Speaker 1: My name is Catherine Hughes, and five years ago I
Speaker 1: gave birth to the most beautiful, gorgeous little boy. His
Speaker 1: name was Riley, and he had soft blonde hair and gorgeous,
Speaker 1: piercing blue eyes. But when Riley was about three weeks old,
Speaker 1: he started to get sick. I really thought it was
Speaker 1: just a cold. At first, it was just a bit
Speaker 1: of a runny nose, a bit of a sniffle, and
Speaker 1: I wasn't too worried. But then a couple of days later,
Speaker 1: I heard this tiny little cough and I'll never forget
Speaker 1: the sound it made. It was so small, so innocuous,
Speaker 1: but it was really a sign of what was to come.
Speaker 1: My husband was way for work, so I decided to
Speaker 1: call out a locum doctor to come visit our house
Speaker 1: one evening. Riley was about four weeks old at the time,
Speaker 1: and Riley appeared perfectly healthy. He was sound asleep and
Speaker 1: you just couldn't tell that there was anything wrong with
Speaker 1: him in between the coughing bouts. So the doctor looked
Speaker 1: at Riley reassured me that I was probably worrying too much,
Speaker 1: that Riley seemed to be perfectly okay. That evening, Riley
Speaker 1: slept and slept and slept and just did not want
Speaker 1: a breastfeed. He didn't want to wake up. He was
Speaker 1: so sleepy. I was feeling really uncomfortable at that stage,
Speaker 1: so my husband flew back in from work and we
Speaker 1: took him to hospital the next morning, and at hospital,
Speaker 1: he was admitted overnight because they were just a bit
Speaker 1: worried that he was not interested in breastfeeding anymore. But
Speaker 1: Riley didn't go home the next day. Each day that
Speaker 1: he stayed in hospital, he just seemed to grow worse
Speaker 1: and worse, and the coughing got more severe. It felt
Speaker 1: like every day there were just more tubes and wires
Speaker 1: and more doctors. Everything just got worse and worse. On
Speaker 1: his fourth day in hospital, we were moved into the
Speaker 1: pediatric intensive care unit. The doctors were concerned that he
Speaker 1: had developed pneumonia, and they were pretty confident at this
Speaker 1: stage that he had hooping cough. When the doctors diagnosed
Speaker 1: Riley with hooping cough, I actually felt a bit relieved
Speaker 1: because I thought that there'd be able to cure him.
Speaker 1: But there is no cure for hooping cough. You just
Speaker 1: kind of hope and pray that they get better as
Speaker 1: they are cared for in hospital, and Riley didn't get better.
Speaker 1: His organs started to shut down. By day five, his
Speaker 1: heart was under a lot of strain, and on day five,
Speaker 1: which was his last day in hospital, he was unconscious.
Speaker 1: They'd put him in a on life support and they
Speaker 1: tried to use echmo to save his life, and I
Speaker 1: just remember looking at his body on the bed. It
Speaker 1: was a big bed, a tiny little four week old
Speaker 1: baby on there, but he was so swollen and just
Speaker 1: covered in so many wires and tubes. It was really
Speaker 1: the most traumatic thing to say. And that afternoon we
Speaker 1: watched as this pink, foamy stuff started coming out of
Speaker 1: his lungs, and the doctors told us that there was
Speaker 1: nothing more that they could do. We'd asked about organ donation,
Speaker 1: but unfortunately, I think his organs were just too ravaged
Speaker 1: from the toxins released by the hooping cough bacteria. So
Speaker 1: at two in the afternoon, after five days in hospital,
Speaker 1: we took Riley off life support and he was just
Speaker 1: hot and swollen and so sick, and they took all
Speaker 1: the tubes and wires out and we had to say
Speaker 1: goodbye to our little baby or because he caught this
Speaker 1: horrible preventable hooping cough, and he was too young to
Speaker 1: be vaccinated. He was only thirty two days old when
Speaker 1: he died, and at the time, pregnancy vaccination hadn't been
Speaker 1: routinely recommended or funded in Australia, so newborn babies up
Speaker 1: Riley were extremely vulnerable to hooping cough and it cost
Speaker 1: him his life.
Speaker 2: Hi, I'm Aaron Welsh and I'm Erin Oman Updike and
Speaker 2: this is this podcast will kill you? Yeah, today it
Speaker 2: is today it is. Yeah. So you just heard from
Speaker 2: Catherine Hughes who was kind enough to come onto the
Speaker 2: podcast and share with you her story, and you're gonna
Speaker 2: hear a little bit more from her later on in
Speaker 2: the episode as well. So thanks again, Catherine. That was yeah.
Speaker 3: Yeah, it's a horribly depressing story that unfortunately isn't the
Speaker 3: only one out there. So today we're obviously talking about
Speaker 3: protessis whoopin cough.
Speaker 2: To get us to this episode, we are drinking.
Speaker 3: A very strong quarantine.
Speaker 2: Yes, it's basically all alcohol. It is call Three Women
Speaker 2: and a Baby and it's called that because the first
Speaker 2: really successful vaccine and that was in widespread use, was
Speaker 2: developed by three awesome women Woo woo girl power. Yeah,
Speaker 2: so what is in three Women and a Baby.
Speaker 3: Well, it's rye whiskey, of course, because whiskey, as we
Speaker 3: all know, is the cure for all children's ailments.
Speaker 2: Of course, don't do that at home. It's not not
Speaker 2: evaluated by the FDA or podcast. We're not being serious.
Speaker 4: No.
Speaker 2: It also has luxardo liqueur and chinar which is an
Speaker 2: artichoke liqueur which.
Speaker 3: Sounds weird, but it's quite tasty in context.
Speaker 2: It's bitter and delicious. Also my band name.
Speaker 3: Bitter. Yeah, that's a good band name actually.
Speaker 2: Garnish with a cherry and enjoy.
Speaker 3: And we'll post the full recipe for this quarantini as
Speaker 3: well as our non outcoholic plasy Burta on our website,
Speaker 3: this podcast will kill you dot Com and all of
Speaker 3: our social media channels.
Speaker 2: Making the plasy burrita is going to be a challenge
Speaker 2: for this one.
Speaker 3: But you'll you'll figure it out up with total faith,
Speaker 3: glad to do like I say, you'll figure it out.
Speaker 3: I'll just be nice jobs.
Speaker 2: Now now this feels like a group project again.
Speaker 3: I also want to give a quick shout out and
Speaker 3: thank you to a Kia and I'm sorry that we
Speaker 3: might have just pronounced your name wrong, but for sending
Speaker 3: us the most adorable gift package from Texas.
Speaker 1: Y'all.
Speaker 2: Oh my gosh, it's adorable. So many great things there.
Speaker 3: Did you guys know something called Techsaroni existed. It's macaroni
Speaker 3: in the shape of Texas. Okay, It's everything I needed
Speaker 3: in life, and I feel like.
Speaker 2: That should be sold in stores across the US. But
Speaker 2: Techsarroni version not like you know, Illinois, Illinois. No, I
Speaker 2: wouldn't eat that. Texas is a great shape for pasta.
Speaker 2: Whow it really is?
Speaker 3: I can't wait. We need to make mac and cheese
Speaker 3: together or something arin.
Speaker 2: Oh my gosh. Yeah.
Speaker 3: Anyways, thank you so much. That was really sweet of you,
Speaker 3: and sorry it took forever for me to check our
Speaker 3: po box.
Speaker 2: We should post pictures, yeah, we.
Speaker 3: Should of us eating macaroni and cheese.
Speaker 2: Yes, okay, cool?
Speaker 3: Cool? Okay?
Speaker 2: All right?
Speaker 3: Shall we jump right in.
Speaker 2: Let's do it. Should we take a quick break first?
Speaker 3: I think we need a breather, right, yeah, So protestis
Speaker 3: aka whooping cough. Let's talk about what these symptoms are.
Speaker 3: So protessis is caused by a bacterium and the name
Speaker 3: of the disease, a colloquial name whooping cough, tells you
Speaker 3: the most characteristic part of these symptoms, and that is
Speaker 3: this very distinctive whooping sound that is not actually during
Speaker 3: the cough, but it's as people try and take a
Speaker 3: breath of air in after an episode of coughing.
Speaker 2: And so is the whoop. Is that all ages that
Speaker 2: have whooping cough? Or is that mostly younger children?
Speaker 3: Good question. We'll talk a little bit more in a
Speaker 3: bit about the differences in symptoms. It can happen in
Speaker 3: people of any age, but it's most typical in younger
Speaker 3: age groups. Okay, and we'll talk about why in a bit.
Speaker 3: That's a really good question though. All right. So the
Speaker 3: bacterium that causes protessis is called Bordodella protessis. It's a
Speaker 3: little gram negative rod so again the gram negative means
Speaker 3: it's pink when we stain it. However, while Borddella protessis
Speaker 3: is the most common cause of whooping cough, there are
Speaker 3: a couple of other very closely related bacteria species, including
Speaker 3: Bordodella paraprotessis and Bordodella bronchosseptica that can in some cases
Speaker 3: cause a very clinically similar disease. But Borddella pertessis is
Speaker 3: the one that, for example, we have a vaccine four
Speaker 3: and kind of the most important of these species.
Speaker 2: Are you ready for questions? I feel like this is
Speaker 2: the aady Okay, So about these different bacterial species. Are
Speaker 2: they as globally prevalent as just Bordetella protessas good question.
Speaker 3: I know that Paraprotesis is pretty widespread globally. I would
Speaker 3: guess that bronchosseptica is as well. One of the big
Speaker 3: differences is that these other species are found in many
Speaker 3: other species of animals as well, whereas Bordadella pertessis is
Speaker 3: a human specific disease. Side note, though, Bordetella bronco septica
Speaker 3: causes kennel cough in dogs. Interesting huh So anyways, protestis
Speaker 3: is transmitted via respiratory droplets. I've seen estimates that the
Speaker 3: are not which, if you'll remember from previous episodes, is
Speaker 3: the number of secondary infections that a primary infection can cause.
