General structure, congenital defects& degenerative diseases

• Skeletal muscle

  • Elongated myofiber cells 1-40 mm long by 10-100μ in diameter
• Normal skeletal muscle

  • Well defined striations provided by the A (anisotropic) and I (isotropic) bands
  • Fibers surrounded by a well delineated, thin connective tissue known as endomysium
  • Nuclei located at the periphery of the fiber
  • Groups of muscles bundles grouped together by slightly thicker connective tissue known as epimysium
  • Highly vascularized and contains numerous capillaries
• Sarcomere


  Functional/structural unit of skeletal muscle, extends from "Z" to "Z" line
• Motor end plate


  Interface between a muscle fiber and the axon
• Types of muscle fibers

  • Type I (Red, oxidative phosphorylation, aerobic, oxygen, rich in mitochondria and myoglobin, slow twitch but fatigue resistant)
  • Type II (White, anaerobic glycolysis, less mitochondria and myoglobin, rapid twitch but prone to fatigue)
• Fixation artifacts

  • Hypercontracted fibers resulting from improper fixation, often mistaken for swelling and hypereosinophilia
• Degenerated muscle

  Appears pale or darker on postmortem examination, due to alterations of myofibers (degeneration or necrosis), hemorrhage and myoglobin stain
• Care should be taken not to mistake myodegeneration with fat
• Expect pale muscle in anemic animals and veal calves
• Arthrogryposis


  Developmental abnormality caused by a problem in the central or peripheral nervous system, resulting in muscle hypoplasia and rigid flexion/extension of limbs
• Arthrogryposis


  • Common in aborted fetuses and stillborns
  • Frequently seen in dysraphism, spina bifida, syringomyelia, hydromyelia
  • In domestic animals, associated with ingestion of toxicants or congenital viral infections during gestation
  • Animals affected with Arthrogryposis generally lack a tail due to concurrent sacrococcygeal agenesis
• Muscle atrophy

  Reduction of muscle size resulting from loss of sarcomeres or decreased number of myofilaments, reversible if source of injury is removed
• Types of muscle atrophy

  • Denervation atrophy (lack of tonic stimuli)
  • Disuse atrophy (intact innervation but reduced movement)
  • Malnutrition atrophy (cachexia, senility, cancer, chronic inflammation)
• Denervation atrophy

  • Laryngeal hemiplegia in horses
  • Polyradiculoneuritis (Coonhound Paralysis) in dogs
• Disuse atrophy

  • Equine with chronic joint injury resulting in partial ankylosis
• Malnutrition atrophy

  • Dog with starvation due to owner negligence
  • Wild duck with chronic lead poisoning
• Muscle hypertrophy

  Increase in size but not number of muscle fibers, in response to increased work demand
• Muscle degeneration and necrosis

  Common sequel to myofiber injury, can be reversible or progress to irreversible necrosis
• Muscle degeneration and necrosis

  • White muscle disease in foal
  • Cow with muscle damage from being down for several days
• Histology of muscle degeneration

  • Cell swelling and hypereosinophilia, loss of striation, fragmentation and rupture of fibers, formation of retraction caps
• Ale muscles


  Found in veal calves
• Conditions affecting muscle

  • Anemia
  • Exsanguination
  • Fat (tongue)
  • White muscle
  • Disease
  • Normal
• Muscle Degeneration and Necrosis

  In contrast to previous slide, degenerated muscle appears darker than normal. A darker color occurs when degenerated muscle coexists with hemorrhage or with extensive release of myoglobin (rhabdomyolysis) into the interstitium.
• Histological changes in degenerating muscle fibers

  • Cell swelling and hypereosinophilia (asterisks), as well as loss of striation, fragmentation and rupture of fibers. Ruptured fibers typically produce the formation of so-called "retraction caps." These retraction caps appear as concavities at the free end of ruptured fibers (arrows).
  • Myofiber calcification is also a frequent finding particularly in some conditions such as white muscle disease
• Gross lesions of degeneration and calcification

  • Note generalized pale musculature and white streaks of degenerated muscle fibers (arrows) intertwined with normal muscle. The glistening appearance of degenerated muscle fibers is due to calcification.
• Microscopic lesions of degeneration and calcification


  • Note the segmental swelling and hypereosinophilia (asterisk) of the degenerated muscle fiber. Also note in the same fiber a segment undergoing dissolution of the sarcoplasm (#). In addition to degeneration, there is focal mineralization or calcification of affected fibers which appear dark purple (arrows).
• White Muscle Disease

  Degeneration and calcification are commonly seen in the muscle of calves and lambs with White Muscle Disease.
• Muscle repair

