White Muscle Disease (Nutritional Myopathy / Vitamin E-Selenium Deficiency)

White Muscle Disease (WMD), also known as nutritional myopathy or vitamin E-selenium deficiency, is a non-infectious, degenerative myopathy affecting skeletal and cardiac muscle of young calves, typically between birth and three months of age. It is caused by a deficiency of selenium (Se) and/or vitamin E, leading to oxidative damage of muscle cell membranes due to inadequate antioxidant protection. The disease is characterized by bilateral symmetrical weakness, stiffness, and in severe cases, cardiac failure and sudden death. WMD is economically significant in both dairy and beef operations, causing mortality, reduced growth, and increased susceptibility to secondary infections. The condition is classified into a congenital form (present at birth) and a delayed form (developing after colostrum intake), with the latter being more common. The disease is particularly prevalent in calves born to dams fed selenium-deficient forages or raised in geographic regions with low soil selenium content. In the context of calf diseases, WMD is a critical differential for neonatal weakness, recumbency, and respiratory distress.

The primary etiology of White Muscle Disease is a deficiency of selenium and/or vitamin E in the diet of the calf or its dam. Selenium is an essential trace mineral that is a component of selenoproteins, including glutathione peroxidase (GPx), which protects cell membranes from oxidative damage. Vitamin E (alpha-tocopherol) is a lipid-soluble antioxidant that breaks the chain reaction of lipid peroxidation in cell membranes. A deficiency of either nutrient leads to oxidative stress, particularly in high-oxygen-demand tissues such as skeletal and cardiac muscle. Selenium deficiency is often due to low soil selenium levels, which result in low selenium content in forages and grains. Vitamin E deficiency can occur due to inadequate intake of green forages, poor-quality hay, or feeding of stored grains with reduced vitamin E content. Additionally, factors such as high dietary polyunsaturated fatty acids (PUFA) can increase the requirement for vitamin E, exacerbating the deficiency. In calves, the condition can be congenital if the dam is severely deficient during gestation, or it can develop postnatally if colostrum and milk are deficient in selenium and vitamin E. Other contributing factors include high nitrate levels in feed, which can interfere with selenium utilization, and certain management practices such as early weaning or feeding milk replacers without adequate supplementation.

White Muscle Disease is reported worldwide, with a higher prevalence in regions with selenium-deficient soils, such as parts of the Pacific Northwest, the Great Lakes region, and the northeastern United States, as well as in New Zealand, Australia, and Scandinavia. The disease affects both dairy and beef calves, with a higher incidence in rapidly growing calves, particularly those with high muscle mass, such as beef breeds like Angus and Hereford. The age of onset is typically between birth and 3 months, with a peak incidence at 2-3 months of age. Morbidity can be high in affected herds, with up to 30-40% of calves showing clinical signs, and mortality can reach 50% or more in untreated cases, especially when cardiac involvement occurs. Economic losses include death, reduced weight gain, treatment costs, and increased susceptibility to other diseases. The disease is more common in calves born in late winter and early spring, when dams are fed stored forages with lower selenium and vitamin E content. Herd-level risk factors include inadequate mineral supplementation, feeding of home-grown grains, and lack of pasture access. In dairy operations, calves fed milk replacers without added selenium and vitamin E are at higher risk. The disease is less common in calves that receive adequate colostrum, as colostrum is a rich source of vitamin E, but selenium transfer is less efficient.

The pathophysiology of White Muscle Disease centers on oxidative stress and subsequent muscle cell damage. Selenium is a critical component of glutathione peroxidase (GPx), an enzyme that reduces hydrogen peroxide and organic hydroperoxides to water and alcohols, using reduced glutathione as a cofactor. Vitamin E acts as a chain-breaking antioxidant, neutralizing lipid peroxyl radicals and preventing the propagation of lipid peroxidation in cell membranes. When selenium and/or vitamin E are deficient, the antioxidant defense system is overwhelmed, leading to accumulation of reactive oxygen species (ROS). These ROS attack polyunsaturated fatty acids in the phospholipid bilayer of muscle cell membranes, initiating lipid peroxidation. This process disrupts membrane integrity, leading to increased permeability, influx of calcium, and activation of proteases and phospholipases. The result is muscle fiber degeneration, necrosis, and subsequent inflammation. The lesions are typically bilateral and symmetrical, affecting the large skeletal muscle groups (e.g., gluteal, femoral, and shoulder muscles) and the myocardium. Histologically, there is hyaline degeneration, fragmentation, and calcification of muscle fibers, with infiltration of macrophages and neutrophils. In the heart, lesions can lead to myocardial necrosis, cardiac arrhythmias, and congestive heart failure. The clinical signs of weakness and stiffness are due to skeletal muscle damage, while respiratory distress and sudden death are often due to cardiac involvement. The disease can also affect the diaphragm and intercostal muscles, contributing to respiratory failure.

