1: and then when these dendritic cells spread to our lymph
Speaker 1: nodes or our bone marrow and our spleen, this virus
Speaker 1: is able to continue to replicate and infect other white
Speaker 1: blood cells. So this virus ends up being at very
Speaker 1: high concentrations in these skin lesions when they appear. And importantly,
Speaker 1: rabbits are not infectious until these skin lesions appear, but
Speaker 1: they also then have virus that spreads throughout their body,
Speaker 1: throughout their lymphatic system and is able to infect a
Speaker 1: number of different organs and potentially reach relatively high loads
Speaker 1: there as well. Now, to answer your question, Aaron, what's
Speaker 1: the difference between these different sentations the less virulent forms
Speaker 1: of maxoma virus and other similar laporoxypox viruses that are
Speaker 1: very closely related, some of which have been used to
Speaker 1: make vaccines against maxomavirus. One thing that they do differently
Speaker 1: is they're not as good at or in some cases,
Speaker 1: they can't at all infect those white blood cells. So
Speaker 1: what they cause is just a localized cutaneous infection causing
Speaker 1: localized cutaneous skin findings, but not causing systemic disease. Okay,
Speaker 1: and that seems to really make one big difference. So
Speaker 1: the virulence we know is at least in part related
Speaker 1: to how well this virus spreads beyond the epidermis and
Speaker 1: dermis and how well it invades and replicates within the
Speaker 1: lymphatic system and becomes a widespread infection.
Speaker 3: Gotcha. Okay, So then that kind of leads me into
Speaker 3: my next question, which is about immunity. So, as we'll
Speaker 3: talk about later on in this episode rabbits, the European
Speaker 3: rabbits that were exposed to mixematosis showed genetic resistance in
Speaker 3: later generations, and so they were able to be resistant
Speaker 3: to this virus separate, you know, from the virus's decreased virulence.
Speaker 3: That's a whole other part of the story or whatever.
Speaker 2: Yeah.
Speaker 3: Yeah, Basically these rabbits were able to resist getting infected.
Speaker 1: Yeah.
Speaker 3: Is the mechanism of resistance the same in the European
Speaker 3: rabbit as this sort of like, does it lead to
Speaker 3: the same reduced disease presence as we see in the
Speaker 3: American rabbits.
Speaker 1: Great questionnairein so the other part of the path of
Speaker 1: physiology of this virus is that mix omavirus mix oma
Speaker 1: viruses all of the different strains have a whole bunch,
Speaker 1: like more than I could possibly list in this podcast
Speaker 1: of proteins that regulate the host immune system in a
Speaker 1: way that facilitates infection. So they have these proteins that,
Speaker 1: for example, inhibit pro apoptotic molecules. What that means apoptosis
Speaker 1: is programmed cell death. That's one of the ways that
Speaker 1: animals immune systems have of targeting and fighting off viruses
Speaker 1: by identifying and killing virally infected cells. Right, while mixomavirus
Speaker 1: has a whole bunch of proteins that it creates specifically
Speaker 1: to prevent that process from happening in a number of
Speaker 1: different ways. They also have other proteins that help to
Speaker 1: interfere with the coordination and recruitment of leukocytes of white
Speaker 1: blood cells, basically down regulating that white blood cell response
Speaker 1: to infections. They have other proteins that block the presentation
Speaker 1: of anogens by those, for example, dendritic cells and other
Speaker 1: anigen presenting cells, so that they block these rabbits ability
Speaker 1: to make antibodies or even recognize the viral antigens. So
Speaker 1: Maxoma virus has a whole host of different mechanisms that
Speaker 1: affect a rabbit's immune response to infection that are really
Speaker 1: important in how much that rabbit is going to be
Speaker 1: able to resist or be susceptible to severe infection.
Speaker 2: So, to answer your questionarin.
Speaker 1: This, it seems like a lot of these specific proteins
Speaker 1: and mechanisms that the Maxoma virus has evolved in the
Speaker 1: American rabbits and are kind of perfectly suited in those
Speaker 1: rabbits to reduce the immune response to.
Speaker 2: A degree that allows for.
Speaker 1: The establishment of an infection but does not impair the
Speaker 1: rabbit's ability to survive and thrive, but also allows the
Speaker 1: establishment of an infection that's actually infectious, right, that has
Speaker 1: high enough tighters in the skin so that this virus
Speaker 1: can be transmitted.
Speaker 3: Okay, So it's like being able to tolerate and coexist
Speaker 3: exactly with Okay.
Speaker 1: Yeah, And so it's thought that then when those same
Speaker 1: kind of proteins were introduced to the European rabbit, like
Speaker 1: that is what allowed for this establishment of a very
Speaker 1: severe infection because of the difference in their immune response
Speaker 1: and how these proteins interacted with that immune response.
Speaker 2: And so, yes, that's one.
Speaker 1: Of the things that tends to change over time.
Speaker 2: As rabbits evolve resistance.
Speaker 3: Oh, it's really interesting.
Speaker 2: I love it. I love it so much. I can't like,
Speaker 2: I get so excited.
Speaker 3: I think this. I swear this is my last one.
Speaker 3: But I was just thinking about it. So, in these
Speaker 3: rabbits that are resistant in some way to Maxima virus,
Speaker 3: whether it's like the American rabbits that you just have
Speaker 3: the skin lesions, et cetera, how long does the virus
Speaker 3: persist in those hosts.
Speaker 1: Oh, that's such a good question, and it's a really
Speaker 1: important part of the story as well. I don't know
Speaker 1: is the short answer to it. And I think it
Speaker 1: depends a lot on what species you're talking about and
Speaker 1: also what strain of the virus you're talking about. But
Speaker 1: it does tend to be the case that, for example,
Speaker 1: in American rabbits, they can have these lesions that persist
Speaker 1: for a really long time. These cutaneous lesions can potentially
Speaker 1: persist for weeks, if not months, but again they don't
Speaker 1: cause any systemic illness. In more resistant European rabbit populations
Speaker 1: or with less virulent virus strains, you can sometimes just
Speaker 1: see a prolonged illness where it lasts maybe fifteen twenty
Speaker 1: thirty days instead of like eight to twelve days. So
Speaker 1: it is variable between species and between strains of virus,
Speaker 1: but it is an important part of the story.
Speaker 3: Yeah.
Speaker 1: Yeah, So yeah, that's I mean, that's an example virus
Speaker 1: Aaron interesting, It's I think there's more to the story.
Speaker 2: I mean, there's a lot more to the story. So
Speaker 2: so can you can you tell us the story?
Speaker 3: I will if I think of more questions along the way,
Speaker 3: I'm gonna ask you.
Speaker 2: Oh good, sounds great, Okay.
Speaker 3: Let me let's take a break and then we'll dive
Speaker 3: into the history of this virus and the European rabbit
Speaker 3: in Australia. The story of rabbits in Australia, not just
Speaker 3: their arrival and spread, but also mix Oma virus and
Speaker 3: then later attempts at biocontrol. It might be one of
Speaker 3: my favorite topics that we've ever covered on this podcast ever.
Speaker 1: Yeah, I mean, we've been talking about doing this, and
Speaker 1: I've been wanting to do it for a very long time.
Speaker 2: So I am really excited.
Speaker 3: I am too because and it's like I said earlier
Speaker 3: on this this is such an incredible story because it
Speaker 3: covers so many different themes, right, Like you could learn
Speaker 3: about it in a veterinary class. You could learn about
Speaker 3: it an ecology class, an evolution class, a virology class,
Speaker 3: an economics class, a pest management class, history class, like
Speaker 3: so many different There are so many different angles to this,
Speaker 3: but I think it's also really fascinating when you put
Speaker 3: them all together and can consider just the full picture
Speaker 3: of this story. So yeah, it's about, you know, not
Speaker 3: just how life finds a way it Also it also
Speaker 3: makes us think about why we choose to use the
Speaker 3: words invasive or pests to describe one species but not another,
Speaker 3: and how those labels or the things defining those labels,
Speaker 3: how they shift over time. I could honestly go on
Speaker 3: and on about how excited I am and all the
Speaker 3: lessons that we're going to learn from the story, but like,
Speaker 3: maybe I should just get to the story itself and
Speaker 3: then we can, you know, discuss the lessons as we go.
