By Kimberly S. Graetz
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 54-117° Fahrenheit, although some Fusarium molds produce toxins at temperatures as low as 41° 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."Continued . . .