Reptile Fight Club - Grilling the Expert w/ Samuel Kerwin

Episode Date: June 26, 2026

In this episode, we have another installment of Grilling the Expert w/ Samuel KerwinWho will win? You decide. Reptile Fight Club!Follow Justin Julander @Australian Addiction Reptiles-http://www.australianaddiction.comIG https://www.instagram.com/jgjulander/Follow Rob @ https://www.instagram.com/highplainsherp/Follow MPR Network @FB: https://www.facebook.com/MoreliaPythonRadioIG: https://www.instagram.com/mpr_network/YouTube: https://www.youtube.com/channel/UCtrEaKcyN8KvC3pqaiYc0RQSwag store: https://teespring.com/stores/mprnetworkPatreon: https://www.patreon.com/moreliapythonradio

Fighters, welcome to Reptata Fight Club. Yeah, we're here for another fun little episode. We're going to be drilling an expert, Samuel Kerwin, but he is not here yet, so we're going to kick off the show and go get here soon. So we catch up a little bit. So how are you doing, Rob? I'm doing great. Excellent. You have a good trip out southeast.

You're going to record on. NPR, I assume? I don't know. I don't think we've made a plan as to it. Oh, okay. But yeah, we went down to basically in and out in New Orleans, checked out some long leaf pine, loose sand upland habitat in central Louisiana. Nice. Checked out the area where Louisiana,

the sort of the L corner of Louisiana and Mississippi, and then went over into some long-league. Pine, upland habitat in Mississippi and met up with Zachary Gray. Okay. Oh, nice. That was really good. Yeah. Yeah.

So that was great. We, principal goal of the trip, I suppose, was a cane break rattlesnake. And Brandon, so went with Eric and Owen, as you alluded to, and Brandon Valentine, our buddy from down in Phoenix. Phoenix area. Yeah. And Aspen wanted to come, but had travel difficulties and was unable to see it through. Yeah, he messaged me. He said he was, yeah, bummed out about that. He was on like standby or something with, you know, family. Yeah. That's a, that's a rough deal. Yeah. So, yeah. He gave it, he gave it the old college try, though. I think he said he waited a couple flights and then he's just like, it's probably not going to happen.

And so he gave up. But, yeah. The good news was he, well, good news, bad news is that he was still at home, right? He was at the airport at home. He hadn't made it halfway and then got stuck, which is good. Oh, yeah. But, yeah, it was certainly an adventure. So Eric and I had gone, I suppose, you know, skipping to the main point of the thing was, yeah,

Canberrake Rattlesnake. Yeah. On the second day, we were. We're in that corner, the L corner at Louisiana, Mississippi. And Eric and I had gone one direction within this state park. And Brandon and Owen had gone another. And we'd both walked for an hour, hour and a half, something. It could not be further from one another.

And then we started wandering back. And then finally the calls came through from Brandon. and in an Owen that they said we found a timber, you know, or came back, although I would say timber rather than cane break. And it really did get into the, from my perspective, I think the northern stuff and inland stuff is timber. And it's really a function of coastal form is what you see that cane break presentation. So they did see a really large, gravity female, but then dipped into a tree hollow and stopped. But I was not particularly optimistic. So we had about 45 minutes to walk to them.

And I was not running because I was like, well, they said it dipped into a tree. Yeah. Not particularly optimistic on it. And that was totally accurate and correct. It was well and truly underground. So we had fully missed it. So, yeah, that was, as always, right, that's kind of an interesting situation. But they got photos and everything.

They got a 10 second video. Oh, okay. In which it's very clear that it is sort of timber form, right? Not all that dissimilar to what we've seen in the Northeast. So, yeah, it was a bummer, but it could have been worse. So we basically we spent the first day in central Louisiana. The big learning out of that habitat was, man, the triggers there produce, at least in me, an atomic reaction. so that both my legs just got

he's sort of instantaneous large welts as opposed to small dots. Right. Yikes. Really something. Cajun triggers. They'll get you every time. Exactly right.

So now I guess we are coming up on or are at 10 days out from having been there and gotten those. So they're just now sort of on the mend, I would say. We also, Brandon, you know, being a desert. guy. I don't know that he's had much, if any, tick exposure. So the first contest of the week was the count of ticks that we each had. So we were counting throughout the days, how many, how many we were pulling off each night. You'll be glad to know that I won the challenge. In suitable form, typical form, I guess. But at a relatively low number, it was really that

Louisiana long leaf habitat was pretty bad for them. So those first couple days and then around the Mississippi, all that water. Yeah. And it's kind of that long grass type stuff. Right. But I think, yeah, the winning number was nine over the course of the week, which is not all that many relative to what we've seen in the Pine Barrens. Nine, nine that had embedded or the... No, nine that I pulled off myself.

Zero properly attached. Oh, that's good. Okay. Yeah. Yeah, absolutely. Did you take any precautions, any poison sprays or, you know, techniques to try to keep them out? That was despite putting duct tape around, duct taping our shoes to our pants. Oh, wow.

Yeah, that did nothing for this. Or who knows? Maybe if I didn't do that, then it would be even worse. You'd have nine in your ankles. Yeah, absolutely right. And it did concentrate the chiggers into my ankles. And maybe that was part of the, uh, blistering, I think is what it actually was, is that the concentration within small areas.

So I had multiple bites within like the size of a less than a penny, right? I would have five or six bites within that size. And I think that's what caused that localized systemic reaction. They really really blow out. So yeah, it was, that was exciting. We saw essentially nothing in the Louisiana long leaf pine other than ticks and sugars. See, if you were a birdo, he'd have something to see. Maybe they'd do something to speak up.

I would say, so that's, we were in habitat because that's what you can do, right? You can't pursue threatened or endangered animals. So we were in habitat where something that would fall in that categorization lives. Right. It would seem appealing, given our various lists and proclivities and things. And did not see any. Yeah. Humorously, you then had provided information later on in the week that could have made things.

And it could have made things a little bit awkward, but, yeah, it wound up not coming to pass. So that was fine. But, and I don't know that we were in the same place. But, yeah, that was interesting. The next day was, yeah, really concentrated on Cane Break Timber stuff. Brandon and Owen got their satisfaction, at least somewhat, with a little limited video. So that put the pressure on for the next day. And we went to a different area.

They're a little bit tough in that area, and as I say, being so inland, it wasn't what I would really be looking for for a life or cane break form. So we actually met up with Zachary Gray, who was on the podcast a couple months ago down in the New Orleans area. And Zachary, we went to a couple different areas, each interesting in their own right. And he spotted this, yeah, a gravette female that was posted up in leaf litter, really beautiful, very placid snake, although it was definitely giving us the veronis vibe in the sense that it was very perceptive to our presence didn't move, didn't rattle, didn't

we're getting a little bit of sort of blood python half-hearted eye movement no not even just the eye movement okay yeah where it definitely was perceptive of us yeah thought it's camouflage was still working because you hadn't grabbed it or something yeah and it took a bunch of pictures literally was sworn by

mosquitoes was taking all the zen that I had. I think the satisfaction of the moment was enough to carry me through literally hundreds, if not thousands of mosquitoes all over my face and my hands. Oh, go. Just all simultaneously. That was, it actually, it was funny. So when got up from the photo session, Eric remarked that my face looked like Will Smith in the movie Hitch. And then he was very concerned that I was about to pop into a systemic real.

reaction totally blow out it took about 10 minutes and it actually went down rather than exacerbating which is good yeah um my goodness yeah you are a dedicated and hurt photographer let nobody doubt that i would be like ah get me out of here now you got to just hold still take take the bites i got my voucher i'm out of here absolutely my bus pass yes indeed the bus pass was highly was very much at risk So we left it alone and came back five minutes later and it was gone. So it was doing the verandah thing where it was like, I know what, I'm going to hold my position. And the second they gave me an opportunity to go, I will.

But it was really cool to see the firm indentation from where it had been rusted down. It was very cool. Went back to Mississippi, had a solid day in the long leaf there. Again, few snakes. we did see a baby a young probably a yearling gopher tortoise which is very good. Great thing about that habitat. I still made the scarlet snake and oh we did again with Zachary kind of just him now having such a keen eye for the spots within particular localities. Put us on a cotton out.

That was my life of Western. Nice. So that was really cool. And then cruised with Owen wasn't feeling that. wasn't feeling well that evening. I had a migraine coming on, which I can understand. After all, I would put him through. I wouldn't say anyone called this trip super enjoyable.

But we did then turn out the local southern coperette as well. So that was really cool. Nice. Owen does need a few Smitty tears because he missed out on the Grand Canyon walk. Yeah, absolutely. Yeah. Well, he got some of them here. He didn't cry, but yeah, he got some of them.

Very cool. But the three pit vipers for the area, theoretically, I think what used to be called Western pygmies, but I think if you really want a Western form, you'd probably go further to the west, more like Oklahoma. We missed out on those. I think my understanding is that the feral hogs have really done a number on all the cisteros that were in that area.

So very rare, very rare to find them. So that didn't come off, but that was so, at this point such that would be so unexpected that I didn't even count out on the list that's something that may be fine right but yeah great trip cool man lots of good times yeah yeah lots of southern hospitality and Eric said yeah Eric was the DJ so yeah was yeah yeah yeah certainly I don't know that Nipper would have approved but that's then it was good music absolutely very cool well well yeah Yeah, we'll have to hear all the details here soon.

We'll either get you guys on here or they'll get something going on. Yeah, absolutely. There's plenty of podcast to get on there. All right. Well, our guest may have something to say about sugar bites or mosquito. I don't know if his expertise translates over there, but welcome to the show, Samuel Kerwin. Thanks for being here. Yeah, thank you so much for having me.

It's a pleasure. Yeah, looking forward to this. So very cool. I don't know. I was hanging out with an ant guy the other week, and he said that carpenter ants have, their venom has the same severity or what's the word I'm looking for? Just like toxicity. Yeah.

Oh, LD50. Same LD50 as Western Diamondback rattlesnake venom. You know, it would not surprise me. Yeah. You know, we always say, like, in toxicology, like, the golden rules dose makes the poison. Right. Like, at a certain amount, like, water, it becomes dangerous. Right.

And there's, there's so much similarities when we talk about, like, venom's across the animal kingdom. Like, bees have incredible amounts of similarities. Like, I think something that we always talk about whenever someone wants to get into the venomous field is like, are you allergic to bees? If so, you probably take caution. Right. You might be a little bit more sensitive. Extra caution. Yeah.

Yeah. Just, just, you know, a red. a red flag, so to speak. So, yeah, I mean, the insect world is daunting to, I think, a lot of the snake venom people. There's so much more variety when it comes to just everything, every layer of the insect world is just crazy to some of us. But yeah, it's really cool. The diversity out there. And, yeah, I mean, the fact that a different chigger will cause your whole, you know, leg to swim, like large bumps to come.

