section name header

Basics ⬇

Outline

BASICS

Definition!!navigator!!

Nutritional myodegeneration (nutritional muscular dystrophy, nutritional myopathy, dystrophic myodegeneration, WMD) is a noninflammatory degenerative disease of skeletal and cardiac muscle associated with dietary deficiency of Se and vitamin E.

Pathophysiology!!navigator!!

  • Se is an important component of GPx, an enzyme found in all animal tissue (high concentrations in liver and erythrocytes) that functions to reduce highly reactive oxygen metabolites that are produced during normal cellular metabolism. Deficiency of GPx increases membrane lipid peroxidation by these metabolites, resulting in membrane degradation and destruction of cells. Severe oxidative damage to myocytes and subsequent rhabdomyolysis underlie the pathogenesis of WMD in Se-deficient foals
  • While vitamin E deficiency may also play a role, deficiency of this nutrient alone is not sufficient to cause clinical disease in foals; vitamin E deficiency likely promotes disease in the setting of Se deficiency
  • Foals born to mares with dietary deficiency of Se are affected; however, not all Se-deficient foals display clinical signs of disease
  • Affected animals may present with acute fulminant disease with myocardial involvement or with subacute, insidious disease; in either case, mortality can be high and animals may not consistently respond to treatment. Comorbidity is common and may mask the underlying primary problem

Systems Affected!!navigator!!

  • Neuromuscular
  • Cardiovascular

Genetics!!navigator!!

There does not appear to be a genetic component.

Incidence/Prevalence!!navigator!!

Dependent on geographic region and diet.

Geographic Distribution!!navigator!!

The regional distribution of cases corresponds to areas where Se-deficient soils predominate. In the USA, the northwest, southeast, and Great Lakes areas tend to have Se-deficient soil. Soil and pasture analysis is recommended to determine whether Se supplementation is needed.

Signalment!!navigator!!

  • Young foals, with the majority of cases diagnosed within the first 60 days of life (most <30 days). Animals up to 1 year of age may be affected, and lesions have been noted in aborted fetuses
  • No breed or sex predisposition

Signs!!navigator!!

Acute Form

  • Sudden death
  • Circulatory collapse
  • Cyanosis
  • Tachycardia, arrhythmia, systolic cardiac murmur
  • Respiratory distress (pulmonary edema, respiratory muscle failure)
  • Inability to rise, often with violent struggling

Subacute Form

  • Profound muscular weakness—hallmark sign
  • Stiff, stilted gait
  • Muscle fasciculation/trembling
  • Inability to rise or stand unassisted
  • Dysphagia and/or poor suckle reflex (milk at nares, ptyalism)
  • Aspiration pneumonia
  • Weight loss or failure to gain due to inadequate dietary intake
  • Swollen, painful muscles—limbs, lumbar, cervical musculature

Causes!!navigator!!

  • Se deficiency

Risk Factors!!navigator!!

  • Geographic area with Se-deficient soil or low Se forage

Diagnosis ⬆ ⬇

Outline

DIAGNOSIS

Differential Diagnosis!!navigator!!

  • Dysphagia
    • Cleft palate
    • Pharyngitis/pharyngeal malformation
    • Botulism
    • Weakness, any cause (e.g. sepsis)
  • Neuromuscular weakness
    • Botulism
    • Tick paralysis
    • Neurologic/neuromuscular disease
  • Stiff gait
    • Tetanus
    • Septic (poly)arthritis
    • Bacterial meningitis
    • Trauma
  • Pneumonia
  • Congenital cardiac anomaly
  • Polysaccharide storage myopathy
  • Glycogen branching enzyme deficiency
  • Neonatal isoerythrolysis
  • Sepsis

CBC/Biochemistry/Urinalysis!!navigator!!

  • CBC—hematocrit normal or increased (helpful to differentiate from neonatal isoerythrolysis, which may also cause pigmenturia)
  • Biochemistry—hyponatremia, hypochloremia, hyperkalemia, hyperphosphatemia, azotemia (prerenal or postrenal), significant increases in CK, AST, and LDH; hypogammaglobulinemia
  • Urinalysis—pigmenturia (myoglobinuria)

Other Laboratory Tests!!navigator!!

  • Whole-blood Se concentration—documents recent Se deficiency; may be used to assess adequacy of supplementation; should be performed prior to supplementation
  • GPx concentration (erythrocyte)—documents Se deficiency in past weeks to months (Se is incorporated during erythropoiesis); should be interpreted according to reference ranges of laboratory performing analysis
  • Cardiac troponin I concentration—can be used to evaluate myocardial involvement

Imaging!!navigator!!

N/A

Other Diagnostic Procedures!!navigator!!

Muscle biopsy—may be helpful to diagnose myopathy in animals with normal whole-blood Se, GPx.

Pathologic Findings!!navigator!!

Pale streaking of major skeletal muscle groups and myocardium (especially left ventricle) seen at necropsy. Histologically, hyaline degeneration and myolysis are seen acutely; chronic cases may display fibrosis and calcification of lesions.

Treatment ⬆ ⬇

Outline

TREATMENT

Appropriate Health Care!!navigator!!