Speaker 3: I've seen estimates ranging anywhere from five to fifteen.
Speaker 2: Wait, I know.
Speaker 5: That's bigger than measles. I was gonna say it, which
Speaker 5: doesn't seem right. Well, but I guess the r like
Speaker 5: the are not is it's an average Yeah.
Speaker 3: But anyways, in any case, this is a highly highly
Speaker 3: infectious disease. It spreads very easily.
Speaker 2: Yeah.
Speaker 3: In general, the incubation period, so the time between when
Speaker 3: you first get exposed and when you start to show symptoms,
Speaker 3: on average is about a week maybe ten days, but
Speaker 3: it can be quite a bit longer. And I think
Speaker 3: the reason that the range can be longer is twofold.
Speaker 3: Partly it has to do with infectious dose how much
Speaker 3: are you exposed to at the outset, But also it's
Speaker 3: very difficult to pinpoint when exposure might be in relation
Speaker 3: to symptoms because the onset of symptoms for this disease
Speaker 3: is kind of insidious, which means it's slow and you
Speaker 3: might not recognize at first, for like a week or
Speaker 3: more that what you're dealing with is actually protessis oh yeah, okay,
Speaker 3: so let's talk about how this little bacterium gets into
Speaker 3: you and causes disease, Okay, and then we'll talk about
Speaker 3: those insidious that's one of my favorite words, insidious symptoms.
Speaker 2: Yeah. Also it's going to end up convincing a lot
Speaker 2: of people that they have whooping cough.
Speaker 3: Probably, I mean, I mean I convinced myself that my
Speaker 3: baby had whooping cough. So you're not alone if this
Speaker 3: convinces you that you have whooping cough.
Speaker 2: Okay, we just apologize in advance, Yeah, we do.
Speaker 3: Uh So, Unlike many of the other diseases that we've
Speaker 3: talked about recently, including like syphilis and E. Coli, even dengay,
Speaker 3: this is a highly highly specific bacterium, So it doesn't
Speaker 3: just go throughout your whole body wreaking havoc. Bordetella. Protessis
Speaker 3: replicates only in association with the cciliated epithelium of your lungs.
Speaker 2: How does it only reproduce there?
Speaker 3: How it has? Okay, So protessis has a lot of
Speaker 3: different virulence factors on its surface, Yeah, that allow it
Speaker 3: to colonize our body and then cause the symptoms that
Speaker 3: it causes. It also has a number of different talks
Speaker 3: which are really ultimately responsible for a lot of the
Speaker 3: symptoms that we see. And so these virulence factors very
Speaker 3: specifically allow it to bind to the epithelium of our
Speaker 3: respiratory tract.
Speaker 2: Okay, And so those are the only.
Speaker 3: Cells that they bind to. Now, Borditella does not invade
Speaker 3: our cells, but it binds to these respiratory cells and
Speaker 3: then it replicates in association with those cells, So like
Speaker 3: next to those cells.
Speaker 2: What this is so weird? Okay, I know, isn't it?
Speaker 3: So this is a very like I don't know how
Speaker 3: much you're going to talk about the evolution of this pathogen. Yeah,
Speaker 3: but it seems to me like based on this, we've
Speaker 3: had a long association with this pathogen. Am I right?
Speaker 2: I'm going to withhold comment until okay the history that
Speaker 2: would be excellent.
Speaker 3: That would be my guess based on the fact that
Speaker 3: this is a bacterium that is highly specialized to these
Speaker 3: cells in our respiratory tract, and it's it's a human
Speaker 3: space pathogen, so it's not found in a bunch of
Speaker 3: other animals. Right, Okay, cool?
Speaker 2: But so are our human respiratory cells that much different
Speaker 2: than any other mammal respiratory cells?
Speaker 3: Oh than any other mammal I have absolutely no idea.
Speaker 3: I mean, I guess they're specific enough that the virulence
Speaker 3: factors that Bordetella protests has doesn't allow them to easily
Speaker 3: colonize other animals.
Speaker 2: Yeah, I'm just wondering what it is about the specificity.
Speaker 3: That's like a great question. I mean, it makes sense
Speaker 3: like that it would if it's going to specify on
Speaker 3: any cells. Respiratory epithelia are great because it's going to
Speaker 3: cause you to cough and sneeze and that's going to
Speaker 3: spread the pathogen really far. So from that perspective it
Speaker 3: makes sense. But the specificity to humans, I don't know, man,
Speaker 3: how does that ever happen?
Speaker 2: Right?
Speaker 3: And again, Bordtella has a number of different toxins that
Speaker 3: it releases that result in a lot of the damage
Speaker 3: and symptoms that we see. So in addition to like
Speaker 3: PILLI which we've talked about before, those sticky things that
Speaker 3: allow it to attach to the respiratory tract, two of
Speaker 3: the important toxins that it has are number one, a
Speaker 3: toxin called protessis toxin. It's a really good name for it.
Speaker 3: That actually blocks the ability of our white blood cells
Speaker 3: to get back into our lymph system. Ooh, So what
Speaker 3: that means is that you have white blood cells coming
Speaker 3: because they recognize bacteria. Right, they're like, oh man, we
Speaker 3: need to come in and help out. But then what
Speaker 3: those white blood cells want to do is then go
Speaker 3: back to our lymph nodes and regroup so that they
Speaker 3: can like figure out a plan of attack kind of
Speaker 3: m hm. So Protessa's toxin blocks their ability to do that,
Speaker 3: So you end up with a ton of white blood
Speaker 3: cells in the blood stream because they've all come out
Speaker 3: to try and figure out what's going on with these bacteria,
Speaker 3: but then they can't get back where they want to be.
Speaker 2: Oh my gosh. Yeah, okay, that's really interesting.
Speaker 3: It is, and it's one of the only systemic symptoms
Speaker 3: of a Bordetella protestis infection. Is this what we call lymphocytosis,
Speaker 3: A lot of white blood cells in your bloodstream?
Speaker 4: Okay?
Speaker 3: Because it is? Yeah, I mean you can get that
Speaker 3: in tons of other diseases, so it's certainly not specific
Speaker 3: at all, but it's one of the only like systemic
Speaker 3: manifestations because this is a very respiratory specific pathogen. And
Speaker 3: then it has other toxins which I forgot to write
Speaker 3: the name of down. Of course, I think tracheal toxin
Speaker 3: is one of them. Actually, that damage directly caused direct
Speaker 3: damage to the scillia of our respiratory epithelia and so ccilia.
Speaker 3: Are these little what do you call this aeron fingers
Speaker 3: like undulating?
Speaker 2: Undulating?
Speaker 3: Yeah, exactly, little projections on these cells that help to
Speaker 3: weep mucus and debris up and out of our respiratory track.
Speaker 3: We talked a lot about them in our cystic fibrosis episode.
Speaker 2: Yeah.
Speaker 3: Anyways, So these other toxins, trichial toxins and others that
Speaker 3: Bordetella produce caused damage to that system. So you're gonna
Speaker 3: get a build up of gunk in your lungs when
Speaker 3: you get infected with protessis. Now we know what it
Speaker 3: does in your body, how it's infecting you. So what
Speaker 3: does it look like when you get infected?
Speaker 2: M h, not good.
Speaker 3: It's not good. So there are three main phases to
Speaker 3: protessis what's called the catarrhal stage, I think that's how
Speaker 3: you pronounce it, the paroxysmal stage, and then the convalescent
Speaker 3: stage aka recovery. So the catarrhal stage is this very insidious,
Speaker 3: nondescript illness, and this is what can make it difficult
Speaker 3: to pinpoint exactly when you might have started showing symptoms.
Speaker 3: And what I think is worst about this phase is
Speaker 3: that the symptoms are quite mild in a lot of cases.
Speaker 3: So these include something like a runny nose, not a
Speaker 3: gunky nose, just kind of a watery, runny nose chariza,
Speaker 3: so like tearing from your eyes, like kind of like
Speaker 3: a like a viral eye infection might be okay, okay,
Speaker 3: like watery eyes, Maybe your eyes get a little red,
Speaker 3: maybe they're itchy, like maybe you think it's allergies. You
Speaker 3: might have some sneezing, And at first it starts off
Speaker 3: with a pretty mild cough, and that's how it begins,
Speaker 3: and in tiny kids actually across the board, if there
Speaker 3: is a fever, which often there isn't a fever at all.
Speaker 3: Even if there is a fever, it's usually pretty mild.
Speaker 3: Like we're talking maybe like one hundred and one, which
Speaker 3: is a pretty low grade fever. If you're talking about
Speaker 3: a kid who's like over age two, you mostly wouldn't
Speaker 3: even be concerned about a fever that low because kids
Speaker 3: get fevers from everything. Like every infection is going to
Speaker 3: give a kid a fever. So if a kid has
Speaker 3: a very low fever, you probably aren't going to be like, well,
Speaker 3: this kid is clearly very sick. You'll be like, oh,
Speaker 3: it's the little fever. They'll get over it, right, but
Speaker 3: that's it. Those are the symptoms. This lasts for like
Speaker 3: one to two weeks. It's super mild. The coughing sort
Speaker 3: of starts to get worse, but at this phase it's
Speaker 3: it doesn't have anything that makes it stand out. It's
Speaker 3: not more frequent at certain times of day, it's not
Speaker 3: super productive. It's just like a kind of normal cough. Okay,
Speaker 3: and again no fever. Then comes the paroxysmal phase, and
Speaker 3: this is the whooping cough of whooping cough. Okay, So
Speaker 3: the cough that starts out as mild in that catarrhal phase,
Speaker 3: it becomes paroxysmal. Paroxysmal means a sudden recurrence, so all
Speaker 3: of a sudden, out of the blue, people will have
Speaker 3: a massive coughing attack. These usually are like between five
Speaker 3: or ten, but they can be up to thirty coughs
Speaker 3: in a row, and they become also these paroxysms, these
Speaker 3: coughing attacks become more frequent at night and overall increase
Speaker 3: in frequency both throughout the day and the night, and
Speaker 3: each one becomes more severe than the last.