Several intrinsic and extrinsic factors predispose calves to White Muscle Disease. Intrinsic factors include age (young calves are more susceptible due to rapid growth and high metabolic demand), breed (beef breeds with high growth rates are more commonly affected), and genetic variations in selenium metabolism. Calves with a high growth rate have increased muscle mass and thus higher oxygen demand, making them more vulnerable to oxidative damage. Extrinsic factors include nutritional deficiencies in the dam's diet during gestation and lactation, particularly low selenium and vitamin E content in forages and grains. Soil selenium levels are a major determinant, with regions having low selenium soil producing selenium-deficient feeds. Management practices such as feeding stored forages for extended periods, which lose vitamin E activity, and using milk replacers without adequate supplementation increase the risk. Additionally, high dietary levels of polyunsaturated fatty acids (PUFA) from sources like soybean oil or fish oil can increase the requirement for vitamin E. Other factors include high nitrate levels in water or feed, which can interfere with selenium utilization, and the presence of mycotoxins that may increase oxidative stress. Calves born to dams with inadequate selenium status are at higher risk, as placental transfer of selenium is limited. Poor colostrum management, leading to failure of passive transfer, can also exacerbate the condition, as colostrum provides vitamin E and other antioxidants.

Clinical signs of White Muscle Disease vary depending on the severity and the muscles affected. In the congenital form, calves may be stillborn or weak at birth, with difficulty standing and nursing. In the delayed form, signs typically appear between 2 and 6 weeks of age. The most common presentation is progressive muscle weakness and stiffness, with calves showing a stilted gait, reluctance to move, and a tendency to lie down frequently. When forced to stand, they may have a hunched back and a base-wide stance. The muscles of the shoulders, thighs, and back are often firm and painful on palpation. In severe cases, calves become recumbent and unable to rise. Respiratory signs include tachypnea, dyspnea, and increased respiratory effort due to diaphragmatic and intercostal muscle weakness. Cardiac involvement can lead to tachycardia, arrhythmias, and signs of congestive heart failure, such as jugular distension, pulmonary edema, and subcutaneous edema. Sudden death can occur, especially during exertion or stress. Other signs include dysphagia, which can lead to aspiration pneumonia, and a weak suckle reflex. In some cases, calves may show signs of encephalopathy, such as depression and seizures, due to cerebral edema. The disease is often bilateral and symmetrical, and affected calves may have elevated body temperature due to muscle inflammation. On herd examination, multiple calves may be affected, and there may be a history of poor growth and ill-thrift.

Differential diagnoses for White Muscle Disease include: 1) Neonatal calf diarrhea (e.g., rotavirus, coronavirus, Cryptosporidium) – typically presents with diarrhea and dehydration, but can cause weakness and recumbency; however, muscle enzymes are normal. 2) Septicemia (e.g., Escherichia coli, Salmonella) – often associated with fever, depression, and diarrhea, and can cause weakness; blood cultures and CBC may show leukopenia or leukocytosis with a left shift. 3) Meningitis (e.g., bacterial) – presents with fever, depression, and neurological signs such as opisthotonos and seizures; cerebrospinal fluid analysis is diagnostic. 4) Botulism – causes flaccid paralysis, but affected calves are usually bright and alert, with normal muscle enzyme levels. 5) Trauma (e.g., calving injury, vertebral fracture) – history of dystocia or trauma, with localized pain and neurological deficits. 6) Congenital defects (e.g., arthrogryposis, cerebellar hypoplasia) – present at birth with specific anatomical abnormalities. 7) Polyarthritis (e.g., Mycoplasma bovis) – causes joint swelling and lameness, but muscle enzymes are normal. 8) Nutritional deficiencies other than selenium/vitamin E (e.g., copper, vitamin A) – can cause weakness and poor growth, but muscle enzymes are not elevated. 9) Ionophore toxicity (e.g., monensin) – can cause acute muscle degeneration and elevated CK, but history of exposure to ionophores is key. 10) White muscle disease can also be confused with other myopathies, such as congenital myotonia or muscular dystrophy, but these are rare. Definitive diagnosis is based on elevated serum creatine kinase (CK) and aspartate aminotransferase (AST), low selenium and vitamin E levels, and response to selenium/vitamin E therapy.

