Ruminate This | Agrarian Solutions

66: Inconsistent Herd Performance? Take A Closer Look at Fumonisin

• Scott Zehr • Season 2 • Episode 66

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0:00 | 27:36

Fumonisin is one of the most overlooked mycotoxins in dairy production, and its impact goes beyond immune suppression. In this episode, Dr. Larry Roth explains how fumonisin disrupts cell-to-cell communication in the gut (often called quorum sensing), which plays a critical role in gut integrity, immune function, liver health, and respiratory resilience. Learn why this mycotoxin is increasingly more common, why many binders fall short, and how targeted testing and smarter mitigation can help explain inconsistent herd performance.

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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. Hey, welcome everybody to another episode of Ruminate This with Agrand Solutions. I am your host once again, Scott Zare, and joined again today with my friend here at Agrarian, Dr. Larry Roth, Vice President of Nutrition. Larry, thanks for jumping in today. Thank you. Good to be here. Larry, there's a term that I've noticed popped up in the in the industry here over the last few years, different companies using it. And the term is quorum sensing. And so I talked to you about this a couple of years back, and and basically quorum sensing is a term that's used to describe how cells within, say, a cow's body communicate with each other. So there's, if I'm understanding everything correctly, there's good quorum sensing that goes on. You know, kind of like you and I talking about stuff on this podcast. That's a that's a good thing. And then there's also bad quorum sensing that happens, like when people talk about how the Dallas Cowboys haven't won a Super Bowl since 1995. To me, that's bad quorum sensing. No, but let's take the jokes out of it. What's an example like inside the cow of good quorum sensing? And then I'm gonna ask you about an example of bad quorum sensing that's gonna fit our topic today, talking about the mycotoxin femonicin. All right. Excellent question. Quorum sensing. Quorum sensing in the body can happen at different levels. We we see the immune system getting turned on when pathogens or beneficial bacteria are picked up in the small intestine. There's like radar receptor sites there. That when it picks up either, say, an E. coli or salmonella or an acidophilus or a biphenobacteria, that immune system goes to a higher level of readiness to defend the body. We think of our cell wall deficient bacteria as initiating some quorum sensing with intestinal cells so that the cells, shall we say, activate the transport proteins to take the garbage out of the intestinal cells. We know that the transport proteins are there to clean up normal metabolites in intestinal cells, and that's also how the intestinal cells get rid of mycotoxins before they're able to cause the cell to die, puncture a hole in the castle wall, and start that sequence of events. So it's so key that body cells are able to communicate. Yeah. So I guess that leads me into femonicin. So this mycotoxin is widely accepted as one of the big five, which we maybe started to say of the big four because we don't really see aflatoxin anymore. But yet it seems like femonicin doesn't come up on our assays that often, albeit the last 18 months, especially in the eastern seaboard here. I'm thinking like Virginia, North Carolina, parts of Pennsylvania, Maryland, we've seen a rise in femonicin. So even though it's one of the big five, it doesn't seem like we maybe know a lot about it when we're in the field. People or the people that we interact with don't know a lot about it. It's just one of these other mycotoxins other than Don or Xorolino. What is it about femonicin that makes it so dangerous to the cow? Well, let me, Scott, before I answer that question, let me broaden that geographical area. We quite often are picking up fumonicin in corn silage and corn grain samples out of Texas, Oklahoma, and Kansas. So we think of fumiticin as being, I'm gonna say, a little bit more of a warm weather mycotoxin. So the states you were mentioning before had had a hurricane come through, and we saw higher levels of fumodicin there. So we we do see it certain parts of the country. Now, why is fumodicin so dangerous to the cow or any animal for that matter? Well, it stops communication between the cells. We talked about how cells are communicating, be it from an immune standpoint, communicates from an energetic standpoint, and it's just like us. Cell communications, cellular communications were to stop, where would we be not in a good spot? So that's kind of what fumatizing does, it stops cells from communicating. Larry, there's a there's a big lesson there to be learned. I'm gonna stop right there because this is applicable to all life. When communication stops, it's never good. Absolutely. That's just a personal note thing to people that are listening. Communication is the key. I didn't mean to cut you off, Larry, but go ahead. So we think of cells communicating so often it's it's nerve action, but it's also immune action when pathogens, different toxins, different metabolites are picked up, the immune system goes to a higher level of readiness. So we can think of fumatism comes in and tries to cut off the communication between cells. Take down the cellular towers, take down the satellites, if we want to think of it from that standpoint. And so when the body is not able