Yeah. Things like that. That's crazy. Yeah. All right. Well, yeah, excited to talk Venom with you. How do you, I guess, how do you fit into this whole thing? Or how did you get into herpetology? Oh, man. I always make the joke where I say poor parenting, where it's just like, you know, you start doing something as a kid and your parents probably don't shut it down soon enough, like wandering around the desert looking for critters. And they're like, he's not going to find anything. And then like a 12-year-old finds a snake. And then, you know, you probably should have stopped the kid from digging around to bushes out in the sun. Sonora Desert, but whatever. It just kind of snowballed into this.

So grew up outside, just doing stuff. I think this is a similar story to so many people in this field. I was saying, are you telling my story or yours? Yeah, right? I mean, I think everyone can connect to that story of just like a kid that wanted to start flip over to rocks and then they see something that, you know, they got really into. And I think I had a moment really early on where I was like, wow, this thing can kill me. Why?

right like how like this thing is just a little snakes on the ground like why can it do this and so from a very young age i was super into just the idea of you know venomous snakes in general and like what they could do and why they could do it so that kind of got me started and here i am talking about it so it's pretty fun yeah yeah where did where did you grow up in the snoring desert um so i kind of bounced i had family both in illinois and arizona like if you go to should uh if you go to let's phoenix um you'll notice there's a lot of like a Italian Chicago-style restaurants. There's a ton of Chicago, like, people going down there. It's like a huge trade back and forth. So I would like, you know, be in Illinois catching snapper turtles and then I would go down to Arizona in the summers and find snakes. And I was mostly around Phoenix for the vast majority. And then I actually ended up doing my undergrad at Arizona State, which allowed me to

just be there in the desert, you know, living. And it's just awesome. And Arizona State's in Tucson, right? Or is that? Yes. Yeah. And it's a crazy place. It's got like five different campuses.

I actually was like on the far eastern side of the valley. So closer-ish to like Mesa area. Okay. Yeah. Okay. So gotcha. Very cool. Yeah.

Yeah. Yeah. The U of A is Tucson. You of A is Tucson. Okay. Oh, yeah. I get the two confused.

Now, I will say that you get them confused as well because I listen to your interview on Snake Talk and he mixed. Oh, yeah. Yeah. No, I do it all the time. I do it all the time. I'll get a little forgiveness here. Yeah, we used to have, I'm from northern Utah, and we'd go down, we'd have a couple

of water polo tournaments down in Tucson at Uve. was that what it was? Yes. Yeah. Arizona states up a little further north. Okay. Cool. Yeah. So were you like, I mean, just kind of general naturalist and had kind of a proclivity to snakes or did you kind of consider yourself like a reptile guy like that was your main or venomous guy I guess oh man it was hard you know I can't say like as a young kid I was ever like a venomous kid like just because you know anytime you're working at facilities like I spend a lot of time working at the the phoenix serpentological sanctuary down there and it you know they're not

going to let like a 15 year old work in the venom room it's a big liability and so I was very much like I am like one of the snake volunteers. Like that was my whole thing. But I always like had the goal of just like I want to work in that venom room. I want to like actually, you know, have that as the role. But I was always always like really into the snakes in general. Even when like, you know, every once in a while that place is a huge crocodileian collection. Yeah.

And every once in a while you'd have to move a crock from pen to pen. And they would just, they just need bodies to help like move his thing. And like that was super cool. is incredible experience. And at the end of the day, I was like, I'm just going to go back in the snake room. You know, that type of thing.

So definitely, yeah, the snakes with the direction of the venomous from as far as I can remember. Yeah, very cool. Well, that's a, yeah,

that's a good place to get your, you know, kind of cut your teeth and get some experience with the, the diversity and things. Did they, they have, uh, so along with their crocodilian collection,

did they have a pretty good extensive, like, uh, exotic collection of snakes or was it most? like natives. Yeah, they had a huge collection. Okay. The facility started early in the 2000s as a home for just like anything taken in

by Arizona Gamewood Fish or other state wildlife departments. And they very quickly realized it's like, oh, it's not just iguanas in like salt ata tortoises. It's actually like, you know, king cobras in people's apartments in New York and like puff adders in, you know, L.A. So their collection grew rapidly. And I think while I was there, it was about 250 venomous. And it was, I think, 115 species with the vast majority being exotics.

Okay. And where did they get their funding? Like, how do they fund the place? Lots of state money was one of the big ones. I mean, they worked so closely with Arizona given fish. Right. You know, if there was a huge case, they would often hold on to the animals while the trial is undergoing, just to, like, have a repository.

And so they were really, really big partners with Arizona given fish. They had a lot of private donors as well. People that just wanted to support the facility. Yeah. Yeah, tons and tons of like different kind of varied sources. That's cool. Yeah. Nice.

Did you have any projects you kind of considered your own or that you really were excited about down there? I think back when I was doing my undergrad, not really. At least at the facility, there was a couple like, you know, I managed to squeeze in some school projects. Like, one of my freshman biology classes, you had to just. design your own, like, experiment with a bunch of, like, you know, your lab mates. And I somehow, amazingly, I still don't know how they agreed to this. I was like, let's do like a defensive behavior study between Western Diamondbacks and Speckle Rattlesnakes in the Phoenix Valley. You can see, like, does one rely on Cripsis more than the other?

I mean, because like the hypothesis is like, well, Speckle rattlesnakes are more relied upon Cripsis. They're not going to rattle or the distance that you can get to them will be shorter before they start rattling. And sure enough, like, the data supported it. And so, like, that was really cool to be able to include some projects and to get some non-snake people into that. I still don't know why they agreed to do that project, bunch of like 18-year-old, you know, freshman biologists in college doing crazy shit. That's cool, though. Yeah, I love that kind of attitude, though, you know, like put a little more research into your things, just so you can say conclusively, you know, we've got so many of those like, I don't know, old wives tales in herbiculture that it's like, you know,

it's nice to have some actual data to support, you know, one way or another. Yeah. That's cool. Even if it seems obvious, like, yeah, of course, the spec's not going to rattle as much as a Western Diamondback, but it's, it's cool to actually have the data to prove that instead of it. Yeah, especially, you know, I think in a field like reptiles in general, which, I mean, I think there, we'd be hard pressed to find a field that has more information, like, misinformation circulating. So getting to put some numbers on a page, it feels good every once in a while for sure. I think one of my favorites that kind of goes around is the idea that baby rattlesnakes are more

dangerous than adults because they can't control the venom output or whatever. And it's like, yeah, yeah. Talk about that one. I'm sure you get some information there. That one's really interesting. I mean, I think every piece of misinformation has. a kernel of truth at the very core, and then it gets built up.

And, you know, my advisor, Dr. Macassie is one of like the, he's got probably more papers on this than the vast majority of researchers in the field. And so him and I, like, make jokes about this all the time. But, I mean, the kernel of truth is that we see venom phenotypes

shifting in a lot of different species from juvenile to the adult stage. The caveat to that is, that the volume aspect of the venom gland is an exponentially increasing factor. So as a snake grows, the volume of venom it contains is exponentially increasing. So even if, you know, the venom of a juvenile is three times as strong, five times as strong, I would much rather take a juvenile bite than an adult. A juvenile might give me 10 microliters of venom. An adult might give me 500 microliters of venom. Okay. So the volumes definitely balance.

other out even if toxicity doesn't. Right. That's cool. So, yeah, that's, I wasn't sure on volumes. That was going to be the question for you there. Yeah. So I'm glad you put that out there. And with, with that, so what am I trying to say here?

That the, oh, replenishing the venom stores, approximately how long does that take? And, you know, is it a, is it a? Do you have an idea on that? Yeah. So it is, the short answer is two-ish weeks. Okay. But it's two-ish weeks if all of the venom has been taken out. Right, right, right.

During a very manual extraction. Yeah, we're actually like compressing the venom glands with our fingers. You know, we're going to see roughly at two, two and a half. We say about 16 days is typically when we see the full replenishment of the venom gland. And we actually measured that using transcriptomics. So we can actually see when do the genes coding for venom start being red, and then when do they stop being red? So one of the proteins of venom stop being produced? And we see that typically is around 16 days.

It's like the max. Now, if a snake in the wild would bite something, it's not going to use all of its venom. I think some estimates from Dr. Bill Hayes out of Loma Linda University estimate like a third-ish of their venom yield might get used in a single predatory bite. varies wildly, obviously. Right. And so that will decrease the amount of replenishment time that we see. So it's pretty linear with venom amount expelled equals like time to replenishment. Right.

Does how long they've gone without a meal play any role in volume injected? It may. Is there just too many unknowns out there, you know, these kind of things? There's a lot of unknowns. I actually, when Dr. Hayes first presented some of this, just about like the venom expenditure studies he was doing, I asked him,

you know, how do you measure that? Because, A, like, first off, you have to get them to bite a mouse. Right.

Well, how do you measure the amount of venom that was injected into the mouse? And his explanation for that was not what I expected. So we can detect proteins using a bunch of different methods. And we can, we can actually like take, like a sample of venom, I can tell you how much of that venom is a very specific protein.

He does the same thing, but he does it on the mouse level. So he can actually wash off any venom that's on the surface of the mouse. And then he can, what he calls, homogenizing the mouse, which is to make all the same. So he puts it in a blender. And then he does it, where he samples it. And then he can say,

here's the proportion of the mass that was venom. And then give you an estimate of this is how much venom was injected into that end. Wow. with pretty good accuracy. Enough to at least give him some good numbers and allow him to make some inferences. Okay. So if he wants volunteers for his studies, don't volunteer for that study.

Yeah. That's impressive. Then you have to consider, you know, the follows to that is, was it one fang? Was it two fangs? Right. Was the duration of like the jaws on the actual animal before the snake released? Was it a holding bite? So it sounds like such a rabbit.

but hold to go down as a researcher that I just I asked him about it, thought it was cool. And I was like, can't wait to see you present on it in the couple of years. We'll let you cover that field. Yeah. That's cool. Yeah. Ah, what an interesting thing. Yeah, I was wondering how they measure that.

