Molds produce mycotoxins to weaken surrounding organisms and give the mold a better chance of survival. Mycotoxins are not seeking to specifically target animal tissues; they are simply made to help their parent mold survive. The animal has defenses to protect itself against mycotoxins in the small intestine. The intestinal lining acts as a castle wall to protect the rest of the body from harmful molecules. High mycotoxin concentrations can overwhelm the animal’s self-defense mechanisms and cause cell death and a breakdown of tight junctions between cells. The loss of intestinal integrity causes leaky gut and enables mycotoxins and other pathogens to enter the body. It is important that products that defend and protect against mycotoxins help the castle wall – the animal’s intestinal lining – stay strong so the animal can defend themselves from mycotoxins.

Ruminal bacteria and protozoa have some capacity to breakdown mycotoxins and render them non-toxic. High concentrations of mycotoxins can overwhelm this ability because mycotoxins are made by molds to harm bacteria and protozoa. The mycotoxins can potentially reduce the beneficial bacteria in the rumen microbiome; thereby resulting in the inconsistent manure and reduced milk components often observed during a mycotoxin challenge. The ruminal environment impacts the ability to breakdown mycotoxins; for example, low ruminal pH conditions, such as associated with high starch diets, often result in lowered mycotoxin breakdown rates. Mycotoxin protection products need to not only protect the animal’s intestinal lining, but also prevent mycotoxins from harming rumen bacteria.

Mycotoxins have been in the environment for thousands of years, and the animal has developed the ability to defend itself from these toxins. Problems begin to occur when the concentration of mycotoxins is too high for the animal’s natural defense mechanisms. DTX helps the cow to maintain her intestinal castle wall defenses against mycotoxins. DTX may also help protect the rumen from mycotoxins and keep the rumen bacteria healthy and digesting feed like she was made to do.

Caroline Knoblock, MSc, – Director of Nutrition, Agrarian Solutions and Larry Roth, Ph.D., PAS – Vice President of Nutrition

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Mycotoxin binders (MTB) work by chemical interactions involving cation exchange capacity with various types of bonds and by their physical structure serving as a “net” to in essence “trap” mycotoxin molecules. The bonding and structural properties of traditional MTB also enable these ingredients to tie-up amino acids and vitamins. Understanding the risks and benefits associated with MTB allows nutritionists to determine the economic feasibility of these ingredients.

Lab-generated in vitro results offer in vivo implications to be considered during ration formulation. Further, the in vitro projects enable new product development and evaluation of modes-of-action. The in vitro research projects included in Kihal et al. (2020, 2021) sought to start to understand how common MTB interact with mycotoxins and dietary nutrients. Using a washout model at multiple pH levels to simulate ruminal and lower tract digestion, both peer-reviewed papers show the effectiveness of different MTB at binding different mycotoxins and nutrients. Each test tube contained one binder and one mycotoxin or nutrient, or sometimes multiple nutrients. Because the animal’s digestive tract is populated by microbes and contains all the nutrients she eats we cannot use the results quantitatively. But what the research does tell us is which mycotoxins and nutrients the MTB may bind in the cow if the opportunity is right.

What do the in vitro Kihal studies tell us about the interaction between MTB and nutrients, including vitamin E, vitamin D, and the B-vitamins 1, 2, 3 and 6, as well as the amino acids methionine, lysine and threonine? The MTB did not bind vitamin D effectively, but 15-60% of the vitamin E was bound by various MTB. An average of 20% of the amino acids were bound by MTB, and yeast cell wall bound the most amino acids at 25% of each. B vitamin binding varied from 0-95% depending on the B vitamin and the MTB.

What does the 68-study meta-analysis in Kihal et al. (2022) tell us about MTB and mycotoxins? One thing is certain – binders are effective at binding aflatoxin. The unfortunate part is we do not see much aflatoxin in the United States anymore. At best, some MTB may bind up to 50% of zearalenone, fumonison, and T2 in vitro, but varies from 5-50%. The MTB have little efficacy against DON, binding 10-20%. What binding efficacy can we expect in the cow, when the MTB are not alone with the mycotoxin as in an in vitro situation?

The Kihal et al. series of research articles (2020, 2021 and 2022) serve as clear indicators that MTB are often more effective at tying up nutrients than protecting the animal against mycotoxins. The research documents enable a nutritionist to rank and make ration adjustments for including various MTB in the diet due to reduced nutrient availability. In contrast, the DTX™ Concentrate is not a MTB, does not tie-up nutrients and is research proven for the ability to defend and protect lactating dairy cows against DON and zearalenone.