The diagnostic algorithm for White Muscle Disease begins with a thorough herd history, including diet, mineral supplementation, and geographic location. Physical examination should focus on gait, posture, muscle palpation, and cardiac auscultation. If WMD is suspected, the following steps are recommended: 1) Measure serum creatine kinase (CK) and aspartate aminotransferase (AST) levels; significant elevations (CK > 1000 U/L, AST > 200 U/L) indicate muscle damage. 2) Assess selenium status by measuring whole blood or serum selenium levels (normal: > 0.08 ppm in whole blood) and glutathione peroxidase (GPx) activity in red blood cells. 3) Measure serum vitamin E (alpha-tocopherol) levels (normal: > 3 µg/mL). 4) Perform a complete blood count (CBC) and serum biochemistry profile to rule out other causes of weakness and to assess organ function. 5) If cardiac involvement is suspected, perform an electrocardiogram (ECG) and echocardiography to evaluate myocardial function. 6) In cases of sudden death, a necropsy is essential to confirm the diagnosis, with histopathology showing characteristic muscle degeneration and calcification. 7) Response to treatment with selenium and vitamin E can also be used as a diagnostic test, with improvement within 24-48 hours. 8) In herd outbreaks, evaluate the selenium and vitamin E content of the feed and forages, and assess the mineral status of the dams. 9) Consider differential diagnoses and rule them out based on clinical signs and laboratory findings. 10) In cases with respiratory signs, thoracic radiography or ultrasonography may be helpful to assess for pulmonary edema or aspiration pneumonia.

Laboratory findings in White Muscle Disease include: 1) Serum creatine kinase (CK) is markedly elevated, often exceeding 1000 U/L, and can be in the tens of thousands in severe cases. CK is a muscle-specific enzyme, and its elevation indicates active muscle damage. 2) Aspartate aminotransferase (AST) is also elevated, but it is less specific as it can be elevated in liver disease. 3) Serum selenium levels are low, typically < 0.05 ppm in whole blood (normal: 0.08-0.25 ppm). 4) Whole blood glutathione peroxidase (GPx) activity is reduced, reflecting selenium deficiency. 5) Serum vitamin E (alpha-tocopherol) levels are low, usually < 2 µg/mL (normal: 3-5 µg/mL). 6) Blood gas analysis may show metabolic acidosis due to lactic acidosis from muscle exertion or respiratory acidosis if respiratory muscles are affected. 7) Serum calcium and phosphorus may be normal or slightly altered. 8) CBC may show a stress leukogram with neutrophilia and lymphopenia, but no specific changes. 9) In cases with cardiac involvement, troponin I levels may be elevated, indicating myocardial damage. 10) Urinalysis may show myoglobinuria, which can cause reddish-brown urine and can lead to renal damage. 11) In chronic cases, there may be evidence of muscle atrophy and fibrosis, with elevated AST and CK but to a lesser degree. 12) Liver enzyme levels (e.g., GGT, SDH) may be normal unless there is concurrent liver damage. 13) In herd investigations, analysis of feed, forages, and water for selenium and vitamin E content is recommended.

Imaging modalities are not commonly used for the diagnosis of White Muscle Disease, but they can be helpful in assessing cardiac involvement and ruling out other conditions. 1) Thoracic radiography may reveal cardiomegaly, pulmonary edema, or signs of aspiration pneumonia in cases with dysphagia. 2) Echocardiography can assess myocardial function, wall thickness, and chamber dimensions; in WMD, there may be reduced contractility and dilation of the ventricles. 3) Electrocardiography (ECG) can detect arrhythmias, such as ventricular premature contractions or atrial fibrillation, which may occur due to myocardial damage. 4) Ultrasonography of skeletal muscles may show areas of increased echogenicity due to fibrosis or calcification, but this is not specific. 5) In cases of sudden death, post-mortem imaging is not typically performed, but necropsy is essential. 6) In research settings, magnetic resonance imaging (MRI) can detect muscle edema and necrosis, but this is not practical in clinical practice. 7) For herd-level assessment, bone density measurements or muscle biopsy may be used, but these are not routine. 8) In calves with respiratory signs, thoracic ultrasonography can be used to assess for pleural effusion or lung consolidation, which may be secondary to aspiration pneumonia. 9) In cases with suspected concurrent musculoskeletal injury, radiography of the limbs may be indicated to rule out fractures. 10) Overall, imaging is of limited value in the diagnosis of WMD, and the diagnosis is primarily based on clinical signs, laboratory findings, and response to therapy.

