This Podcast Will Kill You - Ep 133 Parvoviruses: Who let the dogs (and their viruses) out?

Episode Date: January 16, 2024

This one’s not just for the dogs. It’s also for the cats, the raccoons, the wax moths, the birds, the mice, and so many other critters. Oh, and of course the humans. Even though most of us may be familiar with parvovirus through our canine friends, the world of parvoviruses is much larger. In this episode, we explore that world, focusing first on the biology of these tiny DNA viruses and how they make us sick before tracing the history of their discovery and the pandemic spread of canine parvovirus just a few short decades ago. We are joined by the amazing Dr. Steph Horgan Smith who acts as our veterinary tour guide through the animal world of these viruses and why vaccination against them is so incredibly important. Finally, we round out the episode with some of the latest research on these viruses, featuring some very cool, very promising work on using the dependoparvoviruses as a tool for gene therapy. Tune in to learn where Fifth disease got its name, what role raccoons may have played in the emergence of canine parvovirus, and so much more. See omnystudio.com/listener for privacy information.

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Ross Matthews. You know what kids always say to me? Are you a boy or girl? Oh my God. All the time. I love it. So I try to butcher it up for kids so they're not confused. Yeah, but you're butching it up is basically like Doris Day. Right? No, I turn into Be Arthur.

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on the IHeart Radio app, Apple Podcasts, or wherever you get your podcasts. So it was a Monday in November, I woke up just fiddling, like, ordinarily unwell. I thought it was a strange side of cold or flu. I felt a bit feverish. I had some aches and pains, but I didn't think too much of it. What I did notice at the time, though, was I had a bit of a strange rash on my lower legs that looked like petechiae. So I went down to see my GP and just said, hey, look, I'm feeling unwell.

I've taken the day off work. I've also got these strange little red dots on my legs. Can we just get some bloods and see what's happening? And so that was it. I went and did a blood test. I went home, woke up the next day on the Tuesday. I was still feeling quite unwell, took another day off work, didn't. think too much of it. The little red dots, the patiki, I was still there on my lower legs.

They'd spread a little bit more. They're getting quite numerous, but I'd already done the bloods with my doctor, so I wasn't too concerned. So I just spent the rest of the day in bed. I then work up on the Wednesday. Thought I was feeling slightly better, but still really, really off. The fevers were coming and going, but I'd already taken two days off work. I was a nurse. I didn't want to leave my workplace shot staffed. So I thought, all right, I'm just going. going to crack on with it. I'm going to head into work and I'll see what happens. Within 10 minutes of driving to work, I was like, I cannot possibly do this. I am so unwell. I'm feverish. I'm sweating. I'm covered in this rash. I ended up turning up to work and going, I'm just having, like,

I have to go home. And they said, someone else is already called and sick. Like, you've got to stay for a bit until we can get someone to cover for you. So I just sat around in my, job, just sort of waiting for another nurse to turn up, which was about 5pm at that stage. It was an afternoon shift. So eventually this nurse turned up and I was able to go home and I was really itchy at that stage. So I took an an anihistamine. And I was laying in bed and I realized I was really, really thirsty. So I went up to go get some water. I made it to the fridge and I just hit the ground. And that was that I just completely passed out. I sort of came to and started calling out for help from my family.

And they came downstairs and grabbed me. And my mom at the time had just been diagnosed with high blood pressure. So there was an automatic blood pressure machine just on the kitchen bench. And I just sort of remember kind of vaguely gesturing towards this blood pressure machine going, put it on, put it on. So my mom took my blood pressure. And at the time, I wasn't really able to vocalize or say anything. but my blood pressure was 70 over 40, and I just remember trying to explain to my family,

you need to call an ambulance, this will kill me. And they didn't. I remember being carried into bed, and I woke up in the morning, and I just remember thinking, oh my gosh, I've made it. I'm awake, I'm alive. I honestly didn't expect I was going to wake up,

and of course my family aren't health practitioners. didn't, they weren't aware that that was an incredibly dangerous blood pressure to have and that I might not have made it that night. But thankfully that blood pressure was hopefully only postural and I ended up being okay and I woke up. So I went back to my doctor that day because I was starting to get a really stiff pain in my neck and I was a bit light sensitive and my doctor had warned me to be a bit careful about meningitis. I was in that sort of age age where it was possible and I went, oh yeah, okay, this is a bit of a concern. So I went back to my GP and I said, look, this rush is getting worse. I'm now covered in these patiki eye all over my legs, my arms. I've got this

strange little red sort of rashes all over my torso as well. I was really flush. The fever kept coming. My aches and pains were getting much worse. And he looked at my bloods and he goes, oh, Eliza, your platelets are in your boots. You need to go to the hospital. And I said, oh, okay. But now, do I have to go right now? He said, look, You need to go pretty much today. You have to go get some things when you go home. I expect you to be admitted as an impatient. This isn't looking fantastic.

So make sure you get there as soon as you can. And at the time, the closest hospital to me was also the one that I worked at, which is a lot of fun. So they were able to rule out meningitis in the ED, but they were obviously really concerned about the platelets that I had. And they wanted to admit me because they were, concerned that if the platelets dropped any further, there would be potential for needing a blood transfusion, which was a lot of fun. So I got admitted into a general medical unit. It was one of the

units that was used mostly for managing older people and palliative care. And this particular unit I was admitted into overlooked the ward that I worked at so I could see the comings of goings of my fellow co-workers, which was quite amusing. So what happened? on that first night was obviously I was quite distressed. I'd never spent a night in a hospital before. I was a young and healthy woman. I was only 22. Just graduated basically from nursing. So I was a bit startled and concerned that I'd gotten myself into this predicament so quickly where it suddenly declined so far down. And I was the one now needing care and having nurses look after me. It was a really startling experience. So that was the Thursday. I got admitted. On the Friday, the fevers kept going.

the aches and pains were still there. The patiquiae just kept spreading every time they wanted to take my blood pressure. I would end up with these welts under the blood pressure cuff with a patiki eye, which is bloom from all the bruising they were causing. Eventually, the fever started to drop, and on the Saturday they were like, look, your platelets aren't great, but we can see they're starting to improve. We can look at maybe letting you go home. So my mum came to pick me up, and then I spiked another fever.

And they did my bloods again, and the platelets had dropped. it again and the joint aches and pains kept getting worse. So I was then in the hospital for another night. What kept happening was every time the fever would pick up, the joint aches and pains would get worse and worse. And eventually what had happened was my fingers became quite nalled. I was unable to use my hands. I developed quite severe pain in my knees, my hips, my shoulders, and I lost my ability to walk very well. So I was needing strong pain medication. just to get me up and moving. But what ended up happening was I was even able to attend to my own sort of personal needs in a safe manner.

It was a very humbling experience, I would say, to have that happen to you at such a young age when you'd been like the week prior. So, you know, be the person providing that care to be the one having to receive it so quickly and rapidly. It was quite a challenging experience. It took a long time for the diagnosis of parvovirus to occur. I think it was probably on the Tuesday. So by that time, I'd been sick for over a week. I'd been in hospital for four days when they were finally able to say, oh, we think we've found the cause of what's happening for you.

You have parvovirus. I did say to them, isn't that what dogs have? I get my dog vaccinated for parvovirus. Have I gotten this from an animal? And they said, no, that's not what's happened. Like, there's humans that get parvovirus. It's normally seen in kids in daycare. You've just somehow ended up with it.

The fevers kept coming and going. but I was slowly getting better and eventually I was able to reduce down on the pain medication and by the Friday so I'd been in hospital for just over a week they were able to discharge me home. Finally, that all started to clear but what did happen was they did warm me. I could still get the joint aches and pains for a couple of weeks but it could last a bit longer. I was unlucky and they did last a bit longer. I would have days where I would be absolutely well. I could move about just fine and then suddenly everything would just stop working.

I remember going to a Christmas party and I was feeling absolutely fine that day. I had a couple drinks. I was dancing for about an hour in a club and I sat down because I was like needing to get a breath. I just wanted some water. I sat down and I could not stand back up. My friends had to carry me out of this club and explain to the bounces and the security that no, she's not inebriated. She has this virus and her joints aren't working. She can't move. And I had to be carried into this Uber driver. And this poor Uber driver had to basically carry me into my house

and get my mom to meet me at the door and put me into bed because my legs just stopped working. But for about two months, I was in and out of my physio, having to relearn basically how to lift my arm over my head, how to take a normal stride because my pace would suddenly start getting shuffling. How to open and close my hand well enough because every now and then my hands would just seize and my fingers wouldn't cooperate. It took about two months all up. But in the end, I was completely fine.

The patiki eye all resolved, the rash resolved. The joint aches and pains finally left. It did leave a bit of a lasting impact that now every time I seem to get a virus, I do respond with that sort of viral arthralgia. It's just part of it now. So I know whenever I get a cold or flu or even COVID, the first time I had COVID, it did kick in. But it's never that intense anymore. It's always pretty mild and it's something that can easily be managed with neurofin.

But yeah, it was quite a fun experience. Oh, my gosh. First of all, I had just had no idea about parvoviruses, but also what a wild story. What a wild ride. Terrifying. Terrifying. Honestly. Yeah.

Yeah. Thank you so much for sharing your story with us, truly. My goodness. Thank you. Hi, I'm Erin Welsh. And I'm Erin Alman Updike. And this is, this podcast will kill you. Today we're talking about Parvo. Yeah.

