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LAMENESS AND MUSCLE WEAKNESS INDUCING PLANTS
When lameness or muscle weakness are the predominant clinical signs in horses, plant poisonings that should be considered possible causes are (1) contact with black walnut shavings, (2) ingestion of coffee weed or other Cassia species and ingestion of plants that cause (3) vitamin D-like poisoning-induced calcinosis, (4) chronic selenium poisoning, or (5) oxalate-induced calcium deficiency. Excess oxalate intake decreases calcium absorption, causing a calcium deficiency. As described in the section on calcium deficiency in Chapter 2, if this occurs for more than a few months, it results in shifting leg lameness, bone and joint tenderness, and gradually a reluctance to move. Emaciation, loose teeth, upper respiratory noise due to collapse of the nasal sinuses, enlarged facial bones, and sudden death during exercise may occur.
Black Walnut
Coffee Weed or Coffee Senna
Plant-Induced Calcinosis
A generalized stiffness progressing to lameness occurs in horses from eating plants containing a vitamin D-like substance that, like vitamin D toxicosis described in Chapter 3, results in excessive calcium absorption and deposition in their tissues. Plants that have been incriminated as a cause of this calcinosis in animals include Solanum malacoxylon, golden oat grass (Trisetum flavescens), and day-blooming jessamine (Cestrum diurnum). The only one of these known to cause calcinosis in horses in North America is day-blooming jessamine. Golden oat grass is common in England and Wales, particularly on high calcium- containing soils. It grows well under adverse conditions and on poor soils, and is quite palpable.
Wild Jessamine or Day-Blooming
Selenium Excess
Selenium, has numerous effects on cellular function and is a necessary constituent of the diet. 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. In excess, selenium profoundly inhibits cellular enzyme oxidation reduction reactions, especially those involving sulfate or sulfur-containing amino acids. This antagonistic effect of selenium on sulfate alters the metabolism of the sulfur-containing amino acids methionine and cystine, which affects cell division and growth. These effects are greatest on hoof and hair, which are the body tissues that contain the highest concentrations of these amino acids. With chronic selenium poisoning, this is seen clinically as abnormal hoof and hair growth. Selenium will also cross the placenta of pregnant animals, causing fetal abnormalities through its effect on fetal cellular metabolism.
Causes of Selenium Excess
Selenium excess occurs when excess selenium has inadvertently been added to the animal’s diet, is present at toxic concentrations in its drinking water, or when plants high in selenium content are consumed. There are three types of plants that may accumulate sufficient selenium to cause excess selenium effects. These are (1) obligate selenium accumulator or indicator plants, (2) secondary or facultative selenium accumulator plants, and (3) crop plants, alfalfa, and grasses that are normally good horse feeds but that may contain 1 to 30 ppm selenium, if grown on selenium-rich soils.
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.
Even in high-selenium-containing soils, plant uptake of selenium is variable, depending on the chemical form of selenium in the soil, soil acidity, the climate, and the plant species, and is highest during the period of plant growth. Selenium is taken up by plants more readily the more alkaline the soil. Selenium excess is unlikely from plants grown on acidic soils. Soils high in readily available selenium for plants can be detected and, therefore, the potential for selenium excess in herbivores in these areas recognized, by the presence of obligate selenium accumulator plants, that are growing in that area. Because of this, these plants are also referred to as selenium indicator plants. The high selenium content of these plants gives them an unpleasant garlic-sulfur odor which makes them relatively unpalatable and assists in identifying them. The odor is increased by rubbing their leaves together. Horses will avoid eating these plants if sufficient other feed is available.
These plants are also referred to as obligate selenium accumulator plants because they grow only on soils high in available selenium as they require a high amount of selenium for their normal growth. These plants are capable of accumulating up to 10 times the amount of selenium present in the soil. Some may contain up to 10,000 ppm, or 2000 times the total diet concentration of selenium that is toxic, and thus may cause acute selenium poisoning. However, selenium poisoning is most often caused by secondary, or facultative, selenium accumulator plants and normal horse feeds grown on high-selenium-available soils.
