This Podcast Will Kill You - Ep 68 Coccidioidomycosis: It’s never a spider bite

Episode Date: March 9, 2021

Don’t be daunted by the length of this disease name or just how difficult it looks to pronounce. By the end of the episode, you’ll be saying it right along with us, and bonus, you’ll also be armed with a whole bunch of excellent trivia about this fascinating fungal disease. In this episode, we dive right into all things coccidioidomycosis, also known as Valley fever, which also happens to be the first human fungal pathogen we’ve covered. We’ll walk you through its unusual dual natured lifecycle, its somewhat recent but surprisingly rich history, and the present threat it poses, especially in light of climate change and the United States prison system. This fungus is much more amongus than you may have suspected. We are also so lucky to be joined by Tori, who shared with us her firsthand account of contracting this fierce fungus. See omnystudio.com/listener for privacy information.

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Terms and Conditions Apply. Visit blueapron.com slash terms for more information. I'm Clayton Eckerd. In 2022, I was the lead of ABC's The Bachelor. But here's the thing. Bachelor fans hated him. If I could press a button and rewind it all I would. That's when his life took a disturbing turn.

A one-night stand would end in a courtroom. The media is here. this case has gone viral. The dating contract. Agree to date me, but I'm also suing you. This is unlike anything I've ever seen before. I'm Stephanie Young. Listen to Love Trapped on the Iheart Radio app, Apple Podcasts, or wherever you get your podcasts.

This is Special Agent Regal, Special Agent Bradley Hall. In 2018, the FBI took down a ring of spies working for China's Ministry of State Security, one of the most mysterious intelligence agencies in the world. The Sixth Bureau podcast is a story of the inner workings of the MSS and how one man's ambition and mistakes opened its fault of secrets. Listen to the Sixth Bureau on the IHeart Radio app, Apple Podcasts, or wherever you get your podcasts. So my name is Tori, and I'm from Utah. I had always been a healthy girl with no serious ailments or illnesses.

I spent most of my high school cycling, swimming, running. Exercise was my whole life, and I was always very healthy. At age 19, I created a plan to serve a religious mission and then come home and spend the rest of my life doing Iron Man's and one day making it to the Conna Iron Man Championship. However, those plans would quickly change. In March of 2014, I left on a religious mission to Arizona for 18 months, doing service, outdoors, and teaching. I ran nearly every day of this mission and did quite a lot of bike riding as well. Initially going out to Arizona, we were warned about Valley Fever. We were told always to stay inside if there was a dust storm or if it's extra dusty outside

because Valley Fever was in the spores, the soil, or the dust. While we tried to stay inside from the dust storms, being outside was inevitable and being around the dust was inevitable. Hello, it's Arizona, and we spent so much time outside. Fast forward, it was August 29, 2015. I was 17 days away from going home and seeing my family again and finishing this service. And that day in my life would change forever. I woke up with a bit of chest tightness, but shrugged it off. I still went on our morning run, but could barely

make it more than a quarter of a mile when the chest pain became so intense. I ended up going to an urgent care and sitting in the waiting room for three hours gasping for breath because their computer was down. I was in so much pain I could barely breathe. When the computers finally came up, I was able to get an x-ray by the urgent care doctor. After analyzing the x-ray, nothing of concern showed up. So the doc presumed that the only explanation was something similar to shingles because I didn't have a fever, I didn't have a cough, I didn't have a rash or anything else. I was given steroid shots and pain medications and then sent on my way.

After a few days, I began to have a low-grade fever and some body aches. Progressively, the fevers got worse and the aches more extreme, to which point I felt unable to move my joints. Exactly one week from my initial trip to the urgent care, I was back again with fevers, nausea, a developing cough, consistent chest pain with absolutely no relief and convinced this was more than shingles. I wanted to die with the pain I was experiencing.

Luckily, the computers didn't have issues and I was able to get right into the doctor and he immediately ordered an additional chest x-ray again, just to see. I will never forget that x-ray, as his assistants helped me stand up because I screamed in agony trying to expand my joints and my chest, all of which were screaming back at me tenfold what I was screaming out loud. The x-ray came up on the scream starting from the bottom up.

As I watched it, I saw spider web clouds covering my entire right lung. Even I knew something was wrong. In a week's time, my chest x-ray had dramatically changed. The doctor spent what seemed like years just looking at the x-ray and deemed it appropriate for me to go to the ER and get a stat CT scan and be admitted. When I got there, my O2 SATs were in the 80s at best, and the CT scan that they quickly did showed fluid around my entire right lung and beginning around my lower left lobe. It was clear whatever I was experiencing was spreading quickly. I was quickly treated by teams of infectious disease doctors, pulmonologists, and respiratory

therapists. Blood samples were taken and sent off to labs. In the meantime, I was treated for anything and everything. One of the first things they tested for was valley fever. The blood antigen tests that they did ended up coming back negative for valley fever, oddly enough, but they wanted to test part of my lung tissue to be sure. I was then presumed to maybe have tuberculosis and or a staff infection and was primarily treated for that, along with antifungals for the possible valley fever.

In the coming days, I got sicker and weaker. My cough persisted and became more violent. So much water was in my lungs that each time I was. I coughed, I felt like I was drowning because so much water came up. Every bone hurt and my fever couldn't get under control. I remember multiple mornings being visited by the infectious disease doctor and her sitting by the side of my bed holding my hand and telling me she didn't sleep, worried I wouldn't make it through the night.

On September 12th, three days before I was supposed to return home to Utah, the concoction of medication that they had me on seemed to be stabilizing me and my resting arrow to stats looked as if they could be stable for a short flight home. By this day, the atrophy and amaciation of my once very strong, healthy body was shocking. I could no longer even sit up in my hospital bed without being winded or gasping for air. Standing up was a special task of its own that I could no longer fathom doing on my own. I was wheeled in a wheelchair through the airport to greet my family. The active, vibrant athlete they once knew returned home bruised and beaten by an unknown cause. We later received a call from Arizona that the tissue biopsy did end up growing valley fever,

and that valley fever was indeed the culprit. The year following this infection would be very trying to say the least. I continued to be sick returning to the hospital a few additional times. I lived on the couch, barely even able to get myself up for months, still coughing up water continuously, taking quick, shallow, frightening breaths and too weak to do much of anything on my own. everything caused me to be out of breath, very different from what I grew up knowing. As it stands today, I still get a CT scan about once a year, sometimes every six months, depending on what my infectious disease doctor says.

My lower two lobes of my right lung are dead, as well as the lower lobe of my left lung. I have the equivalent of one lung in my body. The remaining tissue eventually took up the task of providing my body with enough oxygen to live a normal life. When I was able to start moving again, after many years, exercise became a daunting feat. Getting my heart rate up was very difficult and typically resulted in a coughing attack. It took years for me to work up the stamina to ride a bike. To this day, I cannot run and am a mediocre athlete at best. I can enjoy movement for the most part and do what my lungs will allow.