And all the different kinds. Well, a couple of the many different kinds. We will mention the many different kinds and focus on a few. Yep, yep, yep. But there are so many more than I expected. Yeah. It's part for the course. This podcast will kill you. Come on. I know. I know. Why are we surprised by anything at this point? We can't be. We can't be. But it's going to be an interesting episode. I am excited to learn about the history of this virus that I know nothing about. I'm excited to learn about the biology of this virus that I know nothing about. It's really interesting. So I'm excited to tell you about it. And I'm also really excited that we get to talk with another expert. We are. bringing on later in the episode a very special guest, Dr. Steph Horgan Smith, who is a veterinarian, to answer some of your burning questions about parvoviruses and dogs.

Yeah, I'm really excited about that because I am not a vet. Nor am I. But I have a dog, and so I'm interested. But even if I didn't have a dog, I'd still be interested. This is a mess. Let's just get to the quarantine. It's quarantine time, shall we? Yes, we shall.

What are we drinking this week? We're drinking sick as a dog. Yeah, I mean, so named because, yeah, Parvo infects a bunch of different animals, but it is terrifying and deadly in dogs, as we'll learn more about. But before we do that, what is in Sick as a Dog? It is tequila and lime juice and ginger syrup, and it's quite refreshing. Yeah, simple and delicious. Can't go wrong.

What could be better? We'll post the full recipe for that quarantini as well as the non-alcoholic placebo Rita on our website, this podcast will kill you.com and on our social media. On our website, you can find all sorts of cool things. Let me just pull it up to confirm. To confirm. It's still there. It's still functional.

You can find the sources for each and every one of our episodes. You can find transcripts. You can find a submit your first-hand account form, which to all the people that have done that, thank you. It's been amazing. You can find things like our bookshop.org affiliate account, our Goodreads list, merch. There's amazing merch. We have excellent merch. You can find links to Music by Bloodmobile, Patreon.

You know, there's a lot of stuff. So much there. Yeah. Can we get to the actual content now? Can we? Was this a long enough intro? Yeah, I think it is. Okay.

Let's take a quick break and then talk about the biology of parvoviruses. 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 ingredients on a sheet pan, put it in the oven, and that's it. And if there's truly no time to cook, dish by Blue Apron meals are fully prepared.

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dinner with another, and praying your karmic ken or Barbie appears before your shelf life runs out. Trust me, I've been through this ancient and unshakable tradition. I jumped in, hoping to find love the right way, and instead I found chaos, cringe and comedy. And now, I'm looking for healing. Boys and Girls dives into every twist and turn of the arranged marriage carousel, the meat-awquard, the near-misses, the heartbreak, and let's not forget all the jokes. Listen to boys and girls on the IHard Radio app, Apple Podcasts, or wherever you get your podcasts. I want to talk very briefly about parvoviruses as a general, like, group of viruses.

Because I think that understanding some of their common characteristics will be informative to understand how variable the presentation can be when we talk about parvoviruses in different animals with our vet later on. But we'll focus for this biology section on human parvovirus, aka parvovirus B-19. And then I'll briefly mention some of the other parvovarses like canine parvovirus and things like that. But to understand parvoviruses in general at first, parvoviruses are DNA viruses. They happen to be really tiny DNA viruses, which I just find cute. And as always, we're not talking about one virus. The family Parvoviridae includes a number of different genera of viruses that infect a huge range of animals and insects and all kinds of things.

And as a very broad general rule, one thing to know about parvoviruses is that they tend to infect preferentially rapidly dividing cells. That is a key characteristic of parvoviruses, and it makes sense that. then why they infect the cells that they do and therefore cause the diseases that they cause. Very interesting. Yeah. They can infect a wide variety of cells when you look across all the parvoviruses. And different parvoviruses are more specific.

They have a more specific tropism for individual types of cells. But across the board, it's rapidly dividing cells. You know, I find that so interesting to think about like the pros and cons of infecting rapidly dividing cells versus not rapidly dividing cells. And I know it's not like the viruses are not all sat there in a boardroom being like, all right, put that one on the pros list. But, you know, something like rabies that infects nerve cells. Nerve cells. Yeah. Yeah.

It is really interesting. I didn't go with that thought. But it is really interesting, especially because parvovirus is killing and destroying cells. That's what they do, these parvoviruses. So they're infecting cells, and then they're absolutely killing and destroying them. So it makes sense then that for them to be able to have a fresh supply of cells to invade, that they are invading rapidly dividing cells. Again, they didn't make that as a decision, but they kind of go together well with the cell types

that they infect. Oh, and I wonder, too, if it has anything to do with, like, the host immune system and how rapidly they're detected. Like, how do you outrun the immune system? Do you do the sneak and hide approach? Or do you just go in, you know? And go ham. Yeah, go ham. So that is what they do in general. Canine parvovirus and feline panlicopinia virus and a number of others are in the genus proto-parvovirus, as is like porcine parvovirus, a lot of kind of the famous parvoviruses. One that kept coming up in research that I don't know if most people have heard of, but it literally kept coming up was the Aleutian Mink virus disease virus. Yeah.

Of course. Of course. The Aleutian minks. This is in a whole different genera of parvovirus called the amdo parvovirus. There's a few other genera of. of parvoviruses, one of which I will mention, because I'll talk about it at the very end, is called the Dependoparvirus genus. I'm so excited that you're talking about these later.

These are viruses that depend on other viruses. I didn't do that pun, but somebody did. These viruses depend on the presence of other viruses to be able to infect cells. We'll get to it, I promise. and then there's human parvovirus, aka parvovirus B-19. And this is a member of the genera called erythrovirus genus. The reason that it got the name arithrovirus is because this virus, Parvavirus, B-19, and a few other related viruses that infect primates, have very strong tropism,

aka they preferentially infect erythroid precursor cells. What does that mean? our erythrocytes are our red blood cells. So parvovirus B-19 is infecting and replicating in preferentially and close to exclusively, though not entirely exclusively, in the cells in our bone marrow that become red blood cells, like our baby red blood cells. These are cells that are very rapidly dividing, right? Because we make new red blood cells all the time.

So the way I'm going to structure this is let's go over. the nitty, gritty pathophysiology of what is happening in our human bodies when we're exposed to parvo B-19, and then how that effect can manifest in what turns out to be a really wide spectrum of illness. And then I'll briefly touch at the end on some of the other animal parvoviruses. Cool? Mm-hmm. So B-19, can we just call it that? Yeah, sure, why not? Okay, great. It's our podcast. We can do whatever we want. So why do this? So B-19 is a human-specific virus.

That's first off. It's transmitted in respiratory droplets primarily, though since this is a virus that's in red blood cells and their precursors, it can also be transmitted in blood products. And it can cross the placenta during pregnancy and infect a developing fetus, which is an important part of the parvavirus story. But once this virus makes it into our body, it hones in really quickly and specifically on our bone marrow, since it's really specific to these precursor red blood cells. And the reason why this is the cell that it infects is because the receptor that it binds to to be able to enter ourselves happens to be found on our erythroid precursor cells. It's called blood antigen p. Anyways. So once it's in our cells, over the course, of a few days to a few weeks, this virus is just replicating, replicating, replicating. And as it does this, it induces a complex series of changes within the cell, within these

erythroblast precursor cells, that leads to DNA damage, arrest of the cell cycle, so they stop dividing, and death of these cells. And during this time, while this virus is replicating in our blood cells, if you were to change, you were to change. what's called a reticulocyte count. This is some really nerdy fun stuff. Reticulocytes are what we call like immature red blood cells when we look at them on a blood smear. Okay.

And their measurement is something that we check in the case of things like anemia, right? If a person doesn't have enough red blood cells, then they should have an increase in this reticulocyte count because that means their body is going into overdrive to make more red blood cells. They're like making more babies to eventually make more adults. Okay. What is the timeline between reticulocyte and red blood cell? That's a great question. The total lifespan of a red blood cell is usually about 120 days, but I don't actually remember how many days it takes to become a mature red blood cell. It's probably something I should have Googled because it's Googlable. And what happens if you have a low reticulocyte count? Like, what does that mean? Well, great question, because that's what

we see in parvovirus. Oh, the reticulous site count. It really wasn't. But that's what we see. Because parvovirus is infecting these reticulacites and our erythroblasts, the reticulocyte, if you were to check it in someone in an early part of their parvovirus disease course, it drops to almost zero. This virus is attacking and killing off all of these reticulacites, very specifically. So because of that, you also would then see very often a drop, in our hemoglobin. And the hemoglobin is the way that we measure how many red blood cells we have. It's not a direct measurement, but it's the way that we see, do you have enough red blood cells? Usually, this is a pretty small drop by, say, about one point, which is not a lot for most people.

And most of the time, for most people with this infection, this is transient. This virus is killing off a whole bunch of our reticulocytes all at once, but then our body responds. by very quickly making neutralizing antibodies that are highly effective. We neutralize this infection, kick this virus out, and then our reticulocyte count will bounce back, and then eventually so will our hemoglobin. Okay, but if you said, I know that you're poised to say but. I am. You can see the bee on my lips. I can see it. And I'm going to preempt it by asking a question, which is,

So you said that the lifespan of red blood cells like 120 days. And so how, what is the lag time then between when this parvovirus, when B-19 starts killing off those reticulocytes and then when symptoms are being felt? Ooh, Aaron, I just can't wait to tell you. It's, it's so much more detailed than that. Okay, okay. Now I'll let you continue with your butt. Yes. I, by the way, I just Googled it just so that we have a little bit. more information. Okay. According to the Google, it's like two days from when reticulocytes are first sent out of

the bone marrow into our bloodstream to then become red blood cells. But there is also a maturation process within the red, within our bone marrow itself. Okay, because this is all happening within the bone marrow and not in like our circulatory system. Exactly, exactly. So these are, this virus is infecting the cells that are precursors in our bone marrow and causing them to not be able to release any more of those reticulocytes. So then the red blood cells that are mature already in our body are just doing their normal

death process. You know, they die in waves. And then that's why the reticulocytes aren't there for a time period to be able to make up for the natural course of our red blood cells so that hemoglobin drops. And then once we can bounce back because we've fought off this infection, then no problem. Okay. Okay. But sometimes it doesn't happen that way.

