Part II: Notes on Selenium Coutesy Stormy May's Horse Management Newsletter

This article is a follow-up to last issue's How much do you know
about your horse's diet? by Stormy May. Also part of our two-part series on feed rations, check out this issue's book review on Beyond the Hay Days by Rex A. Ewing.

Selenium is a mineral that all horse owners should be aware of. To paraphrase some of the following excerpts, too little selenium (less than .1ppm or .1 mg/kg) and a horse may exhibit signs of tying-up (azoturia) or other symptoms such as anorexia, emaciation, generalized muscle weakness, rapid heart rate, and diarrhea, all of which could ultimately lead to death. Too much selenium (over 5ppm or 5 mg/kg) can lead to "blind staggers" or "alkali disease" which also may result in death. Following, are several excerpts that I found while researching selenium.

From: http://horse.purinamills.com/bulletins/musthaveminerals.htm

How your horse uses it: The trace mineral selenium works in concert with vitamin E to scavenge destructive free-radicals and aid in muscle development.

Where it's found: Most forages contain selenium, but the amounts vary greatly, depending on the area of the country where the forage was grown. For example, the soils of Florida, northern California and western Oregon are low in selenium and produce selenium-deficient crops. In contrast, the soil in parts of Colorado, Montana, the Dakotas and Wyoming contain toxic amounts of the mineral.

Dietary requirements: Horses require only about 0.1 parts per million (PPM) of selenium in the diet. Since soil conditions affect selenium content, it's wise to have your hay analyzed to see how much it supplies. Supplementation in conjunction with vitamin E is useful in treating some cases of tying up.

If he doesn't get enough: A selenium-deficient diet results in reproductive problems, immune deficiencies and, particularly in foals, white muscle disease, where the muscles become weak and useless.

If he gets too much: Selenium poisoning usually occurs when horses graze on plants that contain high levels of the mineral. Horses suffering from acute selenium poisoning--with blood levels of more than 72 PPM--may exhibit colic-like discomfort, increased heart and respiratory rates and head-pressing or staggering behavior. Long-term grazing on plants that contain between 5 and 50 PPM of selenium can lead to chronic toxicity and associated anemia, lameness, a rough hair coat and brittle, malformed hooves. Untreated chronic toxicity can be fatal.

From: http://www.cvm.uiuc.edu/petcolumns/showarticle.cfm?id=181

Many different sources of selenium are available for supplementation, the most important factor is selecting a source of the proper strength and selenium content that is available for digestion. Only one consistent source should be used. A free-choice salt/mineral mix containing selenium is the safest form of supplementation.

The supplementation rate for selenium is generally 1 mg per horse per day. Supplementation can go as high as 2 to 3 mg per day without any ill effects. Doses of 5 mg per day can lead to problems with selenium toxicity.

Clinically, selenium deficient horses will often "tie-up," a degenerative condition of the muscles also known as rhabdomyolysis. It can affect the heart muscle, the muscles of respiration, as well as the large muscles of the back and limbs. It can also cause a decrease in the efficiency of the immune system, leading to opportunistic infections.

From: http://www.neosoft.com/~iaep/pages/nutrition/toxicosis/seleniumtox.html

The condition was called "alkali disease" which in its chronic form resulted in loss of hair from the tail and mane, abnormal hoof growth, lameness, anemia, salivation, grinding of the teeth, paralysis and eventual death. An acute form which can follow consumption of plants with very high levels of selenium results in a condition know as blind staggers which is characterized by elevated temperature, labored respiration, a bloody froth in the mouth and nose, respiratory failure and death.

Most of the early interest in selenium was focused on its role as a toxic element. However, in 1957 Schwarz and Foltz discovered that it was required in the diet of animals and it has since been included in a list of twelve essential trace elements along with chromium, nickel, vanadium, tin, zinc, iron, copper, iodine, managnese, cobalt, and molybdenum. It is now known that the areas where it is deficient far exceed those where selenium toxicity is a problem. Early nutritional studies revealed a relationship between vitamin E and selenium and for a time it was believed that the vitamin could replace selenium in the diet. It was later shown that this was not the case and that some selenium was required irrespective of the level of vitamin E. Further studies have revealed a complex relationship between selenium, vitamin E., lipids, sulfur and sulfur containing amino acids.

