Farmers and veterinarians need to know about molds and mycotoxins Farmers and veterinarians need to know about molds and mycotoxins dairy milkproduction animal health mycotoxin fusarium herd cow aflaxotin t-2 toxin binder mexsil ergot fumonisin silage
Farmers and veterinarians need to know about molds and mycotoxins

WHAT DAIRY FARMERS AND VETERINARIANS NEED TO KNOW ABOUT MOLDS AND MYCOTOXINS

PERSONAL OBSERVATIONS AND PRACTICE REGARDING MYCOTOXIN BINDERS

Farmers and veterinarians need to know about molds and mycotoxins

Farmers and veterinarians need to know about molds and mycotoxins Farmers and veterinarians need to know about molds and mycotoxins dairy milkproduction animal health mycotoxin fusarium herd cow aflaxotin t-2 toxin binder mexsil ergot fumonisin silage Farmers and veterinarians need to know about molds and mycotoxins Farmers and veterinarians need to know about molds and mycotoxins dairy milkproduction animal health mycotoxin fusarium herd cow aflaxotin t-2 toxin binder mexsil ergot fumonisin silage Farmers and veterinarians need to know about molds and mycotoxins Farmers and veterinarians need to know about molds and mycotoxins dairy milkproduction animal health mycotoxin fusarium herd cow aflaxotin t-2 toxin binder mexsil ergot fumonisin silage

WHAT DAIRY FARMERS AND VETERINARIANS NEED TO KNOW ABOUT MOLDS AND MYCOTOXINS

Mycotoxicosis, the manifestation of mycotoxin poisoning, has long been appreciated as an acute cause of poor animal performance. It is only recently that chronic, subclinical mycotoxin load has been appreciated as a cause of poor animal performance and increased disease susceptibility. The adverse effects of mycotoxins are thought to be due to both a direct effect on the animal and indirect by suppression of the immune system.

Molds and mycotoxins are widely distributed in nature, occurring whenever there is sufficient organic matter, temperature and water for them to reproduce. Because of the large volume of feedstuffs that must be stored and distributed on dairy farms, considerable opportunity exists for mold growth to appear. Some, if not all, molds can produce a mycotoxin when subjected to stress. These mycotoxins ingested either in large single doses or in small quantities over a long period of time can have adverse effects on the productive capacity, the reproductive efficiency and the health of the animals. Unfortunately, much of what we know about mycotoxins is conjecture, because definitive studies on their effects in dairy cattle are lacking. Therefore, much of this paper must deal with field experience as it relates to the solution of mycotoxicosis. The focus of this paper will be on the practical and scientific aspects of mycotoxicosis.

In general, it is difficult to make a confirmed diagnosis of mycotoxicosis. There are several general symptoms that may make one suspicious that a mycotoxin problem may exist. Many of these symptoms are general and can be symptomatic of other problems.

None of these manifestations can be considered diagnostic. But when they exist, especially in the absence of more typical explanations, like poor management or presence of infectious disease, the possibility of mycotoxicosis should be explored and steps taken immediately to reduce the potential for mycotoxins to be a problem.

For mold growth to occur, four conditions must exist: (1) there must be an adequate food source; (2) the temperature must be maintained between 12 and 31(C; (3) there must be sufficient oxygen to allow mold growth; and (4) there must be sufficient moisture, at least in some parts of feed, for mold growth. Thus, if the farmer can control the availability of oxygen and moisture, he can go a long way to prevent mycotoxins from being produced on the farm.

Molds produce mycotoxins in response to stress. For example, molds growing on corn, either in the field or in storage, will produce no mycotoxin until subjected to freezing temperatures or until subjected to moisture deprivation. Mycotoxin problems are more pronounced in crops growing under cool, moist conditions and under drought stressed conditions. Unfortunately both of these conditions occur annually in large portions of the world. Mycotoxin production will be in direct proportion to the duration of this stress. Conversely, it is possible that feeds heavily contaminated with molds can be mixed, ground or treated so that obvious mold is not evident. Yet, this feed can be completely contaminated with mycotoxins. Thus, a feed can have molds and still not contain mycotoxins and have mycotoxins without mold. The only way to properly evaluate these situations is the reaction of the cows. Even if mycotoxins are present, it may be difficult to demonstrate their presence or their relative severity.