So that is kind of what is happening in our body. And now that we understand that, we can talk about what it looks like when we have symptoms of this disease and how wide of a range these symptoms can present us. Yeah. There are so many different ways that this can present that there are a lot of different names for the syndromes that are caused by. B-19. The first is erythema infectiosum. I think is how you say that. Or fifth disease, which, are you going to get into this in the history, Erin? I sure am. Okay, good, because I have like a sentence, but I was like, maybe I won't say it out loud. I mean, I have like two sentences. Okay. Well, more than me. So erythema infectiosum or fifth disease is the classic little

kid disease that's caused by parvovirus B-19. The way that it tends to look is this. Early on, like in that early phase of viral infection and replication, which takes maybe a few days to a week after exposure, now we're talking timeline, most kids that get infected with parvo will have a mild, very non-specific illness. You may or may not even notice that they're sick. They'll have some fevers, maybe a runny nose, maybe not, headaches. maybe some nausea, and that's it.

This is the time frame in which people are viremic. So this is the time frame when they're just feeling kind of cruddy that they are getting their friends and family sick. And by the way, if you'd like to ask how infectious is this, how contagious is this disease? Yeah, I'd love to ask that. I couldn't find like an R not reliably, but the attack rates, especially like among household contacts,

are very high. So up to 50% of kids among exposed household contacts who haven't had parvo B-19 will get parvo B-19 and 20 to 30% of adults in like a household or a classroom setting if they haven't yet been exposed. Okay. And so if they haven't yet been exposed. So there is pretty good. Like how durable is the immunity?

Yeah. Great question. As far as I can tell quite durable. And most of the studies of like the epidemiology really just. looks at like zero conversion where like by old age, 85% of people have been exposed and have antibodies to parvo B-19. So what's the rate of asymptomatic versus symptomatic then? Excellent question. I didn't see this exact. I saw one paper that said about 20% of people won't have any symptoms whatsoever. But I think that it's probably even more variable than that

because of especially how different the disease can present in children versus adults. Okay. If that makes sense. Yeah. And we'll get into it. But at least, at least 20% and possibly more percent of the time, people might be entirely asymptomatic. Okay. At least from my reading.

Great question. But that's just the like initial, like I am feeling a little bit cruddy from a non-specific illness and I'm exposing all of my friends. then kids get better and then about two weeks after exposure at least after this initial infection will come a rash and the rash is on the face it's this red splotchiness on the cheeks that usually doesn't extend down to the mouth so what it looks like is like you got slapped on the cheek and your cheek turned red it's literally called a slapped cheek rash Yep. And it really does look like that because it's so isolated to the cheeks and just this kind of red splush on the cheeks.

And then over the course of like one to four days thereafter, it can extend down the body, down the, you know, the arms and the trunk and things. And this rash as it moves looks like a lot of viral rashes. It's like these pink little splotches. They're not usually raised. sometimes they can be kind of lacy looking. And this rash, especially the one that kind of extends down the body, it can kind of come and go. So it can be there for a day or so and then go away for a few days and then come back, maybe under a time of stress. And then eventually, over a few weeks or so, you might not see the rash anymore at all. All right. Why? Why does it come and go and why does it start on your cheeks? Great question. I don't know. As always. But what's interesting is that all of these symptoms that we associate with this specific syndrome, erythema infectiosum or fifth disease, these are immunologically mediated. This is our body's response post-viral. Like if you were to check a viral load at this point, most of the time, you can't find one. in kids with this. So this is all from our bodies, antibodies and immune response causing this rash and these rashes that kind of come and go. Wow. So it's coming in and just like letting somebody spread everything with these very generic mild symptoms. Exactly. Okay. Exactly. Isn't that fascinating? Now, I think we've talked about doing like a whole thing on rashes because I do think it's very interesting.

There's a lot of rashes that we see associated with viral syndromes, and they usually are this immune-mediated kind of rash. And I don't understand why some viruses tend to cause a more specific rash than other viruses. But still in general, there's like a look to these viral rashes. And this is one of those viruses that causes one of these viral rashes with the addition of the specific slapped cheekness of. it. Okay. Yeah, right? Yeah. So no, that's in kids. And in adults, as per usual, when adults get a, quote, childhood illness, it tends to be a bit more severe. And in the case of parvovirus, this comes with joint pain. So adults may still have that initial non-specific illness, or they may not, but the part of parvovirus that's more severe in adults tends to be joint pains and

inflammation. You can see this in kids as well, but almost always if an adult gets parvo B-19, you're going to have some degree of arthritis and arthralgia as like the common presenting feature. Like, why? Why is there a difference? It's immune mediated again. So is it just the difference between a child's immune system and an adult's immune system, which are totally different. Yeah, but what are those differences? Oh, that we could do a whole episode on. Okay. Yeah. But in adults, it's this bilateral arthralgia. It can be the hands, it could be the knees, the ankles, the wrists, really anywhere. And sometimes this can really mimic rheumatoid arthritis. And there was some thought back when that Parvo B-19 might be one of the

kind of triggers for something like rheumatoid arthritis. There's not really a lot of data for that, from what I can tell. Okay. But the symptoms can be really similar. And what's really tough is that for many people, these joint pains resolve over time, but time could mean weeks or months or even years. So the mechanism here is still immunologic. It's our bodies making these antibodies, and then these antibodies getting depotives.

in our joints and causing joint pain and inflammation, very similar to a lot of autoimmune disorders that cause arthritis and arthritis. Okay. Isn't that interesting? That is fascinating. So that is all the mild cases of Parvo B-19. Right. But as we heard in our first-hand account, Parvo is not always a mild illness.

It can also cause very severe disease. both acutely and chronically. So let's get into it. Because this is a virus infecting and destroying, remember, our red blood cell precursors, right? In most people, it results in a transient reduction in hemoglobin. Most of the time, you probably would never even see that because people aren't getting sick enough to have their hemoglobin measured multiple times

over the course of this illness. However, in some people, especially in people who have any kind of baseline either decrease in their red blood cell production capacity or a baseline of a higher than typical red blood cell destruction, this transient small hemoglobin drop can actually result in profound anemia. in what's called a transient aplastic crisis or aplastic anemia. And by profound, I mean that this can cause a hemoglobin drop that is so low that it can be lethal. And if this happens, the symptoms of this disease are vastly different. People are incredibly weak.

They're lethargic. They have very significant pallor, so their skin is incredibly pale, even if they have dark skin, their mucous membranes, the palms of their hands, these things are just like without color because they have no hemoglobin. And if you checked their hemoglobin, they would be incredibly low. And I don't know exactly how low, but I do know that I have seen people present with very, very low hemoglobin in other contexts. And the hematology specialists are always thinking, could this be from parvovirus, B-19? So a normal hemoglobin can range from like 12 to 16 depending on, depending on the situation. And so we're talking about hemoglobin's less than seven, six, five, incredibly low. Whoa.

Yep. Okay. So a big question is like what are the conditions that put you at highest risk of this? Yeah. And the list can be really long. things that result in a decrease in red blood cell production are things as simple as iron deficiency anemia, which many people who menstruate have some degree of iron deficiency anemia. Right.

It can be genetic things like thalassemias. And then we also can see things that cause an increase in red blood cell destruction, like hereditary sphero cytosis, which is when your red blood cells have a slightly different shape. And so as they pass through the spleen, they're more likely to get, like, destroyed. and sheared. Okay. Or not having a spleen altogether or sickle cell disease or chronic hemolytic anemia. There's a whole lot of different things that cause an increase in the turnover of red blood cells.

So instead of existing for 120 days, their lifespan is shorter and therefore this drop in hemoglobin is more significant, even if it's short. That makes sense? Yeah, it does. There are so many different ways for this to have an impact. Right. Okay. The good news is that even in this case, this tends to be a transient phenomenon.

So if it is identified, it can be treated with supportive care, red blood cell transfusions, fluids, supportive care in general. However, even though it's self-limited and eventually most of the time in this aplastic crisis case, people's immune system will mount an antibody response and will, will fight off this infection and their red blood cell count will be able to come back, it can be so severe that it can be fatal. Because this significant anemia can result in heart failure, it can result in strokes, it can really be significant. So it's quite scary. What would some of the signs and symptoms be that somebody would experience when like things are getting

really bad that would prompt them to go to the hospital, for instance? Yeah, it's a great question. Really, it would be things like fatigue, weakness, lethargy. There's nothing that looks particularly infectious per se. So it's not necessarily like fevers, chills, that kind of a thing. It's more about the signs of anemia. So pallor, fatigue, lethargy, those kinds of things. And but by this time, Again, the virus is no longer there, or is it could be? It's a good question. I saw mixed answers to that in some of the literature. But I think that given that this is the time frame in which the virus is still replicating and destroying your red blood cells, you would likely still see some degree of viremia.

Okay. Yeah. Just depends on when in that course of time you get super sick. Mm-hmm. Yeah. So that's one of the severe manifestations. there's more, a few more. Parvovirus B-19 is also one of the torch infections.