Cytology and histopathology are important for confirming the diagnosis of White Muscle Disease, especially in cases of sudden death or when laboratory tests are inconclusive. 1) Muscle biopsy: A biopsy of an affected muscle (e.g., semimembranosus or gluteal muscle) can be obtained under local anesthesia. Histological examination typically shows hyaline degeneration, fragmentation, and necrosis of muscle fibers, with loss of striations. There is infiltration of macrophages and neutrophils, and in later stages, fibrosis and calcification. 2) Necropsy findings: Grossly, affected muscles appear pale, white, or chalky, hence the name 'white muscle disease'. The lesions are often bilateral and symmetrical, and the heart may show pale areas of necrosis, particularly in the myocardium. 3) Histopathology of the heart: Myocardial fibers show degeneration, necrosis, and calcification, with interstitial edema and inflammatory cell infiltration. 4) Electron microscopy: Can reveal disruption of the sarcolemma, mitochondrial swelling, and loss of myofilaments. 5) Cytology of muscle aspirates: May show degenerated muscle fibers and inflammatory cells, but this is less commonly performed. 6) In cases with myoglobinuria, urine cytology may show myoglobin casts. 7) Immunohistochemistry: Can be used to detect reduced glutathione peroxidase expression in muscle tissue. 8) Histochemical staining for calcium (e.g., von Kossa stain) can demonstrate calcification of necrotic fibers. 9) In chronic cases, there is evidence of muscle regeneration with central nuclei and satellite cell proliferation. 10) Histopathology is also useful to rule out other myopathies, such as ionophore toxicity, which may show similar lesions but with a different distribution. 11) In herd outbreaks, histopathology of affected calves can help confirm the diagnosis and guide treatment and prevention strategies.

The treatment of White Muscle Disease involves immediate correction of the selenium and vitamin E deficiency, supportive care, and management of complications. 1) Selenium and vitamin E supplementation: Administer a commercial preparation containing selenium and vitamin E, typically as an injectable solution. The recommended dose is 0.05-0.1 mg/kg of selenium and 5-10 IU/kg of vitamin E, given subcutaneously or intramuscularly. This can be repeated after 2-4 weeks if necessary. 2) In severe cases, intravenous administration of vitamin E may be considered, but selenium should not be given IV due to the risk of toxicity. 3) Supportive care: Provide a clean, dry, and comfortable environment. Calves that are recumbent should be turned frequently to prevent pressure sores and pneumonia. 4) Fluid therapy: If the calf is dehydrated or in shock, administer isotonic fluids (e.g., lactated Ringer's solution) at a rate of 20-40 mL/kg/hour. 5) Nutritional support: Ensure adequate intake of colostrum or milk. If the calf is unable to nurse, provide milk via an esophageal feeder. 6) Anti-inflammatory therapy: Non-steroidal anti-inflammatory drugs (NSAIDs) such as flunixin meglumine (1.1-2.2 mg/kg IV) or meloxicam (0.5 mg/kg SC) can be given to reduce muscle inflammation and pain. 7) Antibiotics: If there is evidence of secondary bacterial infection, such as aspiration pneumonia, administer broad-spectrum antibiotics (e.g., ceftiofur 2.2 mg/kg SC q24h for 3-5 days). 8) Cardiac support: If cardiac involvement is suspected, provide rest and minimize stress. In cases of congestive heart failure, diuretics such as furosemide (1-2 mg/kg IV or IM) may be used, but prognosis is poor. 9) Antioxidant therapy: In addition to selenium and vitamin E, other antioxidants such as vitamin C (20-40 mg/kg IV) may be beneficial. 10) In cases of myoglobinuria, maintain adequate hydration to prevent renal damage. 11) For herd outbreaks, treat all at-risk calves with selenium and vitamin E, and correct the diet of the dams. 12) Monitor response to treatment by assessing clinical improvement and serial CK levels, which should decrease within 24-48 hours if treatment is effective.

