What Vitamin Deficiency Causes White Muscle Disease?

December 24, 2025 •

4 min read

According to studies, white muscle disease (WMD) is a well-documented nutritional disorder in livestock and other animals, most often caused by a dietary deficiency of selenium and/or vitamin E. This condition leads to the degeneration of skeletal and cardiac muscles, which is especially detrimental to young, fast-growing animals.

Quick Summary

This article details the roles of selenium and vitamin E in preventing oxidative damage that leads to white muscle disease in livestock. It covers the causes rooted in environmental factors and diet, identifies the clinical symptoms, and discusses diagnostic methods and effective treatment and prevention strategies.

Key Points

Primary Cause: White muscle disease is caused by a deficiency in selenium and/or vitamin E, leading to oxidative damage and muscle degeneration.
Antioxidant Role: Selenium is a component of the antioxidant enzyme glutathione peroxidase, while vitamin E protects cell membranes from free radical damage.
Affected Animals: The disease most commonly affects young, rapidly growing livestock such as calves, lambs, and foals, but can also occur in adults.
Symptom Variations: Clinical signs depend on whether the heart (sudden death) or skeletal muscles (stiffness, weakness) are primarily affected.
Environmental Factor: Prevalence is highest in regions with selenium-deficient soils, which leads to lower nutrient levels in forages and grains.
Prevention is Key: Proper supplementation of pregnant dams and young animals, informed by soil and forage testing, is the most effective preventative measure.

Understanding White Muscle Disease (WMD)

White muscle disease, or nutritional myodegeneration, is a degenerative muscle disease most frequently observed in young, rapidly growing livestock such as calves, lambs, and foals. The name originates from the pale, calcified appearance of the damaged muscles upon post-mortem examination. The primary cause is a deficiency of the powerful antioxidants, selenium (a trace mineral) and vitamin E, which work synergistically to protect muscle cells from oxidative stress.

The Role of Antioxidants

Both selenium and vitamin E are crucial for antioxidant defense within an animal's body. Selenium is a key component of the enzyme glutathione peroxidase (GSH-Px), which neutralizes harmful reactive oxygen species and protects cellular membranes. Vitamin E (specifically alpha-tocopherol) acts as a fat-soluble antioxidant, protecting cell membranes from lipid peroxidation, a process that damages and ultimately destroys cell integrity. When an animal lacks sufficient levels of these nutrients, free radicals accumulate, leading to widespread cellular damage, particularly in highly active muscle tissues.

Causes of Deficiency

Deficiencies can arise from multiple factors, often related to the animal's geographical location and feed source. The primary cause is foraging on crops or pasture grown in selenium-deficient soil, which is common in many parts of the world. Additionally, poor-quality or improperly stored hay and feed can lose significant amounts of vitamin E over time. Other contributing factors include:

Dietary imbalances: Diets high in polyunsaturated fatty acids can increase the need for antioxidants, precipitating WMD in animals with marginal selenium and vitamin E status.
Soil type and pH: Selenium bioavailability to plants is affected by soil pH. Acidic and neutral soils make selenium less available for plant uptake.
Increased demand: Rapidly growing young animals and pregnant or lactating females have higher nutritional demands, making them more susceptible to deficiencies.
Stress: Factors such as environmental stress, transport, and illness can increase oxidative stress and trigger clinical signs in susceptible animals.

Recognizing the Symptoms

The clinical signs of WMD vary depending on which muscle groups are most affected and the severity of the deficiency. There are two main presentations: a congenital form that primarily affects the heart and a delayed form that affects skeletal muscles.

Congenital (Cardiac) Form:

Sudden death in newborn calves or lambs, often within 2–3 days of birth.
Difficulty breathing and respiratory distress due to heart failure.

Delayed (Skeletal) Form:

Stiffness, weakness, and reluctance to stand or move.
An arched back and a stiff, stilted gait.
Muscle trembling or weakness.
Inability to swallow, leading to a weak suckle reflex and potential aspiration pneumonia, especially in foals.

Diagnosis, Treatment, and Prevention

Diagnosis

Accurate diagnosis requires a veterinarian and relies on a combination of clinical signs, herd history, and laboratory testing. Blood tests will typically show low levels of selenium and/or vitamin E. Elevated levels of muscle enzymes like creatine kinase (CK) and aspartate aminotransferase (AST) indicate muscle damage. Post-mortem examination (necropsy) is often definitive, revealing the characteristic pale, whitish streaks in affected muscles.