to communicate between the different parts, we see the liver loses some of its antioxidant capability, and we see the liver, or excuse me, the immune system is not as strong and active as what it could be. So consequently, we have more pathogens, more metabolites that are circulating through the body, creating more of the oxidative species. Liver isn't able to handle those, and we see cell death in different places. We can see more of the leaky gut because, again, cells at the intestinal level aren't communicating from an immune standpoint to protect themselves, and we lose control of our castle wall. Interestingly, we see this come into play also in the lungs. So lungs are central. We we can go without water for a long period of time, relatively, but we can't go without oxygen. We think of newly weaned cattle that end up in a feedlot. We think of cattle that are in poorly ventilated barns during the winter time, challenges that take place with the lungs. Well, if we don't have communication between cells in the lungs, we don't have good immune function, we're not able to expel pathogens from the lung, we have cell death, and that whole cascade of events starts. So fumaticism is actually quite dangerous for any animal, and for our discussion today for cattle. Yeah, I mean, you just listed off a whole host of challenges there. Leaky gut, liver stress. Obviously, this is all leading to more inflammation. You know, you mentioned the immune system and and it's shutting down the immune signaling. I mean, would you go so far as to say it's immune suppress like immune suppression, suppressing the immune system? We could say we could say that it suppresses the immune system. I'm gonna say it probably is could be termed more stops immune communication. When I think of suppressed immune system, uh we think of an immune system that doesn't have the nutrients that it needs to create the different elements of the immune system to attack pathogens, oxidative species, metabolize and clean things up. What fumodicin does is it stops the different uh uh organs and tissues in the immune system from doing what they're supposed to. So you you could say immune suppression, but I think going back to where our conversation started, uh Pumitacin stops immune communication. I mean it's as you start to get as you start to get into this Scott, it is so amazing how the the body, be it our body or the cow's body, is designed for all of these different parts of the body to communicate. But if those different parts, digestive tract, lungs, liver, immune tissues, lose that ability to communicate, things are literally dead in the water. No, we we talked about the cascade effect with with xoroinone on a previous episode where we think of the direct influence being the estrogenic effect directly impacting repro, but there's a lot of other issues where maybe a little bit of a distinction here with femonicin isn't so much that it's like xoroinone, where it's one direct impact on one region predominantly, and then everything else, this is like 100% affecting all functions with inside that animal, which could lead to honestly a bigger cascade effect if you think of it that way. Yeah, I think that'd be a good way to think about it. Exactly. So when we get into a herd of cows, and again, things don't make sense: inconsistent manure, inconsistent milk production, inconsistent respiratory health, inconsistent repro, just go on down the list. We've kind of got to come back to looking at fumonacin and what might be the levels of fumonicin. So I know we're here today to talk about fumonism, but again, I just want to remind our listeners the importance of testing for mycotoxins, surveilling what's out there for mycotoxin contamination so that we are prepared to put some kind of protection system into play for our animals. Yeah, I mean, exactly right, Dr. Roth. And I'll I'll just remind everybody again if you would like to take advantage of our complimentary mycotoxin sampling program, reach out, email us, podcast at agr.com, and we will get in touch with you on that. So walk us through, Larry. I I think this is really interesting how femonicin' disrupting the cell communication. So walk us through the timeline, if you would, Larry. The first things that are affected. So a cow consumes feed that's contaminated with femonicin, right? So goes down, it hits the rumen, and now this is when the cascade starts. But maybe just think about that femonic as it works its way through the body or that that TMR as it works its way through the body, and just kind of go through the different areas of the cow that are going to be affected. Because it if you're saying the whole animal can be affected, I mean that's that's really what we're saying. But yeah, let's walk us through that. Okay, good. I think that's a great way to look at it, Scott, because that comes into play with how we're going to defend and protect the cow for our conversation today. How we defend and protect the cow against fumaticin. So we think of the primary site where fumaticin starts attacking the cow as being the small intestine. Well, fumaticin comes onto the scene, stops the quorum sensing that you referenced at the beginning of this conversation. Fumaticin stops communication between the cells. Cells aren't able to activate the immune system, and the castle wall is sitting there wide open for invasion, not able to defend itself. So we have cell death at the small intestine level, holes in our castle wall, and bad things start to get into the