2 Equine Muscle Disorders

Additional Muscle Diseases in Horses

• Various muscle diseases can affect horses, including infectious, heritable, toxic, and nutritional myopathies.

Immune-Mediated Myositis

• Strains of Streptococcus spp. are associated with immune-mediated myositis.
• Streptococcus equi subsp equi causes Strangles.
• Immune-mediated myositis can be triggered by natural exposure or vaccination.
• Obvious clinical disease might not always be apparent.
• Intranasal vaccination can be performed using a modified live S. equi vaccine.

Myosin Heavy Chain Myopathy (MYHM)

• Myosin Heavy Chain Myopathy (MYHM) affects Quarter Horses and related breeds.
• MYHM is associated with the MYHI gene.
• Can be caused by immune-mediated myositis, characterized by muscle atrophy post autoimmune events.
• Can be caused by Non-exertional rhabdomyolysis and tying up, not associated with exercise.
• Muscle atrophy may or may not be present.
• MYHM has an autosomal codominant inheritance pattern with variable penetrance.
• N indicates a normal gene.
• My refers to Myosin heavy chain myopathy.
• Diagnosed through testing in Quarter Horses and related breeds.

Strep-Associated Myositis

• M protein (S. equi) has an amino acid sequence similar to myosin, leading to lymphocyte recruitment into muscle.
• Immune-mediated myositis and vasculitis can occur.
• Leukocytoclastic inflammation or infarction can occur.
• IgG or IgA mediate this disease.
• Epaxial and gluteal Muscle atrophy can be observed.
• An SeM ELISA test may show a low result of 1:800.
• Cases have shown improvement after 8 weeks of prednisolone therapy.
• In cases of myositis and infarction, SeM ELISA titers can be very high (e.g., 1:12,600).
• Clinical signs to watch out for include severe petechiation and ulcerations.
• Myocardial and skeletal muscle infarction, as well as PTE (Lung in cross section) have been observed.
• Ventral edema may be present due to vasculitis.
• In a complete blood count, fibrinogen levels may be elevated, around 500 mg/dL.
• Serum chemistry analysis showed creatine phosphokinase at 29,336 mmol / L, and AST at 2290 Units/L.
• Treatments may include administering dexamethasone to reduce inflammation (0.1 mg/kg IV daily), and intravenous fluids to treat pigment.
• Potential for pigment-associated nephropathy when administering intravenous fluids, and LRS 2X maintenance with elevated CK.
• Potassium penicillin addresses primary S. equi infections (22,000 IU/KG IV QID).
• Gastroprotectants, like Omeprazole may be administered to treat poor appetite, steroid therapy.
• Response to therapy can be tracked by SeM titers; an example is SeM titer = 1:25,600 [highest possible value reported].
• Further values include, Day 2 CK = 19,425, Day 3 CK = 14,102, Day 4......CK = 59,464.
• Tachycardia (HR = 80 BPM), colicky, severe pain can be observed.
• Post mortem exams may reveal severe muscle infarction.
• Henoch-Schonlein may be observed.
• For Immune-mediated myositis: treatment consists of Corticosteroids: dexamethasone (HIGH DOSE) 0.2 mg/kg IV daily, Concurrent penicillin therapy, a Mild sedative and analgesic therapy such as Diazepam and butorphanol to manage anxiety and pain

Clostridial Myonecrosis

• This condition that is also known as malignant edema or gas gangrene.
• Bacteria involved include Clostridium perfringens, C. septicum, C. novyi, C. sordelli, and C. chauvoei.
• This is exacerbated by Obligate anaerobic environments, trauma, punctures, High pH, low oxidative potential.
• Spores may exist in muscle tissue, toxin production impairs cellular activity causing severe tissue necrosis.
• Diagnosis is achieved through: Clinical signs and history, non-clotting blood.
• Further diagnostics include: Malodorous fluid, Cytologic analysis via FNA, Anaerobic culture, Fluorescent antibody identification.
• Pain, swelling, and crepitation can be observed.
• Signs include: Poor appetite, Pyrexia, onset generally 48-72 hours after insult.
• This infection can be caused by various factors:
• Various Clostridial spp. infection, Vaccination
• Substances irritating given via intramuscular route
• Such as: Flunixin meglumine, vitamin injections, ivermectin (1980s)
• Spores can be present in muscle tissue; an anaerobic environment and tissue trauma support germination and proliferation.
• Clinical signs can develop rapidly, within 48 to 72 hours, leading to death if underestimated.
• Hematology may show: elevated WBC and neutrophilia, Hyperfibrinogenemia, elevated muscle enzymes, Azotemia, and dehydration.
• Management includes: Fenestration, aggressive fenestration, intravenous fluid therapy.
• Systemic antimicrobial therapy.
  • Penicillin at a high dose of 44,000 IU/kg
  • Metronidazole
  • Oxytetracycline
• Antiinflammatory therapy using corticosteroids is contraindicated.

