2017 Corn silage: 3 things you should know

Corn silage for both beef and dairy fluctuates between 8-10% of the total corn acres in the US: This year’s corn silage can be expected not to be typical, due to challenging weather conditions that prevailed across different states in 2017.

High variability in quality. Depending on the state, severe drought, heat stress or wet conditions will have a great impact on the quality of 2017 corn silage

Extra sampling is recommended. Due to high variability in the quality of corn silage, producers need to take extra samples after fermentation to track quality levels and the amounts of digestible starch (target for starch content over 30 percent), 30-hour neutral detergent fiber digestibility (target over 55 percent) and 30-hour undigested neutral detergent fiber (target under 45 percent).

In addition to testing for quality and starch, tests should also include mycotoxin analysis due to the higher risk of contamination in 2017 corn silage. Testing results can help when building plans to optimize the crop and the ration.

Check out this video for tips on how to prepare a representative silage sample.

Video on preparing representative silage samples

High levels of mycotoxins have already been reported in 2017 corn in several states in the US. DON levels > 5ppm have been reported in South Dakota, Nebraska, Wisconsin, New York and Pennsylvania corn, whereas aflatoxin levels greater than 100ppb have been reported in Georgia, Texas, North Dakota, Nebraska and Oklahoma. According to the 2003 USDA Crop Production Report, the top ten corn silage producing states are: WI, NY, CA, PA, MN, IA, SD, NE and ID.

For an update on Mycotoxins in 2017 crops and technical information on how cows adapt to DON please watch the video below.

 

Reports of DON contamination in US 2017 corn are increasing

As corn harvest advances in the US, reports show that the amount of corn in poor to very poor condition is well over that of last year. Also, high levels of DON are reported in corn in several states.

Minnesota, Pennsylvania have reported DON levels of greater than 1 ppm in corn silage, whereas levels of DON in corn silage in Iowa were greater than 2ppm

 

Aflatoxins: Did you know that in high yielding dairy cows the carry-over rate into milk is greater?

Researchers from Cornell University studied the relationship between the carry-over rate of aflatoxins in milk in dairy cows and the level of milk production. Their findings suggest that the current regulations of 20 ppb total aflatoxin levels allowable in dairy cow feed are not protective to avoid violation of the 0.5 ppb AFM1 regulatory levels for milk in high-producing cows.

A factor, that is considered to be important for influencing regulatory limits of both total aflatoxin and AFM1 is the rate at which AFB1 is converted and excreted as AFM1 into the milk of dairy cows.

The problem is that most previous studies on the carry-over of aflatoxins from feed to milk were in what would be considered today as low-yielding dairy cows, where the carry-over of the ingested AFB1 is closer to 1 to 2%.

However, a study carried out by Churchill et al (2016) at Cornell University revealed that the carry-over rate into milk in high yielding dairy cows is closer to 6.5%.

When linear regression was used to calculate the relationship between ingested and excreted concentrations of aflatoxin and AFM1 in milk of high yielding dairy cows, the results suggested that an aflatoxin level of 15 ppb, was the maximum likely to produce milk with aflatoxin below the US regulatory limits (0.5 ppb AFM1 in milk). Currently the FDA guidelines for aflatoxin (AFB1) in feed for dairy cows is at 20ppb.

Find out more about the carry-over rate of aflatoxins into milk in dairy cows at the end of the video below

 

How cows can adapt to DON – Anco article in milling and grain magazine

Ruminants are regarded as quite resistant to fusarium mycotoxins such as deoxynivalenol (DON) because of the detoxifying potential of rumen microbes. However, the detoxification capacity of rumen microbes depends on a functional rumen. Detoxification capacity for DON by rumen bacteria can be compromised in high producing dairy cows, which are fed greater amounts of concentrates and where feed passage rate is high.