That's insane. It's a big graphic for sure. Yeah. Do you know, is there anything? Certainly I've heard the discourse around it. And I don't recall which way exactly it goes, but the idea, sort of the effects on humans being variable based on the intended normative prey item for a given species. So I think the suggestion was that there is a certain effect when the anticipated prey is a mammal versus an amphibian. And that sometimes it means if it's essentially intended for a totally foreign animal, that might mean it's no impact or it actually might mean that it's worse.

so that things that are eating amphiomas or frogs or whatever might actually be worse going into a mammal than something designed to impact a mammal. Yeah. Oh, man. That one's tough. I've had a few ideas about this for a long time. They're totally unsubstantiated from a data perspective. But I think there's so much of it that goes into how a bite was initiated not only like from the animal's perspective, but from like the human perspective. of like, did I, you know, put my foot next to a bush and the animal who was waiting in ambush did a predatory bite or was an animal that was not an ambush and, you know, the same situation happened and it was a defensive bite. And so, man, the behavior of a bite is super variable. And then tack on to that, all these other factors of what type of animal was waiting for, what posture was the snake in like prior to the bite, what extremity did the human get bit on?

because the human factor is crazy as well. I mean, like every human reacts totally differently to venom's and not totally differently. But there's variation within there, like an atrox bite that's going to suck for everybody. But the levels at which it sucks are going to be very different. Like, did you eat your weaties that morning? Do you have certain amounts of minerals in your blood that might interact with certain toxins? Like, there's, man, the layers when it comes to that is dramatically, I think, understated a lot of times. I think

as snake people, a lot of us focus on like, okay, what was the snake doing? But then it's like, okay, what are the health issues of the human that just got bit? And like, what's their mass? What's their BMI? What's all these other things that go into it? And the MDs that we work with on occasion often stress their

frustration at the, how variations exist all the time. And yeah, it's just snake bite just makes it a little more complicated and exemplifies some of that variation. Right. I'd, I'd, I'd seen some research that tested, you know, defensive bites versus predatory bites. And it seemed like about half of the defensive bites had venom injection, whereas 100% of the predatory.

You know, that was kind of what I, my takeaway from it. Can you confirm or deny those that remembrance? Yeah. I mean, I think that was also a study that was done by Bill Hayes doing like that whole strike behavior stuff. Right. I think that often gets thrown into the realm of like, oh, it was a dry bite type of thing. And I truly don't think there's anything called like a dry bite ever. Okay.

I think if it's a venomous snake, there's... If you're getting something. Yeah. And it could be a small enough amount to cause a blood blister or like a minor, minor rash. But I think if you're going to get hit with fangs that even have even like a residual amount of toxins on there, you're going to suffer something. the only reason I say that is because I have poked myself on fangs before that did not pass through an animal and were just falling out of the mouth while they're feeding. I've also like poked myself with needles that have like very, very dilute amounts of venom in them and had a blister form. Didn't even hit the plunger, just poke myself with what was residual on the tip of the fang or tip of the needle.

I think Bill's work definitely gets at that like venom can be controlled very well. We see it get controlled. We know that venom is a valuable resource. source. Like it is energetically costly to produce, you know, 50 milligrams of protein and a venom gland and have it stored there for a significant amount of time. And it's more expensive if you consider that that is their tool to get more energy. So they're unwilling to use that. And I often, I, to people that are afraid of snakes, I think that that is a great line of dialogue to use with them. Just describing that it's like, you don't want to use it on you. Yeah, it's a tool.

I mean, just like anyone who's out in the wilderness, you know, if they're like hunting squirrels with the 22, you know, they probably don't want to use all their ammo on a bear. They probably just want to try to scare the bear off before they ever try to waste, you know, their resource to survive and live. Okay. Yeah. And is so is there anything known about like the mechanics of a bite, like a maybe defensive bite where they're maybe trying not to use their venom? Or is, you know, a bite, a bite, a bite, you know, what I mean? Does that make sense? Yeah, yeah.

So, mechanics in terms of, like, how the venom is administered and like what choices go into that? Right. Or, I mean, are they controlling it at the pumping out of their venom glands? Or is it like, if the fangs go in, venom's flowing out? Is there control, where is the control lie, I guess? my so a lot of the work that that my advisor and I or really my advisor has done and then I've kind of tacked onto in the past couple of years is really looking at like the physiology of how his venom is made and doing that means that we have to you know look at a lot of venom glands and so that combined with you know it like working in a museum where I'm preserving specimens a lot of times you can very clearly see the musculature that is designed for venom expulsion and it's all based around. around like the actual gland itself. And we call it the compressor glandulae muscle.

And the compressor glandulae, it doesn't necessarily squeeze because squeezing is inefficient. What it does instead, and it's something that almost every human is familiar with, is it rings out. So it actually wraps around and twists in like a torsion motion, just like how you would trying to get the water out of like a wet t-shirt. And it's very, very effective. And it can induce, I think up to, I might be wrong in this. It's been a while. I think it's upwards of 34-ish PSI within the venom gland. The membrane, like the actual fang itself,

because this is also something that I think people assume, is that it's wrapped in that, the fangs wrapped in that sheath. The sheath will slip up once the fang actually punctures something. I don't think, and I don't see any reason why this would be true, I don't think it actually is the trigger mechanism for venom expulsion. Okay. I think it simply allows for easier venom flow because that membrane does actually cover the

external region of the fang. And something that we see when we do venom extractions is if you don't clear that membrane, venom still pools in the membrane. It is just trapped there like a little water balloon. And so then we have to like, you know, be finicky and try to get it around a little water balloon. But venom can still flow without that membrane being lifted or removed from the actual thing. So is the is the membrane resistant?

to puncture from the fang? Yes, in a way. I mean, it's super, super elastic. Right. It's very similar to like, you know, any oral, like, tissue surface that you have, especially like cheeks where, yes, you bite them on occasion, but very, very elastic tissue. And so we often see that it can stretch very, very far.

And we can actually slip it back and then it folds up very, very neatly up in the roof of the mouth when you see those really cool, like fang shots that people take all the time. right very cool yeah this is stuff i mean you maybe think about it in passing but that's really cool to hear the actual uh you know truth behind the thoughts i guess yeah absolutely and while we're there um would you mind going into your master's project a little bit this fell into the box for me of saying i hadn't even considered it as an issue which is amazing right as sort of science of question it was something i'd never considered and the answer that you were able to on earth is pretty amazing.

Yeah, yeah. Man, this has been like a really, really cool thing. And I love getting to talk about this because now in my research I shifted dramatically. There's a few decades of work that kind of laid a lot of the base level information that we went on for my master's work. A few individuals from my advisor's lab, especially I think it was like late 90s. It was 1998 is as far back as some of this work goes. where my advisor was actually teaching an anatomy and physiology class, like a human anatomy and physiology class,

which he doesn't like teaching about the human stuff, but he has to hear once in a while as a professor. And he made this observation when he was doing some cell imaging and just like some histology, some cell staining. And he noticed that there are cells within venom glands that look remarkably similar to the gastrointestinald, system of humans where we have these cells in our stomach that are actually producing acid, which allows for, you know, digestion.

It's a huge part of it. And so he made that observation and he kind of just put it in the back pocket. He said, cool. He had a student that came in, looked at it a little bit more, and he's like, okay, I, yep, these are definitely acid producing cells of some kind. That's about it. That's all they got at that point. In 2006, they had another big stuff.

on it where they did the same thing. They pulled everything apart. They looked at all the stains and they wanted to see, okay, if it is acid secreting, is it the same type of acid secreting that we see in humans? Isn't an actual parietal cell from a human GI tract just now in a snake venom gland? And what they saw suggested, no, it's not the same thing. It's a little bit different. It's maybe a little bit more not necessarily inefficient, but it's not identical. It definitely has a reduced functionality in terms of acid secretion. And then that begs a question, why on earth are you pumping acid into a venom gland? Like what is going on here? Why just there's so many more questions are popping up at this point. And it all comes down to another observation that my

advisor made. He was just on a whim. He took the pH of some venom that he got from some rattlesnakes and found, okay, the pH of these two rattlesnakes, different species, is the same. It's like 5.5. so slightly on the acidic level. He contacted a collaborator that at the time was working on biddis and a bunch of caboons and puff adders. And he asked, you know, next time you take venom, just take a pH reading, let me know what you get. And the advisor was like, his collaborator, sorry, was like, I think it's around 5.5, 5.6. He's like, well, that's super strange. Like you have two, you know, groups of animals, two different continents that are now having the exact same physiological number coming out of an excreted like that are.

file. Again, why? Let's dive into this further. And we started working with the genetics lab down in University of Texas Arlington, the Dr. Todd Castro in his little lab. And they do a lot of evolutionary genetics and transcriptomics. And they found that during that venom production cycle, yes, venom is upregulated. We see tons of venom proteins being produced. We have all these venom genes being transcribed and everything like that. But there's a lot of other things going on the background. Upon venom excretion, there's roughly like 2,500 different genes that get turned on or differentially regulated

within a 24-hour period. And it's a huge shift. And you can actually watch the cells in the venom gland expand and grow to accommodate all of the protein production. The images are insane from some of these studies. And among those are all of these genes that regulate for these acid secretion. creating pumps. And so that study was completed in 2020. And it led us directly into my master's program, which I began in 2021, which is let's solidify why they do this. Let's try to figure out like,

okay, what are the actual mechanics of this and what is it doing for the venom? And then let's also try to turn them off and watch what happens. Like can we turn these off in live snakes? Right. And stop this acid production so that we can really put it in the coffin and support this idea of, you know, why, why potentially the pH is being decreased. What we found was two things. Number one, as soon as Venom is put in that higher pH, because it's at that acidic pH, when you pull it, put it in a little vial. So as soon as you put it artificially at a higher pH, things start destroying themselves

very quickly. And this is mostly due to a couple toxins being protein targeting toxins. So they're very good at destroying protein. Well, venom is also protein. And so they start tearing each other apart. It's a blood bath on a biochemical level. And it just results in a really, really inefficient venom at the end of the day. If you let it sit in that higher pH and then you try to test it again, you see dramatically reduced toxicity across the board.

How high are we talking? What kind of pH does it start to degrade or act on itself, I guess? So we put it, we were doing this at physiological pH of around 7.4. That's really where we wanted to see. that's a super common pH in the biological world. Almost every animal has that as like their blood pH or tissue pH, unless it's like the stomach or other organs. So we saw that decrease to functionality, huge red flag.

Okay, maybe it's just protective. Maybe that's all it is. Maybe it's just trying to prevent the toxins from degrading. These are animals that don't use venom very often. Like some of the snakes are going months and months and months without food. And they also don't live in the most, stable environments. We talk about like biochemical stability. Like we, for us to keep drugs, we have to put them in freezers.

These guys are living in the Sonor Desert. It's probably like 109 right now. And so it just, it goes on and on and on. And I'm like, okay, this is starting to become a much clear picture. The next big question was why? Like other than protection, you know, now you have an acidic venom that's sitting in this tube and it's not really working. Like it's everything's super and efficient, the proteins aren't folded properly, they're not destroying themselves, which means that they're not active. How does it get turned on? And this was like the kind of aha moment for this whole study was, oh, the pH 7.4, that's when they work. So our bodies provide

the perfect environment for these toxins to fold properly and kick on and start, you know, go to town. And this kind of was this really, really cool moment of like, wow, these animals are using our own physiology against us and their own praise physiology against them. And it's such an elegant solution to a really layer problem of toxin production next to your brain over long periods of time. And it's just, it's really, really cool. And man, there's so much more to learn about these things. So much more.

