Speaker 1: Every September. Like many, I feel sick and frightened around
Speaker 1: the anniversary of the nine to eleven attacks. But it
Speaker 1: was the weeks following September eleventh that would forever change
Speaker 1: my life. During that time, I was the victim of
Speaker 1: terrorism when I opened a letter containing a lethal amount
Speaker 1: of anthrax. Around September eighteenth, two thousand and one, I
Speaker 1: headed to work as a desk assistant at NBC Nightly News.
Speaker 1: One of my jobs was opening mister Brocaw's mail. There
Speaker 1: was one letter that looked as if it were written
Speaker 1: by a child. Something seemed unusual. I had never seen
Speaker 1: a letter containing a granular substance. I mentioned the strange
Speaker 1: letter to my friends. Nothing happened for about ten days.
Speaker 1: Then one Friday night, my throat began to swell up
Speaker 1: a cold, I thought, but it worsened over the weekend.
Speaker 1: My glands were soon enormous. Monday morning came and my
Speaker 1: face was barely recognizable. I went to the doctor, who
Speaker 1: said it was a reaction to my acutane medication and
Speaker 1: I should rest in a few days later, I went
Speaker 1: back to work, but I still felt a bit off.
Speaker 1: A week or so after I was sick mister Brokaw's
Speaker 1: assistant became sick. Both of our symptoms were unusual. Authorities
Speaker 1: became involved when Bob Stevens died at the American Media
Speaker 1: Building in Florida at the end of September. The pieces
Speaker 1: slowly began to come together. I soon learned why I
Speaker 1: had been sick anthrax poisoning. Like mister Brocaw's assistant, I
Speaker 1: had contracted cutaneous anthrax. The events over the next few
Speaker 1: months changed my life. I had carried anthrax back on
Speaker 1: my clothes and had contaminated my home. I chose to
Speaker 1: have all of my things destroyed. I lost my most
Speaker 1: personal belongings, all my precious pictures and mementos. I worried
Speaker 1: I might die. I'll have to see doctors the rest
Speaker 1: of my life. I'll never have an overall sense of
Speaker 1: security again. That's what I lost, But what I gained
Speaker 1: was the deep, true appreciation for my family, friends and
Speaker 1: coworkers who support was incredible. WHOA yeah, So that was
Speaker 1: an account of Casey Chamberlain written in two thousand and six,
Speaker 1: and I will post the link to the full account
Speaker 1: on our website. And it was in regard it's two day,
Speaker 1: two thousand and one Anthrax Letters.
Speaker 2: I remember that.
Speaker 1: Oh yeah, I remember that too.
Speaker 2: Hi.
Speaker 1: I'm Erin Welsh and I'm Erin alman Updyke and this
Speaker 1: is this podcast will kill.
Speaker 2: You obviously today we're talking about Anthrax.
Speaker 1: Obviously, Yes, yes we are. This is such first season
Speaker 1: type of material Erin.
Speaker 2: It's big. It's a big one.
Speaker 1: It's a big one, and it makes me. It makes
Speaker 1: me kind of happy that we've already done some of
Speaker 1: the enormous ones, because I think now at this point
Speaker 1: I would be so perfectionistic and so like, oh gosh,
Speaker 1: I didn't get this, and oh I should talk about
Speaker 1: this too, and the episodes would be like eight hours long.
Speaker 2: I'm so, is that not what we're about to get into.
Speaker 1: Okay, Yeah, it's going to be pretty long, but it's
Speaker 1: going to be fun. It's going to be really interesting.
Speaker 1: Scope of this is huge, massive, and we've got some
Speaker 1: very exciting guests to bring on.
Speaker 2: We really do, we really do.
Speaker 1: But first, but first, it is.
Speaker 2: Quarantine any time. You know, I always check my imaginary watch.
Speaker 2: When I say that, like it and.
Speaker 1: It's does that mean it's always quarantiny time on your
Speaker 1: imaginary watch?
Speaker 2: Yes, it is.
Speaker 1: So what are we drinking this real quarantiny time, non
Speaker 1: imaginary quarantiny time.
Speaker 2: We're drinking spore me another? Get it?
Speaker 1: What is in spo me another?
Speaker 2: Well, it's basically a stout float.
Speaker 1: Yeah, and you can kind of go wild with it,
Speaker 1: like you know, coffee stout, coffee stout, chocolate stout, chocolate
Speaker 1: spicy chili stout, I don't know whatever, and whatever ice
Speaker 1: cream you want. I have chocolate chip cookie dough currently,
Speaker 1: so that's what I'm doing.
Speaker 3: Yeah.
Speaker 1: We will post the full recipe for the quarantiney and
Speaker 1: the non alcoholic plus sy Verrita on our website This
Speaker 1: Podcast will Kill You dot Com as well as all
Speaker 1: of our social media channels, so make sure you follow
Speaker 1: us to get to make yourself this for me another?
Speaker 2: Yeah, exactly what other business do we have today? Erin?
Speaker 1: Well, we can just go through the usual suspects. Check
Speaker 1: out our website This Podcast will Kill You dot Com.
Speaker 1: You can find things like all of our sources for
Speaker 1: each episode there, as well as transcripts alcohol free episodes,
Speaker 1: links to our Goodreads list, bookshop dot Org, affiliate account,
Speaker 1: music by Bloodmobile are awesome cool merch There's Patreon links.
Speaker 1: There's honestly so much more.
Speaker 2: Go check it out, and you can also listen to
Speaker 2: this episode and all of our past and future episodes
Speaker 2: on Amazon Music, Apple, Stitcher, or wherever you get your podcasts.
Speaker 1: All right, should we dive in, let's.
Speaker 2: Do it right after this break. So Anthrax. We touched
Speaker 2: on this ever so briefly in our Sweating Sickness episode, Yes,
Speaker 2: which probably just honestly angered people. They were like, what,
Speaker 2: that's all.
Speaker 1: Well, and that's why we're doing it right now, so
Speaker 1: that the full picture.
Speaker 2: Yeah, So anthrax really is the name of the disease
Speaker 2: that is caused by this particular bacterium. But I just
Speaker 2: want to like say up front that there's a really
Speaker 2: good chance that I'll probably just say anthrax at some
Speaker 2: point when I'm referring to the bacteria. So just bear
Speaker 2: with me.
Speaker 1: Oh, I'm going to do that.
Speaker 4: Okay a lot good probably, so we'll both just do
Speaker 4: that and make someone angry. But anyways, the bacterium which
Speaker 4: causes anthrax is known as Bacillis and thracis. This is
Speaker 4: a gram positive spore forming rod shaped little bacterium. And
Speaker 4: we'll talk a lot more about the importance of those
Speaker 4: spores as we go through this. Oh yeah, they're like
Speaker 4: they're the most important thing.
Speaker 2: And this bacterium is related to a pretty large group
Speaker 2: of other bacterium in the group known as Bacillis serious
Speaker 2: ce r e us. But for the most part, what
Speaker 2: I think is so interesting is that Bacillis anthrasis is
Speaker 2: one of the most genetically monomorphic, meaning there is not
Speaker 2: a lot of genetic variation in this species across the
Speaker 2: entire globe.
Speaker 1: It's kind of bananas.
Speaker 2: It really is, like, this is a bacterium that is
Speaker 2: very ubiquitous. It's found across the whole globe. And yet
Speaker 2: if you grab one Anthrax bacterium from like Siberia and
Speaker 2: another from North America, they're going to be so similar.
Speaker 2: It's fascinating. And for the most part, this is the
Speaker 2: only species in the large B serious group that usually
Speaker 2: causes serious disease in humans. But there is a serahvar
Speaker 2: of be serious that can cause a disease very similar
Speaker 2: to anthrax, and will probably touch on that a little
Speaker 2: bit more later in this episode. But where I want
Speaker 2: to start is with the life cycle of this pathogen,
Speaker 2: because by going over its life cycle, we'll learn who
Speaker 2: tends to get infected or affected by anthrax, and we'll
Speaker 2: learn how it's transmitted, and then we can get into
Speaker 2: how it actually causes all of the damage and then
Speaker 2: what those symptoms look like in humans.
Speaker 1: Okay, sounds good.
Speaker 2: So Basillis anthrasis spores are where we're going to start.
Speaker 2: These spores exist in the soil and on vegetation, Like
Speaker 2: I said, pretty much worldwide. They can persist in a
Speaker 2: huge range of environmental conditions across the globe for years
Speaker 2: or in some cases decades or maybe centuries. These spores
Speaker 2: don't really replicate probably asterisk or asterisk. They just mostly
Speaker 2: hang out in the environment, and then at some point
Speaker 2: they're ingested, most commonly by herbivorous mammals, especially large ungulates
Speaker 2: like say cattle or zebras or hippos or antelope or goats, whatever.
Speaker 2: And then, because these herbivores often eat things like spiky grasses,
Speaker 2: for example, they might have small abrasions throughout their gastrointestinal tract,
Speaker 2: and these spores can then enter into the animal's blood
Speaker 2: stream through these little openings, these little like cuts in
Speaker 2: their mucosal lining. Once those spores are introduced into the
Speaker 2: blood stream, they're promptly engulfed by macrophages, which are white
Speaker 2: blood cells, and that is where the trouble starts. The
Speaker 2: spores inside these macrophages are activated back into full fledged bacteria,
Speaker 2: and they begin to replicate, often in the lymph nodes,
Speaker 2: which is where these white blood cells are traveling to.
Speaker 2: And then these bacteria that are replicating burst out of macrophages.
Speaker 2: They travel throughout the bloodstream. They replicate and replicate and
Speaker 2: cause overwhelming infection that almost inevitably leads to the death
Speaker 2: of the host. It's sad, it's absolutely devastating, and in
Speaker 2: many species of animal this generally happens so suddenly that
Speaker 2: very often the first symptom of infection in herd is
Speaker 2: just the sudden death of one animal, followed by many more.
Speaker 2: And it happens so quickly. Incubation period is often as
Speaker 2: short as thirty six to seventy two hours.
Speaker 1: How so fast, so fast.
Speaker 2: And what's important is that when the host die, in
Speaker 2: so doing, they release billions billions of vegetative bacteria. So
Speaker 2: the anthrax bacteria upon contact with the air in the environment,
Speaker 2: these bacteria spoiulate, they form those spores again, they are
Speaker 2: released into the environment and thus complete their life cycle.
Speaker 1: It's just like botulism where we were like, why does
Speaker 1: it kill you? Because it's because it needs to kill
Speaker 1: you in order to be transmitted.
Speaker 2: Exactly, exactly fascinating. Okay, So obviously my favorite question to
Speaker 2: try and answer is like, wh how how how can
Speaker 2: this kill so quickly? Yeah, Aaron, how Okay? Let me
Speaker 2: tell you. So. Basilla's Anthrasis anthrax has a couple of
Speaker 2: different virulence factors, which are the things that bacteria have
Speaker 2: that make us sick or animals sick and like allow
Speaker 2: them to be pathogenic. They have one virulence factor that
Speaker 2: makes a capsule, so it's like a little capsule that
Speaker 2: surrounds the bacterium that makes it really hard for immune
Speaker 2: cells to actually engulf and get rid of those bacteria
Speaker 2: via phagocytosis. Oh okay, so that's one, but it's not
Speaker 2: the most important. Well it is like essential, but the
Speaker 2: other ones are more exciting. The other virulence factor they
Speaker 2: have encodes two different exotoxins. We've talked about toxins a
Speaker 2: fair amount on this podcast, but it's been i think
Speaker 2: kind of a little while. So as a refresher, toxins
Speaker 2: are generally usually proteins that bacteria or other organisms can
Speaker 2: make that cause us harm in some way. In the
Speaker 2: case of Bacillis anthrasis, there's two different exotoxins which are
Speaker 2: called edema toxin and lethal toxin.
Speaker 1: Ooh uh, let me guess what the second one does.
Speaker 2: Yeah, yeah, you're right. And so each of these two
Speaker 2: different toxins is made up of two proteins. They're each
Speaker 2: made up of one part a protein called protective antigen PA,
Speaker 2: and then lethal toxin is made up of PA plus
Speaker 2: lethal factor, which is another protein. And then edema toxin
Speaker 2: is made up of the PA plus edema factor, which
Speaker 2: is another toxin. And they do like what you said,
Speaker 2: like what it sounds like. They do. The protective antigen
Speaker 2: part of each of these toxin protects the toxin itself
Speaker 2: and make sure that the toxin can make its way
Speaker 2: into our cells. And then you have a diema factor
Speaker 2: which causes a lot of inflammation and swelling, and lethal factor,
Speaker 2: which causes mostly cell death, especially of a white blood cells.
Speaker 1: What's the mechanism of cell death?
Speaker 2: Like I knew that you were going to ask, so
Speaker 2: let me scroll to my specific questions. Aaron is going
Speaker 2: to ask me section. Hmm, it's via a cast base
Speaker 2: one dependent cell death program known as pyroptosis.
Speaker 1: I almost wish I didn't ask, I know, I know.