Speaker 2: Okay, And it's kind of almost.
Speaker 3: Hard to describe how terrible these coughs are so I
Speaker 3: actually found a paper from nineteen seventy five that's a
Speaker 3: really nice overview of protesses, and I'm going to just
Speaker 3: read this. The child possessed of the coughing fit is
Speaker 3: a pitiful sight, all the more so as the observer
Speaker 3: is helpless to alleviate or terminate the attack. Each attack
Speaker 3: consists of ten to thirty forceful coughs per spasm, and
Speaker 3: into each cough, the patient appears to concentrate all his energy.
Speaker 3: He leans forward, or, if standing, stands with legs spread,
Speaker 3: grasping the nearest object and leaning far forward, tongue protruded
Speaker 3: to the utmost, saliva and mucus streaming from nose and mouth,
Speaker 3: eyes bulging with tears streaming, his entire body racked with
Speaker 3: the total exertion of each cough. The coughing continues in
Speaker 3: a staccato series. The face becomes more and more cyanotic,
Speaker 3: which means blue, the neck bulges with venus congestion, and
Speaker 3: still the attack continues. Finally, when it seems certain that
Speaker 3: death is imminent, a final cough appears to clear offending
Speaker 3: secretions or mucus from the upper airway, and the first
Speaker 3: opportunity to inspire is offered with a massive effort. Inspiration ensues,
Speaker 3: air rushes into the lungs against a still narrowed glottis,
Speaker 3: and the characteristic whoop is produced.
Speaker 2: Oh my gosh, yeah, just taking a second to like breathe,
Speaker 2: right ah wow.
Speaker 3: Yeah, And so that's kind of a very classic description
Speaker 3: of what these paroxysms look like. They're horrible. I don't
Speaker 3: recommend googling them, but you can find a lot of
Speaker 3: videos of them online.
Speaker 2: Yeah, are the coughs productive? Are you coughing up mucus
Speaker 2: or gunk from your lungs?
Speaker 3: So, yes, and no, there is a lot of mucus
Speaker 3: in your lungs, and so it's thought that these coughing
Speaker 3: spasms are because of that mucus. It's like you trying
Speaker 3: really hard to get that mucus up. But especially because
Speaker 3: this is often a disease of very young infants, they're
Speaker 3: not good at coughing stuff up, so they may or
Speaker 3: may not actually cough anything up, but there is a
Speaker 3: lot of mucus there that could potentially be coughed up. Yeah, okay, Yeah.
Speaker 3: One of the sort of other characteristic things that happens
Speaker 3: after these paroxysms is what's called post tussive vomiting. So
Speaker 3: it's really common to cough so hard that you end
Speaker 3: up vomiting. Oh gosh, Yeah, it's horrific. And these episodes
Speaker 3: are so exhausting. I mean, imagine you are literally unable
Speaker 3: to breathe this whole time, which is why that inspiratory
Speaker 3: whoop is so like, it's so powerful. You're trying so
Speaker 3: hard to get air back into your lungs. That as
Speaker 3: these progress and become more and more frequent throughout the
Speaker 3: ensuing days and weeks, this can last for weeks. People
Speaker 3: tend to become very, very exhausted, so they might be
Speaker 3: sleeping most of the day and only awaken when they
Speaker 3: have these coughing fits and then fall kind of right
Speaker 3: back to sleep.
Speaker 2: It sounds so utterly exhausting.
Speaker 3: Yeah, oh god, and so especially in well in babies
Speaker 3: and in older children and adults. This can lead to
Speaker 3: weight loss because people might stop eating because they're just
Speaker 3: sleeping through like in between every coughing episode.
Speaker 2: Right.
Speaker 3: You can also get a lot of complications from the
Speaker 3: actual force of the coughing. You can burst blood vessels
Speaker 3: in your eyes or under your skin. You can cough
Speaker 3: out like a hernia. You coughing so hard that you
Speaker 3: like result in a hernia through your belly button. You
Speaker 3: can crack ribs, yeah, and often your chest wall will
Speaker 3: get really sore and tender, even if you don't break
Speaker 3: a rib, just because you're working those muscles so so
Speaker 3: hard to cough so much. And then there are a
Speaker 3: number kind of a couple of really important complications that
Speaker 3: can happen on top of this, the most deadly of
Speaker 3: which is a secondary pneumonia. Okay, so that's like a
Speaker 3: secondary Usually it's a secondary bacterial infection because you've been
Speaker 3: sick with protessis for so long, and that often causes
Speaker 3: the most deaths. It's not the only way that you
Speaker 3: can die from protessis, because these paroxysms can be so
Speaker 3: severe that you can have prolonged hypoxia, which means your
Speaker 3: brain isn't getting enough oxygen. That can result in encephalopathy,
Speaker 3: so brain damage, which can cause either long term brain
Speaker 3: damage or can cause death, especially in young infants.
Speaker 2: Yeah.
Speaker 3: Yeah, there's a number of other complications that you can get.
Speaker 3: You can rupture your trichia or your esophagus and get
Speaker 3: air that goes into like your subcutaneous tissue, or you
Speaker 3: can collapse one of your lungs and get a pneumothorax
Speaker 3: from coughing. So hard is that.
Speaker 2: The air and subcutaneous tissue is that in the nineteen
Speaker 2: eighteen flu the yeah the crackles.
Speaker 3: Oh yeah yeah, pop snap, crackle pop under your skin.
Speaker 3: So this phase overall, the paroxysmal phase, can last anywhere
Speaker 3: from one to four weeks. But even as it starts
Speaker 3: to improve and you enter the convalescent phase, it's a
Speaker 3: very gradual improvement. Another name for protestis is actually the
Speaker 3: one hundred days cough uh huh yeah, because symptoms can
Speaker 3: continue for like up to six months. Yeah, uh, so
Speaker 3: that's protestis wow. Yeah. It is technically treatable with antibiotics,
Speaker 3: but the antibiotics work best if you can get treatment
Speaker 3: during that catarrhal phase. Okay, which again is I mean
Speaker 3: a lot of people are never even gonna seek treatment
Speaker 3: during that phase because that phase alone can last one
Speaker 3: to two weeks, right, yeah, And so treatment with antibiotics
Speaker 3: works best if you can get it. If you can
Speaker 3: get treatment during that initial phase. After that the problem
Speaker 3: is that the bacteria have already started releasing all those toxins.
Speaker 3: So while antibiotics are still effective at eliminating the bacterium,
Speaker 3: they don't really help with symptom treatment. Okay, so yeah,
Speaker 3: what they do do is help to prevent further spread
Speaker 3: of the disease. So it is still really important to
Speaker 3: treat with antibiotics, even if you're not treating till later
Speaker 3: in the disease course.
Speaker 2: Right, Is there any anti toxin available.
Speaker 3: As far as I know, No, like there's no antiitoxin
Speaker 3: treatments that we have or anything like that.
Speaker 2: Okay, like there were, like there was for diphtheria before. Yeah,
Speaker 2: well I guess still it is. But yeah, okay, interesting, yep,
Speaker 2: this is making me feel a lot like the diphtheria episode,
Speaker 2: like you can't breathe, yeah, sort of like you have.
Speaker 3: A pseudo membrane covering your throat.
Speaker 2: Yeah yeah.
Speaker 3: Yeah. It's a horrible illness.
Speaker 2: It's really horrible, but vaccine preventable.
Speaker 3: I think we should specify that at the outset of
Speaker 3: this episode. This is a horrible illness and it is
Speaker 3: vaccine preventable.
Speaker 2: It really is.
Speaker 3: No kids should be dying from protessis today, and unfortunately
Speaker 3: they are.
Speaker 2: In theory, it could be a target for eradication.
Speaker 3: Yes, because it's a human specific disease. So Aaron, how
Speaker 3: did we get here? Where did this horrible thing come from?
Speaker 2: I will answer that as well as I can just
Speaker 2: after this break. So if you think back to last
Speaker 2: year during our Vaccines episodes, I talked a little bit
Speaker 2: about Protessis, particularly in the second episode, part two, where
Speaker 2: I talked a lot about the rise of vaccine hesitancy
Speaker 2: or the anti vaccine movement nowadays, and how the Protest's
Speaker 2: vaccine actually played a pretty central role in that. And
Speaker 2: back then I remember promising, Oh, I'm not going to
Speaker 2: go into this too much, because we're going to do
Speaker 2: a full episode on Protessis, And here I am making
Speaker 2: good on that promise. So since I've already talked a
Speaker 2: lot about the history of Protessis, when it comes to
Speaker 2: the rise of the vaccine hesitancy or anti vaccine movements,
Speaker 2: I'm not going to go into too much detail on that,
Speaker 2: So I'll just refer you to Part two of Vaccines.
Speaker 3: Good call.
Speaker 2: But even before I can get to that part of
Speaker 2: the story of protessas, there's so much to cover beforehand.
Speaker 2: So let's go back to the beginning. Throughout history, Protessas
Speaker 2: has been somewhat overshadowed, I would say by some of
Speaker 2: the other big name diseases like smallpox, plague, cholera, tuberculosis,
Speaker 2: et cetera, sort of the ones that did really come
Speaker 2: through a population or a city and just wipe a
Speaker 2: lot of people out. But that doesn't mean that it
Speaker 2: was minor or easily ignored. Protessas has been one of
Speaker 2: the biggest killers of children throughout history, and as I'm
Speaker 2: sure you're going to talk about it, it remains a huge
Speaker 2: problem around the world today. I've talked before about the
Speaker 2: difficulty in retrospectively diagnosing a disease based on historical accounts.