Read more about how to best support them by nutritional means.
In “How cows can adapt to DON” published in Milling and Grain Magazine, September 2017, p 70-71  here

Read ANCO’s article in International Dairy Topics

3 ways to reduce the impact of DON on milk profits, International Dairy Topics, July 2017

Due to their high feed intakes and high concentrate: forage ratios in diets, high producing dairy cows are at risk for negative impacts of the mycotoxin deoxynivalenol (DON) on milk quality and component yields. The extent of the negative response can be managed by nutritional means, through the use of certain phytogenic substances for more consistent milk component yields and low somatic cell counts (SCC).

DON, the most prevalent mycotoxin in animal feedstuffs globally, has been shown to have a negative impact on rumen efficiency. Scientific studies reported that DON negatively impacted certain aspects of rumen fermentative capacity, especially reduced acetate and propionate production. Other reports show negative impacts on SCC in milk.

Find out how plant extracts can help to increase the resistance in dairy cows to DON by nutritional means in an article published in international dairy topics here.

First indications from 2017 US crop reports show that a wet spring and severe draught conditions are affecting grain quality and DON prevalence. Poor to very poor ratings for corn are twice as high compared to last year. Any level of mycotoxins present in corn can be expected to be three times as high in corn DDGS.

Currently 7.6% of corn is being displaced by corn DDGS in livestock rations. The substantial increase in the availability of corn distillers grains has also increased the interest in using these feeds in dairy cattle rations.

A short video by ANCO provides more information on feeding corn ddgs to dairy cows in the link to the article Feeding dairy cows DDGS with confidence.

Feeding corn ddgs to dairy cows with confidence

Rapid expansion of fuel ethanol production capacity has resulted in 36% of Corn being used for ethanol and corn ddgs production in the US today.

This lead to 7.6% of corn currently being displaced by corn distillers grains in livestock rations. The substantial increase in the availability of corn distillers grains has also increased the interest in using these feeds in dairy cattle rations.

Today corn DDGS is found in around 46% of US dairy cow rations. Corn distillers grains can be highly beneficial in formulating cost-efficient rations for high producing dairy cows.

However, with DDGS from 2016 corn greater care needs to be taken to ensure that dairy rations remain profitable. 2017 corn could also be problematic when used as corn distillers grains according to some of the early indicators from July 2017 crop reports.

Find out more in the video below.

Read Anco’s first publication in Pig Progress on gut agility

Anco article published in Pig Progress Magazine

Being able to manage all the risks impacting cost-effectiveness of diets is the holy grail of nutrition. But where best to start – controlling all the risks in the diet or enabling the animal to respond in an effective way to potential risks? Combining inspiration from the industry 4.0 movement with learnings from genetics pave the way to new approaches in pig nutrition.

Read more in: Keep pigs agile to manage the cost-effectiveness of feed by Gwendolyn Jones, Pig Progress, May 2017

Link to online version of the article
http://www.pigprogress.net/Nutrition/Articles/2017/5/Keep-pigs-agile-to-manage-the-cost-effectiveness-of-feed-121496E/

International Poultry Production Magazine – gut agility article in April issue

Boosting gut agility for cost-effective poultry nutrition. Anco article in International Poultry Production Magazine

Poultry producers must continuously adapt – respond faster to challenges and drive production and cost-efficiency. In a fast-moving business environment, operational agility becomes key to profitability and success. New nutritional solutions based on the concept of agility help to manage consistency in the cost-effectiveness of diets and are designed to contribute to the operational agility of modern poultry production systems.

With up to 70% of production costs coming from the cost of feed, consistency in the cost-effectiveness of diets is key to profitability. However, nutritional stressors in the diet, such as dietary changes, reduced nutrient digestibility, endotoxins, antinutritional factors and mycotoxins, often throw a spanner in the works of consistency in performance in response to diets.

Depending on the increased presence or absence of those stressors the same diet can differ in cost-effectiveness. These stressors are often not easy to control for the nutritionist and are part of the reality that animals are facing in modern production systems.

