Difference between revisions of "Muscles Degenerative - Pathology"

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#redirect[[:Category:Muscles - Degenerative Pathology]]
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{{toplink
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|backcolour =CDE472
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|linkpage =Musculoskeletal System - Pathology
 +
|linktext =Musculoskeletal System
 +
|maplink = Musculoskeletal System (Content Map) - Pathology
 +
|pagetype =Pathology
 +
|sublink1=Muscles - Pathology
 +
|subtext1=MUSCLES
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}}
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<br>
 +
==Degeneration==
 +
[[Image:Degenerate muscle fibres.jpg|right|thumb|100px|<small><center>Degenerate muscle fibres (Image sourced from Bristol Biomed Image Archive with permission)</center></small>]]
 +
 
 +
*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, [[Muscles - degenerative#Necrosis|necrosis]] follows
 +
**Vacuolation -> floccular degeneration -> granular degeneration -> [[General Pathology - Degenerations and Infiltrations#Hyaline Degeneration|hyaline]] and [[Zenker degeneration|Zenker’s degeneration]]
 +
*[[General Pathology - Degenerations and Infiltrations#Vacuolar 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
 +
 
 +
 
 +
===Calcification===
 +
 
 +
*Due to:
 +
**Old age - myofibres
 +
**Following necrosis - [[General Pathology - Pigmentation and Calcification#Dystrophic|dystrophic calcification]]
 +
***May be visible grossly as white foci
 +
 
 +
 
 +
===Ossification===
 +
 
 +
*Metaplasia of muscle to bone
 +
*'''Localised'''
 +
**Only in single muscle or a single group of muscles
 +
**May be associated with trauma
 +
**Seen in horses and dogs
 +
**Histologically:
 +
***Central zone - proliferating undifferentiated cells and [[General Pathology - Chronic Inflammation#Fibroblasts|fibroblasts]]
 +
***Middle zone - [[Bones - normal#Normal structure|osteoblasts]] depositing osteoid and bone
 +
***Outer zone - [[Bones - normal#Bone organisation|trabecular bone]] remodelled by [[Bones - normal#Normal structure|osteoclasts]]
 +
*'''Progressive''' (fibrodysplasia ossificans progressiva)
 +
**In connective tissue associated with skeletal muscle
 +
**Secondary involvement of muscle tissue
 +
**In pigs and cats
 +
**Histologically:
 +
***Bundles of dense fibrous connective tissue
 +
***May contain accumulations of cartilage, bone or calcium
 +
**Hyperplastic connective tissue -> compression of adjacent skeletal muscle -> [[Muscles - degenerative#Atrophy|atrophy]]
 +
 
 +
 
 +
===Pigmentation===
 +
 
 +
*[[General Pathology - Pigmentation and Calcification#Lipofuscin|'''Lipofuscin''']]
 +
**Wear and tear pigment accumulating in secondary lisosomes -> converted into compact residual bodies
 +
**Due to old age, past or recent cachexia or starvation
 +
**Mostly stored in skeletal muscle of old high producing dairy cattle
 +
**Masseters and diaphragm mainly involved
 +
**No clinical importance
 +
**Histologically:
 +
***Rounded yellow to brown granules at both poles of nucleus of the skeletal myofiber
 +
*[[General Pathology - Pigmentation and Calcification#Melanin|'''Melanin''']]
 +
**As part of congenital melanosis of calves in fascial sheaths and epimysium
 +
**Grossly - black foci
 +
*'''Myoglobin'''
 +
**After extensive muscle necrosis - '''rhabdomyolysis'''
 +
**Leaks to adjacent tissue after sudden injury
 +
*May also be present after some types of intramuscular injections e.g. iron dextran or tetracycline
 +
 
