Bit & Bridle

Equine White Muscle Disease

Other Names

  • Nutritional Myodegeneration (NMD)
  • Selenium-Vitamin E Deficiency Disease
  • Stiff Lamb Disease (in small ruminants — same nutritional cause)
  • Enzootic Muscular Dystrophy

What is White Muscle Disease in Horses?

White Muscle Disease (WMD), formally known as Nutritional Myodegeneration, is a degenerative muscle condition caused by deficiency of selenium, vitamin E, or both. The disease affects skeletal and cardiac muscle, causing muscle fibre necrosis (cell death) that, in severe cases, can result in an inability to stand, respiratory failure, or sudden death from cardiac involvement.

The name comes from the pale, chalky appearance of affected muscle tissue on post-mortem examination — the degenerated fibres lack their normal dark red colouration. Although the condition is best known in newborn foals, in whom it can be life-threatening, it also affects adult horses, particularly those kept on selenium-deficient pastures without appropriate supplementation.

In the United Kingdom, large portions of the country — particularly the west and upland areas — have selenium-deficient soils, making White Muscle Disease a genuine ongoing concern for horse owners who do not actively supplement or monitor selenium status. In South Africa, selenium deficiency is also regionally significant, particularly in certain highland areas.

Causes of White Muscle Disease in Horses

The primary cause is inadequate dietary selenium and/or vitamin E. These two nutrients work together as antioxidants to protect muscle cell membranes from oxidative damage. Without sufficient levels, the byproducts of normal cellular energy metabolism accumulate and destroy muscle fibres.

Key risk factors include:

  • Selenium-deficient pastures: Grass and forage grown on selenium-deficient soils contains insufficient selenium. Horses grazing these pastures long-term are at high risk without supplementation.
  • Vitamin E deficiency: Vitamin E is naturally present in fresh green grass but diminishes significantly in dried hay and processed feeds. Horses with limited access to fresh pasture may be vitamin E deficient even if selenium levels are adequate.
  • Pregnant and lactating mares: Requirements for selenium and vitamin E are increased during gestation and lactation. Deficient mares produce foals with depleted stores who are immediately at risk of WMD at birth.
  • High cereal/low forage diets: Diets low in quality roughage and reliant on cereals may be inadequate in vitamin E.
  • Older or stored hay: Vitamin E content of hay degrades with storage — hay that is more than 6 months old may contain very little effective vitamin E regardless of initial quality.

Symptoms and Signs

Clinical signs vary depending on the age of the horse and which muscles are most affected:

In foals (most severe presentation):

  • Inability to stand or rise — weakness of the large skeletal muscles of the hindquarters and back
  • Stiffness and pain when attempting to move
  • Trembling muscles
  • Difficulty nursing — weakness of the muscles involved in suckling
  • Dysphagia (difficulty swallowing) if the pharyngeal muscles are affected
  • Respiratory distress if the diaphragm or intercostal muscles are involved
  • Sudden death in neonates if cardiac muscle is severely affected — affected foals may be found dead with no prior signs

In adult horses:

  • Muscle stiffness and reluctance to move
  • Hindquarter weakness or ataxia
  • Difficulty swallowing in cases affecting the oesophageal muscles
  • Sweating and apparent distress
  • Firm, swollen muscles on palpation
  • Dark (red-brown) urine (myoglobinuria) from muscle breakdown products passing through the kidneys
  • Elevated heart rate

Diagnosis

Diagnosis is based on a combination of clinical signs, history, laboratory testing, and response to treatment:

  • Blood selenium levels: Whole blood selenium or glutathione peroxidase (GPx) activity is the most useful measure of selenium status. Low GPx activity confirms selenium deficiency.
  • Serum vitamin E: Measured as alpha-tocopherol concentration in serum.
  • Muscle enzyme testing: CK (creatine kinase) and AST (aspartate aminotransferase) will be markedly elevated in active disease — sometimes to levels hundreds of times normal.
  • Urinalysis: Myoglobin in the urine produces a distinctive brown-red discolouration and is a strong indicator of significant muscle breakdown.
  • Cardiac assessment: Electrocardiography (ECG) and echocardiography may be warranted in foals where cardiac involvement is suspected.
  • Post-mortem: The characteristic pale, white streaking or chalky appearance of skeletal and cardiac muscle is pathognomonic of WMD on gross pathology.