Read more
on how gut agility empowers poultry to cope with nutritional stress factors more efficiently in the latest article published by Anco.

Boosting gut agility for cost-effective poultry nutrition by Gwendolyn Jones
International Poultry Production Magazine, April issue.
http://www.positiveaction.info/magdetails.php?m=6

Mycotoxin kinetics: Did you know how quickly mycotoxins disappear?

Impacts of mycotoxins on farm animal performance and health are generally well known. However, what is often less well known are mycotoxin kinetics and the metabolism of mycotoxins, when they pass through the digestive tract. Based on the current scientific literature, this is also an area of research that still requires greater understanding.

Considering that most dietary mycotoxin solutions will act on mycotoxins in the gut, it is important to understand the time window for action available in the gut. Increasing knowledge of mycotoxin kinetics and metabolism highlights that speed can be a critical characteristic for the mode of action in mycotoxin solutions, as well as the location for mode of action in the animal’s body.

Pharmacokinetics

The pharmacokinetic behaviour of an orally ingested compound determines how readily it is absorbed from the gastrointestinal tract, which concentrations are reached in the various organs, and how long the agent and its metabolites will stay in the body. These aspects are of prime importance for the biological effects and risk assessment.

Mycotoxins have varying bio-availability. Some will be more rapidly absorbed, whilst others will travel further along the digestive tract. This is very important for a number of reasons:

1) Whether absorbed into the systemic circulation or not, the cells of the gastro intestinal tract (GIT) will potentially be exposed to the full range of ingested mycotoxins and in the highest concentrations.
2) Mycotoxins that are rapidly adsorbed can cause damage in other organs and their metabolism can result in more toxic metabolites as well as waste of metabolic energy.
3) The pace at which mycotoxins will be adsorbed from the gut, will affect the time window for dietary mycotoxin solutions to act on mycotoxins in the gut.

Intestinal absorption of mycotoxins in the gut

Mycotoxin uptake and subsequent tissue distribution is governed by GIT absorption. This passage across the intestinal barrier may be maximal, as with aflatoxins or very limited, as with fumonisins (Table 1). The rapid appearance of most mycotoxins in the circulation suggests, that the majority of the ingested toxin is absorbed in the proximal part of the GIT.

Absorption of deoxynivalenol (DON) is on average 55% in pigs, but very limited in poultry (Table 1). The relative tolerance of poultry to DON has been partly attributed to its low bioavailability. However, the potential impact of the remaining DON in the intestinal lumen is still unknown, and the tolerance level within the GIT might be different.

Further details on DON kinetics and metabolism are discussed later in the text.

mycotoxin absoprtion - gut

Kinetics and metabolism of zearalenone (ZEA)

In pigs zearalenone and its metabolites were found in the plasma of a pig less than 30 min after the beginning of feeding.

The first reported mammalian phase I metabolites of ZEA are the stereoisomers of zearalenol (ZOL) – α-ZOL and β-ZOL. α-ZOL is 92 times more oestrogenic than ZEA. β-ZOL is 2.5 times less oestrogenic than ZEA. The metabolization of ZON occurs primarily in the liver, but a variety of organs show metabolization activity, such as intestine, kidney, ovary and testis.

Observations in pigs indicate that ZEA is rapidly and efficiently absorbed after oral intake and metabolised to ZOL and glucuronides of ZEA and ZOL. The glucuronides are efficiently eliminated into the bile, but hydrolysed in the intestine and the aglycones reabsorbed, accounting for the secondary peaks in plasma level. The extensive enterohepatic circulation of ZEA and its metabolites slows the excretion and extends the half-life of this mycoestrogen in the pig. The enterohepatic recirculation of ZEA and α-ZOL was confirmed in a later study on the fate of a single dose of ZEA administered intravenously to young female pigs (Dänicke et al 2005).