Speaker 2: Yeah.
Speaker 3: Okay, So the long and short of it is that
Speaker 3: rabbits were introduced to Australia, They bred like crazy, destroyed
Speaker 3: heaps of vegetation, and eventually the mix Oma virus was
Speaker 3: introduced as a method of controlling rabbit populations.
Speaker 2: All right, So that's the short version.
Speaker 3: That's the short version. Let's go to the long version.
Speaker 3: To do that, we have to go to seventeen eighty.
Speaker 3: This is where the story really begins, because that year
Speaker 3: the first Fleet brought the first European settlers to Australia,
Speaker 3: along with food, tools, agricultural equipment, seeds, alcohol, medical supplies,
Speaker 3: and a few rabbits.
Speaker 2: Just a few, just a few.
Speaker 3: And these are not the rabbits that we need to
Speaker 3: worry about. There's no record specifically describing what happened to
Speaker 3: these First Fleet rabbits, but they were likely domesticated rabbits,
Speaker 3: and if there were any attempts to introduce them into
Speaker 3: the wild, they probably weren't successful. And the same could
Speaker 3: be said more or less for the domesticated rabbits that
Speaker 3: were brought to Australia in the decades after the First
Speaker 3: Fleet's arrival, That is, until eighteen fifty nine. That year
Speaker 3: everything changed. A farmer by the name of Thomas Austen
Speaker 3: got it into his head that hunting wild rabbits on
Speaker 3: his farm would be real, the super fun like, not
Speaker 3: the lame domestic rabbits that were kept in hutches like
Speaker 3: those aren't those aren't fun? To hunt. You want the
Speaker 3: wild ones, and he wanted the wild ones from his
Speaker 3: homeland of England, so he had his brother, who was
Speaker 3: living in Liverpool, send over two dozen wild European rabbits.
Speaker 3: It seems that only thirteen rabbits survived the journey from
Speaker 3: what I gather, But when they got to Austin's farm
Speaker 3: near Geelong in South Victoria, they were let go free
Speaker 3: to breed so that the farm would be stocked with
Speaker 3: nice wild rabbits to hunt. Oh gosh, and since rabbits
Speaker 3: breed like rabbits, that's exactly what they did. So it's
Speaker 3: estimated that one female rabbit produces about seven litters a year,
Speaker 3: with an average of four to six bunnies in each litter.
Speaker 3: So let's say between thirty to forty per year one
Speaker 3: rabbitsh whoa, one rabbit whoa, and by the end of
Speaker 3: a breeding season, those kittens Because did you know that
Speaker 3: baby rabbits are actually called kittens.
Speaker 1: I learned that and it's one of my favorite things
Speaker 1: that I learned while researching this episode.
Speaker 3: It cracks me up. I'm like, wait a second, my
Speaker 3: whole life. No, not bunnies, kittens, kittens, It's not in
Speaker 3: any of the children's books, No, at least not the
Speaker 3: ones I read. Yeah, so these but the kittens that
Speaker 3: were produced in the early in the breeding season, by
Speaker 3: the end of that same breeding season were sexually mature
Speaker 3: and breeding themselves. Oh no, so yeah, a lot of
Speaker 3: rabbits like from thirteen to who knows within one year, right,
Speaker 3: and then you could just see the growth curve on
Speaker 3: that right. Yeah, exponentch exponentch for sure. And also the
Speaker 3: change and environment from England to Australia like those are
Speaker 3: you know, they're pretty different in climates and environments. It
Speaker 3: didn't them down at all, because actually the European rabbit
Speaker 3: is thought to have evolved in the Iberian Peninsula and
Speaker 3: southern France in a Mediterranean climate.
Speaker 2: Yeah.
Speaker 3: Side note, did you know that Spain or Hispania, the
Speaker 3: name may have come from the Phoenician word meaning island
Speaker 3: of rabbits?
Speaker 2: No I did not.
Speaker 3: There's a lot of different proposed explanations for the etymology
Speaker 3: of Spain, but that's one of them. I love it anyway.
Speaker 3: So these rabbits were doing quite well on Austin's farm
Speaker 3: and off of it by eighteen sixty five, six years
Speaker 3: after those thirteen rabbits arrived. Six years Austin wrote that
Speaker 3: he had killed twenty thousand rabbits off his estate, oh
Speaker 3: my god, and that ten thousand still remained in the
Speaker 3: next year's hunt. So this is seven years after their arrival.
Speaker 3: He reported over fourteen thousand rabbits killed.
Speaker 2: Oh my god.
Speaker 3: The next year, eighteen sixty seven, Prince Alfred, son of
Speaker 3: Queen Victoria, killed over four hundred in a three hour
Speaker 3: hunting session. Oh my. And it wasn't stopped because there
Speaker 3: were no more rabbits left. It was too hot. Four
Speaker 3: hundred and three hours.
Speaker 2: I'm sorry. Okay, I have a lot of thoughts.
Speaker 3: I know, the scale of this is really kind of
Speaker 3: hard I think to comprehend. Yeah it Yeah, and Austin
Speaker 3: the farmer definitely helped along the spread of the rabbits,
Speaker 3: or at least likely by introducing them to new areas
Speaker 3: and other people coming in and being like, I want
Speaker 3: rabbits too, this is hunting is really fun. But honestly,
Speaker 3: the rabbits didn't need that much help, and it's not
Speaker 3: like anyone was actively trying to prevent their spread. Instead,
Speaker 3: the arrival of the rabbits was seen as something to
Speaker 3: be celebrated.
Speaker 2: Oh, I know we.
Speaker 3: Can look back at that now and be completely horrified
Speaker 3: because we know how this story plays out, and how
Speaker 3: so many other introduced species stories play out. But let's
Speaker 3: consider the historical context.
Speaker 2: As we always do it. I'll kill you.
Speaker 3: When Thomas Austin imported and released those rabbits, it was
Speaker 3: during the period of large scale colonialism that was taking
Speaker 3: place around the globe from around the fifteen hundreds into
Speaker 3: the early nineteen hundreds, and during that time it was
Speaker 3: a really common practice for colonizers to bring with them
Speaker 3: things that reminded them of home, or things that they
Speaker 3: used to eat or farm, basically anything they thought would
Speaker 3: make their new life easier or more pleasant. Colonialism is
Speaker 3: how so many different species traveled to new places, both
Speaker 3: intentionally or unintentionally, rats, cats, foxes, starlings, so many species
Speaker 3: of plants, pathogens I mean like everything, everything, And the
Speaker 3: worldview that was imposed on the places being colonized was
Speaker 3: the one commonly held by most European or American colonizers
Speaker 3: at the time. That plants and animals were put on
Speaker 3: this earth for humans to eat, or to use for work,
Speaker 3: or to simply enjoy. Biodiversity and the interconnectedness of species
Speaker 3: in an ecosystem. These things weren't really considered by the
Speaker 3: colonizers or even known about. A species' importance was defined
Speaker 3: by how it could be used for humans, the benefit
Speaker 3: that it gave two humans, not its ecological role. Those concepts,
Speaker 3: like the interconnectedness of all the organisms in an ecosystem
Speaker 3: and just how interdependent they were, those may have been
Speaker 3: held by some people, or at least like recognized a
Speaker 3: little bit by some people and some cultures, but they
Speaker 3: were still decades away from being widespread. Ecology as a
Speaker 3: field of study didn't really even get started until the
Speaker 3: nineteen twenties, and the notion that biodie diversity was important
Speaker 3: was even further in the future. And even if someone
Speaker 3: did hold those views back then, they probably weren't in
Speaker 3: a position to argue against those who were in power
Speaker 3: making these decisions. Because introductions of non native species like
Speaker 3: the European rabbit to Australia they were just done casually
Speaker 3: by a few plant or animal enthusiasts. They were encouraged,
Speaker 3: sometimes to the point of being included as a government directive.
Speaker 3: Yes for instance, legislation from New Zealand in eighteen sixty
Speaker 3: one was passed quote to encourage the importation of these
Speaker 3: animals and birds not native to New Zealand, which would
Speaker 3: contribute to the pleasure and profit of the inhabitants when
Speaker 3: they became acclimatized and spread over the country in sufficient numbers.