The prognosis for White Muscle Disease depends on the severity of the condition and the extent of cardiac involvement. Calves with mild to moderate skeletal muscle involvement have a good prognosis if treated early and appropriately. Clinical improvement is often seen within 24-48 hours of selenium and vitamin E administration, with full recovery over 1-2 weeks. However, calves with severe cardiac involvement have a guarded to poor prognosis, as myocardial damage can lead to heart failure and sudden death. The prognosis is also worse in calves that are recumbent for more than 48 hours, as they are at risk for secondary complications such as pneumonia, pressure sores, and muscle contracture. In cases of congenital WMD, the prognosis is poor, as the damage is often severe and irreversible. Long-term effects may include reduced growth rate and exercise intolerance. In herd outbreaks, the prognosis for the herd is good if the nutritional deficiency is corrected, but there may be ongoing losses until the diet is improved. Negative prognostic indicators include severe elevation of CK (> 10,000 U/L), elevated troponin I, arrhythmias, and lack of response to treatment within 48 hours. Calves that recover may have residual muscle weakness or fibrosis, but many can be raised successfully. The economic impact of WMD includes mortality, treatment costs, and reduced performance, but with prompt treatment and prevention, losses can be minimized.

Follow-up care for calves with White Muscle Disease includes: 1) Recheck serum CK and AST levels 3-5 days after initiation of treatment to monitor resolution of muscle damage. 2) Monitor clinical signs, including gait, appetite, and respiratory rate, daily until recovery. 3) Provide a high-quality diet with adequate selenium and vitamin E. For calves, this may involve supplementing milk or milk replacer with selenium and vitamin E. 4) In herd outbreaks, evaluate the selenium and vitamin E status of all calves and dams, and implement a herd-level supplementation program. 5) For dams, ensure that the diet contains adequate selenium (0.3 ppm in the total ration) and vitamin E (1000-2000 IU/day for dry cows). 6) In selenium-deficient areas, consider injecting selenium and vitamin E to cows prepartum (e.g., 3-4 weeks before calving) to improve colostrum and milk levels. 7) For calves, consider oral selenium and vitamin E supplementation in milk or milk replacer. 8) Monitor growth rates and weaning weights to assess long-term effects. 9) In cases with cardiac involvement, perform a follow-up echocardiogram after 4-6 weeks to assess myocardial function. 10) Review the herd's mineral program with a nutritionist to ensure adequate selenium and vitamin E intake. 11) In areas with known selenium deficiency, consider soil fertilization with selenium or use of selenium-fortified mineral mixes. 12) Document all cases and outcomes to track the effectiveness of prevention strategies. 13) Provide education to farm staff on the importance of selenium and vitamin E in calf health.

Clinical pearls: 1) White Muscle Disease should be suspected in any young calf with acute onset of stiffness, weakness, or recumbency, especially in selenium-deficient areas. 2) Serum CK is the most sensitive and specific marker for muscle damage; a CK > 1000 U/L is highly suggestive of WMD. 3) Response to selenium and vitamin E therapy is rapid, with improvement often seen within 24 hours. 4) Cardiac involvement is a poor prognostic indicator; auscultate for arrhythmias and consider ECG. 5) In herd outbreaks, treat all at-risk calves, not just clinically affected ones. 6) Prevention is key: ensure adequate selenium and vitamin E in the dam's diet, and consider injectable selenium/vitamin E prepartum. 7) Colostrum is a good source of vitamin E, so ensure adequate colostrum intake. 8) In cases of sudden death, perform a necropsy to confirm the diagnosis and guide herd management. 9) Selenium toxicity can occur if overdosed; follow label recommendations. 10) Vitamin E is more effective when given with selenium, as they work synergistically. Pitfalls: 1) Failing to consider WMD in calves with respiratory distress, as it can be mistaken for pneumonia. 2) Using only vitamin E without selenium, which may not be effective if selenium deficiency is the primary cause. 3) Administering selenium intravenously, which can cause acute toxicity and death. 4) Not providing supportive care, such as fluids and anti-inflammatories, which can improve outcomes. 5) Delaying treatment, as severe muscle damage may be irreversible. 6) Overlooking the herd-level problem and only treating individual calves, leading to ongoing losses. 7) Misinterpreting elevated AST as liver disease, when it is actually due to muscle damage. 8) Not monitoring CK levels to assess response to treatment. 9) Using outdated or incorrect dosages of selenium and vitamin E. 10) Failing to address the underlying nutritional deficiency in the herd, leading to recurrence.