That's incredible. Yeah. Absolutely. Did you guys wind up seeing where you, did you have the capacity to evaluate reducing, um, Or making more basic the venom within the snakes. Yeah, that was probably the toughest part of the entire study was like, okay, we know what these kind of do. Let's see if we can turn them off in a live snake during that venom production cycle that, you know, they're usually super active. And we used a drug that actually targets these very, very specific pumps.

One of the great things about working research is that you find a bunch of weird drugs that are just like out of the middle of nowhere. like they're not pharmaceuticals. You know, they may have been tried to be used as, you know, some sort of drug product in clinical trials and then they didn't make it, but they're still for certain. Yeah. We found one that does work on these things. And we tried, I think, four or five different methodologies that were as, like,

uninvasive as possible to try to not mess with anything else. And it just kind of led to headaches and headaches as most research does at times. And so we ended up just directly injection. injecting the drug into the venom gland. And we did have some success with that. We actually had venom pH increasing significantly across all of our trial animals up to about 6.5, 6.7 was about as high as we were able to get it. And we saw pretty dramatically reduced venom functionality at that point.

But it was a different type of impaired functionality that we saw with just the artificially improved pH, or officially increased pH. where, you know, there's definitely another role going on. You know, it's not just pump acid into gland. It's more so probably pump acid and help venom be produced type of thing. There's layered functionalities to this in any biological system. If you mess with one thing, other things are going to inevitably start going wrong. And so, you know, that's definitely part of it.

But it was just a really cool look at what a lot of us, I think, forget. about when we talk about venomous snakes. We always talk about the venom itself, but man, the way they produce it is just awesome. Right. So did the LD50 dose go up with those 6.5 animals? Yeah. And so we never did those LD50s just because they're pretty variable in general. So what we actually do is we can assess specific toxin families.

So we can, you know, if I want to assess snake venomatiloprotonase, which are really, really common in snakes that cause tissue damage, and I only want to assess the functionality of those, I can actually do a test in like a test tube that will directly quantify that one toxin family. And so it's a bit more specific and allowed us to pinpoint, okay, which toxins are being more negatively impacted by this increased pH versus others. And there are some toxins that don't care, which is really interesting because those happen to be the same toxins that cause prolonged issues in humans. And they're not just the ones that hit you hard up front. They're the ones that cause issues over the course of like a week or two.

So there's a neat correlation there with the stability of toxins and the effects that we see in humans. So the ones that are stable, both at low and high pH, those are the ones that kind of remain active for a longer period of time. Yes. Yeah. Especially some toxins that have caused some havoc in the U.S. in terms of like the medical field that I've kind of encouraged a couple new anti-venoms to be introduced. We're definitely up there. There's a lot of reports of human patients that, especially, I think, pre-2018, it was a low incidence rate, but it was enough where patients would be clear from the hospital, discharged.

They would have been treated with antivenom, and they will have no severe symptoms at the time. And a few days later, they would come back with a recurrent. of this coagulothopsy or disruptive like hemostatic system where the blood couldn't clot or was either clotting too much. And that was a big issue. It meant that the antivenom was leaving the body before the toxins were actually being degraded or metabolized. And because it's chagiotopathy, we can narrow that symptom down to two major toxin

families that we refer to as serium proteases. And when we were doing our study, the serine proteinases, for two toxin families that did not care about pH changes. They are hyper-stable enzymes. They're incredible at what they do. And it just makes sense that, of course, those are the ones sticking around causing issues. They're incredibly stable,

even in the lab when we try to mess with them. So really, really cool correlation between those two just kind of observations. So how does their effector function differ in the venom gland versus when it's in a person? And how does the venom gland is protected from these serene proteases? So a lot of it is due to targets. So if you, there's one, like really two ways to stop in enzyme. You can either destroy the enzyme itself, causing it to like, you know, fold improperly or actually tear it apart. Or you can remove its target, right?

If you take away the substrate that that toxin acts upon, then it can't do anything. So these are toxins that primarily target things that are in the blood. in the heostatic system themselves. So inside the venom gland, there's no circulation. It's just a actual pocket of space. So there's nothing for them to act upon within that area. Gotcha. And do you notice a more higher presence of these proteinases in,

in like more advanced venomous snake species versus those that just kind of have more of a primitive venom duct? Or is that still unknown? It's an interesting, there's not a really good set pattern on where we typically see, you know, these proteases start to come into play, or at least the serine proteinases. They are oftentimes, if they are present in a venom, they may not be one of the like predominant. toxins. They may be present in a significant amount, but to me, a significant amount in a venom is 10%. And so you could have other proteins that are present in 25, 30 percent that are the predominant

toxin family within that cheese. And that's typically where we see variation on those very, very dominant toxins. There's a lot of other venomes out there where you've got 50, 60 components. and, you know, 45 of them may do something, but they may not be as important as like the three or four very, very big main characters. Okay. So in a typical venom, you're seeing probably up with 50 or so different components or active ingredients, if you will? Yeah, I'll say with vipers, definitely. Okay. Vipers definitely are, they probably reigns supreme in terms of venom complexity.

just generally. There's definitely some vipers that break the rule and decide that they want to be like elapids. And just for comparison, what do you see in an alapid typically? Alpids actually typically have, they'll really be dominated by a couple, like two or three

super, super major toxin families. And sometimes it's only one major toxic family. And we might see variations within the different isoforms or kind of flavors of that toxin within that one species, but they have very, very simple venoms. One of the ways that we visualize venoms is using something called gel electrophoresis, where we can actually separate the venom by all the components based on their actual size.

And what we see with vipers is you have this almost like a ladder where you've got bands just appearing all over the place with varying intensity. Some are super dark, some are very, very light and faint. And if you do the same thing within a lapid, a lot of times what you'll get is one, huge band at the bottom and then a few very, very, very, very light ones just kind of scattered around. But it's nowhere near what we see in the vast majority of vipers, especially rattlesnakes here in the U.S.

Okay. Interesting. That's cool. We've got the most advanced venomous snake, snake venom in the new world. Or in the new world, I suppose. The acidification, right, being maintained in that state, that it does apply to the enzymatic toxins, right? So we're talking principally about viatism.

that this is not an impact that we're seeing in a lapids. Is that fair? Yeah. I mean, there's more variation in the in the venom pH when we get to a lapids. There was a paper that came out about spinning cobras. Well, not just spinning cobras. A lot of cobras. And they're different venom pHs. And it definitely had a wider range. I think the highest I saw there was like 6.2, which is something that you would never really see in a lot of vipers. and that's not a huge jump, but pH is a logarithic scale. So, you know, a change of, you know,

0.5 is actually very, very significant in terms of, you know, what the pH value is inferring. And one of the things I notice is that the lapids that have that very consistent, like pH, that Viper level pH of 5, 5, 5, 6 are all almost always spitting cobras that do have a large amount of enzymatic toxins. So it's almost like,

because they're going to use that enzymatic toxins, they also have to do that viper thing of having acidification in there. Interesting. What about a viper wannabe elapid, like a death adder or something? Do they have? I don't know. Is it a good lifestyle play a role where they're more ambush predators versus like the typan or something that's chasing down its prey? I have actually asked a few researchers down at the University of Queensland where Dr. Brian Fry is to like, you know, next time you guys take venom or if you do ever take venom, like, just give me a pH reading. I mean, it would be interesting to know. I mean, Australia is an outlier for a lot of different reasons. And it would be interesting to see if they follow their trend of just being kind of weird from an animal perspective. But I'm not sure. Australia is kind of a black box for this. be some literature out there, but I have not seen it if so.

Interesting. You think with so many species that are venomous down there and so many lapids that have varying degrees of human impact, they would have a better idea. Yeah, I mean, they have tons and tons of research. Right, right. Their knowledge level is very extensive. I will say the acidification stuff was kind of, it came out of the blue. And it's a bit niche, and it's more of,

it definitely falls in terms of like our researching categories into a very kind of almost ecological like biochemical ecology or biochemical physiology. Right. More than, you know, the human impact side. Because while it's cool to have those correlations and observations, I think an MD is going to look at that and be like, I'm not going to acidify the blood of my patient to try to cure him. Yeah. Has no applicable avenue. This is cool, but whatever. But from an evolutionary perspective, that's really important and interesting, yeah, for sure.

Okay. That makes sense. Yeah, I guess we won't bag on the Australians, especially here. That's one of my favorite places. So got to love the Aussies. Yeah. When you've talked about the master's project before, you mentioned there being hiccups along the way. And I was just wondering if you could talk a little bit about sort of what does the scientific research process

look like and what are the sort of unexpected challenges and trials and tribulations you run into with that? I know Justin can relate. So that's why I think to actually hear about it. And too often, right, I think that doesn't come out. It's focusing on the positive results rather than really getting into the challenges and difficulties you can run into. Yeah.

I think even as researchers, we really want to focus on the positive results sometimes if forget about the headaches. That's what we publish, right? We don't publish negative data usually. Yeah, the headaches in a lot of this research are, you know, they're in the scientific ask, like in scientific context, they're very human where, you know, we just have those moments. We've got to, like, sit down and just put your head up between your hands and just kind of like rethink a lot of different strategies. One of the things I was finding early on in like some of my literature review was, has anyone like,

like tried to alter the venom gland environment during like in a live animal and the short answer is no. I looked for a really long time and I was kind of crestfallen that I had that we just, I thought we had a dead end. And we, I kind of mentioned we wanted to be as uninvasive as possible. But uninvasive as possible still means kind of invasive, especially for this context. Especially when I had the experimental design at the time, it was very dumb. When it worked out, it was great.

It was super smart after it worked. But when I was first trying to develop it, we had this idea of, you know, you have a snake with two venom glands and each venom gland is totally separate. Biologically separate. They're physiologically separate. They can respond to different signals. They have their own venom production. They're not sharing venom at all. Can you give one a treatment and the other one a placebo in the same animal and reduce the animal to animal variation? Yeah. And internal control. Yeah. And at the kind of the front end of that experiment, I was like, oh, this is so cool. And at the middle part of the experiment, I was like, oh, my God, this is so torture because we have to give a drug to each side and not impact the other one and find a way to administer the drug that keeps it in that specific area. And so we tried something at first called osmotic pumps. These look like the pills. And it's a gel membrane with a little balloon inside. and then a little cap on the end. And you can fill it with a certain substance. And the gel will take in water from the surrounding tissue that's been placed in and put pressure on the balloon.