From: http://www.ruralheritage.com/vet_clinic/selenium.htm

"Alkali disease," is characterized by hair loss from the mane and tail, sloughing of hooves, joint erosion, and lameness.

Excessive intake of selenium may result from consuming plant material raised in areas where the soil contains a high level of selenium. The areas with high selenium soils are west of the Mississippi River. Prior to the 1930s, when alkali disease was first proven to be caused by selenium toxicity and the high selenium areas were identified, many horses and cattle died of the disease. Dr. Merl Raisbeck of the Department of Veterinary Science at the University of Wyoming reported that each year before 1930 a vast number of animal deaths in Wyoming were attributed to alkali disease.

Although the number of cases of selenium toxicosis has greatly decreased since 1940, toxicity is still reported. During a recent three-year study in Wyoming Dr. Raisbeck found four substantiated cases of selenium toxicity of horses due to the ingestion of high selenium forage. A few recent cases have also been reported in Colorado and Iowa.

Cases of toxicity due to selenium in the water, excessive use of supplements, or environmental contamination are occasionally reported. The dangers of excessive selenium cannot be ignored.

Requirement Selenium was first shown to be a required nutrient for laboratory animals in the 1950s. Shortly thereafter it was established as a help in preventing muscular degeneration in farm animals. Prior to 1950 white muscle disease was common in calves, lambs, and foals raised in areas where the soil is lacking in selenium. Selenium supplementation and injections have saved the lives of millions of animals.

Although severe selenium deficiency is usually much more common in young animals, it may also occur in older animals. Selenium deficiency may impair reproductive performance and decrease resistance to disease.

In the 1960s researchers discovered that selenium can help prevent tying-up disease in horses, but does not prevent all cases. Since selenium has been widely added to horse feeds, the number of tying-up cases that respond to selenium has been greatly reduced, and tying-up continues to be a problem.

Identifying Deficiency If you live in an area where the soil is known to be lacking in selenium and you feed your horses only home grown feeds, you should use selenium supplementation.

Select a supplement that provides 1 to 3 mg of selenium per day or use a trace mineral salt that is fortified with selenium. Salt products designed for horses contain 30 to 90 ppm selenium. You may add the salt to the feed or offer it free choice.

Free choice feeding of selenized-salt has been widely used for sheep and cattle because supplementing grazing animals is often difficult. Fewer studies have been conducted with horses, but salt appears to be a reasonable source of selenium, particularly for horses that graze. If you use a commercial grain mixture fortified with selenium, you probably don't need a supplement.

If you are not sure whether or not your horses are getting enough selenium, and the horses have muscle problems, selenium may be involved. Your veterinarian can take a blood sample and have it analyzed for selenium or glutathione peroxidase, an enzyme that requires selenium.

Selenium is needed for a horse's normal muscle function and health. Three adages apply: An ounce of prevention is worth a pound of cure—selenium supplementation need not be expensive, but if selenium is needed and not provided, the cost can be great. Use moderation in all things, and good things come in small packages. The horse needs 1 to 3 mg of selenium per day, but 50 mg per day may cause toxicosis.

One mg is 0.0000022 lb. Thus you must exercise care when using selenium supplements. The amount of supplement you add must of course be greater than one mg, because the selenium in the supplement is diluted with carrier. Read the label carefully and add adequate but not excessive amounts to keep your horses healthy.

From: http://www.ansci.cornell.edu/plants/toxicagents/selenium/selenium.html

Alkali disease is more chronic than blind staggers, often taking years to manifest itself. It is caused by feeding on plants and grain that have protein-bound, insoluble selenium. This disease can affect all livestock, but it is detected mostly in cattle and horses. General symptoms include: lack of vitality, anemia, emaciation, stiffness of joints, lameness, rough coat, loss of long hair, and hoof sloughing and deformities. Hoof deformities are a classic sign of selenium and can cause lameness and severe pain for the animal; food and water must be provided to the animal, for it may be hesitant to walk.

The most effective way of preventing selenosis is to remove the animals from the seleniferous area. Treating the soil with sulfates, thus changing the S:Se ratio, can sometimes depress Se uptake by accumulator plants. Results from studies have shown that feeding a higher protein diet may reduce the toxicity of Se; animals fed the same amount of toxic selenium but fed a higher protein diet lived for a few more days than those animals fed a low protein diet. Dilution of high Se feeds with low Se feeds in a mixed ration will help to prevent toxicity. Recognition of seleniferous plants, proper land management, and grazing control are all necessary to completely prevent selenosis.

