67: T-2 Exposure and Hemorrhagic Bowel Syndrome in Dairy

T-2 mycotoxin, often called the assassin toxin, is one of the most aggressive and overlooked feed risks in dairy production. In this episode of Ruminate This, Dr. Larry Roth explains how T-2 disrupts protein synthesis, damages the rumen and intestines, and creates serious health challenges at levels as low as 75 ppb.

They connect T-2 exposure to Hemorrhagic Bowel Syndrome (HBS), gut integrity breakdown, and increased risk from Clostridium perfringens. The discussion also covers feed risks, including refusal management, TMR variability, and why passing down feed can increase mycotoxin exposure.

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Transcript

0:01

Hello everyone, welcome to Ruminate This with Agrarian Solutions. Join us as we explore ruminant nutrition and the impact of mycotoxins. Here we challenge your curiosity and explore new industry insights and research to optimize your herd's health and performance. All right, hey, welcome everybody to another edition of Ruminate This with the Grand Solutions. I'm your host, Scott Zayer, and with me today I have none other than my friend Dr. Larry Roth. Larry, thanks for jumping on today. My pleasure. And Larry, we're gonna talk about something that's near and dear to both of our hearts. I think I've said that before. We're gonna talk mycotoxins one more time. If you're following along this year, you've noticed, Larry, we've we've talked about we did a deep dive on on the mycotoxin Don, you know, the disruptor toxin. We've talked xerolinone, what I would call the imposter toxin. We've also talked fomonicin. I don't remember what my clever name for that was. But today we're going to do a deep dive on T2 slash HT2. And if we're giving them clever names, Larry, I like the term the assassin toxin for this particular fusarium mold derived mycotoxin. Very good. Larry, why is that such a good name to call it? Because that's exactly what T2 does. It goes out and it kills cells, it stops protein synthesis, cells die. And Scott, as as you well know, I think of the digestive tract lining as being the castle wall to protect the animal's body. And if we kill the cells lining our castle wall, it's that much easier for T2 and all these other mycotoxins and even pathogens to get into the body to do their killing. So I think that calling T2 the assassin molecule is a very apt name for it. That's what it's gonna do. Go out and kill something. You know, and it's interesting, you know, these particular mycotoxins they seek out high turnover tissue, room and wall, intestines, mouth and tongue, bone marrow, immune cells, reproductive tissues. And you know, we've seen in my career at least, I've seen some cases where I've gotten calls from farms that we know we have T2 challenges. Maybe we're not yet employing a mitigation strategy. We're we're hedging our bets. And the calls sound like this Hey Scott, we don't really know what's going on, but we have some fresh cows dropping dead, seemingly healthy one day, dead within a couple of days. Sometimes they talk about blood in the manure. What do we do? And there's so many things that it could be, and so you start this investigative pattern, and so many times we've gone back and resampled the forages and found what I would say extremely high levels of T2, 100 part per billion plus T2. We introduced a mitigation strategy that involves our technology DTX, symptoms go away. We don't see it anymore. So that's that's a great story. But your analogy with Don was whatever you put in the mouth of the river eventually flows to the room, and T2HT2 is a speedboat on that river, it's not wasting any time, it's just gonna get there. So tell us a little more about maybe why T2 is so aggressive. Well, T2 stops protein synthesis, and we have to have protein synthesis for these cells to live, any cell. But as you just mentioned, and you cited a number of high turnover tissues, which are going to have a high rate of protein synthesis. If protein synthesis is stopped on those cells, guess what? These high turnover cells, they're dead. And again, we come back to T2 being the assassin toxin. But if those cells are dead, we've lost that line of defense for the animal. You talked about bone marrow, a source of immune elements. If we stop that, so now we've destroyed our castle wall. Now we're dependent more upon elements of the immune system, but T2 is killing the bone marrow cells that make the immune elements. It's just a cascading snowball effect, and T2 usually does not occur at significant levels by itself. It's usually with somebody else. Quite often, Dawn, quite often, xeralinone might be fumaticin. So the T2 kind of amplifies the effect of other mycotoxins. Yeah, I mean, xeralinone, we talked about what it can do once it gets in the liver