Walking up heels and stairs tend to be most difficult. I'm on forever antifungals because for whatever reason, my body being an anomaly doesn't like to fight valley fever. However, today I'm grateful for a body that did fight, though my goals and ambitions changed drastically. I survived and walked today with the equivalent of one lung. Dinner shows up every night, whether you're prepared for it or not. And with Blue Apron, you won't need to panic order takeout again. Blue Apron meals are designed by chefs and arrive with pre-portioned ingredients so there's no meal planning and no extra grocery trip. There, assemble and bake meals, take about five minutes of hands-on prep. Just spread the pre-chopped

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is now the most prolific child killer in modern British history. Everyone thought they knew how it ended. A verdict? A villain? A nurse named Lucy Leppi. Lucy Letby has been found guilty. But what if we didn't get the whole story? The moment you look at the whole picture, the case collapses. I'm Amanda Knox, and in the new podcast, doubt the case of Lucy Lettby,

we follow the evidence and hear from the people that lived it, to ask what really happened when the world decided who Lucy Lettby was. No voicing of any skepticism or doubt. It'll cause so much harm at every single level of the British establishment of this is wrong. Listen to Doubt, the case of Lucy Letby on the Iheart Radio app, Apple Podcasts, or wherever you get your podcasts. Thank you so much, Tori, for sharing your story with us. Yeah, wow. Thank you. Thank you. I'm Aaron Welsh. And I'm Aaron Almond Updike. And this is, this podcast will kill you. And today we're talking about coxidioidomycosis. Ooh, well done. Thank you. We think that's how we're supposed to say it. We've been practicing a lot.

Yeah. If that's the wrong way to pronounce it and it's really bothering you, it's going to be a long episode for you guys. It's going to be terrible. It's going to be worse than Gardia. But listen, I went to YouTube and I found like an actual clinical lecture on coxidioidomycosis. Nailed it. Hopefully. And this is how the person pronounced it. And so we got our pronunciations from a clinical lecture from like a school of public health. So we're trying our best as always, aka in case you have not heard of this, the other name for it is Valley Fever. Yes. This is going to be a cool one because it's our first human fungal pathogen. Which is just, I can't believe it's taken us this long.

We've done chitred. We did chitred. And actually someone asked us recently if we've ever done cortisps, which we haven't done on this podcast, but we did talk a lot about cordyceps on an episode of the Biology of Superheroes podcast. Yes. So definitely check that one out if you haven't listened to that already. Oh, yeah.

But we're not talking about cordyceps today. We're talking about coxidioidomycosis. But before we begin, it's quarantini time. It is quarantini time, my favorite time. What are we drinking this week? We're drinking the dust devil. This is a fantastic name, and it's so fantastic that we cannot take credit for it. I actually found it.

It was the title of a paper. Some of the papers I read for this episode have the greatest titles. This one is Dust Devil, the Life and Times of the Fungus that Causes Valley Fever. Ooh, I love it. Isn't that great? And that's by Lewis Bowers and Barker. Another one of my favorite paper titles for this episode was Cuxidioidomycosis. What a long, strange trip it's been or something to that effect.

Oh, that's adorable. Yeah. It was great. Anyway, what is in the dust devil? It's a tequila-based pear cider situation. Yeah, it's tasty. It's got tequila, of course. It's got like pear juice.

It's got a spiced simple syrup, and we threw in some orange liqueur. And anyway, we will post the full recipe for this quarantini, as well as our non-alcoholic placebo-rita on our website. This podcast Will Kill You.com, as well as on all of our social media channel. So make sure you follow us there. Definitely. What other business do we have to attend to, Aaron? We got some of the most incredible responses from our sweating sickness episode or after our sweating sickness episode.

Yeah, we did. Oh, my gosh. So many people, you know, wrote to us or commented with their different hypotheses as to, like, what caused this, you know, super bizarre disease. And I wanted to shout out one in particular. From someone who wrote us this, like, incredibly detailed email about how they went down into this deep rabbit hole looking into possible causes and came up with a walnut mold, Penerum A, as their hypothesis. Like, I just love it. Like, I love that there are people out there as nerdy as us doing these deep, deep dives on things like what caused sweating sickness. Yeah, and came up with a walnut mold. And like, honestly, I'm, I'm kind of, I kind of buy it.

It seems like quite plausible, like the symptoms line up, a foodborne toxin could very well move along trade routes like we talked about. And I just wanted to say thank you for everyone's responses and this email in particular because I got such a kick out of it. I love it. Do we have more business? I did want to say I finally checked our PO box that I'm really bad about checking. And I wanted to say thank you to Sabrina for your thank you note. Oh my gosh. So adorable. She sent us a thank you card just to say thanks for making the podcast so that she really likes it. And I really like you. It was the sweetest thing. Anyways, that's all. Okay. Let's talk fungus. Please, please. We'll take a quick break and then dive into the biology of coccidiomycosis.

Do I say it right that time? I think so. I think I did. Okay. Coxidioidomycosis, aka Valley Fever, aka our first human fungal pathogen. It's actually two different species of fungi, coxidioidies imidus and coxidioidioidies posodicy, which are, both endemic to desert areas in mostly the southwestern U.S. So coxidioidioidis tends to be more prevalent in California and coxidioidioidis posodicy mostly in Arizona. But these fungi are also found throughout New Mexico, Utah, into Texas. We'll talk a little bit later about how maybe it's all the way up in Washington,

as well as down into parts of Mexico and Central and South America. So let's get into the disease that's actually caused by this fungus. This is a pathogen that is not contagious. So it has not been shown to be spread from person to person or from animal to person because this is also a fungus that can infect other animals aside from humans, especially dogs. But I am not really going to talk anymore about infection in animals like at all. but this is a fungus that's called dimorphic. So it has two entirely different forms that it exists in.

And I have to confess that I know so little about fungus that I still have so many questions about how the heck this is possible. Like it's so fascinating. Okay, let's get into it. In the environment, this fungus exists as a mold. It's called a mycelium. So if you were to grow a whole bunch of it, like very concentrated in like a jar or something and pick it up, it would look kind of like a little cotton puff, like a little ball of white little wispies. Like cotton candy. Yum. Microscopically, if you look at these little wispies in more detail, they look, they're called branching septate hyphy. What does that mean?

They're kind of like, this is the way I'm going to describe it, Aaron. it's like a tree made out of toilet paper. So it's like long, stringy bits that have branches like a tree would, but then they're separated at certain points, like the way that toilet paper is. So it has little septations. Okay. And so what happens is that during times of drought or low precipitation, those like toilet paper squares, which in the fungus are called arthropoconidia or arthropores, they dry in.

out and then they break off super easily. Like if your house got toilet papered and then the wind picked up and broke off a bunch of little squares of toilet paper and then toilet paper flew all around your neighborhood. Yeah. And then what happens is that you as a human breathe those spores in. So that is kind of the life cycle in the environment. So you have these mycelia, these little long branchy, stringy bits that break off when they dry out and then then can become born on the wind in the soil. Excellent. Now you breathe them in.

