JPC SYSTEMIC PATHOLOGY

MUSCULOSKELETAL SYSTEM

April 2025

M-T02

 

Signalment (ACVP/75-25): 2-year-old red Angus cow

HISTORY: This is one of 14 surviving cows from a small herd in Southeast Texas. Sixteen cows died suddenly or after being down for less than 24 hours. The cows had grazed a coastal Bermuda grass pasture that contained toxic weeds. The cow was alert and had a good appetite but would not rise from sternal recumbency.

HISTOPATHOLOGIC DESCRIPTION: Skeletal muscle: 80% of myocytes are characterized by one of the following: swollen up to 90 µm in diameter with pale, often vacuolated sarcoplasm, loss of cross striations, and disorganized myofibrils (degeneration); shrunken and angular with homogeneous, hypereosinophilic, hyalinized sarcoplasm, disorganized fragmented myofibrils, loss of cross striations, prominent contraction bands, and pyknotic nuclei (necrosis). Multifocal aggregates of hyperplastic and hypertrophied satellite cells and macrophages surround and occasionally are intrasarcoplasmic within degenerate and necrotic myocytes.

MORPHOLOGIC DIAGNOSIS: Skeletal muscle, myocytes: Degeneration and necrosis, acute, multifocal, moderate, red Angus cow, bovine.

ETIOLOGIC DIAGNOSIS: Phytotoxic myopathy

CAUSE: Senna sp. (formerly Cassia sp.)

GENERAL DISCUSSION:

• Muscular and myocardial necrosis in livestock caused by ingestion of beans of senna or coffee occidentalis (Senna occidentalis or obtrusifolia); commonly affected species include goats, cattle, horses, and pigs
  • Pigs have been affected with as little as 1% contamination of feed
  • Diaphragm is a commonly affected muscle
• occidentalis is an annual shrub found in the southeastern US, is the most common agent of degenerative myopathy in cattle
• obtusifolia (sicklepod senna, Java bean) also toxic
• Frost makes the plant more palatable; more toxicoses reported late in the year
• Entire plant is toxic, but the seed tegument is most toxic component

PATHOGENESIS:

• Toxic principle in the seed remains unidentified

TYPICAL CLINICAL FINDINGS:

• Anorexia, diarrhea, hyperpnea, tachycardia
• Weakness, stumbling gait that rapidly progressing to ataxia, recumbency, and death
• Morbidity rate may reach 60%; recumbent animals do not recover
• Death attributed to myocardial degeneration and necrosis and heart failure
• Clinical pathology:
  • Myoglobinuria
  • Elevated: Creatine phosphokinase (CK), aspartate aminotransferase (AST), lactate dehydrogenase (LDH), alanine aminotransferase (ALT)
  • +/- hypocalcemia (horse)

TYPICAL GROSS FINDINGS:

• Skeletal muscle: Poorly defined multifocal areas of muscle pallor +/- edema; gross findings may be minimal in spite of histologic findings demonstrating degeneration
• Myocardium not as extensively involved as skeletal muscle
• Heart: Subendocardial to diffuse pale yellow mottling and streaking

TYPICAL LIGHT MICROSCOPIC FINDINGS:

• Skeletal muscle: Monophasic, multifocal, segmental myocyte degeneration and necrosis with intact sarcolemmal sheaths and muscle nuclei; affects type 1 and 2 myofibers; usually no mineralization
• Myocyte swelling
• Sarcoplasm fragmentation
• Proliferation of satellite cells
• Myocardium: Initial small, indistinct vacuoles within myofibrils; contraction bands; progression to degeneration and necrosis
• Liver: Centrilobular fatty degeneration, vacuolation, and necrosis (secondary to heart failure and skeletal muscle injury)

ULTRASTRUCTURAL FINDINGS:

• Mitochondrial swelling and disrupted or excessively branched mitochondrial cristae +/- electron-dense spherical inclusions within affected mitochondria

DIFFERENTIAL DIAGNOSIS: Other toxic myopathies and cardiomyopathies:

Causes of toxic myopathies +/- cardiomyopathies:

