Equine Pasture Grazing Problems
Posted: August 12, 2011
Dr.Ann Swinker, Extension Horse Specialist
Most horses if given the opportunity, will spend 14-18 hours a day eating forages, much like free-running horses (Ralston 1986). There are health and metabolic problems such as colic, gastric ulcers and behavior concerns when horses are fed large amounts of nutrient dense feeds like grain only once or twice a day and have limited access to forages. So it is important to supply equine with a safe constant forage supply.
Because horses have evolved to eat plant material, we must keep in mind that not all plants are safe for them to eat. Poisonous plants and weeds can cause metabolic disturbances or death in horses. Horses differ from other livestock in that anything that impairs the horse's tolerance for exercise and performance diminishes the horse’s value. This paper will cover some disorders created by certain pasture and forage plants.
Fescue toxicosis in the horse has been recognized for decades. However, the mechanism of action and successful management practices are only now being reported. Fescue toxicosis in the horse is due to several alkaloids in the endophytic fungus found in fescue. These alkaloids can cause problems to a pregnant mare and her fetus. Common signs of fescue endophyte toxicity include prolonged gestation, lack of udder development, absence of milk production, abortion, thickened placentas, retained placentas, stillbirths, and foal mortality. One of the most common effects in pregnant mares is reduction of prolactin hormone, which triggers udder development in late pregnancy. Prolactin is released from the pituitary gland and is influenced by other hormones, including dopamine, which inhibits prolactin release. Dopamine is a chemical normally produced in the body, affecting function of glands, muscles, organs, and nerves, and it acts as a neurotransmitter in the central nervous system. It is essential to normal nerve activity in the brain and some peripheral tissues. Its cellular receptor activity is affected by the endophytic fungus toxins.
Fescue toxicosis may be controlled by management or treatment. A rotational grazing technique allows use of fescue for growing horses. Even though endophyte-infected tall fescue hay may be less digestible in the horse than uninfected hay (Redmond et al., 1991), young growing horses being exercised can efficiently use the endophyte-infected fescue on a short-term basis (Pendergraft et al., 1993). Similar techniques can be used in mares. A forage legume, such as birdsfoot treefoil or red clover, seeded with tall fescue will substantially reduce the adverse effects of this poison. The primary method of transmitting the fungus is through infected seed. Fungus-free and fungus-resistant seed is now available and should be used. However, pastures seeded with fungus-free seed may eventually become-infected.
If mares are removed from fescue in late gestation, most signs of toxicosis can be reduced or eliminated. Withdrawal from infected fescue before parturition results in a rise in serum prolactin levels, allowing milk production (Redmond et al., 1991). Mares moved to endophyte-free pasture at 305 to 310 days of gestation delivered live foals and lactated normally.
Fluphanazine has been considered, however Equidone, domperidone has been very promising. Daily oral doses of 1.1 mg/kg body weight of domperidone prevented symptoms of fescue toxicosis in late gestation mares on endophyte-infested fescue forage (Cross et al., 1999).
Alsike clover (Trifolium hybridum) creates a photosensitivity response secondary to damage in the liver caused by alkaloids in the plants. Legume hays have also been implicated in setting up these conditions for skin problems. (Nation, 1989). Chronic or nervous clinical signs and liver disease, including biliary fibrosis and epithelial proliferation, may occur (Nation, 1991). Photosensitivity - Certain plants contain photo-reactive pigments that are absorbed into the blood when a horse eats the plant. In the presence of ultraviolet light from the sun, these then react in areas of non-pigmented skin, and the horse's skin sunburns. Generally, a horse has to consume these plants for a few months before the liver effects are severe enough to allow accumulation of a by-product of plant chlorophyll breakdown in the blood. This compound is called phylloerythrin, and its accumulation in areas of non-pigmented skin causes photosensitivity.
Sweet clover poisoning occurs as a result of molds that grow in poorly managed sweet clover silage or hay that is put up too wet. These molds produce the chemical dicoumarol which blocks normal blood clotting in animals that consume large quantities. Dicoumarol is commonly used in several commercial rodent poisons. If formed, the poison persists in hay or moldy silage and is readily eaten by animals. The signs of sweet clover poisoning include those of abnormal bleeding. The first signs are spontaneous nosebleeds and black tar like manure. Swelling of joints, lameness and difficult breathing can occur later if heavy doses are consumed. Treatment consists of removal of the feed source and administration of vitamin K to restore normal blood clotting. Prevention includes avoiding moldy sweet clover silages and moldy hay that consists primarily of sweet clover.
Slobbers -excessive salivation were observed in horses eating red clover or other legumes infested with Rhizoctonia leguminicola that produces slaframine (Socket et al., 1982). It thrives best in cool conditions with high moisture. Slaframine may be visible on a plant as bronze-colored or black spots or rings, and there is a quantitative lab test for its presence. This toxin is usually stable, it can be found in baled hay. Slaframine can break down over time. In one report, after ten months of storage, the toxin dropped from 100 mg/kg to 7 mg/kg (Hagler and Behlow, 1981). Some of the signs of slaframine are excessive salivation, increased tear production, increased urination, bloating with associated colic, diarrhea, feed refusal, or abortion. Its effects go away almost immediately after taking away the contaminated feed.
Nitrate poisoning can occur in cattle and horses grazing pastures or eating hays that have accumulated high levels of nitrates during growth. Nitrates accumulate in plants when excessive rates of fertilizer have been applied or when plants have been drought stressed. Nitrate levels tend to be higher in the lower one-third of the plant or stalks and accumulate more at night and on cloudy days. Some species of plants that are known to accumulate nitrates include Johnsongrass, sorghum, sweetclover, bromegrass, orchardgrass, lambsquarter, oat hay, rape, barley, wheat and corn. Hay may continue to be dangerous as the accumulated nitrates decrease slowly over time (Stanton, 1995).
