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Selenium Toxicosis in Animals



Karyn Bischoff

, DVM, MS, Cornell University

Last full review/revision Aug 2022 | Content last modified Sep 2022

Selenium imbalances are common in production animals. Both acute and chronic selenium toxicosis (or selenosis) occasionally result from supplement overdose; chronic selenosis can also occur in areas of the world with high soil selenium bioavailability. Acute selenosis is associated with rapid cardiovascular collapse in horses and ruminants, and it can cause poliomyelomalacia in swine. Chronic selenosis, often termed alkali disease, is associated with loss of hair on the mane and tail, hoof deformities, and decreased reproductive performance. Treatment for acute or chronic selenium toxicosis is generally unrewarding; thus, prevention—through monitoring of selenium status, feed quality, and dietary sources of selenium—is key.

Selenium is a metalloid element (atomic number 34) and a required trace mineral for veterinary species, with requirements ranging from 0.1 to 0.38 mg/kg in the diet for most species. Selenium is found in nature in four oxidative states: selenide (–2), elemental selenium (0), selenite (+4), and selenate (+6). Selenate and selenite can be converted into selenide in biological systems. Selenide is found in the selenium-containing amino acids selenocysteine and selenomethionine. Selenium in the food chain originates in plants, which take up the element from the soil. Soil selenium concentrations and bioavailability vary markedly across the US and throughout the world. Relatively high and bioavailable soil selenium concentrations are found in the central states of the US and south-central Canada; lower concentrations are found across the northeastern, western, and southwestern portions of North America. Extensive areas of central Asia, Australia, and Africa as well as parts of South America have selenium-deficient soils, and soil selenium availability globally is expected to further diminish due to climate change.

Selenium deficiency diseases are more widespread than selenium toxicosis. Selenium is integral to numerous enzymes and proteins, including glutathione peroxidase, which prevents oxidative injury, as well as several enzymes involved in thyroid hormone homeostasis. Selenium deficiency contributes to nutritional myopathy, or white muscle disease, affecting predominantly neonatal production animals, as well as hepatosis dietetica in swine, exudative diathesis in growing chickens, and a form of cardiomyopathy in humans known as Keshan disease.

Selenium toxicosis is reported in numerous species, and because of its toxicological importance, the US FDA has set a maximum concentration of 0.3 mcg/g for animal feeds.

The neurologic disease in cattle known as blind staggers, once attributed to selenium, was likely due to polioencephalomalacia resulting from a diet high in sulfur.

Etiology and Pathogenesis of Selenium Toxicosis in Animals

Selenium is a micronutrient, and a certain amount is required in the diet.

For ruminants, the maximum tolerable limit for selenium in forage is 5 mcg/g; for dogs, cats, and fish, it is 2 mcg/g; and for swine, the limit falls in between. The FDA requires animal feeds and foods to contain a maximum selenium concentration of 0.3 mcg/g. Selenium toxicosis usually results from chronic intake of a high-selenium diet; however, occasional occurrences of acute toxicosis are due to oral or parenteral dosing with improperly formulated supplements. Acute selenosis results from overdose of selenium supplements, either orally or parenterally. Miscalculation of dose or improper formulation of parenteral supplements is the most common cause of acute selenium toxicosis. A single selenium dose of ≥1 mg/kg can be associated with lethal toxicosis.

Chronic selenosis is sometimes termed alkali disease because it is associated with alkaline soils in parts of the arid western US. Chronic selenosis is associated with feeds high in selenium or with long-term moderate oversupplementation.