And the cap will ensure that you are only pushing out a certain amount of your drug at a certain rate for as long as it will allow. And so it's a really, really cool little piece of technology that works really, really well in mammals. Yeah. Yes, all zets. Yeah. We use them all the time. Yeah, they're amazing. And they work great in mammals. And, you know, I thought, okay, this is going to be a cinch. It's going to be awesome. It's going to work perfectly. I found out very quickly that when they're administered subdermally just above the venom gland of a snake, they typically don't have enough like just ambient osmotic pressure to actually push any drug out. So what resulting is, is we would take the venom or take the pumps out of the, the, the dermis and we would find that there is a full reservoir there. And so, and it was like after a week. And so we threw that idea out.

And we started trying to do, you know, a bunch of different things. We tried priming the venom glands because the last thing we want to do is puncture them. These things are really, really resilient. And we never saw any adverse effects from doing this. But we ended up having to in the end is actually giving an injection directly into the main

venom gland luminal space and then letting it go from there. We would do two injections per like venom production cycle, and that was pretty good in terms of like actually getting some some pretty good results in the end. Hmm. Interesting. Did you ever consider anything like RNAI or anything like that where you're blocking the genetic or the transcript? Yeah. We did. We thought about that a little bit. We had a we wanted it to be as. Well, I think the very core issue was like, this is a master's project. We got two years. Yeah. You know, let's see what we could do.

Yeah. If it doesn't work quick, get rid of it. Yeah. And it really was a shot in the dark. Like, yes, we had a good idea that this was, you know, what was going on and that we could potentially inhibit it. But I think we really, at the end, we're just kind of hoping that it might, you know, show us some results. now with the confirmation that we have I don't think any of us would

hesitate to try something a little bit more I guess intense as trying like you know inhibitory RNA see if you could block the transcript itself we actually for a moment discussed doing gene knockout snakes where you actually like knock out the whole gene for it that has its own complexities of like

well you have to do embryos and then grow them which is you know bit of a pain. That's more headaches that I want to take on. Yeah. But yeah, I mean, I think now we are, we're interested in potentially doing more in the future, but maybe when our plate is left full or less full, which might be never. Got to pick, got to pick that low hanging fruit first, right? How about an injection through the, through the fang? Yeah. Yeah. Yeah, yeah. we try that as well so we didn't try it we talked about it extensively yeah uh i got talked out of the idea um by my advisor because you know he's been studying venom gland physiology and morphology for a lot

longer than i have right right um you know he he might not like if i say this but before i was even born he was studying it uh and you know we talk about you know snakes having this like really good like big identifiable gland. And yes, it's identifiable. Yes, it's this big pocket of space. But then you go through a little duct that leads into a little tiny accessory gland. And then from there, you have another duct that then leads into the fang. So your injection would have to pass through, go through a like an actual valve into the accessory gland.

Go through another valve and then into the main venom gland. And maybe it's the right fang. And like, let's say the snake has two fangs on one side. And one of them is a looser connection than the other one. and you go through one, it doesn't make it, it pulls up with a maxillary bone and doesn't actually go anywhere. So that was a little bit more variation than I think we wanted to try. Okay.

We did think about that. Yeah. Well, that was kind of my next question too, is, you know, when they replace their fangs, how does, you know, how does that work? That's crazy. Gosh, I don't know. I don't have, yeah, I don't have as much information on that. It's something that I've talked about just like, you know, you have a beer or two at a conference and then you and three other scientists start talking about all these different things and just thrown ideas back and forth.

And Dr. Bill Hayes and I, once again, we're like chatting at a conference. And I was like, I think it goes like this. I think they like they grow in it. Like a fang comes in from where they're all like in development. And, you know, the membrane around like around that maxillary region grows to like accommodate it and accept it. And he's like, no, no, no. I think it goes like this. And so we went back and forth in ideas for a while.

And then we just settled on like, well, we'll have to test it one day to see, you know, what goes on. It's, I think it's going to take someone that's like more of a developmental biologist, individual, someone who's used to doing things like. Tracing. Yeah. Yeah. Just a ton more in-depth, say, like con-focal microscopy could probably come into play, looking at tissue growth and how it's growing, things like that.

But, yeah, something that I'm definitely not a, equipped to answer in the best way. No, that's, that's a, it's fun to think about those things for sure, you know, and just kind of, I mean, somebody with your education and background would have a lot better. I mean, if I'm putting it out there, it's, you know, simple and stupid. I mean, I mean, I think anyone who's seen like the skull of a snake or has like looked very, very closely at how those fangs connect can make a bunch of inferences. I mean, you see like, you know, if you're looking at. a maxillary bone, you clearly see two ports and you clearly see like that they're connected, but you also see like if there's one fang in, it's a very porous connection. And it's bone. It's set in there with bone. But how does that connection grow? When does it grow? What signals it? I mean, there's a million question there that, you know, I always ask. And I, yeah, I think all it

needs is a couple observations and anyone can probably have some good ideas. Right, right. Yeah. Just and I guess one hypothesis can be as good as the next. Yeah, until you get those numbers. You don't know. Exactly. Very cool. Yeah. Absolutely.

So you want to talk a little bit about what you're doing now and then both, well, the whole lab, right? Everyone's getting involved. They talk a little bit about the whole idea of the customer, you know, essentially the viruses and e-cells being hyper-focused. All that stuff. That's mind-blowing. Yeah. Oh, man. I, you know, I got to present this stuff at Copark where obviously you heard it. And I loved getting to present this stuff there because that is a uniquely invested crowd when it comes to, you know, the whole topic of venomous snake bite treatment and, you know, what are the innovations that are coming in the pipeline. I think a room full of, you know, field herpers are going to be very, very attentive to that. that topic to see, you know, how much, how expensive is it going to be? Is it still the same price as moderate antivenom? You know, can I have a little flexibility maybe next time I go out?

Yeah, there's, there's a big shift. And describe, I kind of have to start from square one, kind of like I did with the talk, to really where antivenom begins. And it begins, like using basic rules of immunology way back in the kind of late 1800s with bacterial infections and bacteria, especially diphtheria, will produce toxins in the actual surrounding environment. And a couple of researchers found out that if you take the liquid off of like a diphtheria culture and you inject that into an animal, then that animal will produce antibodies that protects against the toxin that the bacteria produce. And so the first ever antivenom is not an anti-venom.

It's an antitoxin against diphtheria and tetanus. So it's really cool to see how that gets published. And within two years, another researcher saw that and went like, snake venom, easy, easy jump in logic. And like that to me, like some of the early developments are really, really cool to understand. Now, at the time,

they didn't really know that snakes had different venoms, and they're wildly different to the point where you can't just have a cobra antitoxin and then use it in the U.S. Right. Obviously doesn't work like that. But at the time, like they didn't know. And so they were just taking animals that looked similar within a specific region, using them to create this kind of anti-venom by taking the venom,

introducing the large animals, and then just taking that plasma and ejecting it to humans. And that was problematic. You can't just inject full animal plasma into human. Their bodies tend to freak out and not too super well. And so a lot of the innovations in anti-venom from like 1890s, ish all the way to really like 2016, 2018,

we're entirely focused on two things. One is making anti-venoms that are targeting geographic regions with hyper-specificity, but with more specificity than what normally had been done. And then also making it a lot safer.

And like so that humans wouldn't react and go into anaphylaxis when you're trying to treat a snake bite. And the anaphylaxis part got handled pretty early on. There's a couple techniques that we use to kind of clean up antibodies, and they're now pretty safe. Like, the adverse reaction rate is in the single digits in terms of percentages,

nowadays, especially in the U.S. And honestly, at the end of the day, if a medical doctor cannot treat anaphylaxis in a hospital, they probably shouldn't be a medical doctor. Like, you have every toolkit in the box ready to treat some person going into anaphylaxis right in front of you. And so the moral of the story is, anti-venom's work in geographic regions nowadays.

And you can, even with a mild adverse reaction, easily treatable and not even significant anymore. So we have safe products that work in whatever space that they're used in for the most part. This is kind of a rough design, though, still. Like at the end of the day, it's gotten more specific, it's gotten safer, but you are still taking venom, injecting it into a big animal, pulling off plasma and just refining it a little bit. That's it. It's the same formula that was first used in the 1800s. It's not like we've really changed the game. We've just gotten a little better at playing it. And we typically refer to this as kind of like a shotgun approach, right? Where you're not targeting individual toxins. Like I talked before, you know, you can have these hyper complex

toxins or hyper complex venom profiles within, especially rattlesinks in the U.S. And only three or four of those might be main characters. You're going to have a bunch of stuff that's not necessarily toxic. They could be, you know, other peptides that are signaling things. It could be like cellular debris that's produced in the actual venom gland and just pushed out. It's not even part of the venom. Just foreign. Yeah. Yeah. Yeah. Your body's going to mount an immune response to anything foreign. Yeah. And there's a couple people that have done some work on, you know, how can we make modern anti-venoms, like make slight adjustments to even account for that shotgun effect. And in Crowfab, which has been in the U.S. medical system since around the 2000s, like, did a pretty good job at that.

They were one of the first ones to really do this. They did affinity profiling or infinity purification where they actually have a column that's lined with venom toxins, like all the toxins that they really want to target. And they would take this antivenom or plasma straight from the animals and they would feed it through the column. And as it goes down the column, all the antibodies that are actually attacking the targets, will stay in that lined column. And then they can then remove those and have a much cleaner product. That is typically why a crowfab is a much more expensive anti-venom. So it's not just the U.S. medical system,

although that does play a big role in the price. Like, it definitely is a good product. But it's still, you know, the same thing. Like you have a geographic venom that is supposed to cover, you know, how many species in the U.S. and it's supposed to cover all of them with pretty good effectiveness, and even with this purification, it's still really, really variable. And on top of that, you know, in a lab setting, for me to ever see really good inhibition

of a certain venom, whether I'm doing it an animal model or I'm doing it in a test tube, I need almost 100 times the mass of antivenom that I would venom. So if I use a milligram of antirem, or a milligram of venom, I would need 100 milligrams of antivenom to get anywhere close to trying to inhibit that. And from a biological, like, perspective, especially that biochemical perspective, that is horrendous. That is insane that that is the ratio that you need from one to the other. Is that just the antibodies binding to the protein? It needs that ratio?

So that's to see like a totally inhibited effect. So 100, 100% inhibition of like these toxins in a test tube, required. you to get up to that much, if not more, for some of these toxic families. And that goes back into the idea of we have venom variation, right? Yes, this is a geographic polyvail and antivenom. It's supposed to cover everything. But you, like, let's say you have a certain amount of your percentage of antivenom as targeting those serium protenases.

And you have one species that has a ton of them. You might, you're going to need more antivenom to cover that one species. And so, you know, there's so much variability with that. It just adds layers and layers to it. But at the end of the day, it's still the shotgun approach. It's a cleaner shock. You've gone from like birdshot to buckshot at this point, I guess, but you're still doing a shotgun approach.

