Selenium and Vitamin E deficiency

Overview

• Both selenium and Vitamin E play key complimentary but independent roles to protect cells against damage. Skeletal, cardiac and respiratory muscles are the most susceptible to damage.
• Vitamin E deficiency is independent of soil type and more closely reflects forage quality. Fresh legumes and pasture are good sources of vitamin E and stored feeds tend to be poor sources of vitamin E. Stored feeds can lose up to 50 percent of their vitamin E a month. All breeds of sheep and goats are susceptible to WMD and it is most common in newborns or fast growing animals. Kids are more susceptible than lambs, possibly because they have a higher requirement for selenium.

Clinical signs

• White muscle disease (WMD) is a subacute nutritional myopathy caused by selenium (Se) deficiency. In most soils, Se is present in low concentrations, sometimes even below 0.2 mg/kg

Pathogenesis

• White Muscle Disease is a deficiency of either vitamin E or Selenium resulting in excessive oxidative damage to cells.  As the muscle, such as the heart, diaphragm, leg muscles and tongue are used, they produce toxins called free radicals.  Free radicals are extremely damaging to cells in muscles and other organs, as they destroy the cells resulting in pain, inflammation, and weakness.  In food producing animals such as cattle and sheep, muscle cells are the most susceptible.  Vitamin E and Selenium are natural anti-oxidants that scavenge free radicals and eliminate their potency.
• The underlying pathology is thought to be free-radical mediated rhabdomyolysis. Both Se and Vit E have an important antioxidant function and protect cell membranes against damage due to free radicals [13]. Se is an important, redox-sensitive element and is a constituent of GSH-Px, which is essential to neutralize reactive oxygen species produced during oxidation of unsaturated fatty acids. Se forms hydroxy fatty acids which are soluble and can be broken down by beta-oxidation. Vit E is important to prevent transition of fatty acids into peroxides, however, unlike Se, it can’t form soluble hydroxy fatty acids.
• Low Selenium can also contribute to retained placentas, reduced immune systems, poor fertility and simply, poor doing cattle.

Diagnosis and differentials

• Common symptoms were muscle weakness, inability to rise, lethargy and inadequate suckle reflex together with increased serum muscle enzymes and low glutathione peroxidase (GSH-Px) and low to normal serum vit E levels.
• Whole blood glutathione peroxidase (GSHPx), a selenium-containing enzyme, is the standard biochemical test for selenium deficiency.

Treatment and control

• Sodium selenate or selenite may be given by injection, usually combined with Vitamin E and will provide adequate selenium supplementation for up to 3 months. The response to treatment may take 4-7 days.
• Total daily consumption of selenium must not exceed 0.7mg/head/day. Ideally the total diet for sheep and goats should contain between 0.10 to 0.30 ppm of selenium.
• Subcutaneous injections of barium selenate provide adequate supplementation for 9-12 months. Oral dosing using 0.1 mg/kg sodium selenate will provide adequate supplementation for 1-3 months. Intra-ruminal soluble glass boluses provide slow release of selenium for 6-12 months. Selenium and vitamin E are frequently added to concentrate rations for feeding to cattle.
• A beef ranch has suffered 12 acute deaths of 2-4 month old calves in the past six months. The owner of the ranch states that the animals appeared severely weak and depressed just before dying. On some of them, he noticed that they were having trouble breathing and had a frothy nasal discharge. You perform a necropsy on a calf that died yesterday. Findings included bilaterally symmetric muscular atrophy. The skeletal muscle appears pale and dry in appearance with white streaks running along muscle bundles. You also notice that there are several calves in the ranch which are having trouble rising, and their musculature appears swollen, hard, and painful. What is the most likely diagnosis?
• Gossypol toxicity
•  Clostridial myositis
•  Septicemia
•  Oleander toxicity
• The correct answer is vitamin E and selenium deficiency (white muscle disease). The clinical signs are somewhat compatible with the other answers; however the necropsy results are diagnostic for white muscle disease. There is both a cardiac form, in which animals die acutely, and a skeletal muscle form, in which animals don’t die acutely but show clinical signs. In this particular question, the ranch was suffering from both forms. Remember that oleander and gossypol are both cardiotoxic and can cause acute death. Given the necropsy findings, clostridial myositis would be unlikely. Selenium is essential for glutathione peroxidase, deiodinase, and selenoprotein-P to work. Glutathione peroxidase breaks hydrogen peroxide and lipoperoxide into water or harmless alcohols
• Gossypol toxicity
•  Clostridial myositis
•  Septicemia
•  Oleander toxicity
• Selenium is effective in at least partially controlling nutritional muscular dystrophy. Areas east of the Mississippi River and in the northwestern USA appear to be low in selenium. The dietary requirement is ~0.3 ppm. Providing selenium-containing mineral mixture may prevent selenium deficiency if animals are allowed free access. Levels of 7–10 ppm or higher may be toxic.