To answer that question is not an easy undertaking. There has been a great amount of research performed to answer that topic, and it is continuing today. More and more knowledge is being gained, as to the horse’s requirements of the vitamins, trace minerals, carbohydrates, protein, and fat. To understand the scientific literature on the subjects, one must have a working knowledge of physiology and cellular chemistry of the horse. Without that data, the ordinary horse enthusiast, when reading scientific reports, soon becomes lost and mentally wanders through the maze of information, often not reaching the proper conclusions.

To a certain extent it is that way with me. I have been a veterinary practitioner for 50 years. I read all of the latest research as regards the horse, and primarily that material which applies to draft horses and mules. All of this knowledge, plus years of experience, is the basis of one’s practice.

In this article I am going to deal with vitamin E, selenium, and fat, from the aspect of a practioner, and not that of a researcher. I will try to explain in simple terms the research on these three items and how I have approached problems associated with them in the draft horse and mule.

That’s a tall order to fill, and remember, I am doing this from the practitioner’s view. To cover the subject as well as I can, I will attempt to discuss the material in several parts.

Let’s first talk about selenium and vitamin E, their functions and utilization in the body.

Fifty some years ago I learned in vet school that carbohydrates, proteins, and fats are “burned” in the body to produce energy. They are converted to carbon dioxide and water by a process called oxidation. In this process oxygen is used and combined in the cells with carbon-containing nutrients. When oxygen is used in this way, water is formed, plus oxidizing agents, which are very powerful, called free radicals. These free radicals must be destroyed or they damage the proteins and lipids found in the living cells.

Major components of cell walls are unsaturated fatty acids, which are very susceptible to action by these free radicals. The oxidation of these fatty acids would inhibit cellular activity and function and, in effect, would destroy the cell.

Enter vitamin E into the picture. Vitamin E will block the free radical destruction of the lipids, whereby lipid peroxides are formed. To do this, the vitamin E must be in the cell membrane. Even though adequate vitamin E is present in the cell membrane, some lipid peroxides may still be freed in the oxidation process.

Selenium is a part of the enzyme glutathione peroxidase, which is found in the liquid portion of the cell. This enzyme prevents the formation of free radicals and also destroys or counteracts any lipid peroxides that are present in the cell.

Now, it is easy to understand that vitamin E works as an antioxidant in the cell wall and is lipid-soluble. At the same time the selenium glutathione peroxidase enzyme, which is water-soluble and present in the cell’s fluid, removes liquid peroxides which do form and are present there. Therefore, it is very beneficial to have adequate amounts of both selenium and vitamin E present in the cellular structure to prevent tissue or cellular damage from the oxidation process.

This is as simple as I can present it to you, the reader, so that you can understand the importance of vitamin E and the trace mineral, selenium.

There are some synthetic antioxidants which can be added to feeds to aid vitamin E and selenium in the body. However, let’s skip that, as it will somewhat confuse the issue. These products can be added to feeds, usually to grains, that are fed to the horse or mule.

Health researchers and scientists have established that selenium is very essential for proper disease prevention, reproduction and growth of all animals. So where, then, does the horse get the selenium required by it’s body? It is found occurring in various concentrations in the soil and water on our planet.

Generally speaking, the concentrations of selenium found in our water supplies is not of great importance. Selenium found in various forms in the soil is the primary source for all grazing animals. These forms of selenium have various rates of solubility by plants, and plant levels of selenium vary according to the plant species. Some plants grow very well on soils containing high amounts of selenium and can accumulate large amounts of the mineral. This is measured by parts per million (ppm) selenium. These plants, when fed to livestock, can cause a selenium toxicity.

Likewise, some plants are poor accumulators of selenium. A few are buffalo grass, white clover and grama grass.

The soils of the United States and Canada have been tested and mapped as to regional distribution of selenium, which would find its way into grains and other forages. Low selenium areas will have forage and grain containing 0.05 mg. per 2.2 lbs. or more ppm of selenium. In adequate selenium areas forages and grains produced will have 0.10 or more ppm, while variable areas or soils will have 50 percent of forage and grains containing 0.10 ppm selenium.

According to recent scientific data, selenium deficiencies are a problem in 37 states. Nine additional states have mild to moderate deficiencies. Generally speaking, the soils of most of Canada, the Great Lakes region, the Northeastern states, Atlantic seaboard areas, Florida and areas including the western half of Oregon and Washington and the northern half of California, plus an area including the panhandle of Idaho and the western edge of Montana are low in selenium. Scattered across the Great Plains, South, and the Southwestern United States are localized areas where soil is high in selenium, and local accumulator plants contain 50 ppm or greater. Many of these sites are found in South Dakota, just 100 miles from here in Northwest Iowa.