And these are infections that are considered incredibly severe in pregnancy that lead to severe fetal infection and potentially pregnancy loss or significant congenital manifestations in the fetus. So during pregnancy, especially in the second trimester-ish, so like 11 to 23 weeks, a primary infection, so a first-time infection with parvovirus B-19, can cross the placenta and infect the fetus. And in a fetus, it does a very similar thing that it does in a grown person or a child, and that is that it can cause severe anemia.

It can cause this transient aplastic crisis. In the case of the fetus, it's by this virus infecting the fetal liver, because that is the site of red blood cell production for a lot of development in the fetus. But as you can imagine, severe anemia in a fetus can be incredibly dangerous. The anemia can lead to a form of high output heart failure. Because our red blood cells are carrying oxygen,

with less oxygen delivery capacity in the fetus, that fetus's heart has to start pumping overtime in an effort to increase blood flow enough to make up the difference, right? Like your capacity's down. There's not as many trains running, so they're running the trains faster. But eventually, the conductors, the heart, just can't keep up with running trains at this pace. And so it burns out and it can't pump.

And that leads to heart failure. Heart failure leads to blood backing up in the vessels because it's not getting pumped out. And this leads to an increase in pressure in the blood vessels, which leads to leaky blood vessels. which causes edema. And edema in a fetus that gets severe like this is called hydrops fatalis. It's incredibly serious and it is very often fatal. It's a sign of really severe disease. Parvovirus is by no means the only thing that can cause hydrops fatalis, but it is one of them

and that is kind of the mechanism by which it happens in this case. Parvovirus B-19 in a fetus also seems to sometimes infect their myocytes, the heart cells themselves, which is especially fascinating since normally this is only infecting rapidly dividing cells. But apparently the viral receptors in the red blood cells are also on fetal heart cells, which is just interesting. And this can cause a myocytus or an inflammation in the fetal heart and contribute to that development of heart failure. Okay. That's awful. It's awful. It's really scary. And so a parvovirus B-19 infection is one of those that is kind of scary in pregnancy. I will say that it is still very rare. And it's rare not only because it's estimated that about 50% of people by the time that they get pregnant are still able to get infected essentially, like 50% of people are already immune to parvo. But even in those 50% of people, if, If an infection occurs during pregnancy, most sources that I read estimated that it's only about 5% of the time that there's any abnormality as a result, even though it can be up to 30% of the

time that the fetus does end up getting infected. So kind of just like with parvovirus in kids or adults, most of the time it doesn't cause this severe outcome, but some of the times it can. Okay. I have a few questions. Okay. You said torch. What does that stand for?

So torch stands for toxoplasma. The O is other, which includes syphilis, parvovirus, varicella, and listeria. Okay. And then rubella is the R. Cytomagelovirus, CMV, is the C, and then the H is herpesy-symplex virus. Okay. Torch. So these are all viruses that can cross the placenta and then result in pretty severe disease in the fetus.

We've covered quite a lot of these on the phoenix. podcast already. We have. Okay, another question was sort of the timeline of infection in these severe cases where heart failure does happen. What is the timeline of that and follow-up question? Is there any treatment? Excellent question. So the timeline of it, I actually don't fully know in terms of like once the fetus is infected, what's the timeline to development of severe disease? I don't know. Okay. It is infection in the second trimester of pregnancy that we know is highest risk because that's when the fetus is like making a lot of these red blood cells and things like that. Whereas later on, they have enough of a reserve that they might be less affected by an infection.

And earlier than that, they don't have as much of a circulation system yet kind of a thing. But there is treatment that can be done, which is great. Okay. It's definitely not something that is available everywhere, but things like intrauterine transfusions are things that can be done, especially if you identify an infection. And then what you do is you serially monitor with ultrasound to see how the fetus is doing. And if there's any evidence of infection, and then you would be able to treat it with things like transfusions. And it can significantly reduce mortality in the case of the development of hydrops. Okay.

Yeah. Is there a vaccine for humans? No. Okay. Yep. That one's an easy answer, unfortunately. Yeah. There's one more thing that I want to mention, and that is what's called chronic red cell aplasia.

And this is very similar to transient aplastic crisis, except that, like the name, implies, it's chronic. And so in individuals that already have a severe bone marrow deficiency for one reason or another, like they already have leukemia or they've had an organ transplant, so they're on immunosuppressives, or they're undergoing cancer treatment. In these cases, infection with parvo B-19 can cause not a transient, but a chronic anemia that can be pretty profound, but can improve if, like, for example, the chemotherapy is stopped, then things can kind of bounce back. But that's just kind of one last thing.

And in this case, what's interesting is that it does tend to result in a chronic viremia, where this virus is still present. You can still detect it, and it's still causing this damage. Okay. Fascinating. Fascinating is right. So that is kind of most of all of the manifestations of Parvo B-19 in humans. There's a lot.

That's a lot. And that's just the human parvovirus. Right. That's just one virus. It's one virus. One host. There's a few like subgroups of it nowadays, but that's parvo B-19. But this is a huge group of viruses that infect a huge variety of mammals and a lot of pet owners

are probably even more familiar with canine parvovirus or with feline pan-lucopinia virus than they are or were, with human parvo B-19. Now, just like with human parvovirus, these animal parvoviruses are infecting rapidly dividing cells, but in most cases, they happen to have tropisms that are more specific for the lymphoid tissue in the intestinal crypt cells. So this is rapidly dividing lymph tissue

in the intestines of these animals. And because of that, there's some pretty notable differences in the disease course and the mode of transmission when it comes to these animal viruses compared to human parvoviruses. So animal parvoviruses tend to be transmitted fecal-oral because these viruses are infecting the intestinal cells rather than bone marrow cells and then being transmitted in our respiratory secretions.

And as our lovely vet will talk more about later, the symptoms of the disease tend to be more gastrointestinal, but there's a lot more to it than just that. And we'll talk about that later on. But Erin, now can you tell me where the heck this virus came from and how we got to this point? Yeah. I mean, kind of. Or these viruses, I guess. Right. All of them. We'll see what exactly I can tell you right after this break. Anyone who works long hours knows the routine. Wash, sanitize, repeat. By the end of day, your hands feel like they've been through something. That's why O'Keefe's working hands hand cream is such a relief. It's a concentrated hand cream that is specifically designed to relieve extremely dry, cracked hands caused by constant hand washing and harsh conditions. Working hands

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And what's the song that can take you there. Music changes what you feel. And what you feel changes what you do, right? That moment where a song shifts something. inside you, that's where transformation starts. This year, I'm talking to experts across every area of life, like personal finance icon Gene Chatsky, New York Times journalist David Gellis, relationship legend Dan Savage, human connection teacher Mark Groves, and the man who sheet my ear more than anyone, Questlove. They'll bring the strategies. I'll pair them with the right records

and will teach you how to use the music to make change stick. This isn't just a podcast. It's unconventional therapy for your entire year. Listen to DJ. J. Hester Prins, music is therapy, on the IHeart Radio app, Apple Podcasts, or wherever you get your podcasts. Ever feel like you're being chased by the marriage police? Welcome to Boys and Girls, the podcast where dating isn't dating. Arranged marriage is basically a reality show, except the contestants are strangers, and your entire family is judging. You're sipping coffee with one maybe, grabbing dinner with another, and praying your karmic Ken or Barbie appears before your shelf life. runs out. Trust me, I've been through this ancient and unshakable tradition.

I jumped in, hoping to find love the right way, and instead I found chaos, cringe and comedy. And now, I'm looking for healing. Boys and Girls dives into every twist and turn of the arranged marriage carousel, the meat-awquard, the near-misses, the heartbreak, and let's not forget all the jokes. Listen to Boys and Girls on the I-Heart Radio app, Apple Podcasts, or wherever you get your podcasts. I want to start off the history section with possibly the cringiest opener yet, but I couldn't help myself. I can't wait. The history of parvoviruses begins not with a bang, not even with a whimper, but rather a squeak. That's hilarious.

Erin, I just, I don't know. I love it. I had to, I wrote it down and I was like, should I, should I not? Wait, wait. Here's my question. Yeah. Did you write that quote or did you find that quote? I mean, like the whole not with a bang wimp, but with a wimper or whatever. Yeah. That's old, but like I added the squeak part. Oh, I love it. Okay. Thank you. I really loved it. But I said squeak. I say squeak because the first parvovirus

described, which was isolated in 1959, came from a rat. I. It's a, it's. It's. It's. nerdier than you would think. Right? Right. I mean, I don't know how to do it any other way. Oh, I wouldn't want it any other way. Aw. It's discoverers. Killam and Olivier named it fittingly, rat virus. Okay. But like, can you imagine? Can you imagine being a virologist during this time and being able to name something rat virus? Like, what a time. What a time. Wow. Later, presumably because people quickly realized that there wasn't just one rat virus, it became known as Killam rat virus. Okay. Killam and Olivier found the virus while looking for a tumor-inducing virus in rats.

And what they found was rat virus, which did not appear to make the rats sick or cause tumors or seem to be able to infect other species. But the researchers still did find the virus interesting enough to write up. And over the next 10 or so years, their paper describing this rat virus would be referenced in more papers describing similar viruses also newly discovered. First, primarily detected in like immunosuppressed lab rodents or in cell culture lines with a very wide range of pathogenesis from asymptomatic infections to neonatal death and rodents, for instance. Okay. And later they began to find these viruses from non-labular. settings and non-lab mammals, like the greater wax moth, and subsequently a whole bunch more arthropod species, and at least one crustacean. For the most part, these small, seemingly

related viruses didn't make too much of a stir in the virology community until the mid-1960s. Epidemics of enteritis, panleucopenia, and congenital cerebellar ataxia had been popping up in domestic cats for decades. And around 1965, 1966, researchers identify the causative virus as being similar to these small rodent and arthropod viruses that they had found. And they named it feline panlicopinia virus, which I think was also the first real indication that this group of viruses might have a substantial effect on their hosts in like natural settings. But what was this group? It still needed a name. I mean, we know that what it is now, but I'll tell you how we got there.