 +
 
 +
==Necrosis==
 +
 
 +
*Necrosis of an entire myofibre is uncommon
 +
*Segmental necrosis is more typical
 +
*Muscle cell contents may leak into the blood if the cell membrane is damaged
 +
*Creatine kinase (CK) is an enzyme which leaks following injury
 +
**Used to measure the extent of muscle damage
 +
*Often is followed by [[Muscles - normal#Regeneration|regeneration]]
 +
*Histologically:
 +
**Hyaline hypercontracted fiber rounded at cross-section and increased diameter and eosin staining
 +
***May also be an artifact due to hypercontraction of normal fibres at fixation
 +
**Fragmenting portions of fibre -> floccular or granular
 +
**Normal portion of fibre may detach from necrotic part -> retraction caps
 +
**Infarction may cause '''discoid degeneration''' - necrotic fibres detach at '''Z lines'''
 +
**May [[Muscles - degenerative#Calcification|mineralise]]
 +
*[[Zenker degeneration|'''Zenker's degeneration''']] - secondary to systemic disease
 +
**Scattered small segments of necrosis and fast regeneration
 +
**Sacrolemmal tubes are intact
 +
 
 +
 
 +
==Atrophy==
 +
[[Image:Atrophic muscle fibres.jpg|right|thumb|100px|<small><center>Atrophic muscle fibres (Image sourced from Bristol Biomed Image Archive with permission)</center></small>]]
 +
 
 +
*Decreased myofibre or whole muscle diameter
 +
*Myofibrils removed by disintegration -> sacrolemma too large -> forms folds
 +
*Caused by:
 +
**<u>'''Disuse'''</u> (e.g. fracture, failure to use limb, recumbency)
 +
***Slower than denervation atrophy
 +
***Reversible unless too prolonger or severe to cause loss of myofibres
 +
**<u>'''Denervation'''</u>
 +
***Any interference or damage to its nerve supply results in muscle atrophy
 +
****Can be rapid - over 50% of muscle mass may be lost in a few weeks e.g. roarer horses with [[Larynx Degenerative - Pathology#Laryngeal hemiplegia|laryngeal hemiplegia]]
 +
***May be reversible if innervation re-established
 +
***Histologically:
 +
****Fibres become rounded in cross section unless compressed by normal fibres
 +
****Increased concentration of nuclei as they take much longer to disintegrate
 +
****Fibrous stroma of epimysium and endomysium condenses -> more prominent
 +
****End result in muscle consisting of almost only fibrous tissue
 +
***Sometimes replaced by fat tissue -> increased size of muscle = ''pseudohypertrophy''
 +
***Muscle may have a mixture of atrophied and [[Muscles - hyperplastic and neoplastic#Hypertrophy|hypertrophied]] (due to increased work load) fibres if some motor units are not damaged
 +
**<u>'''Metabolisation of muscle protein'''</u> for nutrients during:
 +
***Malnutrition, cachexia, senility
 +
***Gradual onset except for some febrile diseases causing cachexia
 +
***Postural muscles are not affected, sometimes even [[Muscles - hyperplastic and neoplastic#Hypertrophy|hypertrophy]]
 +
***Histologically:
 +
****Some nuclei disappear as myofibre volume is decreased
 +
***Grossly:
 +
****Smaller, darker, thinner muscles
 +
 
 +
 
 +
==Toxic myopathy==
 +
 
 +
*'''Plants'''
 +
**E.g. ''Cassia occidentalis'' (coffee senna), ''Karwinskia humboldtiana'' (coyotillo), ''Eupatorium rugosum'' (white snakeroot), cotton seed
 +
**Lesion an skeletal and cardiac muscle
 +
**Grossly:
 +
***Pale areas with ill-defined borders
 +
***May involve very extensive [[Muscles - degenerative#Necrosis|necrosis]]
 +
**Histologically:
 +
***Segmental necrosis, no calcification
 +
***[[Muscles - normal#Regeneration|Regeneration]] may occur in surviving animals
 +
*'''Drugs'''
 +
**E.g. corticosteroids, cholinesterase inhibitors, vincristine, dimethyl sulfoxide (DMSO)
 +
**'''Monensin''' is a coccidiostat toxic to horses, donkeys, zebras, cattle, sheep, dogs and birds
 +
***Causes muscle necrosis in heart and skeletal muscle
 +
***Grossly:
 +
****Pale streaks, mostly in hind limbs
 +
***Histologically:
 +
****[[Muscles - degenerative#Necrosis|Segmental necrosis]]
 +
****Possibly [[Muscles - normal#Regeneration|regeneration]] in surviving animals
 +
***Can cause rapid onset recumbency and potentially death
 +
***Usually due to mixing errors in feed
 +
**Also from intramuscular injections, e.g. oxytetracycline, lidocaine, chloramphenicol, produce local necrosis
 +
***As [[Muscles - normal|satellite cells]] are destroyes, repair is via fibrosis with some [[Muscles - normal#Regeneration|budding]]
 +
*'''Chemicals'''
 +
**Iron injections can cause local myonecrosis
 +
*'''Mycotoxins'''
 +
**Metabolites cause persistent tremors
 +
**Lesions in skeletal muscle only, possibly secondary to sustained contractions (similar to [[Muscles - degenerative#Exertional myopathies|exertional myopathy]])
 +
**Histologically:
 +
***Tiny foci of [[Muscles - degenerative#Necrosis|segmental necrosis]]
 +
 
