Morphological alterations in oxidative muscles and mitochondrial structure associated with equine atypical myopathy.
Authors: Cassart D, Baise E, Cherel Y, Delguste C, Antoine N, Votion D, Amory H, Rollin F, Linden A, Coignoul F, Desmecht D
Journal: Equine veterinary journal
Summary
# Equine Atypical Myopathy: Mitochondrial dysfunction at the heart of muscle degeneration Equine atypical myopathy (EAM) remains poorly understood despite over 80 years of documented cases, prompting Cassart and colleagues to conduct detailed morphopathological examination of muscle and heart tissue from 32 pasture-kept horses presenting with sudden onset ataxia, myoglobinuria and elevated muscle enzymes. The research team employed multi-level investigation—macroscopic examination, histology, histoenzymology and electron microscopy—to characterise the tissue damage across different muscle types and the myocardium. Respiratory and postural muscles showed the most consistent and severe necrosis, with microscopic analysis revealing monophasic Zenker degeneration predominantly affecting type 1 (oxidative) fibres; crucially, histochemical staining demonstrated severely disorganised NADH tetrazolium reductase patterns, absent calcium precipitation (ruling out inflammation-driven damage) and striking accumulation of lipid droplets within muscle cells. Ultrastructural examination frequently showed that altered mitochondria and intracellular lipid accumulation were the primary or sole abnormalities present, suggesting a primary mitochondrial dysfunction rather than secondary changes. The constellation of findings—preferential type 1 fibre involvement, lipid accumulation, mitochondrial pathology and the absence of inflammatory markers—aligns EAM with toxic myopathies, providing a pathological framework that should prompt investigation into metabolic toxins or environmental factors affecting oxidative muscle metabolism in affected horses.
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Practical Takeaways
- •EAM presents with consistent clinical signs (ataxia, myoglobinuria, elevated muscle enzymes) but diagnosis requires histopathological confirmation showing type 1 fibre necrosis with mitochondrial involvement
- •The disease preferentially affects oxidative muscles (respiratory and postural), suggesting affected horses may show progressive respiratory or postural dysfunction before recumbency
- •Recognition of mitochondrial pathology as central to EAM lesions may guide investigation toward toxic exposures or metabolic triggers, though aetiology remains unknown and requires further investigation
Key Findings
- •Muscle necrosis was most severe and consistent in respiratory, postural muscles and myocardium, with a multifocal monophasic pattern affecting primarily type 1 fibres
- •Histochemical analysis revealed disorganized NADH staining, absent calcium precipitates, and dramatic accumulation of lipid droplets in affected fibres
- •Ultrastructural examination frequently showed primary mitochondrial alterations and sarcoplasmic lipidosis as sole or major fibre modifications
- •Morphological features suggest EAM shares characteristics of toxic myopathies with primary mitochondrial dysfunction as a potential underlying mechanism