Speaker 2: Is this one easy, especially if there's no physical evidence
Speaker 2: like skeletal damage or something like that. But yeah, Protessis
Speaker 2: doesn't have that problem as much as some of the
Speaker 2: other ones because the symptoms, as you describe this whoop,
Speaker 2: the intake of air that's so restricted, it's a pretty
Speaker 2: characteristic and very noticeable, and it also has a tendency
Speaker 2: to just infect children, And so descriptions of a disease
Speaker 2: that mostly impacted children and was accompanied by a horrific
Speaker 2: cough that then breath in afterwards sounded like whooping. It's
Speaker 2: probably whooping cough. Safe assumption, safe assumption. This is where
Speaker 2: I think it's going to get interesting. I think so anyway. Okay, So,
Speaker 2: most historical reviews that I read of protessis say that
Speaker 2: the first definitive or most likely definitive epidemic of the
Speaker 2: disease happened in fifteen seventy eight in Paris. All right,
Speaker 2: so fifteen seventy eight, Like, that's not that long ago.
Speaker 3: No, especially not for a human specific pathogen that is
Speaker 3: so well suited just to our one cell type.
Speaker 2: Yes, so interesting, okay, insulting. The physician who wrote about
Speaker 2: this epidemic called the disease quinta or kintinatusis probably to
Speaker 2: indicate that the severe coughing fits that you mentioned occurred
Speaker 2: every four or five hours.
Speaker 3: Oh okay.
Speaker 2: And he also described it as being a new disease
Speaker 2: and or only referred it to like a couple other outbreaks.
Speaker 2: And he noted that it occurred mostly in children between
Speaker 2: the ages of four and ten, with a violent cough
Speaker 2: that ended in vomiting, cyanosis, and often death. However, there
Speaker 2: are a couple of other possible outbreaks of Protessis that
Speaker 2: date back even for there So, in an ancient Chinese
Speaker 2: medicine treatise dating back to the six hundreds, there is
Speaker 2: mention of something called the one hundred day cough, which
Speaker 2: is the colloquial name for protessis in China today, and
Speaker 2: this in this treatise, it says that the cough will
Speaker 2: last one hundred days and if not cured, eighty to
Speaker 2: ninety percent of people will die. WHOA, So that's very
Speaker 2: very high, very high. And so because of that, because
Speaker 2: of that extremely high reported mortality rate, many researchers dispute
Speaker 2: this inclusion as whooping cough, saying that it seems to
Speaker 2: be too lethal to be whooping cough. And there was
Speaker 2: also no mention made of the fact that it mostly
Speaker 2: happens in children. So even though it is a one
Speaker 2: hundred day cough, now it might have just changed names, right,
Speaker 2: like it might just change diseases rather.
Speaker 3: Yeah, they used to call this thing one hundred day cough,
Speaker 3: and now they call proteste hundred day cough exactly.
Speaker 2: There are also a few other poss earlier, not earlier
Speaker 2: than the six hundreds, but earlier than Paris Protest's epidemics
Speaker 2: in Persia around the fifteenth and sixteenth centuries, and so
Speaker 2: around this time, just for reference, because I didn't really
Speaker 2: know this, Persia span from modern day Iran into parts
Speaker 2: of Central Asia and India, and so in the late
Speaker 2: fourteen hundreds, which is almost a century before the Paris
Speaker 2: Protest's outbreak, there were two epidemic coughs that led to
Speaker 2: vomiting and unconsciousness and death in many people, both children
Speaker 2: and adults, And the fact that adults were affected could
Speaker 2: suggest that this was a new disease for the population
Speaker 2: and hadn't fallen into this pattern of childhood illness yet.
Speaker 2: And there are a few other epidemics in sixteenth century
Speaker 2: Persia that seem even more conclusively to be whooping cough.
Speaker 2: But the take home from all of this, I think
Speaker 2: is that the disease seems to be first recognized in
Speaker 2: humans only five hundred or six hundred years ago.
Speaker 3: WHOA, that's the opposite of what I guessed, Aaron, Yeah.
Speaker 2: So that leads to the question, is this bacterium really
Speaker 2: only five hundred or six hundred years old? Is that
Speaker 2: when it evolved?
Speaker 3: No?
Speaker 2: No, no, definitely not definitely not. So there was a
Speaker 2: research article from two thousand and five that investigated the
Speaker 2: evolutionary history of Bordetella protessis and found that it likely
Speaker 2: evolved from a human specific lineage of the related species
Speaker 2: Bordetella broncho septica around two point five million years ago.
Speaker 3: I'm sorry, Yeah, So so we go from two point
Speaker 3: five million to five hundred, like, yes, what is happening?
Speaker 2: I mean, does that mean that humans have been living
Speaker 2: with this bacterium for since before humans were humans.
Speaker 3: And then it just all of a sudden started causing disease?
Speaker 2: Yeah? I mean, honestly, I don't have a satisfying answer,
Speaker 2: and I couldn't find one in any of the things
Speaker 2: that I read. So I think what a few of
Speaker 2: the articles mentioned is that the most likely scenario is
Speaker 2: that the bacterium probably circulated in a relatively non virulent
Speaker 2: state in parts of Asia, possibly Southeast Asia, for most
Speaker 2: of its history, and then it evolved these virulence factors
Speaker 2: that allowed it to become super prevalent and highly contagious
Speaker 2: and also lethal.
Speaker 3: You know, I bet that is the biggest difference between
Speaker 3: when you asked about parapotessis and bronchoseptica. Yeah, and why
Speaker 3: those don't at least aren't as prevalent. I think it
Speaker 3: is likely just that they don't cause disease as much,
Speaker 3: and it is because of those toxins like bronchoseptica doesn't
Speaker 3: produce protestis toxin, and neither does paraprotessis, and it's thought
Speaker 3: that that's one of the main toxins that causes the
Speaker 3: symptoms that we see.
Speaker 2: That's interesting. Yeah, one of the things that was really
Speaker 2: interesting is in these papers, it's harder to get a
Speaker 2: sense of historical genetic diversity for some of these bacteria
Speaker 2: that have had vaccines used against them, because you can
Speaker 2: imagine certain lineages or certain strains or subspecies or whatever
Speaker 2: have been wiped out in some places, and so the
Speaker 2: genetic diversity that we're left with now isn't necessarily representative
Speaker 2: of its historical diversity.
Speaker 3: Yeah, that's a good point.
Speaker 2: But I thought that was really interesting. But yeah, I mean,
Speaker 2: it probably emerged or started causing epidemics five or six
Speaker 2: hundred years ago, because that's when widespread trade and like
Speaker 2: global travel really kind of got up and running.
Speaker 3: So yeah, fascinating.
Speaker 2: And another point in the column of this being a
Speaker 2: relatively new disease or recently evolved virulence. Is that physicians
Speaker 2: around the time it first started appearing, they were also
Speaker 2: baffled by the disease and seemed to make important notes
Speaker 2: of it. Okay. One physician said in eighteen ninety four
Speaker 2: that quote it is singular that a malady so distinctly
Speaker 2: marked as whoopin cough should figure so little in the
Speaker 2: records of the disease from former times. So no mention
Speaker 2: of it in like ancient Greece or ancient Rome. Sorry,
Speaker 2: which is I had to mention ancient Greece and Rome.
Speaker 2: No mention in the Ebers Ebers Papyrus.
Speaker 3: Oh my gosh, was this even an episode of TPWK? Why?
Speaker 2: I don't know it. It's gonna have an asterisk next
Speaker 2: to it, for sure. And the sudden appearance or apparent
Speaker 2: sudden appearance of whoopin cough caused other problems as well,
Speaker 2: because it kind of popped up all over and in
Speaker 2: such severity it gained all these different names, even within
Speaker 2: the same language, and didn't even get its scientific name
Speaker 2: until nineteen o six, like for the bacterium. Okay, okay,
Speaker 2: but before we get to that, let's talk about a
Speaker 2: few of these names because I know that you're gonna
Speaker 2: be excited for it. They're fine, there are yeah, we've
Speaker 2: had better ones. Okay, there's no mad staggers or whatever.
Speaker 3: The dandy dandy fever.
Speaker 2: Dandy fever. So. There were several English names for the disease,
Speaker 2: including whooping cough, no w chin cough, kink cough, and others.
Speaker 2: Kink cough was apparently the popular name for the disease
Speaker 2: in Scotland, and the word kink i guess was also
Speaker 2: used as a convulsive fit of coughing or laughter, a
Speaker 2: gasping for breath caused by coughing, laughing or crying. The
Speaker 2: whoop and whooping cough it's like from a definition somewhere. Yeah.
Speaker 2: In France it was known as quinta. In Italy it
Speaker 2: was called tussa farina or tossa canina canina because the
Speaker 2: cough could sound like the barking of a dog. Ah okay, yeah,
Speaker 2: And all these names kind of slowed down the accumulation
Speaker 2: of knowledge about the disease, or it made it more
Speaker 2: difficult because it took a while for someone to go
Speaker 2: through and say, ah, yes, the chincoff here is known
Speaker 2: as whoopin cough there, which is the same as quinta
Speaker 2: there something like that. So throughout this time, though the
Speaker 2: disease itself did not slow down after its first appearance
Speaker 2: in Europe in the sixteenth century, it would continue to
Speaker 2: cause epidemics until it fell into this childhood illness pattern,
Speaker 2: so appearing every year every few years, often at a
Speaker 2: particular time of year, and then impacting mostly children. Let's
Speaker 2: talk about that impact. The numbers of infected kids per
Speaker 2: year are more difficult to get a sense for, but
Speaker 2: we do have some census data for a couple of
Speaker 2: places that can give us an idea of the number
Speaker 2: of deaths in Sweden, for example, in the mid seventeen hundreds.
Speaker 2: Sweden seems to be particularly hard hit by whooping cough,
Speaker 2: which I think is interesting history. But so in the
Speaker 2: mid seventeen hundreds there was a death rate of about
Speaker 2: one hundred and fifty one per one hundred thousand people
Speaker 2: every year, which is really high.
Speaker 3: That's very high. One hundred and fifty per hundred thousand
Speaker 3: just from whooping cough.
