MYCOTOXINS CAN BE A PROBLEM FOR PRODUCERS

by: Stephen B. Blezinger
Ph.D., PAS

Part 2

In Part 1 of this series we began a review of mycotoxins and their effects in cattle. Before going on here in part 2, let's consider more background on mycotoxins. While all mycotoxins are of fungal origin, not all toxic compounds produced by fungi are called mycotoxins. The target and the concentration of the metabolite are both important. Fungal products that are mainly toxic to bacteria (such as penicillin) are usually called antibiotics. Fungal products that are toxic to plants are called phytotoxins by plant pathologists (confusingly, the term phytotoxin can also refer to toxins made by plants. Mycotoxins are made by fungi and are toxic to vertebrates and other animal groups in low concentrations. Other low-molecular-weight fungal metabolites such as ethanol that are toxic only in high concentrations are not considered mycotoxins. Finally, although mushroom poisons are definitely fungal metabolites that can cause disease and death in humans and other animals, they are rather arbitrarily excluded from discussions of mycotoxicology. Molds (i.e., microfungi) make mycotoxins; mushrooms and other macroscopic fungi make mushroom poisons.

Let's consider a few more of the different strains.

Fumonisin

Fumonisins occur world-wide in feedstuffs. In contrast to other mycotoxins, fumonisin B1 (the most prevalent of the fumonsins) is relative slowly and poorly metabolized in the rumen. Despite this, fumonisin does not seem to affect rumen metabolism. Target organs damaged by these mycotoxins in ruminants include the liver and the kidney.

Clinical signs of fumonisin toxicity include:

• Reduced feed intake

• Reduced weight gain

• Reduced milk production

• Reduced immune response

• Increased liver sphinganine : sphingosine ratio (altered liver chemistry)

The symptoms of fumonisin toxicity are similar to other mycotoxin strains.

Patulin

Patulin is produced by certain fungal species of Penicillium, Aspergillus and Byssochlamys growing on fruit, including apples, pears and grapes. Fruits stored under conditions that promote bruising and rotting increase the probability of patulin formation. Penicillium expansum appears to be the mold usually responsible for patulin in apple juice and may contaminate the apple pumice waste sometimes used in animal feed.

Patulin was first isolated in the 1940's but is now known to occur world-wide in apple and apple products. Its potential danger to cattle is its presence within fruit pulp and waste products from the fruit industry. These can form a cheap feedstuff for inclusion in ruminant diets, common in dairy rations. Some fruit material is used as a flavoring agent – especially in cows, which are highly sensitive to changes in flavor, where fruit-based material is used to mask certain taints caused by e.g. medication.

Contamination with patulin has also been reported in vegetables, cereal grains and silage. Patulin, however, is not considered a particularly potent mycotoxin. The LD50 in rats has been reported as 15 mg kg1 body and 25 mg kg1after sub-cutaneous injection. Death was usually caused by pulmonary edema. In long-term studies at lower dosage levels, these effects were not observed. It has also been shown to be immunotoxic and neurotoxic. Several studies have found that patulin is genotoxic, i.e. that it causes damage to DNA or chromosomes, in short-term studies.

Symptoms of patulin toxicity include hemorrhaging in the digestive tract in cattle. In 1954, patulin was implicated in the deaths of 100 cows in Japan that ate contaminated feed.

Other Mycotoxins

Other work conducted using dairy cows have shown that feeding a total mixed ration contaminated with deoxynivalenol (DON, 3.5 mg/kg dry matter in trial TMR versus 0.5 mg/kg in uncontaminated control diet) had an impact on metabolic and immune parameters (Korosteleva et al., 2009). The contamination was not severe enough to induce changes in milk production, so could be considered as proof of the negative impact of mycotoxicoses at sub-clinical levels of exposure. The researchers found that, although there was no significant loss in any milk production of feed intake seen for the cows, significant changes in the efficiency of the immune system (when tested by vaccination) were apparent and the cows drank less, resulting in changes in blood serum characteristics.

Symptoms

So with the discussion of the effects of various mycotoxins it becomes necessary to identify the various symptoms so diagnosis can be made. In cattle the most common effects of mycotoxin exposure through feed include:

1. Variable feed intakes

2. Inconsistent milk yield

3. Reduced fertility

4. Scouring

5. Acidosis-type symptoms

6. Lethargy

7. Impaired immune function/poor response to disease or infections

8. Poor rumen function

9. Muscle tremors

10. Bloody feces

11. Lower leg / teat swelling

12. General poor performance without any alternative explanation

Are there safe levels of mycotoxins for cattle?