In broilers, a large proportion of ZEA was changed into. α -ZOL and β -ZOL in the plasma and various tissues of broiler chickens following oral administration of ZEA. This suggests that ZEA was absorbed and metabolized rapidly. The absolute oral bioavailability of ZEA was 29.66% and was higher in broilers than in rats (2.7%) ZEA is excreted largely in the form of α -ZOL in the excreta of broiler chickens. (Buranatragool et al 2015).

In another study, the rate of reduction of zearalenone into α- and β-zearalenol was compared in geese, ducks, guinea-fowl, chickens, laying hens, and quail. Zearalenone reduction was lowest in geese and highest in quail. Although α-zearalenol was the main metabolite formed in all the avian species, the α:β ratio ranged from 1:8 in quail to 5:3 in chicken (Guerre 2015).

In ruminants, the nearly complete recovery of ingested ZON at the duodenum as a-ZOL, b-ZOL and ZON suggests only a minor complete degradation in the rumen under steady-state conditions or some interference with an intensive entero-hepatic cycling of these substances (Dänicke et al 2005b).

Studies in lactating dairy cows revealed that with daily doses of 50, 165 or 544 mg ZEA for 21 days, concentrations of 2.5 ng ZEA and 3.0 ng α-ZOL per ml milk were only detected as conjugated products in cows fed the highest dose of ZEA. Thus, even though minute amounts of ZEA and its metabolites are transmitted into the milk of cows from contaminated feed, this carry-over is minimal. (Metzler et al 2010)

Kinetics and metabolism of aflatoxin

Following ingestion, aflatoxin B1 (AFB1) more than 80% is rapidly absorbed in the intestinal tract in both poultry and pigs. The duodenum was found to be the major site of absorption. From the site of absorption, AFB1 enters the blood stream and is transported to the liver, the major site of metabolism.

Metabolism of AFB1 can be divided into three phases, bioactivation (phase I), conjugation (phase II) and deconjugation (phase III), all of which can occur directly at the site of absorption, in the blood, after entering the liver as the main metabolizing organ, or in several extra-hepatic tissues. Aflatoxin B1 itself is not a potent toxin, and phase I bioactivation is needed to exert toxic effects.
Phase I reactions are mainly oxidation of AFB1 to hydroxylated metabolites such as aflatoxin M1, aflatoxin Q1 and aflatoxin P1 and to the highly reactive AFB1-8,9-epoxide. Cytochrome P450 enzymes (CYPs) are known to play the major role in oxidation of AFB1 to the reactive epoxide in many tissues.

Phase II metabolism includes conjugation of phase I metabolites with glutathione or glucuronic acid and is considered detoxification to enhance water solubility and excretion. Conjugates of epoxide and hydroxylated AFB1 metabolites are readily excreted via the bile into the intestinal tract, where they might be subject to bacterial deconjugation as phase III reaction.
The major route of excretion of AFB1 and its metabolites is the biliary pathway, followed by the urinary pathway. In lactating animals, AFM1 and other metabolites are excreted in the milk.
(adapted from Gratz 2007)

Kinetics and metabolism of deoxynivalenol (DON)

After oral intoxication of pigs, DON starts to appear in the plasma after 30 min. A study on bioavailability of DON in pigs revealed that DON was rapidly absorbed following oral exposure and reached maximal plasma and serum concentrations after 99.1 min. The mean bioavailability of DON was 54%. DON was highly distributed and poorly metabolized. (Goyarts and Dänicke 2006).

In avian, species the levels of DON in plasma following oral administration are relatively low, recent results suggest that DON is highly metabolized, leading to the formation of sulfates, which are a detoxified form of the toxin. This metabolism differs from that observed in some mammal species, in which de-epoxidation is recognized to be the most important step. Although the persistence of DON in tissue and its transmission to eggs are limited, the metabolites of the toxin, especially 3α-sulfate, should be measured (Guerre 2015).