And now we have to talk about what happens in us because it's totally completely different than what happens in the environment. So when you breathe in a spore, literally potentially just one, it only has to be one spore, could potentially infect you. What happens is you breathe it in

and it goes down into the bottom of your respiratory tract and lodges in your terminal alveoli, your terminal bronchial is like right where gas exchange is supposed to be happening. And once it gets there, it begins to enlarge. And it forms what's called a spherial, like a big sphere. Okay. I don't know why it's called that. Like a beach ball in your alveolar. And in this spherial, it begins to replicate and forms thousands of endospores. Ooh. Within the spherial. Within the spherical. Okay.

And then eventually that spherial will rupture and release those thousands of endospores that can go on to travel, form new spherules, which make more endospores, et cetera, et cetera. That's cool. So it brings its own little like reproductive machinery. Yeah. It just, it does it all on its own. It's asexually reproducing, just boop, boop, boop, make it a bunch of little endospores. but that's completely different than how it lives and replicates in the environment, in the soil. And it gets even weirder because if, for example, you take a sample of someone's sputum, like gunk that they coughed up when they were infected with coxidioides, and that's a whole bunch of endospores inside a spherial, if you left that on the counter, it would grow mycelium. It would grow into the environmental form, which by the, by the same.

the way would be highly infectious if it dried out. So there's some kind of cues that it's using. Yeah, some kind of cues to know that it's in a host versus in the external environment. I wonder what those cues are. Me too, Aaron. Me too. But we're going to focus on what happens when it's inside of your body. If somebody is a fungus researcher, it would be awesome to know more details about that fungus because who boy. But in general, once this happens inside of our lungs, our body reacts to this fungus. It's going to induce an immune response. It's going to recruit a lot of inflammatory cells. And that's going to kind of result in the symptoms that we see. So let's talk about those. Yeah. If you have any symptoms at all,

which about 40% of people who get infected with coxidioides will. 60% of people won't have any symptoms at all. If you have these symptoms, most commonly, it presents as an acute pneumonia. And I think we've talked very peripherally about pneumonia in the past. I'm actually going to talk kind of a lot about pneumonia in this episode, which is exciting. Yeah. But pneumonia is basically just the way that we say there's an infectious cause. of inflammation and fluid filling up the air sacs of the lungs.

Okay. So it's inflammation of the lungs, but pneumonia is used specifically to mean an infectious cause of that inflammation. So with coxidioidomycosis, do I get that right? I think so. Honestly, it's like we've said it and I've thought it so many times and it's starting to sound weird. I know.

One to three weeks after inhalation of the spores, you have basically pretty typical pneumonia symptoms. Fever, a cough that's quite productive of like gunk, very profound fatigue, like just feeling very exhausted, and probably chest pain, especially when you take really deep breaths. With coxidioides infection, it's also really common to have a headache, and the chest pain tends to be very severe. And with this type of pneumonia, the fatigue can last for months and months. So even as the pneumonia resolves, that fatigue can persist. Okay. If you were to take a chest x-ray or a chest CT scan, which would be very likely to happen if you went to the ER or the doctor's office, it would look like pretty much most other causes of pneumonia, which means it would look like there's fluid in some portion of your lung, either in just one lobe or maybe in like the middle.

region, which is called the hylar region around the trachea, like where the trachea divides. You might have some swollen lymph nodes along that region. That's a little bit more common with a coxidioides pneumonia than other types of pneumonia. One other thing you might have that's not as common with other forms of pneumonia is you might have some skin changes, like some red, painful, swollen bumps along your shins that are called erythema nodosum, or another red splotchy rash that can occur kind of across your body that's called erythema multiform? Question. Okay.

What else causes those two things? So a number of different, these are not specific to coxidioides infection. These are both caused by an immune response to this infection, not from like a disseminated fungus. So there's actually a number of different infections that can cause similar findings, like different viruses and bacteria. Okay. But I mean, like, I guess what's the mechanism? Like, why does that happen in these different infections?

That's a really good question. That I don't know the specifics of it, aside from the fact that whatever specific immune response is being generated, that's what then causes this. Okay. And this is only like an occasional sign of disease. Okay. Yeah. Yeah. So it's also kind of person specific. Like some people might be more likely to have this immune response than others. Mm-hmm. Yeah. But most of these people, with this presentation will recover and be pretty much fine with or without any treatment. And keep that in mind, ding, ding, ding, ding with or without treatment, because it'll become really important later on. Okay. But some people won't.

So there's a few other forms that this disease can take. Some people will go on to have a chronic form of pneumonia that's called chronic progressive pneumonia. And I had a hard time finding the exact percentage of people that go on to have like a chronic pneumonia, which basically would be all the same things that you had with this pneumonia. So cough, potentially coughing up blood because you have so much inflammation and infection. You'd go on to have weight loss because you've essentially been sick for so long that you're just not eating. You feel really, really bad. The fatigue is extreme. And on X-ray, you still see those same pneumonia changes. But based on everything that I read, it seems like it's likely

less than 5% of the time. But I didn't get a hard number on chronic pneumonia. Okay. But even if the pneumonia resolves or is treated and goes away, sometimes all of the fluid and gunk that's left behind from the infection can kind of persist and what it does is contract into like a cavity that our body kind of walls off and it just stays there. And this can happen like five to 10 percent of the time. So you'd still see like a nodule or a cavity if you looked at an x-ray of a person with this. This is in their lung. In their lung. And now most of the time, that's all and nothing ever happens beyond that. But in 30 to 60% of people with these nodules, they actually still have an active infection. It's just not spreading or doing anything. So if you tested them for coxidioides, you would find it.

And so this could potentially reactivate or have like waxing and waning symptoms. Wait a second. So the fungus is still there in that nodule, but it's been walled off. It's been walled off. So it's like that Edgar Allan Poe story. the cask of a Monteado. Do you ever talking about? I probably have read it, but I don't specifically remember it. It's the one where they wall the guy up inside. Oh, yeah.

They wall him up and like leave him. Yeah, I was going to say it's kind of like TB. But yeah, also that. I feel like that says a lot about our personalities. Yeah. is not uncommon in other fungal infections as well. Fungal infections are very difficult to kind of treat and deal with, and our immune system doesn't always do a great job of responding to them. Now, there's something else that can happen that gets a lot worse. So in somewhere between 1 and 5%

of cases, the infection can spread beyond the lungs and result in what's called disseminated disease. So overall, if you look at everyone who gets infected with coxidioides, the percentages are like somewhere between 1 and 5%. But if you look just at people who are in some way immunocompromised, whether that's from HIV infection that has a low CD4 count or some kind of congenital immunodeficiency, someone who's on immunosuppressants because of an organ transplant or whatever, in this group, it's like 30 to 50% of people could go on to develop disseminated disease. Okay. So it's like...

