There is increasing evidence indicating that molds and mycotoxins are involved in the syndromes in Kentucky, Ohio, Pennsylvania, and West Virginia this spring. There have been some positive screens for the mycotoxin zearalenone in pasture and horse urine, and some positive ergot alkaloids found in forages–particularly fescue–and in horse urine. There is a continuing effort to make sure “all bases are covered” in trying to come to a conclusion of what has been causing early fetal loss, late-term gestation loss, red bag deliveries of foals, pericarditis (fluid in the sac around the heart), eye problems, and possibly decreased immune system functions and growth rates in horses.

One agronomist said, “Every 24 hours we can shorten this deal is a benefit to the industry.” A meeting tomorrow (May 17) in Lexington should offer some early results of pasture testing.

Several pasture specialists and veterinarians have thought all along that one single thing probably isn’t the cause of the rash of horse health problems seen this spring. When mycotoxins affect other livestock species, it is known that “1 + 1 = 6” in many cases. That means one mycotoxin might not be seen at extraordinarily high levels, and another mycotoxin also might not been seen at high levels, but when those two are combined, their effects are greatly exaggerated.

Unfortunately with horses, the study of mycotoxins is largely virgin territory. Fescue toxicosis and moldy corn poisoning have been researched, but forage (and/or feed) problems are not seen as often in horses as they are in other species such as cattle, sheep, and swine.

Lon D. Lewis, DVM, PhD, Diplomate American College of Veterinary Nutrition, in his 1995 book Equine Clinical Nutrition: Feeding and Care, has a large section on mycotoxins, equine ergotism, and fescue toxicosis. In his book he stated:

“The largest and most common group of toxins affecting horses is the mycotoxins, of which some are present primarily in harvested feeds; others occur more commonly in unharvested feeds; and some occur in both harvested and unharvested feeds.”

He noted that diagnosis of the causative mycotoxin is important in preventing continued and future exposure, although he added that there frequently was “no single sign or symptom on which a diagnosis can be based on.”
In his section explaining mycotoxins, Lewis said that mycotoxins “are sporadically produced secondary metabolites of molds. These include many useful antibiotics (such as penicillin, griseofulvin, cephalosporins, and ionophores), which at therapeutic levels are more toxic to bacteria than to animals. Molds are ubiquitous, terrestrial, filamentous one-cell fungi. They are an integral part of the natural decay process of plant materials. Those that produce mycotoxins grow in many feeds; the major feeds affected in the United States are tall fescue pasture, harvested corn, peanuts, and cottonseeds, but they include all cereal grains and forages.

“Their growth and toxin production occur primarily in feeds containing over 12-20% moisture, during times of high relative humidity (greater than 70%) when oxygen is available, and generally under alkaline conditions at temperatures of 54-117ƒ Fahrenheit, although some Fusarium molds produce toxins at temperatures as low as 41ƒ F. Moisture levels above 13-14% are, however, the single most important factor that determines whether mold growth and mycotoxin production occurs. Stress, such as drought or inappropriate application of fertilizers or pesticides, can weaken a plant’s natural defenses against molds, and insect and mechanical damage may allow entry of mold spores past a plant’s normal physical barrier, allowing increased mold colonization.”
An important part of Lewis’ writings underscored that, “Under optimum conditions, mycotoxins can be produced within hours and reach a maximum concentration within one to two weeks.” He said the amount of mycotoxin produced varied greatly depending on which mold was involved and environmental conditions.

“Mycotoxicosis in animals often occurs as an outbreak during a specific season and is often associated with a particular climatic event, such as a wet harvest season preceded by a drought. Although feed contamination with most mycotoxins occurs during storage, some mycotoxins (such as ergot alkaloids, slaframine, and some Fusarium species-produced mycotoxins) may be produced in the field.

Lewis said that there are more than 300 “chemically different mycotoxins with different sites of action, mechanisms of toxicity, and, as a result, effects” He said clinical syndromes associated with mycotoxicosis in animals included acute death, debilitation, interference with reproductive efficiency, decreased feed efficiency and growth, and poor condition.

He noted in his book that in general, mycotoxicoses:

1) Are not transmissible fom animal to animal, but frequently affect more than one animal in a herd.
2) Are usually associated with a particular feed and season.
3) Are usually not responsive to treatment of any kind.