Speaker 2: So the specific mechanisms of action of both lethal toxin
Speaker 2: and a dema toxin are absolutely fascinating and they've been
Speaker 2: studied in great detail. I have a ton of papers
Speaker 2: that people can read if they want to know this
Speaker 2: specific like cell like receptor by receptor detail of how
Speaker 2: these work, but essentially to go over just the broad
Speaker 2: strokes of it for the sake of this podcast. The
Speaker 2: toxins both together have actions both in the early phase
Speaker 2: of infection, where these toxins serve to downregulate and suppress
Speaker 2: our immune response. This is what allows for Basillis anthrasis
Speaker 2: to persist and replicate within our bodies so that you
Speaker 2: have a huge number of bacteria in the blood. And
Speaker 2: then later in the course of infection, these two toxins
Speaker 2: together create the edema, so the swelling, vascular collapse, and
Speaker 2: eventually shock that does lead to death, which, like you said,
Speaker 2: erin is pretty much an essential part of the natural
Speaker 2: history of this pathogen.
Speaker 1: And it's also like for at least in the twentieth century,
Speaker 1: there was the prevailing thought that, oh, pathogens will evolve
Speaker 1: to be more mild. That's just the way evolution works.
Speaker 1: And this is case in point that does not happen.
Speaker 2: Yeah, I mean not for a pathogen like this, right, Yeah,
Speaker 2: something where the host has to survive in order to transmit. Yes,
Speaker 2: but this is not a directly transmitted pathogen. This is
Speaker 2: essentially an environmentally transmitted disease.
Speaker 1: It's fascinating. This is why like mode of transmission and
Speaker 1: virulence I think are just still two of the like
Speaker 1: the most fascinating topic or one of the most fascinating topics.
Speaker 2: Oh, I agree, absolutely amazing. Last point I want to
Speaker 2: make about these virulence factors, and this gets back to
Speaker 2: what we were talking about with these this new serivar
Speaker 2: of Bacillis sirius that we've seen both of these virulence factors.
Speaker 2: So the capsule and the two toxins, both of them
Speaker 2: are required in order for anthrax to be pathogenic like
Speaker 2: to cause anthrax. But both of these virulence factors are
Speaker 2: encoded on plasmids, which there are circular little pieces of
Speaker 2: DNA that are not part of the main genome, which
Speaker 2: means they can be passed back and forth from bacterium
Speaker 2: to bacterium.
Speaker 1: But how often does that happen, the passing back and forth.
Speaker 2: It's a really good question, especially in a bacterium like
Speaker 2: Basillis anthrasis, which for the most part we think doesn't
Speaker 2: replicate well in the environment. How often is it going
Speaker 2: to be even coming in contact with other bacteria to
Speaker 2: be transmitting and passing plasmids. I don't know the answer
Speaker 2: to that. It's a really interesting question though.
Speaker 1: So I know that like they there has been some
Speaker 1: evidence that they form biofilms, but I don't know if
Speaker 1: that's just from like one individual bacterial cell.
Speaker 2: Yeah, and from what I understand, while Basillis anthrasis can
Speaker 2: in theory replicate in the soil, like they don't need
Speaker 2: to be inside of a host to replicate necessarily, they're
Speaker 2: really bad competitors, right, So in the most part in
Speaker 2: the en even if they could try and replicate, they're
Speaker 2: just not good at it, and so they get out competed. Okay, cool, yep,
Speaker 2: fun question Aron. Okay, So now what does this actually
Speaker 2: look like in humans? Yeah, that's what we usually talk
Speaker 2: about on this podcast. And how do humans get exposed?
Speaker 2: There are a few different ways that humans can become infected.
Speaker 2: There's three main routes that you can get infected. Cutaneous
Speaker 2: anthrax when spores enter through breaks in your skin. You
Speaker 2: can get gastrointestinal anthrax if you ingest the spores, very
Speaker 2: similar to how most animals become infected, or you can
Speaker 2: inhale the spores, which results in inhalational anthrax. So let's
Speaker 2: go through each of these one by one. The cutaneous
Speaker 2: form worldwide, by far, is the most common in humans.
Speaker 2: Something like ninety to ninety five percent of cases worldwide
Speaker 2: are cutaneous anthrax. So this is when spores enter through
Speaker 2: like a cut in your skin, just like in animals.
Speaker 2: Like I described, for the main transmission cycle or main
Speaker 2: life cycle of this pathogen, the replication still happens in macrophages,
Speaker 2: but in the case of cutaneous it tends to be
Speaker 2: those macrophasas that stay locally in the skin surrounding where
Speaker 2: the spores were introduced, or in nearby lymph nodes. So
Speaker 2: let's say you get a cut on your arm, then
Speaker 2: maybe you'll get swelling in the lymph nodes under your armpit. Okay,
Speaker 2: the first symptom that you usually see is just a
Speaker 2: little bump that's it, just a little bump. It's generally painless,
Speaker 2: but it's often quite itchy. And this happens anywhere from
Speaker 2: one to twelve days after exposure. But usually that little
Speaker 2: bump starts to get swollen, like all around it. There
Speaker 2: starts to be some swelling, more than you would expect
Speaker 2: from something like a regular bug bite. And then this
Speaker 2: bump gets surrounded either by small little vesicles, little fluid
Speaker 2: filled blisters all around the bump, or like one large,
Speaker 2: like one or two centimeter blister that kind of encompasses
Speaker 2: that initial bump.
Speaker 1: Anyone right now who has a bug bite is staring
Speaker 1: at it.
Speaker 2: I don't it's gonna get worse. I keep going, hopefully
Speaker 2: your bug bite won't. And this blister, it's filled with
Speaker 2: clear fluid. So it looks at first, especially a lot
Speaker 2: like the kind of blister that you might get on
Speaker 2: the back of your heel after you walk all day
Speaker 2: in new shoes. You know, those really like taut fluid
Speaker 2: filled blisters.
Speaker 1: Oh I'm familiar, uh huh.
Speaker 2: But unlike those blisters on your heel, it is surrounded
Speaker 2: in a wide margin by what they call gelatinous edema.
Speaker 1: Okay, so.
Speaker 2: Swelling that makes your skin feel like there's like jello
Speaker 2: underneath it.
Speaker 1: That is disturbing.
Speaker 5: Mm hm.
Speaker 1: Often you're just like m hmm, yeah, it is.
Speaker 2: Often people might also have some like low grade fever,
Speaker 2: maybe they're feeling kind of crappy, and then this vesicle,
Speaker 2: this blister enlarges and eventually it pops, just like the
Speaker 2: blister on your heel, except that this blister leaves an ulcer,
Speaker 2: a pretty sizable one potentially, and this ulcer progresses into
Speaker 2: a black eshkar, which is kind of like a really
Speaker 2: really gnarly looking scab. Okay, that's the best way I
Speaker 2: can describe it. It's like completely black. It's basically entirely
Speaker 2: dead necrotic tissue. That's pretty characteristic of cutaneous anthrax.
Speaker 1: How deep is that?
Speaker 2: Good question? It not necessarily that deep, but they can
Speaker 2: be quite large, like encompass a pretty large area. They
Speaker 2: don't tend to scar.
Speaker 1: Oh interesting, okay, yeah.
Speaker 2: But what's much worse even is the edema. So the
Speaker 2: swelling is still present and often it continues to grow,
Speaker 2: and especially if the lesion, instead of on your arm,
Speaker 2: was near your face or your neck, the swelling can
Speaker 2: get so intense that it can block your airway.
Speaker 1: Oh my god, and it's still gelatinous.
Speaker 2: Yeah, it's like a gelatinous your face.
Speaker 1: Just imagining pressing down on my skin and just feeling
Speaker 1: like jello underneath it. That would be very alarming, very say.
Speaker 2: The least that's very alarming is a good description. And
Speaker 2: while cutaneous anthrax is the least lethal of the three forms,
Speaker 2: and in many cases these esh cars heal over the
Speaker 2: course of two to three to six weeks, especially if
Speaker 2: this edema is near the face or neck, it can
Speaker 2: be fatal because of just how much swelling you get,
Speaker 2: or if this extends beyond just a local infection and
Speaker 2: does cause a more systemic infection. So, if cutaneous anthrax
Speaker 2: is untreated, mortality ranges from five to twenty percent, although
Speaker 2: I have seen estimates as high as like thirty or
Speaker 2: more percent. With antibiotics, though, mortality is less than one percent,
Speaker 2: so that's excellent.
Speaker 1: Which antibiotics, by the way, I always remember.
Speaker 2: A whole range of antibiotics. You can use kind of sillin,
Speaker 2: you can use clindamycin, you can use doxycycleankins.
Speaker 1: Yeah, resistance very little, great, yes, figured.
Speaker 2: So moving on to the next most deadly form, and
Speaker 2: that would be gastrointestinal anthrax in a lot of ways.
Speaker 2: You can actually think of gastrointestinal anthrax as cutaneous anthrax,
Speaker 2: but in your guts, so jello, guts, jello, Yeah, guts,
Speaker 2: not exactly, but kind of let me go into detail. Okay,
Speaker 2: So gastrointestinal anthrax is really how anthrax is spread in
Speaker 2: its enzootic cycle, right. Herbivores are most often infected while
Speaker 2: grazing on grass or ingesting soil that's contaminated with anthrax spores.
Speaker 2: So while humans could be infected that way, most commonly
Speaker 2: humans get infected with gastrointestinal anthrax by ingesting meat that
Speaker 2: is contaminated with the spores. And there are two different
Speaker 2: forms of gasterintestinal anthrax depending on where the spores enter
Speaker 2: your body and break through your mucosa, either oropharyngeal so
Speaker 2: in the back of your throat, or truly intestinal in
Speaker 2: your intestines, but pathologically, both essentially result in ulcer formation,
Speaker 2: not dissimilar to the ulcers that you see on the skin,
Speaker 2: but as you can imagine, ulcers in your throat or
Speaker 2: your intestine are a much bigger problem than on your
Speaker 2: skin because they can lead to perforation your face.
Speaker 1: Sorry, it just sounds really painful. It's not. The ulcer
Speaker 1: is not painful, right, that's what they say.
Speaker 2: I don't know. They look awful, so gosh, supposedly they're
Speaker 2: just itchy.
Speaker 1: It just still seems highly uncomfortable.
Speaker 2: I'm gonna get more uncomfortable.
Speaker 1: Wonderful. Okay, that's what this podcast is about.
Speaker 2: So remember when I said that often the bacteria travel
Speaker 2: to your lymph nodes and you get a lot of
Speaker 2: swelling in your lymph nodes. If this happens in your guts,
Speaker 2: you get swelling or lymphatinopathy in the lymph nodes in
Speaker 2: your throat potentially if we're talking oralpharyngeal infection, or in
Speaker 2: the mesentary which is the connective tissue that holds your
Speaker 2: guts in place. We have a ton of lymph nodes
Speaker 2: in there, and if those become severely inflamed and very swollen,
Speaker 2: that can lead to potentially intestinal obstruction. It can also
Speaker 2: lead to acieties, which we've talked about at a fair
Speaker 2: number of times on this podcast. But that's basically the
Speaker 2: build up of fluid in your abdomen because the blood
Speaker 2: vessels and the lymph nodes, the whole lymph system that
Speaker 2: should drain fluid gets congested. Because of all this swelling,
Speaker 2: you can through these ulcers or through just ischemia. Because
Speaker 2: of all this swelling, you can get perforation of the bowels,
Speaker 2: which is a pretty serious emergency. And because we're talking
Speaker 2: about becoming infected through the mucosa, so through a cut
Speaker 2: in your gastrointestinal tract, rather than through your skin, which
Speaker 2: is quite thick, this disease is far more systemic than
Speaker 2: cutaneous anthrax, so it makes its way to your bloodstream
Speaker 2: much more easily than from our skin, and for that reason,
Speaker 2: the mortality rate is much higher. It's usually twenty five
Speaker 2: to sixty percent if untreated.
Speaker 3: I have a.
Speaker 1: Question, yes, Sarin, So you mentioned that basillisanthrasis is not
Speaker 1: a good competitor. Does any of that potentially have anything
Speaker 1: to do with the gut microbiome and not being able
Speaker 1: to establish there or is it not really that because
Speaker 1: it's perforations in your gut.
Speaker 2: Yeah, so that's a really interesting question. I haven't read
Speaker 2: anything on this. I don't know that there's been study,
Speaker 2: so I can't answer it like with data, but I
Speaker 2: can tell you based on what I know of the
Speaker 2: life cycle it enters our gut as spores. It's not
Speaker 2: establishing an infection in our gut, okay, so it's not
Speaker 2: going to be competing with anything any other bacteria that
Speaker 2: live in our gut that are commensals. And what's really
Speaker 2: interesting about this pathogen is that even though it's not intracellular,
Speaker 2: so it doesn't live its life inside of our cells,
Speaker 2: it does necessarily have to enter macrophages, we think, in
Speaker 2: order for the spores to reactivate and become you know,
Speaker 2: replicating bacteria again.