So it's disproportionate who is likely to get a disseminated infection. Right, right. But even in people who are otherwise immunocompetent, somewhere between like 1 to 3% of people will go on to develop this systemic infection. Okay. So once this fungus spreads from beyond your lungs, so it like makes its way from your alveolite out into your bloodstream,

it can go literally anywhere. And in fact, in theory, any organ or any system. But there are a few places that it goes most commonly. The skin is one of them. And this results in kind of ulcerations or nodules or big kind of like blisters that burst open that you see on the skin. It can go to the lymph nodes, which would cause a lot of lymph swelling. It can go to the joints, which would cause a lot of joint pain. but the most severe and terrifying manifestation is if it goes to the meninges, which is the lining

of our central nervous system. So this means it's managed to cross the blood brain barrier and result in meningitis, which if untreated, is fatal over 90% of the time. And this also tends to happen months or even years after an initial respiratory pneumonia type infection. Months or years. Yeah, so it's a long process of this fungus making its way through our body and wreaking havoc. So is it possible that somebody becomes infected and then doesn't know for years and years that this is what they have? I don't think for years and years, but potentially yes, because, for example, if they form like a nodule and they're otherwise immunocompetent, then their immune system can keep that at bay.

if they then become immunosuppressed for some reason later on, this could be reactivated. Okay. Yeah. Gotcha. Yeah. So, yeah, so that's kind of like the general overall biology of coxidioidomycosis. Well said. Thank you.

It is treatable with antifungals. But the thing is, and I'll talk a little bit more about this, in the current event section. It's a very underdiagnosed cause of pneumonia, even in regions where it's endemic, like where we know that it's definitely circulating. So a lot of people who present with pneumonia just get antibiotics and then they're sent on their way home. So that's why a lot of people just recover without ever actually getting the proper treatment

because they just got antibiotics and then they felt crappy for like three months and then they got better. Maybe that was a fungus. But there are guidelines for when you should treat versus when you don't necessarily need to treat if you think someone's going to clear it. But they're not clear. There's not a good consensus. We don't have good evidence-based guidelines on exactly how to treat coxidioidomycosis. It seems interesting considering, well, I'll talk about the history a bit, but like... I can't wait to hear about the history. Erin, can you please tell me all about it?

Because I read like a tiny bit by accident and I was like, what? Wait, are you ready now? Yes, I'm ready now. Oh, okay. I'm not, so let's take a quick break first. Prominently displayed at the Institute of Parasitology in Buenos Aires is a head. Oh. A human head.

stored in formalin and labeled as Exhibit 1. Oh, gosh. When this preserved head was discovered in 1948, there was no identifying card to describe who the head once belonged to, when it was removed for storage, and why it was preserved. I'm sorry, someone just came across a head. Like in a jar in formalin, yeah.

Okay. Uh-huh. Not creepy at all. Well, and the guy who came across this head, Dr. Flavio Niño, didn't need any sort of card to tell him who it was. Hmm. He recognized it immediately as being the head of Domingo Escura, removed and preserved after Escura's death 50 years prior. What? Aaron.

Okay. So we've got the who and the when, but the why remains. Why was this head removed and placed in Formalin? In 1898. Yeah. And as far as I know, still on display in 2021. What? Because it turns out that this head's original owner, Domingo Eskura, was the first described

case of coxidioidomycosis. So someone preserved his head. So someone preserved his head. Okay. Yeah. In January, 1888, Domingo, who was then a 30,000. two-year-old member of the cavalry in northern Argentina, he woke up from a nap and noticed what he thought was a spider bite on his right cheek. Spoiler alert, it's never a spider bite. It's never a spider bite.

It's never a spider bite. Unless you're in Australia, that might be a different story. But like, it's never a spider bite. Never a spider bite. That's our, that's our title. That's our He tried various treatments to heal the lesion, but nothing seemed to work. The original lesion grew larger and rougher, his lymph nodes swelled, and new lesions appeared all over his face and neck. Eventually, he sought help at the military hospital, where they promptly diagnosed him with lupus vulgaris and discharged him with a prescription for nitric acid. But, of course, the nitric acid didn't do anything. No. So when the lesions continued to get worse, he was sent to a hospital in Buenos Aires.

This time, he was diagnosed with mycosis fungoides. Aaron, what is that just like briefly? I googled it and I can't remember now. It's a type of T-cell lymphoma. So it's a type of cancer of the skin that manifests with a lot of skin issues. It's interesting because it has myco. Yes. And so it makes you think that it's fungus.

related, but it's also mycosis fungioides. I know. It's very confusing, but yes, it's a type of T-cell lymphoma. Not infectious, not contagious, not whatever. Okay. Okay. And so these treatments once again failed. And then he was put under the care of Alejandro Posadas, who was a 21-year-old intern with a mustache that makes Salvador Dallis look like tame. It is. An incredible, it might be the most incredible mustache I've ever seen. Whoa. Yeah. At this point, when Posada's first met Domingo, Domingo had a large purple, fungal-like mask covering

his right cheek and vegetations on his nose, his arm, his trunk, and his extremities. He must have been in incredible discomfort. And Posadas, trying to find out what exactly was going on, put some of Domingo's lesions under the scope and noticed that it was riddled with a multi-nucleated giant cells and then some smaller cells with granular contents. He put two and two together and figured that these cells were a type of protozoan. Okay. They weren't.

He tried, though. He tried. But that they were probably the ones responsible for Domingo's condition. Okay. And he published his findings in 1892. So this is like the first time that what would later turn into coxidioidomycosis was described. This unique, but kind of like, you know, lonely case and that it was singular, right? Yeah.

Could have gone unnoticed for years. And this is what just really gets me. It didn't. Like I feel like so many times we've come across, oh, and then, you know, finally someone had to look back hundreds of years and link together. all these cases. Yeah, like it was lost for decades or whatever, and then they found the same thing and then saw it in some record somewhere. Yeah. Yeah. But yeah, this case wasn't lost to time or whatever, because a couple of years before Domingo Iscura noticed his spider bite, that wasn't actually a spider bite. Yeah. Another guy by the name of Joas Furtado Silveria had immigrated

from the Azores to San Francisco, where he began working as a farm laborer. And soon after his arrival, he noticed a sore on his neck that just wouldn't go away. He ended up seeking medical help, nothing made it better, and he eventually deteriorated until he died much more quickly, actually, than Domingo Ascura. He had to endure much more horrifying treatments, like carbolic acid, coterization, bromine plus cocaine, Oh, yeah. And it seemed to suffer much more before his death in 1895. And before he died, a couple of doctors popped a bit of tissue from his neck lesion under a scope.

And once again, they saw giant cells and granulated cells of various sizes, which they realized were just like the ones that Posadas had written about. They were like, hey, that reminds me of this. I am very impressed. I know. I know. And they did, though, they did disagree with the diagnosis of mycosus fungoides, but they did notice the connection between the two conditions. And once again, said these cells were likely responsible. They also believed that they were a new species of protozoan, which they weren't.