Deficiency of Se is much more common in the eastern United States where the soil content of Se is low. There are many different diseases that affect the different species, all of which will be addressed in the species sections. There is one disease that is consistent in all livestock species, and that is Nutritional Muscular Dystrophy, or White Muscle Disease (WMD). Nutritional muscular dystrophy is caused by the deficiency of Se and/or vitamin E and S-containing amino acids. The disease is characterized by degeneration of the skeletal muscles, causing stiff gaits, and other problems.

The nutrient requirement for horses is 0.10 mg/kg. Nutritional muscular dystrophy is the known disease that affects horses with Se deficiency. Similar to sheep, there are three different patterns of NMD that can occur. The first is acute, with death occurring within 24 hours. The foal's tongue may be paralyzed, making in unable to suckle. The second case is more common and is induced by exercise. Older foals are more susceptible to this form; they show an unsteady gait and general muscle weakness, rapid heart rate with arrhythmia, and labored breathing. After a few days, it is difficult to make them stand and they salivate excessively. Mortality from this condition is only about 30-45%. The third condition affects mostly older animals, and is the result of chronic Se deficiency. Affected animals show anorexia, emaciation, generalized muscle weakness, rapid heart rate, and diarrhea.

From: http://horse.purinamills.com/bulletins/poison/lamenessinducing.html

A number of detrimental effects occur if the diet contains less than 0.1 ppm (or mg/kg) selenium. However, greater than 5 ppm in the total diet is harmful and causes chronic selenium poisoning of livestock; greater than 25 to 50 ppm may cause acute selenium poisoning and sudden death due to pulmonary congestion and edema.

Selenium-rich soils occur in areas of low rainfall, where minimal leaching of selenium from the soil is likely to occur. In North America this occurs primarily in the Rocky Mountain and Great Plains regions. In a recent survey, selenium excess attributable to native plants was reported in only eight states (California, Colorado, Idaho, Montana, Oregon, South Dakota, Utah, and Wyoming). In contrast, in all 50 states except four (Delaware, Rhode Island, West Virginia, and Wyoming), selenium deficiency, was reported to be a problem.

Acute selenium poisoning most commonly occurs as a result of the inadvertent addition of excess selenium to the diet.

More common than the acute is a chronic selenium excess. Traditionally, chronic selenium excess has been divided into two syndromes referred to as blind staggers and as alkali disease. Both syndromes are associated with the chronic ingestion of forage and crop plants that have accumulated 5 to 50 ppm selenium in their dry matter.

Excess selenium consumption results in the substitution of sulfur in keratin by selenium. This results in defective formation of keratin, the principal protein present in the hoof and hair. Initially, affected horses lose the long hair from the mane and tail; it breaks off at the site where excess selenium is incorporated in the hair shaft. This gives the horse a roached mane and bobtailed appearance, and is the reason the syndrome has been referred to as "bob-tail disease." Lameness develops as a result of inflammation of the coronary band and abnormal hoof wall formation affecting all feet. Initially, affected horses walk stiff-legged, with tenderness followed by pronounced lameness. Horizontal rings or ridges that may progress to full-thickness cracks through the hoof wall causing severe lameness are characteristic. Some horses may slough the hoof wall entirely. Chronic selenium excess has also been associated with anemia, liver cirrhosis, emaciation, and degeneration of heart, bones, and joints in horses and cattle.

A diagnosis of selenium poisoning is best confirmed by submitting samples of feeds ingested for analysis and then determining the selenium concentration in the total diet as described in Chapter 6. A selenium concentration in the total diet dry matter greater than 5 ppm (5 mg/kg) should be considered potentially toxic. A serum selenium concentration above the normal of 0.09 to 0.3 ppm is suggestive of chronic selenium excess, although 1 to 4 ppm is typically present, whereas serum levels up to 25 ppm have been reported in acute poisoning. Excess selenium in liver or kidney is also indicative of selenium excess.

Stormy May, a graduate of the United States Pony Club, and professional equine video producer, is dedicated to promoting the harmonious relationship between human and horse through quality riding instruction and educational videos, workshops, and other products. www.stormymay.com

She also produces the Horse Management Newsletter.

Part I:
How much do you know
about your horse's diet?
by Stormy May