Carlos Brilofsky proposed the name parvovirus rati or rati for a Latin naming system for rat virus. Parvo from the Latin parvus for small. And he suggested that this group of small DNA viruses be designated the parvoviruses. Very small. You know, seems reasonable. Yeah. But somehow this seemingly innocuous. reasonable suggestion got a whole lot of people upset. I saw the phrase, quote, somewhat rancorous

debate used to describe it. Interesting. Yeah. And so on one side was the pro-parvovirus, and the other side was pro-Picodna virus, kind of like in parallel with pecorna viruses, small RNA viruses. But then like you have pecornaviruses and pecorna viruses and Pocodna viruses, like all you have to do is have one typo. And then it's- Also, Pocodina sounds silly. I mean, I know. But I mean, if it had been that, we wouldn't think it sounded silly today. I would still think it sounds silly.

I would, I can, I'm going to stand by that. I'm going to die on that hill. Well, in any case, to quote from a paper, reason and clarity prevailed. and the name parvovirus was adopted. I like that. Throughout the rest of the 1960s and into the 1970s, the parvovirus family continued to grow, one by one, with the first human parvoviruses,

adenovirus associated viruses or adno-associated viruses, aka AAVs, so-called because they're dependent upon adno-viruses for their own replication. The Dependoviruses. The Dependoviruses. These were discovered in the mid-1960s. Oh, okay. But, and I know you'll talk more about these later, and I'm really excited for that. These are considered non-pathogenic, question mark.

We'll see if that stands, I guess. But a human pathogenic parvovirus was just around the corner waiting to be identified. In 1975, researchers were evaluating a newly developed test that was used to detect hepatitis B virus. in donor serum, and they found a different antigen that had, like, precipitated with this test. And this was not, definitely not, the hepatitis B antigen. And it more closely resembled a parvovirus than a hepatitis virus. So they wrote it up, a new human parvovirus that seemed to infect a not small proportion of samples that they tested, but whose pathogenicity was totally unknown. And I feel like, okay, this does happen from time to time.

And I know we've talked about it on the podcast before. But it does seem uncommon for a pathogen to be discovered before, not discovered, but like the pathogen was discovered not an association with a particular disease. Right. Like completely independently of, yeah. Yeah. Yeah. I don't think that that happens very often, at least from what we've talked about on the podcast. But it is really interesting.

And I feel like in this case kind of makes sense. Yes. Yeah. For sure. Yeah. So this virus would become known as B-19, which the name allegedly comes from the fact that the virus was found in specimen 19 of panel B. So boring. But logical.

Yeah. Now that parvovirus B-19 was identified, all that was left to do was find out like, did it make people sick? What did it make people sick with? Yeah. So, Erin, you mentioned aoplastic crisis in people with sickle cell anemia and many other types of blood disorders. Instances of aplastic crisis often happen in families concurrently and are often preceded by symptoms of viral infection. And so for decades, physicians have thought, okay, maybe it's triggered by some sort of infectious agent, but we just don't know. what it is. Then in the early 1980s, researchers found parvovirus B-19 or antibodies to parvovirus B-19

in the serum of people with sickle cell anemia who were experiencing aplastic crises. And the evidence that this virus was the principal cause of a plastic crisis as well as hemolytic anemia began to mount. But along, I love that still, it's like we're finding the most severe manifestations first for this and not like. like literally the most common cause or the most common manifestation. But making the link between B-19 and the most common and often mild manifestation did happen like shortly after. So researchers were finding B-19 in simultaneous outbreaks of aplastic crises and erythema infectiosum. And then they were like, okay, let's look for just in erythema infectiosum in children. And,

And of course, they found the virus again. As you mentioned, erythium-infectioism is also called fifth disease. I love this. I love this. I love it so much. I don't know why because it's silly, but I really like it. So silly. It never would have occurred to me that this was the reason why it was called this.

Yeah. Like it's just what. Okay, so the earliest possible mention of this common infection of childhood comes from the late 1700s, early 1800s, with the description of a disease called Rubiola Sin Katar. So it wasn't called Fifth Disease then. Right. And, you know, it's, that seems to be debated whether it was actually Fifth Disease, but whatever.

The first real reference to Fifth Disease, or Arethia Mephtheusum, comes from 1890 when Shamer described a childhood rash characterized by the slapped cheek appearance. The disease came to be known. known in Western Europe as arithema infectiosum, and then in 1905, fifth disease, to distinguish it from the other four rashy illnesses common in childhood. Measles, scarlet fever, rebella, and epidemics, pseudoscarlatina, Duke's disease, which is a variant of scarlet fever related to staphylacal exotoxin. Yeah, apparently people are now like Duke's disease doesn't exist.

Fourth is not real. And now there's also a sixth disease. Roseola. Okay, but are people still using one, two, like first, second, third, fourth, sixth? So first, second, third, no. Okay. Fourths, no, I've never heard anybody use. But fifth and six, yes. I can't get over it. So yeah, eryema, infectiosum, B-19, whatever, that was fifth. It seems like the most confusing naming system, because not only do you have to remember the order, Like, it's just why? Yeah.

Well, it's also in part because we now, we have vaccines against measles. We don't get scarlet fever because we can treat bacterial infections. Rubella, we also have a vaccine against. So really, it's just, like, it's just fifth that's left. And then, yeah, roseola as well. But still, like even pre-vaccines, a kid would come in and you would go, oh, that's measles. Oh, wait, no, that's first or is that second? I don't know.

Like, you know what I mean? Well, wasn't it more just like, oh, yeah, that's. this rash is first, this rash is second, this rash is third. I mean, maybe there is a method to the order of these, but I feel strongly opposed. Well, anyway, over the first half of the 20th century, people would have plenty of reason, at least to remember the name Fifth Disease, because it grew more and more common. So one paper said, quote, fifth disease is, now annoyingly familiar to pediatricians, school administrators, and public health officials throughout the United States.

Wow. End quote. Yeah. It was clear that it was an infectious disease of some sort, contagious, just given the nature of outbreaks, but the root of transmission and the causative agent, Porvovirus B19, wasn't linked to it until like 1983, 1984, which is kind of amazing. Yeah. Yeah.

And it took another 20 or so years after that, 30 years since the discovery of B-19, that another human parvovirus was discovered. So we're still very much in an active area of research and discovery with human parvoviruses. But these are only one branch of this big parvovirus family, arguably not even the most famous branch. So should we get into the famous one? Let's. Okay. Throughout the 1960s and into the 1970s, additional parvoviruses were isolated from new animal species and the known host ranges of parvoviruses were expanding, like feline pan-lucopinia virus,

which was also found in mink and raccoons. But despite the creeping realization that parvoviruses were, A, globally distributed, and B, that the name of a specific virus, like raccoon parvovirus, for example, might not capture the full host range of that virus. The public, I think for the most part, was unfamiliar with this new group of pathogens. Maybe, maybe, you know, feline panlicopinia virus, but that's it. Until 1978, when blurbs about a deadly new disease in dogs began popping up in newspapers, First, small little paragraphs on like page 12 or whatever, but later, as the extensive spread of this disease became apparent, these articles began showing up in countries around the world simultaneously, making headline news.

From an article in the Schenectady Gazette on May 27, 1978, quote, a serious viral disease affecting dogs has been reported to have reached this area, a representative of the Capitol Disciate, strict veterinary medical society said the virus has been identified as belonging to the coronavirus group. It causes, yeah, it causes acute gastroenteritis exhibiting vomiting and several hemorrhagic diarrhea resulting in severe dehydration and an imbalance of the dog's electrolytes, which leads to death. The veterinary society recommends that any dog exhibiting symptoms be immediately taken to a veterinarian for treatment, especially dogs who have been to dog shows or among

other groups of dogs, such as at classes, etc. The progress of the disease and its serious effect on the dogs is extremely rapid after the first sign of symptoms. Dogs have died within 12 hours. According to a report in the American Kennel Gazette Pure Bread Dogs Magazine's April 1978 issue, the problem with this virus became widely known in February following a specialty show sponsored by a national parent club, and it has rapidly spread throughout the country since then. end quote, long quote. Yeah. It was, I found it very like jarring to see coronavirus, like suggested. Obviously it wasn't a coronavirus. It was part of a virus, but I saw that and my heart went like. I know. Another one. No. Yeah, it gave me this little jolt of anxiety. But yeah, so this would, this is what the first, one of the first descriptions of parvovirus. And so I want to read some snippets from later news articles.

to kind of trace the spread of parvo and awareness of it. That's kind of fun, like history through headlines. I don't know. This is from a Canadian press article from October 25th, 1978, titled Virus Kills Dog in Five Days. Quote, dog owners are being warned to watch for signs of a new virus, which can kill a healthy animal in five days. Veterinarians say they don't know much yet about the virus,

called enteritis, except that it is an intent. intestinal infection and appears to dehydrate a dog, mainly through vomiting and diarrhea. Enteritis has been found from the Maritimes to Saskatchewan and is reported to be widespread in the United States. It does not pose a threat to other animals or to humans. Gary Thompson, a pathologist at the University of Guelph, said the problem first appeared among show and kennel dogs, but now has shown up among dogs who get no further than their own neighborhood. End quote. No further than their own neighborhood. I know. It's really scary to like read about the spread. A few months later, in January 1979, there's an article from the Associated Press titled, quote, new virus infects

dogs, cats may be to blame, end quote. Oh my gosh. So rude. Right. And this article mentions that scientists are calling the virus canine parvo virus and that it is similar to quote unquote feline distemper, aka feline pan-lucopinia, which is also confusingly called cat plague. It's just like, what? Why do you have to have so many names? I know. Also, distemper is like a different thing. It's a completely different thing.