“The only treatment for mycotoxicosis is symptomatic and supportive, including a mycotoxin-free diet that is at least 10-20% higher in protein and vitamins than would otherwise be required for that animal. This may assist in overcoming a prior mycotoxin damage-induced decrease in the utilization of these nutrients.”

Lewis noted that susceptibility to mycotoxins varies tremendously between species, with younger animals more susceptible and severely affected than older animals at similar levels of intake.

“The mycotoxins most commonly implicated in health problems in domestic animals are aflatoxins, fumonisins, and zearalenone, and, to a lesser extent, trichothecenes, ochratoxins, tremorgenic mycotoxins, and ergot.

The only mycotoxicosis that commonly affects horses is caused by the fumonisins, causing leukoencephalomalacia or moldy corn poisoning, and the mold Acremonium coenophialum, which causes fescue toxicosis. Less commonly, horses may be affected by ergot, aflatoxins, and tremorgenic mycotoxins that cause grass staggers.”

Lewis noted that at least 42 species of grasses–most of which grow in North America–can contain endophytic molds. “These molds, or their mycotoxins, have the potential to cause disease in horses and other animals.

“Zearalenone at concentrations as low as 0.7 to 5.6 parts per million is a well-known cause of reproductive problems in swine and much less commonly in cattle, but isn’t known to affect horses.”

Lewis in his section on equine ergotism said, in part, “Ergot is the common name for the hardened mycotoxin-containin sclerotia of the mold Claviceps purpurea and C. paspali. It is unique in that it is the only mycotoxin produced during the flowering and seed maturation, and not in the mature plant or seed and, therefore, not during their storage. Ergot formation and, therefore, epidemics and cases of ergotism, are most likely to occur during damp weather around plant flowering time. Conversely, ergot formation and spread are inhibited by periods of drought.”

Lewis said ergots can be found in ryegrass.

“Ergot production by Claviceps purpurea is toxic to all animals, including people, and was responsible for the death of thousands of people in the Middle Ages who ate contaminated rye bread, causing what was referred to as St. Anthony’s Fire. Although ergot contains many compounds, its alkaloids are its toxic principle. These include the hallucinatory drug lysergic acid diamine (LSD), which may be responsible for the behavioral effects ergot causes. Ergot alkaloids also are strongly vasoconstrictive, causing dry gangrene of the extremities, and inhibit prolactin, which may be responsible for the reproductive effects of ergot poisoning.”

Ergot alkaloids in livestock can cause numerous problems, including abortion, reduced birth weight and viability, and agalactia similar to fescue toxicosis.

“Cattle and sheep, which appear to be the most sensitive to ergot, may demonstrate any of these clinical effects (behavioral, dry gangrene, and reproductive effects). Horses are rarely affected by ergotism, but may shown any of these clinical effects, with behavioral changes being most common. Horses fed over one pound of ergot showed only transient symptoms. However, dry gangrene of the legs, difficulty in swallowing, slow respiration, weak pulse, and death of horses ingesting large quantities of ergot-infected ryegrass was reported nearly 100 years ago. No udder development, thickened fetal membranes that required manual rupturing, dystocia, poor cervical dilation, uterine contractions, retained placenta, and uterine rupture were reported in mares consuming oats containing ryegrass seeds contaminated with Claviceps purpurea and ergot. Abortions and prolonged gestations also occurred. Embryonic death and anestrus occurred in mares rebred. Affected foals were unable to stand, were icteric (jaundiced), and had no sucking reflex. These effects are similar to those occurring as a result of fescue toxicosis. Despite tube-feeding and blood or plasma transfusions, 21 of 33 ergot-affected foals died within the first five days of life. Icterus, enlarged livers, and splenic and adrenal hemorrhage were evident on necropsy. Other well-documented accounts of ergotism in horses haven’t been reported.”

Equine Clinical Nutrition: Feeding and Care was published by Lea & Febiger, Williams and Wilkins. Reprints of chapters (quantities of 100 or more) can be purchased from the company by calling Jen Kullgren at 410/528-8573. The book can be purchased through the company by calling 800/638-3030 or on-line at https://www.lww.com. The chapter cited in this article was Chapter 21, Feed-Related Poisonings of Horses