Speaker 2: Yes, wow. So that calculates to about twenty seven hundred
Speaker 2: children per year in a population of one point eight million,
Speaker 2: which is what it was in Sweden then, oh god,
Speaker 2: and so, as I mentioned, these numbers are on the
Speaker 2: on the high end for deaths due to whooping cough,
Speaker 2: but it was still a really bad problem in other
Speaker 2: places as well. So in London the annual death rate
Speaker 2: was around twenty nine per one hundred thousand around that
Speaker 2: same time in the mid seventeen hundreds, calculating to about
Speaker 2: two hundred and thirty eight deaths per year in that
Speaker 2: population of seven hundred thousand. Okay, And these numbers for London, though,
Speaker 2: would increase over the course of the eighteenth century the
Speaker 2: next one hundred years, almost doubling and even occasionally surpassing
Speaker 2: the number of deaths caused by measles.
Speaker 3: Whoa.
Speaker 2: Yeah. So this trend in increasing virulence was repeated across
Speaker 2: a wide geographic range, which is kind of interesting because
Speaker 2: I think we have this idea that diseases tend to
Speaker 2: decrease in virulence over time, as we saw syphilis do,
Speaker 2: for instance, after its first appearance in Europe in the
Speaker 2: late fifteenth century. But for whipping cough, this increase in
Speaker 2: virulence was probably due to a combination of an influx
Speaker 2: of new susceptibles every year or every few years, increasing
Speaker 2: population density overall, and a bunch of other things like
Speaker 2: poor nutrition, poor air quality, ineffective treatment that may have contributed,
Speaker 2: and it probably could be also or was a big
Speaker 2: part of it, that physicians just got better at diagnosing
Speaker 2: the disease and correctly attributing cases and deaths to it
Speaker 2: over that time as it kind of grew in infamy.
Speaker 2: That makes sense, okay, In any case. By the time
Speaker 2: that microbiology as a field started and grew, protessis was
Speaker 2: high up on the list of diseases that desperately needed
Speaker 2: a cure or treatment of some kind, just as it
Speaker 2: did in the seventeen hundreds. The mortality due to protessis
Speaker 2: and the prevalence of protessis grew also in the eighteen hundreds,
Speaker 2: with about ten percent of infections leading ending in death,
Speaker 2: and that number would be higher for children of working
Speaker 2: classes or who just had poor nutrition or in lower income.
Speaker 2: But one issue in trying to control the disease was
Speaker 2: knowing what the disease was, what was it caused by.
Speaker 2: So if you didn't know what was causing this, how
Speaker 2: could you even try to stop it. Physicians did recognize, though,
Speaker 2: that it was contagious which I think is interesting. As
Speaker 2: we've talked about again, there is like if you read
Speaker 2: some of these old medical treatises, it's like, oh, you know,
Speaker 2: we can't ignore the fact that there is some sort
Speaker 2: of environmental component to this, but it does seem to
Speaker 2: be contagious.
Speaker 3: So I do think that's so interesting, just that whole
Speaker 3: aspect of it. Before, you know, before we knew that
Speaker 3: bacteria or viruses were things that were transmissible from person
Speaker 3: to person. Just this idea that you could still somehow
Speaker 3: have a contagious disease despite that is so fascinating.
Speaker 2: Yeah, So there were two researchers named Bourdette or Bordet
Speaker 2: b rd Et and Jean Jus I guess think that's
Speaker 2: right spell ge Nngou, and these two guys had struggled
Speaker 2: to isolate the bacterium because even though the symptoms of
Speaker 2: the disease could last for a really long time, there
Speaker 2: was apparently a really narrow window in which you could
Speaker 2: actually culture the bacterium. But another issue was that it
Speaker 2: only grew in the long It had that super high
Speaker 2: specificity that you mentioned towards the long epithelial cells, so
Speaker 2: you couldn't pick it up for the blood of someone
Speaker 2: who is infected, and even if you were able to
Speaker 2: get a little like you know, muca sample, Yeah, the
Speaker 2: bacteria would quickly die outside the body. Yeah, But they
Speaker 2: kept at it, and they first saw the bacterium under
Speaker 2: the microscope in nineteen hundred and six years later, were
Speaker 2: finally able to grow the bacterium in a lab using
Speaker 2: a special broth.
Speaker 3: Wow. Nineteen o six.
Speaker 2: Uh huh, nineteen oh six, that's like kind of late, but.
Speaker 3: That's amazing that, like they were able to do it
Speaker 3: considering where it grows and how difficult it is to culture.
Speaker 3: I mean it's still hard to culture.
Speaker 2: Yeah, no, it's it's amazing. Also, Bordet had isolated this
Speaker 2: bacterium like when they could finally first grow it from
Speaker 2: his son's sputum oh.
Speaker 3: Was his son? Okay?
Speaker 2: I don't know, Okay, but there was one really sad
Speaker 2: treatise that I read from eighteen twenty two, I think
Speaker 2: something like that, and the physician who wrote it lost
Speaker 2: several of his children to whooping cough and I think
Speaker 2: was inspired to research more about it after that horrible experience. Anyway, Okay,
Speaker 2: so then this development of being able to actually culture
Speaker 2: the bacterium in a lab was super important because it
Speaker 2: really laid the groundwork for trying to make a vaccine,
Speaker 2: and that was the big target, like from the outset. Yeah,
Speaker 2: and the vaccines themselves, like ones for protesters, weren't that
Speaker 2: far behind. Just a few years after announcing they were
Speaker 2: able to culture the bacterium in the lab, these two
Speaker 2: dudes announced that they had developed a vaccine, Bordet and
Speaker 2: Jean Ju. And then not far behind was someone named
Speaker 2: John Zahorski at Washington University in Saint Louis, OH. And
Speaker 2: he said, I've got a vaccine too, And neither of
Speaker 2: these vaccines would really prove to be that reliable, that stable,
Speaker 2: you know, that effective, And it would take another couple
Speaker 2: of decades for an effective and reliable protest's vaccine to
Speaker 2: come onto the market. During those decades, the prevalence of
Speaker 2: protessis remained high, with between five thousand and eight thousand
Speaker 2: deaths annually.
Speaker 3: And that's just in the US.
Speaker 2: Okay, Wow, And then three awesome scientists come onto the scene.
Speaker 2: These are whom are quarantine is named after.
Speaker 3: Can we I feel like I imagine when you said
Speaker 3: three awesome scientists like the Western Doors opening and like
Speaker 3: some spurs. Can we throw that sound effect in?
Speaker 2: Thanks? Yeah, let's do that. How do their partner? I
Speaker 2: don't know.
Speaker 3: I don't know, okay, anyway, So.
Speaker 2: Walking through the saloon doors is Pearl Kendrick, Grace l
Speaker 2: and Loney Gordon. All Right, Pearl Kendrick was born. I
Speaker 2: love the name Pearl. I think it's wonderful.
Speaker 3: It's very adorable.
Speaker 2: She was born in eighteen ninety three in Wheaton, Illinois. Yeah,
Speaker 2: I have no idea where that is to me either,
Speaker 2: and from I probably should. And from the start, Pearl
Speaker 2: was fascinated by evolutionary biology and disease, and after she
Speaker 2: graduated with a degree in zoology, she taught school during
Speaker 2: the week and then, in her free time on the weekends,
Speaker 2: took a train down to New York City to volunteer
Speaker 2: as a research assistant in a lab that worked on typhus.
Speaker 3: Oh my god, I already am going to love these
Speaker 3: three women like it's gonna hurt my heart how much
Speaker 3: I love them?
Speaker 2: Oh my gosh, Well, I just love it. It's like
Speaker 2: in my free time, unnerd after our own hearts. I
Speaker 2: love it right, Yeah, and she ended up loving her
Speaker 2: lab time her research so much. But she was like,
Speaker 2: you know what, this is what I want to do
Speaker 2: full time. I don't want to be a teacher. I
Speaker 2: want to work in a research lie full time. And
Speaker 2: so that's exactly what she did.
Speaker 3: Wow.
Speaker 2: She started out working at the state health departments, first
Speaker 2: in New York and then in Michigan. And then in
Speaker 2: Michigan she worked at a microbiology lab in Grand Rapids
Speaker 2: while also earning her PhD at Johns Hopkins. On the side,
Speaker 2: what she full time full time job. She's double time,
Speaker 2: full time.
Speaker 3: Oh my god.
Speaker 2: And while she was at this microbiology lab in Grand Rapids,
Speaker 2: she hired and mentored a scientist named Grace Eldering. Eldering
Speaker 2: was inspired to study science due to an extremely bad
Speaker 2: case of whooping cough that she had as a kid.
Speaker 2: Oh so, she, like Kendrick, worked first as a teacher
Speaker 2: after graduating, but then applied for this job in the
Speaker 2: Michigan lab where she would work with Kendrick, and together
Speaker 2: these two made headlines for their many developments in the
Speaker 2: world of protessis wow. For instance, in the early nineteen thirties,
Speaker 2: they developed a diagnostic test for the bacterium, which was
Speaker 2: great because that could be used to determine how long
Speaker 2: an infected child was contagious, and that was then super
Speaker 2: important for quarantine and controlling the spread of the disease. Yeah.
Speaker 2: Then came their work on the whole cell protest's vaccine.
Speaker 2: So up to this point there had been, as I mentioned,
Speaker 2: several vaccines for protests produced, but because it was so
Speaker 2: difficult to culture in the lab, only a very limited
Speaker 2: number of vaccines could be made, so it was often
Speaker 2: like a one sample, one vaccine, Like it wasn't an
Speaker 2: effective or efficient way to make vaccines. Yeah, Kendrick and
Speaker 2: Eldering found a way around this, but didn't have the
Speaker 2: resources to widely administer the vaccine. But a visit from
Speaker 2: Eleanor Roosevelt in nineteen thirty six, she was first Lady
Speaker 2: at the time, change all that.
Speaker 3: I'm like, my heart is fluttering. There should be feeling
Speaker 3: so hard. Can we can we make a movie?
Speaker 2: Yeah, okay, let's do it. I would watch it. So
Speaker 2: Eleanor Roosevelt was super is she had like read about
Speaker 2: their work and she's like, I want to go to
Speaker 2: this lab and visit you and learn more about it.