In ruminants, the low recovery of DON at the duodenum as de-epoxy-DON and DON would indicate either a nearly complete degradation of the molecule in the rumen and/or absorption at this site of the digestive tract (Dänicke et al 2005b). However, detoxification capacity for DON by rumen bacteria can be compromised in high producing dairy cows, which are fed greater amounts of concentrates and where feed passage rate is high. Both conditions will affect rumen pH and the time available to degrade DON into non-toxic metabolites. Low rumen pH has a negative impact on the rumen microbes that would otherwise detoxify DON. Jeong et al (2010) report that high concentrate to forage rations reduce the amount of DON detoxified by rumen bacteria by 14%. Similarly, Hildebrand et al (2012) observed that DON can negatively influence rumen fermentation and microbial protein synthesis to a greater extent in high concentrate rations than in low concentrate rations.

The rank order of sensitivity of animals to ingested DON is pigs > poultry/ruminants. Intestinal explants (cultured tissue samples) from poultry and pigs possess a similar ability to intestinally absorb DON, suggesting that the difference in their sensitivity to ingested DON does not rely on their ability to intestinally absorb DON.

It is more likely that the sensitivity of animals to oral DON relies on the localization of the intestinal bacteria in their gut in relation to their ability to generate 9,12-diene DON or DOM-1, the non-toxic de-epoxide derivative of DON (Maresca 2013). The presence of high bacterial contents that can convert toxic DON into its non-toxic de-epoxide metabolite DOM-1 before the small intestine in ruminants (rumen-associated bacteria) and poultry (crop-associated bacteria) hugely decreases the amount of native DON reaching the small intestine.

In pigs, due to the high absorption of DON by the small intestine, bacterial transformation of DON in DOM-1 could only be possible if a part of the ingested DON reaches the colon and/or in the case of intestinal/hepatic excretion of absorbed DON.

Differences between animal species

Mycotoxin metabolism can occur in both the liver and the digestive tract. Intestinal metabolism, be in the gut epithelium or by gut microorganisms, may limit the toxic effects of mycotoxins within the GIT. This is especially true for ruminants which can convert many mycotoxins into non-toxic metabolites. Greater resistance to zearalenone, DON or ochratoxin in ruminants has been attributed to the detoxifying role of the microbial population in the rumen. These mycotoxins are effectively transformed into non-toxic metabolites by rumen microorganisms before absorption. However, in non-ruminants, intestinal biotransformation of mycotoxins takes place predominantly in the large intestine and thus provides little detoxification prior to absorption. (Grenier and Applegate 2013)

Scientific data suggest that the toxicokinetics of fusariotoxins in avian species differs from those in mammals. The use of radio labelled DON, T2-toxin, and zearalenone revealed high biliary excretion of these toxins whereas the amount of the parent compound in plasma was low. This observation and the low level of radioactivity found in tissues led to the conclusion that fusariotoxins are weakly absorbed and rapidly eliminated in birds.

Metabolism appears to play a key role in avian species. For instance, the metabolic pathways of DON in avian species strongly differ from what was reported in rat, pig, cattle and sheep, which could contribute to the reported difference in sensitivity to DON. De-epoxidation of DON, which is the main detoxification mechanism in mammals, appears to play a less important role in avian species. In avian species, it seems that sulfation is a key protective mechanism. (Guerre 2015)

Speed matters

The message from the scientific literature is that the potential time window for action on some mycotoxins in the gut is short – for zearalenone in pigs 30 minutes or less, before they get absorbed into the blood system.
The consequence is that speed is of great importance, when it comes to solutions that act on mycotoxins in the gut to counteract their harmful effects. The alternative is that they also should be able to act on the mycotoxins or reduce their impact outside of the animal’s digestive tract, i.e. in the blood system or other target organs for mycotoxins in the animal.

Adapt vs attack – strategies for counteracting mycotoxins

Traditionally, feed additives have been developed to attack mycotoxins in the animal’s digestive tract directly to counteract harmful effects from mycotoxins in the animal. However, both mycotoxin binders and mycotoxin deactivators have their limitations.

