Muscles Degenerative - Pathology

Degeneration

Degenerate muscle fibres (Image sourced from Bristol Biomed Image Archive with permission)

• Different types of degeneration
• May, or may not, be reversible
• Cloudy swelling, hydropic, vacuolar, granular and fatty change
• Occur following many different types of insult and are usually segmental
• If regeneration does not occur after formation of small vacuoles, necrosis follows
  • Vacuolation -> floccular degeneration -> granular degeneration -> hyaline and Zenker’s degeneration
• Vacuolar degeneration:
  • Due to swelling of organelles or due to glycogen or fat accumulation
  • May be caused by hypokalaemia, hyperkalaemia or necrosis
• Histologically:
  • Swollen
  • Hypereosinophilic
  • Lost cross striations

Exertional myopathies

• Caused by intensive and exhaustive activity of major muscle masses
• Glycogen used up -> local heat and lactic acid -> muscle degeneration
• Other forms include capture myopathy, racing greyhounds, sheep chased by dogs

Equine rhabdomyolysis

• Azoturia (Monday morning disease)
  • Acute
  • Due to exercise following a prolonged period of rest
  • Clincal signs:
    • Unable to move
    • Sweating
    • Tremors
    • Swollen and hard lumbar, gluteal and femoral muscles
  • Myoglobin leaks from muscle cells -> leaks into urine -> urine is dark red/brown (myoglobinuria) -> damages renal tubules
  • Grossly:
    • Salmon pink muscles -> dark, moist, swollen +/- pale streaks
  • Histologically:
    • Segmental myofibre necrosis
      • Multifocal and monophasic, but may be multiphasic if repeated bouts
    • Both, type IIA and IIB fibres affected; type IIB preferentially affected in acute disease
    • Minor inflammatory reaction and calcification

• Tying-up
  • Similar to azoturia but much milder
  • Grossly - normal muscle
  • Histologically - same as azoturia

Neuromuscular junction diseases

Aquired myasthenia gravis

• See congenital MG

Botulism

• Caused by:
  • Ingestion of Clostridium botulinum toxin which inhibits acetyl choline release
• Diagnosis by demonstration of toxin in faeces, ingested material or serum

Circulatory disturbances

Congestion

• Localised or generalised stasis -> dark red muscle
• E.g. in ruminal tympany (bloat) - congestion of muscles cranial to thoracic inlet
• May resemble haemorhage grossly

Ischaemia

• Firstly segmental necrosis
• -> death of satellite cells
  • Causes regeneration but myoblast precursors have to be recruited from viable fibres
• -> death of all cells
• Mostly healed by fibrosis and scar formation
• May attempt regeneration by budding

Main causes:

• Vascular occlusion
  • Infarction from embolism is rare due to collateral circulation
  • Extension of infarcts depends on size of vessels occluded
    • Small capillaries -> segmental necrosis
    • Large arteries -> whole muscle areas, including sattelite cells, are killed
  • Healed by fibrosis
  • May be due to:
    • Blockage of iliac arteries by aortic-iliac thrombosis in horses
    • Blockage of aortic bifurcation in cats
    • Dirofilaria immitis arteritis in dogs
    • Vasculitis due to bluetongue virus in sheep
    • Equine purpura haemorrhagica
      • Non-contagious, sporadic
      • Grossly:
        • Subcutaneous oedema
        • Scattered haemorrhagic foci throughout skin and muscles
        • Vasculitis -> infarcts of muscles
      • May cause myoglobinuria if extensive
      • Possibly immune mediated
      • In horses post streptococal infection, especially strangles
• External pressure
  • During prolonged recumbency, e.g. anaesthesia, inability to rise, or due to too tightly fitting bandages or casts
  • Post anaesthesia myopathy especially in horses
    • Dorsal recumbancy -> gluteals and longissimus ischaemia
    • Lateral recumbancy -> triceps brachii, pectoralis, deltoideus and brachiocephalicus ischaemia
  • Caused by pressure on muscle > perfusion pressure of capillaries
  • Downer cows - vetral recumbency -> ischaemia of pectoral muscles and muscles of limbs tucked under the animal
  • Pregnant ewes with twins or triplets -> internal abdominal oblique muscle ischaemic necrosis -> potential rupture
• Muscle swelling where it cannot expand
  • E.g. supracoracoid muscle infarction in some breeds of turkeys after flapping their wings
    • Surrounded by inelastic fascial sheath and bone

Trauma

• Due to:
  • Direct transection of myofibres
  • Compression of myofibres
  • Secondary from haemorrhage (bruising)
    • May increase muscle pressure -> ischaemia -> necrosis
  • Partial rupture - e.g. of diaphragm in road traffic accident
  • Complete rupture - e.g. quadriceps of racing greyhounds
  • Myorrhexis (tearing) - e.g. slippery floor causing 'splits' in cattle -> adductor muscle tear
• Healing is by regeneration
• Fibrosis (scarring) will compromise function
• During fractures, fragments may cause further trauma if moved