Although there have been about 400 mycotoxins identified, there are probably as many that have not been fully characterized. Also, pure mycotoxin may have little animal impact. However, the same mycotoxin, given at lower dose, but in conjunction with another mycotoxin, may have a devastating effect on the health and productive ability of the animal. Apparently different mycotoxins can potentiate the effect of other mycotoxins.

In general, animal symptoms include: poor milk production, poor feed consumption, poor body condition, diarrhea, quantities of mucous in the manure, anestrus, poor reproductive performance, abortion, high disease incidence and general lethargy. However, presence of two or more mycotoxins may completely change the symptomology of the mycotoxicosis. Also, many of these are general symptoms and are the symptoms of other toxicosis, parasites, disease, management or simply poor environmental conditions. Many herds where mycotoxins have been a persistent problem have been labeled as "poor managers." Thus, someone with experience and a consistent analytical approach needs to sort out whether the problem is mycotoxins or other factors. At the end of the day, this may be difficult to prove. Normally, we believe that mycotoxins should be considered only after other causes of poor performance have been fully explored. This does not mean that the mycotoxin needs to be demonstrated before melioration takes place. For various reasons, it may be impossible to demonstrate a toxin. Rather, if mycotoxin is suspected, the suspect feed should be removed, or at least the quantities of the suspect feed decreased, and a toxin binder should be added to the ration. Then cow performance should be evaluated. If health and production improve, then one should keep pursuing the avenue of mycotoxins. If no change in cow performance occurs, obviously another track should be taken.

Mycotoxins tend to accumulate in the liver, causing liver toxicosis. Increases in the liver enzymes, particularly SGOT (serum glutamic acid oxalate transaminase) and LDH (lactic dehydrogenase), along with increased serum cholesterol levels and decreased white cell counts without elevated body temperature are considered indicators of mycotoxins. Immune system depression is another classic symptom of mycotoxicosis. Many of the reproductive and health effects are believed to be the result of the general immune suppression. However, there is also a "mycototic abortion" syndrome, where ingestion of molds and mycotoxins directly results in the termination of gestation. Additionally, evidence exists that abortions now identified as neospora canium abortions may in fact be potentiated by mycotoxin.

In general, mycotoxins are toxic to rumen bacteria, although it is thought that rumen microorganisms detoxify between 80-90% of ingested mycotoxins. The other major site of mycotoxin action tends to be in the intestines, both large and small. Depending on the toxin, malabsorption of nutrients, excessive mucous production, tissue erosion, hemorrhage and tissue necrosis have been reported. This often leads to loss of appetite, severe diarrhea and weight loss.

Mycotoxin problems tend to be typical of the farm or herd. Whether this is because of large amounts of inoculum present either in the fields or in the storage structures, or whether there is bad management of the feed and feeding program is not known. However, the author has personally seen herds with apparently excellent feed preservation and feed management that still had highly contaminated feeds. Farms that have a history of mycotoxicosis should add toxin binders as a regular management practice.

Again, a word of caution: many of these symptoms are not of themselves diagnostic. Also, not all mycotoxins manifest these symptoms, and combinations of mycotoxins can produce symptoms that are more severe or less pronounced than those listed. A diagnosis of mycotoxicosis is not a panacea. Often, depending on the type of mycotoxin and the degree to which the liver has been damaged, recuperation is slow, or in the case of cows with severely damaged livers, it does not occur.

Unfortunately, dairymen outside the US and Canada face more challenges from mycotoxins. The primary sources of mycotoxin tend to be corn, barley, wheat, cottonseed, sorghum, by-product feeds which have been miss handled and silages. In Asia, copra meal also has a large potential to be contaminated. These feeds may be of either national origin or imported. There are some cases of other ingredients being contaminated, but these feeds are by far the largest culprits. Silages continue to be the major source of mycotoxin contamination in many parts of the world. Also, although aflatoxin receives the major amount of attention of laboratory tests, we would like to suggest that they are not the largest problem. Rather, we believe molds of the Fusarium species cause far more mycotoxin problems.