Since mycotoxins are so common in feeds and forages it can be assumed that some exposure (of either one sole strain or a combination of strains) is fairly common. With this we recognize that some of the factors that make diagnosis difficult also contribute to the difficulty of establishing levels of safety. Mycotoxin effects are moderated by factors such as sex, age, duration of exposure and environmental and production stresses.

One area of particular concern is that a low level of several mycotoxins can be more problematic than high levels of an individual mycotoxin, due to a synergistic relationship. So even if the feed samples tested come back as being ‘low', there may still be an issue.

Partial degradation of certain mycotoxins in the rumen does mean that they are less toxic to cattle than to most other animals but some of these degradation products can be more toxic than the original mycotoxin.

Management Aspects

So as we work to understand these compounds and how they affect the animals for which we are responsible we have to consider the practical considerations. We'll begin with silage.

Managing silage to reduce mycotoxins exposure

In any fermentation storage system, temperature and the presence of moisture is sufficient for toxin production. But oxygen will act as the switch, which turns mycotoxin production on or off during storage. The amount of mycotoxin in contaminated silage samples increases as the ensilement method changes from airtight, upright silos to concrete capped and uncapped silos. The highest forage concentrations of mycotoxins are found in horizontal storage methods, such as bunker silos and feed piles, which are left open to oxygen.

Greater amounts of mycotoxins are found where there has been poor management of the upright or bunker silo, as this results in oxygen entering the stored feed. In scientific studies, well managed bunker silos, covered with plastic and weighted with tires, did not have significantly greater levels of mycotoxins than well managed upright silos. In a plastic covered storage system, oxygen penetration is slowed but not eliminated. The longer the silage is stored, the greater the opportunity for significant fungus growth and mycotoxin contamination. In one study the levels of DON increased in the silo slowly over time even when properly covered.

There is no such thing as an oxygen-proof silo. We would all like to think this is true but, in practical terms, our current technologies are not perfect. If you examine a plastic layer under a microscope, you will see many tiny holes through which oxygen slowly flows. This is especially true of plastic that is stretched for wrapping haylage bales. Any damage to the plastic further increases the flow of oxygen from a trickle to a river and must be repaired as quickly as possible.

A checklist of practices to prevent mycotoxin contamination in silage:

1. Purchase corn and other feed varieties resistant to foliar, ear rot, and stalk rot diseases

2. Purchase varieties resistant to ear and stalk boring insects.

3. Harvest corn and haylage at the recommended maturity and moisture level for your storage system. DO NOT let corn stand in the field after reaching maturity or killing frost.

4. Be sure chopper knives are sharp and cut at the correct length to improve packing

5. Harvest forages as quickly as possible and pack tightly with the proper weight of tractor matched to the right number of packing hours and filling rate.

6. Be sure the silo is sealed to exclude oxygen. Use plastic covers secured by tires on bunkers.

7. Patch any holes in plastic covers, bags, or wrapped bails as soon as possible

8. Discard obviously spoiled feed or layers of feed.

9. Since mycotoxins are highly soluble in water, do not allow rain to wash through upper layers of spoiled feed.

10. Clean out leftover feed from feeding bunks regularly.

11. Consider the use of an inoculant in silage or acid additive in high moisture corn to enhance fermentation and control during storage.

12. Match the rate of feed removal from the silo face to the size of the herd. For example bunker silo faces should be removed at four to six inches and upright silo face at three to four inches per day. Use the higher rate during the warm seasons.

13. When confronted with a toxicity problem, stop feeding the contaminated feed.

14. In consultation with your veterinarian or nutritionist, consider the use of a mycotoxin adsorbent to be mixed with the feed.

Conclusions

Obviously the problem with mycotoxins is widespread and complex. In the next part of this series we will discuss more of the practical steps that can be taken to address this very common problem.

Copyright 2014 – Dr. Stephen B. Blezinger

Steve Blezinger, Ph.D., PAS is a management and nutritional consultant with an office in Sulphur Springs, TX. He can be reached by phone at (903) 352-3475 or by e-mail sblez@verizon.net. For more information please visit us on Facebook at Reveille Livestock Concepts.







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