64: How DON Mycotoxin Slows the Rumen and Erodes Dairy Performance

In this episode of Ruminate This, Scott Zehr is joined by Dr. Larry Roth (VP of Nutrition, Agrarian Solutions) for a discussion about DON (deoxynivalenol/vomitoxin)—one of the most common and most misunderstood mycotoxins in dairy rations.

Rather than causing an obvious crash every time, DON often works like a “pause button” on rumen microbes. It doesn’t necessarily kill bacteria, it slows microbial function and disrupts fermentation, reducing the cow’s ability to convert the TMR into energy and microbial protein. The result can be a quiet, cascading problem: lower feed efficiency, reduced intake, erratic manure, and performance erosion that shows up long after the damage begins.

Scott and Larry discuss how DON can:

• Disrupt rumen microbial balance by interfering with protein synthesis and slowing fermentation
• Push undigested nutrients “down the river” into the hindgut, leading to undesired hindgut fermentation
• Create signs that look like acidosis, when the real issue may be hindgut acidosis driven by poor rumen breakdown
• Weaken gut barrier integrity, increasing permeability and contributing to leaky gut
• Trigger immune activation and force nutrient reallocation, pulling glucose and energy away from milk and reproduction to support inflammation control
• Compound other stressors, making DON a major player in stacked inflammation 

They also discuss why the same DON ppm level can hit two herds very differently, and why ongoing mycotoxin testing can help connect the dots before a slow decline turns into a full-blown crisis.

If you’ve ever wondered, “Is this really rumen acidosis… or something else?” This episode will change how you diagnose digestive, immune, and performance problems in high-producing dairy cows.

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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. I'm your host, Scott Zayer, and today I am happy to be joined by none other than our vice president of nutrition here at Agrarian, one of my friends in the company here, Dr. Larry Roth. Larry, thanks for joining us. Good to be here. Larry, you know, we we are going to dive into a topic today that is near and dear to both of our hearts. One, because we work at Agrarian and we believe in defending and protecting cows for a lifetime. And one of the main things that we do to defend and protect that cow for a lifetime is mitigate mycotoxins we feel in a way that is probably better than anybody else out there, with some unique things that we do with our specialized bacteria, L-form bacteria. You know, and I've asked you this question before: what is a mycotoxin? And I'm I'm gonna I'm gonna just kind of give the people an overview. So, right, mycotoxins aren't these bad actors that the world has put in your cow's TMR with the sole purpose of hurting your cow's production and health. They're just the byproduct of a mold that's just trying to survive, Larry. And unfortunately, our cattle in the US and abroad are are the collateral damage. And producers, producer's bottom lines ends up being the collateral damage of mycotoxins. But what I do want to kind of bring out today is let's talk about a specific mycotoxin today, Larry. And we're gonna start with Don. And we have discussed in the past some things that Don is kind of known for, like disrupting rumen microbial balance. But I want to take it a step further with you, if you could, and and help the audience really understand what Don is and what it does, both directly and indirectly. So I guess my first question for you is why is Don actually so disruptive to the rumen microbial balance? And what is it doing once it gets in the rumen? All right, excellent. All right, thank you, Scott. Great way to start off our conversation. You know, I think we have to stop for a moment and say with our ruminants, what makes them unique from the non-ruminants, the pigs and the chickens, is we have this 55-gallon fermentation vat between their ribs. And so we have to think about everything that comes into that fermentation vat and its effect on microbial balance and the resulting fermentation in the fermentation products. So, what does Dawn have to do with all of that? Well, Dawn is something that we might call it static. It kind of stops the bacteria where they are. It's not sidal in killing the bacteria, but it think of it as slowing them down and stopping them where they are. They're not dead. So talk about genetics for a moment. Rhizomes are ribosomes are in the in the cell and they generate proteins that cause all kinds of things to happen within the cell. Well, Dawn happens to kind of tie up these ribosomes so we don't get the proteins created. So the microbes, when I say microbes, I'm talking about bacteria and protozoa. They slow down. They're not dead, but they're not functioning like they should be. And they're supposed to be almost like a paralysis. You could you can think of it that way. Slowing them down, they're really not doing anything, they're not functioning at the level that they should be. So consequently, we're not turning the diet into energy and into microbial protein. So if the cells aren't increasing in number, we're not creating the microbial protein that