The secondary selenium accumulator plants may cause either acute or chronic excess selenium intake and, as a result poisoning. In contrast to the obligate selenium accumulator plants, the secondary accumulator plants do not require selenium for growth, but may accumulate up to several hundred ppm of selenium when grown on soils high in available selenium. The toxic effects of selenium in ruminants varies, depending on the amount and rate of its absorption, the individual animal’s susceptibility, the type of selenium present in the plant, and the interaction of selenium with other elements, such as sulfur, arsenic, or copper, in the diet. These minerals, and possibly others, competitively interfere with selenium absorption by ruminants. If this also occurs in horses, adequate amounts of these minerals in their diet may help reduce selenium poisoning for them, although currently this hasn’t been demonstrated.
Two-Grooved Milkvetch
Golden Weed
Woody Aster
Prince's Plume
White Prarie Aster
Broom, Turpentine, Snake or Match Weed
Gumweed or Resinweed
Saltbush
Indian Paintbrush
Beard Tongue
Effects of Selenium Excess
Acute selenium poisoning from plant ingestion is not common since animals rarely eat plants containing excessively high levels of selenium (over 50 ppm), as they generally are distasteful. Acute selenium poisoning most commonly occurs as a result of the inadvertent addition of excess selenium to the diet. However, when livestock are forced to graze plants high in selenium content, or consume a diet containing high levels of selenium, they can rapidly accumulate levels of selenium in their tissues that will result in death. Blood serum selenium levels greater than 72 ppm cause severe capillary damage in the lungs, liver, and kidneys. As a result of this, affected animals frequently die before clinical signs are evident. Death results from respiratory failure attributable to lung congestion and edema.
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.
Blind staggers is primarily a problem of cattle and sheep resulting from the ingestion of selenium accumulator plants. Affected animals characteristically exhibit aimless wandering, circling, disregard for objects in their way, loss of appetite, and apparent blindness. The disease progresses to the point that animals show front leg weakness and inability to stand. Weight loss accompanies a loss of appetite and decreased feed intake. Teeth grinding, indicating abdominal pain or colic, is common. Death results from respiratory failure, which usually occurs unless the plants causing the disease are removed from the animal’s diet early in the course of the disease. Recent evidence suggests that the blind staggers syndrome may be due to chronic locoweed poisoning and not to excess selenium.
Alkali disease from chronic selenium excess commonly affects horses, cattle, pigs, sheep, and poultry that consume forages or cereal crops grown in seleniferous soil or diets to which excess selenium has inadvertently been added. Early Great Plains and Rocky Mountain settlers referred to the condition as alkali disease because they noted that it occurred only in livestock grazing semiarid regions with high alkali soil, which we now know is soil high in readily available selenium for plant uptake. Poisoning is likely to occur after high-selenium-containing plants or a diet high in selenium have been consumed for several months. 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.
Diagnosis of Selenium Excess
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.
Generally, the more chronic the selenium excess becomes, the lower the levels in the tissues. Hair and hoof sample, however, retain high concentrations and are useful in the diagnosis of chronic selenium excess. It is important to collect hoof and hair samples from the areas where the hoof is cracked or the hair broken off, because this is where selenium is incorporated in the keratin. Hoof wall or hair containing in excess of 5 to 10 ppm selenium indicate excessive selenium intake. However, hair selenium content is affected by intake of other minerals and external or surface contamination.
Treatment of Chronic Selenium Excess
Successful treatment of excess selenium intake depends on its early recognition and on removal of horses from the source of excess selenium. Feeding a low-selenium, highprotein diet rich in the sulfur-containing amino acids cysteine and methionine will help counteract selenium’s effect. Good-quality alfalfa hay, provided it does not contain high levels of selenium from being grown on selenium-rich soils, is relatively high in protein, which is high in cysteine and methionine. Any cereal grain, except corn, may be fed with 15 to 20% cottonseed, rapeseed, or fish meal, which will increase the protein content of the grain mix to 15 to 20%. Corn, soybean meal, and bran are low in these sulfur-containing amino acids and, therefore, are not preferred. In addition, ensure that the total diet contains at least 10 and preferably 25 ppm copper, as copper is necessary to reduce the toxic effects of selenium. Recovery from chronic selenium excess will occur gradually as the horse’s affected hooves grow out, if the horse is fed a diet low in selenium and attention is given to regular trimming of the cracked and overgrown hooves.
Providing feeds, such as grain or hay, known to be low in selenium when horses are grazing pastures containing plants high in selenium assists in preventing excess selenium ingestion.
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