Speaker 1: Okay, so it's able to sort of like sneak in
Speaker 1: under the guys of macrophages and then get to high
Speaker 1: enough volume or whatever.
Speaker 2: Right.
Speaker 1: Interesting, Yeah, and it does.
Speaker 2: And I do also think it's interesting that for the
Speaker 2: most part, it does need we think at least it
Speaker 2: needs a break in the mucosal lining. It can't just
Speaker 2: like other bacteria that we've talked about on this podcast do.
Speaker 2: It can't burrow its way through our mucosa on its own.
Speaker 2: It has to enter through a wound of some kind
Speaker 2: that's already there. And so I wonder if that plays
Speaker 2: a lot into why different animals are differently differentially susceptible
Speaker 2: based on what they're eating, and how likely they are
Speaker 2: to have some kind of.
Speaker 1: How much ruffage is exactly how much captain crunch they
Speaker 1: ate because like these abrasions everywhere.
Speaker 2: That's so true. Oh that's really really interesting. Okay, Anyways,
Speaker 2: that's castro intestinal anthrocs. Do you have any more questions
Speaker 2: about that one?
Speaker 1: I don't think so.
Speaker 2: Symptoms you have, you know, abdominal pain, nause of, vomiting, fever, diarrhea,
Speaker 2: and then you pretty much die very.
Speaker 1: Rapidly, and you die because of all the same things
Speaker 1: like or your body is it diarrhea?
Speaker 2: What? Yeah, we're going to talk a little bit more
Speaker 2: about the mechanisms when we get to the next form,
Speaker 2: which is the deadliest form, which is inhalational anthrax.
Speaker 1: The most terrifying.
Speaker 2: Yes, the most absolutely the most terrifying, and the reason
Speaker 2: that most people who have heard of anthrax are probably
Speaker 2: most terrified of it because they think of anthrax and
Speaker 2: they think of bioterrorism, and that that means that they're
Speaker 2: thinking of inhalational anthrax. So whether they know it or not,
Speaker 2: So the inhalational form, in this form, you have a
Speaker 2: biphasic illness, so you have two different parts to this infection.
Speaker 2: The first part happens about one to six days after exposure.
Speaker 2: It starts pretty non specifically fever. I feel cruddy, my
Speaker 2: muscles ache, maybe I have a cough since I inhaled
Speaker 2: something into my lungs, be some chest pain. And then
Speaker 2: within two to three or four days, your fever will increase,
Speaker 2: but you'll become short of breath. You won't be able
Speaker 2: to breathe, you can't get in enough air. You might
Speaker 2: get cyanosis because you Cyanosis is when your skin turns
Speaker 2: blue because you literally don't have enough oxygen. Often your
Speaker 2: lymph nodes and your neck will get so swollen that
Speaker 2: those will further obstruct your windpipe. So then when you
Speaker 2: breathe in it might sound like which is called strider.
Speaker 2: And about half of people will progress to complications like
Speaker 2: meningitis because these bacteria have crossed the blood brain barrier.
Speaker 2: If you get meningitis, it's essentially one hundred percent chance
Speaker 2: that you're going to die, even with treatment. But even
Speaker 2: if not, as this bacteria replicates throughout your body because
Speaker 2: of those toxins, what happens is that you very rapidly
Speaker 2: progress to shock. So shock we've talked about a lot,
Speaker 2: But it's essentially there's a lot of ways that it
Speaker 2: can happen. But what it means is that you're not
Speaker 2: getting blood and oxygen perfusing your tissues. So in this case,
Speaker 2: it can happen kind of in a lot of different ways.
Speaker 2: You're losing a lot of fluid because of these toxins
Speaker 2: and their actions both on your blood vessels and also
Speaker 2: on your lymph system, essentially just causing a lot of
Speaker 2: swelling and in some cases actual bleeding and bleeding out
Speaker 2: of places that you're not supposed to bleed. So in general,
Speaker 2: with inhalational anthrax, whether because of the meningitis or whether
Speaker 2: because of the shock, death usually happens within twenty four
Speaker 2: to thirty six hours of that second stage of the illness.
Speaker 1: Okay, that's terrifying, horrifying.
Speaker 2: It's very horrifying. And what happens in inhalational anthrax, and
Speaker 2: the difference between inhalational anthrax and cutaneous and gastrointestinal anthrax
Speaker 2: is that in the case of inhalational when these spores
Speaker 2: are inhaled, they're engulfed by macrophasas that live in the
Speaker 2: bottoms of our lungs, the little alveoli which are where
Speaker 2: gas exchange happens, and these macrophasas take those spores to
Speaker 2: a set of lymph nodes that are right along the
Speaker 2: center of our chest called the media stynum, and that
Speaker 2: is where they germinate and begin to replicate, and from
Speaker 2: there they very rapidly produce a huge, huge amount of bacterimia,
Speaker 2: so tons of bacteria that are able to go throughout
Speaker 2: your whole bloodstream, a huge amount of toxin, and then
Speaker 2: the shock and the death. So this is an inhaled spore.
Speaker 2: So it's a quote li lung thing, but it's not
Speaker 2: really a lung.
Speaker 1: Disease, right, it's just the avenue of entry exactly right.
Speaker 2: So in general, mortality rate in some outbreaks has been
Speaker 2: as low as forty six percent. That's with really good treatment.
Speaker 1: As low as forty six percent.
Speaker 2: Yeah, that was the US in two thousand and one.
Speaker 2: The death rate was forty six percent, But it's usually
Speaker 2: as high as eighty five to ninety five percent. And
Speaker 2: like I said, if it progresses to meningitis, it's nearly
Speaker 2: one hundred percent. It's treatable, especially early on in the infection,
Speaker 2: but often especially if it progresses to meningitis, antibiotics alone
Speaker 2: often aren't enough because of the high level of toxemia
Speaker 2: because of the toxins themselves. So yeah, really briefly, there's
Speaker 2: also actually a forethroot that has been documented pretty rarely,
Speaker 2: but that is injectional anthrax, and this has been documented
Speaker 2: in several places throughout Europe because of contaminated heroin, which
Speaker 2: is very scary. And the reason that this is different
Speaker 2: than just cutaneous anthrax, even though it's a needle going
Speaker 2: through the skin, is that it ends up producing a
Speaker 2: deeper soft tissue infection, which is more likely to result
Speaker 2: in systemic infection and therefore has a higher mortality rate
Speaker 2: because it's introduced much deeper than just a superficial skin
Speaker 2: infection would be.
Speaker 1: Gotcha. So it's not the needle, it's the heroin itself, right.
Speaker 2: Yeah, it's been from contaminated heroin, not from like needles
Speaker 2: that were dropped in soil or something like that.
Speaker 5: Right.
Speaker 2: Yeah.
Speaker 6: Wow.
Speaker 2: Yeah. It is treatable in animals and in humans, so
Speaker 2: that's exciting, and there is a vac technically, yes, yes,
Speaker 2: that's for animals and for humans, but it's not a
Speaker 2: great vaccine for animals or for humans.
Speaker 1: Yeah, low protection or Yeah, for.
Speaker 2: Reasons that we don't fully understand, it doesn't produce super
Speaker 2: long lasting immunity. So even for animals, they have to
Speaker 2: get boosters like every year. For humans, the vaccines that
Speaker 2: we have, at least the one that we have in
Speaker 2: the States, you have to get a dose at times
Speaker 2: zero and then again at two weeks and four weeks,
Speaker 2: and then six months, and then twelve months and then
Speaker 2: eighteen months, and then every year after that.
Speaker 1: That's a lot of Yeah, compliance must be challenging to
Speaker 1: achieve on.
Speaker 2: That, Yeah, it definitely can be. So speaking of the
Speaker 2: anthrax vaccine and animals, we wanted to bring on a
Speaker 2: very special guest to help us explore a huge area
Speaker 2: of this disease and this microbe that we've really just
Speaker 2: barely touched on so far, and that is the impact
Speaker 2: of anthrax on domestic and wild animals, you know, aarin,
Speaker 2: so that we don't have to just speculate about how
Speaker 2: much captain crunch a cow versus a deer is eating.
Speaker 2: So we consulted an expert. We were so thrilled to
Speaker 2: get to chat with doctor Johanna Salzer, veterinary medical officer
Speaker 2: at the CDC. So we'll let her introduce herself.
Speaker 3: So I'm Johannah Slzer. I'm a veterinary Medical Officer and
Speaker 3: Bacterial Special Pathogens Branch at the US Centers for Disease
Speaker 3: Control and Prevention. I serve as both a veterinarian and
Speaker 3: an epidemiologist.
Speaker 2: Yay, We're so thrilled to get to talk to you today.
Speaker 2: So we wanted to ask you, you know about because
Speaker 2: you are both a veterinarian and you know infectious disease
Speaker 2: epidemiologists researcher, we wanted to ask you about anthrax in animals.
Speaker 2: So could you tell us a little bit about what
Speaker 2: the course kind of in general of anthrax as a
Speaker 2: disease looks like in animals other than humans.
Speaker 3: Sure so. So antrax affects different animal species differently, So
Speaker 3: there are some animals that are more affected and have
Speaker 3: more severe disease than others. So usually when we think
Speaker 3: about anthrax and animals, we think about herbivores, so cattle, sheep, goats,
Speaker 3: and wild herbivores such as zebras and buffalo and other antelope.
Speaker 3: And in these animals when they either ingest or inhale
Speaker 3: the bisilcanthracist spore, they have a pretty rapid onset of
Speaker 3: disease and pretty severe. And so usually the first sign
Speaker 3: of disease in these animals is actually said in death.
Speaker 3: And so usually the first sign of that you have
Speaker 3: an outbreak of anthrax in a herd is when animals
Speaker 3: are found dead and the carcasses present with you know,
Speaker 3: lacar ric or mortis or reduced rigor mortise and dark
Speaker 3: blood that can be oozing from the mouth or nostrils
Speaker 3: or anus marked bloating and often this rapid decomposition of
Speaker 3: the carcass.
Speaker 1: Interesting, that's awful. Yeah, So looking now more specifically, are
Speaker 1: there any big differences in how this disease happens among
Speaker 1: different animal species? Like are some animals more susceptible or
Speaker 1: seem to be more susceptible or is it just a
Speaker 1: difference in exposure risk?
Speaker 3: Yeah, so some animals are considered more resistant. So species
Speaker 3: like pigs, dogs, cats, carnivores, some of your scavengers. So
Speaker 3: actually some of the animals that would maybe feed on
Speaker 3: a carcass are the animals that if they are infected,
Speaker 3: they have less severe disease and it's more rarely fatal.
Speaker 2: Interesting, that's fascinating. So I mean, because this is a
Speaker 2: disease that can you know, these really massive outbreaks and
Speaker 2: like you were saying, just really rapid death and decomposition
Speaker 2: of the carcasses leading to further outbreaks. What do control
Speaker 2: efforts kind of look like and entail once an outbreak
Speaker 2: has been identified and how does that control differ for
Speaker 2: an outbreak maybe in livestock versus wildlife.
Speaker 3: Yeah, so the two primary tools that we have for
Speaker 3: controlling anthrax are livestock vaccination and vaccination programs for anthrax,
Speaker 3: especially in areas that are known to be endemic. So
Speaker 3: vaccination it has been done in wildlife, but it is
Speaker 3: pretty challenging right because most of the time it would
Speaker 3: involve darting of an animal and then proper carcass disposal.
Speaker 3: When you do have an animal that suspected are confirmed
Speaker 3: to diet of anthrax, the carcass disposal so the recommendations
Speaker 3: are either to concinerate or burn a carcass, and if
Speaker 3: that's not possible, then to bury. And even with livestock
Speaker 3: this can be a challenge. There are places where anthrax
Speaker 3: is endemic that there's just not much top soil you're
Speaker 3: not able to actually physically bury an animal or perhaps
Speaker 3: there's a burned band or other reasons. You wouldn't burn
Speaker 3: a carcass with wildlife. It's even you know, a bigger
Speaker 3: challenge because you have to find the carcass fairly quickly
Speaker 3: before scavengers do, and that's that's often nearly impossible with wildlife.
Speaker 3: And wildlife there are also larger carcasses, right you're talking
Speaker 3: about elephants or hippos buffalo one of the outbreaks that
Speaker 3: we recently consulted on in Namibia, some of the recommendations
Speaker 3: were just to bury the carcasses when possible, and to
Speaker 3: just minimally move them to try to prevent further like
Speaker 3: environmental contamination.
Speaker 1: In places where there's like mixed cattle and wildlife grazing.
Speaker 1: I know that that's been happening a lot, like integrated farms.
Speaker 1: Would that practice increase the risk to domestic animals or
Speaker 1: decrease the risk almost to the wildlife, because maybe an
Speaker 1: anthrax operate could be identified more quickly even if there
Speaker 1: are more like susceptible individuals. I was just thinking about
Speaker 1: how that practice might affect either the risk or like
Speaker 1: control measures for anthrax in those in those animal populations.
Speaker 3: Yeah, I mean that is a perfect example of where
Speaker 3: vaccination and good vaccination programs like our strongest weapon against anthrax.