body. We'll come back to that, but let's continue with your question about fumaticism. Fumoticin is now into the body. We have so many different cells in the body that are related to immune regulation, producing the elements of the immune system that go out and attack and destroy the bad guys, be it pathogens, toxins, metabolites, what have you. Well, now the body's not able to defend itself, either small intestine level, or the wall has been breached there throughout the body. So bad stuff, a scientific term for you, is going all through the body, not able to defend itself. Now we end up with the fumaticism reaching to the liver. Well, the liver does so much for simple nutrient metabolism, does so much for breaking down these oxidative species that are breaking down membranes and causing so much damage and havoc throughout the body. But the liver cells aren't able to communicate amongst themselves to make all of this happen because fumodicin is there and stopping this communication process. We've talked earlier about the lungs. So now fumaticin is going through the blood system, affecting immune tissues, affecting the liver, and eventually reaching the lungs, where again, lungs aren't able to clear pathogens and toxins. We have death of lung membrane cells. And I I think, Scott, we we could say that the lung lining is again kind of like the castle wall in the digestive tract. And so now you've got so many bad things happening throughout the whole animal that we may lose the animal. If not, just poor performance may actually lose the animal because the communication between cells has been compromised. And so the animal is not able to defend and protect itself adequately. That's tremendous when you think about it in the way you just described it. Yeah, I I recently visited a farm that in the past has had femonacin present in the diet. And Larry, on the records, when I was looking at the health records, I was just listening to you going through, and I see pretty high incidence of indigestion, pretty high incidence of ketosis, pretty high incidence of pneumonia in in the cows, way higher than I should see in a in a mature herd. Just makes me wonder how much of that is from the fumonicin. So I think that's a great question. Anytime we start seeing these problems show up, especially when they're kind of erratic, we want to start thinking about fumonacin. But then, Scott, we were kind of saying the same thing about xeralinum. So that's where the surveillance program testing for mycotoxins becomes so important. Let me follow up on that for a moment. The challenge is that the feed ingredients that we have typically used to bind fubinicin are pretty ineffective. But where DTX concentrate or cell wall deficient bacteria are not binders, rather, they help the cells to communicate so that mycotoxins can be repelled right there at the intestinal cells. That's how we're going to try to defend against fumatics and help the cells to communicate, help maintain the integrity of the small intestine, the castle wall, to heat mycotoxins out right there. Well, Larry, you just brought the human morality side of this full circle in the sense that good communication is always going to beat out bad communication. And because what you just said with the L-form uh bacteria technology we have in DTX, which is good quorum sensing, it's good talking, good communication between those receptor sites in the small intestine. And we're able to reject those mycotoxins before they get a chance to mess the communication up. And what we've seen with the cell wall deficient bacteria we have here at agrarium, actually, some of the very early research that agrarian did was with chicks, day-old chicks, and going with some four different levels of fumaticin, including a final fumaticin level that was really quite high. And what we saw was improved chick survivability and chick growth. And these chicks are so fast growing. We talk about cell development and all of that with our ruminants being important. Well, with that chick, it is such a higher relative growth rate. And we saw that the cell wall-deficient bacteria helped defend and protect the chicks, so we had not only greater survivability but improved growth and feed efficiency. So we know from field experience that the DTX concentrate is effective when cows are challenged with fuminicin. Got the chick research. So here's a great opportunity. If nutritionists, dairy producers, veterinarians find that they've got fuminicin contamination, let's talk about what DTX, the cell wall deficient bacteria, can do for helping to defend and protect the animal against fumonacin. I I think that's such an important point, though, to bring up the chick research, because we do dedicate this platform, I would say, 99% of the time to cattle here in the US. But you know, the chick research is some pretty good data, and our swine data is pretty profound as well. And, you know, we use the same technology in all three of those species across the globe. Right. Yeah. And again, I realize our main audience is on the ruminant side, but I think that with the chick data, we've got kind of challenged animals, challenged from high growth rate, and we can take some of those results and transfer them over to our ruminants. Exactly. Yeah. So Larry, you know, you describe very, very well for us kind of the path of destruction, if you would, that Fromonacin leaves behind in its journey through the cow's body. And you know, everything you just described from the lungs, the intestinal