It's fine. And thought that they looked similar to coxidia. And so they named it coxidioides. Oh, that makes sense. Okay. Yeah. And these two researchers who were doing this study, Ricksford and Gilchrist, presented all these findings at a meeting of the California Academy of Medicine in 1894. Okay. And so begins the modern history of coccidioidomycosis.

But before I keep going on that path, you know that I have to ask, but what about the not-so-modern history? So these two, Domingo and Joas, were not the first two people to get infected. Of course not. Little fungus, right? If we've learned nothing from this podcast, we've learned that that is absolutely not the case. Absolutely not the case. Okay, so we have to go back, way, way back. So you mentioned that coxidomycosis is caused by these two species of fungus,

coxidioidioidus and coxidioidioidus and coxidioidioidus, pizodosy. And even though it was relatively recently that coxidioidioidus Pesodicy was recognized to be a separate species, it was like 2002, I think. It turns out that this species is actually much older than Cuxidioidioidus imitus. And it's likely that imitus evolved from Pesodicy. And there seems to be still a little bit of debate about the geographic origins of Cuxidioidioidioidus Pesi. But most papers I read seem to agree that it is thought to have originated somewhere in southern Arizona or northern Mexico, maybe around like 800,000 years ago. And then more recently, like, well, not recently to us, but like more recently, 365,000 years ago, Cuxidioides Imitus, which is found most commonly and has the most diversity in the Central Valley of California, that's thought to have diverged from. Pesodicy when like the glaciers and the inland sea of that area of California retreated.

So it kind of like trapped it there in this little like, you know, really home. Exactly. Little allopatra speciation. There we go. Wow. Keeping isolated by the Sierra Nevadas. Yeah. Yeah.

And the next big moment in the evolutionary history of this little fungus is the arrival of humans in North America. And there's a cool paper from. 2001. So it might be a little bit out of date, but current papers still do reference it. And it traced the genomic diversity of different isolates of Cuxidioides-Pasodicy, so the older one all throughout the regions that it's been found in North America and South America, and found that based on the types of and the levels of diversity in the South American isolates, it seems that during the Pleistocene, ancient humans who migrated down from

from North America to South America also brought the fungus with them along those migration routes. Okay. Okay. Yeah. But their estimate of when coxidioides, Pesodicy arrived in South America is like a little bit broad. So anywhere between 9,000 and 140,000 years ago. No big deal. No big deal. I mean, those are pretty big range. So they also say, okay, yeah, it could have been like his.

species of rodent or it could have been before. But that does seem to be like the direction that how it happened. Okay. Okay. And I will say that a lot of this genomic analyses of like the evolutionary history and stuff are kind of plagued by these problems of low of like sampling bias. So like because Arizona has been so extensively sampled, is it just that we think it originated there because we see the most diversity. If we sampled more in Guatemala, for instance, might there be, might that point to a Guatemalan origin? Totally. That totally makes sense. Yeah. So in any case, ancient humans in North and South America were no stranger to this fungus. And to further show this, there's a skeleton from Arizona from around 1,000 to 1400 CE that has

signs of destructive lesions and also microscopic examination show that there were spherules and endospores that resembled coxidioides imitus or posodicy. It's an older paper, so everything was called imitus. What? Yeah. That's so cool. We haven't had bones in a while, Aaron. I know. And they were like, well, you know, it's not, like this may not necessarily cause like actual lesions on the skeleton necessarily, but they were like, we, weird, they were pretty confident it wasn't just contamination from the soil because that you could imagine would be a big problem. Yeah. And then in prehistoric middens, so like old trash heaps essentially, in California, coxidioides imitis was found at higher rates than in surrounding soil, which could suggest that

the people who used the middens had the disease. That one's a little bit more hand. wavy to me. Yeah, definitely. All right, so coxidioidomycosis has probably been around and infecting people and animals for hundreds of thousands of years before it was first described. And Domingo and Joas just happened to be the first two people whose unfortunate encounter with this fungus was documented. But they definitely weren't the last. And these two reports, instead of being lost and forgotten, somehow ended up kicking off this era of coxidioidomycosis research that picked up steam significantly throughout the 20th century. And so after, and part of it is because after those first two cases happened, more steam

to kind of like steadily trickle in and the geographic patterns of this disease, like, you know, how they kept popping up in the same areas, that helped physicians kind of make the link between them all. Got it. In 1900, so just a few years after Ricksford and Gilchrist named their new microbe, a physician also working in San Francisco named William O'Fills, O-P-H-U-L-L-S, who, by the way, had a scar on his cheek from a duel back in Germany. Love it.

He later became the dean of the Stanford School of Medicine. Wow. With a dueling scar on his cheek. So cool. In 1900. In 1900. And so Ophils was like, wait a sec, this is not a protozoan. It's definitely a fungus, you guys.

It's going on. And so he did a bunch more research on it, describing its life cycle, its various morphologies, its root of transmission, and proposing a name for the disease, which he called coxidioidal granuloma. But this disease, coxidioidal granuloma, was. often was like the more severe of the ones that you described, right? So it was like super painful, disfiguring, debilitating, sometimes fatal. And that makes sense that that would be the one described first. Right. And that was, so that's a disseminated infection.

So that's an infection that has gone to the skin and presumably also to other organs, which would be why it would be fatal. Right. Exactly. But that's not the only form of disease that coxidioidioidus causes. And it's certainly not. not the most common. Right.

So. So. East of San Francisco, residents of the San Joaquin Valley were plagued by a mild illness, which usually consisted of respiratory symptoms, a high white blood cell count. And sometimes those painful lumps or those red lumps, erythema nodosum. People called it San Joaquin Valley fever. And no one could figure out what was causing it. A physician named Mernie Ada Gifford had been working on the problem as part of her job as the chief assistant health officer of Kern County in California. And she spent months trying to link it to Ascarus roundworms.

But then she finally found coxidioides from a guinea pig that had been experimentally infected from like someone spewed him. which is poor guinea pig. I know. And she knew that coxidioides was the pathogen responsible for coxidioidal granuloma, but the people she was seeing, like, her patients were nowhere near that sick, like, at all. So could there still be a connection, or was this just, you know, contamination? She showed her research to her former teacher, mentor, Ernest Dixon, and asked him whether he thought the two diseases could be caused by the same thing.

