Molds are one-celled fungi that facilitate the breakdown and decay of plant materials. Mycotoxins are "sporadically produced secondary metabolites of molds," according to Equine Clinical Nutrition by Lon D. Lewis, DVM, PhD, Dipl. ACVIM. Antibiotics (such as penicillin) are types of useful mycotoxins, which at therapeutic levels are more toxic to bacteria than to animals. There are other types of mycotoxins that can be harmful or fatal to horses.
Some fungi live inside plants in a symbiotic relationship. They make the plant more resistant to drought, frost, and insect infestation while they derive nutrients from the host plant. Many of these affected plants are forages and feedstuffs that horses consume. Under optimum conditions (usually including high moisture), mycotoxins can form in plants within hours, and they can reach maximum concentration within one to two weeks.
What are Mycotoxins?
Horses have an increased risk of encountering mycotoxins when fed grain products, which readily support fungal growth. Kyle Newman, PhD, is director of Venture Laboratories, an analytical lab for the feed industry and author of The Mycotoxin Blue Book. He explains that mycotoxin contamination has been detected in feeds, forages, and bedding.
"Mycotoxins are secondary products of metabolism, although not all fungi produce mycotoxins," he says. "There are estimates that over 300 secondary metabolites from molds are toxic to humans and animals."
Gary Osweiler, DVM, PhD, professor of veterinary toxicology at Iowa State University, has been a noted authority on equine mycotoxins for the past four decades.
He says, "Mycotoxins generally are produced when crop conditions are adverse."
Newman explains that mycotoxin production might occur when conditions favor fungal growth on crops in the field, at harvest, in storage, or during the processing of feed.
"Mold and subsequent mycotoxin contamination of a feedstuff or forage can increase in extreme environmental conditions such as drought, excessive precipitation, or sudden frost," Newman says. "Physical damage from storms, birds, or insects also allows fungi to penetrate the plant tissue. Molds that are present in the field before harvest proliferate if moisture content remains high through inadequate processing and storage conditions.
"A large number of the predominant mycotoxins are produced by the Fusarium molds, which thrive in temperate climates worldwide and are common contaminants," he adds. "A wet growing season followed by cool weather increases the likelihood that fungi, especially Fusarium and its mycotoxins, will be present in grains. High moisture levels in grains encourage fungal growth, while cool temperatures may increase mycotoxin production."
Osweiler says other molds, such as Aspergillus and Penicillium, grow and produce toxins at moisture levels as low as 13%. Aspergillus spp. fungi require environmental temperatures greater than 70°F to produce aflatoxins (a form of mycotoxin). Aflatoxins are potent mycotoxins.
Osweiler notes a difference in mycotoxin risk between grain types: "Feed grains that include corn, milo, wheat, barley, rice, and cottonseed seem most susceptible. Oilseeds such as soybeans, canola, and flax seem less affected, partly because they have seed coats that are resistant to damage, but also because there is somewhat less available carbohydrate to support mold growth."
Strategies for Prevention
Based on descriptions of climatic conditions that favor mycotoxin growth, you might consider the geographical area where you live to gain an impression of how your forage might stack up as a risk factor. Purchase of hay or commercial grains from outside sources makes it more difficult to determine if there has been contamination with mycotoxins.
To minimize the risk of fungal and mycotoxin contamination in the feed, hay should be properly dried and cured. Osweiler stresses that storage conditions, particularly of grains and supplements, are critical to protecting a horse from mycotoxin ingestion.
"Aflatoxins (from Aspergillus spp.) can be formed in storage at moistures above 14%, while Fusarium toxins usually are not produced if stored grain moisture is less than 22%," says Osweiler.
"Grains should be reasonably free of dust and/or screened, with a minimum of split, broken, or checked kernels," he continues. "Probably the best storage strategy is to put up dry feed (less than 14% moisture) sealed in bags until shortly before use. Grain that is dry and clean, with a low amount of dust and fine particles, is not likely to deteriorate much in storage. As long as moisture is less than 14%, mold growth is slow, making mycotoxin production unlikely."
Newman cautions, "A cool, dry place is important for storage, especially with sealed bags as these bags can form 'hot pockets' where water vapor condenses in a bag. Even though the overall moisture of the bag or container is low, there could be pockets of high moisture for mold growth."
Osweiler recommends that storage bins be clean and dry before new batches of feed are delivered.
Newman suggests, "Feed containers should be kept in cool, dry places, and feed should be rotated at least monthly in dry climates."
Osweiler describes the tenacity of mycotoxin contamination in feed, "Our common mycotoxins are very stable, only destroyed by temperatures that begin to char the grain. Ammoniation is known to reduce or destroy much of the aflatoxin content of grains, but is not very effective against fumonisins or deoxynivalenol (DON). Adsorbents (that bind the mycotoxins) such as calcium aluminosilicate are effective against aflatoxins, but are less effective against other mycotoxins. When added to mixed feeds, these adsorbents might reduce aflatoxin absorption by half."