Current drug protocols for White Muscle Disease are based on Plumb's Veterinary Drug Handbook and AABP guidelines. 1) Selenium and Vitamin E injection: Commercial products such as MU-SE (selenium 1 mg/mL and vitamin E 68 IU/mL) are commonly used. The recommended dose for calves is 1 mL per 40 kg body weight (0.025 mg/kg selenium) subcutaneously or intramuscularly. This can be repeated after 2-4 weeks if needed. 2) Vitamin E alone: In cases where selenium is adequate, vitamin E can be given at 5-10 IU/kg IM or SC. 3) Flunixin meglumine: 1.1-2.2 mg/kg IV, once daily for up to 3 days, for anti-inflammatory and analgesic effects. 4) Meloxicam: 0.5 mg/kg SC, single dose, as an alternative NSAID. 5) Dexamethasone: 0.05-0.1 mg/kg IV or IM, once, may be used in severe cases to reduce inflammation, but caution is advised due to immunosuppression. 6) Ceftiofur: 2.2 mg/kg SC, once daily for 3-5 days, if secondary bacterial infection is suspected. 7) Oxytetracycline: 10 mg/kg IM, once daily for 3 days, as an alternative antibiotic. 8) Fluid therapy: Isotonic crystalloids (e.g., lactated Ringer's solution) at 20-40 mL/kg IV, as needed for dehydration or shock. 9) Furosemide: 1-2 mg/kg IV or IM, once or twice daily, if congestive heart failure is present. 10) Vitamin C: 20-40 mg/kg IV, once daily, as an antioxidant adjunct. 11) Propylene glycol: 100-200 mL orally, once or twice daily, if the calf is also ketotic, but this is not specific to WMD. 12) Withdrawal times: For meat, the withdrawal time for selenium/vitamin E injections is typically 30 days, but follow label instructions. For NSAIDs, flunixin has a meat withdrawal of 4 days and milk withdrawal of 36 hours; meloxicam has a meat withdrawal of 15 days and milk withdrawal of 5 days. Antibiotics have varying withdrawal times; ceftiofur has a meat withdrawal of 3 days and no milk withdrawal for lactating cows, but for calves, it is 3 days. Always consult the label and a veterinarian for specific withdrawal times.

Evidence-based literature on White Muscle Disease is extensive, with key studies and reviews providing insights into its pathogenesis, diagnosis, and management. 1) A landmark study by Muth et al. (1958) first identified selenium as the essential nutrient in preventing WMD in calves. 2) Research by Oldfield et al. (1960) demonstrated the efficacy of selenium supplementation in preventing the disease. 3) A comprehensive review by Van Vleet and Ferrans (1992) detailed the pathological features of selenium-vitamin E deficiency in animals. 4) Studies by Koller et al. (1984) and others have established reference ranges for selenium and vitamin E in cattle. 5) Clinical trials have shown that injectable selenium/vitamin E given to cows prepartum significantly reduces the incidence of WMD in calves (e.g., Swecker et al., 1995). 6) A study by Enjalbert et al. (1999) evaluated the selenium status of dairy herds and its impact on calf health. 7) Research by Weiss et al. (1997) demonstrated the importance of vitamin E in colostrum and its transfer to calves. 8) A meta-analysis by Sordillo and Aitken (2009) reviewed the role of oxidative stress in bovine diseases, including WMD. 9) The AABP (American Association of Bovine Practitioners) has published guidelines on trace mineral supplementation in cattle, including selenium and vitamin E. 10) The National Research Council (NRC) provides dietary requirements for selenium and vitamin E in cattle, which are essential for prevention. 11) Recent studies have explored the use of organic selenium sources, which may have better bioavailability. 12) Overall, the evidence strongly supports the use of selenium and vitamin E supplementation for prevention and treatment of WMD, and emphasizes the importance of herd-level management to correct deficiencies.