Treatment

If diagnosed early, treatment can be effective. A veterinarian will typically administer an injection containing a sterile emulsion of selenium and vitamin E. Supportive care, such as keeping the animal warm and providing assistance with feeding, is also crucial. For long-term management, dietary supplementation is necessary. However, animals with severe heart muscle damage have a poor prognosis.

Prevention

Prevention is the most cost-effective and reliable strategy for managing WMD. Focus should be on ensuring adequate intake of selenium and vitamin E for breeding females and young stock, especially in regions with selenium-deficient soils.

Supplementation during gestation: Administering selenium and vitamin E to pregnant dams can improve nutrient status in newborn offspring.
Mineral mixes: Providing selenium-fortified mineral mixes or salt is an effective method for supplementing animals, particularly on deficient pastures.
Forage analysis: Regularly testing soil and forage for selenium content helps determine if supplementation is needed.
Proper storage: Storing hay and other feedstuffs correctly can preserve their vitamin E content.

Comparison of WMD in Different Species


Feature	Calves	Lambs & Kids	Foals	Poultry
Primary Cause	Selenium and/or vitamin E deficiency	Selenium and/or vitamin E deficiency	Selenium deficiency, less commonly vitamin E	Vitamin E and/or selenium deficiency
Susceptible Age	Young, fast-growing calves and neonates	Newborn or fast-growing animals	Newborn foals (up to one year), occasionally adults	Chicks and young waterfowl
Common Signs	Stiff gait, weakness, arched back; sudden death	Stiffness, arched back, pneumonia; sudden death	Weakness, poor coordination, difficulty nursing/eating	Locomotor difficulties, weak muscles
Affected Muscles	Skeletal and cardiac, especially legs, back, heart	Skeletal and cardiac, hindquarters, diaphragm	Skeletal (legs, chewing) and cardiac	Skeletal (breast) and cardiac, sometimes smooth muscle
Geographic Risk	Areas with selenium-deficient soils	Areas with selenium-deficient soils	Areas with selenium-deficient soils	Dependent on regional feed sources

Conclusion

White muscle disease is a serious but largely preventable condition caused by a deficiency of selenium and vitamin E. Both nutrients act as essential antioxidants, and without adequate levels, muscle tissue is highly susceptible to oxidative damage. Livestock owners in at-risk geographic regions must be proactive in testing their soil and forage, and implementing a strategic supplementation plan for their animals, especially pregnant dams and young stock. While treatment is possible with veterinary intervention, prevention through proper nutrition is the most effective approach to protect animal health and avoid significant economic losses. For more information on managing selenium in livestock, consult resources from extension services like the Michigan State University Extension.

Frequently Asked Questions

The main cause of white muscle disease is a deficiency in the trace mineral selenium and/or the fat-soluble vitamin E, which are both crucial antioxidants for protecting muscle tissue from damage.

Young, fast-growing ruminants like calves, lambs, and goat kids, as well as foals and poultry, are most susceptible to white muscle disease.

Yes, older animals can also be affected by a more chronic form of white muscle disease, particularly with prolonged low dietary intake of selenium or vitamin E.

In white muscle disease, the affected muscles appear pale, dry, and often have white, chalky-looking streaks or patches due to calcium deposits and tissue degeneration.

Diagnosis is confirmed by a veterinarian using blood tests to measure selenium and vitamin E levels and to check for elevated muscle enzymes like CK and AST. Necropsy can also provide a definitive diagnosis.

Common symptoms include muscle stiffness, weakness, inability to stand, trembling, an arched back, and difficulty breathing. Sudden death can occur if the heart muscle is affected.

Prevention involves ensuring adequate dietary intake of selenium and vitamin E through fortified feed, mineral mixes, or injections, especially for pregnant females and young animals in high-risk areas.

Selenium deficiency is geographically linked because many regions have low selenium concentrations in their soil, resulting in forage and grains with insufficient levels of the mineral.

Yes, early and prompt veterinary treatment, often involving injections of selenium and vitamin E, can help improve the prognosis for affected animals. Supportive care is also necessary.

The congenital form affects the heart muscle and often causes sudden death in newborns, while the delayed form affects skeletal muscles, leading to stiffness and weakness in slightly older animals.