I told. We'll do it someday, I swear. We will. Yeah, it's been on our list. Yeah. But this was clearly not the same exact virus as feline pan lucopinia virus, since A, this is like the first time. that people were seeing it in dogs.

And also, there were studies from the 1960s showing that experimental infection of dogs with feline pan-lucopinia virus were unsuccessful. Like, the dogs didn't get infected. Nor was it the minute virus of canines. I'm assuming it's minute, not minute. Yeah. I think it's minute because they're little viruses. They're little viruses.

I was like reading it. I was like, oh, wait, I guess I never considered. Anyway. English is rough. Right. Yeah. Yeah. But the minute virus of canines is now called canine parvovirus type 1. And that was discovered in 1967 and not really considered to be of great concern. Like it did seem to possibly cause infertility and pregnancy loss in dogs, but not enteritis or this super high mortality. from its first identification and description as, you know, quote-unquote show dog disease, which was what it was called in its early days, to canine parvovirus that took less than a year. And another big development was not far behind, a vaccine.

Once researchers made the link between this new deadly canine parvovirus and feline pan-lucopinia virus, the next natural step was to wonder whether the vaccine, for feline pan-lucopenia virus, which had been developed in the late 1960s, would work on this new virus. Seemed like they're related, it's worth a shot. The answer can be found in another news article title from March 1980, again by the Canadian press. Quote, cat vaccine helps quell dog disease, end quote.

Oh, full 180. I love it. I know. I do have some, I do have more from that article. article, quote, some Canadian veterinarians in an effort to quell a disease that killed an estimated 1,000 dogs in Canada last year, have turned to an unlikely source for help. They're using a cat vaccine, which, although not yet licensed for use in Canada, has met with success and is licensed for use in the United States, end quote. An unlikely source. And unlikely source. I'm like,

actually, it's like fairly likely. Be likely. I love it, though. But it's okay. So this was excellent news, right? Especially since this new canine parvovirus, we're starting to show signs of being able to infect cats. But where did it come from? Were cats to blame? No. And so, okay, we have this vaccine, control as possible, but we have a lot of unanswered questions about the origins of canine parvovirus. And so now I want to get into a bit of the history of canine parvovirus type 2, I should say, not as the general public was reading about it like over coffee and cereal,

but as the virologists and evolutionary biologists piece together using molecular clues. Love it. The canine parvovirus that began making headlines around the world in 1978 was, like I mentioned, the second canine parvovirus to be identified. Hence the type 2 attached to its name. Most people call it K9 parvovirus because it is like the one, you know, but anyway. But it's number two. It's number two.

And K9 parvovirus type 2 did not evolve from the minute virus of canines, aka K9 parvovirus type 1. And it probably comes as no surprise that 1978 was certainly not the first year that it began circulating in dogs. researchers tested CERA from dogs from 1974, 1976, and found antibodies to the virus.

And it's pretty amazing, maybe not surprising for this COVID world, that within a few years, this virus had become global, a true pandemic virus.

Like, yes, it had been circulating, but I think that, like, the earliest signs were 1974, 1976. And then it was global.

It's this, I feel like, I don't know, I don't know why I feel this way, but it feels especially impressive that it's dogs and that it's spread. But I guess like wild animals, yeah, I don't know. Yeah. No, and I think it actually, that aspect of it was really concerning to a lot of people because we have, all these countries have specific like quarantine restrictions and like legal limits on can you bring a dog in here? Can you bring this animal? How many animals can you bring in? You know, like the contact, signs of disease steps, like how did this happen? Yeah. And I'm not going to

talk about it from like a disease control perspective, but that is something that I think still people are making sure, like where were the cracks in the system. Yeah. Yeah. Yeah. But anyway, so once this virus had become pandemic, it underwent some genetic tweaking. to reach its full potential, as pandemic viruses do. A few amino acid changes here and there led to a new genetic variant called parvovirus type 2A, which emerged in 1979, so just like a year after sort of the first rumblings in newspapers and so on. And in a short time, just a couple of years, really, parvovirus type 2A completely replaced parvovirus type 2.

Wow. Yeah. Since then, there have been a few more variants, like B and C and so on, and I'm not going to get into those. Type 2A was definitely, from a pandemic virus perspective, a level up from type 2. Not only was it better adapted to its canine hosts, it also had an expanded host range, able to infect cats and wild carnivores. And it seemed deadlier. after a decline in cases of canine parvovirus in like 1980 and 1981, as herd immunity kind of slowed transmission a bit, things exploded again in 1981, 1982.

But this time the disease seemed more severe. Quote, pups collapsed suddenly in a shock-like state and died with or without interrach signs. Many pups also developed an acute, rapidly progressing illness with exceptionally severe. hemorrhagic enteritis that was not commonly seen in the initial outbreaks, end quote. Goodness. Yeah. Fortunately, though, another improved vaccine was developed pretty quickly. But the sudden shift with a new deadly variant was obviously really concerning. Yeah.

Because it kind of begged the question, like, okay, what next? Yeah. Would this virus keep evolving until it could escape a vaccine, until it could infect other animals outside of its existing host range, could that eventually include humans? And as always with this podcast, to understand where we might be going, we have to look back at where we came from.

Perhaps untangling the origins of canine parvovirus type 2 would help researchers to predict whether or not this virus was likely to expand its host range beyond what currently existed. Initially, when canine parvovirus type 2 first appeared, most scientists thought it had jumped hosts from cats, the feline pan-lucopinia virus evolving to infect dogs. And maybe even it was like the vaccine strain of that virus that had sort of turned into a virus capable of infecting dogs. But it doesn't have a whole lot of support.

And it seems actually unlikely. So first, canine parvovirus type 2 was unrelated to those vaccines. strains. Well, that's, that's a big fat no then. That's a big fat no. Second, despite the long history of cats and dogs being in proximity, this was the first detected instance of this virus, or another kind of similar virus hopping from one species to the other, at least that we know of. Of course, there's always that, you know, hedge. But the third reason, I think, is the strongest, which is that intermediate viruses between feline pan-lucopinia virus and canine parvoinia virus and canine parvoin, Parvovirus type 2 have not been detected in domestic cat or dog populations.

And that's what we would expect to see if the virus evolved from cats to infect dogs. We would see those in between strains. So canine parvovirus type 2 is seen as a host range variant of feline parvovirus. So if it didn't come from cats, like where did it come from? How is that possible? Yeah. Well, the answer is a different host range variant of feline pan-lucopinia virus. So feline panlucopenia virus is actually comprised of a bunch of strains of virus, which can infect

other hosts besides cats, including mink, raccoons, and foxes. And so maybe this taxonomy is, like, I read a paper about like the history of the taxonomy of parvoviruses, but it was from 2008, so maybe this is a little bit out of date. But in any case, that was my understanding of the organization of these viruses. Yeah. So researchers think that canine parvovirus type 2 may have evolved from one of those feline panlicopinia virus variants. So like dogs somehow got into contact with raccoons, mink, foxes, whatever, and then that virus infected dogs and then, yeah.

I feel like this just shows the problems with the way that we name things and the way that we name viruses. Because like the parvov viruses especially seem like, What a mess. What a mess. And it's clearly named after like the first animal that it was detected. Right. Which is just what? And like also why like this one is called pan leukopinia virus.

And then this one is called parvovirus. And then this one is called like something else. And I'm just like, stop it. I know. Stop. Well. Anyways. Anyways.

It's just me. No, it's not. It's definitely not just you. And so I don't think that at least I couldn't get a clear answer on what they think that animal was. That was the source of sort of like the initial spillover, I guess. But like don't blame the cats. Don't blame the cats. Okay.

We can blame the raccoons though because it does seem there is some research to suggest that once canine parvovirus type 2 emerged from whatever, you know, feline pan-licopinia virus variant, it then further evolved possibly in raccoons. So like spilled over from dogs into raccoons and then kind of, you know, evolve, tweak things a little bit more to become canine parvovirus type 2A. Ah. Yeah. So the parvovirus that infects raccoons seems to fall between canine parvovirus type 2 and type 2A. Oh my gosh. Oh, okay.

This is like a lot of nitty-gritty, and I'm done. So you're welcome. But the bottom line is that we don't know exactly which animal feline panlicopinia virus jumped from into dogs, probably not cats. And the other bottom line is that canine parbo virus type 2 evolved into type 2A, possibly with the help of raccoons. But why is all this nitty-gritty important? Why am I like stumbling over the taxonomy of all of all. all of this. Because anytime a pandemic virus emerges, we want to know how it happened. We want to be able to trace that roadmap to understand how a virus mutated, how it was able to come into contact with another host, aka spillover, how it continued to evolve to infect that host, and how it was able to rapidly spread around the world, looking at both the biological properties of a virus, as well as the societal or political or infrastructural properties that allowed the pandemic to happen. I also think that the canine parvovirus pandemic is especially interesting given that it's a single-stranded DNA virus, where we tend to think of RNA viruses as the ones of pandemic potential because of their high rate of mutation.