Inpatient medical treatment is needed for foals with moderate to severe neuromuscular weakness. Mildly affected foals may be treated and monitored on the farm.

Nursing Care!!navigator!!

Fluid therapy (avoid potassium-containing fluids in hyperkalemic foals) and plasma are often required.

Activity!!navigator!!

Affected foals should be strictly rested to avoid additional undue muscle damage.

Diet!!navigator!!

Important for prevention of Se deficiency (see Prevention/Avoidance). Feed should be analyzed to ensure appropriate levels of Se.

Client Education!!navigator!!

  • Feed should be analyzed, and additional feed or supplements used to correct/prevent Se deficiency
  • Prophylactic treatment of mares and foals in the same geographic area is recommended

Surgical Considerations!!navigator!!

N/A

Medications ⬆ ⬇

Outline

MEDICATIONS

Drug(s) of Choice!!navigator!!

  • Se—0.06 mg/kg deep IM divided into 2 sites (semimembranosus/semitendinosus recommended; do not use cervical, gluteal muscles); can be repeated 3 days and 8–10 days later. This corresponds to 1 mL of a vitamin E/Se combination product containing 2.5 mg Se/mL for a 45–50 kg foal
  • Vitamin E (oral)—500 IU vitamin E/mL; recommended dose is 1–2 IU/kg PO daily
  • NSAIDs—flunixin meglumine (1 mg/kg IV SID–BID) or ketoprofen (2.2 mg/kg IV SID–BID) may be used to reduce muscle pain and swelling; associated with gastric ulcers in neonates
  • Broad-spectrum antimicrobials—affected foals often have FTPI due to decreased colostral intake (recumbent/weak, dysphagia); concurrent aspiration pneumonia common (antimicrobial therapy best directed with results of bacterial culture of percutaneous transtracheal aspirate)

Contraindications!!navigator!!

Anaphylactoid reactions may occur with IV administration of commercial vitamin E/Se preparations; this is not recommended.

Precautions!!navigator!!

See Prevention/Avoidance.

Possible Interactions!!navigator!!

N/A

Alternative Drugs!!navigator!!

N/A

Follow-up ⬆ ⬇

Outline

FOLLOW-UP

Patient Monitoring!!navigator!!

  • Rapid decreases (24–48 h) in plasma CK concentration indicate cessation of muscle damage; AST and LDH decrease much more slowly (weeks)
  • Monitoring of whole-blood Se and GPx concentrations is recommended to gauge efficacy of supplementation

Prevention/Avoidance!!navigator!!

  • Prevention via monitoring of dietary and animal Se status and supplementation of pregnant mares is effective and recommended in Se-deficient areas or on farms where cases have been documented.
  • Since nutritional myodegeneration is associated with a high mortality rate (even with appropriate treatment), prevention of the disease is preferred
  • Farms in known Se-deficient areas should practice routine feed analysis; all dietary components (forage and grain) should contain at least 0.10 ppm Se, preferably 0.30 ppm
  • Pregnant mares should be supplemented with dietary Se at the rate of 1–3 mg Se/mare/day through provision of a trace mineral salt (15–30 ppm) or in the ration at 0.50 ppm. Supplementation of mares in this fashion has been shown to prevent myopathy in foals and is more effective than supplementation of foals at birth (as they may be born diseased). Alternatively, IM administration of commercial vitamin E/Se preparations may be used for prevention

Possible Complications!!navigator!!

  • Selenium toxicity may occur with overzealous supplementation; the toxic dose is 200 µg/kg in foals
  • Concurrent aspiration pneumonia and FTPI/septicemia are common
  • Fibrosis of severely affected muscle groups may result in permanent gait deficits in recovered animals

Expected Course and Prognosis!!navigator!!

  • Guarded prognosis
  • Acute form, >90% mortality; subacute form, 50–75%
  • Animals that do not respond to therapy within 2–5 days have a poor prognosis for recovery

Miscellaneous ⬆ ⬇

Outline

MISCELLANEOUS

Associated Conditions!!navigator!!

  • Septicemia
  • Aspiration pneumonia

Age-Related Factors!!navigator!!

N/A

Zoonotic Potential!!navigator!!

N/A

Pregnancy/Fertility/Breeding!!navigator!!

See Prevention/Avoidance.

Synonyms!!navigator!!

WMD

Abbreviations!!navigator!!

  • AST = aspartate aminotransferase
  • CK = creatine kinase
  • FTPI = failure of transfer of passive immunity
  • GPx = glutathione peroxidase
  • LDH = lactate dehydrogenase
  • NSAID = nonsteroidal anti-inflammatory drug
  • Se = selenium
  • WMD = white muscle disease

Suggested Reading ⬆ ⬇

Lofstedt J. White muscle disease of foals. Vet Clin North Am Equine Pract 1997;13(1):169–185.

Streeter RM, Divers TJ, Mittel L, et al. Selenium deficiency associations with gender, breed, serum vitamin E and creatine kinase, clinical signs and diagnoses in horses of different age groups: a retrospective examination 1996-2011. Equine Vet J Suppl 2012;43:31–35.

Author(s) ⬆

Author: Teresa A. Burns

Consulting Editor: Margaret C. Mudge