Other adsorbents, such as yeast glucans, have been shown to be effective against a number of mycotoxins, and they have lower usage rates than aluminosilicates. However, such compounds with binding capabilities are not necessarily cleared by the FDA as mycotoxin binders because of the ambiguity in defining a mycotoxin binder.
"Most feed producers use mold inhibitors to prevent fungal growth on the finished feed," notes Newman. "This works if mycotoxins are not already present from fungal growth on the feed ingredients prior to harvest, during drying, or storage. If fungi are already present in high numbers or were present and have subsequently produced the toxins and died off, then mold inhibitors won't work."
Osweiler says that appearance and smell of the feed are helpful indicators if you aresensitive to subtle changes, but you can't rely on these assessments alone.
He stresses, "One should never presume that there are 'safe' molds. On the other hand, normal-appearing feed can contain mycotoxins, and the appearance of mold may be masked in prepared or pelleted feed, or the molds killed by processing, yet the toxin remains."
Newman recommends that you avoid visibly moldy feeds and not feed screenings (fines) since these are often heavily contaminated with mycotoxins.
Laboratories can test grain to detect common mycotoxins. Osweiler offers advice for prevention: "Good sampling of a grain supply with occasional testing for major mycotoxins is a step that most horse owners don't take, but is a strategy that could improve the relative safety of grains."
Newman adds, "Most commercial feed manufacturers test either raw materials, finished feed, or both. However, testing is not a 100% guarantee as a few kernels of mycotoxin-infested corn may be missed in testing, yet still pose a health risk to a horse."
Toxicosis by Mycotoxins
A small amount of mycotoxin might have minimal effects, or it could be fatal, depending on the type. Paracelsus (1493-1541), the father of modern toxicology, professed, "All things are poison, and there is nothing without poison. Only the dose makes a thing not a poison."
Each mycotoxin has an individual character in how it causes a horse to react. Osweiler stresses, "Mycotoxins are a group of unique and widely different compounds with respect to poisoning, so their effects are correspondingly diverse. We need to remember not to lump all mycotoxins as identical siblings, but as very individual characters with their own set of toxicity and risk factors."
According to Osweiler, toxicity effects vary greatly, depending on type of mycotoxin and dose ingested.
"Clinical signs can be trivial, such as feed refusal or mild salivation, or may be potentially fatal," he says. "Common effects range from liver damage to fatal, necrotic equine leukoencephalomalacia (ELEM, a softening of the white matter of the brain) from fumonisins, to acute or chronic hepatic disease from aflatoxins, or dramatic salivation with some diarrhea caused by slaframine in molded red clover."
Early in investigating the cause of mare reproductive loss syndrome (MRLS, see www.TheHorse.com/emag.aspx?id=3526), mycotoxins were incriminated as a possible source of the problem. Since that time, thanks to work done by Newman and others, mycotoxins have been eliminated as a cause for foal loss associated with MRLS.
Newman says that usually not all horses fed the same mycotoxin-contaminated feed will become ill. Although it is not clear why this happens, he notes that some individuals have a greater resistance to toxicity, just as not all people exposed to a cold virus will develop a cold. It seems likely that nutritional and immune statuses play a role in susceptibility.
He also comments that many have tried to implicate mycotoxins as a possible cause of colic, but to date, no definitive proof of this exists. Newman reports that one of the first signs of toxicity is feed refusal and/or reduced feed intake.
Other clinical signs include immunosuppression, increased susceptibility to disease, organ damage (often identified by abnormalities in blood chemistry profiles), poor reproductive performance, excessive salivation, incoordination, and edema. These signs are variable and dependent on the specific mycotoxin present, and any of these symptoms might be easily confused with other common horse ailments.
Osweiler describes the onset of clinical signs, "Each mycotoxin has a probable onset of signs after ingestion, depending on the mycotoxin and on the dosage. Many have immediate effects; others' effects are cumulative. Fumonisins can induce irreversible, fatal leukoencephalomalacia (ELEM) in as little as a couple of weeks, or may take as long as several months for clinical signs to appear. This duration of onset is similar for aflatoxins. Conversely, slaframine (red clover poisoning or slobbers) usually has a rapid onset with short duration, but it is not a life-threatening condition. In instances related to toxicity with slaframine, endophyte, or zearalenone, a horse quickly returns to normal once the contaminated feed is eliminated."
Fumonisin (Fusarium spp.) Fumonsins thrive in moldy corn and cause moldy corn poisoning, also known as blind staggers. This mycotoxin, at amounts more than 5 ppm (parts per million), has profound effects such as lameness or staggering, seizures, and by the time clinical signs are observed, fumonsin toxicity is usually fatal.
Osweiler says, "What is striking is the long ingestion time required, followed by dramatic CNS (central nervous system) disease and death in a day or a few days. Fumonisin poisoning can be largely prevented by keeping corn content low in the diet and using only clean, screened corn."
Aflatoxins At levels greater than 50 ppb (parts per billion), aflatoxins cause signs such as feed refusal, fever, weight loss, sluggishness, liver damage, jaundice, bloody diarrhea, kidney damage, birth defects, tumors, and suppressed immune function.