Genetic Diseases

• Hyperkalemic Periodic Paralysis (HYPP), Atypical (seasonal) myopathy, and Nutritional myodegeneration are muscle diseases in horses.

Hyperkalemic Periodic Paralysis (HYPP)

• HYPP primarily affects Quarter Horses.
• The condition is traced back to descendants of a horse named Impressive.
• HYPP was first identified in horses in 1985.
• In humans it is called Adynamia episodica hereditaria, and Gamstorp’s disease.
• Clinical signs of HYPP include, Twitching, Muscle fasciculations, and Prolapse of the nictitating membrane.
• Manifestations of HYPP can be confused with other conditions, including, Colic, exertional rhabdomyolysis, laminitis, cardiac disease, seizures, tetanus, and esophageal obstruction.
• The onset of symptoms occurs at around 2 to 3 years of age.
• Males are affected more often than females.
• Episodes typically last 15 to 90 minutes.
• Stress is a common trigger.
• Pathogenesis
• Caused by Sodium ion channel mutation, Cytosine to guanine substitution
• Coding: leucine instead of phenylalanine
• Results in increased intercellular sodium.
• Loss of electrical gradient, Channels remain open or re-open frequently
• Low resting membrane potential resulting in K+ leakage from the cell
• Risk factors include Diet that are high in potassium, > 1.1 %, Alfalfa, Molasses, Electrolyte supplementation, Anesthesia, Sedation, and Stress
• Diagnosis
  • During an episode:
    • Serum potassium can be measured, levels of 5-12 mEq/L (affected horses) vs N = 2.5-4.0 (normal).
    • Normokalemic variant can be observed.
  • At baseline:
    • DNA testing can be performed.
    • KCl challenge is another diagnostic option, Enteral 88-160 mg/kg
    • EMG can be run.
• Clinical Management for mild/ moderate disease consists of:
  • Grain or corn syrup increases insulin secretion.
  • Acetazolamide 2.5-3.0 mg / kg PO tid
  • With proper management an episode is mostly avoided.
• For severe cases:
• Administer: Calcium gluconate (0.2-0.4 mL/kg) in 5% dextrose, 5% dextrose alone 6 mL/kg IV (500 kg = 3 L IV), Sodium bicarbonate 1-2 mEq / kg.
• Tracheostomy is necessary in severe cases.
• General control measures include:
  • Low potassium diet
  • Plain grass hay
  • Regular exercise or pasture
  • Acetazolamide 2.5 mg/kg PO bid
  • Hydrochlorthiazide 0.5-1.0 mg/kg PO bid

Acquired: Atypical Myopathy: Box Elder Trees

• Atypical Myopathy or Seasonal Pasture Myopathy (SPM), is usually highly fatal.
• Characterized by acute, severe myonecrosis.
• Primarily occurs in Midwest during fall months, with cool, wet weather.
• Sparse pasture and limited grain put horses at risk.
• Atypical myopathy is a seasonal pasture myopathy with outbreaks during the Fall.
• Related to the Box elder tree and hypoglycin A in maple trees.
• In Europe sycamore maple = A. pseudoplatanus causes deficiencies in multiple acetyl-CoA dehydrogenases (MAD)
• Non-exertional rhabdomyolsysis may result.
• Treatment
  • Consists of High volume crystalloid therapy using Balanced electrolyte solution/
  • Status of electrolytes should be monitored through Calcium supplementation.
• Supportive care such as NSAIDs and Vitamin E (antioxidant) may be administered.
• Prognosis should be guarded.

Nutritional Myodegeneration

• Also known as White Muscle Disease.
• It is caused by Vitamin E and / or selenium deficiency, commonly affecting foals between birth and 2 months.
• Can cause acute death, evidence of muscle pain or myocarditis, and elevation of CK / AST levels.
• Dysphagia occurs in less severely affected foals.
• Blood analysis often shows Elevated muscle enzymes with serum selenium and E levels below normal.

Summary of Muscle Diseases

• Myosin Heavy Chain Myopathy (MYHM): This genetic muscle disease is characterized by marked muscle atrophy in Quarter Horses and related breeds; it can be immune-mediated
• Clostridial myonecrosis: Results from the proliferation of Clostridium organisms in muscle tissue, often from resident spores or inoculation.
• HYPP: A heritable condition in Quarter Horses with significant economic impact on the breed due to an autosomal dominant inheritance.
• Box elder ingestion: Results in a toxic myositis known as atypical myopathy, which can be life-threatening.
• Nutritional myodegeneration: A serious condition of foals in geographic regions of selenium deficiency.