And, you know, like that's cool. It works. But it only works in the U.S. really because we have infrastructure, just a point. Right. We can dump 20-something vials in a person. There was an Eastern Diamondback bite in Florida by an influencer. And I think he got 88. vials of anti-mower.

I think it was earlier this year or like late last year. Yeah. I just remember like watching the whole bite kind of play it on social media and I was just like, that is not going to be good. And I think they ended up giving him almost 90 vials. And if each vial is retailing for, you know, $13,000 or $15,000, I think I probably would have let the bite take me at that point. Like that's just insane. Like that's astronomical. Yeah.

And so that goes to highlight, like, you need that much antivenom for a single bite. That is outrageous. Yeah. Because each one of those influencers, they got the cash, you know. Gosh. Oh, boy. I just, I would pale to see what that. Right.

Right. But if each vial of antivenom contains 75 milligrams of, like, crude protein. And that snake bite was probably only, you know, 30 milligrams of venom. that's a huge, that's a huge amount. That's like a one to 300 ratio. Yeah, right. It's crazy. Wow.

And so there's a need for a shift in how we do things. I think that that is kind of this long-winded way to say that. Like we're here at this point. You know, it works in the U.S. We don't think about it as much in the U.S. But there are other regions where, like, you know, you don't have any vitals to give to a patient. You have maybe two. And you better hope that two is enough.

So that they can make it through the night and maybe you'll give them one more. What about like cell-based synthetic approaches like hybridomas or something that are producing targeted, you know, specific antibodies that work? And then you could kind of mix them in a cocktail depending on, you know, the venom components in the region. So it's super interesting to bring that up because that's kind of where like a lot of this is going for the most part. So we in collaboration with a bunch of different labs. Oh my gosh. I think there's four countries involved. The vast majority of the labs are in Europe. And the big kind of brainchild of the projects are really in Copenhagen, Denmark. The Denmark Technical Institute, Denmark Technical University, I think the lab is currently headed by Dr. Andreas Laustin.

And this is a antibody development lab. They're not just a snake venom lab. A lot of them. have never even like seen any of these animals before. And sometimes like we'll like send them pictures of stuff from our lab and they're like freaking out and they love it. And you know, we love to chat with them at conferences. But they really study antibodies, study how anybody's interact with things,

you know, can we create better antibodies? And they reach out to us along in collaboration with a Mexico lab, talking about like doing some work with these nanobodies. And nanobodies was kind of a foreign concept. to me, I didn't know much about them. And we talk about antibodies being the things that have always been used. And those are like those really classic Y structures that we see all over the place.

They're probably one of the most abundant antibodies in humans. But not all mammals are created equal in the immunological sense. Camelids like llamas, alpacas, camels themselves, actually produce things called nanobodies. And so it's the same kind of basic structure where you have those two kind of parts of the why that are binding to different antigens and inhibiting them. And then you have that kind of big stem part. But those two little top regions are really small. They're only about a quarter of the size of what we think about in like an IgG or

immunoglocloglin you find in a human. And so that became really, really ideal for a couple of reasons. But one of the big ones was the whole idea of you're injecting an antivenominty to a patient. you're injecting it into the bloodstream. The venom itself is not in the bloodstream. It's in muscle tissue. It's in lymphatic tissue. And so the antibodies are really good at binding up, you know, anything that's in the blood.

But that's why you have to keep redosing antivenom is because it's like you'll have toxins leaking into the blood throughout the course of a bite. The nanobodies are small enough that they have really good distribution qualities and they can get around to some of the areas that the actual antibodies can't. And so that was a really problem. thing. They're also a lot more stable, which means that they have a longer shelf life. So another like kind of win for them. And one of the things that this lab did, and I had to, I did a lot of reading to kind of catch up to where they were and just understand some of the basics that they were sending me. These guys found a way to really start at the same place that everyone else did. Let's take whole venoms from an area, you know, like Africa. And let's try to

take whole venoms from a bunch of different elapids. So mambas and cobras primarily, let's inject it into these camels. But instead of just taking off the plasma and using these nanobodies, let's pick out the best ones possible. And so they started off with tens of

thousands of different nanobodies that they got from these animals. And now you could have 3,000 nanobodies coding for one single toxin, but they only wanted the best, right? They only wanted the most efficient, the best at binding, things like that. So they did something called phage, display campaigns. This is like where stuff gets crazy. I had to do it. This is where like my knowledge

kind of fell off a cliff and I had to, you know, find a way to somehow keep up in conversations with them, where you are encoding the genetic, the genetic code for each of those, you know, 3,000 nanobodies is given to bacteriophages or viruses that prey predominantly upon bacteria. They will present a physical copy of that externally and then you can allow them to sort themselves out based on how well that nanobody that they're presenting actually binds to your target toxin. Because they carry the blueprint genetically for that antibody that they sorted out, the nanobody, sorry, you can take that genetic code and implant it into E. coli populations and then just like you know, you have a batch of bacteria in brewing beer, you can have all these E. coli producing a nanopausea.

bodies in a cell culture, these huge bioreactors. And so your antivenom doesn't come out of an animal, comes out of a spigot at the bottom of a bioreactor, which is just incredible. And it kind of, they took it even further. And they said, okay, if I have a snake that has these three toxins and I've got these three nanobodies, if I stick them together and put them in the animal, does it save the animal's life? And it did amazing.

I mean, every, every test we ran was incredible. And we did a lot of the animal testing in Colorado. And it was just, it felt like every day we were doing it was just like a breath of fresh air just to watch how well it was working on some of these mice. It was incredible. I'm curious just as a detail of that study and you can continue on beyond there. But when you're doing these protection studies, are you dosing the venom via injection and then dose? I mean, everything's kind of controlled and. Yeah.

Or are you testing different routes of venom exposure or areas where you're injecting? Like, how is that? Is there a standardized protocol for that? There's a couple steps that we take. Typically, first step is, does the thing work if you stack the deck in its favor? Right, right. So in this case, pre-incubation studies are the, that is the first thing we did. We have this product, we had this drug.

It looks like it works at a test tube. Does it work in an animal? And first things first, let's take the actual nanobodies and let's take the venom. Let's allow them to mix and interact. And then let's introduce them to the animal intravenously. And if you introduce the venom alone to the animal intravenously, like especially like a mamba, they die within about 30 seconds. It is, it's kind of insane.

Because we would inject regularly three times the lethal dose. So for that mouse, he would get his own personal dose. and usually it's like a 20 gram mouse, you would give him micrograms of a certain venom. And that is enough to kill it in roughly 30 seconds through the intravenous route of administration. It's actually kind of alarming when you give the injection. And by the time you put the mouse down,

it is totally paralyzed. It's a little eye-opening as people who work with venom sticks. You don't want to mistake that mouse for your hand. Yeah. And so we just want to see it doesn't work, first and foremost. And we had great results. almost everything worked just across the board for that pre-incubation. There was a couple of species that we were actually testing that we didn't think we would get

100% indivition and we didn't. And so it was nice to see like, okay, our line of thought is correct, right? The ones that we aren't confident about are the ones that are not showing confident results. That's good to see. At least we're like on the right track in terms of how we're thinking about this. We then went on to those kind of rescue assays. And these are where you were giving a challenge dose.

In this case, again, three times a lethal dose. You cannot give it intravenously because they die way too fast. Right. And so you're moving to a more realistic model where you're either giving it subcue, so in the scruff behind the neck, or you're giving it IP or interperitoneal where you're actually going into the body cavity and injecting some dose there as well. Right.

And what we saw is if you wait five minutes, which five minutes seems super, super short, but this is a mouse, things move real quick in a mouse from a path, like a pathology perspective. So you would give that that 3x LD50. and you would watch symptoms start to appear really, really fast, and you would hope that five minutes came when the mouse hasn't died, and then you'd inject that IV kind of rescue cocktail of nanobodies or even just a single nanobody, if it's a more simple venom.

And we would watch very clearly that you would have very good outcomes for the most part. And, you know, not every trial was 100%, you know, all the mice survived. But what was super important is we actually did the same things with the currently used antivenom. in that region and we were out competing at almost every mark. And that that was like kind of like, okay, we're on the right track for sure type of thing. That's cool. Wow. Yeah, that's encouraging when you're besting the positive control.

Yeah, it's great to see. Great to see. And I think even now, something that excites me about this project, because I mean, obviously this tip of the iceberg, we got to keep going with it, keep doing a ton of stuff, is yes, you know, we were out competing. But like, not by huge margins. What's different about the nanobodies is that these are individual components that, like you were saying, it'd be cool. If we can mix and match, we can mix and match these. So if, you know, we're working on a dendaraspus, you know, a mamba that's got some unique toxins in it. And the cocktail doesn't represent that.

We can alter the cocktail to, you know, better reflect that mamba venom. And you will see much improved results from what you got with just like the standard cocktail we're using for everything else. Right. And as far as you mentioned the stability, what kind of increases on stability? Because, I mean, that's a big concern is, you know, people that by the time they get a bite, their anti-venom is outdated and maybe rusted shut or something in the viality. There's two answers to this. The first answer is biological. Biological stability is increased for sure.

but biological stability of current antibodies is also phenomenal. Antivenom from 1970 is probably great. Probably works perfectly. As long as it hasn't been left out in the sun for 50 years, it's probably doing awesome. And the other answer is pharmaceutically. The FDA puts expiration dates on stuff and they want to keep. you to replenish. And those expiration dates come from, you know, whatever, you know, safety measures that they did with those initial kind of trials.

And a lot of it is, you know, so you keep buying it because it's not like there's enough bites to actually, like in the U.S. especially to have this huge rotating, you know, freezer full of antiphon. And you're not depleting the shelves. You know, it hits that date and you have to move it off. And so that that's really a lot of that. Yeah, I know. It's incredible. You can't have that as a stockpile just in case kind of thing.

you know, like where it's better than nothing? I don't know. That seems like a tragedy. Yeah. Private facilities do for sure. I know Jim Harrison over at the Kentucky Reptile Zoo. You know, he gets bit more than most people, but he's often, you know, statistically, he's definitely put himself out there, you know, doing more of

extractions than almost anyone in the world, especially on a daily basis. Man, the guy's a machine. Right. It's honestly kind of a surprise he doesn't get bit more. and really is a testament to his experience. And, you know, he has tons of antivinam in him and Kristen Wiley. Like, they hold on to every vial. And they know that it can save lives still.

It's not something that, you know, you should ever throw away. Dr. Leslie Boyer, who was at the University of Arizona for the longest time running the Viper Institute, which is like a toxicology program down there. She had a walk-in freezer that was full of antivenom. And none of it was like current. It was all expired going all the way back to, think the 1950s. Wow.