And then she added that several of the patients she had treated had also presented with erythema nodosum. And for Dixon, this was the clincher. A few years back, Dixon had a young med student working in his lab named Harold Chope, who on day one of the job, poor guy, opened an old petri dish, like full of an old coxidioidies, culture and then breathed in a bunch of the old spores. So he like, he brought it up to look at it closely, breathed on it and it just, it like, of course. All of the spores went airborne and then right into his. And breathed it. Oh, yeah. Yeah. Poor guy. Oh, yeah. Within nine days, Chope was in the hospital with severe chest pain, bad cough, yellowish sputum streaked with

blood. And there didn't seem to be much of a chance that he would recover. And, like, a bunch of newspapers picked up this story, and he was presented as this heroic young researcher, you know, martyred for the cause of disease, I don't know. But he hung in there. Okay, good. Eventually, he would be discharged from the hospital and sent, somewhat ironically, to Arizona to recuperate. Oh, gosh. But before that happened, he developed erythema nodosum, which is the same symptom that Gifford had observed in some of her patients with San Joaquin Valley fever. And to Dixon,

this was strong evidence that the two diseases, so San Joaquin Valley fever and coxidioidal granuloma, were caused by the same pathogen. Yeah. And that the Valley fever was just a mild form of, yeah. Right. I mean, it's almost like all of the times that we've had people who were reckless enough to intentionally infect themselves with whatever thing that they were studying to try and prove, but this poor kid just did it. Right. I mean, in some ways, you know how in a Rocky Mountain Spotted Fever episode, we talked about how like everyone got Rocky Mountain Spotted Fever or one of the other tick-borne pathogens. It's kind of the same thing. Right. Like a bunch of people got infected who were researchers who worked on this. It was sort of like a right of passage. I mean, it is very

infectious, like one single spore, and you can get infected. So it's not that surprising. It's not that surprising. And so Dixon was like, I've solved the puzzle. And he presented this hypothesis at a meeting of the California Medical Association. And he never once acknowledged that it was actually Gifford who had come up with the idea. Yeah, which is really frustrating. That is infuriating. Eventually in the 1950s, her contribution would be recognized, but like still really annoying. Yeah. So now that researchers had a better picture of the disease caused by coxidioides, they could start digging into questions like, where does this happen? What animals does this happen to? How often does it happen? And so on. And these massive questions would almost all be taken up by another of Dixon students. So Gifford was one of Dixon students.

a guy named Charles Smith. Also, Harold Chope's frat brother. This is just perfectly illustrates how, you could say, either incestuous or connected, the world is. It's a small world. If you have a very specific study organism. Everyone knows everyone. And Smith spent the late 1930s wandering all over Kern and Tulare counties in a truck named the flying, the flying clematospore.

Nope. Mm-mm. Yeah. Don't call it that. A clematispor is a thick-walled hyphal cell that functions as a spore. That's what I have in parentheses. Uh-uh. I love it.

And he was just like looking for people who had developed erythema no dosum. Okay. He was like, okay. Like I want to know. And so what he found what he was looking for. because over 18 months, he saw over 400 people who reacted to a skin test with cuxidioidin. And this is in two counties in California. Like, I feel like that's kind of substantial.

Erin, I can't wait to tell you about the current events. Oh, I have a little bit of a taste of it. It's horrifying. And he found that a good chunk of the people who seemed to have been infected at one point were just 80. asymptomatically infected and that the disease was much more prevalent than previously thought and that people who were new to the area or, and I saw this in a lot of the early studies weren't white, seemed to be more likely to develop severe disease. And I know that like these studies were back from the early 1900s and so I don't know what their reasons were. But

that's like a very common thing that you see even in, in the early 1900s. And so I don't know what their reasons were. But that's like a very common thing that you see even in literature from today. Yeah, all of the literature from today still says the same thing. And I agree. I don't know exactly what they're basing that on. Right, right. Yeah. So Charles Smith was also infamous for hating to wash glassware, like in the lab.

He was like, I hate, he hated doing it. And so that is how through a series of serendipitous accidents. I don't know. involving dirty wasterman tubes, he developed a complement fixation test for the disease. Like accidentally, figured out. Accidentally. He like left him on the counter and he was like, I'll wash them later, I'll wash them later. And then they formed these little like buttons. He was like, oh, that can be, anyway.

This was a huge step forward, though, this complement fixation test because it became the standardized way to test for exposure to the disease. and it allowed for these large-scale prevalent studies without the need for growing the fungus and lab animals. Why was so much focus placed on coxidioidomycosis? Because it kind of seems like it was. I mean, like, yes, it could absolutely be deadly and debilitating, but there were also so many other diseases that were in constant circulation.

Yeah. This is still pre-anibiotic and pre-most vaccines. Right. But coxidioidomycosis did pose a big threat to california. California's rapidly growing population. Why was it growing? The Dust Bowl. The Dust Bowl.

Throughout the 1930s, tens of thousands of families picked up from their eroded and parched farms in the prairies and headed to California. And this enormous influx of people meant a whole new bunch of susceptibles for coxidioides. And so the disease became much more visible. That makes sense. And so, Aaron, I really, to like, side note, really still want to do an episode on the Dust Bowl. Can we do it?

And if you, listeners, can't wait until that episode comes out, go read the worst hard time because that's an amazing book. Okay. So if the Dust Bowl was indirectly responsible for coxidioidomycosis becoming more visible and fueling more research in the 1930s than in the 1940s, that role would go to World War II. as the U.S. got ready to enter the war, a bunch of airfields were established for training purposes, and what better place than the southwestern U.S.? Smith, so like Charles Smith from before, took this opportunity to set up a prospective epidemiological study where he began skin testing all of the newly arrived personnel to these airfields. He made notes of how living conditions impacted disease risk, like,

tense. And even though on Smith's recommendation, the airfields implemented dust control strategies, there was still plenty of coxidioidomycosis cases for Smith to make detailed study on all the ways the disease could manifest, the incubation period, the timeline of disease, and so on. And what this and other research conducted during this time ended up showing was that this disease was essentially endemic in a good chunk of the southwestern United States. And the other thing that the 1940s would do was to firmly establish coxidioides as a pathogen of incarcerated populations. Oh, yeah. Oh, yeah. During World War II, specifically between the years of 1942 and 1945, the United States set up concentration camps, previously known as internment camps, in the Western

States and other places as well, for the forceful relocation and incarceration of around 120,000 people of Japanese ancestry, 62% of whom were U.S. citizens, actually. At least one of these camps, which had a population of 13,000, was located on the Gila River in southern Arizona, which was a hot spot for coxidomycosis. And the high prevalence of this disease was known before the camp was established, of course, and so no one was too surprised when cases began popping up at the camp or nearby at the prisoner of war camp where German prisoners were being held. And I didn't see any solid numbers for infection rates or like total number of cases at these concentration camps, but I did see that at the prisoner of war camp, where Charles Smith visited,

I think at least once, he estimated that between two-thirds to three-quarters of new arrivals would become infected within one year of arriving. Oh, my God. Based on living conditions and just the super high indemnicity of the pathogen. And there do seem to have been some deaths at that camp. And, Aaron, I'm sure you're going to talk a whole lot more about how coxidioidomycosis is still super prevalent at prisons. And maybe about some of the ethics of intentionally building or maintaining prison

facilities where infection is a certainty. There's so much there in. Oh, boy. But yeah. But at the time that these concentration camps and other prisons were first being built, there weren't any effective treatments for the disease and no vaccines. And I know that treatment is still more art than science even today. But the big increase in cases during World War II in endemic areas allowed Smith and other researchers to notice that infection with the fungus did seem to protect you from getting it again, which then spurred on some vaccine work. And alongside this vaccine research, which ultimately did seem to produce a vaccine. I read a paper word that was like, oh, and then they all injected themselves with this vaccine, and it seemed to work. Oh. I don't know.