 +
 
 +
==Endocrine myopathy==
 +
 
 +
*[[Adrenal Glands - Pathology#Adrenal Hyperfunction|Hyperadrenocorticism]]
 +
**Muscle weakness is a clinical sign
 +
**-> [[Muscles - degenerative#Atrophy|muscle atrophy]]
 +
***Type II myofibre atrophy is non-specific
 +
***Type IIB myofibre atrophy is preferential in hyperadrenocorticism
 +
*[[Thyroid Gland - Pathology#Hypothyroidism|Hypothyroidism]] can cause muscle atrophy
 +
 
 +
 
 +
==Nutritional myopathy==
 +
[[Image:White muscle disease.jpg|right|thumb|100px|<small><center>White muscle disease (Image sourced from Bristol Biomed Image Archive with permission)</center></small>]]
 +
[[Image:White muscle disease histo.jpg|right|thumb|100px|<small><center>White muscle disease (Image sourced from Bristol Biomed Image Archive with permission)</center></small>]]
 +
 
 +
= [[White muscle disease|'''White muscle disease''']]
 +
*Very important economic disease of sheep, cattle and pig
 +
*Caused by:
 +
**Deficiency of selenium, vitamin E or both
 +
**Exacerbated by rapid growth, unaccustomed exercise or other dietary factor
 +
*Pathogenesis:
 +
**Oxygen free radicals (OFR) can damage cell membranes
 +
**Vitamin E usually mops up OFRs
 +
**Selenium as part of glutathione peroxidase neutralises effects of OFRs
 +
**If Vit E or Se are deficient -> the balance shifts to membrane damage, calcium entry and mitochondrial damage -> cell swells and dies -> segmental muscle [[Muscles - degenerative#Necrosis|necrosis]]
 +
*Grossly:
 +
**Lesions are bilaterally symmetrical in hard working muscles (vary with species)
 +
**Early lesions are pale areas and streaks
 +
***Difficult to see especially in pale muscles
 +
**Later becoming calcified necrotic areas
 +
***More obvious
 +
**Pigs also have lesions in their [[Myocardial - Pathology#Hyaline degeneration|heart]] and [[Liver - general pathology#Hepatosis dietica|liver]]
 +
*Histologically:
 +
**[[Muscles - degenerative#Necrosis|Segmental necrosis]] +/- [[Muscles - degenerative#Calcification|calcification]] and [[Muscles - normal#Regeneration|regeneration]]
 +
**Multifocal and multiphasic lesions
 +
 
 +
==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 [[Muscles - degenerative#Necrosis|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
 +
 
 +
 
 +
===Porcine stress syndrome===
 +
 
 +
*='''Malignant hyperthermia'''
 +
*Pigs, dogs, humans
 +
*Possibly a cellular defect resulting in high intacellular calcium ion concentration
 +
**-> Activates myofibrillar ATPase -> rapid intracellular glycolysis -> increase in body heat -> denature protein -> cell death -> leakage of cellular content -> oedema
 +
*Grossly:
 +
**Muscles are pale, soft and exudative
 +
*Histologically:
 +
**Segmental hypercontraction
 +
**Monophasic, multifocal [[Muscles - degenerative#Necrosis|segmental necrosis]]
 +
*Inherited
 +
*Triggered by halothane anaesthesia, stress of handling, transportation or slaughter
 +
 
 +
 
 +
==Neuromuscular junction diseases==
 +
 
 +
===Aquired myasthenia gravis===
 +
 
 +
*See [[Muscles Developmental - Pathology#Myasthenia gravis (MG)|congenital MG]]
 +
 