and so on. Well, if there's not a castle wall there to defend the liver, because the T2 is destroying it, makes it a lot easier. And it can happen so fast because of these high turnover cells that T2 is so effective at. So that's why, Scott, the situation that you laid out a moment ago, hey, everything's fine today, problems come overnight. And then maybe the problems disappear because we got into that one specific spot in our fermented feeds, or it could be a dry feed, dry corn grain, where we got some T2. And we don't have to have very high levels of T2 for it to cause major issues. So before I get into what I consider my money question for this episode, some of the early signs of T2 that we might see on the farm. I read an article and doing some research here prepping for this. Sometimes these symptoms or these early signs are mistaken for just maybe acidosis type thing or or bad feed type thing, swollen gut, grinding teeth, bloody manure, cows off feed, sudden drop in production. What does that sound like, Larry? Anything and everything that always goes wrong with a cow. Exactly. Exactly. And so that's that's where sometimes diagnosing the exact problem can be a bit of a challenge. And of course, Scott, as as you know, I like to encourage people to do routine sampling, sample our fermented feeds going into storage, and then on a routine monthly basis, sample our TMRs so that these things don't become a surprise to us. Yeah. Larry, I have uh talked to you a lot about this next question over the last couple of years. It's been a theory in my head anyway. So hemorrhagic bowel syndrome. Boy, if you were a nutritionist in the 90s and early 2000s, that was your almost your biggest fear. And it probably to some degree still is in some cases. I think we don't hear about it quite as much anymore. But I've asked you this question a number of different times. I'm gonna ask it again publicly. Is it possible some of these things we thought some of these instances we thought we just chalked it up to HBS? Or could it have been actually caused by T2 poisoning? That is an excellent question, Scott. And the short answer to that is yes, it could have been T2 poisoning. My hesitancy in answering your question was I think that HBS and T2 are probably more interrelated than maybe we give it credit to for. So for example, I think that's good, yeah. Yeah, I think that's fair. T2, again, you know, I sound like I just keep repeating myself, takes out those high turnover cells, digestive tract lining, rumen lining, bone marrow, immune type cells, and now the animal is more susceptible to what we have traditionally associated HBS with Aspergellus fumigatus and Clostridium perfynes type A. So again, it's a bit of a chicken of the egg which comes first, those organisms that I just mentioned, or the T2, and they may come along at right at the same time, or maybe T2 came first, whatever. But I think it all comes back to watching our feed hygiene, watching for Aspergillus fumagatus, watching for Costridium perfingis type A, watching for T2, and having a strategy in effect to reduce the likelihood of these organisms, mycotoxin occurring, or at least reducing the ability of these bad guys to wreak havoc upon the cow. Again, it comes back to feed hygiene and always watching for T2 to rear its ugly head. I think a good simple analogy I I like to use when I talk about this, Larry, is at the end of the day, my theoretical question of could some of those HBS things could have actually been T2 and we just weren't diagnosing it, it's almost irrelevant because at the end of the day, all three of those things are going to be causative in the HBS symptoms, or at least could be. So I always tell people think of it like all three agents are riding in the same car, and it really doesn't matter who gets out the door first to go to battle. Yep. At the end of the day, how do we, like you just said, how do we create a strategy to mitigate the risk associated with those issues? Yeah. So how do we do that? I think part of it comes back to minimizing dirt coming into our feeds. Back to the aspergellus, you know, we've associated that fumigatus with alfalfa hay stored on the ground while that brings in dirt, the way that we make our halage, the way that we make our corn silage, not tracking dirt and manure into it, watching our feeding equipment, just good plain hygiene, and then watching for the T2. But again, the challenge with T2 is in the lab, it's quite often hard to create it. So we don't have a complete understanding of what is it that makes the pubesarium mold decide that it's going to make T2. Okay. And and Scott, we don't really need very much of the T2 to cause issues. And let's complicate this further. The body starts to do some metabolism of the T2, and it creates the metabolite HT2, which is even