It was incredible collection. And when you tested that product, you can still inhibit a lot of toxins with it. Right, right. So the biological answer, the pharmaceutical answer. Yeah. Yeah. That's cool. What about a, you know, a vaccine for snake bite?

Is that a possibility? You know, there's currently vaccines for dogs and their efficacy is great for, I think, about a month or a few months. The trouble is, yeah, the issue with, like, you know, veneration in general is, yes, you can have an immune response to it and you can stop it from an immune, immunological kind of action. Right. But it's kind of inverse of a disease where diseases, you get introduced to a viral load, and then the viruses typically replicate, or bacteria, they typically replicate and then grow an abundance in her body. So they start slow and kind of snowball. Venom is the opposite, right?

You are kind of hit with an avalanche that kind of trickles away as your body starts dealing with that issue. And so because it's not that kind of snowballing, your body's immune system cannot really recognize an antigen and then mount an immune response before pathology start kicking in, like we can do with diseases like a cold, where by the time we're hitting symptoms, our bodies are starting to mount an immune response and develop those those kind of adaptive immune system reactions. Yeah, Venom is just a different animal entirely where it's too rapid for the adaptive response

to take hold. Yeah, that's typically why you see that efficacy of the vaccine is about a month. Right. Because you have that really, really good immune response that you've learned from that vaccine and then your body starts like putting it in the back pocket. But if you get bit, you know, three months after that, then it has to pull that memory out of the back pocket and then reproduce the immune response. And by the time that that's happened, you know, you should be getting antivenom.

Yeah, you don't have weeks to wait for your antibodies to respond. Yeah. Yeah. Yeah. And it's a great, yeah, it's a great, like, example of, like, why antivenom works. Antivenom is just an artificial immune response that you're mounting rapidly in replace of your own. That's all it is. Right.

Yeah. You're just putting antibodies in that would normally. normally bind if you had time to create them in your body. Yeah, pretty much. Interesting. And I'm curious, like, evolutionarily, you know, some of these animals that are resistant to bites, what are the squirrels or whatever, you know, kind of have an arms race? You know, how are they, has that been investigated?

Or even seemingly the ability for the same species to be resistant to its own bite. or one of its condoms. Yeah. So probably the answer that's going to cover most taxa is bait. Bate molecules in general. So like I was saying before, these toxins can be inhibited either by destroying them or you can remove their targets. You can also like fake out their targets. And so let's say a toxin is targeting collagen and you have the molecule that's called alpha-2 macroglobulin.

floating around your blood. That has two little bait regions of collagen built into this molecule. And so if one of these toxins comes and targets that, instead of it causing damage, it's like a tripwire. It triggers that and that break in the end and the protein. And then the protein folds in on it and traps it. And so you have this like kind of bait and switch and they're going to be a decoy. So instead of them hitting the important stuff, they're hitting this kind of fake trap molecule instead. And we see that in a lot of different animals where they've, they develop decoy molecules to help kind of mitigate any impacts from venom being

introduced to the system. Right. Oh, that's cool. What about some sort of, you know, pill you could take to introduce that into the bloodstream rapidly and bait? So that's, that is, I think, a really hot topic. And I really think in the next couple years, we're going to be seeing a lot of crazy stuff because a lot of it's published. You can see that there's some good candidates for that

exact thing right now. The nanobodies are cool. The nanobodies are really awesome. The idea of a modular antivenom is super cool. However, no matter how good your antivenom is, it leaves a gap, right, from bite to hospital. It's still an anti-venom. It still has to be administered in a place where it can be done, where if you do have a reaction, someone's there to treat that reaction to the antivenom. So there's a black hole there that has existed since the dawn of time from, you know, from when you get, you know, that bite to when you get treatment for that bite. And that is going to be kind of what is being targeted by companies like ophyrics. And this idea of a small molecule inhibitor that is orally available. Ophyrics, it was a company started by Dr. Matt Lewin, who was like an MD and, man, he's got tons of alkaliates. I can't remember all of his titles. But it was him working in, you know, a bunch of other countries, I believe he was in Africa for a while and just kind of seeing the impact of snake bite on some of the populations down there. And the issue was not that like, you know, I didn't exist in the country. It's that it's so far away.

And I think a lot of us have had that moment in the back of our head. We're thinking like doing field work in the middle of nowhere. Like, okay, how far is it to that nearest hospital? Like, you know, we got to think about that every once in a while. And usually it's a few hours, you know, hopefully not a couple days away. But that is something that these people, you know, that's their reality is, you know, their treatment is so, so far away that do you even go in the first place? And, you know, I was talking about, God, I got a way back to just venom in general. You know, you have a lot of venom profiles.

You've got a lot of different toxins that we see across snakes, but you see a lot of similarities as well. We typically have, you know, I could probably name 10 major toxins that are going to be like the most important ones across the world. And that's 10 for almost every species of snake to kind of have some similarity within that pool of 10. And so if you have a molecule that you can take, just as a pill, that attacks one of those 10, you know, families, then you've got something that can effectively target some of these really, really bad bites that is readily. available in places that, you know, have that long distance to more proper treatment. And so ophyrics is spearheading a drug called vraspidim. Vrasbidivis very, very cool.

It targets what we call phospholipase atus. These are really, really common toxins. We see them in just about everything has some level of PLA2s. I mean, we have PLA2s in our body. And in terms of snakes, they can cause tissue damage. like in an atrox, they will cause, like, necrosis, so actually cause the cells to die off. But if you see it in a Mojave Rattlesnake,

that Mojave Rattlesnake has a PLA2 that doesn't cause tissue damage. It becomes a neurotoxin in the Mojave Rattlesnake. So it's a generic neurotoxin. Tiger Rattlesnakes have the same thing. We see it in coral snakes. And like half the coral snake diversity in the Americas has significant amounts of the phospholipase A2. We see it in cobras all the time.

We see different types of it in, you know, of go boboons and puff adders, and we see it going all the way through Africa. We see it a ton in trimorosuris, like species of green tree vipers and that whole clade in Southeast Asia is full of phospholipase atos. And so that is a huge one to target. If you've got a drug that can do that and you can show those results and actually talk to the FDA and get something approved, that will be revolutionary. That will be a first of its kind.

But that alone only cover. is one out of those 10 kind of major important toxins. And so what we're seeing is a few different toxins, a few different toxins, but these drugs that are coming out of the woodwork. And they're not just like random drugs. These are drugs that a lot of times have been studied kind of similar to the drug I used in my master's research for some sort of pharmaceutical purpose. A lot of them are anti-cancer drugs that never made it through the FDA's process.

And so the orphan drug, like association, I'm not sure the exact title, they can take these drugs and then use them for other things. If they didn't work super well at this, can they work for this? And so for Raspid, it was one of those drugs. It didn't really quite work for cancer research. It showed promise, but not enough to really push it through. But the properties can apply here. And so that paired with something that could target, you know, tissue damaging enzymes that we see as well or something that can target other types of neurotoxins. If you can have a combination pill that could be a blanket coverage that you could carry in your pocket, every field herper would. I think we would probably get a little too risky, honestly.

I think people would start freehandling a lot more. But just the idea of having that is pretty exciting for a lot of reasons. We're definitely due for an advancement as well. You know, something that's less expensive that you could carry in your backpack. You know, that would be fantastic. I always I've talked about this a few people like how nice would it be to go to like REI or any outdoor store and see a snake bike kit that actually works. Right. It's not just a suction cup and a razor blade.

Like that would be awesome. I'm thinking tired of telling people like, oh, that thing you bought on Amazon sucks. You know, it's horrendous. I don't actually use it thrown away. So I want to get people options. Like I think it's sometimes it's annoying and frustrating and honestly a little depressing. Right. And sometimes for me, a bit embarrassing because I'm in the field of research for this, when people are like, well, what can I do if I get bid out in the field? And I say nothing. I'm like, go to a hospital. Like, I want a better answer than that.

So I'm right there with you. I study a lot of neglected tropical diseases that there's no treatments for. Even though we've identified several that could work, they just, nobody's going to take them to market because there's no money in it. You know, it's kind of a kick in the pants a lot of times. But what do you do? Keep going. Keep going. Yeah. One of these days, I think we're all going to be really happy to actually have a good answer for people. And to set some minds at ease. Yeah. Well, speaking of herping, do you get out herping much?

And if so, what's been your favorite find? Herp-wise. Oh, man. I don't get out as much as I used to back when I lived in Arizona. I, you know, I had this moment when I moved to Colorado, like after I'd been here a few years. where I was like, man, I had way more snake species at my fingertips down there. I feel like I didn't see as many. Nicklegged them.

Yeah. Yeah. Right. Our lab is very interesting in, I think, one of the best ways where we sit at a crossroads of so many different fields and we do so much. We have so many very, like, grad students that come in the lab. Right. And we get to do so many cool things.

I spend so much of my time, especially nowadays. days cooped up in the lab, you know, messing with mice, you know, doing all these like very kind of, I don't want to say boring, but definitely tedious like an experiment where I'm just, you know, putting stuff in tubes and then watching for a color to change and doing whatever, where I get so antsy at times, especially during the school year where I have to teach and do other stuff. I just, I want to go out and do things. And, you know, we're lucky enough to where we have field projects ongoing. And if I get a spare week, I'm like, cool, I'm dipping out to the western slopes and meet up with our field crew and looking for con color and like

in some of those areas. So every once in a while I get to, you know, kind of stretch my legs a little bit and go out in the field. Just like last month, I met up with our field crew out in like Grand Junction area. They're doing a huge study right now on con color across the entire range. It's just a big like, let's see how the population is doing. Let's do Mark Recapture. So there's a ton of cool work. And it's always fun to meet up. with people who are like experts on this one species. Yeah. And just to be like, all right, point me in their direction, right?

Take me to where they are. I just want to find stuff and take photos. Yeah. And so it's very like low stress herping sometimes. Yeah. And then, of course, you know, just going to talk to them about their, you know, all the stuff that they're finding out there is so much fun. Yeah.

You know, I get to do my cruising out in the planes every once in a while when the weather is good and wants to work with us. Right. But yeah, I miss being Arizona where, you know, herping was, I don't want to say easy, but definitely more accessible, I think. You've got more options down there, especially year round. And then, you know, being over in Colorado is kind of, it feels a little boxed in sometimes for the herps. But yeah, I get to go out whenever I get the opportunity to. I've done a few, you know, trips where I've gotten lucky enough to be with some people where we've done Taiwan a bit.

We spent a couple weeks out there. And Taiwan is, man, it was my first time in Asia. And after that trip, I just couldn't wait to go back. I mean, it's an incredible place, incredible country. I think we got to see so many cool parts. We did incredible out there. We got Dina Kistradon and Avofos, Makaziah, Zaya, and one night, which is incredible. I mean, finding, like, the, like, I think one of the Holy Grails for us out there was the Ovovis species.