There are several reasons that corn, barley and wheat have the potential to be contaminated. First, in various parts of the world they often harvested after standing for prolonged periods in wet weather conditions. These are ideal conditions for Fusarium species to initiate growth. Secondly, these grains are often stored in grain bins where little or no aeration and re-circulation occur. Also, significant amounts of U.S. corn, especially that grown in the mid-western region of the U.S., is contaminated with mycotoxins every year. Unfortunately, some of this corn, because it will not pass quality tests for the U.S. market, is price discounted and sold into markets where testing is less stringent. If the price of these grains is significantly below the prevailing market, it should be suspected that some mycotoxin contamination might exist. This grain should be purchased only after it has passed a minimum number of mycotoxin tests. If the feed smells moldy, then reject it as a source of grain for the milking herd. The best advice in dealing with this situation is to know the supplier. Grain dealers will not knowingly sell a bad load of feed to a good client. However, if the purchaser is buying strictly on price and is dealing on a one-time-only or hit-or-miss basis, the dealer will be more inclined to sell grain based on the lowest purchase price.

The situation is largely the same with cottonseed, except that in cottonseed, aflatoxin is by far the greatest danger. Each year both in the U.S. and in Latin American countries, dairy farmers will experience aflatoxin toxicity with some herds due to infected cottonseed. In every case, this will be traced to the cottonseed being stored at too high a humidity or to cottonseed that got rained on after storage. The same advice applies to cottonseed as to corn. Reject obviously contaminated supplies and buy from a known dealer.

As mentioned, silages continue to be the major source of mycotoxin problems. In many countries, this can be traced to the dependence on hand labor to empty trucks from the field, to distribute the silage in the bunk and to remove silage from the bunk. This is further complicated by improper sizing of silo stacks for the size of the herd. Silages usually contain molds of the Fusarium types and are contaminated by the zearalenone, deoxynivalenol acid (DON), Fusarium toxin and T-2 toxin. Unfortunately, corn silage, both because it contains the greatest amount of inocula and because it is the most poorly buffered, is the greatest danger. Alfalfa and grass silages are generally limited to DON and T-2 toxin.

In order to make high quality silages, it is necessary to fill quickly and pack continuously. This is nearly impossible if hand labor is used to unload trucks and/or distribute the silage. However, far more dangerous as far as molds are concerned is the practice of hand unloading of bunker silos. It is the recommendation of almost all experts in the field that 15 cm of silage be removed daily from across the entire face of the silo in order to prevent mold growth. Typically what happens in many world areas is that bunker silos are unloaded by taking a two-meter wide strip across the top and then moving down the face. This often results in parts of the face being subjected to aeration for more than a week. Obviously, this will encourage mold growth. In order to really and truly reduce mycotoxin problems this practice will have to be changed.

What is a dairy farmer to do if he suspects that he is feeding mycotoxin contaminated feeds? The first step would be to try to remove the offending feedstuff. This is especially critical if the suspected toxin is aflatoxin or T-2 toxin. However, many times, either because the silage is contaminated or because supplies have been purchased in large quantities, complete removal of the feed is impossible. If there are alternative feeds available, the amount of the suspect feed should be reduced. If the feed is silage, attempts should be made to remove as much mold as possible from the stack and amounts of the feed reduced. Daily treatment of the silo face with a mold inhibitor, such as propionic acid, will help to reduce mold growth. In all cases a proven mycotoxin binder should be added to the ration whenever mycotoxin is suspected. Even feed not obviously contaminated by molds may still contain some mycotoxin. Levels of vitamin A and E should be increased both because toxin binders may bind some of these vitamins, but also because they will help to protect the immune system.

Toxin binders vary in their ability to bind toxins, and some toxin binders can bind one type of toxin and not bind any of another type of toxin. In general, bentonite products have a disadvantage in that although they may bind the target mycotoxin they will also bind other minerals and vitamins. Other binders may bind the mycotoxin temporarily, but the mycotoxin may be released when further subjected to conditions in the rumen and/or the small intestine. For this reason, a binder of proven scientific effectiveness should be selected.