is the ideal amino acid balance for the cow so that we get milk production, we get immune support, and we get reproduction. Things are just kind of slowed down and not functioning. And so consequently, if our fermentation has been slowed down in the rumen, we're not going to get the rumen turnover, and we're not going to get as much feed intake as what we want. And to me, everything starts right there. What happens to our fermentation balance and we've slowed it down? Mm-hmm. So, I mean, let's just I guess run this out before we move on a little bit more about Don. If you're telling me we're not getting the fermentation done correctly in the rumen, and we have digestion or something happening somewhere else, right? Is that what we would call hind gut fermentation? Okay. Great question. Is that is that we have undigested starch in the in the sm in the hind gut causing what issues? To me, the digestive tract is like a river. Whatever ends up in the river at the headwaters is going to flow all the way down. So ideally, we would have fiber and starch being fermented in the in the rumen. The fermentation products are going to be absorbed for energy in the rumen. The microbial protein flows on down to the small intestine, broken down and absorbed as amino acids. But if we're not breaking down digesta, be it both fiber and starch in the rumen, those nutrients are going to flow on to the hind gut, and we have fermentation taking place there that we don't want to have taken place. So, Scott, I have a boring life. One of the things I like to do is screen manure, and when we do that, we have an idea of what's happening in the hind gut. And so we notice that with cows who are challenged by Dawn, that quite often, not always, but quite often, feed intakes can be a little bit lower than what we want. And we notice a more erratic manure. Well, right there we're having one of our two of our key things. Less ruminal fermentation, cows aren't going to eat as much, not breaking everything down in the rumen like it should be. Nutrients flow to the hind gut. Maybe we have our erratic manure. So we're we're starting to put all of these dots together why we see what we do. Yeah, it's a pretty distinct cascade effect there, you know. And I and I I always come back to, you know, as we learn more about Don, and maybe this is just a me thing, Larry, but boy, I can remember being on the dairy in the early 2000s, and it was like you wanted to the word the the word acidosis was like a trigger for nutritionists. And when we would see symptoms to me that looked like the cows were acidotic, and the nutritionist is saying, Ain't no way I'm feeding your cows to be acidotic. It just makes me wonder, Larry, over the course of time, how many how many nutritionists got replaced with another nutritionist because the dairyman didn't understand or somebody didn't understand that maybe what's going on here is is a don issue that's causing things to look like acidosis. Exactly. And and again, we go back to the manure screening. We have too much fermentation taking place in the hind gut. Well, that's because we got acidosis, we've got too low rumin pH, we're not having fiber fermented like it should be in the rumen and starch, and so and we make a conclusion that we've got acidosis when really it's not acidosis. It's more of a hind gut acidosis because we got nutrients flowing down the river to the hind gut. So we're trying to make a diagnosis, and we're not understanding everything that's happening there in the rumen. Yeah. So I I think that you're right, Scott. There are probably decisions that have been made in the past that were incorrect because we've got Dawn messing ruminal fermentation up. Oh, so we've got acidosis. So that means we need to feed a little bit more fiber, right? But Dawn has unfortunately a greater effect upon fiber fermenting bacteria than it does the start. So we've just increased our fiber in our diet. Now we're slowing it down. Fiber fermentation down, excuse me. So we get less energy there. And you can you can just see how there's a cascading effect that goes on with all of this, not really understanding how Dawn is negatively impacting the rumen microorganisms. Larry, you talked about this cascade effect, and it just makes me think in terms of, you know, let's go back to your river analogy. I I live in an area of New York right near the Black River, and it it's one of the largest rivers in the in the in the country, I think. It carries quite a bit of water, and it it can it connects into Lake Ontario and the St. Lawrence Seaway, and that water that flows in there ends up in the ocean. It takes some time for something that's put into the Black River down at the mouth to make its way all the way to the Lake Ontario, up the St. Lawrence Seaway and out to the ocean, to the point where you might not even notice that anything actually was wrong in that water until it's way too late. And you know, I go back to I made this comment to you once before. I think there's only been one time in my career that I truly felt like we were dealing with an acute Don issue. And when I say acute, I'm talking like a smoking gun kind of issue where we did some sampling, the Don was, I think it was like 16 ppm in the diet. There was like a