Alkaline soil is more conducive to plants which accumulate selenium. Plants grown on acidic soils are less likely to take up toxic amounts of selenium. I hope the reader understands that the amount of selenium which a horse or mule can receive from his forage depends on the availability of selenium in the soil, the pH of the soil, the species of plant growing on this soil, growing conditions, and grazing conditions.

There are certain plants which require selenium for their growth, and these plants are named obligate selenium accumulator or indicator plants. These plants may store up to 10 times the amount of selenium in the soil and become very toxic to the horse or animal which ingests it. Some of these plants are: Milk Vetches; Prince’s Plume; Woody Asters; and Golden Weeds.

A second group of plants known to store high amounts of selenium are called secondary selenium accumulator plants. They do not require selenium for their growth, but will store it if weather conditions are favorable for their growth on high selenium-available soil. Some of these plants include: Asters; Saltbursh; Broom Weed; Indian Paintbrush; Snakeweed; Beard Tongue; Gumweed; Ironweed; Bastard Toad Flax; and Turpentine Weed. Alfalfa and some grasses grown under these conditions can amass 1 to 30 ppm of selenium, and their consumption as horse forage can cause chronic selenium poisoning.

Scientific research has established that the selenium requirement for an idle horse is purported to be 0.10 mg. per 2.2 lbs or kg. of diet dry matter or forage. A number of bad effects are seen in horses which receive less than this amount in their diet. It has also been determined that 5 ppm or greater in the diet is very harmful to the horse or mule and will result in chronic or acute selenium poisoning. In the horse, consumption of forage containing 25 to 50 ppm will cause acute selenium poisoning, often resulting in the death of the animal.

Occasionally, acute selenium poisoning or toxicosis will occur because horses and mules are found to eat plants which are selenium accumulators. This occurs in drought areas and where pasture or rangeland is overgrazed, forcing the animals to ingest the plants that normally they would not eat. This forage would contain 50 ppm or greater. Ingestion of 500 to 1000 ppm in the forage, or 2-11 mg. of selenium/kg. of body weight, will cause acute poisoning. Parenteral administration of 0.8 to 2 mg./kg. will also cause the acute phase of poisoning.

In cases of acute toxicity the horse or mule is usually found dead. However, in those cases seen alive the first symptoms noticed are fear, nervousness, depression, and difficult breathing. As the condition rapidly progresses, one sees muscle weakness with trembling, staggering, coma, and death. Blood serum levels in these cases will be 25 ppm or greater.

There is no treatment for acute selenium toxicity.

Chronic selenium toxicosis or poisoning is often known locally as “alkali disease” or “bob-tail disease.” This condition is caused in the horse or mule by ingesting a dry matter diet containing 5 ppm or greater of selenium. I have had occasion to see and participate in many of these cases.

Symptoms of this condition as seen in horses and mules are varied and different from animal to animal.

In the most sub-acute cases the hair becomes rough and coarse, and the animal appears unthrifty, with a failing appetite.

Many of these animals will show signs of fear and nervousness. They will “shy” away from people or objects which normally would not alarm them. This nervousness, fear, and anxiety will increase as time goes on.

Some animals will walk aimlessly about and act as if they cannot see; however, they can.

An interesting symptom, I have noticed in some horses, is that the third eyelid will become prominent, and the eye will appear to bulge. The upper and lower eyelids will appear to be swollen.

The throat region behind the jaws will become swollen, and when the head is held erect the area will seem swollen, and the muscles will appear to be “stiff”.

Some horses will have difficulty in eating and swallowing. This is especially seen in those animals exhibiting the “thickened neck.”

Transverse or horizontal lines will often show up in the skin of the neck and chest area.

The horse will walk with a “stilted” gait. He will not reach out and travel freely, and he’s sore-footed and lame. As the condition progresses, the animal will become quite stiff and may “rope walk” with all four legs and feet and develop a staggering gait.

The coronary band will swell on these affected horses, and circular horizontal cracks will appear in the hoof wall on all four feet. If the crack goes completely around and through the hoof wall to the sensitive laminae, the hoof below the crack will slough off. In time the toe will grow long in the unattended hoof, just like a chronic founder. The hooves on these animals will deteriorate sometimes quite rapidly, and subsoler abscesses may be present.
Selenium horse

Hair will become brittle and break off, giving the mane a “roached” appearance and the tail the “bob-tailed” look. This leads to the term “bob-tailed disease.”

Some afflicted horses may show problems in flexing the hocks and bending the knee. Long term chronic cases will have damage to these joints.

The diagnosis of chronic selenium poisoning can be made from the signs and symptoms alone. As I told one Ph.D. veterinarian over the phone one day, “Any old rancher in South Dakota knows that when a horse loses his mane and tail hairs and walks like a foundered animal, he has selenium poisoning.” This gentleman had a Ph.D. in the subject, he told me, and yet couldn’t recognize the condition in a band of horses when he saw it! Another symptom that is extremely diagnostic, if present, is the thickened neck and throat area. If one sees this symptom and the “bob-tailed”-roached symptom, you could diagnose the condition with both eyes closed or turn in your vet license! Throw in the transverse hoof wall cracks on all four feet plus some lameness, and you are an idiot if you do not know what’s wrong with the horse!