Careful record keeping is a must in these situations in order to know if the remedies that have been started are having the desired effect. Often farmers think the situation is getting better when in fact it is the same or worse. Often dairy farmers think that what they are doing to lessen the effects of mycotoxin is positive, when a study of the numbers indicates that nothing is really happening. Pay close attention to production per cow, feed consumption, diarrhea, abortions, heat cycles and body condition. If these cannot be demonstrated to improve, then either the wrong feed has been identified, the feed is contaminated several orders of magnitude more than suspected, the wrong toxin binder has been utilized, or the problems are not caused by mycotoxins.

Dealing with mycotoxins is difficult because we are just beginning to learn about their effects, treatment and prevention. Better managers will have the records to indicate whether a problem exits and whether initiated remedies are having the desired effect.

It has long been established in disease situations that the presence of the disease must be demonstrated before treatment should begin. This is certainly desirable in situations where mycotoxins are present. There are, however, several caveats that must be applied to mycotoxin testing.

The following is a list of the most well described mycotoxins, their origin, and their approximate safe levels of inclusion as ppm or ppb per total dry matter. This list is by no means exhaustive, nor can the levels of mycotoxin assumed to be safe be tolerated by cattle under all circumstances. It is well known that lower levels of several mycotoxins have a greater effect than one mycotoxin in high dosage. Also the safe levels of mycotoxin listed below are at acute intakes. Feeding of lower levels for prolonged periods of time may result in the same or more severe symptoms.

1. Aflatoxin is the mycotoxin that is best recognized and best characterized. It is produced by molds of the Aspergillus species and is a potent carcinogen. This is the reason aflatoxin levels are regulated in raw milk in the United States. Symptoms include: decreased appetite, decreased production, weight loss, high liver enzymes, loss of liver function, abortion and ultimately death. Although aflatoxin is perhaps the most dangerous of the mycotoxins, it really does little practical damage. This is because its effects are severe and dramatic, which makes the change to aflatoxin contaminated feeds noticeable. It is quickly associated with feed changes, and the offending feed can either be reduced in quantity or removed. Also, feed companies readily appreciate the damage that aflatoxin can do and regularly screen for its presence. Thus, aflatoxin is really not the severe problem that it could be if left unscreened.

If liver damage is not severe, animals usually recover in 4-10 days after the offending feed has been removed. On a practical basis, 20 ppb can probably be well tolerated by mature milking cows, but only about 10 ppb in growing cattle and 4 ppb for calves. For chronic feeding, these levels should be reduced by one half.

2. Deoxynivalenol (DON) is produced by molds of the Fusarium species. Much of the data in dairy cattle concerning the effects of DON are conflicting. High doses of pure DON have caused no noticeable problems; however, lower doses of DON in association with other mycotoxins have resulted in lower milk production with increased morbidity. In addition nervous symptoms, diarrhea and intestinal hemorrhage have been reported. For this reason DON is often referred to as a "marker" mycotoxin, i.e., presence of DON is usually associated with other mycotoxins that may not be easily identified. Levels of DON below 500 ppb are probably safe for consumption by dairy cattle.

3. Zearalenone is a mycotoxin with estrogenic activity which is also produced by molds of the Fusarium species. Lowered milk production, abortion, short heat cycles, nymphomania and feminization of bulls have been reported when feeding zearalenone infected silages. Zearalenol is a compound similar to zearalenone but is reported to provoke 5-10 times the estrogen response. Levels of zearalenone below 250 ppb are probably safe to feed adult dairy cattle if no other molds are contaminating the feed.

4. T-2 toxin (one of the trichothecenes) is also produced by several molds of the Fusarium species. T-2 is found not only in corn silage but also in some haylages. Symptoms in cattle include lowered milk production, diarrhea, hemorrhagic bowel, sterility, and lesions in the intestine, ovaries and uterus. Immune function is severely depressed. Consumption of large quantities can cause acute death. Consumption of greater than 100 ppb are probably dangerous for cattle. Diacetoxyscirpenol (DAS) is a closely related compound that produces many of the same effects. Fifty ppb is the safe suggested limit for this toxin.

5. Fumonisin has been reported relatively recently, and the effects are still relatively unknown. It has been implicated in liver and kidney damage, decreased immune function and high mortality rates in cattle. It is tumorgenic in swine and horses, but this has not been demonstrated in cattle. Fumonisin is thought to potentiate the toxicity of other trichothecene toxins. Safe levels have been estimated to be below 50,000 ppb. Five thousand ppb is the maximum safe level for horses.