Speaker 2: And she was really impressed by all of the progress
Speaker 2: that they had made. And it's funny in reports, like
Speaker 2: not in reports, but I think in a letter or
Speaker 2: something from that time, either Kendrick or Eldering said that
Speaker 2: Eleanor Roosevelt was like one of the only people who
Speaker 2: had visited the lab who actually understood what was going on.
Speaker 3: That's really funny.
Speaker 2: I love that. So then, so yeah, Elean Risvelt was
Speaker 2: so impressed that she was like, all right, I'm gonna
Speaker 2: give you guys all the funding that you need. And
Speaker 2: they were like, oh great. Sweet. So then within a
Speaker 2: few years, mass production of the protesta's vaccine began. What boom,
Speaker 2: that's it. Just kidding, Yeah, like there's a third woman.
Speaker 2: There's a third woman. She's coming out of the scene.
Speaker 2: So yeah, there was, there was. They had the ability
Speaker 2: to mass produce these vaccines, but the demand still way
Speaker 2: outpaced the supply, so they needed to find a way
Speaker 2: to increase the amount of bacteria that could be cultured
Speaker 2: in the lab. Okay, they put out an ad for
Speaker 2: a position and hired a dietitian named Loney Gordon on
Speaker 2: the spot. Interesting, Loney also came into science sort of
Speaker 2: through these back channels as well, like working first getting
Speaker 2: her degree in this, and then working as a dietitian
Speaker 2: and then this and that, and they were then lucky
Speaker 2: enough that she applied for this position because her job
Speaker 2: was basically to try some different broth recipes until they
Speaker 2: could find one that worked well for the for Bordeteller protests.
Speaker 2: And she got there like she wasn't that long actually,
Speaker 2: until she found that adding sheep's blood to a broth
Speaker 2: did the trick. So suddenly, with this new recipe, Kendrick,
Speaker 2: Elderling and Gordon were able to start manufacturing this wholesale
Speaker 2: protestsvaccine in large enough quantities not only for the state
Speaker 2: of Michigan, but also for other states as well.
Speaker 3: Wow, and this is in the nineteen.
Speaker 2: Thirties, This is in the nineteen thirties, early nineteen forties.
Speaker 3: Yeah, three women kicking booty. Yeah, at the time when
Speaker 3: it was like vaccine, I can't that is so so cool.
Speaker 2: It's so inspiring. I love it.
Speaker 3: We do need to make a movie out of.
Speaker 2: This, seriously. And also they didn't stop there, like they
Speaker 2: weren't just like, oh, this is good enough, let's patter
Speaker 2: ourselven in the back. And you know, they were always
Speaker 2: seeking new ways to improve the production or efficacy of
Speaker 2: the vaccine, and so they started to play around with adjuvants, which,
Speaker 2: if you remember from The Vaccine's episode, adjuvants are basically
Speaker 2: chemicals that are added to a vaccine that can increase
Speaker 2: the effectiveness by stimulating the immune system in certain ways.
Speaker 2: The team from Michigan used aluminum hydroxide in the Protests vaccine,
Speaker 2: which and correct me if I'm wrong, stimulates macrophages to
Speaker 2: basically do better at their jobs.
Speaker 3: Yeah that sounds about right.
Speaker 2: Okay, they like pick up the antigens and interact with
Speaker 2: the lymphocytes and concentrate in lymphos and so on.
Speaker 3: Yeah, exactly, So they're able to like increase the amount
Speaker 3: of immune response by driving your cells to that area
Speaker 3: kind of Yeah.
Speaker 2: Yeah, which makes it a longer lasting and more effective
Speaker 2: and yeah, better vaccine. And so this new and improved
Speaker 2: wholesale Protests vaccine with this adjuvant was put to the
Speaker 2: test in nineteen forty three and it was shown to
Speaker 2: be super successful provided lasting and effective protection against the disease.
Speaker 2: And then a couple years later, in order to reduce
Speaker 2: the number of shots that children would have to get
Speaker 2: for vaccines, the PROTESTES vaccine was combined with ones for
Speaker 2: diphtheria and tetanus in the mid nineteen forties, and that's
Speaker 2: why we called it the DTP vaccine.
Speaker 3: Yep.
Speaker 2: And this vaccine was widely administered throughout the whole world,
Speaker 2: and as a result, the incidents of protessis fell and fell.
Speaker 2: Here's some numbers. Yes, before the protests vaccine, there were
Speaker 2: an estimated two hundred and seventy thousand cases of protessis
Speaker 2: annually in the US.
Speaker 3: Two hundred and seven thousand.
Speaker 2: Two hundred and seventy thousand.
Speaker 3: Oh, I'm sorry, two seven zero.
Speaker 2: Two seven zero zero zero zero. Wow. That's the number
Speaker 2: of cases in the nineteen eighties. So this is after
Speaker 2: the vaccine had been in use for approximately forty years,
Speaker 2: and before the vaccine hesitancy movement really began. There were
Speaker 2: between twelve hundred and four thousand cases per year.
Speaker 3: Wow.
Speaker 2: That's a drop of almost ninety nine percent.
Speaker 3: Wow. Wow. Wow.
Speaker 2: And So, as I mentioned earlier in that part two
Speaker 2: of our Vaccines episode, I went into a lot of
Speaker 2: detail about how this pushback against the DTP vaccine began,
Speaker 2: and so I'm not going to do that here, but briefly,
Speaker 2: there was a global decline in vaccination rates with the
Speaker 2: DTP vaccine, and the fears were mostly based on the
Speaker 2: protessa's component of the vaccine, and so, as you might expect,
Speaker 2: the decline in vaccine coverage led to outbreaks. So in Sweden,
Speaker 2: for instance, the annual incidents of protessas cases went from
Speaker 2: seven hundred whoa total in nineteen eighty one to thirty
Speaker 2: two hundred and nineteen eighty five just four years later.
Speaker 3: Wow.
Speaker 2: In Japan there were two hundred and six cases in
Speaker 2: nineteen seventy one. In nineteen seventy nine there were thirteen
Speaker 2: thy one hundred and five.
Speaker 3: Cases whole mackerel m HM.
Speaker 2: Obviously something had to be done to get people to
Speaker 2: vaccinate again, or to somehow, you know, reduce these fears
Speaker 2: whatever it was. So and so, because so many people
Speaker 2: were not vaccinating out of fear that the whole cell
Speaker 2: PROTESTE vaccine would lead to deadly side effects in their kids,
Speaker 2: one solution was just to make a new vaccine, which
Speaker 2: is how we got the acellular protestas vaccine. So instead
Speaker 2: of these whole killed bacteria, which is what the you know,
Speaker 2: the name gives it away. The previous vaccine was it
Speaker 2: included just these these toxins, these antigens from Berttella protessis
Speaker 2: and the efficacy and I'm sure you're going to talk
Speaker 2: more about this, but the efficacy of this vaccine wasn't
Speaker 2: as high as the whole cell version, but it was
Speaker 2: associated with fewer adverse reactions, and so that replaced the
Speaker 2: P component of the DTP vaccine and it became DETAP
Speaker 2: to stand for acellular protessis in the nineteen nineties.
Speaker 3: Yeah, which Aaron means that we got at least one
Speaker 3: whole so vaccine.
Speaker 2: Cool.
Speaker 3: Yep. Probably a bunch actually, because we were pretty much
Speaker 3: done getting our vaccinations by the time they introduced DETAP
Speaker 3: in nineteen ninety two.
Speaker 2: Oh yeah, yeah, excellent. One of the things that I
Speaker 2: find interesting when doing the research for some of these
Speaker 2: episodes is that I get to read these articles that
Speaker 2: were written all like over a really long time span. Yeah, so,
Speaker 2: like some were written in the eighteen hundreds, seventeen hundreds whatever,
Speaker 2: translated from this and that, and you can see how
Speaker 2: the language used and the sentiment about a topic can
Speaker 2: really changes over time. In helps especially apparent for protessis.
Speaker 2: In more recent articles protessis has always described in the
Speaker 2: introduction as this re emerging problem that highlights the difficulties
Speaker 2: in educating the public and how quickly progress can be undone.
Speaker 2: But in these older articles or chapters from before the
Speaker 2: nineteen seventies, but like after the vaccine was developed, it
Speaker 2: was written about as a great triumph of modern medicine
Speaker 2: in many of them. Wow, And there was one line
Speaker 2: that really stuck with me when reading one of these
Speaker 2: old articles, and it was the one that you mentioned earlier,
Speaker 2: the one from nineteen seventy five. The author says, quote
Speaker 2: as recently as nineteen forty eight, protessis remained a leading
Speaker 2: cause of death in children under fourteen years of age
Speaker 2: in the United States. Now the disease has become almost
Speaker 2: a medical curiosity. The Center for Disease Control, for example,
Speaker 2: no longer routinely reports protessis. So aarin that was nineteen
Speaker 2: seventy five, This is twenty twenty. Tell me just how
Speaker 2: much that statement is no longer true.
Speaker 3: Yeah, you're not gonna like it. Let's take one more
Speaker 3: quick break.
Speaker 6: Okay, let's just go straight to the facts.
Speaker 2: Let's do it.
Speaker 3: Twenty eighteen, United States of America. You want to guess
Speaker 3: how many cases of protesters there were.
Speaker 2: Is it more than five thousand?
Speaker 4: Oh yes, Oh, my gosh, fifteen thousand, Okay, fifteen thousand
Speaker 4: cases of protessis in the US in twenty eighteen, including
Speaker 4: five deaths.
Speaker 2: And cases of a vaccine preventable illness.