worse for destroying tissues than its origin T2. If you follow my reasoning there. So we don't need much of the original T2 to have all of these issues. So we go out, we sample our feeds, we do a good job, but then we get that one little pocket of T2, and it devastates the cow so very quickly before we have a chance to say, Oh, I gotta go test my TMR, oh, I gotta go test my corn silage to see what happens. Because by the time we go to do that, we've already worked through those bad feeds. So that that's where I I think, Scott, we need to continually have a program in place to protect against T2. If we if we're trying to protect against it after it's already caused us mischief, we're behind. We're behind. We had a gentleman that worked for us at agrarian for a number of years named Greg Muchmore. And Greg, when he would talk with me about the different mycotoxins, and and Greg, previous to working for us, we had a career as a nutritionist, T2 was about the only one he talked about that would make him like sweat and get nervous. And like, hey, you know, it's one of those moments where you gotta slow down and really listen to what I'm about to say, kind of moments. He took it very seriously, and I remember him telling me all the time that T2 kills white blood cells. I mean, that alone raises a pretty big red flag, too. I mean, just the the amount of destruction this molecule can do inside our animals. You know, I I think when I first met Greg, I kind of, you know, maybe had a little reaction of, okay, this seems a little dramatic, but as we've gone along, as I've gone along in my career, I think it's important when we have a herd that is in our routine sampling program. And I encourage anybody listening to contact us, podcast at agrsol.com, and and visit with us about our routine sampling program. I I get a little nervous when I see levels of t2 because it, as you said, it doesn't take a lot, and also not only is that t2 riding in the same car as aspergillus fumigatus and clostridium perfringes A, it's also riding in the same car with usually Don and Xorolinone and sometimes Spimonisan. Yep. Again, it's we usually use the term synergistic with things that are working together for good. And so I don't know what the term is for things working together for bad, but that's what's happening here. You get everything bad coming along at just the wrong time for the animal, and that's why these issues with T2 can happen so very quickly. So that that's again going back to the beginning, when you referred to T2 as being the assassin mycotoxin, I think that's a very appropriate name. You know, and I I'm gonna come back to something that we talked about earlier this week. You know, so many times when we have challenges on the farm and we start to try to diagnose and investigate and make determinations, we lose sight. I think sometimes we do at least of the fact that you know these animals are a biological system, and within this animal is another biological system. And these are biological bad agents. Yep. That are, you know, their purpose in life isn't to harm our cattle, but once they get there, we need to pay real close attention. And and I think one of the neat things in the story here, Larry, and I I haven't brought this up in either one of these past three podcasts where we've deep dived on the toxins, is a biological solution that we have. And just expand on that a little bit. Okay. Excellent. Well, I like how you talked about the cow being a biological system because that's what she is, and she has many biological systems within her the rumen, the small, the large intestine, the liver, that all have their own unique ways of working. The immune system, that's a biological system. And with biological systems, I think that there's more, I'm gonna go ahead and say variability than there is with just a plain chemical system. You know, we're we're in a factory and we're trying to make some chemical, okay? That that's a lot more static, a lot more predictable. So we need to be, we need to have some flexibility to protect our cows, flexibility to take into account many different causative agents that could cause, shall we say, T2 poisoning or cause HBS, because we're we're thinking of T2 being an integral part of HBS. Well, that's where our biological solution, the DTX, comes into play, in that we've got a bacteria, specialized bacteria, the cell wall deficient bacteria takes up residence in the digestive tract lining and through the quorum sensing communicates across different cells. Hey, you need to elevate your transport proteins, which clean the garbage out of the cells. That's all these transport proteins do is serve as garbage man. Hey, there's something in the cell that should not be here. If we don't get this garbage, this trash out of here, the cell is going to die. And