Leave your saddle sitting in a corner of your tack room after you and your horse are caught in a rainstorm, and you'll get an eye-opening look into the world of fungi and molds. Within days, your leather tack will have sprouted a patchy coat of green and white fur created by spores from the air and the surrounding environment migrating onto the wet, nourishing surface.
It's not only tack that's vulnerable to mold growth. Given the right conditions, your horse's feed can also become contaminated with fungi and molds. And while most of these microscopic spores are relatively harmless, a few can wreak havoc on your horse's respiratory and digestive systems. The most dangerous are the species of molds that exude poisons called mycotoxins as part of their metabolism. Some types of mycotoxins are potentially fatal to horses--and they can be very difficult to detect.
The Basics of Mycotoxins
Mycotoxins can accumulate in a wide variety of places. The process begins when mold infestations take hold in pasture, hay, or maturing grains. Sometimes molds start to grow after the crop is harvested, especially when moisture levels in the plants are too high. These molds often produce metabolites that can cause reproductive, digestive, neurological, and athletic problems in your horse.
Just what can mycotoxins do? At the least they can be responsible for a loss of appetite, feed refusal, decreased digestive efficiency, and a generally unthrifty appearance. In some horses, they can trigger allergic reactions, ranging from mild to severe. At worst, mycotoxins can be responsible for paralysis, skin hypersensitivity, reproductive failure, brain lesions, and a gradual deterioration of organ function, which in turn can affect breathing, feed efficiency, and growth rates in youngsters. The impact of mycotoxin-infected feed can be especially high on horses used for high-intensity sports and on gestating or lactating broodmares, because they usually have a higher grain intake than other equids.
One of the most well-recognized of the mycotoxicoses in humans is ergot poisoning. Ergot is a fungus that grows on any seed, with fescue being the most common source in the United States. The mycotoxin it exudes causes what doctors in the Middle Ages called "St. Anthony's Fire;" now it's called ergotism (symptoms include LSD-like hallucinations, muscle cramps, convulsions, miscarriages, and gangrene). Toxins on yellow rice have been known to cause cardiac problems, and several types of mycotoxins have been linked to an increased incidence of cancer.
Factors that influence the concentrations of mycotoxins in horse feed include late frosts, high humidity, drought, and delayed harvesting. Cool, wet weather conditions are often the worst-case scenario, allowing molds to thrive in hays and cereal grains (especially corn).
In practical terms, it's virtually impossible to prevent mold growth. It has been estimated that up to 50% of forages and grains fed to horses contain traces of some type of mycotoxin. That's not unreasonable, considering the billions upon billions of mold spores in the air, soil, and water at any given moment. But horse owners should learn to spot the conditions in which these invisible compounds are most likely to accumulate to dangerous levels.
Let's have a look at the five most serious mycotoxins that are likely to contaminate your horse's feed.
Most North American broodmare owners are aware of the dangers of grazing pregnant mares on tall fescue pastures. Tall fescue is frequently infected with an endophytic (growing within a plant) fungus called Acremonium coenophialum, which can cause delayed labor, retained placenta, agalactia (lack of milk production), and abortion in late-term broodmares. The pasture grass, which grows vigorously in the spring and fall, is widespread throughout the United States, although the endophyte that infects it tends to thrive in hot, humid climates.
It should be noted that ingesting infected fescue--either as fresh pasture or as hay--poses little threat to mature horses not being used for breeding. Most horses can graze pastures heavily infected with the fescue endophyte and emerge unscathed.
However, there have been some studies indicating that young, growing horses will not thrive on endophyte-infected fescue. And if you have broodmares, fescue toxicosis is a serious matter. The best treatment for fescue toxicosis is to remove broodmares from all pasture suspected of having endophyte-infected tall fescue at least 60 days before they are due to foal.
There are varieties of "guaranteed endophyte-free" fescue with which you can seed your pasture, but even then, it's worth testing the grass because it is difficult to completely eradicate previously infected varieties. For information on testing, contact your county's cooperative extension agent. Non-infected fescue tends to be less vigorous than infected fescue, so it is often overgrown by the hardier endophyte-infected variety after several years.