6. Ergot is a mold that infects the flowering portion of many grains and grasses. Abortion storms and lowered fertility are associated with consumption of ergot infected feeds. Although dramatic in its effects, ergot is probably not an industry wide problem. Cattle fed less than 0.5% (5,000 ppm) of dry matter as ergot showed no adverse reproductive effects, but cattle fed at 1% (10, 000 ppm) had increased abortion rates with calves that were born alive being weak and debilitated

7. Ochratoxin is a mycotoxin produced almost always on grains and almost always as a result of poor storage conditions by molds of the Penicillium family and by Aspergillus ochraceus. Controlled studies in dairy animals are lacking, although cattle fed Ochratoxin contaminated feed had enlarged livers and kidneys at slaughter. Safe levels are assumed to be less than 10,000 ppb.

While many other mycotoxins that infect feed are known, they are usually a problem in areas of the world other than the Americas.

Mycotoxins, especially those produced by Fusarium species, may result in great losses in productivity. Although aflatoxin is widely recognized as a potent mycotoxin, it is probably not the problem that either feed dealers or veterinarians believe it to be.

All obviously moldy or damaged feed should be avoided. Silages are one of the largest sources of mycotoxin contamination. Silages need to be well managed from the time of ensiling through the feed out process. Silages should be treated with a mold inhibitor in situations where at least 15 cm of silage cannot be removed from the face. A mycotoxin binder should be added to the feed mix whenever moldy feed is being utilized or whenever mycotoxins are suspected. Mixing should occur for sufficient time to insure complete distribution of both the suspect contaminated feed and the mycotoxin binder.

Lastly, be ever vigilant. Mycotoxins, even in low doses but fed continually for long periods of time, reduce productivity and reproduction while increasing morbidity. Constant monitoring and good on-farm feed management, including good mixing and inclusion of mold inhibitors and binders, will reduce the economic impact of molds and mycotoxins.

We have been involved as a dairy consultant to both farmers and feed dealers on the continents of North and South America, Europe and Asia. In each of these areas we have found evidence of what we believed to be mycotoxicosis. Mycotoxins seem to be a more consistent problem in areas where high levels of by-product feeds are used in concentrates and/or where silages have been mismanaged. The diagnosis of mycotoxicosis has been complicated by the fact that in many areas, even in the United States, identification of mycotoxins is not always possible. This is for various reasons, including inability of laboratories to provide adequate testing. In a few instances even when there was confirmed mycotoxin, particularly in cases of zearalenone or T-2 toxin, and a "mycotoxin binder" was added, the recovery of the herd has proven to be intractable. Personally, we feel that this is due to the inability of the selected (available in the market) binder to adequately combine with the mycotoxin and sequester it from digestion.

We can divide the types of binders available in the market into four basic types based on the manufacturers' description: bentonites, aluminosilicates, zeolites and cocktail products. Cocktail products generally include several types of clays as well as vitamins and other minerals. Chemically, these binders are all clays and have more or less the same chemical composition. However, morphology, purity and ability to form chemical bonds with mycotoxins differ widely among both the types of these clays and their manufacturing process.

Our opinion about which type of clays perform better is based solely on field experience, but they are supported by in vitro binding experiments. We have found the clays that identify themselves as phyllosilicates, a subclass of aluminosilicates, are definitely superior to the others especially when treating mycotoxins of the fusarium species. In our opinion the absolute best of these products is a phyllosilicate of Mexican origin which is known by the trade name of Mexsil (r) . We have used this product at dosages of 150-250 g per head per day in several difficult situations involving fusariums with outstanding results.

In any case, a binder selected for use should have research data that indicates, both in vitro and in vivo, that it binds mycotoxins and keeps the mycotoxin sequestered throughout the digestive process. Additionally, there should be data indicating if there is binding of minerals and/or vitamins. With this information in hand, one can determine the level of extra supplementation that might be necessary.

In many cases, when reproductive parameters are subpar or when there is a high level of digestive upsets than we consider normal, we recommend mycotoxin binders of the aluminosilicate type as a prophylactic. While the economic benefits of this action are hard to measure, reproductive records definitely show improvement. Generally, records also show improved animal health.

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