Low levels of nitrates can cause abortion without any other symptoms. Severely affected animals develop muscle tremors, lose coordination and become weak. Moving these animals will initiate difficult breathing commonly followed by collapse and death. Nitrate poisoning is often confused with prussic acid poisoning but is distinguished by a marked difference in blood color of affected animals. Animals poisoned by nitrates will have chocolate brown blood while those poisoned by prussic acid will have bright red blood. Treatment by a veterinarian can be effective if initiated early. Prevention includes mixing affected forages with normal forages to dilute the nitrate levels. Raising the cutter bar 10-12 inches to avoid cutting the lower one-third of the plant and not cutting drought-stressed forages for several days after a rain also helps reduce problems. If high nitrate levels are suspected, samples of the forage should be submitted to a competent laboratory for analysis before the forage is fed. Horses can tolerate a higher amount of nitrate levels in feed than cattle.
Prussic acid poisoning is caused by a poison called cyanide that can be produced in several types of plants under certain growing conditions. All species of farm animals may be affected with this acute poisoning. The plants most commonly involved in prussic acid poisoning are Johnsongrass, sundangrass, common sorghum, in addition to black cherry and choke cherry. Johnsongrass is the most toxic of the sorghums and commonly causes poisoning when subjected to frost or drought conditions. Very young, rapidly growing plants are more likely to produce the poison. Feeding or grazing of these forages should be delayed until they are more mature. Feeding forages following heavy nitrogen fertilization, plant injury by trampling or stunting of plant growth due to adverse weather should be avoided. If large amounts of forages containing prussic acid are eaten, death can occur within a few minutes. Excess salivation, difficult breathing, muscle tremors and rapid heart rate all signal the onset of prussic acid poisoning. Shortly after these symptoms are seen the animal may go down and death will likely occur due to respiratory paralysis. Animals that live one to two hours after the onset of these signs will usually recover.
Prussic acid is quite volatile and there is little danger from feeding well-cured hay. The following prevention measures will best control the problem: Do not graze pastures that are less than 18-24 inches tall or green chop plants over 18 inches tall for three days after a killing frost. Feed grain before allowing animals to graze fields that may be high in prussic acid.
Colic - Alfalfa pasture is commonly involved in causing cattle to bloat. Cattle in early stages of bloat will show signs of abdominal pain, which include restlessness and kicking at the belly. Legumes tend to produce gas in the Equine digestive system. Horse do not bloat but do colic just another name for a sever stomachache.
Metabolic Disorders related to feeding forages: Because horses are living longer we are having reports of metabolic and hormonal dysfunction (Peripheral Cushing's disease) in horses. Clinical signs of metabolic syndrome include obesity-associated laminitis and abnormal fat deposition. In addition, insulin resistance appears to be one of the criteria defining metabolic syndrome. When a horse has a history of chronic laminitis, the first concern would be addressing the metabolic issues contributing to the problem, usually obesity and/or pituitary dysfunction, both of which are treatable.
Horses that are truly insulin resistant/glucose intolerant there is no one "type" of hay guaranteed not to trigger a bout of laminitis. It depends more on the harvest conditions, not the species of grass, whether a batch of hay contains sufficient non-structural carbohydrates (NSC: starches, water soluble sugars and fructans) to cause problems. Most horses tolerate more than 20% NSC without adverse effects, and most grass hays, especially those from the Eastern states, contain only 7-18% NSC, with an average of 12%. Even legume hays, on average, contain less than 15% NSC. Oat hay, on the other hand, averages 22% NSC. (Equi-Analytical Laboratories' web site.)
Grasses accumulate NSC throughout the day, with the highest concentrations achieved late in the day if the sun shines. If temperatures are above freezing and adequate water is present, NSC are converted to cellulose and other structural carbohydrates overnight, resulting in very low sugar concentrations by daybreak. If this process is disrupted by drought or freezing temperatures overnight, NSC concentrations can increase significantly.
The grasses continue to "respire" after cutting until the hay is baled and "cured." The longer the hay is dried in the field, the lower the NSC will be. Sugars and fructans are water soluble, so if the hay is rained on or soaked in water, the overall NSC will also be reduced. "Warm season" grasses, such as coastal Bermuda and crabgrass, tend to accumulate lesser amounts of sugars than the "cool season" grasses like fescue, orchard grass, and timothy under adverse conditions.
If a horse is sensitive to NSC content, the "safest" hays are coastal Bermuda or timothy cut early in the day, after a warm night and recent rainfall. Hay dried in the field for at least a day or two--even rained on a bit--is considered safer. Western hay producers tend to cut their hay later in the day to prevent excessive drying, and they bale more quickly than is possible in the humid East, all of which tends to preserve a higher NSC content.
Laminitis is inflammation within the sensitive laminae of the feet. It can occur for many reasons, but as a nutritional problem it is commonly linked to grain-rich diets, ingestion of too much rich pasture, and obesity. Grain overload or a diet rich in high-carbohydrate feed (grain or lush pasture) initiates a series of metabolic and endocrine (hormone) disturbances in the body. A diet abundant in carbohydrates upsets normal intestinal bacteria, allowing more endotoxins from harmful bacteria to be absorbed into the bloodstream than can be neutralized by the liver.
In Conclusion, When feeding horse forages there are a few things to keep in mind. There are molds and fungi that can produce toxins in forages that can make your horse sick or cause death. Learn to recognize clinical signs, and understand climatic conditions that may cause plants to be affected. Buy feeds and hays from reputable dealers and lab test suspicious feed.
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