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

Cassart, Dominique; Baise, Etienne; Cherel, Yann; Delguste, Catherine; Antoine, Nadine; Votion, Dominique; Amory, Hélène; Rollin, Frédéric; Lindén, Annick; Coignoul, Freddy; Desmecht, Daniël

doi:10.2746/042516407x157765

Cited by 66 publications

(116 citation statements)

References 17 publications

(24 reference statements)

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“…Atypical myopathy occurs in horses of all age groups kept on pasture. Clinical signs are very similar to those in nutritional myodegeneration (weakness, stiffness, muscle pain, recumbency, myoglobinuria) (Cassart et al, 2007). However, dysphagia has never been described in atypical myopathy and affected horses can eat and drink well (Brandt, 1997).…”

Section: Discussionmentioning

confidence: 75%

Nutritional myodegeneration as a cause of dysphagia in adult horses: three case reports

Ludvíková¹,

Jahn²,

Lukáš³

2007

Vet. Med. - Czech

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Three cases of nutritional myodegeneration caused by selenium deficiency in adult horses are described. Difficulty in eating and drinking was a common clinical sign in all horses. Blood biochemistry revealed a marked elevation of muscle enzymes and low glutathione peroxidase activity or low selenium concentration in whole blood in all cases. The treatment with sodium selenite and vitamin E was instituted in all horses. Two of them were euthanized because of continuing muscle injuries, one patient was cured. The post-mortem examination of euthanized horses revealed pale muscles that were distributed with bilateral symmetry on hind and thoracic limbs, diaphragm, tongue, masticatory and intercostal muscles and the myocardium. Histopathology revealed the areas of degeneration and necrosis. Large groups of regenerating fibres and pronounced lymphoplasmocytic reaction among the groups of intact fibres were also present. The clinical outcome of the disease is probably influenced by timely diagnosis and treatment.

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Section: Discussionmentioning

confidence: 75%

Nutritional myodegeneration as a cause of dysphagia in adult horses: three case reports

Ludvíková¹,

Jahn²,

Lukáš³

2007

Vet. Med. - Czech

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“…Adicionalmente são descritos aspectos histoquí-micos e ultraestruturais musculares compatíveis com alterações mitocondriais e lipidose sarcoplasmática, sendo denominada de miopatia atípica ou mioglobinúria atípica (Cassart et al 2007, Aleman 2008.…”

Section: Discussão E Conclusãounclassified

“…Esse último aspecto pode predispor ao aparecimento da miopatia nutricional. De forma semelhante, Cassart et al (2007) e Aleman (2008) observaram que, na miopatia atípica, o surgimento dos sinais clínicos também não está relacionado com atividade física e incluem sinais semelhantes como fraqueza, tremores musculares, relutância em se locomover e andar rígi-do, dor a palpação muscular, taquicardia, taquipnéia, dispnéia, elevação da atividade sérica de CK, mioglobinúria e alta mortalidade. Portanto, os animais desse estudo apresentaram manifestações clínicas compatíveis tanto com a miopatia nutricional quanto com a miopatia atípica, não sendo possí-vel diferenciar clinicamente essas duas enfermidades, fato esse que está de acordo com os pressupostos de Valberg et al (1999) e Votion et al (2006).…”

Section: Discussão E Conclusãounclassified

“…O grupo das miopatias não associadas ao exercício inclui as de causa nutricional (deficiência de vitamina E e Se) (Lofestd 1997), metabólica (deficiência da enzima I de ramificação do glicogênio e por acúmulo de polissacarídeo) (Valberg et al 1992, Ward et al 2004, tóxica (Martin et al 1981, Bezerra et al 2000, Cassart et al 2007), traumática, inflamatória (bacterianas, virais, parasitárias e imunomediadas) (Peek et al 2003, Sponseller et al 2005, Lewis et al 2007, Aleman 2008, associada a anestesia (miopatia isquêmica e hipertermia maligna) (Aleman 2008), induzida por esteróides, neoplásicas e síndromes paraneoplásicas (Aleman 2008).…”

