Equis ISSN 2398-2977

Toxicity: selenium

Introduction

• Cause: ingestion of selenium accumulator plants; accidental toxicity by excess selenium supplementation, either oral or parenteral.
• Signs: chronic and acute syndromes; lameness, coronary exudate, abnormal hoof wall growth, pedal bone rotation, hair loss.
• Diagnosis: diet analysis, hoof wall analysis for selenium levels; radiography.
• Treatment: adjust diet accordingly.
• Prognosis: depends on severity of injury to hoof wall, acute toxicity usually fatal.

Pathogenesis

Etiology

• Selenium Selenium is an essential element but has a narrow therapeutic range.
• As a component of gluthathione peroxidase, selenium acts as an antioxidant. Large amounts of selenium interfere with this mechanism and cause severe oxidative tissue damage.
• Selenium replaces sulfur in sulfur-containing amino acids (methionine, cysteine and cystine) → weakened structure of the keratin in hoof and hair - cause of systemic toxicity not understood.

Predisposing factors

General

• Alkaline soils in low rainfall.
• Grazing animals.
• Supplementation with feeds containing selenium (selenium is often combined with Vitamin E in supplements for horses with muscle disease).

Specific

• Grazing pastures grown on soil with high selenium levels and/or grazing pastures containing selenium accumulator plants.
• Periods of drought.

Pathophysiology

• Chronic or acute ingestion of feed or forage containing in excess of dietary requirements:
  • Acute poisoning: single oral dose of 3.3-6 mg/kg, 115 ppm in feed for 5 weeks.
  • Chronic poisoning: >5 ppm dry matter; 10 ppb in water.
  • Selenium Selenium intake: 0.5-2.0 mg/kg bodyweight.

Timecourse

• Acute toxicity can occur after a single dose, whereas chronic toxicity often develops over prolonged periods (>30 days).

Epidemiology

• All animals exposed to high selenium at risk of development of clinical signs.

Diagnosis

Treatment

Prevention

Outcomes