Herbivores are susceptible to selenium toxicosis through the ingestion of high-selenium forage. Certain forage plants and weeds accumulate selenium under specific conditions. Selenium indicator plants are known to preferentially grow in alkali soils in the dry climates of the western and central US. Indicator plants can accumulate selenium concentrations of several thousand mcg/g. These indicator species include many species of Astragalus (locoweeds) as well as Xylorhiza spp (woody aster), Stanleya spp (prince’s plume), Oonopsis (false golden weed), Machaeranthera spp (tansy aster), and Haplopappus spp (golden weed). Other plant species are termed facultative indicators; they do not require high selenium conditions to grow, but in high-selenium soils they can accumulate selenium concentrations >50 mcg/g. Facultative indicator plant genera include Atriplex spp (saltbush), Aster spp, Castilleja spp (prairie fire), Grindelia spp (gumweed), and Comandra spp (bastard toadflax). A few common crop and forage species are relatively selenium tolerant and can accumulate selenium, including Medicago sativa (alfalfa), Triticum spp (wheat), and Hordeum vulgare (barley).

Historically, irrigation and mining operations have mobilized water-soluble selenate and selenite, leading to localized high selenium concentrations in wetland areas and resulting in selenium toxicosis in local aquatic birds. Oversupplementation or improper supplement formulation are other possible causes of chronic or acute selenium toxicosis in domestic animals. Brazil nuts (also known as paradise nuts) have been associated with selenium toxicosis in humans, and they are possible sources for captive animals, such as psittacine birds. Some household items contain relatively high selenium concentrations, including dietary supplements, dandruff shampoo, consumer electronics, and photocopier toners.

Absorption. Selenium absorption in the digestive tract can reach 98%; however, it varies with the form of selenium and other dietary constituents. Selenium can be absorbed via various mechanisms, including passive diffusion for selenite, carrier molecules for selenate, and active amino acid transport for selenomethionine and selenocysteine.

Distribution. Selenium in plasma is bound to selenoprotein P, albumin, and glutathione peroxidase. Highest tissue concentrations occur in the kidneys and liver under normal circumstances.

Elimination. Selenium homeostasis is regulated through fecal and urinary elimination.

Mechanism of Action. A primary biological function of selenium is its role as part of the cytosolic antioxidant system; however, many of the clinical effects of selenium toxicosis are related to oxidative injury. The pathophysiology of selenium toxicosis remains a topic of debate; multiple mechanisms are likely at play. Theorized mechanisms include the following:

  • Selenium is believed to induce oxidative injury through multiple pathways involving glutathione:

    • Selenium interacts with glutathione, leading to the depletion of thiol substrates of the enzyme and thus a decrease in free radical scavenging.

    • Selenium increases the formation of reactive oxygen species, leading to oxidative injury.

  • Selenide, similar to sulfur, has an oxidation state of –2 and can substitute for sulfur in critical proteins, causing dysfunction. Replacement of sulfur with selenium in keratin likely causes the integument defects of chronic selenosis.

Clinical Findings of Selenium Toxicosis in Animals

Chronic selenosis is associated with hair and hoof abnormalities. Bilateral alopecia or hair fragility and breakage along the mane, tail, and the nape of the neck are described in production animals. Similarly, feather loss, particularly affecting the head, and onychomadesis (sloughing of claws) has been observed experimentally and in the field in chickens and wild aquatic birds. Histologic lesions of the skin include degeneration of keratinocytes and atrophy of hair follicles. Hoofed animals develop lameness and hoof deformities. Erythema and swelling of the coronary band is associated with separation of the hoof wall, which can slough off or remain attached as new growth occurs beneath, resulting in the appearance of transverse hoof cracks. Hoof lesions are associated with dyskeratosis of the primary laminae leading to accumulation of keratin debris that distorts the hoof wall. The accumulation of defective keratin leads to circumferential cracks in the proximal hoof wall. Reproductive performance can be decreased in less affected production animals. Selenium toxicosis in aquatic birds and poultry is associated with decreased egg hatching and teratogenic effects in embryos.

In acute selenium toxicosis, some animals die peracutely without developing obvious clinical signs; others quickly become debilitated and weak, often with rapid progression to cardiogenic shock. Signs of abdominal pain have been described in production animals, with profuse sweating in horses and vomiting in swine. A rapid decrease in blood pressure coincides with increased heart rate and respiratory rate. A garlic odor to the breath has been commonly described. Animals can die from cardiovascular collapse and pulmonary edema within hours or days of selenium overdose. Swine with acute selenium toxicosis develop ascending paralysis progressing to tetraplegia; however, they remain alert and willing to eat. These paralyzed pigs generally do not recover.