  • Skeletal muscle has the remarkable ability to repair providing that the sarcolemmal tube and myosatellite cells remain intact.
  • Macrophages clean cell debris within 12 hours of necrosis.
  • The sarcolemmal tubes (endomysium + basal lamina) serve as scaffolding for the myoblasts and as a barrier to prevent fibroblasts from getting into the sarcoplasm.
  • Myosatellite cells and myoblast undergo mitosis and prove the elements necessary for the formation of new sarcomeres at the edges of ruptured myofibers. Eventually the edges become bridged by newly formed sarcomeres.
• If sarcolemmal tubes are disrupted, regeneration can occur but is generally complicated with fibrosis (scars).
• Myopathies (Degenerative Diseases of Muscle)

  • Nutritional: White Muscle Disease
  • Metabolic: Porcine Stress Syndrome, Malignant Hyperthermia
  • Exertional: Azoturia, Captive Myopathy, Compartment Syndrome
  • Traumatic: Downer Cow, Crush Syndrome (HBC)
• White Muscle Disease (Nutritional Myopathy)


  White Muscle Disease (WMD) is a very common condition causing important economic losses in farm animals. It has variable morbidity and mortality affecting up to 50% of animals. WMD typically affects rapidly growing, young, well thrift sheep, cattle, pigs, and is less common in foals and goats. It is also seen in captive minks (WMD / steatitis).
• Causes of White Muscle Disease

  WMD is associated to Vitamin/Selenium deficiency but it is exacerbated by other factors such as exercise, environment (climatologic conditions may be involved), nutrition and some toxicants. The occurrence of WMD is unpredictable and the theory of a geographic predisposition has been recently challenged. WMD is occasionally found in neonates.
• White Muscle Disease in pigs

  WMD in pigs may be independent or coexist with other Vitamin E or Selenium deficiency syndromes (mulberry heart, hepatosis dietetica).
• Pathogenesis of White Muscle Disease

  The pathogenesis of WMD is related to the oxidation of cell membrane lipids (lipoperoxidation ) by free radicals due to lack of oxygen radical-scavengers such as tocopherol (Vitamin E) and selenium containing enzymes (glutathione peroxidase/reductase). Membrane peroxidation induces a positive influx of Ca++ into sarcoplasm and mitochondria. A considerable amount of energy is required to remove Ca++ out of the cell. Once cell energy is exhausted, myofibers degenerate and Ca++ accumulates up 50 times normal amounts. Intracellular enzymes such as CK leak out from the cell into serum; finally degenerated myofibers undergo necrosis.
• Muscles affected in White Muscle Disease

  Since muscle activity relates to the production of free radicals, muscles with higher physiological activity such as diaphragms, intercostal, tongue and heart are more severely affected (type I fibers).
• Gross pathology of White Muscle Disease

  • It is difficult to see in mild cases but in severe cases (fatal), affected muscles appear pale with calcifications. The heart is also affected appearing as a pale myocardium. Note pale discolored myocardium (arrows) in the left (L) ventricular wall. For still unknown reasons, WMD always affects the left side of the bovine heart while in sheep degeneration and calcification is typically seen in the right side.
• Confirming calcification in White Muscle Disease

  Von Kossa stain is often used to confirm calcification (insert top). Calcified fibers appear dark.
• White Muscle Disease in foals and pigs

  • WMD Foal: The pale muscle (W) was obtained from a foal few days old that died of WMD. Note the normal color of equine muscle (N).
  • WMD Pig: Pigs are also susceptible to develop WMD. WMD in pigs may be independent or coexist with other Vitamin E or Selenium deficiency syndromes such as mulberry heart and hepatosis dietetica. The musculature of this pig with WMD was slightly pale.
• Porcine Stress Syndrome (PSS) / Malignant Hyperthermia


  Porcine Stress Syndrome (PSS), also known as Porcine Malignant Hyperthermia and Pale Soft Exudative Pork is a hereditable, life-threatening, hypermetabolic syndrome. It is most common in Landrace, Pietran, Hampshire, and Yorkshire. Clinically, PPS is characterized by respiratory and metabolic acidosis, myoglobinemia, hyperkalemia, high blood lactate, hyperthermia, cardiovascular collapse and death. Stress such as fighting, exercise, heat can trigger PSS.
• Pathogenesis of Porcine Stress Syndrome

  The pathogenesis is related to an inherited defect in the intracellular uptake, storage and release of Ca ions. Excessive Ca++ in the cell (consumption of ATP) progresses to degeneration and necrosis of fibers. Denaturation of sarcoplasmic proteins leads to movement of intracellular water into the interstitium (see gross lesions).