1950s. And then it sort of dropped. Yeah. But it seems like, it seems like this vaccine research was being done at the same time that the U.S. was looking into this as a potential bio-weapon. Not to weaponize it, but to see how feasible it was for other people to weaponize. And also, like, how worried should we be about this? Should we make a vaccine? Just in case, et cetera. And then finally, treatment emerged in the 1960s in the form of amphiterericin B, like we talked about in our organ transplant episode. And since that one can be a bit toxic, later development of anti-terrorismosal.

thifungal azoles was kind of a relief. And I say kind of because, yeah, all the problems you talked about. And then the next time we really saw like a huge increase in interest in coxidioidomycosis was, of course, during the AIDS pandemic in the 1980s, where that seemed to be suddenly this fungus that was like, oh, generally it causes mild infection, became like an absolute killer disease. Yep. So it's been about 130 years since this pathogen and the disease that it causes was first described. And we've learned quite a lot since that time about its ecology, its epidemiology,

disease course treatments, et cetera, et cetera. But there's still quite a bit that we're trying to figure out. And it's becoming more and more of a pressing issue with like the steadily growing number of cases, climate change, expansion. mansion into new areas, disproportionately high rates and incarcerated populations. So, Aaron. Oh, here we go. Tell me, where do we stand with coccidiomycosis today?

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This season, an epic battle of He Said She Said, and the search for accountability in a sea of lies. Listen to Love Trapped on the IHeart Radio app, Apple Podcast. or wherever you get your podcasts. I should say really quick in case I didn't say it clearly in the biology section, since you mentioned how we still don't really have perfect treatment. It's especially true for people who don't have a lot of risk factors

for a disseminated or severe disease. People who we know are high risk, who have certain chronic diseases, etc., like are probably going to need, are definitely going to need to be on treatment, possibly for their entire rest of their life. So, and that we do know. But it's the kind of lower risk people that it's a little bit tricky. So I'm really excited to get into some of these details, Aaron. Unsurprisingly, and as always on this podcast, the number of reported cases greatly underestimates the actual number of cases.

But let's talk at least briefly about what those reported cases are. And then I want to do something that I haven't done in a long time, which is math, to kind of just kind of emphasize why it is that we know how underreported this disease is. Okay. Sounds great. I'm excited. Me too. It was really fun, and it took me way too long to do this math.

So like you said, the number of cases has been steadily increasing. And while there's a thought that maybe this is just better recognition, the data actually doesn't support that. So this is definitely increases in cases, not just increasing in reporting. So in 2011 was actually the greatest number of reported cases in the U.S. And I'll just say up front, I really only have data for the U.S. that's where this is like more well reported and where cases seem to be the highest in the world.

So in 2011, there were 22,641 cases reported. The vast majority of those are in California and Arizona, but several other states as well. And then in 2018, so the most recent year that I could find data for, there were 15,611 cases reported. That's a lot of cases. That's a lot, but you're like 15,000. It's not. The real number is probably 150,000 or more. So it's like literally an order of magnitude. An order of magnitude. And let's talk about why, because it gets fun.

There have been a number of studies that have tried to estimate how much of the share of community acquired pneumonia is accounted for by coxidiotomycosis. And they've done this in a number of different ways. And what they have found is that in endemic areas, especially in Arizona and parts of the Central Valley of California, coxidiotomycosis accounts for up to 30% of all community-acquired pneumonia. 30%. Okay. So sidebar, pneumonia.

Pneumonia is very, very common. Yeah. There's a lot of different types. of pneumonia, and we often differentiate them by saying, is this a community acquired pneumonia? Like, did you get this in your normal everyday life in the, quote, community? Or is this a hospital acquired pneumonia? Like you were in a health care facility, and that's how you got it. The reason that we do that is partly because hospitals don't like it when you get sick inside of them, but also because it tends to be different organisms that are more likely to cause a community

acquired versus a hospital-acquired pneumonia. So it can help clinicians to decide how to treat this pneumonia. Uh-huh. Uh-huh. But there are a lot of different potential causes. There's viral pneumonias that don't need any antibiotics. There are bacterial pneumonias, a lot of different types of bacteria. And then there are these fungal pneumonias. I'm getting excited. But overall, pneumonia as a blanket diagnosis is one of the leading infectious causes of hospitalization and death for adults in the United States. It's the second leading cause of hospitalizations, period, among adults in the U.S. And there are like four and a half million doctors' visits annually for community-acquired

pneumonia. This is what's so interesting because coxidioidomycosis is not contagious. Right. And so like these are all individual exposures, not like someone standing next to someone on a bus. And then coughing and whatever. Right. Exactly. Wow.

And 30%. That's wild. 30%. And community acquired pneumonia is estimated to cause between like 23 to 27. So let's split the difference and call it 25 cases per 10,000 adults every year that require hospitalization. So that's just the ones that are bad enough that someone ends up in the hospital. Yeah. That's a lot.

that's a lot. So if we back up to knowing that coxidiotomycosis, 30% of all of these community acquired pneumonia cases are going to be caused potentially by coxidiotomycosis. And estimates range across its geographic range from like 17 to 30%. So if we again like split the difference, we can do some math here. And we can say, okay, if there's 25 cases per 10,000 adults per year that require hospitalization, and there's 39 million people in California, not all of them maybe in superendemic regions, but whatever, it's Aaron's math. And let's say only 20% of those cases are actually caused by coxidiotomycosis. That's almost 100,000 cases of pneumonia requiring hospitalization every year in California

caused by coxidionomycosis. That's requiring hospitalization. That's a lot. That's a lot. Yeah. So that is how we can get to these estimates of what is the true burden likely. And so now the question is, if we know that 30% of these cases, or. or 17 to 30% of these cases are caused by coxidioids.

But only 15,000 are reported. Like, why do we still have such a big discrepancy? And it turns out, because in the cases where they've looked into this, we find that oftentimes anywhere from 15 to 30%, often less than 15% of the time, do we actually test someone with a community-acquired pneumonia for the pathogen. Is that just because, like, in general, if you're looking at the U.S., it's most likely to be

these other pathogens. And so you just either give someone like some sort of antibiotics or be like, oh, it's viral or whatever, and it's just, like, faster? Like, does it cost a lot of money to test? Is it a lot of resources? Like, what's the argument against testing, I guess, is what I'm trying to figure out? So you're asking a lot of good questions. And the answer is it's all.

of those things and then some. So part of it is certainly if you live in New York State, are you going to test everyone with pneumonia for coxidomycosis? No, that would be completely not indicated. But even in places, like they've done studies in California and Arizona, where this is highly endemic, and they've found that less than 15% of all community acquired pneumonia cases have an identified pathogen detected. Part of it is that it is very difficult to be able to get the proper samples that you need to be able to do this test isn't always easy. But also, if someone is coming in and isn't all that sick, you take a look at their x-ray and, you know, they're not going to be hospitalized. They're just going to be treated kind of as an outpatient.