 +
 
 +
===Botulism===
 +
 
 +
*Caused by:
 +
**Ingestion of [[Clostridium species|''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 ([[Forestomach - Nutritional Pathology#Bloat/ Tympany|bloat]]) - congestion of muscles cranial to thoracic inlet
 +
*May resemble haemorhage grossly
 +
 
 +
 
 +
===Ischaemia===
 +
 
 +
*Firstly [[Muscles - degenerative#Necrosis|segmental necrosis]]
 +
*-> death of satellite cells
 +
**Causes [[Muscles - normal#Regeneration|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 [[Muscles - normal#Regeneration|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 [[Muscles - degenerative#Necrosis|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|''Dirofilaria immitis'']] arteritis in dogs
 +
***Vasculitis due to [[Reoviridae#Bluetongue Virus|bluetongue virus]] in sheep
 +
***[[General Pathology - Haemorrhage#Purpura haemorrhagica|'''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 [[Streptococci|streptococal]] infection, especially [[Respiratory Bacterial Infections - Pathology#Strangles|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 -> [[Muscles - degenerative#Ischaemia|ischaemia]] -> [[Muscles - degenerative#Necrosis|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 [[Muscles - normal#Regeneration|regeneration]]
 +
*Fibrosis (scarring) will compromise function
 +
*During [[Bones Fractures - Pathology|fractures]], fragments may cause further trauma if moved

Revision as of 20:10, 18 August 2008

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()Map MUSCULOSKELETAL SYSTEM (Map)
MUSCLES



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
  • 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


Calcification


Ossification

  • Metaplasia of muscle to bone
  • Localised
    • Only in single muscle or a single group of muscles
    • May be associated with trauma
    • Seen in horses and dogs
    • Histologically:
  • Progressive (fibrodysplasia ossificans progressiva)
    • In connective tissue associated with skeletal muscle
    • Secondary involvement of muscle tissue
    • In pigs and cats
    • Histologically:
      • Bundles of dense fibrous connective tissue
      • May contain accumulations of cartilage, bone or calcium
    • Hyperplastic connective tissue -> compression of adjacent skeletal muscle -> atrophy


Pigmentation

  • Lipofuscin
    • Wear and tear pigment accumulating in secondary lisosomes -> converted into compact residual bodies
    • Due to old age, past or recent cachexia or starvation
    • Mostly stored in skeletal muscle of old high producing dairy cattle
    • Masseters and diaphragm mainly involved
    • No clinical importance
    • Histologically:
      • Rounded yellow to brown granules at both poles of nucleus of the skeletal myofiber
  • Melanin
    • As part of congenital melanosis of calves in fascial sheaths and epimysium
    • Grossly - black foci
  • Myoglobin
    • After extensive muscle necrosis - rhabdomyolysis
    • Leaks to adjacent tissue after sudden injury
  • May also be present after some types of intramuscular injections e.g. iron dextran or tetracycline


Necrosis

  • Necrosis of an entire myofibre is uncommon
  • Segmental necrosis is more typical
  • Muscle cell contents may leak into the blood if the cell membrane is damaged
  • Creatine kinase (CK) is an enzyme which leaks following injury
    • Used to measure the extent of muscle damage
  • Often is followed by regeneration
  • Histologically:
    • Hyaline hypercontracted fiber rounded at cross-section and increased diameter and eosin staining
      • May also be an artifact due to hypercontraction of normal fibres at fixation
    • Fragmenting portions of fibre -> floccular or granular
    • Normal portion of fibre may detach from necrotic part -> retraction caps
    • Infarction may cause discoid degeneration - necrotic fibres detach at Z lines
    • May mineralise
  • Zenker's degeneration - secondary to systemic disease
    • Scattered small segments of necrosis and fast regeneration
    • Sacrolemmal tubes are intact


