JPC SYSTEMIC PATHOLOGY
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: Approximately 50% of myocytes are swollen up to 100 um in diameter with pale, often vacuolated sarcoplasm, indistinct cross-striations and disrupted myofibrils (degeneration), or shrunken and angulated profiles with homogeneous hypereosinophilic hyalinzed sarcoplasm, disorganized fragmented myofibrils, loss of cross-striations, prominent contraction bands and pyknotic nuclei (necrosis). Multifocal aggregates of hyperplastic and hypertrophied satellite cells surround affected myocytes, which occasionally contain intrasarcoplasmic macrophages and satellite cells. Rarely, myocytes have basophilic sarcoplasm with internalized, “rowed” vesiculate nuclei (regeneration). Surrounding affected myofibers are few scattered macrophages and rare neutrophils.
MORPHOLOGIC DIAGNOSIS: Skeletal muscle, myocytes: Degeneration and necrosis, acute, multifocal, moderate, with rare regeneration, red Angus cow, bovine.
ETIOLOGIC DIAGNOSIS: Phytotoxic myopathy
CAUSE: Senna sp. (formerly Cassia sp.)
- Ingestion of beans of senna or coffee occidentalis (Cassia occidentalis or obtrusifolia) by goats and cattle
- Annual shrub found in the southeastern US and is believed to be the most toxic of the Senna species
- obtusifolia (sicklepod senna, Java bean), S. roemeriana (twin leaf senna), S. fistula (senna of commerce, golden shower tree), S. lindheimeriana, and S. tora are 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
- Toxic principle is unknown
- Uncoupling of oxidative phosphorylation and depression of mitochondrial respiration within myocardial fibers > energy loss, cell swelling and degeneration of the sarcotubular system
TYPICAL CLINICAL FINDINGS:
- Anorexia, diarrhea, hyperpnea, tachycardia
- Weakness rapidly progressing to ataxia, recumbency, and death
- Death is attributed to myocardial degeneration and necrosis and heart failure
- Clinical pathology:
- Elevated creatine phosphokinase (CK), aspartate aminotransferase (AST), lactate dehydrogenase (LDH)
TYPICAL GROSS FINDINGS:
- Skeletal muscle: poorly define pallor of muscle mass; gross findings may be minimal in spite of findings demonstrating degeneration
- Heart: Subendocardial to diffuse pale yellow mottling and streaking, +/- subepicardial hemorrhages (especially near coronary arteries), +/- pericardial effusion
- Lungs: Diffuse congestion and interlobular edema
- Trachea and bronchi: May be filled with serous to frothy fluid
TYPICAL LIGHT MICROSCOPIC FINDINGS:
- Skeletal muscle: Monophasic, multifocal, segmental myocyte degeneration and necrosis with intact sarcolemmal sheaths and muscle nuclei; usually no mineralization
- Myocardium: Initial small, indistinct vacuoles within myofibrils; progression to degeneration and necrosis
- Lungs: Edema and marked congestion
- Liver: Centrilobular fatty degeneration and necrosis (secondary to heart failure)
- Kidney: Tubular degeneration with protein casts
- Mitochondrial swelling and disrupted or excessively branched mitochondrial cristae +/- electron-dense spherical inclusions within affected mitochondria
- Mitochondrial collapse, cellular swelling, glycogen loss
DIFFERENTIAL DIAGNOSIS: Other toxic myopathies and cardiomyopathies:
- Coyotillo (Karwinskia humboldtiana)
- Summer pheasant’s eye (Adonis aestivalis) (cardiac glycoside; endocardial hemorrhage)
- Vitamin D containing plants (Cestrum diurnum, Trisetum flavescens, Solanum malacoxylon) (mineralization is prominent)
- White snakeroot (Eupatorium rugosum)
- Oleander (Nerium oleander) (southern and southwest US; most species susceptible)
- Gossypol (cottonseed)
- Lupine (Diaporthe toxica) (sheep)
- Water hemlock (Cicuta douglasii) (sheep)
- False lupine (Thermopsis montana) (calves)
- Vitamin E / selenium deficiency
- Selenium toxicosis (pigs, cattle, sheep, others)
- Ionophore toxicosis (monensin, maduramicin, others)
- Toxicosis reported in cattle, sheep, goats, horses, pigs, poultry, and rabbits
- Pigs had no gross lesion, but microscopic degeneration in the heart and diaphragm with vacuolation and segmental hypercontraction of fibers
- Cooper BJ, Valentine BA. Muscle and Tendon. In: Maxie MG, ed. Jubb, Kennedy, and Palmer’s Pathology of Domestic Animals. Vol 3. 6th ed. St Louis, MO: Elsevier; 2016: 219-220.
- Haraguchi M, Calore EE, Dagli MLZ, et al. Muscle atrophy induced in broiler chicks by parts of Senna occidentalis Vet Res Comm. 1998;22:265-271.
- Jones TC, Hunt RD, King NW. Diseases due to extraneous poisons. In: Veterinary Pathology. 5th ed. Baltimore, MD: Williams and Wilkins; 1997:770-771.
- Rissi DR, L Barros CS. Pathology in Practice. J Am Vet Med Assoc. 2017;250(1):51-53.
- Sebastian MM. Role of pathology in diagnosis. In: Gupta RC, ed. Veterinary Toxicology: Basic and Clinical Principles. Ney York, NY: Elsevier; 2007:1120.
- Valentine BA, Skeletal Muscle. In: Zachary JF, ed. Pathologic Basis of Veterinary Disease. 6th ed. St. Louis, MO: Elsevier; 2017:925.