History

A 3-month-old Angus-cross heifer in a 500-head beef herd developed an illness of short duration, which included signs of depression, lethargy, ataxia, and progressive weakness. The calf died and underwent necropsy the same day. No other animals at the farm had similar clinical signs.

Clinical and Gross Findings

At necropsy, the heifer was in fair body condition with adequate subcutaneous and abdominal adipose tissue; hydration status was fair. Autolysis was minimal. On cut surfaces, the iliopsoas and adductor muscles of the hind limbs were mottled pink to pale tan with irregularly shaped, variably sized, dark pink areas. The ventricular myocardium was mottled with irregular, primarily subendocardial, light tan areas and few pale tan streaks (Figure 1). Pinpoint to 2-mm-diameter hemorrhages were scattered throughout the ventricular epicardium, mainly surrounding coronary vessels. The liver was diffusely mottled yellow-tan and friable. The gallbladder was distended by approximately 150 mL of viscous, dark green-black bile. The forestomachs contained green forage. In the abomasal mucosa, multiple pinpoint ulcers with hemorrhagic margins were evident.

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Photographs of a section of adductor skeletal muscle (A) and a portion of cardiac muscle (external and cut surfaces; B) obtained from a 3-month-old calf that developed signs of depression, lethargy, ataxia, and progressive weakness and subsequently died. Notice the irregular pale tan to pink mottling in the skeletal muscle tissue and irregular pale tan mottling of the interventricular septum and right ventricular free wall.

Citation: Journal of the American Veterinary Medical Association 235, 7; 10.2460/javma.235.7.827

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Formulate differential diagnoses from the history, clinical findings, and Figure 1—then turn the page →

Histopathologic Findings

Histologic examination of sections of skeletal muscle revealed marked myofiber degeneration and necrosis; these pathologic changes were evident throughout all sections of skeletal muscle examined. Severely affected myofibers were shrunken and hypereosinophilic and had fragmented to flocculent sarcoplasm with loss of striations. Other myofibers were swollen and hyalinized with pyknotic nuclei. A few swollen myofibers contained central, granular, basophilic stippling (dystrophic mineralization). There was loss of scattered myofibers with empty myotubes remaining. Some intact myofibers were hypercontracted, and some had centrally located nuclei. The endomysium and perimysium were expanded by edema and infiltrated by macrophages and fewer lymphocytes, plasma cells, and neutrophils. Macrophages infiltrated and replaced some necrotic myofibers (Figures 2 and 3). Scattered cardiac myofibers were shrunken and hypereosinophilic with pyknotic nuclei.

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Photomicrograph of a longitudinal section of skeletal muscle obtained from the calf in Figure 1. Notice the necrotic myofibers that have hypereosinophilic, flocculent sarcoplasm with loss of cross-striations and pyknotic nuclei. Fragmented myofibers are infiltrated by macrophages with fewer lymphocytes and neutrophils. H&E stain; bar = 100 μm.

Citation: Journal of the American Veterinary Medical Association 235, 7; 10.2460/javma.235.7.827

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Photomicrograph of a transverse section of skeletal muscle obtained from the calf in Figure 1. Among the necrotic myofibers, many are swollen and hyalinized with pyknotic nuclei, whereas others are shrunken and flocculent with variable infiltration by macrophages. H&E stain; bar = 100 μm.

Citation: Journal of the American Veterinary Medical Association 235, 7; 10.2460/javma.235.7.827

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Morphologic Diagnosis

Severe, multifocal to locally extensive, monophasic skeletal muscle necrosis and multifocal, monophasic myocardial necrosis.

Comments

Histologic lesions in multiple sections of skeletal and cardiac muscle from the calf of this report were consistent with monophasic, multifocal myonecrosis. On the basis of these lesions, nutritional or toxin-related myopathies were considered as differential diagnoses. In ruminants, nutritional myopathy associated with selenium and vitamin E deficiency is commonly polyphasic and associated with marked mineralization.¹ However, in this calf, lesions were monophasic and with minimal mineralization, which suggested that nutritional myopathy was a less likely cause of myonecrosis. Also, selenium and vitamin E deficiency is usually a herd problem because of dietary inadequacies, but in this instance, only 1 animal in the herd was affected. Thus, toxicants such as ionophores or poisonous plants were considered more likely causes of myopathy.

Plants associated with myonecrosis and myocardial necrosis in cattle include white snakeroot (Eupatorium rugosum), coffee senna (Cassia occidentalis), coyotillo (Karwinskia humboldtiana), western water hemlock (Cicuta douglassi), false lupine (Thermopis montana), and gossypol (Gossypium spp).^1,2 Histologic lesions associated with plant or ionophore toxicoses are morphologically similar.¹ Therefore, a history of exposure or identification of the associated toxicant (eg, detection of excessively high concentrations of ionophores in the feed) is necessary for a definitive diagnosis. For the herd at this farm, there was no history of exposure to ionophores, and only a single animal was affected; ionophore toxicosis was therefore considered unlikely. However, cattle at the farm had been exposed to white snakeroot in the past, with 6 clinical cases of white snakeroot toxicosis reported over the last 30 years. For each of those previously affected bovids, a diagnosis was made on the basis of clinical signs and known exposure to white snakeroot. Other plants known to cause necrosis of skeletal or cardiac muscle were not found on the farm, and the cattle were not given gossypol in their feed. Because of the calf's clinical signs prior to death and pathologic findings at necropsy, historical evidence of white snakeroot on the farm property, and lack of known exposure to other potential toxicants, white snakeroot toxicosis was considered to be the most likely cause of death. Given the high clinical suspicion of white snakeroot toxicosis and history of white snakeroot exposure of cattle at the farm, further testing was declined by the calf's owner.

White snakeroot is a perennial plant that is found in the southern, eastern, and Midwestern United States. It grows in shaded and wooded areas and matures in late summer and early fall.³ The plant is typically 2 to 4 feet in height and has oppositely located, heart-shaped, serrated leaves; white flowers; and white, branched roots.⁴ The toxic metabolite of white snakeroot is trematol or trematone.^3,4 Clinical signs of white snakeroot toxicosis include reluctance to move, incoordination, tremors, signs of depression, progressive weakness, recumbency, and death.^3–5 Following ingestion of the plant, the onset of clinical signs varies from < 2 days to 3 weeks.³ Trematol is excreted in the milk of cows that ingest white snakeroot, which decreases the cows' susceptibility to its toxic effects but may result in intoxication of suckling calves.³ For the calf of this report, a lactogenic source of trematol was suspected. Consumption of cows' milk containing trematol can cause milk sickness in humans.^3,6 Clinical signs of milk sickness in humans include weakness, anorexia, abdominal pain, and vomiting. Terminal cases can progress to delirium, coma, and death.^3,6