Speaker 3: You're asking Aaron, like identifying a wildlife case early then
Speaker 3: could trigger vaccination in livestock. Yeah, And I think that
Speaker 3: actually is the case in Taxess where you do have
Speaker 3: a lot of wildlife mingling with livestock from a veninary perspective. Like,
Speaker 3: one of the things I most love about working on
Speaker 3: anthrax is because it is one of those diseases, much
Speaker 3: like Rabi's, that if you could protect the animal and
Speaker 3: prevent the disease in animal, you protect people and anthrax.
Speaker 3: Working on antras and livestock specifically and protecting livestock you
Speaker 3: know also in turn can not only protect people but
Speaker 3: also wildlife, which is one of the things that you know,
Speaker 3: I find so fascinating by anthrax, Like it really much
Speaker 3: like Raby's has this the connectivity is so tight between
Speaker 3: human and animal health and with anthraxs you also have
Speaker 3: this environmental piece where you have to have all these
Speaker 3: the right environmental conditions for the sport to survive too.
Speaker 3: So it's kind of the poster health for one health
Speaker 3: and approaching you know, using a one health approach to
Speaker 3: disease control.
Speaker 1: Thank you so much, doctor Salzer for taking the time
Speaker 1: to chat with us. It was so fantastic and we
Speaker 1: really appreciate it.
Speaker 2: Yeah, we do. It was absolutely thrilling. So, Aaron, after
Speaker 2: all that, what can you tell me about the history
Speaker 2: of anthrax? Like, where did this come from? And how
Speaker 2: did we get here?
Speaker 1: I can't wait, but let's take a quick break first.
Speaker 1: For many of us, especially those that remember watching the
Speaker 1: news coverage in two thousand and one on the Anthrax letters.
Speaker 1: More on that later, anthrax holds a very specific meaning,
Speaker 1: that of a bioterrorism agent, and that reputation or perception
Speaker 1: of anthrax hasn't diminished over the years, despite the fact
Speaker 1: that anthrax poses a much more real threat as a
Speaker 1: disease of livestock and wildlife that it has as a
Speaker 1: bioweapon so far bioweapon angle itself, that's relatively new. Throughout
Speaker 1: its very long history, anthrax has been many things, a
Speaker 1: punishment from the heavens, an agricultural disease, an occupational hazard,
Speaker 1: and now a potential weapon of bioterrorism. So my goal
Speaker 1: for the history section is to take us through these
Speaker 1: different phases of anthrax and let's begin at the beginning,
Speaker 1: the evolutionary origins. Yes, so, as you mentioned aaron, Basilla santhrasis,
Speaker 1: it's kind of a funky little pathogen. It's not super diverse.
Speaker 1: It reproduces clonally primarily. And actually this incredible lack of
Speaker 1: diversity meant that it was only in the past few
Speaker 1: decades or so, past two decades or so, with the
Speaker 1: development of next generation sequencing technology, that researchers were able
Speaker 1: to get a full picture of its lutionary history and
Speaker 1: relationships among different strains or clades. Before it was too difficult.
Speaker 2: Yeah, because they were just too similar across exactly. Yeah, fascinating.
Speaker 1: So what did they find. Well, first of all, they
Speaker 1: found that Basilis anthrasis likely evolved several tens of thousands
Speaker 1: of years ago. I couldn't actually find like a very
Speaker 1: good estimate of when it first emerged or diverged, but
Speaker 1: in any case, several researchers believe that it evolved from
Speaker 1: an insect pathogen or insect commensal.
Speaker 2: Oh mm hmm, like some of the really.
Speaker 1: Exactly Basillis thuringentsa. I don't know what syringiensis, thank you. So, yeah,
Speaker 1: it evolved from this insect pathogen or commensal, and it
Speaker 1: diverged from Basilla sirius after acquiring those virulence plasmids. Okay,
Speaker 1: it's thought that Basilis anthrasis emerged in sub Saharan Africa,
Speaker 1: but the location of where it's spread from and then
Speaker 1: this burst of diversification is likely to have happened somewhere
Speaker 1: in the Fertile Crescent, which is where the domestication of
Speaker 1: livestock primarily happened.
Speaker 2: That makes sense, makes.
Speaker 1: Sense, And it's unclear exactly how this bacterium got to
Speaker 1: the Americas. But there are a couple of hypotheses which
Speaker 1: are not mutually exclusive. So when an introduction could have
Speaker 1: come during the Holocene by ungulates traveling over the Bearing
Speaker 1: land Bridge and then you know, down into the Americas.
Speaker 1: And another source of introduction is thought to be European
Speaker 1: trappers who brought it into the Eastern Us. But overall,
Speaker 1: like you said, anthrax is a very slow moving creature,
Speaker 1: evolutionarily accumulating mutations slowly. And this quality of Anthrax has
Speaker 1: made it a lot easier to trace not only its history,
Speaker 1: but it also has as great forensic value in tracing
Speaker 1: the source of an anthrax bioweapon, such as in the
Speaker 1: case of the two thousand and one anthrax letters, so
Speaker 1: like pinpointing exactly where this particular strain came from, which
Speaker 1: is pretty interesting. But anyway, I'm getting ahead of myself
Speaker 1: a little bit. And so now that we've got the
Speaker 1: evolutionary history out of the way, let's check in with
Speaker 1: ancient history and antrax.
Speaker 2: This really is like it first season.
Speaker 1: It super is. I'm overwhelmed. Anthrax seems like it was
Speaker 1: definitely known in ancient times. The fifth and maybe sixth
Speaker 1: Biblical plagues, the plague of livestock and the plague of boils, respectively,
Speaker 1: which always makes me think of Brooklyn ninet nine the
Speaker 1: plague of boils. Anyway, anyway, those have often been held
Speaker 1: to be anthrax as well as Render Past Like I
Speaker 1: know that I mentioned these biblical plagues in the Render
Speaker 1: Pest episode. Yeah, and in ancient writings in India from
Speaker 1: five hundred BCE or so describing did the diseases of animals?
Speaker 1: Anthrax seems to be one of those diseases described. It
Speaker 1: was also known in ancient Greece and in ancient Rome.
Speaker 1: The poet Virgil wrote about animal plagues, one of which
Speaker 1: sounds an awful lot like anthrax. Here's a quote for you.
Speaker 1: A terrible plague once sprang up there and raged on
Speaker 1: through the warmer part of autumn, not only destroying one
Speaker 1: flock of sheep after another, but killing animals of all kinds.
Speaker 1: Nor did the victims die an easy and uncomplicated death.
Speaker 1: After a burning fever had raged through in animal's veins
Speaker 1: and shriveled its flesh, the fluids again became abundant and
Speaker 1: virtually dissolved the bones. Oh yeah, it sounds rough, no
Speaker 1: matter what it is and right, and one of these plagues,
Speaker 1: one of Virgil's plagues, supposedly wiped out almost half of
Speaker 1: both the human and animal populations of Rome, and the
Speaker 1: disease continued to be a major problem in the area
Speaker 1: for centuries, popping up over and over again. This tendency
Speaker 1: of anthrax, which is like to haunt certain farms or regions,
Speaker 1: gave rise to almost like a mythology around the disease,
Speaker 1: and it meant that generational knowledge was required, so families
Speaker 1: or villages had to remember like where the bodies were buried,
Speaker 1: so to speak, and pass that information down so that
Speaker 1: future generations could avoid grazing livestock in those areas.
Speaker 2: Not even so to speak, but like literally.
Speaker 1: Literally and not even so to speak. Yeah, actually side note,
Speaker 1: I saw a really cool paper about how the spots
Speaker 1: where carcasses are actually end up being an attractant to
Speaker 1: animals because like, if an animal dies of anthrax, that
Speaker 1: nutrient influx into the soil will actually help plants grow
Speaker 1: like better and faster, thus attracting other animals, thus influencing
Speaker 1: the transmission chain at.
Speaker 2: What time frame though, Because I was reading about how
Speaker 2: for the first year.
Speaker 1: The second year, the second year, the first year it's avoidant,
Speaker 1: the second it's attractant, the third year the preference goes away.
Speaker 2: Fascinating, I know, because it seems like after two years
Speaker 2: is when infectivity goes down. So that second year is.
Speaker 1: When crucial trick. Isn't that so ugh? It's just evolution ecology,
Speaker 1: It's just magical. Ah. But this tendency to like, you know,
Speaker 1: haunt certain areas led to for instance, in France, some
Speaker 1: of these areas being referred to as the cursed fields,
Speaker 1: the cursed fields, so widespread trade of animals and animal
Speaker 1: products ensured that these cursed fields could spring up anywhere,
Speaker 1: and by around one thousand CE, anthrax was really well
Speaker 1: established throughout the Old World. Germany and the British Isles
Speaker 1: experienced major outbreaks of anthrax in the tenth, thirteenth, and
Speaker 1: fourteenth centuries, and these episolotics resulted not only in the
Speaker 1: deaths of livestock, but also in the humans and dogs
Speaker 1: and birds and other animals that fed on the cattle
Speaker 1: carcasses or they ended up starving due to food shortages
Speaker 1: or nutritional deficiencies.
Speaker 2: So does that mean that anthrax moved around the world
Speaker 2: from livestock trading exactly?
Speaker 1: Yeah, well livestock trading and fur trading, wow, and like
Speaker 1: wool and so on. So it is. This is what's
Speaker 1: so interesting to me is that you know, for a
Speaker 1: lot of diseases that are human specific, they moved around
Speaker 1: the world due to human travel, but it was also
Speaker 1: it was almost an inevitability. But like with anthrax, I
Speaker 1: feel like we really lent a helping hand, right Like, it's.
Speaker 2: What this is blowing my mind right now?
Speaker 1: Actually yeah, I mean, it turns out this is one
Speaker 1: of like the big ones like oh Capital b capital O.
Speaker 1: It's it has been I mean, and it has really
Speaker 1: had like a huge impact on history and ecology, and
Speaker 1: it's just really fascinating to me.
Speaker 2: Let me give you an example, oh please.
Speaker 1: In sixteen thirteen in southern Europe, a massive outbreak of
Speaker 1: anthrax is estimated to have killed around sixty thousand people
Speaker 1: and untold numbers of livestock. What uh huh. Over the
Speaker 1: next one hundred years, so like, between the sixteen hundreds
Speaker 1: and seventeen hundreds, anthrac's outbreak seemed to grow stronger and
Speaker 1: deadlier in some ways, which probably definitely had something to
Speaker 1: do with this increased movement and trade. And one of
Speaker 1: these places of trade was the New World. Even if
Speaker 1: anthrax had been brought over across the Bearing Land Bridge
Speaker 1: around ten thousand years ago, it greatly spread in prevalence
Speaker 1: an outbreak intensity following European colonization. It seems that anthrax
Speaker 1: began to be perceived as a problem in the New
Speaker 1: World by the fifteen hundreds, but the biggest and most
Speaker 1: devastating outbreak of what was likely anthrax didn't occur until
Speaker 1: the seventeen seventies in what is now Haiti. In this outbreak,
Speaker 1: an estimated fifteen thousand people died of anthrax and untold.
Speaker 1: Thousands of cattle and other livestock also perished, and a
Speaker 1: major component of this anthrax outbreak that contributed to its
Speaker 1: deadliness was the fact that an earthquake occur in the
Speaker 1: middle of the outbreak, making food even more scarce than
Speaker 1: it was before, and so out of desperation, people began
Speaker 1: to eat the livestock that had died of anthrax, which
Speaker 1: of course led to even more cases.
Speaker 2: Yeah, I feel like it's important to also point out
Speaker 2: that cooking the meat doesn't kill the spores.
Speaker 1: Oh no, these spores are like.
Speaker 2: They're like prions practically.
Speaker 1: I know. Nevertheless, they persisted. Yeah, a hardcore spore, my gosh. Okay, So,
Speaker 1: although this seventeen seventy outbreak of anthrax may have been
Speaker 1: the most devastating, it certainly wouldn't be the last. But
Speaker 1: before I go into more of those, let's talk names
Speaker 1: real quick. Okay, I'm not going to go through all
Speaker 1: the different names, because there are very many, but I
Speaker 1: will go over some of the patterns that we have
Speaker 1: seen in these names, and so one is that they
Speaker 1: often called out that grazing animals were most commonly infected,
Speaker 1: so like cowsickness, goat sickness, etc. And another is that
Speaker 1: the skin condition caused by anthrax, which is like the
Speaker 1: most common manifestation, as you pointed out, also made an
Speaker 1: appearance in many of the names. And the word anthrax
Speaker 1: itself comes from the Greek anthracos, meaning coal or carbuncle,
Speaker 1: and many other names call out the black color that
Speaker 1: can often result from the anthrax skin condition.
Speaker 2: Right, Yeah, it's a very characteristic. Yeah.
Speaker 1: And the Latin word anthrax also means carbuncles or malignant boils.