Fescue is not the only grass that can be contaminated with endophyte fungus--perennial ryegrass can also be endophyte-infected. If you have perennial ryegrass in pastures in which broodmares graze, have it tested. Endophyte-free seed is available.
First identified about 30 years ago when they killed thousands of birds in the United Kingdom, aflatoxins are now among the most studied of the mycotoxins. Horses can ingest aflatoxin when they eat contaminated corn, peanut, or cottonseed products, although other high-energy grains also can be susceptible. Aflatoxins are primarily produced by a strain of Aspergillus flavus mold (among others) when conditions are warm and humid, so they are most commonly found in grain crops grown in Texas, Florida, Georgia, and other southern states (see Figure 1 on page 74).
Historically, problems with these mycotoxins have been most severe when crops suffered drought stress through the end of the growing season. Infestation with insects, such as the corn ear worm, can make matters worse because the insects bore into the grains and allow the mold easy access.
The tough-as-a-cement-mixer digestive systems of cattle are considerably more tolerant of aflatoxins in their feed than those of horses (although calves have fewer defenses, often suffering reduced growth rates and liver damage). Equine clinical signs of aflatoxicosis include feed refusal, diarrhea, colic, anemia, immune suppression, oral inflammation, and liver damage. Aflatoxins are also thought to be associated with an increased incidence of cancer in animals.
Grains can be screened for aflatoxins by using a blacklight to detect kernels or grains that glow with a bright greenish-yellow fluorescence, indicating the presence of A. flavus mold. The test is most successful when it's performed on cracked grains rather than whole grains, and it should be remembered that not every A. flavus infection causes a significant build-up of aflatoxins. (When researchers spot a batch of grain that might be infected, they can follow up with a chemical test to confirm aflatoxin levels.)
Equine leukoencephalomalacia (ELEM), commonly known as moldy corn poisoning or "blind staggers," is the mycotoxin-related syndrome with which many horse owners are most familiar. First identified in 1891, this syndrome is the product of a fungus called Fusarium moniliforme, which often invades cornfields in the Midwest. The fungus looks gray or cottony white, with affected kernels of corn turning gray to brown (see Figure 2 on page 74). But F. moniliforme can be present with little or no outward signs in the corn.
F. moniliforme produces fumonisins, which increase in concentration when corn crops are stressed during the growing season. Outbreaks of ELEM are usually associated with drought or very wet conditions at harvest that favor fungal growth. When consumed daily in sufficient quantities over a week or more, fumonisins can trigger liver or neurological problems in horses after three to four weeks. Affected horses usually show incoordination and a reduced response to external stimuli at first, followed by circling or aimless wandering, hyperexcitability, pressing the head against solid objects, blindness, and partial paralysis. Eventually, they go down and are unable to get up. Any neurological signs should immediately be brought to the attention of a veterinarian.
These clinical signs are a result of extensive brain damage (necropsies reveal a rather shocking liquefying of portions of the cerebral cortex, the outer portion of the brain); and horses exhibiting these clinical signs usually die within 24-48 hours. Those which survive often suffer from life-long neurological defects.
For reasons which aren't yet clear to researchers, some horses with ELEM end up with liver disease rather than neurological damage. Clinical signs of liver disease include weight loss, unthriftiness, and jaundice (evidenced by yellowing of the skin and whites of the eyes). The good news is that this form is believed to be more reversible than the neurological form of ELEM. However, if more than half of the liver becomes damaged, hepatic disease can become chronic, resulting in a horse which loses weight even when given plenty of feed.
Horses are more vulnerable to moldy corn poisoning than any other livestock species, sometimes showing symptoms after exposure to levels as low as five parts per million. To a large extent, the survival rate depends on how much of the toxin horses ingest and over what length of time, but the survival rate is estimated at less than 50%. Since corn kernels infected with F. moniliforme are more brittle than healthy kernels, they tend to crack and break during harvest and drying, and end up in the screenings (waste material separated by a screen). For this reason, fumonisins are often found in higher concentrations in these screenings, so they should never be fed to horses.
