Member:
lisabel
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Posted on Wednesday, Oct 21, 2009 - 5:19 pm:
I have a friend with a horse who is now day six after onset of Atypical Myopathy. Against all odds, it looks like the horse is going to make it. The owner would dearly like to hear some success stories and perhaps write to someone who has tried rehabilitating a horse who has survived this disease.
I haven't seen the horse and haven't gotten a thorough description of the symptoms, but from what she says, her vet is not in doubt about the diagnosis.
This is (was?) a competitive endurance horse. What can the future be expected for him? What is the likelihood of full recovery. If not full recovery, what kind of limitations can be expected? Is there cause to be concerned about a re-occurance?
Any help and advice will be sent on with gratitude.
Location, BTW, is on the island of Falster in Denmark. No known incidences of other cases at this time.
Thanks, Lisa
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Moderator:
DrO
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Posted on Thursday, Oct 22, 2009 - 9:26 am:
Hello Lisa,
I have never seen a case of Atypical Myopathy (AM) but from what I read it can be quite severe even resulting in death. I cannot answer any of the specific questions about your friend's horse and her veterinarian is likely to be the best source of that information. AM has really just been described in the past decade and still remains quite a mystery. The two most informative pieces of information I have seen are these two. The first is a review of the conditions under which AM most occurs:
Vet J. 2009 Apr;180(1):77-87.
Atypical myopathy in grazing horses: a first exploratory data analysis.
Votion DM, Linden A, Delguste C, Amory H, Thiry E, Engels P, van Galen G, Navet R, Sluse F, Serteyn D, Saegerman C.
Equine Teaching Hospital, Department of Clinical Sciences, Faculty of Veterinary Medicine, University of Liège, 4000 Liège, Belgium. dominique.votion@ulg.ac.be
Over the last decade, atypical myopathy (AM) in grazing horses has emerged in several European countries. An exploratory analysis was conducted to determine horse- and pasture-level indicators or factors associated with AM in Belgium. Belgian cases of AM confirmed by histology (n=57) were compared to their healthy co-grazing horses (n=77) and to pastured horses not involved with AM as controls (n=386). The pastures where confirmed cases were grazing (42 pastures; 38 sites; 44 incidences of AM) were compared with those of the controls (216 pastures; 96 sites; no incidence of AM). Statistically significant (P< or =0.05) exploratory variables, identified by means of adjusted odds ratios, suggested that indicators or factors associated with individual horses (young age, inactivity, body condition poor to normal), management practices (permanent pasturing, spreading of manure) and pasture characteristics (humid, sloping pastures, accumulated dead leaves, presence of waterway) may increase the risk of AM. Specific interventions based on these factors might help to reduce the incidence of AM.
This second report is of interest because it is the first look into a possible mechanism. It is a bit technical but suggests that the problem is an acquired problem that impairs energy production in the muscle's cells leading to muscle cell death. What is currently known about the epidemiology suggsts a toxin or nutriitonal deficiency.
Neuromuscul Disord. 2008 Apr 10;
Acquired multiple Acyl-CoA dehyDrOgenase deficiency in 10 horses with atypical myopathy.
Westermann CM, Dorland L, Votion DM, Velden MG, Wijnberg ID, Wanders RJ, Spliet WG, Testerink N, Berger R, Ruiter JP, Kolk JH.
Department of Equine Sciences, Medicine Section, Faculty of Veterinary Medicine, Utrecht University, Yalelaan 114, 3508 TD Utrecht, The Netherlands.
The aim of the current study was to assess lipid metabolism in horses with atypical myopathy. Urine samples from 10 cases were subjected to analysis of organic acids, glycine conjugates, and acylcarnitines revealing increased mean excretion of lactic acid, ethylmalonic acid, 2-methylsuccinic acid, butyrylglycine, (iso)valerylglycine, hexanoylglycine, free carnitine, C2-, C3-, C4-, C5-, C6-, C8-, C8:1-, C10:1-, and C10:2-carnitine as compared with 15 control horses (12 healthy and three with acute myopathy due to other causes). Analysis of plasma revealed similar results for these predominantly short-chain acylcarnitines. Furthermore, measurement of dehyDrOgenase activities in lateral vastus muscle from one horse with atypical myopathy indeed showed deficiencies of short-chain acyl-CoA dehyDrOgenase (0.66 as compared with 2.27 and 2.48 in two controls), medium-chain acyl-CoA dehyDrOgenase (0.36 as compared with 4.31 and 4.82 in two controls) and isovaleryl-CoA dehyDrOgenase (0.74 as compared with 1.43 and 1.61nmol min(-1)mg(-1) in two controls). A deficiency of several mitochondrial dehyDrOgenases that utilize flavin adenine dinucleotide as cofactor including the acyl-CoA dehyDrOgenases of fatty acid beta-oxidation, and enzymes that degrade the CoA-esters of glutaric acid, isovaleric acid, 2-methylbutyric acid, isobutyric acid, and sarcosine was suspected in 10 out of 10 cases as the possible etiology for a highly fatal and prevalent toxic equine muscle disease similar to the combined metabolic derangements seen in human multiple acyl-CoA dehyDrOgenase deficiency also known as glutaric acidemia type II.
I was really looking for prognostic information but did not find any specific references but the case reports I read were not encouraging.
DrO
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