• Coyotillo (Karwinskia humboldtiana)
• Gossypol (cottonseed) (pigs especially affected)
• Lupine (Diaporthe toxica) (sheep)
• Water hemlock (Cicuta douglasii) (sheep)
• False lupine (Thermopsis montana) (calves, horses)
• White snakeroot (Ageratina [formerly Eupatorium] rugosum) (horses, ruminants)
• Rayless gold­enrod (Isocoma pluriflora) (horses, ruminants)
• Vitamin E / selenium deficiency (M-M11)
• Selenium toxicosis (pigs, cattle, sheep, others)
• Ionophore toxicosis (monensin, maduramicin, others; horses particularly susceptible) (M-T01)
• Box elder (Acer negundo) or Sycamore seed (Acer pseudoplanatus) (horses), known as atypical myoglobinuria
• Honey mesquite (Prosopis glandulosa)(sheep and goats), affects muscles of mastication

Causes of toxic cardiomyopathies:

• Summer pheasant’s eye (Adonis aestivalis) (cardiac glycoside; endocardial hemorrhage)
• Oleander (Nerium oleander) (cardiac glycoside; southern and southwest US; most species susceptible)

Causes of toxic metastatic mineralization:

• Vitamin D containing plants (Cestrum diurnum, Trisetum flavescens, Solanum glaucophyllum [formerly malacoxylon]) (M-T01; metastatic mineralization)

COMPARATIVE PATHOLOGY:

• Senna toxicosis reported in numerous species
• Pigs had no gross lesions, but microscopic degeneration in the heart and diaphragm with vacuolation and segmental hypercontraction of fibers
• Senna sp (Cassia sp) have caused skeletal muscle lesions in birds including poultry, ostriches, quail, and other African wild birds
• Gross changes may not be noted, histological lesions (loss of striations, macrophage infiltration, mineralization) are minimal; peripheral neurophathy common

REFERENCES:

1. Abdul-Aziz T, Fletcher OJ. Chapter 5: Cardiovascular System. In: Abdul-Aziz T, Fletcher OJ, Barns HJ, eds. Avian Histopathology. 4th ed. Madison, WI: Omnipress; 2016: 145.
2. Barnes HJ, Abdul-Aziz T, Fletcher OJ. Chapter 4: Muscular System. In: Abdul-Aziz T, Fletcher OJ, Barns HJ, eds. Avian Histopathology. 4th ed. Madison, WI: Omnipress; 2016: 109.
3. Cooper BJ, Valentine BA. Muscle and Tendon. In: Maxie MG, ed. Jubb, Kennedy, and Palmer’s Pathology of Domestic Animals. Vol 1. 6th ed. St Louis, MO: Elsevier; 2016: 219-220.
4. Cullen JM, Stalker MJ. Liver and Biliary System. In: Maxie MG, ed. Jubb, Kennedy & Palmer's Pathology of Domestic Animals. Vol 2. 6th ed. St. Louis, MO: Elsevier; 2016:341.
5. Duncan M. Perissodactyls. In: Terio KA, McAloose D, St. Leger J, eds. Pathology of Wildlife and Zoo Animals. London, UK: Academic Press; 2018:438.
6. Robinson WF, Robinson NA. Cardiovascular System. In: Maxie MG, ed. Jubb, Kennedy & Palmer's Pathology of Domestic Animals. Vol 3. 6th ed. St. Louis, MO: Elsevier; 2016:36.
7. Schmidt RE, Struthers JD, Phalen DN. Pathology of Pet and Aviary Birds. 3rd ed. Hoboken, NJ: John Wiley & Sons, Inc.; 2024: 202.
8. Stockham SL, Scott MA. Fundamentals of Veterinary Clinical Pathology. 2nd ed. Hoboken, NJ: Wiley; 2013.: 610.
9. Stacy NI, Hollinger C. Introduction to Comparative Clinical Pathology. In: Terio KA, McAloose D, St. Leger J, eds. Pathology of Wildlife and Zoo Animals. London, UK: Academic Press; 2018:85.
10. Swayne DE, Barnes HJ, Abdul-Aziz T, Fletcher OJ. Chapter 10: Nervous System. In: Abdul-Aziz T, Fletcher OJ, Barns HJ, eds. Avian Histopathology. 4th ed. Madison, WI: Omnipress; 2016: 471.
11. Valentine BA, Skeletal Muscle. In: Zachary JF, ed. Pathologic Basis of Veterinary Disease. 7th ed. St. Louis, MO: Elsevier; 2022:1009, 1019, 1025-1029.

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