Speaker 1: The French word for the disease was sharbone like carbon
Speaker 1: like coal or charcoal, and the whole body forms of anthrax, though,
Speaker 1: were of course called by many different names because no
Speaker 1: one yet knew that the diseases were linked.
Speaker 2: Right, that's what's so interesting about these ones that have
Speaker 2: such varied manifestations. Yeah, who connected cutaneous anthrax to inhalational anthrax?
Speaker 1: Uh huh? Oh, well, I'm gonna tell you that. Oh good,
Speaker 1: I can tell you his name, I can tell you
Speaker 1: how he did it. And another characteristic, or another parallel,
Speaker 1: was that many of these names included a reference to
Speaker 1: the spleen in the disease's name, So like in South Africa,
Speaker 1: the disease was referred to as spleen illness and in
Speaker 1: German spleen fire or inflammatory death of the spleen. Does
Speaker 1: the spleen I mean, does that a.
Speaker 2: Lot of It's a giant lymphoid organ There we go.
Speaker 1: As I've talked about before, the names that people use
Speaker 1: for a disease can tell us about the importance of
Speaker 1: the disease to humans or what they saw as it's
Speaker 1: defining characteristics. And maybe it was because of the economic
Speaker 1: importance of livestock, the fact that humans could also become ill,
Speaker 1: or the terrifyingly random and rapid way it killed. It's
Speaker 1: pretty clear that anthrax, in all of its various forms,
Speaker 1: was not an overlooked disease. By the seventeen hundreds, widespread
Speaker 1: global trade and population growth had led to, among other things,
Speaker 1: increasing urbanization and industrial specialization, and that also included textile production.
Speaker 1: So rather than wool or leather products being processed at
Speaker 1: the same place where the farms were, they were sent
Speaker 1: to textile mills where many people worked. The animal products wool, hides, skins, etc.
Speaker 1: Began to be transported long distances and aarin can you
Speaker 1: guess who.
Speaker 2: Hitched a ride anthrax sports exactly.
Speaker 1: At some of these busy textile mills in France, a
Speaker 1: physician named and I'm going to need your help with
Speaker 1: this pronunciation. Air okay, Nicholas, Okay, Nicholas, and then Fournier
Speaker 1: foh you are, and I er, yeah, that was great perfect.
Speaker 1: Fournier started to notice that some of the workers began
Speaker 1: to show signs of illness similar to those experienced by
Speaker 1: the animals where the materials came from, and the rate
Speaker 1: of these conditions was substantially higher than it was in
Speaker 1: the general population. And it wasn't just inflamed skin that
Speaker 1: these workers were experiencing, but also the GI symptoms or
Speaker 1: the full body manifestations of anthrax. Fournier, inspired in part
Speaker 1: by his older colleague, began to question whether these diseases
Speaker 1: with different names, thought at the same time to all
Speaker 1: be distinct diseases, were really all the same thing. He
Speaker 1: noticed a common thread binding the affected people together. They
Speaker 1: all had some connection to animal hair or animal parts,
Speaker 1: either eating or working or cleaning whatever, some sort of connection,
Speaker 1: and he published his findings and his description of anthrax
Speaker 1: in a booklet that may not have been very popular
Speaker 1: at the time of publication. But it would go on
Speaker 1: to greatly influence other researchers and physicians and veterinarians that
Speaker 1: came after him, And it would also mark him, at
Speaker 1: least in my eyes, as pretty dang ahead of his time,
Speaker 1: because all of these observations and hypotheses that he was
Speaker 1: making were taking place in the mid seventeen hundreds. Wow,
Speaker 1: the birth of germ theory was still about one hundred
Speaker 1: years away.
Speaker 2: That is truly remarkable.
Speaker 1: Yes, it reminds me a lot again of the botulism dude.
Speaker 1: I can't remember his name. Remember, he made all of
Speaker 1: these amazing achievements.
Speaker 2: Yet he's the one who did like all of the things,
Speaker 2: like he discovered the pathogen, did the test, did the
Speaker 2: thing found, a treatment, found a use.
Speaker 1: Blah blah blah everything. Yeah, yeah, he was cool. Only
Speaker 1: I can remember his name. Like I said, limited space here, okay,
Speaker 1: oh okay, but speaking of germ theory, shall we jump
Speaker 1: one hundred years into the future.
Speaker 2: I just want to give Fournier like a second more
Speaker 2: credit because I am still blown.
Speaker 1: Away, Okay, a moment of appreciation for Fournier.
Speaker 2: Nice job, dude, Okay, Okay.
Speaker 1: There's no we were gonna get away with not laughing
Speaker 1: about that one. Okay, Anthrax actually played a pretty huge
Speaker 1: role in the development of germ theory. What, yes, this
Speaker 1: is again where I was like, what this bacteria has
Speaker 1: so much beneath the surface?
Speaker 2: Okay, keep going, Okay.
Speaker 1: Basilla Santhrasis was one of the first bacterial species actually
Speaker 1: that was really intensively studied. It was used as one
Speaker 1: of the first case studies to develop cox postulates what
Speaker 1: to understand the ecology of the disease and the role
Speaker 1: that the environment played, what, and to develop a vaccine?
Speaker 2: Like why don't I know any of this, Aaron? It
Speaker 2: feels like I should know this.
Speaker 1: I think it was all overshadowed by two thousand and one. Yeah,
Speaker 1: but yeah, I think also there's a question in that
Speaker 1: as to why not just why don't you know all this?
Speaker 1: But why anthrax? Why was it so heavily studied?
Speaker 2: I mean because those killing people and their cows.
Speaker 1: Those are a couple of the reasons. So definitely, yeah,
Speaker 1: cause these huge episolotics that led to loss of life,
Speaker 1: loss of like wealth, et cetera. It was terrifying, you know,
Speaker 1: just a very threatening disease in terms of the symptoms
Speaker 1: and the mortality rate, and also how it seemed to
Speaker 1: appear randomly, so like untangling that mystery seemed to have,
Speaker 1: you know, would have placed it at high priority. Another reason, though,
Speaker 1: is that anthrax cases continued to rise in people who
Speaker 1: worked with animals or animal products, not just livestock farmers,
Speaker 1: but tanners and butchers and wool sorders as well. Yeah, definitely,
Speaker 1: and number four this is a very practical reason. But
Speaker 1: the Anthrax bacillis is actually like quite large ye so yeah,
Speaker 1: so it was large enough to be easily seen under
Speaker 1: a mid eighteen hundred's microscope, and it also turns out
Speaker 1: it's pretty easily stained as well. But still, the discovery
Speaker 1: of the Anthrax bacillis begins probably earlier than you might expect,
Speaker 1: in the eighteen fifties. Why this is like before germ theory. Really,
Speaker 1: it's like the very very beginning of germ theory in
Speaker 1: that time. So like eighteen forty nine eighteen fifty the
Speaker 1: French and a German researcher both observed the bacteria independently
Speaker 1: at like nearly the same time, and no one knows
Speaker 1: like priority doesn't really matter, but it still led to
Speaker 1: this huge controversy in both France and Germany trying to
Speaker 1: claim to who first discovered the Anthrax bacillis. And I
Speaker 1: think it's interesting because this controversy between France and Germany
Speaker 1: was just a preview of the contentious rivalry that would
Speaker 1: emerge between the French Louis Pasture and the German Robert
Speaker 1: Koch when it came to anthrax and all other things microbiology. Okay,
Speaker 1: so observing the rods in the blood of infected humans
Speaker 1: or animals was pretty easy, like those two earlier microbiologists did,
Speaker 1: But isolating those rods and growing them in a lab
Speaker 1: is a whole nother story. Yeah. Yeah, And so by
Speaker 1: recognizing that the Anthrax bacillis and other microbes were living things,
Speaker 1: early microbiologists were faced with the enormous hurdle of figuring
Speaker 1: out how to feed and shelter them, how to keep
Speaker 1: them happy enough to grow in an artificial setting outside
Speaker 1: of an animal. Yeah. An anthrax, because it has this
Speaker 1: like pretty unusual life cycle, proved to be quite technically challenging.
Speaker 2: Yeah, that's why it's surprising that it was so one
Speaker 2: of the first.
Speaker 1: Yeah, it's surprising that it was one of the first.
Speaker 1: But I also think that the way that it was
Speaker 1: studied was rather ingenious. Okay, so Robert Cooch, like, I'm
Speaker 1: not going to go into too many details, but what
Speaker 1: he did was he developed a culture slide. It was
Speaker 1: like a little had a little dip in it that
Speaker 1: not only allowed the bacillas to live, but it also
Speaker 1: allowed an observer to closely watch its every move. And
Speaker 1: this slide is how he was able to observe that
Speaker 1: the rods at the edge of the liquid suspension, those
Speaker 1: that were like more exposed to air, they were undergoing
Speaker 1: shape changes.
Speaker 2: Stop it.
Speaker 1: Yes, they were turning into long filaments and they started
Speaker 1: to look granular.
Speaker 2: Stop it.
Speaker 1: In other words, if they were transitioning into perfectly formed spores.
Speaker 2: He oh, I am losing it right now. Okay, but
Speaker 2: this is the eighteen hundreds and we're talking about looking
Speaker 2: through a microscope and watching a Bacterium sporiulate. Yeah, what
Speaker 2: the heck?
Speaker 1: Eighteen seventy six, I'm dead now, I know, because the
Speaker 1: implications for that discovery were enormous. So like, not only
Speaker 1: did this answer a whole host of questions, why did
Speaker 1: the basillas seemed to disappear in blood and tissue samples
Speaker 1: after the animal died because it did turn into his bore.
Speaker 1: Why greazing animals seemed.
Speaker 2: To be the most affected because they ate so much
Speaker 2: of it in the soil.
Speaker 1: And how on earth this bacterium survived in the soil
Speaker 1: and was able to cause seemingly random outbreaks.
Speaker 2: Oh my gracious.
Speaker 1: It's I mean, it's amazing. So you know, another reason
Speaker 1: why anthrax became a model organism is because Coke published
Speaker 1: his super detailed protocol for cultivating these anthrax withcilli And
Speaker 1: so for that reason, everyone was able to go out
Speaker 1: because like you said, it's globally distributed, or find a
Speaker 1: farm that had an anthrax outbreak, get some blood, and
Speaker 1: then you know, work with it in the lab. So,
Speaker 1: I mean, it's really weird to think about now because
Speaker 1: a anthrax is so deadly, and b were like that
Speaker 1: should be under high you know, like highly control substance, but.
Speaker 2: Three or four, like you can't just do that, you
Speaker 2: can't just do that.
Speaker 1: But they just did that. And so anthrax was used
Speaker 1: not only to develop Cox postulates, but also the principles
Speaker 1: that researchers would use to ensure that the bacterial species
Speaker 1: they were working on was indeed the species they thought
Speaker 1: it was so things like morphology, lab requirements, staining principles,
Speaker 1: life cycle illustrations like it was used as a model
Speaker 1: for all of those things.
Speaker 2: Wow.
Speaker 1: And Koch's anthrax research also caught the eye of none
Speaker 1: other than Louis Pasture. Among his many achievements. Pasture is
Speaker 1: often credited with developing the first anthrax vaccine, but in
Speaker 1: doing the research for this episode, I learned that he
Speaker 1: actually was not the first. The first was a veterinarian
Speaker 1: named Jean Joseph Henri Toussaint, who used heat and chemicals
Speaker 1: to develop a strain of anthrax that would produce an
Speaker 1: immune response in an animal without killing it. Heat and
Speaker 1: chemicals like again ahead of its time eighteen hundreds, late
Speaker 1: eighteen hundreds. He successfully tested his vaccine on twenty sheep
Speaker 1: and published his findings, and Pastur came across Pussant's vaccine
Speaker 1: work and decided to test it out. So in a
Speaker 1: public and highly publicized demonstration, he injected anthrax into two
Speaker 1: groups of sheep, one that had been vaccinated and the
Speaker 1: other not. I mean, newspapers were like came from all over.
Speaker 1: It's been now made into a movie like. This was
Speaker 1: a huge demonstration and thank goodness it worked. All of
Speaker 1: the sheep who had not been vaccinated died and those
Speaker 1: that had lived.
Speaker 2: Wow.
Speaker 1: And this public demonstration was not only a very exciting
Speaker 1: demonstration of theory in action and the life saving power
Speaker 1: of vaccines, but it also firmly placed Pasture as the
Speaker 1: creator of the anthrax vaccine because he.
Speaker 2: Was like, I'm gonna do it loudest.
Speaker 1: Well, not only did he do it loudest, but he
Speaker 1: also was like, oh no, my vaccine is way better.
Speaker 1: I used a much better like thing. You know, Touissant's
Speaker 1: method is unreliable and unscientific and blah blah blah. And
Speaker 1: poor Toussaint, he who was both less well known and
Speaker 1: less powerful than Pasture, was also suffering from a neurodegenerative
Speaker 1: disease that would go on to kill him at the
Speaker 1: age of forty one, and so he didn't have the
Speaker 1: ability to really assert his claim to fame.
Speaker 2: That's very sad, Errands.
Speaker 1: Very sad Pasture did not create the first anthrax vaccine.