Speaker 2: Oh my god, Oh my god. It's giving me palpitations.
Speaker 3: I know, I know, I know. It just they there
Speaker 3: just wasn't the knowledge of Yeah.
Speaker 1: It's so hard to hear that though, to go back
Speaker 1: and be like, oh my god, you intentionally ruined the world.
Speaker 2: I mean, we've been doing it for so long.
Speaker 3: But I was gonna say so so many stories like yeah, yeah, yeah,
Speaker 3: And so all of this is just to say that
Speaker 3: if Thomas Austen hadn't brought over the rabbits when he did,
Speaker 3: it was probably just a matter of time before somebody
Speaker 3: else did. Yeah.
Speaker 1: Yeah.
Speaker 3: Just as certain species were valued for their potential for
Speaker 3: profit or enjoyment by humans, others were seen as hurting
Speaker 3: humans or human interests pest species, and this term is
Speaker 3: still plenty in use today, typically in an agricultural context,
Speaker 3: and it's separate from terms used to describe a species origin,
Speaker 3: like native or non native slash introduced, which refers to
Speaker 3: where a species evolved, or the term invasive, which disc
Speaker 3: vibes of species that's been introduced and is detrimental to
Speaker 3: the native species in an area. So a pest species
Speaker 3: can be native or invasive. And there are a lot
Speaker 3: more terms dealing with these concepts, but I don't want
Speaker 3: to overwhelm with terminology and definitions. But this concept of
Speaker 3: pest species is entirely defined by the meaning to humans
Speaker 3: for the most part, and it has origins all the
Speaker 3: way back to the agricultural Revolution ten to twelve thousand
Speaker 3: years ago, when people began to interact more with the
Speaker 3: plants and animals that disrupted their crop yields or their
Speaker 3: livestock numbers, and that gave rise to this term pest
Speaker 3: from the Latin pestis for plague, and people devised ways
Speaker 3: to deter those pest species like scarecrows, manual removal, fences, poisoning,
Speaker 3: hunting and trapping, introduction of animals to control them, et cetera.
Speaker 3: Some species may have been considered pests almost universally or
Speaker 3: at least wherever they were found, like mosquitoes, but for
Speaker 3: many others, the label of a species as pest depended
Speaker 3: on who you asked. Yeah, for instance, wolves and sheep,
Speaker 3: So if you're a sheep farmer, you may consider wolves
Speaker 3: to be a pest species because they sometimes eat your sheep.
Speaker 3: But for other people, sheep are the real pests, changing
Speaker 3: an ecosystem with their grazing, reducing habitat for other species.
Speaker 3: Over time, the concept of pest species changed. It expanded
Speaker 3: to include things like pathogenic microorganisms and parasites and arthropods
Speaker 3: that carried disease, and it also shifted as our understanding
Speaker 3: of ecology and biodiversity grew, and so species that were
Speaker 3: once viewed as pests lost that label as their importance
Speaker 3: to an ecosystem was recognized, and others that were once
Speaker 3: highly valued earned the pest label, and then some as
Speaker 3: they wreaked havoc on the landscape, like rabbits in Australia.
Speaker 3: Rabbits in Australia, and the switch from valued animal to
Speaker 3: dangerous pests for rabbits in Australia was sudden and nearly complete. Wow,
Speaker 3: these guys are we need them gone. In the first
Speaker 3: few years after their arrival in eighteen fifty nine, people
Speaker 3: were thrilled. Like I said, Hunting them was forbidden for
Speaker 3: several months out of the year to try to protect
Speaker 3: their numbers.
Speaker 2: Oh my, oh my.
Speaker 3: And one man was fined ten pounds for killing a
Speaker 3: rabbit on someone's property.
Speaker 2: Oh my gosh.
Speaker 3: But within ten years of their introduction, their rapids spread
Speaker 3: at hundreds of kilometers a year, and enormous population explosion
Speaker 3: was looked on. Was looked at in absolute horror. As
Speaker 3: the rabbit spread, they consumed any vegetation visible, whether it
Speaker 3: was grass or shrubs or the bark of a tree,
Speaker 3: leaving almost nothing left for the prized sheep that many
Speaker 3: people farmed, let alone than native animal species. Millions of
Speaker 3: acres in land were forfeited in the late eighteen hundreds
Speaker 3: because they had been rendered useless by rabbits. Wow. And
Speaker 3: remember that guy who was fined ten pounds for killing
Speaker 3: a rabbit. A few years after that, his son was
Speaker 3: spending five thousand pounds a year to try to control
Speaker 3: the rabbits on his land.
Speaker 2: That's so sad.
Speaker 3: Yeah. And there was also legislation that was introduced in
Speaker 3: the eighteen eighties requiring all farmers to control the rabbit populations,
Speaker 3: and if they didn't, they would be fined Wow.
Speaker 2: Yeah.
Speaker 3: As rabbits spread even into areas that people had said,
Speaker 3: you know, oh, there's no way they can survive here.
Speaker 3: This is surely is not suitable land for rabbits, people
Speaker 3: began to realize that physical barriers might be needed, some
Speaker 3: stronger efforts that might need to take place. In the
Speaker 3: early nineteen hundreds, construction began on a giant rabbit proof
Speaker 3: fence in Western Australia, and when fence number one was
Speaker 3: completed in nineteen oh seven, it was the longest continuous
Speaker 3: fence in the world. Wow. It was eighteen one hundred
Speaker 3: and thirty three kilometers or eleven hundred and thirty nine miles.
Speaker 4: Wow.
Speaker 3: Yeah, over a thousand.
Speaker 2: It's a lot and supposedly rabbit proof.
Speaker 1: Huh uh huh, Well.
Speaker 3: No, maybe not so much. Later it was I think
Speaker 3: named the Emu Fence, and it did seem to have
Speaker 3: some effect in other pest species quote unquote, but rabbits
Speaker 3: not so much. When it was constructed, it seems that
Speaker 3: rabbits could be found on both sides of the fence,
Speaker 3: and a fence that long it would have been really difficult,
Speaker 3: if not impossible, to maintain effectively. Yeah. There were two
Speaker 3: other rabbit proof fences that were constructed around the same time,
Speaker 3: and it brought the total length of fencing to over
Speaker 3: thirty two hundred kilometers or two thousand miles, so a
Speaker 3: pretty substantial effort. But fences weren't the only thing that
Speaker 3: people were trying to use to control rabbit populations. Poisons,
Speaker 3: especially strychnine and arsenic which would be two potential great
Speaker 3: topics for future episodes.
Speaker 2: Yep, they would be.
Speaker 3: They were a popular choice, as was ripping, which was
Speaker 3: the term used for tearing up the large underground burrows
Speaker 3: or warrens that the rabbits were living in. This is
Speaker 3: one of the only species, it seems, that creates these
Speaker 3: large family warrens or burrows, which is actually really important
Speaker 3: to the transmission of mix andmatosis. Also, predators were introduced,
Speaker 3: like foxes and cats to other sometimes invasive species, but
Speaker 3: nothing seemed to put a dent in the rapid expansion
Speaker 3: of rabbit. So let's talk about some of the characteristics
Speaker 3: of these rabbits that made them so successful at establishing okay,
Speaker 3: And it's really a mixture of both rabbits themselves and
Speaker 3: the Australia they entered into in eighteen fifty nine. So
Speaker 3: first I already mentioned what efficient breeders rabbits are off
Speaker 3: the charts. Second, many of the places in southern Australia
Speaker 3: they first moved to were similar in climate to the
Speaker 3: places they evolved. I mentioned that as well. Third, they
Speaker 3: can move surprisingly long distances just individual rabbits, but also
Speaker 3: allowing for the spread. Fourth, when they were brought over,
Speaker 3: they left most of their pathogens and parasites behind, and
Speaker 3: there didn't seem to be any in Australia that could
Speaker 3: affect them, so what we call parasite escape.
Speaker 1: It's always the case with invasive species.
Speaker 3: It often is. Yet and then there was also predator escape,
Speaker 3: which is something that happens also a lot with other
Speaker 3: invasives species. So for decades, many farmers had been poisoning
Speaker 3: dingoes and other native predators who were considered pests because
Speaker 3: of livestock at that time, and so rabbits entered into
Speaker 3: this low predator environment, And it also might have taken
Speaker 3: some time overall for predators to even recognize the rabbits
Speaker 3: as potential prey. Number six, there were already lots of
Speaker 3: burrows dug by batongs, bilbi's and wombats that.