It is well known that adsorption is not an effective strategy for most mycotoxins. Only certain bentonites work well with aflatoxins and some yeast cell wall components have been proven to bind zearalenone, based on specific structural fits. For other types of mycotoxins, particularly DON, binding strategies do not work effectively.

Biotransformation of mycotoxins is another strategy that directly attacks mycotoxins to transform their structure into non-toxic metabolites. Again, this strategy is very specific to certain target mycotoxins. On top of that, it takes time to complete the biotransformation of mycotoxins and time to do so in the digestive tract is limited. Find out how long it takes to transform mycotoxins in vitro in this scientific paper.

The question is, how does the animal deal with the mycotoxins left untouched by the highly specific feed solutions mentioned above?

A third and more cost-effective strategy to counteract mycotoxins focuses on disarming mycotoxins by supporting the animal’s resistance to the harmful effects of mycotoxins. This strategy empowers animals to adapt to nutritional stress factors such as mycotoxins and reduces the extent of the stress reactions generally seen in response to these stressors . Find out more about stress reactions

This strategy is not a direct attack on mycotoxins, but it helps the animal to shield itself efficiently from the negative effects of a broader range of mycotoxins, when challenged. It is non-specific for mycotoxins, but highly specific on the side effects of the most important mycotoxins.

References

Buranatragool et al (2015). Dispositions and tissue residue of zearalenone and its metabolites α-zearalenol and β-zearalenol in broilers. Toxicology Reports 2 ,351–356

Dänicke et al (2005). Kinetics and metabolism of zearalenone in young female pigs. Journal of Animal Physiology and Animal Nutrition 89, 268–276

Dänicke et al (2005b). Effects of Fusarium toxin-contaminated wheat grain on nutrient turnover, microbial protein synthesis and metabolism of deoxynivalenol and zearalenone in the rumen of dairy cows. Journal of Animal Physiology and Animal Nutrition 89, 303–315

Devreese et al (2013). Overview of the most important mycotoxins for the pig and poultry husbandry. Vlaams Diergeneeskundig Tijdschrift, 82

Goyarts and Dänicke (2006). Bioavailability of the Fusarim toxin deoxynivalenol (DON) from naturally contaminated wheat for the pigs. Toxicology Letters, Volume 163, Issue 3, Pages 171–182

Gratz (2007). Aflatoxin Binding by Probiotics, Experimental Studies on Intestinal Aflatoxin Transport, Metabolism and Toxicity, Doctorial Thesis; University of Kuopio, Finland

Grenier and Applegate (2013). Modulation of Intestinal Functions Following Mycotoxin Ingestion: Meta-Analysis of Published Experiments in Animals, Toxins 5, 396-430

Guerre (2015). Review: Fusariotoxins in Avian Species: Toxicokinetics, Metabolism and Persistence in Tissues, Toxins, 7, 2289-2305

Hildebrand et al (2012). Effect of Fusarium toxin-contaminated triticale and
forage-to-concentrate ratio on fermentation and microbial protein synthesis in the rumen. Journal of Animal Physiology and Animal Nutrition 96, 307–318

Jeong et al (2010), Effects of the Fusarium mycotoxin deoxynivalenol on in vitro rumen
fermentation, Animal Feed Science and Technology, 162, 144–148

Maresca (2013). From the Gut to the Brain: Journey and Pathophysiological Effects of the Food-Associated Trichothecene Mycotoxin Deoxynivalenol. Toxins (Basel); 5(4): 784–820.

Metzler et al (2010). Zearalenone and its metabolites as endocrine disrupting chemicals.
World Mycotoxin Journal, 3 (4): 385-401

Vekiru et al (2010). Cleavage of Zearalenone by Trichosporon mycotoxinivorans to a Novel Nonestrogenic Metabolite, Applied and environmental microbiology, vol. 76 no. 7 2353-2359