Larry Roth, Ph.D., PAS – Vice President of Nutrition, Agrarian Solutions and Caroline Knoblock, MSc, – Director of Nutrition

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Heat stress and mycotoxin contamination are harmful enough alone, and especially so when experienced together by dairy cattle. Heat stress occurs when cows cannot dissipate the heat they produce and try to compensate physiologically in ways that result in less milk and poorer reproduction. Why does this happen?

Heat stress results in a cascade of events whereby cows attempt to alleviate internally produced heat via increased respiration; however, there are also consequences including reduced feed intake, lowered nutrient intake, altering of digestive pH, increased digestive pathogen levels and leaky gut syndrome. The immune system attempts to defend an animal during a nutrient restricted time, and nutrients are re-partitioned from productive purposes (growth, milk production and reproduction) to simply keeping the animal alive.

Consuming a mycotoxin-contaminated diet compounds the negative heat stress effects as another inflammation-source to which the cows must respond, and once again diverting nutrients from profitable utilization.

How do we protect our cows from this deadly duo? Cooling systems involving air movement and moisture for evaporative cooling are essential during heat stress periods. It is also critical to feed palatable diets with additions to restrict wild yeast and mold growth from metabolizing nutrients in the TMR as well as creating internal issues.

Dairy producers and nutritionists also cite supplementing Select DTX™ Concentrate as a profitable practice when feeding a mycotoxin-contaminated diet during heat stress periods. Independent research indicated that DTX feeding may protect cows from harmful mycotoxin effects and with the reduced inflammation enable nutrients to be re-partitioned to profitable uses.

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Enhancing reproductive success may be one of the most crucial factors for improving dairy profitability. A recent third-party study with over 920 cows, proved supplementing DTX™ Concentrate to early-lactation Holstein cows challenged by mycotoxins improved the first-service pregnancy/service by 28.6% for artificial insemination (A.I.) and 15.6% for embryo transfer (ET) services at first pregnancy check (28-34 d post-service). Why did DTX Concentrate supplementation improve reproductive success?

The mycotoxin TMR contamination levels (approximately 1.56 ppm DON and 147 ppb ZEA) experienced by cows in this study were not excessive. Even moderate levels of mycotoxins disrupt the intestinal lining, causing reduced nutrient absorption and increased nutrient demand from the subsequent immune response. Improving nutrient absorption and efficiency enables the cow to use nutrients for productive purposes that can result in reproductive success.

Researchers have repeatedly demonstrated that achieving less severe negative energy balance post-fresh significantly enhances reproductive success. Further, glucose is a key carbon source for rapidly developing cells, such as follicles, and a glucose shortage due to nutrient re-partitioning and deprivation due to mycotoxin exposure would also negatively impact first service conception rate. In addition, glucose and other nutrients are necessary for the rapidly developing egg after conception to avoid early-pregnancy loss.

The enhanced pregnancy success per service observed in cows supplemented with DTX in the recent study could be attributed to heightened mycotoxin defense, which facilitated better nutrient absorption, efficient nutrient allocation, and increased availability of glucose for the rapid development of follicles. Consequently, leading to a higher number of cows conceiving and maintaining pregnancy.

The cow prioritizes nutrient allocation to maintenance, growth (depending upon age), milk production, and lastly reproduction. Nutrient shortages and re-partitioning due to mycotoxin exposure, even at medium risk levels, could have profound negative reproductive effects due to the cow’s hierarchy of nutrient utilization.

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Written By: John Doerr, Ph.D., PAS, Dpl. ACAP Vice President, Science & Technology

As well-known as mycotoxins have become in animal agriculture, there are some recurring myths needing correction so a producer can make good choices when faced with a possible threat to the herd or flock:

Mycotoxin = aflatoxin. False. Aflatoxins are just one kind of over 2000 known mycotoxins. Zero aflatoxin does not mean that there are no mycotoxins. A corollary is that when a test for 6 or so different mycotoxins is performed and the results are negative, the feed tested is ‘safe’. False. While we don’t see some of the odd mycotoxins very often, or if they are not part of the test panel, the animals may still be at high risk. For example, one called beauvericin has been known for over a decade, but little was known about its effects on domestic species. In a 2016 study, Schoevers [E. J. Schoevers, et al. (2016). Toxicity of beauvericin on porcine oocyte maturation and preimplantation embryo development. Repro. Toxicol. 65:159-69] reported that this toxin has serious impact on developing pig embryos shortly after fertilization of the ovum. At this time, we may not have similar studies for poultry or cattle, but the implication that they are also at risk is reasonable. Does your mycotoxin test include beauvericin?