Atrophy

Atrophic muscle fibres (Image sourced from Bristol Biomed Image Archive with permission)
  • Decreased myofibre or whole muscle diameter
  • Myofibrils removed by disintegration -> sacrolemma too large -> forms folds
  • Caused by:
    • Disuse (e.g. fracture, failure to use limb, recumbency)
      • Slower than denervation atrophy
      • Reversible unless too prolonger or severe to cause loss of myofibres
    • Denervation
      • Any interference or damage to its nerve supply results in muscle atrophy
        • Can be rapid - over 50% of muscle mass may be lost in a few weeks e.g. roarer horses with laryngeal hemiplegia
      • May be reversible if innervation re-established
      • Histologically:
        • Fibres become rounded in cross section unless compressed by normal fibres
        • Increased concentration of nuclei as they take much longer to disintegrate
        • Fibrous stroma of epimysium and endomysium condenses -> more prominent
        • End result in muscle consisting of almost only fibrous tissue
      • Sometimes replaced by fat tissue -> increased size of muscle = pseudohypertrophy
      • Muscle may have a mixture of atrophied and hypertrophied (due to increased work load) fibres if some motor units are not damaged
    • Metabolisation of muscle protein for nutrients during:
      • Malnutrition, cachexia, senility
      • Gradual onset except for some febrile diseases causing cachexia
      • Postural muscles are not affected, sometimes even hypertrophy
      • Histologically:
        • Some nuclei disappear as myofibre volume is decreased
      • Grossly:
        • Smaller, darker, thinner muscles


Toxic myopathy

  • Plants
    • E.g. Cassia occidentalis (coffee senna), Karwinskia humboldtiana (coyotillo), Eupatorium rugosum (white snakeroot), cotton seed
    • Lesion an skeletal and cardiac muscle
    • Grossly:
      • Pale areas with ill-defined borders
      • May involve very extensive necrosis
    • Histologically:
      • Segmental necrosis, no calcification
      • Regeneration may occur in surviving animals
  • Drugs
    • E.g. corticosteroids, cholinesterase inhibitors, vincristine, dimethyl sulfoxide (DMSO)
    • Monensin is a coccidiostat toxic to horses, donkeys, zebras, cattle, sheep, dogs and birds
      • Causes muscle necrosis in heart and skeletal muscle
      • Grossly:
        • Pale streaks, mostly in hind limbs
      • Histologically:
      • Can cause rapid onset recumbency and potentially death
      • Usually due to mixing errors in feed
    • Also from intramuscular injections, e.g. oxytetracycline, lidocaine, chloramphenicol, produce local necrosis
  • Chemicals
    • Iron injections can cause local myonecrosis
  • Mycotoxins
    • Metabolites cause persistent tremors
    • Lesions in skeletal muscle only, possibly secondary to sustained contractions (similar to exertional myopathy)
    • Histologically:


Endocrine myopathy


Nutritional myopathy

White muscle disease (Image sourced from Bristol Biomed Image Archive with permission)
White muscle disease (Image sourced from Bristol Biomed Image Archive with permission)

= White muscle disease

  • Very important economic disease of sheep, cattle and pig
  • Caused by:
    • Deficiency of selenium, vitamin E or both
    • Exacerbated by rapid growth, unaccustomed exercise or other dietary factor
  • Pathogenesis:
    • Oxygen free radicals (OFR) can damage cell membranes
    • Vitamin E usually mops up OFRs
    • Selenium as part of glutathione peroxidase neutralises effects of OFRs
    • If Vit E or Se are deficient -> the balance shifts to membrane damage, calcium entry and mitochondrial damage -> cell swells and dies -> segmental muscle necrosis
  • Grossly:
    • Lesions are bilaterally symmetrical in hard working muscles (vary with species)
    • Early lesions are pale areas and streaks
      • Difficult to see especially in pale muscles
    • Later becoming calcified necrotic areas
      • More obvious
    • Pigs also have lesions in their heart and liver
  • Histologically:

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


Porcine stress syndrome

  • =Malignant hyperthermia
  • Pigs, dogs, humans
  • Possibly a cellular defect resulting in high intacellular calcium ion concentration
    • -> Activates myofibrillar ATPase -> rapid intracellular glycolysis -> increase in body heat -> denature protein -> cell death -> leakage of cellular content -> oedema
  • Grossly:
    • Muscles are pale, soft and exudative
  • Histologically:
  • Inherited
  • Triggered by halothane anaesthesia, stress of handling, transportation or slaughter


Neuromuscular junction diseases

Aquired myasthenia gravis


Botulism

  • Caused by:
  • 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)
    • 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
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