integrity, the liver health, you know, I put all these things together, and I I'm I'm thinking about the herd that I referenced and and the the different health challenges they had. And and honestly, it reminds me of that term of we used to use a marketing, it was a marketing piece we had at agrarian, and it was avoid the roller coaster. Don't let your herd, you know, get on that roller coaster. And I feel like that's kind of what it would be like if we were dealing with some Femonicin challenges, right? We have the cows just going up and down, erratic intakes, you know, just starting their lactation off, not very good. And and then, you know, maybe there's a change in the Femonicin levels and they they start to rebound and then they crash again. And but you know, kind of bring us home from that perspective of one, the things that Producers need to look closely for and in that roller coaster ride that we're trying to help them avoid. Okay, perfect. Let's do that. So I think we have to start with feed intake. That to me, that that's where everything starts. Number one. Right there with feed intake. And I always like to use this analogy. If a group of us went to a nice buffet bar and one of us was not feeling well, that person's probably only going to go up once. Might go up to the dessert bar a couple times, but only going to go up once. So cows that don't feel good because the immune system is not communicating, because they have lost integrity at the small intestine level, they're not eating like what they should. And then they start to feel a little bit better. So the roller coaster effect can start right there at the feed bunk. And if cows are eating, are they having off-feed days? Is it showing up in irregular manure? We start to look there. And then what's so neat about these dairy cows is they're producing milk each day. And so we we have that daily marker of what's happening with the cow. What's her milk production day to day? Go back to your roller coaster. Cow's not eating, milk production is down, she's having to defend herself against all of these cells, all of the pathogens, toxins that got into the body because we lost some small intestine integrity. Well, milk production is down. Again, glucose is a key fuel for the immune system, and so many cells, no glucose, no lactose. Milk generally has a relatively constant lactose level. So no glucose, no lactose, no milk. That's simple right there. And again, we don't have glucose. So now different uh body tissues, such as the udder, are not able to defend themselves. We see things like mastitis start to to flare up. And then we go to our transition cows that are under such a challenge with inflammation from so many different natural sources. Reproductive tracts trying to heal itself. Mammary gland is starting to produce smell, so many inflammation loads on the transition cow. But she's not able to resolve that because we have fumaticins stopping communication between cells at small intestine level, immune level, and liver level. And then we get into some of these winter conditions where we don't have as much ventilation as what we would like. We start to have ammonia, and that can lead to pneumonia. I think it's so interesting how those two words sound alike and they're so related. So we have a our lung cells are compromised. Fumodicin is keeping the lung cells from communicating to adequately defend and protect the lungs, and things start to spiral down. And then what is the final thing, the tip of our pyramid with the dairy cow? Reproduction. So if the base of our pyramid has been compromised because cells aren't communicating due to gamutin contamination of the diet, well, the repro is going to suffer. Reproductive cells aren't communicating. Glucose is over here going to fuel the immune system, so we don't have glucose contributing carbons to the rapidly developing follicle cells and later on embryo cells. And again, that spiral downward just accelerates itself. Oh, yeah. I mean, you summed it up well. And and again, it's you know, we we all know Repro is the first to go and the last to come back. And it's very much that natural hierarchy of that cow and how she's going to allocate her nutrient pie for the day. Well, I appreciate you very much taking time out of your day today with us, Larry, to go through Fromonicine. I think there's some really good insights here for nutritionists and producers across the country. And, you know, I just I just think we go back and we, you know, we talked about Don being the the rumen disruptor toxin, and we talk about xorolinone being that, you know, the the estrogen imposter. And really what it sounds like is femonicin is is quite the saboteur toxin and how it disrupts that communication. I think that's a great way to think about that, folks. So, Larry, well, we are going to have you back in the chair again as we're gonna dive into, I'm just gonna say it, the last of the big four. And uh, and that's gonna be T2HT2, which I think some people have heard of. I think many people have probably heard of it. Doesn't always pop up a lot, but when it does, we certainly want to be paying attention at what levels and what issues we're seeing from it. Not one to mess around with. Exactly. All right. Well, thank you, Larry. You have yourself a good couple of weeks. We'll talk to you again, and I'll be talking to everybody else soon. All right, thank you, Scott. Mike, thank you for listening to Ruminate This with Agrarian Solutions. Look for our next episode in two weeks.