that part of the castle wall is gone. And that that's all that we're doing is we're triggering the animal to work the way that it is supposed to. Protect against the toxins, kick them out of the cells so that the digestive tract lining cells are not killed, maintain the integrity of the digestive tract lining. That's what we're doing. It's really quite simple, Scott. The cow has this ability to do it. We just need to activate it, take it to a higher level of readiness so that the cow can work. In contrast, we look at in vitro studies that suggest that traditional clay binders and yeast cell wall products are relatively ineffective for chemically tying up T2. So we don't want to be reliant upon something that is not that effective, the binding, chemical binding offered by some of these feed ingredients. We want to go to the biological system that communicates through the different intestinal lining cells. Hey, we don't want that mycotoxin, in this case today, T2 building up in our cells because it's going to cause bad things to happen. Let's get it out of here. Let's kick it back into the digestive tract contents, the river, and let it flow on out. I think you brought up a really good point, Larry. And I'll phrase it up this way, you know, as we wrap up this episode and and kind of this mini-series on the deep dive of these four major mycotoxins. Again, going back to the biological system that is that cow, right? When we have a biological challenge, a biological solution, in my way of thinking and and how we've described this, is a more logical solution than a chemical solution would be. Yep. Exactly. I'd just like people to to ruminate on that for a minute. Let's just help the cow to function the way that she is supposed to. Yep. Yep. Take her to a higher level of readiness. Yeah, and I'm not to get too carried away with this, but when we take this biological approach to a biological challenge, the downstream effect of that, if you would, of letting a cow be a cow, right? It comes right back to helping her allocate nutrients to productive purposes. Yep. And that's that's really, I know you said that, you know, all we're I like the way you phrased it up. All we're really doing is quite simple. We're helping the cow be a cow, right? We're we're talking across these these cells. And I'm gonna follow up with another simple statement, Larry. All we're doing is allowing that cow to use the nutrients the way we'd like them to be used. Exactly. Exactly. Put them into productive purposes, not just trying to stay alive, even though that's important, but let's take that those stressors off of her so that these nutrients that cost a lot of money can go to productive, profitable purposes. With some animals, it's gonna be gain. With others, it's gonna be milk production, with others, it's gonna be reproductive success. Larry, I'm gonna ask you your back of the napkin summary for today's episode and the takeaway for the listeners to go home with. T2 is an assassin molecule that stops cells from protein synthesis. And so this is especially true for high turnover cells, those that are lining the digestive tract, small intestine, rumen, large intestine, bone marrow cells that are important to the immune system. So T2 takes out our highly most important cells, high level of turnover, so that now the cow is that much more susceptible to invasion and destruction by other mycotoxins and by other pathogens. T2 is the assassin. All right, Larry, I appreciate you coming on today to shed some light in this whole series, really doing the deep dives. I feel like there's still a lot of questions in the field around mycotoxins in general, especially not named on at this point. And I hopefully the listeners were able to walk away from the series with a better level of understanding on how they work and a better level of understanding on how we assist that cow via cow. If you have further questions, folks, or would like to subscribe to our newsletter, you can do that by going to our website. And if you do that, you'll get articles from Dr. Roth and Caroline Kenoblach, our director of nutrition, talking about things like this. I believe you guys have an article about T2 coming out soon. If you have questions about specific toxin stuff or you want to talk to us about our sampling program, reach out podcast at agr.com. You can also go to the website and fill out the contact us form, and we will get back to you. Thank you again, everybody, and I look forward to talking to everybody again soon. Just a reminder of our new battle rhythm here on Ruminate This. We will be having episodes on the second and fourth Monday of every month. Thank you and have a great day. All right, thank you, Scott. Thank you for listening to Ruminate This with a Gray and Solutions. Look for our next episode in two weeks.