Then a lot of times you won't do a ton of testing because you'll say this is most likely what it is. If you don't get better, then come back. Right, right. That makes sense. It's a lot. And that's why, you know, we do distinguish at least between is this hospital equestalston. or community acquired, like we're trying to narrow down what is the most likely pathogen that's causing this and how are we going to treat it.

Yeah, so it's very interesting when you think about that and then you think of how many people might have had this infection, went to the doctor, got antibiotics, took them, got better. The antibiotics didn't make them better, but most of these cases resolve on their own without any treatment. But I'm-hmm. So that's kind of how we get to those numbers. But like you already touched on Erin, and since this is T-PW-K-Y, you'll also be unsurprised listeners to know just how huge their disparities are in who gets infected, probably in who

gets diagnosed and who gets treated. So we've already mentioned a number of different. groups that are at risk, like people who are immunocompromised in some way or another. People who are pregnant have a much higher risk of having disseminated disease. And like you mentioned, Erin, it's been shown, and a lot of the literature states that African Americans and people of Filipino descent tend to be more at risk for disseminated disease, so that's severe manifestation of disease. but a lot of the studies that showed this that are cited in the more recent literature were done in like the 1940s.

And I'm not sure what the kind of explanation would be. If we think about people during the Dust Bowl time coming in, because one thing that we have seen in places like Arizona today, where Arizona has a large elderly population of people who came from somewhere else in the country and moved to Arizona when they were old. so they never had any exposures. Those people seem to be at higher risk for infection. So is that what was driving these studies early on? I really don't know, but I do think that we really need to ask ourselves, like, as a community of people researching and writing papers about cuxidioidomycosis, is how much of this disparity is true today and how much of it is due to differences in health care access among vulnerable or marginalized populations or among

health care providers in adequate diagnosis and treatment and all of that. So I don't know the full answer to that. So definitely exposure. And certainly people who work in certain situations that put them in close contact with soil are at much higher risk for contracting disease, like agricultural workers, construction workers, people who work. in the soil or have contact with the soil. But the other place, this is a massive issue, Erin, that you mentioned, is for incarcerated individuals. California Central Valley, which is coxidioides territory, is home to a lot of prisons.

The incarcerated population of California from 1980 to 2000 increased eightfold. And so what you're saying, Aaron, is like, we already. knew this was a problem back in the 1940s. I mean, we've known it for decades for almost a hundred years. But then they were like, let's build a bunch of prisons right on top of all this. 89% of people who are incarcerated in these prisons in the Central Valley are brought from non-endemic areas of California. Yeah.

Which means that they have not previously been exposed potentially. Oh, yeah. So in the last several decades, there have been quite a number of outbreaks in prisons that have resulted in a large number of deaths and in fact continue to result in deaths annually. And there's a few papers that say, you know, we've tried this type of medical restriction where if you have these certain diseases, then you can't be put in prisons in this particular area. But it turns out there have also been studies from the CDC that show that that really doesn't actually work to reduce exposure or cases. So there's another program to try and risk stratify people using skin testing, where if they've never been exposed to coxidioides and don't have a positive skin test, then they can't go to certain prisons. But that was a small study, and I'm not sure that any of that has actually been implemented. yet today. It's an interesting approach because it seems like another solution would be to not

have prisons. I mean, the whole prison system, that's a whole other aspect. I was going to say, that's like the problems with the prison system are not something we're going to get into right now. It's like scales and scales and scales of different levels of this. Exactly. Honestly, Erin, that's still a thing. So it doesn't. Yeah. Yeah. Oh my gosh. Yeah. And so we've kind of covered a lot of sort of frontiers on things that we need to do a better job of, right? Diagnosing deciding who and when and how to treat the problem of all of the prisons in the Central Valley. But also, let us not forget that this is an environmental pathogen. So what about climate change?

It's not good. It's not great. There have been a number of recent studies that have modeled what the environmental risk factors are for infection, which is awesome. And unsurprisingly, it seems very related to rainfalls. So larger rainfalls, heavier rainfalls in the winter, followed by drier summers, results in what they called in these papers a grow and blow phenomenon. Okay. where a lot of the fungi can grow and exist in the environment during that wet winter, and then they get dried out in this dry summer, and then you get increases in infection

because of the dry soil blowing in the air. You're basically recreating Harold Chope's old dried out peachy dish. Yeah, exactly. And so this sort of climate modeling has been shown to be like in line with retrospective data on where we see cases. And so these match up really well, both in Arizona and in California. So now the kind of question going forward will be, can we use this knowledge to try and predict out to the future when we might have like a bad year for coxidioidies infection, something like that. Yeah. But that still doesn't answer the question of like climate change

specifically. And so one thing that I wanted to mention that I think is really important in thinking about this is that we've seen in the last decade or so a number of cases pop up in areas that aren't generally considered endemic like Washington State, which has had also a steady increase in the number of confirmed endemic cases of coxidioidomycosis. Where in Washington State? Oh, good question. I don't actually know like what county it was in Washington State. But even in 2017, it was still only 12 cases.

but they have identified that those cases were endemic. They weren't from travel. So we don't have a truly great handle on what the distribution of this fungus is worldwide to begin with. But we know that climate change is very likely to have some effect. But since we don't exactly know where it is, it's hard to say exactly what that's going to do, if that makes sense. Yeah. No, that's so. Totally.

But yeah, so there's a lot of room for research here. Oh, yes. It's an open petri dish. Just don't breathe it in. Just don't breathe it in. So, yeah, that's coxidioidomycosis. Sources? Sources.

Okay. I want to shout out a paper by Derasinski and Murals. Coxidioidomycosis, what a long, strange trip it's been. definitely wins my favorite title, I think. That was a very useful paper, as was a book from 1980 by David Stevens called Cuxidioidomycosis, a text. And I have a bunch more that I will put on the website. I also have quite a number of papers, many of which are just titled Coxidioidomycosis, which I found hilarious. Straight to the point. Straight to the point. Let's know, no messing around. You can find our list of sources from this episode and every single one of our episodes on our website. This Podcast Will Kill You.com under the episodes tab.

Thank you to Bloodmobile for providing the music for this episode and all of our episodes. And thank you to the exactly right network of whom we're very proud to be a part. And thanks again, Tori, so much for sharing your story with us. We really appreciate it. Yeah. And thank you to you, listeners, for listening to this podcast. We hope you enjoyed this one. I feel like maybe some people might not have ever heard of it. So hopefully this was a fun new one for people. Yeah. It's kind of niche, but then it's like also really interesting. I don't know. I had a lot more fun than I thought I was going to have in the research. Me too. To be honest. I feel like we put this one off for a while and I'm glad that we did it. Yeah. It was a good one. Yeah. Okay. Well, until next time, wash your hands. You filthy animals. I'm Clayton Eckerd. In 2022, I was the lead of ABC's The Bachelor. But here's the thing. Bachelor fans hated him. If I could press a button and rewind it all I would.

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