Speaker 2: Sorry, what's a batongue?
Speaker 1: And what's bill b I know what a wombat is.
Speaker 3: My words alone can't do it justice. They are adorable,
Speaker 3: small mammals. You should look them up. I can't. I
Speaker 3: was like, these are new mammals I've never heard of.
Speaker 2: There.
Speaker 1: I feel like Australia has a lot of mammals I've
Speaker 1: never heard of. Oh my gosh, I love them.
Speaker 3: So we just took a break so that Aaron could
Speaker 3: look up batongs and bilbie's and I recommend that you
Speaker 3: do the same because they're adorable. They're adorable.
Speaker 1: Okay, getting back to it. So the bilbi's and the
Speaker 1: batongs built these burrows.
Speaker 3: These burrows, and so then when the rabbits came in,
Speaker 3: they were like, oh, sweet, free real estate. We're just
Speaker 3: going to move right in.
Speaker 2: And that was that.
Speaker 3: And number seven human mediated changes to the landscape like
Speaker 3: clear cutting of trees and the promotion of pasture lands
Speaker 3: is also paved the way for rabbits. And there's just
Speaker 3: the fact that it was like I already said this
Speaker 3: attitude of oh, we can't wait to have these rabbits.
Speaker 3: Let's promote their growth anything that you know, we want
Speaker 3: to have here to make our lives better is going
Speaker 3: to be great.
Speaker 2: Yeah. Yeah.
Speaker 3: And so all of these factors combined meant that by
Speaker 3: the time people recognized there might be a problem, it
Speaker 3: was already way too late. Yeah. I want to read
Speaker 3: another quote about rabbit population growth in Australia from the
Speaker 3: time quote. Rabbits overran the town in search of water.
Speaker 3: They ate the gardens and burrowed under the houses. Shopkeepers
Speaker 3: had to wiren at their premises. The servants at the
Speaker 3: hotels brushed them off the steps. The inspector of stock
Speaker 3: hunted two or three from under his bed each morning.
Speaker 3: School children killed so many on the way to and
Speaker 3: from school that the mayor had to employ a man
Speaker 3: with a cart to gather them up. Oh, what it's like.
Speaker 3: It is still hard for me to imagine it is.
Speaker 2: It's unimaginable.
Speaker 1: I can't picture that many little bun buns m m.
Speaker 3: But also not everyone saw rabbits as this threatening menace.
Speaker 3: They were also seen as an opportunity. The profession of
Speaker 3: rabbiter sprung up when bonuses were introduced for rabbit scalps
Speaker 3: starting in the late eighteen hundreds, and rabbits did pretty
Speaker 3: well into the nineteen hundreds. Even after this bonus system
Speaker 3: was scrapped, in the first few decades of the twentieth century,
Speaker 3: upwards of a million rabbits were killed each year and
Speaker 3: canned for food to be sent to soldiers fighting in
Speaker 3: World War One and World War II. Okay, although the
Speaker 3: rabbit industry certainly was raking in some money, the cost
Speaker 3: of lost farmland and sheep grazing areas it vastly outweighed
Speaker 3: that some and in the late eighteen hundreds, the governments
Speaker 3: of Australia and New Zealand, where rabbits had also been introduced,
Speaker 3: decided to search for a solution. On April twenty sixth,
Speaker 3: eighteen eighty eight, these governments got together to establish the
Speaker 3: Royal Commission of Inquiry into Schemes for Extermination of Rabbits
Speaker 3: in Australasia oh wow aka the Intercolonial Rabbit Commission. The
Speaker 3: goal of this commission was to quote make a full
Speaker 3: and diligent inquiry as to whether or not the introduction
Speaker 3: of contagious diseases amongst rabbits for promoting their destruction, will
Speaker 3: be accompanied by dangers to human health or to animal
Speaker 3: life other than rabbits. Pretty interesting, yeah. They offered a
Speaker 3: twenty five thousand pounds award, which in nineteen ninety eight
Speaker 3: in Australian dollars because that's when the book I read
Speaker 3: was from was about two million Australian dollars, so that's
Speaker 3: quite a big reward. Yeah, yeah, the Elmer Fudd reward.
Speaker 2: That's funny.
Speaker 3: Thank you. He sounds so surprised.
Speaker 2: I forgot about Elmer Fudd.
Speaker 3: So yeah, anyone who could come up with a successful
Speaker 3: and feasible strategy for the destruction of rabbits would get
Speaker 3: this money. Hundreds of people from all over the world
Speaker 3: wrote in with their different suggestions on how to kill
Speaker 3: the rabbits. One of these people was none other than
Speaker 3: Louis Pasture.
Speaker 2: Actually, I did think, I think I saw that.
Speaker 3: So exciting, and he suggested at chicken colera virus, but
Speaker 3: no one, including Pasture, took home the prize. He was
Speaker 3: really angry about it. He was like, my solution is
Speaker 3: the best. This is discrimination against the French because the
Speaker 3: people who were judging were Germans and they have this competition.
Speaker 3: Well it was like, oh, over the top for sure,
Speaker 3: but also his chicken cholera wasn't that deadly to rabbits?
Speaker 3: Didn't seem to be super transmissible, and it wasn't restricted
Speaker 3: to rabbits, so like he shouldn't have gotten the prize.
Speaker 2: No, it's not a great option, sorry.
Speaker 3: Louis, but it was really fascinating to me to read
Speaker 3: about this introduction of this idea, the concept of you
Speaker 3: using an infectious disease as a method of control. It
Speaker 3: seemed so early. Yeah, but actually people have been trying
Speaker 3: to use other organisms to control pest species for a
Speaker 3: long time. It's mostly been through the introduction of predators
Speaker 3: like cats and mongooses, and after germ theory, some pathogens
Speaker 3: as well. And there are many potential benefits to biological
Speaker 3: control methods over traditional methods of control. For instance, they
Speaker 3: can be highly specific to just the target species, unlike poisons.
Speaker 3: They are often the only practical means for control if
Speaker 3: the species is already established in a large area and
Speaker 3: over diverse habitat. They can be self perpetuating and the
Speaker 3: cost benefit is low. Right, you just cook up some
Speaker 3: incubate some virus, and release it.
Speaker 2: Let's see what happens, and see what happens.
Speaker 3: Yeah, but there are also risks. So we now know
Speaker 3: that biological methods of control are rarely effective, or if
Speaker 3: they are, it isn't for very long. They are self perpetuating,
Speaker 3: which means difficult to control. You kind of just let
Speaker 3: them loose, and there are often unf foreseen consequences which
Speaker 3: can lead to ecological cascades that have enormous long term
Speaker 3: impacts on an ecosystem.
Speaker 2: Yeah.
Speaker 3: So it's like, while biological control methods can potentially solve problems,
Speaker 3: they can also create new ones. For example, mongooses. This
Speaker 3: is like a classic example. Right throughout the second half
Speaker 3: of the eighteen hundreds, they were introduced to many islands
Speaker 3: in the Caribbean as well as Hawaii to try to
Speaker 3: control rats in the sugar cane, which were also invasive.
Speaker 3: But instead they just ate iguanas and ground nesting birds
Speaker 3: and snakes and cause enormous population declines and some extinctions,
Speaker 3: and that led to a lot of indirect effects and
Speaker 3: ecological cascades. Yep, yeah, I mean you can just there
Speaker 3: are so many examples of biological control gone wrong.
Speaker 2: Oh yeah, look at all of Hawaii.
Speaker 3: Yeah, any island at all pretty much is really susceptible
Speaker 3: to these types of ecological collapses caused by an introduced Yeah. Okay,
Speaker 3: but since this is the classic story of biocontrol gone
Speaker 3: mostly right. I would say, I think it's about time
Speaker 3: that we meet the Mixoma virus in this part of
Speaker 3: the story. So, the Mixoma virus was first observed in
Speaker 3: eighteen ninety eight by an infectious disease researcher named doctor
Speaker 3: Giuseppe Sanarelli in Uruguay. It's one of the very first
Speaker 3: viruses described, coming shortly after the word virus was used
Speaker 3: to describe the filterable transmissible agent causing tobacco mosaic disease,
Speaker 3: which is all which is what we always learn as
Speaker 3: the first virus.