Speaker 1: Maybe that's the take home. No, it's not really. There's
Speaker 1: lots of other take homes, but let that be one
Speaker 1: of them. Anyway. Vaccine credit aside The important thing was
Speaker 1: that there was now an anthrax vaccine, and the administration
Speaker 1: of this vaccine to livestock all over the globe did
Speaker 1: a great deal to reduce the incidence of the disease,
Speaker 1: but it did still happen. And here is where I
Speaker 1: want to revisit anthrax as an occupational disease. At this
Speaker 1: point in anthrax's history, it was still viewed primarily as
Speaker 1: a rural agricultural disease, despite Fournier's work in the French
Speaker 1: textile mills of the seventeen hundreds, because people just ignored
Speaker 1: that work straight up. But this characterization of anthrax as
Speaker 1: just agricultural that was about to change.
Speaker 2: Okay.
Speaker 1: By the late eighteen hundreds, the textile industry in Europe
Speaker 1: had become very centralized, even more so than one hundred
Speaker 1: years prior, with large factories where different types of wool
Speaker 1: and hair and skins would be imported from all the world.
Speaker 1: In these factories, a disease started to show up with
Speaker 1: increasing prevalence in the workers who would sort the wool.
Speaker 1: Wolfsorter's disease, as it's called. One day you felt fine,
Speaker 1: the next you got a fever and pneumonia like symptoms
Speaker 1: and then you collapsed and died. And during these outbreaks,
Speaker 1: no one yet knew that Wolfsort's disease was actually a
Speaker 1: type of anthrax. And that's because anthrax at the time,
Speaker 1: like I said, was still thought of just as a
Speaker 1: disease of agriculture. And at the same time, most anthrax
Speaker 1: cases tended to be cutaneous rather than inhalational. Yeah, and
Speaker 1: Wolfsort's disease is inhalational. Remember how scrapy like, which is
Speaker 1: the pre on disease of sheep, increased in prevalence and
Speaker 1: geographical distribution because of the wool trade. Yeah, yeah, anthrax also,
Speaker 1: And there was like around this time, which is like
Speaker 1: all so similarly, when wool demand grew so much and
Speaker 1: scrapey became a huge problem and also more widely distributed.
Speaker 1: That high demand for exotic furs and wolves grew so
Speaker 1: much that some farmers became more reluctant to lose out
Speaker 1: on a profitable fleece from a goat or sheep that
Speaker 1: died prematurely, perhaps from anthrax, Oh dear, yep, And so
Speaker 1: they would shear the animal anyway and send off the hair,
Speaker 1: which often still had bits of blood or skin attached. Yeah,
Speaker 1: the wool. Sorder would then comb the wool using newly
Speaker 1: developed machinery, which would often result in the dirt and
Speaker 1: dust and blood and skin particles turning a bit aerosolized.
Speaker 1: Oh god, yeah, just like a haze of anthrax.
Speaker 2: Oh God.
Speaker 1: And I think to us now, Wolfsort's disease may seem
Speaker 1: like an isolated problem limited to a various part of
Speaker 1: the population, but that wasn't the case at all. Wolfsorders
Speaker 1: made up a huge part of the occupational community, and
Speaker 1: to give you some sense of how much of an
Speaker 1: impact occupational anthrax had during this time, considered these stats
Speaker 1: from Italy. Between eighteen ninety and nineteen oh four, thirty
Speaker 1: six thousand, four hundred and thirty six cases of anthrax
Speaker 1: were registered among tanners, brushmakers, and woolworkers, with seven three
Speaker 1: hundred and eight deaths.
Speaker 2: WHOA, that's a lot. That's a lot.
Speaker 1: And so it makes sense then that there would be
Speaker 1: many epidemiologists hard at work on this problem. But among
Speaker 1: all of these epidemiologists, John Henry Bell may have been
Speaker 1: the most influential in getting wolfsorders disease to be widely
Speaker 1: recognized as a form of anthrax. It was also one
Speaker 1: of the first to push for workers' rights or at
Speaker 1: least call out the responsibility of the employer in providing
Speaker 1: a safe work environment and minimizing the risk of disease.
Speaker 2: Oh kidd it, h huh.
Speaker 1: As a physician, Bell would often be called upon to
Speaker 1: perform autopsies on those who died of woolsorters disease, and
Speaker 1: he became increasingly frustrated with what seemed to him to
Speaker 1: be careless employers who refused to acknowledge their own responsibility
Speaker 1: in the disease and so under cause of death he
Speaker 1: started to put things like employer's neglect and not properly
Speaker 1: washing or disinfecting imported mohair. Whoa yeah, and so you know,
Speaker 1: not employers don't want to be blamed for the death
Speaker 1: of their employees or you know. And also I think
Speaker 1: that his voice was loud enough and he was prominent
Speaker 1: enough in the community to really like raise the alarm
Speaker 1: on this wow And so in effect he started this
Speaker 1: activist movement among the woolfsorts to protest these working can
Speaker 1: conitions and to fight for protections from anthrax. And this
Speaker 1: also marked one of the first occasions of an infectious
Speaker 1: disease being recognized as an occupational hazard. So interesting, so.
Speaker 2: Many pieces to this anthrax puzzle. Err, I know, gosh.
Speaker 1: Practices like vaccination or increased sanitation of wool reduced the
Speaker 1: incidence of anthrax among these workers, but it did still
Speaker 1: pop up, and not just in the wool sorders. For instance,
Speaker 1: early shaving brushes were made of like animal hair, and
Speaker 1: some of these carried anthrax spores on them, And so
Speaker 1: when somebody would use a brush on their face that
Speaker 1: they had tiny little cuts from shaving, oh no, yeah,
Speaker 1: the spores would get in there and cause cutaneous anthrax.
Speaker 2: No thank you.
Speaker 1: And horse hair was often used as an ingredient in
Speaker 1: plaster and often or at least occasionally contain anthrax spores.
Speaker 1: By the early nineteen hundreds, the perception of anthrax had
Speaker 1: evolved into one of both agricultural and industrial importance, and
Speaker 1: several tools had been developed to combat the disease. Vaccines,
Speaker 1: which I'm not going to go into the history of,
Speaker 1: except to say that new and improved ones had been developed.
Speaker 1: Better sanitation practices and serum were all variously used and
Speaker 1: seemed to make a pretty substantial dent in slowing transmission.
Speaker 1: Anthrax seemed to be turning into a disease of the past,
Speaker 1: not quite. The world wars of the twentieth century really
Speaker 1: showcased how inventive and cruel and brutal and relentless humanity
Speaker 1: could be when it comes to killing other humans, and
Speaker 1: one of these methods of murder happened to be bioweapons.
Speaker 1: Long before the two thousand and one anthrax attacks in
Speaker 1: the US, there had been previous attempts to develop anthrax
Speaker 1: into a bioweapon by nearly every country involved in these
Speaker 1: global conflicts. Anthrax is always has always been near the
Speaker 1: top of the list of potential bioweapon agents because of
Speaker 1: its high mortality rate, its relatively easy manipulation in the
Speaker 1: lab thanks to its model organism status, its durability, its
Speaker 1: ability to survive an explosion, and the existence of a
Speaker 1: vaccine which could protect those who were administering the bioweapon.
Speaker 2: That is a gross part that I did not realize
Speaker 2: was a criteria for what makes a good bioweapon. Mm hmmmmm, Yes,
Speaker 2: that's so gross.
Speaker 1: Yeah, gross is Yeah, it's the right word. Research was
Speaker 1: carried out in many countries to work on how best
Speaker 1: to use antrax as a weapon, maybe in warfare, with
Speaker 1: shrapnel bombs, or as a massive civilian attack using high
Speaker 1: altitude bombs or atomizers, or may you know, lace some
Speaker 1: anthrax in lindseed cakes and then drop those into German
Speaker 1: fields where they would be eaten by the cattle, killing
Speaker 1: cattle and then humans that ate the cattle. It's a
Speaker 1: very specific example that I'm giving because that was an
Speaker 1: actual British operation called Operation Vegetarian during World War Two.
Speaker 1: I know, like I wrote this, and I'm like, am
Speaker 1: I reading this right?
Speaker 2: Yeah?
Speaker 1: Yeah. Scientists dealt with things like the logistics of how
Speaker 1: high a bomb should be deployed to impact the widest area,
Speaker 1: which way the wind was going, or which form of
Speaker 1: the bacillis, so we should we do like a liquid
Speaker 1: suspension or a spore form it would be most likely
Speaker 1: to cause death or be the most stable, or how
Speaker 1: to protect those deploying the weapon. So we know that
Speaker 1: people worked on anthrax as a bioweapon during these wars
Speaker 1: and researched it as a possibility, but did anyone ever
Speaker 1: try it out well. The first instance of anthrax being
Speaker 1: used as a bioweapon is often cited as a part
Speaker 1: of a World War One German sabotage program in which
Speaker 1: anthrax was supposed to be administered to Allied draft animals
Speaker 1: like horses, mules, reindeer, et cetera. In nineteen seventeen, German
Speaker 1: spy Baron von Rosen was captured in Norway and accused
Speaker 1: of smuggling a bioweapon anthrax filled glass capillaries concealed in
Speaker 1: sugar lumps. So these anthrax sugar cubes. In nineteen ninety eight,
Speaker 1: they were analyzed and anthrax genetic material was found, so
Speaker 1: like maybe there was something to it. However, in twenty
Speaker 1: seventeen a paper came out that suggests that those anthrax
Speaker 1: colonies were actually just lab contamination, and so we'll never
Speaker 1: really know if the sugar cubes held anthrax were not
Speaker 1: actually but we do have solid evidence of weaponized anthrax
Speaker 1: being tested on humans from Unit seven thirty one, and
Speaker 1: so this is the infamous unit of the Japanese Army
Speaker 1: that in World War II carried out bioweapons testing on
Speaker 1: human and animal subjects, and also where no one was
Speaker 1: ever punished because the US made an immunity deal to
Speaker 1: get access to all their research in exchange for immunity cool.
Speaker 2: Which is the episode where you talk a lot about
Speaker 2: that one.
Speaker 1: Hantaviruss I believe anyway, thousands of people, primarily in the
Speaker 1: historical region Manchuria, were intentionally dosed with anthrax to observe
Speaker 1: how quickly it killed or the dose necessary medicalized torture
Speaker 1: that mostly resulted in death. There were anthrax shrapnel bombs
Speaker 1: that were blasted at people tied to stakes nearby, with
Speaker 1: different body parts exposed to test dose and site of entry.
Speaker 1: What the actual I know and many Many other countries,
Speaker 1: including France and England and Germany and Canada and the US,
Speaker 1: performed similar horrifying experiments on weaponized anthrax on animal subjects
Speaker 1: throughout World War II. As you can expect, as we
Speaker 1: all expect, research into anthrax as a bioweapon did not
Speaker 1: cease with the end of World War II, nor did
Speaker 1: it end in nineteen seventy two, when nearly every country
Speaker 1: around the globe signed the Biological Weapons Convention, which banned research, development, possession,
Speaker 1: and deployment of biological weapons. In nineteen seventy nine, in Serdloftsk, Russia,
Speaker 1: approximately one hundred people maybe more fell ill and died
Speaker 1: within a few days of anthrax. Most of the people
Speaker 1: were workers at a ceramic plant located across the street
Speaker 1: from a biological research facility whose main project was you
Speaker 1: guessed it, aerosolized anthrax. Yeah, well, bioweapons with aeroed anthrax
Speaker 1: is the main yep. And the Soviet government claimed at
Speaker 1: the time, oh, that's ingestional anthrax, that they just got
Speaker 1: it from eating tainted meat. And then they also happened
Speaker 1: to destroy all of the victim's medical records. And then
Speaker 1: later investigations though, like they invited American researchers to come
Speaker 1: in and investigate the source of this outbreak, and that
Speaker 1: revealed that a filter that was preventing the fine anthrax
Speaker 1: powder from escaping the building had been removed and no
Speaker 1: one had noticed, And so the drying machines with this
Speaker 1: mound of like anthrax were turned on, basically blowing these
Speaker 1: anthrax spores into the outside air. Oh no, yeah, downwind
Speaker 1: was as you can guess, the ceramic plant. There's a
Speaker 1: whole book on this written by one of the American
Speaker 1: researchers who helped to uncover the truth about this incident.
Speaker 1: It's called Anthrax The Investigation of a Deadly Outbreak looks fascinating.
Speaker 1: I didn't read it, but I'll post it anyway. Around
Speaker 1: the same time as the speredlofsk incident, an enormous outbreak
Speaker 1: of anthrax was taking place in what was then Rhodesia
Speaker 1: now Zimbabwe, the largest epidemic of the last two hundred years.
Speaker 2: Oh my god.
Speaker 1: Between nineteen seventy eight and nineteen eighty four, one hundred
Speaker 1: and one thousand, nine hundred and ninety cattle and seventeen thousand,
Speaker 1: one hundred and ninety nine people were stricken with anthrax
Speaker 1: and nearly two hundred people died.