Vomitoxin, a.k.a. Deoxynivalenol
In the case of horses, vomitoxin is a bit of a misnomer since horses can't vomit; but in other livestock species, this mycotoxin triggers vomiting and total feed refusal when it is present at high concentrations. The toxin is produced by a fungus called Fusarium graminearum, which infects corn (often growing in the silk at the top of the ear in cool, wet weather) and wheat. An infected corn cob will have pink or reddish mold at the top when the husk is peeled back (see Figure 3 on page 74). Once the corn is shelled from the cob, it is difficult to see whether it's infected.
Pigs are particularly vulnerable to deoxynivalenol (DON) toxicosis, ruminants and poultry are quite resistant, and horses are somewhere in between, according to Susan L. Raymond of the Equine Research Centre at the University of Guelph. At high enough concentrations, horses can suffer lethargy, intestinal lesions, ataxia, and a loss of appetite. DON can also alter the normal function of the immune system. Depending on the concentration of DON, sometimes the immune system is suppressed, and other times it is overstimulated.
An estrogenic (having estrogen-like effects) mycotoxin, zearalenone can cause abortion, uterine prolapse, and other reproductive problems in pigs and other livestock species. It was not thought to affect horses prior to a 1994 study by D.T. Barnett, R.A. Mowrey, W.M. Hagler Jr., D.G. Bristol, and R.A. Mansmann at the Department of Animal Science at North Carolina State University 1. The study implicated zearalenone in some cases of feed-related colic in horses. The mycotoxin appeared in about 40% of the hay and grain samples taken from farms where colic related to feeding had been a problem.
Zearalenone often appears together with DON in the same batch of grain. A mycotoxin produced by F. graminearum fungus, F. culmorum, and others, zearalenone can be found in all types of cereal grains, and is suspected to also grow in forage and hay. The growth of the fungus is effectively halted if the grain is dried to 15% moisture or lower.
What can you do to limit your horse's exposure to mycotoxins?
As Raymond points out, mold and fungus growth and mycotoxin build-up in feeds is a very regional problem, but 21st Century global trade has meant wider distribution of many types of molds. Levels of molds in a product are not always indicative of mycotoxin levels. This is because some molds produce no mycotoxins at all, and sometimes molds are destroyed by a treatment, but their mycotoxins are unaffected. As yet, there is no effective way of removing mycotoxins from a feedstuff once they've been produced in it.
Factors that can magnify the effects of mycotoxins include heat stress, exposure to more than one mycotoxin at a time, overcrowding, exposure to disease, drug interactions, and malnutrition. Often, the debilitating effects of mycotoxins increase with repeated exposure.
As a general rule, young horses are more vulnerable to the effects of mycotoxins than mature horses, although traditionally ELEM has been reported to affect older horses more severely.
The good news is that severe moldy corn poisoning might be more rare than we thought in years past. A recent study by Raymond, Trevor K. Smith, and Swamy Haladi at the University of Guelph in Ontario, Canada, indicated that the palatability of Fusarium-infected grain is so low that horses generally refuse to eat it, thus saving themselves from poisoning2.
Raymond's team studied the effects on appetite and metabolism when nine mares consumed Fusarium-contaminated grain on a daily basis. The animals were split into three groups of three; each group spent 21 days on a specific dietary regimen and then rotated to the next, so in the end all nine horses had been exposed to all three diets. The first was a control diet of corn and wheat, with no contamination; the second was a blend of corn and wheat naturally contaminated with Fusarium mycotoxins (deoxynivalenol, zearalonone, and fusaric acid); and the third was a blend of the contaminated grain, along with 0.2% of a product called Mycosorb from Alltech Biotechnology Center in Nicholasville, Ky. (Mycosorb is extracted from yeast cell walls and is marketed as limiting a horse's absorption of mycotoxins in the gut.)