However, there are those who cannot make a diagnosis from symptoms alone. They need the lab. Hoof, hair, and blood samples can be taken and sent to determine the levels of selenium in the tissues. Hoof samples should be taken from the tissue at the edge of the crack. Hair samples are taken at the point of the break of the mane and tail hairs. Selenium levels in the blood 1-4 ppm; hooves 8-20 ppm; hair 11-45 ppm, together with any or all of the above listed symptoms are diagnostic for chronic selenium poisoning.

Successfully treating an individual or band of horses depends on removing the animals from the excessive source of selenium. If one is feeding forage, one will have to discard it and procure some which is known (tested) to be low in selenium. In selenium-deficient areas selenium-fortified salt or mineral is often fed. Occasionally, hay is purchased from a selenium-rich area, and without thinking, the two are fed together, with a resulting chronic selenium toxicosis.

Feeding a high protein diet of good quality alfalfa hay which has a low selenium content is very good therapy. Do not feed corn, soybean meal, or bran. Instead, feed any other cereal grain and add cottonseed, rapeseed, or fish meal to bring the protein content of the grain mix to 15 percent.

Naphthalene orally can be used in the treatment of selenium toxicity by giving 4 to 5 grams orally for five days. Wait five days, then repeat the 4-5 grams for five more days.

Make sure the total diet contains at least 10 to 25 ppm of copper. Copper will reduce some of the toxic effects of selenium, so make sure you add it to the ration of the affected animals.

Arsenic is also used in treating this chronic condition. Inorganic arsenic at 5 ppm in the drinking water is recommended along with salt containing 35- 40 ppm arsenic.

The altered hooves will have to be treated symptomatically, as well as the subsoler abscesses if they are present. Corrective trimming of the hooves must be done to avoid damage to the joints and the sensitive laminae.

Recovery in these animals suffering with chronic selenium poisoning will take up to a year or longer. The selenium-free ration must be maintained throughout this period.

And now, as an after-thought, I’d like to throw in a little story. A while back my friend, Maury Telleen, sent me a letter with a little enclosure entitled, “The Plants That Killed Custer” by Dr. B. Ira Judd. It is a very interesting paper, in that in 1934 he saw the results of selenium poisoning first hand in South Dakota while working on his doctoral degree at the University of Nebraska. According to his paper, he saw cattle kneeling to graze, because their feet were sore, and he saw horses with shovel hooves 3 feet long. He also saw hairless hogs.

According to his paper, a group of people went there to study the selenium-absorbing plants. He said the area around Pierre, South Dakota, was the works.

He states that in 1856 an animal scientist, T.C. Madison, described a disease in cavalry horses at Ft. Randall in Nebraska Territory, whereby the afflicted horses’ manes and tail hair fell out, and their hooves came loose and were deformed. He related that they developed a “staggering gait and died within a month or two.”

According to Dr. Judd, in 1921 a soil scientist, C.C. Lipp, reported trouble in areas of South Dakota, Nebraska, and eastern Wyoming, where steers had such sore feet they knelt to graze.

Dr. Judd learned that several plants absorb selenium. They included locoweed, ground cherry, gum weed, and brushy plants such as the wild woody aster, gum weed, and ground cherry. Sound familiar?

Dr. Judd disclosed that Major Reno’s troops were stationed in South Dakota, and there was a lack of hay that winter and spring. He states that Reno’s horses, on the way to the Little Big Horn, could have grazed on these plants, including locoweed and other selenium-bearing species. He also states the march to join Custer was made at the time of the year when these native plants were the most succulent, and their poison content was high.

Dr. Judd tells that there was a mule packer with Reno, named Ed Alderson. He was a veteran packer, and he knew his stock. He stated the horses and mules were in trouble. “Many were almost useless because of lameness and sore feet. Some lost hair and behaved as locoed animals. Others staggered and died a few days later.” Alderson said the pack train was slow and averaged only 10 miles a day instead of the planned 30.

Dr. Judd reasons that “the horses ridden by the Indians came from beyond the selenium belt and were fresh and rested while Reno’s horses were jaded and suffering from selenium poisoning.” He feels the outcome of the battle might have been different, had it not been for the selenium poisoning.

(Judd, B. Ira.“ The Plants That Killed Custer.” The Cattle-man, August 1978 65:160-161.)

Well, make up your own mind, but this is a very good example of what selenium toxicity in the horse can do.

In the next issue of The Draft Horse Journal, I will discuss adding fat to the ration of the draft horse and what happens when there is too little vitamin E and selenium in the horse’s diet.