Speaker 1: Right.
Speaker 3: Yeah. Sanarelli had imported some lab rabbits from Brazil to
Speaker 3: run some experiments, and some of them became super sick,
Speaker 3: with swollen eyes and ears and faces, and he decided
Speaker 3: to name this disease miximatosis maxa, from the Greek word
Speaker 3: for mucus and oma for tumor, tumor mucus mucus tumor.
Speaker 3: This disease seemed especially deadly to the European rabbits in
Speaker 3: the lab, but not the ones native to South America,
Speaker 3: and for about ten years after Sanarelli published his findings,
Speaker 3: there was pretty much just like silence on the mixmatosis front.
Speaker 3: But then interest picked up. Other researchers, of course, grew interested,
Speaker 3: and over time we learned a lot more about the virus,
Speaker 3: the role of arthropod vectors in its transmission, the reservoirs
Speaker 3: of the virus in North and South America, how immunity worked,
Speaker 3: how specific its host range was, and importantly, how lethal
Speaker 3: the virus was in some species, like the European rabbit,
Speaker 3: but not others.
Speaker 2: Yeah.
Speaker 3: One of the people who became interested in this rabbit
Speaker 3: disease was a Brazilian researcher named doctor Hanrique Aragau, who
Speaker 3: spent his career at the Oswaldo Cruz Institute. Think back
Speaker 3: to our Shagas episode. Yeah, Aragao had worked unidentifying the
Speaker 3: reservoir of Maxoma virus in South America and also the
Speaker 3: role of arthropod vectors, and he was so impressed with
Speaker 3: the virus's ability to cause disease that in nineteen eighteen
Speaker 3: he wrote to the Australian government saying, you should use
Speaker 3: this virus as a control strategy for your rabbit problem. Wow,
Speaker 3: which by then the rabbit problem was like internationally famous.
Speaker 2: Yeah.
Speaker 3: His suggestion was considered and then dismissed, mostly on the
Speaker 3: grounds that not enough research had been done to determine
Speaker 3: whether it would be effective or whether the virus could
Speaker 3: be dangerous to humans or other animals. Okay, but while
Speaker 3: it got the official no at first, the idea wasn't
Speaker 3: entirely dropped, especially since some people were just getting so
Speaker 3: desperate for anything to work, and so in nineteen twenty
Speaker 3: seven a series of experiments were carried out to see
Speaker 3: how transmissible and how specific it was. Could this actually
Speaker 3: be something we could use? The results weren't encouraging. Basically,
Speaker 3: it didn't seem like it would spread among rabbits easily,
Speaker 3: and even if it did, it was likely to result
Speaker 3: in a situation where rabbits would evolve resistance or tolerance
Speaker 3: and the virus would decrease in virulence, and researchers still
Speaker 3: couldn't be sure that it wouldn't spread to the native
Speaker 3: animal species or humans and cause a huge catastrophe. All
Speaker 3: fair points, and the idea was shelved yet again, And
Speaker 3: that could have been the last time that we ever
Speaker 3: heard about miximatosis if doctor Gen McNamara hadn't come across
Speaker 3: the idea totally independently from doctor Ericau. Doctor McNamara was
Speaker 3: a pediatrician from Australia who in nineteen thirty three was
Speaker 3: awarded a fellowship to study polio in New York. While there,
Speaker 3: she visited the lab of doctor Richard Schope, whose name
Speaker 3: may sound familiar from our HPV episode. He discovered the
Speaker 3: chop papolloma virus that had given rise to the jacalobe
Speaker 3: myth and was one of the first people to link
Speaker 3: viruses to causing cancer jacalobes. Okay, yeah, but at the
Speaker 3: time of McNamara's visit, Shope was working on a vaccine
Speaker 3: against maxoma virus using the immunologically related fibromavirus. He showed
Speaker 3: McNamara the rabbits that were infected with maxoma, and when
Speaker 3: she saw how lethal it was, she was like, uh,
Speaker 3: this could be useful. So she wrote home to her
Speaker 3: family quote, I had a lovely day out at Princeton
Speaker 3: the branch of Animal and Plant pathology. There is a
Speaker 3: man there I would love to take home to work
Speaker 3: on her animal diseases. Shop is his name, and he
Speaker 3: has something which kills rabbits, though he has not tried ours.
Speaker 3: I'm going to send some to Ivan to give him
Speaker 3: the chance to become famous by killing off the rabbits.
Speaker 3: I love that, and so she sent some samples of
Speaker 3: the Maxoma virus. They were destroyed upon arrival because things
Speaker 3: had been ramped up a little bit more seriously at like,
Speaker 3: you know, let's not introduce species gential pathogens. But nevertheless,
Speaker 3: she persisted and eventually convinced the Australian government to set
Speaker 3: up some experiments, commissioning doctor Charles Martin and Cambridge to
Speaker 3: examine the virus' potential. Martin's experiments showed more promise than
Speaker 3: the nineteen twenty seven ones, but there was still a
Speaker 3: great deal of hesitation to introduce it to Australia, not
Speaker 3: just on the grounds that it might not work, but
Speaker 3: that if it did work, there might be unintended consequences.
Speaker 3: But just like last time, more field experiments were set up,
Speaker 3: and just like last time, they weren't overwhelmingly successful. And
Speaker 3: maybe that really would have been the end of it.
Speaker 3: But the landscape, which was already drastically altered by years
Speaker 3: of rabbit population growth, it had grown even more rabbit
Speaker 3: infested during World War II, when so many people left
Speaker 3: to fight in the war rabbit control on some of
Speaker 3: these farms like slipped, like there was no way. You
Speaker 3: just didn't have the human power to control the rabbit populations.
Speaker 3: And so by the end of the nineteen forties people
Speaker 3: were desperate for something to reduce rabbit numbers. And McNamara
Speaker 3: was like, Okay, I'm going to say it again, mix thematosis.
Speaker 3: The last field trials were wrong, they were done in
Speaker 3: the wrong place, there were no mosquitoes there. You need
Speaker 3: to do it again. And it turns out that the
Speaker 3: fourth or the fifth or whatever time it was, I've
Speaker 3: lost count. This time was the charm.
Speaker 2: Oh yeah.
Speaker 3: In nineteen fifty, field experiments were set up where rabbits
Speaker 3: in different areas were inoculated with the virus and then
Speaker 3: let loose to bring it back to the burrow and
Speaker 3: the rabbits living in there. The first year results weren't
Speaker 3: too impressive, and the researchers in charge, Francis Ratcliffe and
Speaker 3: Lionel Bowl. Francis Ratcliffe, by the way, was the author
Speaker 3: of the second quote that we read in the intro.
Speaker 3: They nearly pulled the plug, but then reports sick rabbits
Speaker 3: began to come in from southeastern Australia in areas where
Speaker 3: the virus had been released. In some places, over ninety
Speaker 3: percent of the rabbits had died within a month of
Speaker 3: the virus showing up.
Speaker 1: Wow, yeah, in a month.
Speaker 3: In a month, it's again hard to imagine. So it
Speaker 3: seems that heavy rains had led to a big mosquito
Speaker 3: season and the mosquitoes were able to pick up the
Speaker 3: slack where a direct contact among the rabbits alone had failed.
Speaker 3: And around this time is when doctor Frank Fenner, who's
Speaker 3: one of the authors of that great book that I
Speaker 3: read about this, he joined the team as the virologist,
Speaker 3: and Fenner would go on to uncover so much about
Speaker 3: viral evolution and resistance and also played a major role
Speaker 3: in the eradication of smallpox in Australia, So he was
Speaker 3: kind of a big name in microbiology out there. So
Speaker 3: everything seemed to be going great with the Maxoma virus.
Speaker 3: People were celebrating over the corpses of millions of rabbits
Speaker 3: in anticipation of the return of vegetation. Wow. But then
Speaker 3: there was a development that almost brought the whole thing
Speaker 3: to a stop, an outbreak of encephalitis cases of unknown
Speaker 3: cause in humans appeared alongside the rise in miximatosis and
Speaker 3: the rabbits, which made people terrified that like, okay, this
Speaker 3: virus that you introduced is now infecting and killing humans.
