Skeletal muscle necrosis in a pig

Skeletal muscle necrosis in a pig

Whats your diagnosis #5

History: An 18 week old female pig was found down and on her side and not able to get up.

Gross Findings:

The muscles of the right shoulder and neck including the subscapularis, infraspinatus, and the supraspinatus muscles had multifocal white streaks running parallel to the direction of the muscle fibers.  The bilateral epaxial musculature including the longissimus dorsi contained similar white streaking.


Skeletal muscle:  There are extensive areas of myofiber necrosis exhibiting sarcoplasmic fragmentation, hypercontraction of sarcomeres, hypereosinophilia, proliferation of satellite cells, and infiltration with large numbers of macrophages.  There is extensive mineralization of necrotic myofibers, and regeneration of myofibers characterized by centralizationand rowing of satellite cell nuclei.

At  low power there is marked fragmentation of skeletal muscle fibers and infiltration by large numbers of smaller dark cells

At higher power the smaller cells are proliferating satellite cells and infiltrations of macrophages

There is marked fragmentation of myofibers

Several myofibers are mineralized- granular basophilic material within the cytoplasm


Skeletal muscle (subscapularis, infraspinatus, supraspinatus, longissimus dorsi):  Myocyte degeneration, necrosis, mineralization, and regeneration, diffuse, severe, with histiocytic infiltration.


Causes for this lesion include vitamin E / Selenium deficiency, exertional rhabdomyolysis, Cassia spp (senna or coffee senna plant), coyotillo (Karwinskia spp), Gossypol toxicity (cotton seeds), and ionophore toxicity.

This pig was from a pig farm where diet is strictly controlled.  Under the circumstances ingestion of toxic plants is less likely.  The gross lesions are not typical for porcine stress syndrome and there has been no other cases of PSS from this herd, making this a less likely cause of the observed lesions.  Exertional rhabdomyolysis is similar in pathogenesis to PSS, but can occur without the mutation in the ryanodine receptor.  We don’t have a detailed history of this pig’s activities, so while we cannot exclude this differential we have no reason to think it more likely than any other cause of muscle necrosis.   Vitamin E/Se deficiency or ionophore toxicity is more likely under the circumstances.  In intensively managed herds improperly mixed rations are a far more likely to cause this lesion than any of the others on the differential list.  We were not able to test the feed or the tissues for Vit E/ Se or ionophore levels.

About Brian

Anatomic Pathologist, VetPath Services, Stone Ridge, NY- musculoskeletal, oral/dental, and sinonasal diseases
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