Speaker 3: Yep. So let's talk about that. Well, first, really briefly,
Speaker 3: we'll talk about it across the globe, and then we
Speaker 3: really need to spend some time talking about this vaccine
Speaker 3: preventable disease aspect. The World Health Organization didn't have super
Speaker 3: great numbers more recently, like in the last couple of years,
Speaker 3: but for example, in twenty fourteen, it was estimated that
Speaker 3: there were twenty four over twenty four million cases of
Speaker 3: protessis worldwide and over one hundred and sixty thousand deaths
Speaker 3: in children under age five years. What one hundred and
Speaker 3: sixty thousand deaths from pertessis in children under age five
Speaker 3: in twenty fourteen, Oh and there are gosh, yeah, So
Speaker 3: this is not a disease that has gone away, and
Speaker 3: in fact, it's been on the rise for a number
Speaker 3: of years now, probably since the nineties. It's been kind
Speaker 3: of increasing every year and there's a number of reasons
Speaker 3: for that. So let's start talking about this vaccine. You
Speaker 3: mentioned that in the late eighties early nineties is when
Speaker 3: we pretty much switched from a whole cell vaccine to
Speaker 3: an a cellular vaccine. That's really important. The acellular vaccine
Speaker 3: does not provide as long lasting immunity as the whole
Speaker 3: cell vaccine, So that means that immunity, while it still exists,
Speaker 3: is not for your whole life when you get the
Speaker 3: acellular vaccine. However, and this is really important, especially I
Speaker 3: think in talking to people who are vaccine hesitant, who
Speaker 3: maybe sometimes use that as an excuse. While it doesn't
Speaker 3: provide long lasting immunity, wouldn't it be better just to
Speaker 3: get infected with the disease that kills people to begin with.
Speaker 3: Even getting infected with Pertessis does not provide lifetime immunity.
Speaker 2: Interesting.
Speaker 3: Yeah, this is a very interesting aspect of Protessis that
Speaker 3: I didn't realize until starting to research this. So, yeah,
Speaker 3: even getting infected doesn't provide lifelong immunity. Does it provide
Speaker 3: longer immunity than getting a vaccine? Yes, most likely, but
Speaker 3: it's still you can get reinfected with bordetella. Protessis. Even
Speaker 3: if you get infected as a child and survive that infection.
Speaker 2: Is the infection less severe in subsequent infections, So.
Speaker 3: Overall, great question overall whether you get infected and survive,
Speaker 3: which again not everyone does. If you get infected or
Speaker 3: you get vaccinated, then the disease that you get subsequently
Speaker 3: is most likely to be less severe. So even though
Speaker 3: vaccination doesn't provide lifelong immunity, it's massively protective against serious
Speaker 3: illness and death from protessis. Even with the whole cell vaccine,
Speaker 3: immunity does wane, but it's usually over like maybe ten, fifteen,
Speaker 3: twenty years, whereas with the acellular it might be seven
Speaker 3: to ten years that your immunity starts to wane. So
Speaker 3: that means that if you got your last vaccine, say
Speaker 3: when you went to kindergarten, then by the time you
Speaker 3: get to high school, you might not be immune anymore,
Speaker 3: or at least not completely immune. Your immunity has waned.
Speaker 3: So what we see is, while we have these really
Speaker 3: high numbers of protessis today in the United States and
Speaker 3: across the globe, it's not just because of vaccine hesitancy.
Speaker 3: It's not only an unvaccinated people. We also see increasing
Speaker 3: we see actually a shift in the age groups of
Speaker 3: people who get infected. So, while you talked about kind
Speaker 3: of throughout the last five hundred years of this disease,
Speaker 3: it's been mostly a disease of children, right, not babies necessarily,
Speaker 3: but children. This is a disease of childhood. Maybe like
Speaker 3: one to two year olds up to like ten year
Speaker 3: olds were the majority of people who got sick before
Speaker 3: the introduction of any vaccine. Now today the largest numbers
Speaker 3: of people who get sick are actually adolescents and young adults.
Speaker 3: So in twenty eighteen in the US, thirty percent of
Speaker 3: those fifteen thousand cases were in people age eleven to nineteen.
Speaker 2: Wow, okay, I have a question about sort of the vaccine.
Speaker 2: Now when you go to the doctor and you because
Speaker 2: I know the TEENNUS vaccine, you need.
Speaker 3: To get re upped every yeah, ten.
Speaker 2: Years, when they give you that booster. Is it DTaP
Speaker 2: or is it just tetanus?
Speaker 3: Good question. It used to be just td which is
Speaker 3: tetanus and diphtheria. Now it's recommended that adolescents get at
Speaker 3: least one booster of t DAP, which is the adult
Speaker 3: version of tetanus, diphtheria, and acellular protessis. But it didn't
Speaker 3: used to be the case. So because we thought, oh,
Speaker 3: this provides a long enough immunity that because the whole
Speaker 3: cell vaccine did.
Speaker 2: Yeah.
Speaker 3: But now it's recognized that immunity wanes faster than we
Speaker 3: may be expected, and that's part of the reason that
Speaker 3: we see an increase in the number of cases in
Speaker 3: older age groups. But this is really important because the
Speaker 3: other group that's massively affected besides adolescence are the very
Speaker 3: very old who are immunocompromised and tiny babies who are
Speaker 3: too young to be fully vaccinated right And in those
Speaker 3: groups over up to fifty percent of them will be hospitalized.
Speaker 3: And in that age group is where we also see
Speaker 3: the highest mortality rates. So while infants under the age
Speaker 3: of six months were only nine percent of the total
Speaker 3: cases of protessis in the US in twenty eighteen, forty
Speaker 3: two percent of those babies were hospitalized.
Speaker 2: Two questions, how old do you have to be to
Speaker 2: get the first protestis vaccine? Second question, when you go
Speaker 2: in for your tetanus booster, do you have to specifically
Speaker 2: ask for tap?
Speaker 3: First question is easy. You get your first d tap
Speaker 3: at around two months of age, as early as six weeks,
Speaker 3: but usually at around the eight week two month mark.
Speaker 3: And it's a series of like four vaccines usually, so
Speaker 3: you get it at two months, at four months, at
Speaker 3: six months, and so that's why up to six months
Speaker 3: you haven't gotten your full dose of it, So you're
Speaker 3: still at risk, okay, And in those kids and in
Speaker 3: older adolescents, it's more likely to present with an atypical course,
Speaker 3: which we kind of touched on a little bit. We
Speaker 3: hinted at in the biology section. But once you have
Speaker 3: some antibodies that you've built up against this infection, you're
Speaker 3: less likely to have that characteristic whoop of the whooping
Speaker 3: cough oh okay, because you have a less kind of
Speaker 3: intense infection. But what's also scary is that in tiny
Speaker 3: infants this can also present with just apnea, which means
Speaker 3: cessation of breathing entirely. So you don't have the coughing,
Speaker 3: you don't have the whoop. You just have babies who
Speaker 3: stop breathing, which is terrifying.
Speaker 2: Yeah, that's horrifying.
Speaker 3: Yep. Your second question was do you have to specifically
Speaker 3: ask for a tea DAP at this point the recommendation
Speaker 3: is if you haven't, If you are an adult who
Speaker 3: hasn't had a tea DAP booster at any point in
Speaker 3: your life, then you should get one. And then after
Speaker 3: that you would just get your regular tetanus and diphtheria
Speaker 3: every ten years. But let's talk about a couple of
Speaker 3: specific groups that should get boosters and can talk to
Speaker 3: their physicians about this.
Speaker 2: Yeah, would you just go to your physician and say, hey,
Speaker 2: can you check my tighters?
Speaker 3: Absolutely check that you could do that. Yeah, check my records.
Speaker 3: Have I had one recently? If not, most physicians will
Speaker 3: be like, yeah, let's give you a tea DAP because
Speaker 3: certainly not going to hurt you.
Speaker 2: I was gonna say, is there any harm in like
Speaker 2: getting an early booster.
Speaker 3: No, there isn't. And there are a few groups who
Speaker 3: should really consider getting boosters. Number one, anyone who's going
Speaker 3: to be in contact with a tiny baby pregnancy. It's
Speaker 3: now recommended and it's in a lot of countries. It's
Speaker 3: standard practice that during pregnancy, in the third trimester, so
Speaker 3: between like twenty seven and thirty six weeks, we give
Speaker 3: tea DAP boosters. And this has been hugely important in
Speaker 3: preventing illness in that tiny baby age group, so pre
Speaker 3: two months, where that baby is entirely unvaccinated. If you
Speaker 3: vaccinate during pregnancy, then you can pass annabodies, maternal antibodies
Speaker 3: onto the baby, right, which is it's massively protected.
Speaker 2: It's amazing and didn't used to.
Speaker 3: Be standard practice. Unfortunately. That's pretty much all I have
Speaker 3: aaron about the state of protesters today. I tried to
Speaker 3: find some current research on what's going on and the NIAID.
Speaker 3: The NIH page was last updated in twenty sixteen.
Speaker 2: WHOA, right, come on, come on, But well, it's it's
Speaker 2: hard because it's like with many of the other diseases
Speaker 2: that we do an episode on, it's like, oh, and
Speaker 2: then there's a new drug therapy, there's a new vaccine
Speaker 2: in development, there's a new something. But this is like,
Speaker 2: we have antibiotics that can work if you if you
Speaker 2: give them early enough, and we have a vaccine that works.
Speaker 2: So maybe the progress needs to be made in public
Speaker 2: education in access, like reducing the barriers to vaccine access.
Speaker 3: I would say there could still be work to be
Speaker 3: done on creating a more effective vaccine that produces longer
Speaker 3: lasting immunity as well, especially since we're seeing waning immunity
Speaker 3: and kind of developing a better immunization schedule perhaps for
Speaker 3: older children and adults. But what's hard is that it's
Speaker 3: easy to give vaccines to small kids because they come
Speaker 3: to the doctor on a regular schedule. Once kids get
Speaker 3: older and become adults, we don't necessarily go to the
Speaker 3: doctor on a regular schedule. So it's really hard. Even
Speaker 3: if you have an effective vaccine to give a booster,
Speaker 3: it's hard to get that booster to everyone to actually
Speaker 3: create the herd immunity that we need to protect the
Speaker 3: vulnerable people in our population.