Speaker 3: A few researchers working on the Maxoma virus knew that
Speaker 3: it couldn't be the cause of this illness, and so
Speaker 3: to reassure the public, researchers doctors Frank Venner, McFarlane, Burnett,
Speaker 3: and Clooney's Ross injected themselves with Maxoma virus and publicized
Speaker 3: the outcome, which was nothing but a slight red spot
Speaker 3: near the site of injection of no encephalitis.
Speaker 2: What was causing the encephalitis.
Speaker 3: It was actually found to be a relative of the
Speaker 3: Japanese encephalitis virus. It was given the name Murray Valley
Speaker 3: encephalitis virus after where the outbreak took place, and it's
Speaker 3: transmitted by mosquito mosquitos which.
Speaker 1: Were so prevalent, which we're also transmitting Magsimitata's Oh.
Speaker 2: My gosh, I love it.
Speaker 1: I don't love that people got encephalitis, but like.
Speaker 3: All the pieces fall into place, yeah, oh my gosh. Yeah.
Speaker 3: Nineteen fifty one, though, was the first year to show
Speaker 3: real promise in mixamatosis as a control agent for rabbits.
Speaker 3: But even though things were looking good, the disease seemed
Speaker 3: to be largely restricted to two areas along rivers and lakes.
Speaker 3: But the next year it exploded far beyond that. And
Speaker 3: with like you said, this estimated case fatality rate of
Speaker 3: ninety nine point eight percent, It obliterated, obliterated any rabbit
Speaker 3: population it came into contact with. Wow. And within a
Speaker 3: few years of the virus's release, Australia's rabbit population dropped
Speaker 3: from an estimated six hundred million to one hundred million.
Speaker 2: Wow. Yeah.
Speaker 3: And this drop in population was not, of course, you know,
Speaker 3: consistent or equal across the entirety of the rabbit infested areas,
Speaker 3: due to differences in climate and so, like mosquitoes might
Speaker 3: not breed as well in more hot and arid regions,
Speaker 3: and so they didn't experience as much of a decline.
Speaker 3: And also despite how huge an impact the virus was
Speaker 3: having on the rabbits, researchers on the project knew that
Speaker 3: it was just sort of the honeymoon phase. It was
Speaker 3: only a matter of time before resistance popped up, an
Speaker 3: attenuation crept in and they were expecting it to happen eventually,
Speaker 3: but it showed up a lot faster than they thought,
Speaker 3: like years and years faster by nineteen fifty two and
Speaker 3: nineteen fifty three. So two and three years after the
Speaker 3: virus was introduced, less deadly strains of the mix Oma
Speaker 3: virus or attenuated strains, had been discovered in some of
Speaker 3: the wild rabbits two to three years after wow, and
Speaker 3: later research showed that attenuated strains had popped up independently
Speaker 3: all over the continent during the nineteen fifties. And so
Speaker 3: let's talk about the trend towards decreasing virulence. Why was
Speaker 3: it evolving to become less deadly. Well, if you're a
Speaker 3: virus that's transmitted by direct contact, and you kill your
Speaker 3: host before your host can pass it on, you won't
Speaker 3: survive as the virus. The strains that will survive are
Speaker 3: those that are less deadly, where the host maybe stays
Speaker 3: alive a few days longer to infect a few more rabbits.
Speaker 3: And this with the fast rabbit reproduction cycle, and how
Speaker 3: many there were, this evolution happened on a much faster
Speaker 3: timescale than people expected. And for their part, the severe
Speaker 3: bottleneck and rabbits meant that genetic resistance would be selected
Speaker 3: for those were the ones that survived to reproduce and
Speaker 3: pass along resistance alleles. Genetic resistance and rabbits also showed
Speaker 3: up in the mid nineteen fifties, also decades ahead of predictions,
Speaker 3: and some fascinating lessons were learned about host pathogen coevolution
Speaker 3: in terms of the virus. Although the general trend was
Speaker 3: towards decreased virulence, a study examining trends in viral evolution
Speaker 3: across Australia and Europe where it had been released showed
Speaker 3: that there were multiple different evolutionary pathways the virus had taken. Eventually,
Speaker 3: all of these Maxoma virus strains seemed to have evolved
Speaker 3: to be less deadly, so it converged on this phenotype
Speaker 3: of being less deadly. But if you looked at them genetically,
Speaker 3: they didn't show those same patterns of genetic alterations, right,
Speaker 3: They weren't constrained by evolution in that way.
Speaker 1: They did it in like a bunch of different ways.
Speaker 3: They got to the end result, but they took a
Speaker 3: bunch of different paths to get there. It's so interesting. Yeah,
Speaker 3: and research in the nineteen nineties showed that although in
Speaker 3: general there had been a trend towards less deadly strains,
Speaker 3: there were some strains that seemed to have evolved way
Speaker 3: back to super high virulence. And those highly virulent strains
Speaker 3: had apparently been selected for because they could overcome the
Speaker 3: rabbit's resistance. They were the ones that were causing lesions
Speaker 3: where the virus could spread, whereas the less virulent ones
Speaker 3: were just kind of existing in the rabbits and then
Speaker 3: petering out right.
Speaker 1: Because it was this interplay between this rapidly evolving virus
Speaker 1: and an animal with a very short generation time that
Speaker 1: was rapidly evolving resistance is.
Speaker 3: It's so interesting, and I think it really also makes
Speaker 3: us rethink. I feel like there's, especially in COVID times,
Speaker 3: been this assumption that all pathogens evolved to be less deadly,
Speaker 3: they've to be benign, and that is absolutely not the case.
Speaker 3: It really is more about transmission.
Speaker 1: Yeah, exactly, although they evolved to be optimally transmitted, which
Speaker 1: could vary depending on how something is transmitted and how
Speaker 1: their host reacts to it and how much resistance they have.
Speaker 3: Like oh my goodness, Yaren there's no hard and fast
Speaker 3: rule which is what we love about ecology. Okay, So
Speaker 3: all of that is super fascinating, but there's also some
Speaker 3: really interesting tidbits from the rabbit side of things too. Yes, First,
Speaker 3: a study published in twenty nineteen showed that in rabbit
Speaker 3: populations that had been exposed to MaxMa virus across Australia, France,
Speaker 3: and the United Kingdom over the past sixty years, the
Speaker 3: same alleles in the rabbits had been selected for, and
Speaker 3: that most of the alleles were immunity related genes.
Speaker 2: Interesting.
Speaker 3: Yeah, And so the rabbits showed a common genetic basis
Speaker 3: for the evolution of resistance, but the virus did not.
Speaker 2: Oh my gosh, that's cool.
Speaker 3: Isn't that really fascinating? So there was existing genetic variation
Speaker 3: in all of these rabbit populations all around the world,
Speaker 3: and that certain alleles were the ones that were present
Speaker 3: in all of these populations from the beginning were the ones.
Speaker 1: Gosh, yeah, that is interesting, huh, super cool.
Speaker 2: Yeah.
Speaker 3: And then there's one more thing, okay, and so this
Speaker 3: is something called a sire effect, and it was found
Speaker 3: in about rabbit resistance in these in these miximatosis rabbits. Okay,
Speaker 3: so essentially when a dough an unselected dough female rabbit
Speaker 3: mated with a buck that had recovered from miximatosis, had
Speaker 3: been infected and then recovered, the kittens were more resistant
Speaker 3: than expected. The risk of death had been reduced by
Speaker 3: about twenty five percent.
Speaker 1: But only in that direction, like only a selected dough
Speaker 1: and a selected a resistant buck, but not the other
Speaker 1: way around.
Speaker 3: At least I didn't see like I would assume that
Speaker 3: there would be some maternal antibodies, yeah, passed in. But
Speaker 3: this is the dough is unselected and then the buck
Speaker 3: had been exposed. And it's not just in the litter
Speaker 3: that was produced when the dough in that buck had
Speaker 3: made it, but also future offspring.
Speaker 2: Like of that dough with other bucks.