Speaker 2: Whoa.
Speaker 1: This outbreak, which was obviously economically devastating, took place at
Speaker 1: a time of great civil unrest in the country, and
Speaker 1: there has been a lot of speculation that the surge
Speaker 1: in anthrax cases was due to the intentional release of
Speaker 1: anthrax as a bio weapon. And while there's not a
Speaker 1: whole lot of physical evidence that's the case, there is
Speaker 1: a good deal of circumstantial evidence. And I'll post a
Speaker 1: great review that goes over this outbreak and all the
Speaker 1: different sort of hypotheses. Okay, this is a long episode.
Speaker 1: Just a couple more bioterrorism incidents, and then I'll throw
Speaker 1: it back to you, okay. In nineteen ninety three in Japan,
Speaker 1: a liquid culture of anthrax was sprayed from the rooftops
Speaker 1: by a religious cult, but no one got sick because
Speaker 1: it turns out it was the strain of anthrax used
Speaker 1: to vaccinate animals and was therefore harmless. Kay, great news.
Speaker 1: And then finally the two thousand and one Anthrax Letters.
Speaker 1: And I'm just going to go over the basics here,
Speaker 1: like some very surface level stuff because this episode is
Speaker 1: very long as is, and be there might be a
Speaker 1: time in the future where I give this topic the
Speaker 1: time that it truly deserves, which is my way of
Speaker 1: throwing in like a very vague potential teaser. S. Stay tuned, Yes,
Speaker 1: definitely stay tuned for more updates on that, but okay,
Speaker 1: the Anthrax Letters. The first victim of the Anthrax Letters
Speaker 1: was Bob Stevens, editor for tabloid publisher American Media, in
Speaker 1: Boca Ratonne, Florida, on October fourth, two thousand and one,
Speaker 1: a couple of days after opening a letter that contained
Speaker 1: a threatening note. He checked himself into a hospital due
Speaker 1: to trouble breathing. The next day. He died. A few
Speaker 1: days after his death, one of his coworkers developed cutaneous anthrax.
Speaker 1: Then cases of anthrax started popping up in New York
Speaker 1: City news outlets, studios for NBC News, and headquarters of
Speaker 1: the National Inquirer, all from letters containing anthrax spores. Anthrax
Speaker 1: letters arrived at US Senators Tom Dashel and Patrick Leahy's offices,
Speaker 1: and then postal workers in New Jersey, in Washington in
Speaker 1: DC became sick with inhalational anthrax. In total, twenty two
Speaker 1: people became sick due to these anthrax letters, eleven with
Speaker 1: cutaneous anthrax and eleven with inhalational anthrax, and five of
Speaker 1: those with the inhalational form died pretty quickly. It seemed
Speaker 1: likely that the person responsible had access to a highly
Speaker 1: secure scientific facility where the deadly so called AIM strain
Speaker 1: was kept, and genetic testing also supported this, which created
Speaker 1: this like very strange situation right where like everyone who
Speaker 1: worked at you SAMRID, which is United States Army Medical
Speaker 1: Research Institute of Infectious Diseases much easier to say you SAMRID.
Speaker 2: Yeah, the longest acronym of all time, yep.
Speaker 1: But everyone who was working there, you know, they were
Speaker 1: treated as both suspect and they were also these essential
Speaker 1: assistants to the case because they would be the ones
Speaker 1: performing the genetic tests and the analyzes that would reveal
Speaker 1: where the anthrax from the letters came from. It's like
Speaker 1: a really strange thing to think about.
Speaker 2: Yeah, that's bizarre.
Speaker 1: Yeah. And the investigation itself into who was responsible for
Speaker 1: the anthrax letters, it has so many twists and turns
Speaker 1: and you know, at least a couple of dead ends.
Speaker 1: But years after the letters were mailed, super sensitive genetic
Speaker 1: tests were developed that allowed investigators to identify not only
Speaker 1: the strain of anthrax used in the letters, but the
Speaker 1: specific flask where those spores had come from.
Speaker 2: That is amazing.
Speaker 1: I know, it's just such an interesting, like course of investigation.
Speaker 2: Yeah.
Speaker 1: The more technology you have and then I don't know,
Speaker 1: and also the characteristics of anthrax itself, like or the
Speaker 1: basilis anthrasis right, the fact that it's so clonal, the
Speaker 1: fact that it doesn't really like evolve very much or
Speaker 1: is like so consistent.
Speaker 2: Yeah, that you can identify it down to the flask,
Speaker 2: that's incredible.
Speaker 1: Yeah, exactly. And it turns out that these anthrax spores
Speaker 1: had come from a flask at you Samrid that was
Speaker 1: under the care of researcher Bruce Ivans, and Ivan's motive
Speaker 1: was thought to be that he wanted to save the
Speaker 1: anthrax vaccine program, which was in danger of being shut down.
Speaker 1: And so you know, if there were suddenly a bunch
Speaker 1: of deadly anthrax cases, then the need for the program would,
Speaker 1: you know, become clear or something. And throughout the investigation,
Speaker 1: Ivans never confessed. I believe that there was no physical
Speaker 1: evidence found connecting Ivans like home or car to the
Speaker 1: anthrax envelopes, and Ivans himself died of an acetamnifin overdose
Speaker 1: in two thousand and eight, but the circumstantial evidence does
Speaker 1: seem pretty strong, and like I said, there's a lot
Speaker 1: more to the story that I didn't do it justice.
Speaker 1: And even if we never have a conclusive answer as
Speaker 1: to who sent those letters, one thing is for sure.
Speaker 1: The two thousand and one anthrax letters forever seared anthrax
Speaker 1: as a dangerous bioweapon in the minds of the public. Yeah,
Speaker 1: so it started out as an agricultural disease, transformed into
Speaker 1: that of an occupational hazard and now a bioweapon. Since
Speaker 1: two thousand and one, we've learned so much more about
Speaker 1: the ecology of this Bacillus, how it infects wildlife, how
Speaker 1: it interacts with plants and may not be as dormant
Speaker 1: in the soil as we previously thought. How anthrax may
Speaker 1: not just be a disease caused by basilisanthrasis, the role
Speaker 1: that Necrophagius flies may play in transmission, the risk that
Speaker 1: a warming climate plays, and expanding the geographical distribution of
Speaker 1: his pathoges. Oh my goodness, and so on and so forth. Clearly,
Speaker 1: despite being one of the longest studied bacterial species, there
Speaker 1: are still many many mysteries to uncover. So erin, where
Speaker 1: do we stand with anthrax today?
Speaker 2: Oh my goodness. I will try to bring us up
Speaker 2: to speed right after this break.
Speaker 3: Wow.
Speaker 2: Okay, those were a lot of questions that you left
Speaker 2: open for me, Aaron, So let me just say, off
Speaker 2: the bat, I'm not going to be able to answer those,
Speaker 2: but we're going to call in some backup. So historical
Speaker 2: analysis reveals, and I think this is really interesting. For
Speaker 2: every ten anthrax cases in animals that leave anthrax carcasses,
Speaker 2: essentially that tends to result in one human cutaneous anthrax case.
Speaker 2: H there is one case of human gastrointestinal anthrax for
Speaker 2: every three thousand, just over three thousand anthrax infected animals
Speaker 2: that are eaten.
Speaker 1: Wow, wait for every three thousand anthrax infected animals that
Speaker 1: are eaten.
Speaker 2: So we didn't get into this in the biology erin
Speaker 2: But while we don't fully know exactly the infectious dose,
Speaker 2: it's estimated to be quite high, especially for gastrointestinal and
Speaker 2: inhalational anthrax. Humans are actually probably pretty resistant to anthrax infection.
Speaker 1: That is very interesting, I know, okay.
Speaker 2: And we also know from historical data that in humans
Speaker 2: there are about one hundred thousand cutaneous cases for every
Speaker 2: enteric or gastrointestinal case that occurs worldwide. Wow. And inhalational
Speaker 2: anthrax today is extremely uncommon, Okay. So that's what we
Speaker 2: do know. Globally overall, we have a fairly poor understanding
Speaker 2: of global risk and incidents of anthrax. But we do know,
Speaker 2: like I said, that human infection largely results from interactions
Speaker 2: with animals or animal products, and so outbreaks in human
Speaker 2: tend to occur both temporally and spatially in association with
Speaker 2: outbreaks in animals. And we also have a lot of
Speaker 2: good data that shows that in most parts of the world,
Speaker 2: widespread distribution of vaccines for domestic animals and livestock is
Speaker 2: really effective at reducing infection in animals and in humans.
Speaker 2: But like we've talked about in pretty much every episode
Speaker 2: of this podcast, our estimates of incidence and prevalence are
Speaker 2: only as good as the surveillance that we do. And
Speaker 2: in the case of anthrax, even though in almost every
Speaker 2: country it's a global presence and it's a notifiable disease,
Speaker 2: we still just don't have excellent data in a lot
Speaker 2: of cases. And I think this is probably at least
Speaker 2: in part because it's not specifically a human disease and
Speaker 2: it can often infect wildlife. It's really hard to get
Speaker 2: a handle on something as big as that, understanding everything
Speaker 2: from the course of the disease to the ecological characteristics
Speaker 2: in so many different ecosystems. It's a massive challenge. Oh yeah.
Speaker 2: So anthrax is really I think probably especially fun for us, Aaron,
Speaker 2: because it's an environmental pathogen that really requires a large
Speaker 2: scale interdisciplinary approach to understanding and control. And because of that,
Speaker 2: we wanted to talk to someone who is an expert
Speaker 2: in this type of interdisciplinary research when it comes to anthrax.
Speaker 2: Understanding the disease dynamics in wildlife, evaluating the climate and
Speaker 2: environmental patterns and the distribution of anthrax, identifying the challenges
Speaker 2: and predicting outbreaks, and most of all, working across fields
Speaker 2: to most effectively control the incidents of this devastating disease.
Speaker 2: Were so lucky to get to chat with spatial epidemiologist
Speaker 2: Morgan Walker. And we'll let her introduce herself right now.
Speaker 5: My name is Morgan Walker.
Speaker 6: I am a spatial epidemiologist at the University of Florida.
Speaker 6: I work in doctor Jason Blackburn's lab and we are
Speaker 6: house jointly in the Department of Geography and the Emerging
Speaker 6: Pathogens Institute at UF and my research focuses on the space,
Speaker 6: shoot and poral patterns of diseases and disease spread, especially
Speaker 6: of bacterial zoonoses, which are acterial diseases that can affect
Speaker 6: both animals and humans, one of which is anthrax.
Speaker 1: Awesome, thank you so much for joining us. We're so
Speaker 1: excited to talk with you.
Speaker 5: Thank you so much for having me.
Speaker 1: So we want to just start off by asking, you know,
Speaker 1: a very basic general question, what is the current worldwide
Speaker 1: distribution of b anthrasis? Like, I know, it's a big one.
Speaker 1: And so because there are presumably patterns in the distribution
Speaker 1: of this pathogen, we also wanted to ask you, you know,
Speaker 1: what are some of the environmental or climatic determinants of
Speaker 1: its distribution. What are some of the patterns that we see.
Speaker 6: Yeah, so it is definitely a big one. It's distributed
Speaker 6: pretty much globally. Some of the areas where it is
Speaker 6: endemic or where we typically see cases are areas like
Speaker 6: Central Asia, the midwest of the United States, extending up
Speaker 6: into the northwest territories of Canada, sub Saharan Africa, southern
Speaker 6: eastern Europe, and southeastern Australia. And part of the reason
Speaker 6: why it has such a wide range is because it
Speaker 6: can form a protective spore around it, which makes it
Speaker 6: really hearty and really resistant to a variety of environmental
Speaker 6: and climatic conditions. But it survives best in soils with
Speaker 6: slightly alkaline phs and soils where there's high calcium concentrations,
Speaker 6: and in soils where there's lots of organic matter present,
Speaker 6: so fertile soils excellent.
Speaker 2: So then what types of kind of environmental or ecological
Speaker 2: patterns do we know of that are tied to an
Speaker 2: increased risk of anthrax outbreaks, either among animals or even humans.
Speaker 5: That's a great question.
Speaker 6: It's something that we're definitely still researching and trying to
Speaker 6: figure out, because if we have a better idea of
Speaker 6: why an outbreak happens, we can do better predicting when
Speaker 6: they're going to occur and how intense they're going to be.
Speaker 6: There's not a clear consensus at this point what the
Speaker 6: mechanism is that leads to an outbreak, because outbreaks have
Speaker 6: happened in such a variety of geographies and a variety
Speaker 6: of ecological conditions into such a wide variety of animal species.
Speaker 6: But what we can't say at this point is it
Speaker 6: seems to be that in the mid to high latitudes
Speaker 6: of the world, the pattern that precedes an outbreak is
Speaker 6: that there will be a wet spring followed by a
Speaker 6: hot dry period, and then there will be a rainfall event.