date and time where they started on some corn and there was a crash in milk, and all systems pointed to this was a big time smoking gun. But the way you've described it, and when I think of the river analogy you used, that's not normal. That's maybe, you know, there's probably a reason I've only seen it one time in my career. To me, it sounds like what you're describing is a slow erosion of the riverbank. It takes a lot of time for these symptoms to potentially show up in ways that we can measure, you know, like profitability or certain KPIs. Where am I at with that? Is that about right? I think that you're right with that. The the challenge I would have is that word acute. I think you were right to use the word acute in the situation you were describing. I think in most of our other situations, we have subacute or I don't know if I want to say subclinical, but maybe subacute, in which we are adding another inflammation source to the cow who's already having to deal with so many other sources of inflammation. Yeah. And we're kind of getting to that final straw that breaks the camel's back. That final little bit of inflammation that she can't deal with. And then things just get exagger just exaggerated. Things just get bigger from that point because we went beyond the point of what the cow could handle. And then everything else starts to become more of an issue. So we've reduced fiber fermentation a little bit in the rumen. What could be wrong with that? We've reduced starch fermentation a little bit in the rumen. What could be wrong with that? Well, now we don't have as much microbial protein presented to the small intestine to be broken down to amino acids and absorbed. We've sent more nutrients to the hind gut to be fermented. What could go wrong with all that? Then we add in things like leaky gut that can come from a number of different non-mycotoxin-related situations, but we do have that. And so we've been focusing upon Dawn so far in our discussion and its effect upon ruminal fermentation. Let's talk about Dawn and what it can do to the intestinal lining, contributing to leaky gut. So we get more and more inflammation challenges on the cow. How many of these inflammation sources can she deal with? Because she's a high-functioning biological unit, but how many inflammation challenges can she handle? Where we're asking her to do so much more, she's producing what, 120, 140 pounds of milk. She's got a much greater glucose need than the cow who's down there at 50 pounds. Completely different needs. And we're asking her to do all of this biological and physiological work, but yet she's also trying to stay alive and deal with all these mycotoxin-related inflammations as well as other types of inflammation challenges going on. Because I I don't think we talk about this aspect enough of Don increasing the permeability of rumen and intestinal walls and loosening those tight junctions in the epithelial tissues. And we talk about it a lot in it as it pertains to like T2 HT2 toxin. But you know, it it just I'm gonna come back and and maybe sound a little bit silly. There's a reason it's called a toxin, and you know, and so expand on that a little bit. I mean, there's I guess I I'd like to hear your take on this because when we think of like T2 HT2 affecting the mucosal tissues and the soft tissue linings and the small intestine, we think of creating ulcers and and really some pretty nasty stuff. I don't think I've ever really heard you talk about Don being that aggressive, but I guess and probably in high enough levels, it'd probably be something similar to what we see with T2HT2. But just walk us through the cascade effect of weakening those epithelial cells and and increasing the permeability in the rumen and small intestine. You bet. All right, so think of the small intestine lining as being the castle wall to keep the barbarians, the bad stuff in the digestive tract, and out of the body. But Don can weaken our castle wall, reduce the viability of that castle wall. Now we got greater permeability. The tight junctions that were supposed to be tight between intestinal cells are now open. We got an interstate highway for all of the mycotoxins and other digests to flow into the body, and now the immune system has to deal with all of these invaders. So now we have glucose that we were hoping was going to go for follicle development and supporting embryo development, that now glucose plus go to lactose creation for milk. Now that glucose has to go to support the immune system. So we've reallocated nutrients from productive purposes to dealing with the increased permeability due to the leaky gut due to the don, they're at the digestive tract lining. And then we have the liver, the body's biochemical factory. So we got leaky gut, we've got stuff ending up in the in the body that shouldn't be there, the immune systems have to deal with that. But these metabolites, these toxins that flow on to the liver, the biochemical factory has to deal with that, and the liver is not as efficient at metabolizing other nutrients. Oh, and by the way, we don't have as many nutrients to go to the liver because we don't have the ruminal fermentation that we wanted. So it's one great big cycle that we see going on. And little bits