Speaker 2: It still seems like an upward battle.
Speaker 3: It's an upward battle, for sure. It always is with
Speaker 3: diseases though, isn't it.
Speaker 2: Yeah, Yeah, But there's a lot of amazing work done
Speaker 2: in this upward battle, and for you know, pushing for
Speaker 2: VACUS vaccine education information and for just promoting the use
Speaker 2: of vaccines. And so one of these amazing people who's
Speaker 2: working on this you heard from earlier, Catherine Hughes, and
Speaker 2: we wanted to have her talk a little bit about like,
Speaker 2: for Riley.
Speaker 3: As traumatic as it was, I'm sure to go through
Speaker 3: and to relive it, you have really turned this into
Speaker 3: a lot of advocacy and done amazing things as a
Speaker 3: result of this tragic situation. So can you tell us
Speaker 3: a little bit about sort of what that's been like
Speaker 3: for you to kind of take the worst possible situation
Speaker 3: and try and make something good out of it.
Speaker 1: I really believe that life can be measured in years,
Speaker 1: but it can also be measured in impact, and so
Speaker 1: when Riley died, we felt devastated that his life was
Speaker 1: so short in years, but we thought that perhaps we
Speaker 1: could somehow extend his life by making sure that it
Speaker 1: had an impact on the world. So we sort of
Speaker 1: were loaded with that really strong urge to do something
Speaker 1: to create a legacy for Riley. But we were also
Speaker 1: filled with this sense that what happened was so unfair
Speaker 1: and that it was preventable, and that it shouldn't happen
Speaker 1: to other babies and other families. So we were really
Speaker 1: driven to spread awareness and we started our campaign, which
Speaker 1: is called the Light for Riley Campaign. We were really
Speaker 1: determined to shine a light on the importance of vaccination
Speaker 1: and the dangers of hooping cough. It was when Riley
Speaker 1: was really sick in hospital that I sort of jumped
Speaker 1: on my phone and began googling, you know, all the
Speaker 1: information I could find out about hooping cough and that's
Speaker 1: when I learned that other countries were offering pregnant mums
Speaker 1: a hooping core vaccine during pregnancy, and I felt so
Speaker 1: upset that this hadn't been offered to me in my pregnancy.
Speaker 1: I'd had the flu vaccine in pregnancy. I knew I
Speaker 1: was the type of mum to say, you know, yes,
Speaker 1: you know, if you recommend it, I'll do it. And
Speaker 1: we know now that babies are born to mums who
Speaker 1: have this hooping core vaccine in pregnancy, the chance of
Speaker 1: them catching hooping cough is drastically reduced. So I truly
Speaker 1: believe Riley would probably still be here with us today
Speaker 1: if this pregnancy hooping core vaccine had been offered to me.
Speaker 1: So with that knowledge, it was very instinctive for us
Speaker 1: to embark on our life for Riley campaign. We've you know,
Speaker 1: done media interviews and social media campaigns, and we travel
Speaker 1: around to pregnancy expos where we talk to pregnant mums
Speaker 1: about the importance of getting vaccinated. And we've seen really
Speaker 1: good uptake of this vaccine in Australia. So around eighty
Speaker 1: percent of mums saying yes to this pregnancy vaccine. But
Speaker 1: then again, that's still twenty percent of babies who have
Speaker 1: been born at risk of contracting this disease, which is
Speaker 1: always circulating around our community. So there's so much more
Speaker 1: that we want to do.
Speaker 2: It's incredible work that you're doing, and it's also really
Speaker 2: inspiring because this must not be an easy thing to do.
Speaker 2: In your experience with the Light for Raley campaign, what
Speaker 2: do you feel like have been the biggest challenges you've
Speaker 2: had to overcome.
Speaker 1: I think we've had two challenges with our Light for
Speaker 1: Raley campaign. The first is just coping with grief while
Speaker 1: trying to put ourselves out there. Grief is a funny
Speaker 1: thing and I think it's different for person, but that's
Speaker 1: certainly been a challenge trying to manage grief and advocacy.
Speaker 1: And the second challenge we've faced was, you know, for
Speaker 1: want of a better word, being attacked by the anti
Speaker 1: vaccine movement. This happened within a day of Riley's death,
Speaker 1: where we're getting messages on Facebook from anti vaccine activists
Speaker 1: and we've had an incredible amount of blog posts and
Speaker 1: Facebook messages and comments and all sorts of things from
Speaker 1: the anti vaccine movement. I truly believe that Riley's death
Speaker 1: is a bit of an uncomfortable truth for them. Riley
Speaker 1: was unvaccinated who was too young to be vaccinated, and
Speaker 1: it's probably scary for them to realize that unvaccinated children
Speaker 1: die from vaccine preventable diseases. We've also seen a lot
Speaker 1: of conspiracy theories about us. We've been told that we're actors,
Speaker 1: that we've been paid by Big Farmer. We've been told
Speaker 1: that Riley never existed. We've been told that we murdered him,
Speaker 1: all sorts of stuff. And again, I think it's just
Speaker 1: because anti vaxes can feel very uncomfortable when it comes
Speaker 1: to facing the truth. The best way for us to
Speaker 1: deal with the anti vax movement is really to give
Speaker 1: them as little attention as possible. We don't respond to them.
Speaker 1: For the most part, we ignore them. The people that
Speaker 1: we want to focus on, of those who are on
Speaker 1: the fence or just don't know much about vaccination, they're
Speaker 1: really the people that we want Riley's message to get
Speaker 1: across to.
Speaker 2: What sort of future plans do you have for the
Speaker 2: Late for Riley campaign? Do you have anything that's currently
Speaker 2: in the works or anything upcoming.
Speaker 1: In twenty sixteen, we launched our charity, the Immunization Foundation
Speaker 1: of Australia, and so that's kept us really busy. I
Speaker 1: absolutely love being a director of this foundation because we're
Speaker 1: not just focused on hooping cough, but on immunization in general.
Speaker 1: We want all babies and all families to be protected
Speaker 1: from these potentially deadly vaccine preventable diseases. So we'll continue traveling.
Speaker 1: I do lots of speaking and workshops. We present to schools.
Speaker 1: We've got puppet shows for kids to make them feel
Speaker 1: more comfortable with the process of vaccinating. We're looking to
Speaker 1: collect more stories about families who have suffered through vaccine
Speaker 1: preventable diseases, because we believe it is so important that
Speaker 1: people know these stories. Because vaccination is almost a victim
Speaker 1: of its own success. We don't see these stories around
Speaker 1: so much because vaccines work so well, but as parents,
Speaker 1: we need to know why we vaccinate. And we're also
Speaker 1: looking at hopefully being able to donate some vaccines overseas
Speaker 1: later this year as well to children in developing countries.
Speaker 2: That's wonderful. What an inspiring campaign. Where can our listeners
Speaker 2: learn more or read more about Like for Riley and
Speaker 2: some of the work that you're doing through the campaign.
Speaker 1: If you go to our Facebook page, which is just
Speaker 1: like for Riley on Facebook, you can read all about
Speaker 1: Riley's story there and then also on our website which
Speaker 1: is www. Dot IFA dot org dot au.
Speaker 3: Thank you so much for sharing your story not only
Speaker 3: with us and our listeners, but with everyone around the
Speaker 3: world with your campaign and all of the work that
Speaker 3: you're doing. It's really incredible.
Speaker 2: Yeah, this was really wonderful. Thank you again, so so much.
Speaker 2: We really appreciate it.
Speaker 1: Thank you. Thanks, it's such a pleasure to speak to
Speaker 1: you guys. And apologies for my terrible Australian twang. Hopefully
Speaker 1: it doesn't ruin your whole podcast.
Speaker 2: I love it, perfect, We love it.
Speaker 3: I think we need a little bit more twang on
Speaker 3: our for sure. For sure.
Speaker 2: That was fantastic. It's so inspiring to hear yet another
Speaker 2: awesome woman doing incredible work on protessis. Yeah, should we
Speaker 2: uh get into sources? Let's okay, I have somehow accumulated
Speaker 2: an unbelievable number of sources for this one. There was
Speaker 2: a like consolidated No, there was no like usually I'm like, oh, great,
Speaker 2: there's a book. I'll read that book. But there was
Speaker 2: no single book this times, so it was much more
Speaker 2: of a digging down the rabbit hole. But I'll mention
Speaker 2: a few of these. So one was from Aslana Body
Speaker 2: at all from twenty fifteen, and that was about these
Speaker 2: possible epidemics in Persia. A couple great articles about just
Speaker 2: the history of protessis won by James Cherry from twenty fifteen,
Speaker 2: another by Chow at All from twenty sixteen. And the
Speaker 2: evolutionary paper came from Dievatapoulos at all two thousand and five.
Speaker 2: And the title of our quarantiny three Women and a
Speaker 2: Baby came from a title of a chapter of a
Speaker 2: book in between Hope and Fear, A History of Vaccines
Speaker 2: and Human Immunity from by Michael Kinsch And that one
Speaker 2: I mentioned also on our vaccines episode. Yeah, and honestly,
Speaker 2: there are a bunch more, and I'll just put them
Speaker 2: all on our website. Sorry, that was a really long list.
Speaker 3: Yeah, I have a number. We'll post all of them
Speaker 3: on our website this podcast will kill You dot com
Speaker 3: under the episodes tab. All right, So thank you to
Speaker 3: Bloodmobile for providing the music for this episode and all
Speaker 3: of our episodes.
Speaker 2: Thank you again to Catherine Hughes for being so amazing
Speaker 2: and coming onto our podcast and be willing to share
Speaker 2: her story, and we hope that you all enjoyed it
Speaker 2: as well, and we will post links to Light for
Speaker 2: Riley in our show notes and on our website, so
Speaker 2: keep an eye out for that.
Speaker 3: And thank you to you all for listening. As always,
Speaker 3: we love making this podcast, so thanks for letting us
Speaker 3: do that.
Speaker 2: Yes, we do well with that.
Speaker 3: Wash your hands, you filthy animals.