Neurotoxicosis in horses associated with consumption of Trema micrantha.
Authors: Lorenzett M P, Pereira P R, Bassuino D M, Konradt G, Panziera W, Bianchi M V, Argenta F F, Hammerschmitt M E, Caprioli R A, de Barros C S L, Pavarini S P, Driemeier D
Journal: Equine veterinary journal
Summary
# Trema micrantha Poisoning in Horses: A CNS-Focused Toxicity Trema micrantha, a highly palatable tree species distributed across the Americas, has previously been documented as causing hepatic necrosis and encephalopathy in livestock; however, this 2018 retrospective case series of 14 horses reveals a distinctly different pathological presentation. All affected horses displayed severe neurological deterioration—including ataxia, pronounced sialorrhoea, involuntary locomotion, and recumbency—within 24 hours to 9 days of consuming potentially toxic quantities of T. micrantha leaves, with necropsy revealing diffuse yellowish discoloration and liquefactive necrosis predominantly affecting the brainstem (particularly the pons), cerebellum, and spinal cord alongside severe vasculitis, but notably minimal to absent hepatic involvement. Microscopically, the lesions represented severe vasculitis and necrosis of both white and grey matter, with spinal cord damage particularly evident in the lumbar and sacral intumescences. Whilst the specific neurotoxic mechanism remains unidentified and the study's reliance on retrospective owner observations presents methodological limitations, the findings establish that T. micrantha poisoning in equines manifests as a primary neurological disease rather than secondary hepatic encephalopathy. Practitioners in regions where this species grows should consider T. micrantha as a differential diagnosis in acute-onset ataxia and neurological deterioration, particularly when pasture assessment reveals access to unfamiliar vegetation, and counsel owners on the danger of its highly palatable leaves.
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Practical Takeaways
- •Recognize that T. micrantha leaves, despite being palatable to horses, cause rapid-onset neurological signs including ataxia and sialorrhoea that progress to recumbency and death within days of consumption
- •Counsel horse owners in regions where T. micrantha is present (throughout the Americas) to prevent access to this tree, as there is no identified treatment and poisoning is often fatal
- •Be aware that CNS lesions may occur without significant liver involvement, so hepatic parameters alone should not be used to rule out T. micrantha toxicity in horses with acute neurological signs
Key Findings
- •All 14 horses with T. micrantha consumption presented with ataxia, sialorrhoea, involuntary movements, and death within 24 hours to 9 days
- •Diffuse yellowish discoloration and severe vasculitis with liquefactive necrosis were observed throughout the brain and spinal cord, with most severe lesions in the pons
- •T. micrantha poisoning causes predominantly neurological disease with minimal to absent hepatic lesions, distinguishing it from previously reported hepatic presentations
- •The mechanism of action of the plant toxin in the CNS remains unidentified