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MYCOTOXINS ▶▶▶


in in vitro models, which simulated the capacity of an actual cow rumen to degrade the mycotoxins under normal pH (6.8) and a lower pH (5.8), simulating acidosis. For DON and NIV, the microbial degradation was slower when pH was de- creased; a delay in degradation is of concern when the pas- sage rate is accelerated due to high feed intake, allowing some mycotoxins to reach the intestine intact. For enniatin B (ENNB) on the other hand, degradation was weak under both conditions. With a normal pH, the maximum degradation achieved was 75%, and a lower pH worsens it by degrading only a maximum of 20% of the initial concentration.


Mycotoxins’ effects on the intestines In addition to looking at the prevalence of mycotoxins and how they are degraded in real-world conditions, for the first time an in vitro model using calf intestinal epithelial cells (CIEB) was used to determine the toxic effects on the intes- tines of Fusarium toxins (DON, NIV and fumonisin [FB1]) and enniatin B (ENNB) – selected for their relevance for dairy cows since they were highly prevalent in silage samples – on the in- testines (Figure 2). All mycotoxins caused cells to die or deacti- vate, increasing the possibility that mycotoxins or other harm- ful substances like gram negative bacteria could reach the bloodstream and cause systemic infections. NIV and DON had the greatest detrimental effects. Even at concentrations of 138 ppb NIV and 172 ppb DON, the cell viability was reduced by 25%. Furthermore, the ENNB and FB1 led to the same 25% re- duction at 1,500 ppb and 3,383 ppb, respectively. For NIV and


DON, the numbers align with trials on pig and human intesti- nal cells. Although it is not always easy to translate in vitro re- sults to in vivo results, the fact is that intestinal cells of rumi- nants are as sensitive as those of pigs and humans, according to the author.


Three tips to mitigate risks of mycotoxins Taken together, these studies clearly indicate risks for dairy farmers. Mycotoxin degradation is incomplete even in ideal conditions and is significantly compromised during high feed intake and acidosis. Given the prevalence of mycotoxins in maize silage, failing to implement a mycotoxin risk manage- ment strategy for ruminants could result in losses in produc- tion and, subsequently, profit. Follow these three tips to en- sure mycotoxins do not compromise the health of your herd. 1. Test early and often. It’s important to understand the mycotoxin load in your silage feeds because of the number and diversity of mycotoxins it may contain. Sampling and analysing silage and feed for mycotoxins is essential for creat- ing the right detoxification strategy. 2. Bind and deactivate. After analysis, nutritionists, techni- cians and farmers need to consider the load of mycotoxins coming from the feed and establish the level of risk. Once this is done, the right combination of binders and deactivators can be determined and added to feed. 3. Support. Support bovine gut health with the right mix of probiotics and phytogenic feed additives to improve nutrient absorption and immunity.


Figure 2 - Cytotoxicity of fumonisin b1, nivalenol, deoxinivalenol and enniatin b1 over calf intestinal epithelial cells through the WST-1 assay.


Deoxynivalenol 100 100 Nivalenol


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0 0.001 0.01 1 10 100 1000 10000 100000 Concertraion [ppb] Fumonisin B1 100 100


0 0.001 0.01 1 10 100 1000 10000 100000 Concertraion [ppb] Enniatin B1


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0 0.001 0.01 1 10 100 1000 10000 100000 Concertration [ppb] 54 ▶DAIRY GLOBAL | Volume 7, No. 3, 2020


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Metabolic acticity (%)


Metabolic acticity (%)


Metabolic acticity (%)


Metabolic acticity (%)


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