Treatment

Treatment must be prompt, particularly in foals:

  1. Selenium supplementation: Injectable selenium (sodium selenite or selenium/vitamin E combination products) is the primary treatment. The dose is calculated carefully by weight — selenium toxicity is possible if overdosed, so administration should always be by a vet.
  2. Vitamin E supplementation: High-dose oral vitamin E (natural d-alpha-tocopherol is preferred for bioavailability) is administered alongside selenium treatment.
  3. Supportive care: Severely affected foals may need assisted nursing, IV fluids to protect the kidneys from myoglobinuria damage, and careful management to prevent pressure sores from recumbency.
  4. Rest: Exercise must be strictly restricted during recovery — exertion worsens muscle damage when enzyme levels are elevated. The horse should be kept quiet and comfortable.
  5. Anti-inflammatory medication: NSAIDs (such as phenylbutazone or flunixin) may be used to manage pain and inflammation.
  6. Nutritional review: The entire herd’s nutritional programme should be reviewed following a case of WMD — other horses in the same environment are likely deficient too.

Prevention

Prevention is highly effective and straightforward:

  • Test before you supplement: Have selenium and vitamin E blood levels checked in your herd, particularly broodmares and youngstock. Supplementation without knowing baseline levels risks toxicity.
  • Supplement pregnant mares: Mares in late pregnancy should receive selenium and vitamin E supplementation if blood levels are low, to ensure foals are born with adequate stores.
  • Use balanced compound feeds: Many quality compound feeds include selenium at appropriate levels for the forage base in a given region. Check with your feed supplier.
  • Provide good quality fresh forage: Access to fresh green grass or good quality, relatively recently harvested hay supports vitamin E intake.
  • Slow-release selenium boluses: In high-risk environments, vets may recommend selenium boluses given to mares before foaling for reliable, sustained release.
  • Soil supplementation: Some properties top-dress pasture with selenium fertilisers to increase grass selenium content — this approach requires consultation with an agronomist and vet.

Prognosis

Prognosis depends heavily on severity and speed of treatment. Mildly affected horses and foals that receive prompt selenium and vitamin E supplementation and appropriate rest often recover fully. Severely affected foals — particularly those unable to stand or with cardiac involvement — carry a guarded to poor prognosis. Foals born moribund (effectively dead at birth due to cardiac WMD) do not survive.

Adult horses with moderate disease generally recover well with treatment and management changes, though complete resolution may take several weeks.

When to Call the Vet

Call your vet urgently if:

  • A newborn foal is unable to stand or nurse
  • Any horse shows sudden muscle weakness, stiffness, or inability to move
  • You observe dark brown-red urine (myoglobinuria)
  • A horse in a known selenium-deficient area shows unexplained muscle problems
  • You are unsure whether your mares’ selenium and vitamin E levels are adequate before foaling season

Do not administer selenium injections without veterinary guidance — selenium toxicity from overdose is serious and can be fatal.

Frequently Asked Questions

Is White Muscle Disease the same as tying-up?

They share the common feature of muscle damage and elevated CK/AST, but are distinct conditions. White Muscle Disease is caused by a specific nutritional deficiency (selenium/vitamin E) and results in primary muscle fibre necrosis. Tying-up (exertional rhabdomyolysis) is typically triggered by exercise in horses with certain management, dietary, or genetic predispositions. The treatment approaches differ significantly — a horse with WMD should rest and receive selenium supplementation, while management of tying-up involves dietary and exercise modification.

Can White Muscle Disease be prevented with regular feeding?

In many cases, yes — a well-formulated diet that includes supplementary selenium and vitamin E appropriate to your region will prevent the disease. However, feeding alone may be insufficient if selenium levels in the forage base are very low and feeds are not specifically fortified. The most reliable prevention is to measure blood selenium and vitamin E levels, then supplement accordingly under veterinary guidance.

How long does recovery take?

Mild cases may show significant improvement within 1–2 weeks of supplementation and rest. More severe cases can take 4–8 weeks for muscle enzyme levels to return to normal. The horse should not return to full work until CK and AST levels have normalised, confirmed by repeat blood testing.

Can White Muscle Disease affect the heart?

Yes, and this is one of the most serious aspects of the disease in foals. Cardiac muscle (myocardium) relies on the same antioxidant protection as skeletal muscle. When selenium and vitamin E are severely deficient, cardiac fibre necrosis can occur, leading to heart failure and sudden death — sometimes the first sign an owner sees is a dead foal. Echocardiographic evaluation is warranted in any foal with suspected WMD to assess cardiac involvement.