Each horse was examined on a daily basis and weighed once a week. Blood was also drawn and serum IgA, IgG, and IgM levels (three types of immunoglobulin, or antibody) were analyzed to provide the research team with a picture of how these mycotoxins might be affecting the immune response.
The most significant effect of the deliberately contaminated diet, says Raymond, was that there was a dramatic decrease in feed intake. Although the horses ate all of their hay, they were hesitant to eat the moldy corn, consuming only about 36% of what they were given. On the other hand, horses consumed 63% of the contaminated feed treated with Mycosorb. Serum analyses showed that the mares' livers adapted to the toxicity of the mycotoxins, with liver function returning to near-normal levels by Day 21 of Fusarium mycotoxin consumption. (Horses consuming the Mycosorb showed no alteration in their serum chemistry.)
While it's encouraging to know that horses exhibit some nutritional wisdom when faced with contaminated grain, Raymond emphasizes that it still pays to be vigilant, particularly when it comes to proper storage of feed. If you have any doubts about whether your feed might be contaminated, don't feed it. Either have it tested and feed it only after it has been proven safe, or throw out the feed.
Since corn is more susceptible than other grains to various forms of mold, you might choose to eliminate corn from your horse's diet. But other grains also have some potential to be infected with molds or fungi, so it's difficult to achieve zero risk. (Reputable feed mills, well aware of the dangers of moldy corn poisoning, go through several steps to ensure their grain is fumonisin-free, including the application of a non-toxic mold inhibitor to all processed corn products.)
As a general rule, poor growing seasons (which tend to produce damaged kernels) and a high moisture content are the biggest risk factors for moldy grain. Therefore, choosing a feed with naturally low moisture--such as a pelleted ration--might be wise in a year when the growing season has been particularly tough. Most pelleted feeds have a moisture level of only 12-13%, making them resistant to mold as long as they're stored in a cool, dry environment.
If you prefer a sweet feed or other molasses formulation, you might want to seek out one that is sold in paper bags, which "breathe" and allow moisture to escape. Try to use up your feed supply within a couple of weeks, especially in hot, humid weather, and discard any feed that has gotten wet or has been sitting in storage for more than six weeks in the summer.
If you suspect mold growth on your pastures, you might choose to remove your horses from them and feed hay exclusively, or you can try supplementing the diet with a mycotoxin-binding product. While the Food and Drug Administration does not recognize the term "mycotoxin binding agent," there is a significant amount of data supporting the use of silicate clays and/or Mycosorb (yeast cell walls) to help minimize the harmful effects of certain mycotoxins.
Of course, you should always store your hay and grain in a dry environment to minimize the chances of mold growth, inspect it thoroughly before you feed it, and immediately discard any feed that is suspect. Pay attention to your horse's eating habits; his refusal of a feed that looks and smells perfectly normal to you might be an indicator of the presence of molds and/or mycotoxins.
1 Barnett, D.T.; Mowrey, R.A.; Hagler, W.M.; Bristol, D.G.; Mansmann, R.A. Correlation of Selected Mycotoxins to the Incidence of Colic in Horses. Proceedings of the 14th Equine Nutrition and Physiology Symposium, 242-247, 1995.
2 Raymond, S.L.; Smith, T.K.; H.V.L.N. Swamy. Nutritional Treatment of Naturally-Induced Fusarium Mycotoxicosis in Horses. Annual Conference of the Nutraceutical Alliance. Guelph, Ontario, Canada, May 10-11, 2002.
About the Author
Karen Briggs is the author of six books, including the recently updated Understanding Equine Nutrition as well as Understanding The Pony, both published by Eclipse Press. She's written a few thousand articles on subjects ranging from guttural pouch infections to how to compost your manure. She is also a Canadian certified riding coach, an equine nutritionist, and works in media relations for the harness racing industry. She lives with her band of off-the-track Thoroughbreds on a farm near Guelph, Ontario, and dabbles in eventing.
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