Speaker 3: Yeah, so even if a dough later mates with a
Speaker 3: buck that was not immune, if she had previously mated
Speaker 3: with a recovered buck within seven months of his infection,
Speaker 3: those offspring are also partially immune. What I know, Okay,
Speaker 3: I'll post more papers about this. It's really fascinating and
Speaker 3: it's probably something to do with epigenetics. It's not even
Speaker 3: the mechanism is known.
Speaker 2: Yeah, that's oh my god, that is really bizarre.
Speaker 3: This shows like also This is such an incredible system
Speaker 3: to have studied because there's so much known about it.
Speaker 3: You can watch these things happen in real time. There's gos.
Speaker 3: Just the more you dig, the more you find, the
Speaker 3: more questions you have.
Speaker 2: Yeah, I have so many.
Speaker 3: Okay. So, despite the increasing resistance in rabbits and decreasing
Speaker 3: virulence in the virus, rabbit populations continued to decline or
Speaker 3: at least even out throughout the nineteen sixties, and part
Speaker 3: of that was due to the introduction of the European
Speaker 3: rabbit flee in nineteen sixty six, which was even more
Speaker 3: successful as a mechanical vector than the mosquito, and it
Speaker 3: was also somewhat due to the reactivation of the virus
Speaker 3: in rabbits with lesions, which allowed it to spread to
Speaker 3: rabbits who were newly susceptible. And by the nineteen eighties,
Speaker 3: rabbit populations were under pretty good control in some places,
Speaker 3: not eliminated by any means, but at least more manageable maybe.
Speaker 3: But in drier and hotter regions where mosquitoes weren't as
Speaker 3: prevalent and the European flea didn't survive well, rabbits were
Speaker 3: still a huge problem, and so the Spanish rabbit flea,
Speaker 3: which was adapted to that type of dryer and hotter environment,
Speaker 3: was introduced also was decently successful. But the story of
Speaker 3: rabbits in Australia was not over, and let's be honest,
Speaker 3: it may never be. Rabbit populations had begun to recover
Speaker 3: despite all of these interventions, and by nineteen ninety one
Speaker 3: it was close to half of the pre mixematosis population.
Speaker 2: Whoa yeah.
Speaker 3: The rabbit hemorrhagic disease virus a kelisi virus, also incredibly
Speaker 3: specific to rabbits, was explored as a possible rabbit control
Speaker 3: agent in the nineteen nineties after first being discovered in
Speaker 3: China in nineteen eighty four, and in nineteen ninety five
Speaker 3: it actually escaped into wild rabbit populations in Australia from
Speaker 3: an island where field studies were taken place, so it
Speaker 3: was like whoopsie, yeah, but they would have been planned
Speaker 3: to be released anyway. It was just a little head
Speaker 3: of schedule. Yeah, And the rabbit hemorrhagic disease virus proved
Speaker 3: to be pretty successful as a control agent, especially in
Speaker 3: those hotter, drier areas where control had previously been challenging,
Speaker 3: and there have been repeated introductions of that virus since
Speaker 3: so I've presented the story of rabbits in Australia as
Speaker 3: one of a villain rabbits and a hero the Mixoma virus,
Speaker 3: but as always, it's way more nuanced than that, and
Speaker 3: those roles could easily be swapped in other places where
Speaker 3: rabbits aren't considered pests. It's true that these introduced rabbits
Speaker 3: did and continued to do tremendous damage to ecosystems in
Speaker 3: Australia by reducing overall vegetation and destroying new plant growth,
Speaker 3: including trees. They have eliminated some plant species such as
Speaker 3: Acacia trees and species of grass in some areas, and
Speaker 3: the overall reduction in vegetation has also led to the
Speaker 3: erosion of topsoil, which has impacts on the establishment of
Speaker 3: new plants, drought tolerance, potential for windstorms and wildfires, and
Speaker 3: further destruction of habitat. This destruction is also not equal
Speaker 3: across Australia. For instance, in arid rangelands, where plants often
Speaker 3: have long lifespans and very slow growth periods, rabbits eat
Speaker 3: seedlings and destroy plants that were decades old. The recovery
Speaker 3: times for these areas is much much longer than others,
Speaker 3: and it's unclear whether complete recovery is even possible. And
Speaker 3: while initially the concern was primarily for the impact of
Speaker 3: rabbits on sheep or other livestock, many other species suffered
Speaker 3: at this destruction of habitat. Rabbits limited resources for many
Speaker 3: other herbivores and out competed them, in some cases, completely
Speaker 3: driving out native burrowing herbivores from rabbit infested areas like bilbies, batongs,
Speaker 3: common wombats, spectacled hair wallaby, western gray kangaroo, and Southern
Speaker 3: hairy nosed wombat.
Speaker 2: Oh my goodness.
Speaker 3: And then there are many social and cultural aspects of
Speaker 3: rabbit control. Some feel the introduction of mixomavirus and rabbit
Speaker 3: hemorrhagic disease virus is inhumane, and efforts have been made
Speaker 3: towards finding a better way to achieve reduced rabbit populations,
Speaker 3: like maybe through sterility. And there are also many people
Speaker 3: whose livelihood relies on or is supplemented by hunting rabbits
Speaker 3: for meat or pelts, and there have been calls to
Speaker 3: prevent the introduction of rabbit hemorrhagic disease virus in some
Speaker 3: areas where rabbits are used for this purpose. These aspects
Speaker 3: have led to questions of how to weigh the role
Speaker 3: of the rabbit as a resource against its role as
Speaker 3: an environmental pest, which is a conflict that comes up
Speaker 3: often in questions of conservation. At this point, the war
Speaker 3: on rabbits in Australia has been going on for nearly
Speaker 3: one hundred and sixty years. These introduced rabbits now occupy
Speaker 3: seventy percent of the continent, impact over three hundred native
Speaker 3: plant and animal species, and cost an estimated two hundred
Speaker 3: million Australian dollars every year in lost production. Wow. Miximatosis
Speaker 3: has been used as a control agent for rabbits in
Speaker 3: several other countries, and its story, as as well as
Speaker 3: that of invasive rabbits, is likely far from over. But
Speaker 3: let's talk more about where we stand today with maximatosis.
Speaker 3: What are those other rabbit populations impacted? Should we be worried?
Speaker 3: What's going on?
Speaker 1: Let's get into all of that after a quick break.
Speaker 1: So maxoma virus today, like you said, Aaron, it is
Speaker 1: not only a story of Australia Mixoma virus was also
Speaker 1: introduced in France to control rabbit populations in France, and
Speaker 1: from there it spread across Europe and into the UK,
Speaker 1: so Maxoma virus is now found pretty well distributed around
Speaker 1: the world. It's endemic of course to North and South America,
Speaker 1: but it's also found across Europe, into the UK and
Speaker 1: of course in Australia, and at this point in much
Speaker 1: of the world where Maxoma virus has been introduced, it
Speaker 1: has sort of established itself as an endemic pathogen. Now
Speaker 1: it causes occasional episode and primarily it is these medium
Speaker 1: virulence strains that tend to predominate, so as it turns
Speaker 1: out as this virulence kind of decreased, it was also
Speaker 1: found that when strains became really mild, where they caused
Speaker 1: very little disease and rabbits could recover really quickly, they
Speaker 1: only had transmissible tighters for a very short period of time,
Speaker 1: so it wasn't very infectious, and like you talked about
Speaker 1: a lot aarin, when rabbits died very quickly from infection,
Speaker 1: they were also really poor sources of infection, which in
Speaker 1: the case of Maxoma virus isn't very surprising since something
Speaker 1: like a mosquito or a flea doesn't tend to feed
Speaker 1: from dead things, and rabbits don't hang out with their
Speaker 1: dead friend's bodies for very long. So both these highly
Speaker 1: virulent strains that wipe out rabbits very quickly and these
Speaker 1: very very mild strains where rabbits survive infection and recover,
Speaker 1: both of those tend to be poor sources of virus transmission,
Speaker 1: and so it's these medium virulence strains often called like
Speaker 1: three A or four. There's like a grading scale, so
Speaker 1: it's these grade three and four strains that tend to predominate.