Speaker 6: So basically just it will brain really hard, and then
Speaker 6: a few days after that rain event there will suddenly
Speaker 6: be cases popping up. And we are still researching why
Speaker 6: exactly that pattern leads to outbreaks, but in areas like
Speaker 6: West Texas, we see both on the ground and anecdotally
Speaker 6: when talking to land managers that those conditions seem to
Speaker 6: allow the populations of biting fly populations to explode. So
Speaker 6: we think that biting flies are mechanical vectors of the disease,
Speaker 6: which essentially means that when a biting fly bites an
Speaker 6: animal that is actively fighting an infection and has the
Speaker 6: solo sand brasis circulating through its bloodstream, it can get
Speaker 6: the bacteria on its mouth parts and then fly to
Speaker 6: another animal, bite it and infect it.
Speaker 1: That's like such an interesting mechanism of dispersal because it's
Speaker 1: like a vector but not a vector, but not a vector, yeah,
Speaker 1: in the way that we like traditionally think of vectors. Yeah,
Speaker 1: so you know, and I know that you said that
Speaker 1: we're still sort of working out the exact risk factors
Speaker 1: for an anthrax outbreak, But how do we monitor how
Speaker 1: risk of exposure to anthrax changes over time? And then
Speaker 1: also how does that risk in general differ between you know,
Speaker 1: let's say some groups of wildlife or some groups of
Speaker 1: domestic animals and humans as well, Like, how does the
Speaker 1: risk change for those different groups?
Speaker 6: Yes, so globally, the use of active surveillance or continually
Speaker 6: monitoring risk in a population for antas, it's really limited,
Speaker 6: especially because areas can go long time periods about seeing
Speaker 6: an outbreak, so people will get into a habit of
Speaker 6: not really worrying about it, and so they're not actively monitoring.
Speaker 6: It's much more common to do you sort of passive surveillance,
Speaker 6: which means that on the animal side of things, if
Speaker 6: a land manager sees an animal that is exhibiting clinical
Speaker 6: signs of anthrax, they might have that animal tested, or
Speaker 6: they might have that animal carcass tested if the animal
Speaker 6: actually succumbs to disease. And then on the human side
Speaker 6: of things, passive surveillance pretty much looks like waiting for
Speaker 6: humans to get infected to come into a clinical setting
Speaker 6: because they need to be treated, and then that's how
Speaker 6: cases get reported. So almost all mammals are susceptible. However,
Speaker 6: the animals that we typically see diet of antacts are herbivores,
Speaker 6: so that's why it's a big problem in livestock amongst cattle, goats,
Speaker 6: and sheep, whereas carnivores actually very rarely succumb to anthrax,
Speaker 6: so it does differ amongst animal groups. And then for humans,
Speaker 6: risk is definitely sort of dependent on occupation and behavior,
Speaker 6: so obviously if you're land manager that's trying to handle
Speaker 6: an outbreak and dispose of the carcasses, that's something that
Speaker 6: will put you at risk. But also it's not uncommon
Speaker 6: in certain areas of the world for people who are
Speaker 6: raising livestock. If they see an animal that's sick, they
Speaker 6: might go ahead and slaughter that animal just so that
Speaker 6: they can try to recover some of the financial investment
Speaker 6: that they've spent. And then once they are slaughtering the animal,
Speaker 6: handling infected animal meat outputs you at risk for continuous anthrax.
Speaker 5: And then if you go.
Speaker 6: On to sell that meat and people eat it and
Speaker 6: it might be undercooked, they can also become infected that way.
Speaker 2: Got it. So, as a pathogen that spends part, if
Speaker 2: not the majority, of its life cycle in the external environment,
Speaker 2: like not being pathogenic necessarily, it seems like very likely
Speaker 2: that global climate change is going to or maybe already
Speaker 2: has begun to impact the distribution of Basilla's and racis
Speaker 2: in some way. So could you talk a little bit
Speaker 2: about what some of the models are predicting in regards
Speaker 2: to the impact of a warming climate on either a
Speaker 2: shift or expansion in the range of this pathogen, and
Speaker 2: what might that mean for the kind of shifting landscape
Speaker 2: of risk.
Speaker 6: Yes, So this moment in time, there's a lot of
Speaker 6: uncertainty in the face of climate change when thinking about
Speaker 6: the soles and racis, because there could absolutely be range
Speaker 6: expansion where we see that new areas are now suitable
Speaker 6: for the bacterias to survive, but at the same time,
Speaker 6: some models predicted there will be range contraction. Additionally, some
Speaker 6: people hypothesize that outbreaks could become more intense because those
Speaker 6: weather patterns that I talked about earlier, where there's a
Speaker 6: really wet spring and then a hot dry period that
Speaker 6: could happen more frequently, or it could be on like
Speaker 6: larger scales. But at this point it's really difficult to
Speaker 6: know exactly what's going to occur.
Speaker 5: We don't really have enough data.
Speaker 6: And because antax, there's a lot of stigma around it,
Speaker 6: so it's actually under reported globally. So we're still kind
Speaker 6: of working on getting highly accurate maps of just where
Speaker 6: cases are occurring today. So projecting that into the future
Speaker 6: is something that's pretty difficult at this point to do.
Speaker 1: Gotcha, gotcha. Yeah, Fortunately for Basilla Santhrasis, we do have
Speaker 1: various methods of control or prevention sometimes treatment. So we
Speaker 1: have like a vaccine, we have antibiotics, and we have
Speaker 1: also just improved sanitation and monitoring measures, and so we
Speaker 1: wanted to ask sort of how do the use of
Speaker 1: these different control measures differ between wildlife and domestic animals
Speaker 1: for instance, or just between animals in general and humans. So, like,
Speaker 1: for instance, let's say that there's an outbreak in wildlife,
Speaker 1: how might different control strategies be used in that outbreak
Speaker 1: compared to one in livestock for instance.
Speaker 6: Yes, so that is the good news. There are different
Speaker 6: control strategies. And for livestock, there is a vaccine that's
Speaker 6: very effective and it's been in use for decades and
Speaker 6: it's easy to administer.
Speaker 5: But the downside of that is that.
Speaker 6: The vaccine is most effective twenty one days after vaccination,
Speaker 6: so it might not be most effective to administer in
Speaker 6: the middle of an outbreak. And then additionally, the vaccine
Speaker 6: has to be readministered annually, so that is time consuming
Speaker 6: and can sometimes be difficult. In terms of wildlife, the
Speaker 6: vaccine is safe for wildlife. That is an off label use,
Speaker 6: meaning that there haven't been that many clinical trials done
Speaker 6: to confirm the safety and efficacy of vaccine and wildlife,
Speaker 6: but it has been used for a variety of species
Speaker 6: and seems to be effective. The problem with that is
Speaker 6: that the vaccine is an injectable vaccine, so if you
Speaker 6: can't get close to the wildlife in question, that makes
Speaker 6: it very difficult. Can dart So if you have a
Speaker 6: dart and you put the vaccine in it and then
Speaker 6: you can shoot the animal, that is a way to
Speaker 6: administer it. And that's sometimes used for wildlife that are
Speaker 6: like on some of these closed franches that have like
Speaker 6: exotic wildlife species that are expensive animals. Sometimes people try
Speaker 6: to do that, but they also have to weigh the
Speaker 6: risk of then you can potentially injure the animal with
Speaker 6: a dart versus administer in the vaccine.
Speaker 2: Right. Interesting.
Speaker 1: Yeah, So you know, with these different control strategies, does
Speaker 1: their effectiveness vary regionally?
Speaker 5: Yes.
Speaker 6: Vaccine use is a strategy that varies regionally and by
Speaker 6: country and sometimes even within countries. In the former Soviet Union,
Speaker 6: for example, they have a legacy of really high vaccination
Speaker 6: of livestock, so that's still in place in many countries
Speaker 6: in Central Asia and Eastern Europe, whereas a lot of
Speaker 6: areas in for example to here, in Africa and South
Speaker 6: and East Asia, the amount of vaccinations going out to
Speaker 6: livestock are really low, sometimes around like zero to five percent.
Speaker 6: So one of the methods of control during an outbreak
Speaker 6: is proper carcass disposal. So it's very important to try
Speaker 6: to dispose of the carcass in a way that will
Speaker 6: minimize the amount of bacterial that gets leached out into
Speaker 6: the environment.
Speaker 5: How we recommend that people do that.
Speaker 6: The best method is through burning, and if you can't
Speaker 6: burn the animal thoroughly, we recommend that people bury it.
Speaker 6: If you can't bury it, we recommend decontamination.
Speaker 5: With a bleach spray.
Speaker 6: But regionally, especially in areas if they're experiencing an outbreak
Speaker 6: in the hot, dry season, it might be too dangerous
Speaker 6: to try to burn the animal carcass because of the
Speaker 6: danger of wildfires.
Speaker 2: So with anthrax, it's one of these examples of a
Speaker 2: system that there are so many different angles where not
Speaker 2: only can you study it, but you kind of have
Speaker 2: to because you have you know animal hosts, you have
Speaker 2: a human disease, you have the genetics or the microbiology
Speaker 2: of the pathogen itself, but then you have the environmental aspects.
Speaker 2: You have all these different regional aspects of different cultural practices.
Speaker 2: It's so much and then there's like public health big
Speaker 2: scale on top of all of that. So could you
Speaker 2: talk a little bit about how interdisciplinary research is just
Speaker 2: so crucial for a disease like anthrax and kind of
Speaker 2: what interdisciplinary research looks like in practice.
Speaker 6: Yeah, So interdisciplinarity is really important for anthrax because, as
Speaker 6: I donostics, there are many different agencies and research groups
Speaker 6: and stakeholders all involved, and our lab aims to be
Speaker 6: a part of the practice by being involved in so
Speaker 6: many different pieces of the puzzle. So we do things
Speaker 6: from working outbreaks on the ground with land manager, to
Speaker 6: then taking those samples that we collect back to the
Speaker 6: lab and doing diagnostics to hold genome sequencing, to then
Speaker 6: mapping the outbreak and trying to analyze it, to then
Speaker 6: also working with partners internationally to try to mutually educate
Speaker 6: ourselves about the disease and also to help inform them with.
Speaker 5: Prevention of the disease.
Speaker 6: So there's definitely a lot of components to go into it,
Speaker 6: and it's difficult to coordinate, and it's as many public
Speaker 6: health issues are.
Speaker 5: There's so a lot of progress to be made.
Speaker 6: As I mentioned, there's a lot of sigma around anthrax,
Speaker 6: so it goes under reported globally. And it's also really
Speaker 6: difficult to determine the exact distribution of vaccination and how
Speaker 6: many vaccines are going out to animals. So to more
Speaker 6: accurately understand where cases are occurring as well as vaccination,
Speaker 6: we really need more accurate reporting, which takes interdisciplinarity and
Speaker 6: the cooperation between many different groups and agencies.
Speaker 1: That was so awesome. Thank you so much, Morgan, and
Speaker 1: thank you to doctor Saltzer as well. That was just
Speaker 1: so great. I loved it.
Speaker 2: We were so lucky to get to have both of
Speaker 2: you on. Thank you.
Speaker 1: Yeah, all right, this was a really fun episode to do.
Speaker 1: It was super interesting, so many different angles.
Speaker 2: I feel like I learned a lot.
Speaker 1: Yeah, absolutely, Speaking of learning a lot and learning a
Speaker 1: lot more, should we do sources?
Speaker 2: Let's these sources?
Speaker 1: Okay, So for this episode, I have a lot of
Speaker 1: sources and I will list all of them on our website,
Speaker 1: but I do want to shout out a book that
Speaker 1: I used called Death in a Small Package, A Short
Speaker 1: History of Anthrax by Susan Jones.
Speaker 2: Yeah. I also had quite a number of sources Aaron
Speaker 2: a couple that I wanted to give a special shout
Speaker 2: out to. There was a paper it's a little old
Speaker 2: now from nineteen ninety eight by the World Health Organization
Speaker 2: that is Guidelines for the Surveillance and Control of Anthrax
Speaker 2: in Humans and Animals. It's just a really nice kind
Speaker 2: of overview of just how broad anthrax is. And then
Speaker 2: a couple of really great papers by doctor Colin Carlson
Speaker 2: really focusing on how important interdisciplinary research is for anthrax.
Speaker 2: So there's a paper from twenty eighteen called Spores and
Speaker 2: Soil from Six Sides, Interdisciplinarity and the Environmental Biology of Anthrax.
Speaker 2: And Morgan Walker wrote an awesome paper that came out
Speaker 2: in twenty twenty called Ungulate Use of locally infectious Zones
Speaker 2: in a re Emerging Anthrax risk Area. You'll find the
Speaker 2: list of all of our sources from this episode and
Speaker 2: every one of our episodes on our website This podcast
Speaker 2: will kill you dot com, Yes you will.
Speaker 1: Thanks again so much to our absolutely wonderful guests. It
Speaker 1: was such a joy yeah to chat with you, it
Speaker 1: really was.
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Speaker 2: this episode and all of our episodes.
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Speaker 1: next time, wash your hands.
Speaker 2: You filthy animals.
Speaker 1: Obu bon bu bu bu bu bu