History

At a farm located in the Pantanal region of the state of Mato Grosso, Brazil, a herd of 400 1.5-year-old male mixed-breed oxen were introduced to a recently cultivated paddock composed of Urochloa brizantha and other weeds. Fifteen days after being introduced to that pasture, 22 cattle developed staggering gait and recumbence. After 15 deaths within 3 to 4 days, the pathology service team from the Federal University of Mato Grosso was called to investigate the cause of mortality. During the investigation, 7 additional cattle were found in recumbency; 2 of them were euthanized (with an IV overdose injection of pentobarbital solution) and necropsied. The herd was reallocated to another pasture. The remaining 5 cattle that were found in recumbency died within 2 days.

Clinical and Gross Findings

Close observation of the herd revealed cattle reluctant to move, with muscular weakness; some of the cattle would go down when required to race or walk long distances. Recumbent cattle appeared alert and would eat and drink until late in the clinical course. The primary gross lesions occurred in skeletal muscles. Gross changes consisted of varying degrees and extension of muscle pallor affecting 1 or multiple muscles (Figure 1). Muscles in the hind limbs were most frequently affected. Samples from all organs and various muscle fragments were collected and fixed in neutral-buffered 10% formalin for morphologic studies.

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Postmortem images of the affected hind limb muscles from a 1.5-year-old mixed-breed ox that was showing reluctance to move, muscular weakness, and recumbency and was euthanized. A—Biceps femoris showing pale discolored areas in part of the muscle (arrows). B—Muscle adductor. The whole muscle is pale white (arrows).

Citation: Journal of the American Veterinary Medical Association 2025; 10.2460/javma.24.08.0543

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Histopathologic Findings and Diagnostic Confirmation

Microscopically, the skeletal muscles had extensive areas of monophasic hyaline myodegeneration and coagulative necrosis characterized by sarcoplasm loss of cross-striation or fragmentation, swelling, and vacuolation. Additionally, floccular degeneration and loss of the sarcoplasm through ruptured sarcolemmal membranes (Figure 2) were observed. Neutrophil infiltration was minimal. Occasionally, macrophages and lymphocytes accumulated within and around degenerated fibers. The pasture examination revealed an intense invasion by Senna obtusifolia.

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Photomicrograph of a section of skeletal muscle of the ox described in Figure 1. Panels A and B depict longitudinal and transverse sections, respectively, showing myofiber loss of striation and fragmentation, swelling and vacuolation of the sarcoplasm, floccular degeneration, and loss of the sarcoplasm through ruptured sarcolemmal membranes (arrows). H&E stain. Bar = 50 µm (panel A) and 20 µm (panel B).

Citation: Journal of the American Veterinary Medical Association 2025; 10.2460/javma.24.08.0543

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Morphologic Diagnosis and Case Summary

Morphologic diagnosis: severe, multifocal, monophasic skeletal myodegeneration and myonecrosis.

Case summary: toxic skeletal myodegeneration and myonecrosis.

Comments

The most frequent causes involved in toxic myodegeneration leading to necrosis of cattle are coffee senna (Senna occidentalis or S obtusifolia) and ionophores.¹ However, others, such as gossypol, a substance present in cotton seeds and the plants Ageratina altissima, Isocoma pluriflora, Laburnum anagyroides, Lupinus sp, and Thermopsis montana, are also described.^1–3 In Brazil, the only known plant responsible for causing toxic myodegeneration and necrosis in cattle is S occidentalis.⁴ Yet, recently, outbreaks of poisoning by ingestion of S obtusifolia have been reported.^3,5 Senna occidentalis and S obtusifolia belong to the family Caesalpinioideae, are native American shrubs with pantropical distribution, and are often found as invasive to pastures and cereal crops such as soy, maize, and sorghum.^2–3

Senna occidentalis poisoning in cattle was reproduced with the administration of leaves, stems, pods, or seeds.⁴ Leaves, stems, and green pods of S obtusifolia were also experimentally toxic to cattle.^3,5 Some authors consider S occidentalis to be more toxic than S obtusifolia.^3,5

The low availability of good-quality forage in pastures and high rate of infestation by Senna spp are factors that lead cattle to ingest these plants. These conditions have been reported in field outbreaks of poisoning by S obtusifolia.^3,5 Other conditions that bring animals to consume the plant are the high stocking rate of cattle in pastures invaded by S obtusifolia or providing green chopped forage mixed with this plant. These conditions have also been observed in field poisoning by S occidentalis.^2,3

Clinical signs often include muscle weakness, staggering gait, and reluctance to move, which progresses to decubitus followed by death. The lesions caused by Senna spp poisoning are similar to those observed in this outbreak.^2–5 These lesions could result from mitochondrial damage, leading to a mitochondrial metabolic impairment.² The myotoxins of Senna spp are water soluble but have not been completely identified. The anthraquinones isolated from Senna spp can impair mitochondrial metabolism and may cause the toxic effects of S obtusifolia and S occidentalis. This observation is consistent with the description of muscle mitochondrial damage and possible uncoupling of oxidative phosphorylation experimental poisoning with S occidentalis.²

Hepatic lesions have been observed in Senna spp poisoning in cattle. Hepatocellular vacuolization, individual hepatocellular necrosis, and centrilobular necrosis have been described. Hepatic centrilobular necrosis has been attributed to consuming large amounts of the plant.^2,3,5

The mechanism that triggers hepatic injury appears to be similar to that causing muscle lesions because the affected hepatocytes had ultrastructural changes and a decreased mitochondrial function as those observed in the affected muscular tissue. This observation suggests that the same toxic principle can cause muscle and liver damage and that the extension of the damage depends on the amount of the plant consumed.^2,3,5

The differential diagnoses in Senna spp poisoning in cattle must include, mainly, myotoxic plant poisoning, ionophore poisoning, and nutritional myodegeneration (white muscle disease) due to vitamin E and selenium deficiency. In myotoxic plant poisoning, due to similar clinical and pathological findings, the diagnosis should be based on identifying the toxic plants in the field, the amount of the toxic plant in the pasture, and the presence of signs of consumption by the animal. Observing plant fragments in the stomach has limited diagnostic value since rumination destroys plant parts, preventing their subsequent identification. The observation of plant parts in the stomach is only helpful in plants with hard parts, such as Stryphnodendron spp, or when animals die quickly after ingestion (before rumination), such as in poisoning by Manihot spp or other cyanogenic plants.³ In ionophore poisoning, despite the similarity of the pathological findings, there is normally a history of ionophore consumption associated with clinical evidence characterized mainly by congestive heart failure, which was not observed in the present study. Nutritional myodegeneration primarily affects young animals and presents with remarkable calcification of muscle fibers and low serum levels of vitamin E and selenium.^1–5 Each differential diagnosis was considered and ruled out on the basis of the specific epidemiological, clinical, gross, and histopathologic findings of this case.

Disclosures

The authors have nothing to disclose. No AI-assisted technologies were used in the generation of this manuscript.

Funding

The authors are grateful for the funding provided by the Conselho Nacional de Desenvolvimento Científico e Tecnológico, Pró Reitoria de Pesquisa of the Universidade Federal de Mato Grosso, and Fundação de Amparo a Pesquisa do Estado de Mato Grosso.