But, hey, don't forget about the single-stranded DNA viruses. That's not. Yeah. So clearly, the story of parvoviruses is very much ongoing. We're finding new parvoviruses or variants of existing parvoviruses and new species. And canine parvovirus very much remains a threat to domestic dogs and cats and wild animal populations around the world. But before we get into where we are with the human side of parvoviruses today, we wanted to bring on a very special guest. who can share some insight from the veterinary side of things. We'll take a short break here and then jump in.

So far in this episode, we've covered a lot of ground. But what we haven't gotten into, and this is probably especially obvious to those dog and cat owners out there, is the animal side of things. Like we've mentioned, parvoviruses are quite a diverse group. And if we went into each and every one of them, we'd be here all day and probably tomorrow too. So instead, what we're going to do is spend a bit more time on two parvoviruses in particular,

canine parvovirus and feline pan-lucopinia virus. And to help us do that, we've enlisted the help of the amazing Dr. Steff Horgan-Smith. Dr. Steph graduated from Ontario Veterinary College in 2011 and now owns and runs a veterinary hospital in York region in Ontario, Canada. And we are so excited to chat with her today. And just to note, this interview was recorded on November 20th, 2023. Dr. Steph, thank you so much for joining me today. I can't wait to talk about parvoviruses from the veterinary side of things.

Thank you for having me. I'm very excited. So let's just like jump right into it. We talked a little bit about cana and parvovirus throughout the biology and the history, but we didn't really get into like what it looks like in dogs. So what are some of the signs and symptoms of infection? So the classic what we see in clinic is with puppies, really. It's mostly in puppies. Adult dogs can get it, but their immune system is definitely better at fighting it off. So the classic is a puppy that comes in and by the time we see them that they're sick, they're vomiting, they're having some diarrhea, and most of the time that diarrhea is bloody. They're sometimes eating by that point or not. They're pretty sick and flat. So as soon as we get a puppy that's vomiting diarrhea, we're all testing for parvo. A lot of them are actually pretty painful in their stomach and their intestinal tract just from the virus kind of getting through that area. When we talked about parvo B-19, which is one of the viruses that infect humans, we talked about it being spread through respiratory droplets.

But that's not the same for dogs. So how is parvo spread between dogs? So in dogs, it's actually more fecal oral. The virus has shed way more in feces. And so the virus itself is pretty stable in the environment and will last on surfaces or toys or shoes that I've walked through with virus attached and can be spread to other dogs that way. It can be passed in utero sometimes from mum to puppies, but that's, I would say, not as common. We see it mostly in puppies that are out in the environment and they're catching it that way. Durability, it's pretty dang durable, right? Like months, even longer? Up to a year in the right conditions. Okay. So if there's organic material that's still left over, it's going to survive in that

organic material. So actually scrubbing cleaning is a big one and making sure that all the organic material is gone. UV rays will actually kill the virus eventually. So indoors, it can stay a long time. We talked a little bit about how one of the newer variants that emerged, well, you know, several decades ago, could also be spread to cats. But what about other animals? So, yeah, there are reports. They're not sure if it's a canine parbovirus or a feline like panloquipenia, which type. But there have been reports in like coyotes, wolves, pumas, bobcats even, and then raccoons and skunks. So all of those animals seem to get some type of parvo.

And then separate to the canine and feline parvovirus, porcine parvovirus is a really important virus in pigs and pig production. Because mostly it actually just causes fetal death. So it changes your litter size. So yeah, there's a vaccine for that also. So at least we can help try and prevent that. Prognosis. So canine parvovirus, obviously. very severe disease, but like what is the prognosis and how does that vary based on the age of

the dog or puppy and other factors like overall health status or breeds or anything like that? Yeah, the younger the puppy, the more susceptible they're going to be to the virus because it's infecting those rapidly dividing cells. It runs through the immune system and the bone marrow and infects all their immune cells and then to the GI tract. And it just wipes out the villa, all the little intestinal villa that are absorbing all the puppy's food. So then we basically supportive care have to just keep that puppy alive until the cells regenerate in, you know, that kind of 10 to 14 day mark where the new cells grow up from the crypts. that's where survival kind of depends on how young they are, how prone to other complications like hypovalemic shock or low blood sugar because they can't keep up their sugar and stuff.

And then unfortunately, with veterinary medicine, cost comes into it. So what level of care an owner can do? If they can do intensive management in a hospital setting for two weeks, that's pretty pricey. but generally survival is about 90%. It kind of goes down from there, again, depending on age of the puppy. But if we have to do outpatient treatment, it can work, but survival is a little bit lower than kind of the ideal gold standard. But obviously, not everybody has that much money to keep a puppy in intensive care for two weeks.

It's a lot. Right. And treatment is sort of, like you said, just supportive. Does that just mean like fluids and monitoring? Yeah. Yeah, so that puppy is hooked up to IV fluids, nutritional support. So either a feeding tube or down right into their belly, we do that. They're getting their electrolytes checked all the time to make sure that those are staying normal and supplementing whatever they need. And then keeping them in the hospital, keeping them monitored. That's always been our classic main treatment. There is actually a new monoclonal antibody that has been licensed. That sounds quite exciting. It's showing some really promising quick turnaround. that maybe those puppies won't be as sick for as long, which is amazing in so many ways. So that's really exciting that we might actually have a specific treatment where it's blocking

the virus from being able to get into the cells. So that's really exciting, potentially on the future horizon. That's amazing. Oh, that's really cool. Yeah, it's really cool. Oh, I love that. In the history section, I talked about how canine parvovirus likely evolved from a related parvovirus, one of the host variants of the feline panlocopenia virus. Can you tell me a little bit

about that virus? And what are some of the signs and symptoms and cats? Yeah. So that one actually is maybe a little bit more similar to the human one because it can be infectious through any body secretion. So saliva or potentially respiratory droplets as well also can be fecal oral. So it kind of just ranges anything. Anything. But yeah, that one, again, it's going to infect those rapidly dividing cells. We see not as severe gastrointestinal symptoms with cats. What a lot of the time we see is sometimes the queen gets infected, so then vertical transmission to the kittens or very, very young kittens while they're still nursing. One of the classic symptoms that we learn about and we see sometimes is the virus actually goes and starts affecting their cerebellar development.

So that specific part of the brain, kittens are still developing that for like about two weeks after they're born. So even if they get infected really young, they can get this cerebellar hypoplasia where it just doesn't develop completely normally. And they'll have these tremors because that's movements and fine movements is part of what the cerebellum helps with. So these kittens will grow up and they'll have these intention tremors probably for life. But if they recover from the virus, then they can survive. They can kind of be normal. But yeah, they get this very specific symptom that you can kind of look at them later and say, oh, that cat probably had panlicoppedia when it was a kitten because it has this very specific intention tremor.

Is panlicopenia in kittens as severe as canine parvo is? is in puppies? Is the prognosis pretty similar? No, I'll say, for whatever reason, we see it more in extra young kittens, so when they're still nursing. And so unfortunately, some of those kittens, when they're that young, they kind of just get this fading kitten, and some of them will just not survive. And then, again, with the cerebellar hypoplasia, but we just don't see it as often as we would, like a parvo puppy. I think partly because of how we keep cats in general, they're not out in the environment meeting other cats, right? So if they're picking it up, it's because someone in their households has it and hasn't been vaccinated for it. So it's not as widespread as

puppies who are seeing other dogs all the time or being introduced to other environments. Okay. So when do puppies and kittens get vaccinated for parvovirus or panlicopinia? And how many rounds of vaccination are there? So luckily it's the same for cats and dogs. so we can talk about it at the same time. We start at anywhere between six to eight weeks to get that vaccine into them. That's where it's a bit tricky depending on the whole situation with mom, because if mom is well vaccinated, she's giving those puppies or kittens her maternal antibodies in the milk,

and they are still active at definitely six to eight weeks for most of those babies. We start then just in case mom doesn't have great immunity. We want to catch those ones that are not getting immunity from mum, but then we have to re-vaccinate every four weeks up until they're about 16 weeks old. At 16 weeks old, mom's maternal antibodies won't be there anymore and will be stimulating that puppy or kitten's own immune system to fight the virus. It's generally a series of three to four vaccinations starting at 6 to 8 weeks. Parvo's the main reason that most vets will recommend being really,

careful with where you take your new puppy until they get at least a couple vaccines into them because parvovirus can be anywhere. It can be shed and then just left in the environment. So that's the main reason why we have to be careful with where puppies are going and who they're meeting right when they're really young. During COVID, the last 10, 20, 30 years even, we've seen a big upward trend, especially here in the U.S., but I think globally as well, in vaccine hesitancy and anti-vaccine sentiment for human vaccines. But have you seen something like this as well for people and their pets? Yes, we definitely have clients that are vaccine hesitant and just not 100% sure what the science is and what's going on. But the one thing I will say about parvo vaccination,

and especially in dogs but in cats as well, it's really effective. Getting those puppies in when they're young and bringing them back every month for that booster vaccine. I couldn't find an actual number when I looked at it, but there's very rare breakthrough actual parvovirus infections in dogs that have been fully vaccinated. They do need re-vaccination, though. The immunity, we don't know exactly how long it lasts in every dog. Their own immune system is going to be different.

So we generally do a boost. booster at a year later. And then re-vaccination is every one to three years after that. So I have one last question for you. And it's not about parvovirus, but it's instead about this new canine respiratory illness that seems to be popping up throughout the United States, at least, all over. It's here in the front range in Colorado. What do we know about this infection? And why has it gotten people so concerned? I hate to say, but we're not sure yet. It's all right. We say it all the time on the podcast. We don't know. We don't know.