I mean, it's just incredible seeing them out there, meeting up with, locals. What's the common name on those? I believe it's Ali Shan Habu, otherwise known as like the strawberry snake. Okay. Yeah, Latin name is Ovophis Makaziah Zaya, which is one of the cooler Latin names. I don't know my Asian viparids very well. I really didn't know that much about it. I think one of my big targets was most definitely like Naya Atro, the Chinese cobra on Taiwan, just because like, you know, seeing a cobra is an Americanist. Always cool. Always cool.

And then Dina Kistrianicudis, the Chinese cotton mouth, was just awesome to find as well. But yeah, the strawberry snake, at least that's the common name that we were calling at the time was something that I really didn't know much about. It's a very kind of not reclusive species, but one that's really strange. Like you would only find it, like the locals of things, you only find it when it's like raining out. And that's like, that's when it crosses. the road, which is, you know, obviously a little different. I'm used to going out like after a rain. So kind of switching up, you know, our, our styles a little bit. But yeah, it resulted in some really awesome finds. It's an incredible trip. With that same group, I've done Peru on the western

coast of Peru, which is like the part of Peru, like, herpers don't go to like the western part very often. I think a lot of times you think about Peru, you're going into the Amazon. And we did not do super well. I think most of them just got sick, which I mean, you have to have one bad trip at least at least once in your life. That was pretty rough. But then, you know, hopping over the next time into the Amazon and, you know, getting to help out a researcher from Florida State University down there in kind of that Napa River Valley was really awesome. Stumbling across like a huge lechesis on the trail. It's just, I think a holy grail for a lot of herpers within the Americas. That's just something that is just incredible. That's like a night that I'll just never

forget. But yeah, I'm looking forward to doing more. I've got a trip coming up in August. I'll be going with the Asclepiest Snakebite Foundation to West Africa in Guinea. This is a team where it's mostly actually MDs and medical professionals who go to the snakebite clinic out there. And they assist the Ghanaian physical. Oh my God, the Ghanaian physicians in treating snake bites. And, you know, they work to kind of help mitigate, you know, snake bite mortality rates out there. But we also get to work with them and collect venom from anything we find.

So the locals will actually call this for snake calls. Obviously, most of the times it's puff adders. I mean, like that's the predominant thing across almost all of Africa. Green mambas, the Western green mambas are also very common out there as well. Cool. And the clinic has actually been brought in the past couple of years. two black mambas, which for Guinea is incredibly rare. And I believe one of them was the first live black mamba caught in the country.

And so the fact that that facility has enough really good connections with the locals to work with them on that level is awesome. So I'm excited to just go out there. You know, it's a tough, it's tough herping in those regions. But I mean, just getting to be there in that environment will be awesome. And to like watch these physicians really, really work on the ground and talk to them. and, you know, had that discussion of like, hey, we're developing these treatments. What types of data to use a physician want to have? And, you know, like, what do you want to see in your treatments as a physician?

And so that's like the big goal of the trip. And then also, you know, mamba's is awesome. That's just hard to ignore. Some of the biddest as well. You know, Gaboon viper or something would be really a cool thing to see in the wild. Yeah. I know one of the MDs is. actually a huge herper. He's a very, very adamant herper. And sometimes, like, when he's

down there, he's like, oh, well, there's an atheros spot that's like five hours away. We could make a day trip. And the other MDs who are like, not snake food, people are like, not doing that. Like, what are you? What's wrong with you? Right. And so I know, I know, waiting for the herpetologist to get there. So yeah, he was, him and I were talking about it a little And he's like, yeah, there's a local guy who told me that he's got this one spot. Cool. I'd be down. I'd be down.

Right. Yeah. Well, I mean, yeah, use those connections. Well, you know, you can or have those. Us lay folk don't get those kind of connections really out. I know. It's a crazy place. This is a connection that's very surreal to me.

I was mentioning, I've been wanting to do venom for a long time. And I've actually been doing anti-venom stuff almost just as long. Back when I was working at the sanctuary, we actually had a cobra bite back in 2017, 2016. And it was like one of the first cobra bites that an Arizona physician had ever treated. They did an amazing job. Problem was it, a fly-in antivenom from Denver. And, you know, as a facility that has a bunch of venomous snakes, that's not great.

And so then we started up the Phoenix Repetological Sanctuary, anti-venom bank, which is one of the largest anti-venom banks in the American Southwest. And being a part of that project was so cool. I got to meet so many physicians and really learn the ins and outs of like, okay, what is anti-venom? Why is it doing all this stuff? And we got to a point where I met up with Dr. Leslie Boyer. And her and I talked a lot just about the whole, you know, world of snake bite and what

the challenge is facing it. And she was like, you know, there's a clinic in Guinea that is really cool. Cool. And so now fast forward 10 years. Leslie Boyer is sitting on the, is like one of the medical advisors for Ophyrics as a company. Yeah. Working on for hospital. I get to work with around that project and also like do this clinic. And it feels very full circle.

That's so cool. Yeah. Yeah. And man, I, part of me wishes that a lot of these MDs would go to more of these like HIRP conferences. Because I like having conversations with them is super eye opening, especially as like, people who, you know, were on the field a lot. And just getting to do that. But, man, hearing their perspectives on things is so cool.

And I've tried to convince them to come to, like, biology of the pit vipers and biology the snakes and a lot of those conferences. And they're like, oh, well, you know, like maybe next time. Yeah. Yeah. So, yeah. Wow. Man, what a great field you're in and how some of really exciting work.

We really appreciate you coming on here and talking about this. stuff. It's so fascinating and just exciting, you know. Yeah. Just thoughts of what could be. Yeah. And I think like I mentioned, we're definitely, and you said it as well, we're in a turning point. This is like definitely the corner that we're kind of coming around right now. And man, give it, give it a decade. And I think this field is going to look a lot different than what we currently have for the better. Thank gosh. Yeah. Yeah. Yeah. It's about time, right? Yeah. And 100 years in the way you made in the making at this point.

A lot of time with a horse serum. Mm-hmm. Yeah. Yep. That's exciting. Yeah. Well, yeah, good luck to you. And, yeah, hopefully we see those advancements sooner than later, right?

Yeah. It's the cool. Right. Rob, did you have any other questions? No, this has been fabulous. Yeah. Yeah. Yeah.

Well, where can people find or track your progress or see your, aside from Google Scholar? Is your publications? Do you have any place to you post? I'm mostly, in terms of social media, just on Instagram, should be pretty easy to find for the most part. Toxic underscore Sam, we'll get you there. I get a lot of weird looks when I mention that name sometimes. But yeah, I use social media sometimes.

I think like many herpers, my social media is almost entirely snake pictures and skeletons that I articulate on occasion. That's about it. Oh, very cool. Yeah. Yeah, I'm kind of a, I've got a little bit of a dead zoo behind me. I don't know if you can see it, but it's on the shelf there. That's awesome. But yeah, I like some different skulls and things, but yeah, I thought that would be really cool to do an articulation or some like wood burning or carving of a skull would look really neat too. Oh, yeah. I got a really cool Aboriginal painted crocodile skull that I brought back from Australia with me, which is pretty sweet. Yeah.

Yeah, that's something I need more of. I think, you know, being a grad student, you learn to move around light in terms of belongings. I'm with, yeah, I'm excited to. A heartbreaking story of the grad school student moving. We had a grad student at Utah State that he had a collection of things that he'd found out in the wild or whatever and had him his pets in his apartment. And then he got a job somewhere, finished. his PhD and then just euthanized all his pets, put them in the collection that Utah State and left. I'm like, oh, my gosh.

That's so, that was one of the things that made me decide not to be a herpetologist. I'm like, I can't be that call. I'm sure not all herpetologists are that way, but yeah, the pickling and the, yeah, that kind of got me a little, you know, I'm like, I don't know if I could do that too well. Yeah, yeah. Every once in a while, like, you know, having a main. maintaining a beetle colony kind of gets on me. It's a little annoying. But, you know, when they take a skinned animal down to a skeleton in 24 hours, you're like, all right, I kind of love you

guys. This is very helpful. Yeah. Yeah. Very cool. Well, thanks again for coming on. And we're a good pleasure. Yeah. I'm trying to think if there's anything really cool, you know, at the end of the show, we like to kind of say if there's anything really cool that you've seen in Herpetology, herpetulture, anything like that in the last little bit. I'm excited about a, they're going to air a program on the Kimberly on the 17th of June. So I'm really excited to see that. I hear there's footage of rough scale pythons and some other Kimberly endemics. So on PBS in June 17th.

So I'm looking forward to that next week. That's awesome. Yeah. Yeah. So it should be fun. Yeah. I don't know. I think there's a lot of advancements coming up and like as follow-ups of some of our research that I'm hoping we'll get the light of day here soon.

So in terms of like media, that's where a lot of my attention is. Yeah. You know, media in terms of, I guess, scientific publications. Yeah. We'll keep an eye on your profile. See if you got any publications coming out soon. Good stuff. Yeah.

Yeah. I pre-ordered someone's field. guide of the reptiles and amphibians of Utah. Oh, very cool. Yeah. Yeah, I'm glad to see it's finally out. And I think they even put a price to it. It was like, was it, was it $21 or something?

Yeah, $295, something like that. Yeah. Bob kept it low, low price. That's impressive. Yeah, I got two advanced copies that I've had a chance to peruse. It costs 50 bucks to send one to Nipper, so I'm not sure how we want to work that.

I might just wait till he's in country and give him a box to take home or something. But yeah, it's a little tricky there. Sorry, Nipper. But yeah, excited to have that out and hopefully in hand sooner than later. We're thinking mid-July is when the main shipment arrives from China and then I'll pick up a bunch of boxes at the IHS meeting. Do you happen to be going to that, Sam? Unfortunately not I'm going to

I had time for one conference this summer and I'm doing JMIH instead Right yeah So I Got a lot of friends going down to IHS but Yeah I'm really couldn't make it Very excited to be there

I mean it's the 50th And the 50th one So it should be a pretty big production But looking forward to it And not to mention the new library down there It's just fantastic Yeah I was down there for biology of the pit vipers last year, which it was super cool to be down there, but during a conference, it's a bit noisy in the library.

And I kept sending myself, like, I got to come back when it's not a conference. Yeah, yeah. We've been there a few times where it's just been, you know, five or six of us at most. And just, yeah, just jaws down on the ground. And Bob, Bob pulled out some books that were, you know, know worth a lot of i think you know paid tens of thousands of dollars for some of these books and it's pretty cool to see these old you know prints and lithographs and stuff in the books it's amazing what a collection never never ceases to amaze me what he's got to do yeah for sure yeah

good stuff all right well thanks again and we'll thank eric an hona and the mpr crew for hosting us and uh we'll catch you next time for reptile fight club