Lecture 13- Disease of equine muscle 2

Definition: rhabdomyolysis

Disruption of skeletal muscle integrity → myalgia, weakness, myoglobinuria, ↑ muscle enzymes, risk of AKI

Definition: myopathy

General muscle disease; subtle signs; NOT associated with ↑ muscle enzymes

Non‑exertional myopathy/rhabdomyolysis

Occurs without exercise; includes infectious, immune‑mediated, nutritional, toxic, traumatic/anesthetic, genetic causes

Clostridial myositis etiology

Clostridium spp.; C. perfringens >> C. septicum, C. chauvoei, C. sporogenes; ubiquitous; requires inoculation + low oxygen → exotoxin production

Clostridial myositis clinical signs: local

Swollen/hot → cool/insensitive; skin sloughing; crepitus; malodorous serosanguinous fluid; “cooked” muscle appearance

Clostridial myositis clinical signs: systemic

Depression, fever, toxemia; tremors, ataxia, dyspnea; recumbency → coma → death

Clostridial myositis diagnosis

History + signs; CBC: hemoconcentration, stress leukogram, toxemia; CK/AST moderately ↑; U/S: fluid + hyperechoic gas; aspirates: rods; anaerobic culture

Clostridial myositis treatment priorities

Stabilize shock/toxemia; create unfavorable anaerobic conditions; high‑dose antimicrobials; supportive care

Clostridial myositis antimicrobials

K‑pen 44,000 U/kg q2–4h until stable; metronidazole 15 mg/kg q6–8h

Clostridial myositis surgical therapy

Debridement; fenestration

Clostridial myositis prognosis

Guarded to poor

MYHM inheritance

Autosomal codominant; 1 allele = disease; 2 alleles = severe; 80% homozygotes affected vs 20% heterozygotes

MYHM mutation

MyH1 gene mutation in type 2X fibers → immune attack on altered myosin chain

MYHM epidemiology

Quarter Horses + related breeds; prevalence 7–8% (higher in reining/cutting)

MYHM triggers

Often unknown; respiratory infection; vaccination; immune stimulation

MYHM phenotypes

Immune‑mediated myositis; non‑exertional rhabdomyolysis; calciphylaxis (systemic calcinosis)

IMM clinical signs

Rapid symmetrical atrophy; stiffness; depression; weakness; recumbency

IMM diagnosis

Genetic test; biopsy: lymphocytic infiltration; CK/AST variable ↑

IMM treatment

Corticosteroids (dex → pred taper)

IMM prognosis

Good for heterozygotes

Non‑exertional rhabdomyolysis (MYHM) signs

Severe pain; cramping; stiffness; swelling over back/hindquarters; myoglobinuria; rapid recumbency

Non‑exertional rhabdomyolysis diagnosis

Genetic test; biopsy: myonecrosis; CK/AST markedly ↑

Calciphylaxis signs

Muscle atrophy; firm painful plaques; organ failure; skin lesions

Calciphylaxis diagnosis

Genetic test; biopsy: mineral deposits; Ca×P > 65 mg/dL; CBC: neutrophilia

Calciphylaxis prognosis

Grave

MYHM treatment protocol

Dex 0.05 mg/kg ×3d → pred 1 mg/kg ×7–10d taper; monitor CBC; treat rhabdo; avoid respiratory vaccines; extend vaccine intervals

MYHM prognosis

Heterozygous: recovery 2–3 months; homozygous: severe atrophy + recurrence possible

Nutritional myodegeneration etiology

Selenium/Vit E deficiency in mares → foals affected; Se deficiency in acidic/volcanic soils; Vit E deficiency with no grass/poor hay/heated pellets

Nutritional myodegeneration signs: subacute

Weakness; dysphagia; aspiration pneumonia; stiffness; trembling; difficulty rising

Nutritional myodegeneration signs: acute

Rapid weakness; recumbency; death; tachycardia; arrhythmias; respiratory distress; pulmonary edema

Nutritional myodegeneration skeletal muscles

Gastrocnemius, semitendinosus/membranosus, biceps, lumbar, gluteal, neck, diaphragm, intercostal, tongue

Nutritional myodegeneration cardiac form

Acute myocardial decompensation

Nutritional myodegeneration clinical pathology

Moderate–marked ↑ muscle enzymes; low Se (<0.07 ppm) or Vit E (<2 ppm); ↑K, ↑P, ↓Na, ↓Cl, ↓Ca; dehydration; biopsy: myonecrosis

Nutritional myodegeneration treatment

Stall rest; injectable Se; oral water‑dispersible Vit E; manage complications; supplement Se/Vit E; high‑quality forage; monitor levels

Nutritional myodegeneration prognosis

Guarded

Hypoglycin A myopathy etiology

Box elder tree seeds containing hypoglycin A; fall/early spring; windy/rainy; wooded pasture >12h; young/new pasture horses

Hypoglycin A myopathy signs

Sudden onset; rapid progression; weakness; sweating; fasciculations; stiffness; tachycardia/pnea; myoglobinuria; collapse; death from cardiac/resp failure

Hypoglycin A myopathy diagnosis

Marked ↑ CK/AST; myoglobinuria; hyperglycemia; lactic acidemia; ↑ troponin I; PM: multiple acyl‑CoA dehydrogenase deficiency; lipid accumulation

Hypoglycin A myopathy prognosis

Hypoglycin A myopathy treatment

Aggressive fluids; DMSO; Vit E; Vit C; NSAIDs

Other toxic myopathies

Ionophores; chemical toxins; toxic plants

Traumatic/anesthetic myopathies

Post‑anesthetic myopathy; malignant hyperthermia; fibrotic myopathy

Most common cause of rapid topline atrophy in AQH/APH

MYHM immune‑mediated myositis → 40% muscle loss in 48h; epaxial/gluteal atrophy; weakness; recumbency; CK/AST ↑; CBC normal

Calciphylaxis Ca×P threshold

Ca (mg/dL) × P > 65 mg/dL → systemic calcinosis risk