Section: Introductionunclassified

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Aspectos morfológicos de biópsias musculares em equinos com miopatia sob forma de surto

et al. 2011

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Pesq. Vet. Bras. 31(7):579-585, julho 2011 RESUMO.-As miopatias em equinos são classificadas de acordo com aspectos clínicos, morfológicos e moleculares, em três grandes grupos: não associadas ao exercício, associadas ao exercício e devido alteração da condução elétrica do sarcolema. Apesar dos avanços no diagnóstico, a literatura ainda relata surtos de miopatia em equinos sem etiologia esclarecida em diversos países. O objetivo desse estudo foi descrever as alterações histológicas e histoquímicas de biópsias musculares de equinos acometidos por miopatia. Sete equinos da raça Quarto de Milha, com 18-24 meses de idade, apresentaram sinais clínicos de miopatia. Dentre esses animais, cinco apresentaram sinais subagudos leves a moderados e dois apresentaram sinais hiperagudos severos e decúbito lateral. Foram realizadas biópsias musculares utilizando a técnica percutâ-nea, por agulha tipo Bergström, no músculo glúteo médio em todos os animais acometidos. As amostras foram processadas por meio de técnicas histológicas (HE, Tricrômio de Gomori modificado) e histoquímicas (PAS, NADH, ATPase). Nos quadros clínicos mais leves, a principal alteração encontrada foi a presença de fibras vermelhas rajadas do tipo I e Equine myopathies are classified according clinic, morphologic and molecular features in three groups: Non-exertional, exertional, and abnormal muscle membrane conduction. In spite the advances in diagnostic, the literature has reported outbreaks of equine myopathy without clear etiology in several countries. The aim of this study was to describe the histological and histochemical findings of muscle biopsies in an outbreak of equine myopathy. Seven 18 to 24-month-old Quarter horses showed clinical signs of myopathy. Five horses presented mild clinical signs and two horses had severe clinical signs with recumbency. Muscle biopsies were obtained from gluteal medium muscle by percutaneous technique with Bergstrom needle in all affected horses. Muscle samples were processed by histological (HE, modified gomori-trichrome) and histochemical (PAS, NADH, ATPase) technics. In animals with mild clinical signs, ragged red fibers type I and IIA, related to the oxidative metabolism dysfunction of mitochondria, was the main abnormality found. Muscle fiber atrophy and presence of subsarcolemmal aggregates in type I and IIA muscle fibers were also observed. More severe affected horses presented inflammatory infiltrate, proliferation of collagen, phagocytosis, necrosis and calcification. Based on the morphological findings, vitamin E therapy response associated with the low mortality when compared with atypical myopathy reports, We concluded that this outbreak was triggering for mitochondrial lesions, characterized by ragged red muscle fibers, probably due a breakdown homeostasis in vitamin E and Se, being compatible with nutritional myopathy diagnosis.INDEX TERMS: White muscle disease, nutritional myopathy, atypical myopathy, ragged red fibers.

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“…In animals, outbreaks of fatal MADD have been recorded in horses with atypical myopathy in particular weather conditions (Finno et al 2006;Cassart et al 2007;Westermann et al 2008;van der Kolk et al 2010;Valberg et al 2012). In these cases, an exogenous factor was predicted to cause MADD, and a genetic mutation of ETF and ETFDH has never been recognized.…”

Section: Introductionmentioning

confidence: 99%

Multiple Acyl-CoA Dehydrogenation Deficiency (Glutaric Aciduria Type II) with a Novel Mutation of Electron Transfer Flavoprotein-Dehydrogenase in a Cat

et al. 2013

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Multiple acyl-CoA dehydrogenation deficiency (MADD; also known as glutaric aciduria type II) is a human autosomal recessive disease classified as one of the mitochondrial fatty-acid oxidation disorders. MADD is caused by a defect in the electron transfer flavoprotein (ETF) or ETF dehydrogenase (ETFDH) molecule, but as yet, inherited MADD has not been reported in animals. Here we present the first report of MADD in a cat. The affected animal presented with symptoms characteristic of MADD including hypoglycemia, hyperammonemia, vomiting, diagnostic organic aciduria, and accumulation of medium-and long-chain fatty acids in plasma. Treatment with riboflavin and L-carnitine ameliorated the symptoms. To detect the gene mutation responsible for MADD in this case, we determined the complete cDNA sequences of feline ETFa, ETFb, and ETFDH. Finally, we identified the feline patient-specific mutation, c.692T>G (p.F231C) in ETFDH. The affected animal only carries mutant alleles of ETFDH. p.F231 in feline ETFDH is completely conserved in eukaryotes, and is located on the apical surface of ETFDH, receiving electrons from ETF. This study thus identified the mutation strongly suspected to have been the cause of MADD in this cat.

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

Abstract: The morphological features gathered here reveal that EAM shares most of the characteristics of toxic myopathies.

Cited by 66 publications

References 17 publications

Nutritional myodegeneration as a cause of dysphagia in adult horses: three case reports

Nutritional myodegeneration as a cause of dysphagia in adult horses: three case reports

Aspectos morfológicos de biópsias musculares em equinos com miopatia sob forma de surto

Multiple Acyl-CoA Dehydrogenation Deficiency (Glutaric Aciduria Type II) with a Novel Mutation of Electron Transfer Flavoprotein-Dehydrogenase in a Cat

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