There's, yeah, it's been around, there's been reports of some kind of respiratory infection since, I would say, late spring in different parts of the U.S. We've been tracking it. I personally haven't seen any reports. I'm up in Ontario. I haven't seen too many things here. But it started with, is it kennel cough or some type of kennel cough kind of organism that is just not responding to normal treatment? Most of the labs that we use have a pretty extensive respiratory panel. So if we get samples, we can send that out to our labs and try to see all the common stuff is on there, including influenza, portatella, pear influenza, things that cause kennel cough and other common respiratory infections. And it's testing negative for all of those. And then it just seems to be, unfortunately, the dog's own immune system, whether they get this cough and it just lingers. but they're okay otherwise.

I've heard reports of it lasting for like six to eight weeks in some dogs. And then some unlucky ones, it does seem to turn into more of a pneumonia. And those dogs are needing some of them. Hospitalization, pretty intensive management to help get them through it. So they haven't really even found what the difference is between those cases, why some dogs are just getting a cough or, and then some of them are getting quite sick with pneumonia. it's a bit scary that we don't know still what it is. Yeah, for sure.

It's very scary. It definitely has echoes of like the early parvovirus news articles. Like there's this mysterious thing that's spreading, you know, and we don't know what it is. But anyway, well, thank you so, so much for taking the time to chat and answer all of our questions about canine parvovirus and pan-lucupinia virus. I mean, I feel like we definitely could have talked for hours, and I really, really appreciate it. You're very welcome. I'm glad that I could help and hopefully shed some light on the canine and feline pet side of parvovirus. Thank you so much, Dr. Steph, for walking us through that. I love getting to hear about animal diseases from someone who actually knows. Yes. Yeah, totally.

Yeah, I really appreciate it. That was great. Thank you. So let's talk a little bit about where we stand with parvoviruses today. Let's do it. Again, here I'm going to focus on human parvovirus B-19, in part because I couldn't find data on, like, the prevalence of feline panleukopinavirus or canine parvovirus, too. Like, except studies that were like this country in these years, you know what I mean? That was like very specific. Like the point is those viruses are everywhere all the time. Yeah.

The end. So for humans, the story is almost exactly the same. I couldn't get a handle on breaking things down much more than letting you know that when we look at serology studies by age, by the time someone is about six years old, anywhere from, like, like 2 to 15% of kids will have antibodies. But by the time you get to adulthood, over 60% of adults have antibodies to Parvo B-19. And by the time you get to be geriatric, over 85% of people have antibodies.

So like everyone gets Parvo at some point. And there is, at least in temperate regions, seasonal variation in parvovirus infection. So peak incidence tends to be late winter, early spring, which makes sense. That's when a lot of viruses circulate. And like we have seen with other childhood infections, there can be these outbreak years, where every three to four years or so will see an increase in infections overall. And they call these epidemic years.

Okay. Now, during these outbreaks in these epidemic years, we see that about 10% of all the cases, will occur among children that are about five years old, and 70% of them will be in kids between age 5 to 15, and then 20% of cases are in people older than 15. So that's like the age breakdown, where the youngest of kids might be a little bit more protected, and it's that middle, like, school age kids that are the highest risk for infection. Okay. Now, what I wanted to be able to get a handle on is, like, what percentage of kids or

people who get infected will have more severe manifestations like a plastic crisis. Yeah. I don't know. Okay. I don't know. I mean, we try. But that is parvo B-19 epidemiology. When I tried to get a handle on where we stand in terms of vaccines or treatments, I also

didn't find very much. It was kind of disappointing. I found one paper that was talking about a few different vaccines that are kind of in trials, which are made from these what are called virus-like particles, is kind of weird and interesting. Basically, like, parvo proteins, parvo-virus proteins, do weird stuff, essentially, and, like, form these little nuggets that look like viruses. And so people are taking these and trying to use them to make vaccines.

I don't know. I don't know a lot of details about it. But apparently they haven't worked great so far in clinical trials. And so a paper that I found, which is old now, like 2013, was trying to make different virus-like particles that would cause less illness in people and still be able to induce a good immunity. But they were still in animal model stages. and I really couldn't find anything more recent. So if someone knows of more actual parvo B-19 vaccine research going on, hit me up.

I'd like to know. Okay. But I have more to talk about. I'm not done. I know. I'm excited. Because I want to give a shout out to some very important parvoviruses that we haven't talked in detail about. And that is the adeno-associated viruses, the Dependoviruses, or A-AVs.

And these are parvoviruses that can't infect cells without a concommonant co-infection with either an adenovirus or a herpes virus. What? Yeah. It's, I, I, yep, keep going on. I love it. I love it. We mentioned this concept even, like very briefly in our hepatitis B episode. Yep.

Because hepatitis D is a similar virus that requires. requires the presence of hepatitis B persistently to be able to cause infection because it needs hepatitis B to leave the cells or whatever. So, okay, these AAVs are super tiny parvoviruses, and their genomes, essentially, they're very simple. They encode for like a capsid protein and a couple of other proteins, and that's it. They're really basic. And they generally are considered, to everyone's knowledge, asterisk, to not cause any disease in humans. But they infect humans quite readily in the presence of a helper virus. They're really efficient at getting into our cells and replicating and specifically

integrating into our genome and laying latent, particularly in this one specific place on chromosome 19, at least when we're talking about wild type AAV. And this characteristic, being able to infect ourselves and get into our DNA and hang out there, makes them an ideal candidate for gene therapy. Uh-huh. Amazing. So Aavs have actually been the kind of leading platform for gene therapy thus far. And I think I've probably said the words, I don't know, associated virus on this podcast in the past. because additionally, one of the COVID virus vaccines is an adno-associated virus vector vaccine.

But I didn't even really know what that meant before researching this episode. So essentially, you can make recombinant AAVs that use this same capsid protein, but you can replace the rest of their tiny little genome with genes that code for whatever proteins you want. And now you have this really efficient little machine that needs some help from an adenovirus to get into ourselves, but then can be in ourselves churning out whatever proteins we asked it to make and not causing any disease. This is pretty cool. It's like a whole new world of like I just, I love it. Yeah.

There are already gene therapy platforms that are out there that are being used for things like spinal muscular atrophy, some forms of congenital blindness, and there are more in the pipeline for so many genetic conditions. It's phenomenal. You can read a lot more about it. I have a few papers, but there's even more out there. But one last thing. There was an asterisk. Yeah, I saw that. Historically, this adeno-associated virus or adeno-associated viruses in general have never been shown to cause disease. But just these past years in 2022, the end of 2021, 2021, 2021, and 2022 and 23, it has recently been shown that Aav2 has been associated with some pretty severe outbreaks of hepatitis among kids. So in like 35 different countries, several hundred kids got very super sick and in some cases died.

and after some really intense investigation and these extensive case control studies in a few different countries, what they have found so far is that Aav2 is at least associated in some ways with these outbreaks. But what's really interesting is that we don't know still if there's a causative link as to why kids got so sick or whether AAV2. existing was a marker of like a primary adenovirus infection. But we don't often see as severe disease with primary adenovirus infections. One really interesting part of this story, and I know this is like such an abbreviated story. It's like, wow. But one part of it is that some thought was that this all happened kind of just post-pandemic, right? Like obviously COVID

still exist, y'all. But once all of the restrictions from COVID were lifted, one hypothesis is that susceptible kids may have had a higher chance at all of a sudden at the same time being exposed to both an adenovirus and Aavv2 at the same time that caused this like synchronized wave of severe disease where previously kids might have been exposed to one virus and then another and then another like on a larger time scale if that makes sense right so it's we still like this is very early these papers were just published like few months ago yeah but it's really interesting because it shows just how much we still don't know about so many viruses that exist yeah And like down the line repercussions.

Yeah. Yeah. It's fascinating. Yeah. But again, you can read so much more. I've got papers. We've got sources for you. Let us go through some of those sources.

I have, Erin, I have so many for this. I like kept finding little snippets here and there and just trying to piece through it all. Whatever. I'll just name a few of them right now. And then the rest. I'll post. So there's one by Carmichael from 2005 called an annotated historical account of canine parvovirus. By Parrish and Kauqua from 2005, the origins of new pandemic viruses, the acquisition of new host ranges. And by Thurn from 1988, human parvovirus B-19, historical and clinical review.

Love it. I actually, most of my papers were kind of old for this, but they were. solid. So there was a paper called Human Parvovirus B-19 in clinical microbiology reviews from all the way back in 2002. And another one on Parvo B-19 from the New England Journal of Medicine from 2004. A few others on more specific aspects like parvo in pregnancy, et cetera, and then a bunch on the AAVs, both as platforms for gene therapy and this association with hepatitis, et cetera. Plus I threw in a few on canine and feline parvoviruses as well. You can find all of the sources from this episode and all of our episodes on our website, this podcast will kill you.com and all of our social media channels. Thank you again so much to Eliza for sharing your story with us.

Thank you again, Dr. Steff, for providing our veterinary expertise for this episode. Thank you to Bloodmobile for providing the music for this episode and all of our episodes. Thank you to Tom Brigh Fogel for the incredible audio mixing. Thank you to exactly right. And we have so many people to think, especially thank you listeners. Thanks for listening to all these thank yous. I hope you learn more about parvoviruses. Yeah.

Yeah. And a special thank you, as always, to our wonderful, generous, amazing patrons. Your support really means the world to us. It does. We love it. Thank you. Well, until next time, wash your hands. You filthy animals. This season on Dear Chelsea with me, Chelsea Handler, we've got some incredible guests like Kumail Nanjiani.

Let's start with your cat. How is she? She is not with us. She. Great, great, great way to start. Maybe you will cry. Ross Matthews. You know what kids always say to me?

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