Animals overdosed with selenium supplements often have cardiac lesions, including areas of pallor in the myocardium, along with epicardial and endocardial petechiae. Chronic myocardial necrosis with areas of fibrosis is possible in animals with chronic selenosis. Pulmonary edema is a common sequela to myocardial damage. Skeletal muscle pallor and hemorrhage have been described in horses. Microscopically, foci of striated muscle pallor and hemorrhage correspond to myofiber degeneration and necrosis. The primary lesion reported in swine is poliomyelomalacia—degeneration of gray matter in the ventral horn of the cervical and lumbar spinal cord.

Diagnosis of Selenium Toxicosis in Animals

When clinical signs and lesions suggest selenium toxicosis, definitive diagnosis is based on assessments of selenium concentrations in serum, blood, tissue, feed, forage, and supplements. Glutathione peroxidase activity can be used to diagnose selenium deficiency, but is less useful in the diagnosis of selenium toxicosis.

Antemortem testing:

  • Measurements of serum and plasma selenium concentrations reflect the selenium associated with plasma proteins, which can fluctuate relatively rapidly along with exposure patterns.

  • Whole-blood selenium concentrations account for selenium associated with plasma proteins and selenium incorporated into erythrocytes. Erythrocyte life span varies in different species but is usually >100 days; thus, whole-blood selenium concentrations are more stable over time.

  • Both blood and serum selenium concentrations increase immediately after parenteral supplementation.

  • Keratin from the hoof wall has been used as a long-term indicator of selenium status. However, the selenium concentration varies as the hoof grows because of differences in selenium exposure over time, necessitating careful sample selection and cautious interpretation of selenium concentrations from the hoof wall.

Postmortem testing:

  • The liver and kidneys are the most common postmortem samples used for selenium analysis.

  • Kidney selenium concentrations are higher than liver concentrations; however, in cases of toxicosis, this ratio can be reversed.

  • The liver selenium concentration increases rapidly after parenteral selenium supplementation.

Treatment and Control of Selenium Toxicosis in Animals

  • Elimination of exposure

  • Low-selenium, high-quality diet

  • Supportive hoof care

Besides eliminating exposure, there is no specific treatment for selenium toxicosis. Treatment of food-producing animals with severe chronic selenosis is unlikely to be cost-effective.

Treatment of chronic selenosis consists of a low-selenium, high-quality diet, with high protein and balanced micromineral composition. Supportive hoof care, including pain control and therapeutic trimming, is critical. Prevention is key. A good-quality diet with a balanced micronutrient profile, regular assessment of the diet and the production animals themselves for selenium, and cautious and appropriate supplementation are keys to preventing selenium imbalances. Chronic selenosis can be prevented in selenium-deficient areas of the world by avoiding oversupplementation. Where selenium is abundant and bioavailable in the soil, regular forage sampling, careful pasture management, and a system of pasture rotation can be used in strategies to prevent selenium excess.

Supportive care for acute cardiac collapse has generally been unsuccessful. Both acute and chronic clinical selenium toxicoses have grave prognoses.

Key Points

  • Selenium deficiency is more common than toxicosis, but toxicosis does occur.

  • Chronic selenosis is most common in areas of the world with high soil selenium bioavailability; it can also occur as a result of long-term oversupplementation. Clinical signs include hair loss, particularly affecting the mane and tail, as well as hoof deformities.

  • Acute selenium toxicosis occasionally results from oral or parenteral supplement overdose and is characterized by rapid cardiovascular collapse in horses and ruminants, and with poliomyelomalacia in swine.

  • Treatment for acute or chronic selenium toxicosis is usually unrewarding.

  • Prevention, through monitoring selenium status and dietary sources of selenium, is key.

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