Aflatoxins flourish in grains such as corn, milo, and peanuts, particularly when day and night temperatures exceed 70°F with high humidity, coupled with insect damage and/or drought.
Osweiler reports that aflatoxin is always dangerous since its effects can be progressive as well as cumulative.
He notes, "Aflatoxin may be passed in a mare's milk, and foals are much more susceptible to toxicity than adults."
DON (deoxynivalenol or vomitoxin) This is found in corn and wheat affected by alternating warm and cool temperatures, especially in the central United States and Canada. This mycotoxin inhibits protein synthesis, and it produces signs of feed refusal and weight loss as well as decreased performance. It possibly contributes to immune suppression.
According to Newman, a published case report cited weight loss and elevated hepatic enzymes in horses with the probable cause being straw contaminated with DON. It was reported that in 2002, approximately half of a study group of 104 Warmblood-type riding horses stabled in Germany suddenly lost weight. Further examination of nine of the affected horses revealed marked elevation of liver enzyme activity of both GDH (glutamate dehydrogenose) and GGT (gamma glutamyl transferase). Analysis of the horses' feed, hay, and bedding revealed DON concentration ranging from 0.5 to 2.7 ppm in the straw.
Once the horses were removed from the contaminated bedding, they gained weight and general condition became progressively better (Zeyner et al., 2002). FDA levels of concern for DON are 2ppm for wheat entering the milling process for humans and 1ppm for the finished product for humans. The concern level for DON in wheat for livestock is 4 ppm (Wood, G.E., 1992).
Ryegrass tremorgens This is an endophyte responsible for ryegrass staggers. It proliferates well in hot, dry conditions coupled with drought or overgrazing that is followed by brief, moist periods of dew or rain, such as during late summer and fall in the northwestern United States.
Newman describes what one might see: "Ataxia, loss of coordination, head shaking, and collapse are common signs, while some animals may appear normal at rest, but when disturbed or stimulated, they freak out. The neurological effects are temporary, lasting less than a week upon removal of the animal from affected forage, but the lack of coordination could cause a horse to run through a fence or wall, or fall into water and drown."
Slaframine This grows on red clover and other legumes. It thrives best in cool conditions with high moisture. Slaframine might be visible on a plant as bronze-colored or black spots or rings, and there is a quantitative lab test for its presence.
Slaframine induces a condition of excessive salivation referred to as "slobbers," while other signs include increased tear production, increased urination, bloating with associated colic, diarrhea, feed refusal, or abortion. Although this toxin is somewhat stable and might be found in baled hay, over time it will degrade. Its effects abate almost immediately with removal of contaminated feed from the horse's diet.
Endophyte Fescue Toxicosis from this is caused by an infection of the seed with an endophyte. Because fescue is generally a hearty plant, it is a favored pasture grass, particularly in the eastern United States. Fescue endophyte with its ergot alkaloids does not develop in all fescue pastures, but when it is present, it is known for its association with reproductive problems, such as lowered sperm count, prolonged gestation length, early embryonic death, lack of mammary development or lactation, red bag foals (presentation of the placenta prior to the foal), retained fetal membranes, stillbirths, or weak/dysmature foals.
A horse with fescue endophyte toxicity might have reduced weight gain, a rough hair coat, higher than normal body temperature, and decreased performance. In some cases, fescue endophyte toxins (ergot alkaloids) elicit necrosis of the tail or ears due to decreased blood flow related to constrictive effects on the blood vessels.
Osweiler suggests, "We recommend that pastures or hay from fescue sources either be endophyte-free or managed closely to reduce the endophyte. If this is not possible, it is a good idea to test the pasture or hay periodically at the beginning of grazing season."
It is also suggested that fescue pastures be mowed periodically to prevent seedheads from developing.
A pregnant mare should be removed from endophyte-contaminated fescue pasture by at least 300 days of gestation, preferably 60 days prior to foaling. In the last two weeks prior to her expected foaling date, the mare can be treated daily with domperidone to limit the adverse hormonal effects of fescue endophyte toxicity.
"Horses are very sensitive to the fumonisins, and probably next most vulnerable to aflatoxins," says Osweiler. "However, they are relatively sensitive to forage mycotoxins, the fescue ergopeptides, and the toxin slaframine produced on red clover or other legumes."
While this problem seems complicated, it really is quite simple. There are molds that can produce toxins in feedstuffs and forages that can make your horse sick or cause him to die.
It is important to know the source of your grains and hay, buy from reputable dealers, have feeds tested, watch for clinical signs, and understand conditions that can cause molds to grow or plants to be affected in the field.
Ask your county extension agent for more information about mycotoxins in your area.
About the Author
Nancy S. Loving, DVM, owns Loving Equine Clinic in Boulder, Colorado, and has a special interest in managing the care of sport horses. Her book, All Horse Systems Go, is a comprehensive veterinary care and conditioning resource in full color that covers all facets of horse care. She has also authored the books Go the Distance as a resource for endurance horse owners, Conformation and Performance, and First Aid for Horse and Rider in addition to many veterinary articles for both horse owner and professional audiences.
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