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Home / Equine Research Bank / Equine Vet J / Morphological alterations in oxidative muscles and mitochond...
Equine veterinary journal2007; 39(1); 26-32; doi: 10.2746/042516407x157765

Morphological alterations in oxidative muscles and mitochondrial structure associated with equine atypical myopathy.

Abstract: There is a lack of well documented studies about muscular lesions in equine atypical myopathy (EAM). Objective: To characterise morphopathological changes of striated muscles and myocardium, to progress understanding of this disease. Methods: Thirty-two horses age 0.5-7 years kept on pasture were referred for a sudden ataxia/myoglobinuria syndrome. Clinical examination (stiffness, muscle pain, muscle fasciculations, abnormal gait, recumbency, myoglobinuria, tachycardia, sweating) and plasma CPK, LDH and AST levels were consistent with extensive myonecrosis and, together with anamnestic data, with so-called 'equine atypical myopathy' (EAM), a disease of unknown aetiology reported since 1939. Macroscopic and microscopic (histology, histoenzymology, ultrastructure) lesions were evaluated. Results: Necropsic examination revealed large areas of muscle necrosis, the extent and severity of which varied between cases and muscles, but which were clearly more constant and severe in respiratory and postural muscles and in the myocardium. Histology highlighted a multifocal and monophasic process compatible with Zenker degeneration/necrosis that mostly and segmentally affected type 1 fibres. Histochemical evaluation revealed a weak and disorganised pattern of NADH tetrazolium reductase staining, the absence of calcium salts precipitates and a dramatic accumulation of lipid droplets. Ultrastructural examination often revealed fibres of which the sole modifications were altered mitochondria and sarcoplasmic lipidosis. Conclusions: Taken together, the data suggest that a primary alteration of mitochondria should be considered, although secondary mitochondrial abnormalities have yet to be ruled out. Conclusions: The morphological features gathered here reveal that EAM shares most of the characteristics of toxic myopathies.
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Publication Date: 2007-01-19 PubMed ID: 17228591DOI: 10.2746/042516407x157765Google Scholar: Lookup
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  • Journal Article

Summary

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The research explores the pathological muscular changes in horses suffering from equine atypical myopathy (EAM), specifically focusing on muscle and myocardium transformations. It highlights the possibility of primary mitochondrial alteration in EAM.

Background and Objective

  • The research centers on equine atypical myopathy (EAM), an illness of unknown cause that has been reported since 1939. There’s a scarcity of well-documented studies on muscular lesions in EAM. The study aims to characterize the morphopathological changes of striated muscles and myocardium to enhance the comprehension of this disease.

Methodology

  • Thirty-two horses aged between 0.5 to 7 years, kept in pastures, were examined for a sudden ataxia or myoglobinuria syndrome.
  • Clinical examinations showed symptoms such as stiffness, muscle pain, abnormal gait, recumbency, myoglobinuria, tachycardia, and sweating. The symptoms, along with data from the medical history, were in line with extensive myonecrosis and so-called ‘equine atypical myopathy’.
  • Macroscopic and microscopic (histology, histoenzymology, ultrastructure) lesions were evaluated to understand the changes and alterations.

Results and Findings

  • The necropsic examination showed vast areas of muscle necrosis, the breadth and severity of which varied among cases and muscles. However, the damage was more pronounced and frequent in respiratory, postural muscles, and the myocardium.
  • The histology revealed a multifocal and monophasic process compatible with Zenker degeneration/necrosis that primarily and segmentally affected type 1 fibres.
  • The histochemical evaluation brought out a weak and disorganized pattern of NADH tetrazolium reductase staining. It showed no calcium salts precipitates and a significant accumulation of lipid droplets – these observations pointed towards altered energy metabolism.
  • On an ultrastructural level, fibres often showed the only modifications were altered mitochondria and sarcoplasmic lipidosis (excessive fat in the cell plasma).

Conclusions

  • The data collated from the research led to the thinking that primary alteration of mitochondria could be part of the problem. However, the possibility of secondary mitochondrial abnormalities couldn’t be discounted.
  • The morphological features aligned EAM close to toxic myopathies, suggesting similar underlying issues.

Cite This Article

APA
Cassart D, Baise E, Cherel Y, Delguste C, Antoine N, Votion D, Amory H, Rollin F, Linden A, Coignoul F, Desmecht D. (2007). Morphological alterations in oxidative muscles and mitochondrial structure associated with equine atypical myopathy. Equine Vet J, 39(1), 26-32. https://doi.org/10.2746/042516407x157765

Publication

Equine veterinary journal
ISSN: 0425-1644
NlmUniqueID: 0173320
Country: United States
Language: English
Volume: 39
Issue: 1
Pages: 26-32

Researcher Affiliations

Cassart, D
  • Department of Pathology, Faculty of Veterinary Medicine, University of Liège, Sart Tilman B43, B-4000 Liège, Belgium.
Baise, E
    Cherel, Y
      Delguste, C
        Antoine, N
          Votion, D
            Amory, H
              Rollin, F
                Linden, A
                  Coignoul, F
                    Desmecht, D

                      MeSH Terms

                      • Animals
                      • Female
                      • Horse Diseases / metabolism
                      • Horse Diseases / pathology
                      • Horses
                      • Male
                      • Mitochondria, Heart / metabolism
                      • Mitochondria, Heart / pathology
                      • Mitochondria, Heart / ultrastructure
                      • Mitochondria, Muscle / metabolism
                      • Mitochondria, Muscle / pathology
                      • Mitochondria, Muscle / ultrastructure
                      • Muscle, Skeletal / metabolism
                      • Necrosis / veterinary
                      • Oxidation-Reduction
                      • Rhabdomyolysis / metabolism
                      • Rhabdomyolysis / pathology
                      • Rhabdomyolysis / veterinary

                      Citations

                      This article has been cited 14 times.
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                        doi: 10.1177/10406387211020721pubmed: 34092152google scholar: lookup
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