here, little bits there have a greater aggregate effect when they all come together. So we want each part of the body to function the way that it should be. Maximum ruminal fermentation in the rumen, nutrients not flowing to the hind gut, the right balance of bacteria in the small intestine and large intestine. We don't want pathogens, we don't want mycotoxins affecting digestive tract wall permeability. We don't want invaders getting into the body, reallocating nutrients from productive purposes to immune support. We don't want metabolites ending up in the liver causing bad things to happen there and not metabolizing nutrients the right way. So it we're we're dealing with a biological system, the cow, in which she has many biological systems. The rumen, the small intestine, the large intestine, the immune system, the liver. All of these things have to be working together in the right way. And little pokes here, little pushes over there, they come together for a greater effect. And now the cow is not living up to her genetic potential for milk production. Then the diet is there, the nutrients are there, but they're not being fermented in the proper way in the rumen, they're not being absorbed in the proper way in the small intestine, they're unfortunately being fermented in the hind gut, we got leaky gut, we got the immune system going crazy, trying to defend the cow's body, and we got the liver, the body's biochemical factory not working the way it should be. What could go wrong with all of this stuff? You know, Larry, I know you love a good sports analogy, and football is often cited as the ultimate team sport because it takes 11 men on offense, all going the same direction, everybody doing their job, same on defense, same on the special teams. And all it takes is one offensive lineman missing a block or a twist or a stunt or misreading a blitz by a quarterback and not changing the protection to wreck the whole system. And boy, what you just told me was that the biological system that is a cow is really the ultimate team sport. And the you know, the the job from a nutrition perspective is to just give each one of those systems the tools that it needs to do its job. Quite frankly, the way God intended. Absolutely. Absolutely. And yeah, when you're asking when you're asking different parts of that biological system to do the job of another part, what could go wrong? Yeah. What could go wrong with bringing in the wide receiver that's 160 pounds and lining them up in the backfield to to pick up blitzes against uh the big NFL linebackers? Yeah. What could go wrong? Yeah, what could go wrong? But that's what happens with our cows. Yep. And so it's little bits here, little bits there. And I think that's Scott, why some herds we see relatively lower to medium risk levels of Dawn having greater effects on cows, greater negative effects than higher levels at a other dairy. Because maybe it's just Dawn at this dairy versus multiple mycotoxins here. What all challenges is the cow trying to deal with? And now we're putting just one more challenge. So Dawn can affect each part of the cow's body. It's not just a rumen influence, it can influence each part of the cow's body. So I I want to bring up Don resistant microbes. You know that so there's a thought that some bacteria can tolerate Dawn, but it's maybe not the necessarily the good guys. Maybe not necessarily the most efficient good guys. So there are some organisms that can tolerate Dawn, but now we're going from being dependent or shall we say utilizing the most efficient organism to now it's the low efficient but tough, durable organisms that are t tolerant to Dawn. Anyhow, we've lost feed efficiency. We've lost our ability to fully make use of the diet that has been most correctly formulated because we don't have the most efficient organisms fermenting that diet in the rumen. That makes sense. You know, speaking of feed efficiency, I mean it when you walk through the list of things that we know Don can impact. Obviously, if we're if we're seeing symptoms like erratic manure that's leading us to believe there's hind gut fermentation, we inherently know, intuitively know that we're not being as efficient with the TMR as we can. Uh I'm one Larry. I don't like to I don't like to put a number on toxin levels. That's just me. And I I've kind of arrived that way after working in this space for for the last number of years because of one of your comments you just said. Why is it that a herd that is consistently at 1.5 ppm Don seemingly not having any issues? Yep. And yet that you know the the neighbors herd at 1.5 ppm are having all kinds of problems. They're not making any milk, they're not getting cow's bred, and it's because of those stacked challenges and how that cow is is allocating nutrients. However, you know, everybody likes to talk numbers. I don't, so I think there's a lot of value in knowing the levels on a part per million basis of Don in your TMR, in your corn silage. But I think the the benefit of knowing it's there outweighs to some degree the actual level. And if we know it's there, we can now put on our Sherlock Holmes glasses and go see if there's any clinical symptoms showing up. Yeah, yeah. I think that'd be fair to say. We're putting