Speaker 1: But at the same time, more virulent strains like you
Speaker 1: mentioned Aaron. In some populations where rabbits have developed a
Speaker 1: lot of resistance or evolved a lot of resistance, these
Speaker 1: more virulent strains still exist, and so in different areas geographically,
Speaker 1: all of these different types of strains can actually co exist,
Speaker 1: which is so fascinating. And if you think about it
Speaker 1: on an even larger scale, like the large scale evolution
Speaker 1: and ecology of this virus, it's not just the intrinsic
Speaker 1: virulence of the virus and the resistance of the rabbits.
Speaker 1: It's also larger scale things like weather. Right, turns out
Speaker 1: that cold weather increases effective virulence and warmer totures make
Speaker 1: it easier for rabbits to survive infection.
Speaker 3: It's just so many, se many things.
Speaker 1: Nutritional status of the little bun buns, whether they have
Speaker 1: any co infections or other parasites that they're dealing with.
Speaker 1: Predator abundance, because especially in the wild, predators are going
Speaker 1: to tend to remove sick rabbits that when you're looking
Speaker 1: at experimental trials, those rabbits might have survived for longer.
Speaker 1: It depends on seasonal influences.
Speaker 2: There are so.
Speaker 1: Many things that contribute to this continually evolving story of
Speaker 1: the co evolution of mixomavirus and rabbits.
Speaker 3: It's so true. It really excites like the little ecology
Speaker 3: part of my brain where I'm like, but what about this?
Speaker 3: But what about that? How do you put this into
Speaker 3: a model? And then I'm like, no, I don't want
Speaker 3: to do any more modeling, No more.
Speaker 2: Don't worry.
Speaker 1: Lots of people are doing the modeling here and we
Speaker 1: could just get to read about it.
Speaker 3: Thank goodness, Thank goodness, other people are doing the models.
Speaker 3: But I think this topic almost more than any other
Speaker 3: one we've covered, just was such a perfect example of
Speaker 3: how this is truly a snapshot. This is constantly evolving.
Speaker 3: All of the moving parts of this are constantly evolving.
Speaker 3: What's climate change going to do to the areas where
Speaker 3: our thing is going to get hotter and drier and
Speaker 3: there are going to be no more mosquitoes at all?
Speaker 3: And the Spanish flea, the Spanish rabbit flea can't survive, Like,
Speaker 3: what's going to happen?
Speaker 1: Right?
Speaker 2: I know?
Speaker 1: And it does seem you asked earlier on Aaron, like
Speaker 1: how many other species of rabbits and hares are we
Speaker 1: talking about here? And I don't know exactly, but I
Speaker 1: do know that there are more and more case reports
Speaker 1: and studies showing that, for example, the Iberian hair has
Speaker 1: now been found to be infected with miximatosis and have
Speaker 1: outbreaks that have caused deaths of hundreds of Iberian hairs,
Speaker 1: which are a totally different species in the IBERIANSLA and
Speaker 1: so like, how much more could this spread?
Speaker 2: We don't know yet?
Speaker 1: Yeah, right, how do we try and keep it under control?
Speaker 1: There are vaccines, which is great. It seems from what
Speaker 1: I could tell, there's like two different groups of vaccines
Speaker 1: that exist. Both of them are live attenuated vaccines, so
Speaker 1: live virus that are grown in a lab to be
Speaker 1: not as virulent. One of them comes actually from the
Speaker 1: Shope fibroma virus, which again is that related virus that
Speaker 1: doesn't cause severe disease, just causes like a one big
Speaker 1: fibroma and it kind of tends to cause some cross
Speaker 1: protection against Maxoma virus. Think cowpox inoculation and small prox protection,
Speaker 1: same idea, right, And then there are also a live
Speaker 1: attenuated vaccines that are made from various strains of the
Speaker 1: Maxoma virus. These tend to produce a stronger and longer
Speaker 1: lasting immune response, but because they're from Maxoma virus, can
Speaker 1: also have the potential.
Speaker 2: For mild disease.
Speaker 1: So, from what I could gather, in settings where you're
Speaker 1: raising a lot of rabbits, whether it's for you know,
Speaker 1: domestic rabbits or for pelts or whatever it is, these
Speaker 1: two vaccines are often used in combination from what I
Speaker 1: can tell, so like one dose of the shop fibromavirus
Speaker 1: and then a few months later the Maxoma virus so
Speaker 1: that you have really good protection.
Speaker 2: And the last thing that I want to just.
Speaker 1: Briefly mention because first of all, this blew my mind
Speaker 1: and I think it's incredibly cool. But also I'm mentioning
Speaker 1: it because inevitably people will ask, like, how does this
Speaker 1: relate to my life in specific as a human being
Speaker 1: who maybe doesn't care.
Speaker 2: That much about rabbits.
Speaker 1: Fair enough, let me tell you, because this is incredible.
Speaker 1: So remember that little tiny spoiler I dropped at the
Speaker 1: top that maxoma virus can replicate in a wide variety
Speaker 1: of cells in vitro and is very adept at replicating
Speaker 1: in inhuman cancer cells. Mm hm, Well, turns out there's
Speaker 1: a lot of research into using maxoma virus as a
Speaker 1: cancer fighting viral infection, essentially something that could potentially be
Speaker 1: used in combination with chemotherapy to treat various cancers.
Speaker 2: That is.
Speaker 3: Fascinating, fascinating, erin, where are we in that research?
Speaker 2: Very early stages?
Speaker 3: Okay.
Speaker 1: There's also work being done to investigate maxoma virus as
Speaker 1: a treatment for chronic rejection of things like organ transplants
Speaker 1: and other diseases that have like a chronic vascular inflammatory
Speaker 1: component because of all of its immunosuppressive properties.
Speaker 3: Oh oh, that's interesting. It's kind of like the way
Speaker 3: there's been research into human parasite infections, yes Exactlyssance, Yeah.
Speaker 2: So very early stages.
Speaker 1: Actually, the paper that I found that went into this
Speaker 1: was actually kind of old at this point, and I
Speaker 1: didn't find anything like more up to date. But we'll
Speaker 1: post it and y' all can do your own research,
Speaker 1: because I think it's really like a cool future direction.
Speaker 3: See, it's like one more lesson one person's pest is
Speaker 3: another person's pet, or potential cancer curing micro exactly exactly.
Speaker 2: I love it, And that makes mix sematosis.
Speaker 3: What a journey.
Speaker 1: Seriously, I think this has just been so interesting.
Speaker 3: It really has been. And do you know what else
Speaker 3: is so interesting that I feel like we only talked
Speaker 3: about just a little bit in this episode what the
Speaker 3: rabbit hemorrhagic disease virus.
Speaker 2: The rabbit hemorrhagic disease virus. We barely even got into it.
Speaker 3: It's true, we barely did. And if you're kind of
Speaker 3: bummed that we didn't really talk about it as much
Speaker 3: as you wanted us to, maybe you're in luck because
Speaker 3: next week you can hear all about it. When we
Speaker 3: interviewed doctor Robin Hall, who is a veterinary virologist. What
Speaker 3: a cool title at CSIRO, which is the Commonwealth Scientific
Speaker 3: and Industrial Research Organization in Australia.
Speaker 2: It's gonna be so awesome.
Speaker 3: I am so excited about it.
Speaker 1: Yeah, me too, Okay, but for now sources sources.
Speaker 3: I mentioned the book Biological Control of Vertebrant Pests earlier
Speaker 3: by Fener and Fantini, and I also watched a couple
Speaker 3: of really fascinating YouTube videos on this. One is called
Speaker 3: one hundred and sixty Year Battle against one of Australia's
Speaker 3: worst invasives, and another is called The Rabbit in Australia.
Speaker 3: And I will post links to those as well as
Speaker 3: to a bunch of papers also that I read.
Speaker 1: I have a number of papers. Two of my favorites,
Speaker 1: just about the mixoma virus itself, were both by Peter Kerr,
Speaker 1: one from twenty twelve, one from twenty fifteen. I will
Speaker 1: post both of those, and then that paper on it
Speaker 1: was titled the Current Status and Future Directions of Mixsoma Virus,
Speaker 1: A Master in Immune Evasion. That was the twenty eleven
Speaker 1: paper that really detailed kind of the future possible directions
Speaker 1: of mixoma virus that I thought was so interesting. We
Speaker 1: will post the sources from this episode and all of
Speaker 1: our episodes on our website, this podcast will Kill You
Speaker 1: dot com.
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