Monogastrics absorb mycotoxins differently that ruminants. True. But differences occur within each of those groups. Even within one type of animal (e.g., the dairy cow) different breeds have different susceptibilities to specific mycotoxins. And, within a single breed, there is considerable variation animal to animal on absorption and impact, usually dependent on health, environmental stress, genetics, etc. But, almost without exception, all animals do absorb mycotoxins in the same general region of the intestinal tract.

The rumen will detoxify key mycotoxins. False. Early research was performed in vitro with rumen fluid; some research confirms that a portion of deoxynivalenol (DON) is converted to a less toxic form. But zearalenone is converted in the rumen to an alternative form that is many times more estrogenic than the primary molecule. And while some research implied aflatoxins might be broken down, one must then explain how a conversion product of aflatoxin in the liver, aflatoxin M1, can show up in milk.

High levels of mycotoxins are needed to affect animals. False. First exposure may be acute…a sudden problem from a portion of one ingredient for a short time…or chronic…low to moderate levels over a long period of time. Each will impact the herd or flock. And, when there are multiple mycotoxins, low amounts generally produce the most noticeable synergistic effects.

If the toxin is below FDA levels, it’s okay. False. FDA’s primary mission is to protect humans from problems related to their food, and secondarily to protect animals from chemicals that may harm them or contaminate the milk, meat, or eggs they produce. But the line between what causes possible harm to a cow or pig and what impairs efficient production is not clear cut. Whether your Holstein produces 90 lbs of milk or 70 lbs of milk is not FDA’s concern.

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Written By: John Doerr, Ph.D., PAS, Dpl. ACAP Vice President, Science & Technology

Back in the early 1960’s, when the news of aflatoxin was just ‘going viral’, a team of agricultural engineers went to work on determining the rules for correct sampling of corn. From that, the statistical methods approach for obtaining samples developed and has been a useful guide, but it is often the least followed in practice. It’s 2022. What do we do today about the sampling issue?

Fact: 80% of all error in toxin analysis comes from the sampling. That means that in the worst case when your test report says 100 ppb of T-2 toxin, the real value could be as low as 20 or as high as 180 ppb. What does that mean for your Holstein, Duroc, or Cobb700?

Fact: for low error, accurate analysis of shell corn, about 5 kg of properly sampled grain is required. After coarse grind, 1 kg is sampled for additional fine grinding from which the 50 gram analytical sample will be taken. Look at it another way…that 5kg initial shell corn sample equals about 4.3 kg dry matter. Translate that into sampling pelleted feeds (not too hard) or wet rations, such as dairy TMR or high moisture corn. Now it becomes significantly problematic.

Fact: commercial laboratories aren’t too concerned about what amount of sample you want to send; rather, they have set limits on their drying capacity. You send in 4.3 kg dry matter basis of a 60% moisture feed/forage, the lab is getting almost 11 kg wet weight basis. They will NOT dry that much.

Some guidance: Typically, your goal is to provide a minimum of 500 gm of representative sample. That’s also about what you can pack into a 1L zip bag. Representative? Probing a grain delivery truck or stream sampling from bulk storage bins just means randomizing small collections, mixing well, and then taking your submission sample. Forages, wet feeds…again, small (!) collections and combining very carefully; dairy TMR if mixed too much will undergo particle separation and the result will not reflect the feedstuff. Of course, you’ll have to live with some error which means you have to learn to interpret your mycotoxin report correctly. Given the potential error range, using some arbitrary ppb or ppm number will be the wrong approach. Instead, based on history or professional guidance, categorize your results as to low, moderate, or high risk and take action accordingly. That’s not foolproof, but it does a better job than fixating on some ppb amount. Example: some official ‘guideline’ tells you 500 ppb DON is the limit for a breeding animal. Your test comes in at 499 ppb. That does not mean your animal is safe! And those guidelines rarely allow for the fact that a majority of animal feeds contain multiple mycotoxins, most of which have high capacity for synergy.

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