another dot on the wall to help us connect the dots so that we get a picture of what's going on. If we don't know what's there for mycotoxins, we're not as able to fully deduce what our challenge truly is. And I think if we know these mycotoxin levels over time, it helps us to see what is shifting in the diet, what's shifting in the cow's performance, performance, and we're better able to truly figure out what is happening. So the more information points I can have, the more likely I am to truly determine what the challenge or challenges are. And if nothing else, we start to eliminate potential challenges. Exactly. Exactly. And I think that's a big one. And I'm going to do a callback to a previous episode we did right now, and that's going to be episode 59, folks. It dropped on November 3rd. Nine months of pain, all because testing came too late. If nothing else, if we were testing regularly, we could have maybe just ruled mycotoxins as not a contributing factor. And in best case scenario, rather than suffering through nine months of diagnostic struggles, we could have determined that hey, there is significant reason to investigate mycotoxin-related issues, and potentially we could have treated that situation nine months before we did. Yep. Absolutely. Yeah. I just I think about some of those situations, and I and I go back to when I was on the dairy with my father, and I I just remember the emotional toll that it would take on myself and my father when things weren't going right, and it felt like we were just beating our heads against the wall. And turns out we were just dealing with a mycotoxin problem that could have been solved relatively easily. The last thing I want to get to is can you expand on Don interrupting the rumen liver immune communication? Talk us through that. What does that mean? All right. Well, part of it is if we lose control of the rumen in that we have fermentation now not occurring. So now we've got nutrients ending up in the small intestine that might be utilized by bacteria that are pathogens or going on to the hind gut. Now we have destruction taking place of the intestinal lighting, and now we have items due to gut permeability that are ending up in the liver, where the liver's trying to deal with these as toxins, and liver isn't functioning as properly as what it should be. So again, it comes to our river analogy, making sure we use nutrients in the proper spot so they don't end up in other places to contribute to pathogens and undesirable organisms attacking the gut lining. Then anytime these pathogens, these mycotoxins or other digesta products end up in the body, we have these oxidative products created because we have cell membranes being destroyed. Think of it as we got cannonballs now bouncing around the body, destroying membranes, creating more of these oxidative species. We need more antioxidants to stop the cannonballs, and all of this contributes to what the liver is trying to deal with. So again, a challenge in this part of the body results in challenges in other parts. Yeah, they they can handle that challenge, but they're not going to be as efficient as what they could be. And overall, we're losing because now the liver is trying to detoxify instead of most efficiently process nutrients as possible. Yep. That makes perfect sense. And if I were to break it down into five key points that I'd like the listener to take home and I'll ask you to expand or comment, it's disruptive because it stops microbes from doing their job, which is then going to help shift rumen pH and microbial composition, weakening the gut barrier integrity, activating the immune system. And at the end of the day, that's going to quietly erode performance, and oftentimes long before we ever see obvious symptoms. No, I think it's that right there. Rumen organisms aren't functioning the way that they should be. They're slowed down, hitting the pause button. We have things passing out of the rumen that shouldn't be, that now feed pathogens. We lose our castle wall integrity, liver doesn't function the way that it should be, and we have more inflammation to deal with throughout the body, and nutrients are going to non-productive purposes instead of productive. And gradually this happens over time so slowly that we don't really notice it until one day we say, Wow, our milk production is way off. Wow, our preg rates are way lower than what they used to be. It was a slow, gradual decline down. You know, and that's like the definition of drift. To go back to your river analogy, think of the boat that's on the edge of the ocean, right? And if you're sitting in the boat, you almost don't even realize you're drifting. Maybe some other people can see it, but all of a sudden you wake up and there's no land in sight. And you just quietly drifted away. And there you go. So, well, I think we have brought this conversation home. Larry, again, thank you so much for taking time out of your day. We're gonna see everybody again in two weeks, and we will bring you some more information, a similar deep dive on another mycotoxin. All right, see everybody in two weeks. Thanks, Larry. All right, thanks a lot. Bye. Thank you for listening to Ruminate This with Agrarian Solutions. Look for our next episode in two weeks.