Equine atypical myopathy

Equine atypical myopathy, also known as atypical myoglobinuria, or EAM is a fatal disease of horses (equidae) characterized by acute rhabdomyolysis.[1][2][3][4] It is caused by the ingestion of the seeds or young shoots of sycamore tree.[5][6][7] EAM has a high fatality rate.[8][9][10][1]

Cause

Atypical myopathy is a commonly fatal form of equine rhabdomyolysis caused by the toxin Hypoglycin A (HGA).[10][3][5] HGA is a naturally-occurring amino acid contained by trees and shrubs of Sapindaceae family.[7] Horses can become poisoned by eating sycamore seeds or seedlings of Acer pseudoplatanus in Europe and Acer negundo in North America.[11][4][12][13]The amount of HGA in sycamore seeds may vary.[6] The toxin affects to the functioning of horse’s muscle cells by slowing down or stopping the energy production.[9]

Even if atypical myopathy is not contagious it can affect either to individual horse or several horses in the same stock.[14] Some horses may be more resistant to the toxin than others due to genetic differences and different grazing habitats.[15]

Changes in weather conditions and temperature may contribute to the propensity of being affected, which is the reason why many cases are reported during autumn and spring.[9][1]

Diagnosis

Diagnosis can be confirmed by clinical examination and laboratory tests. In most cases treatment needs to be started before getting the laboratory test results as the confirmation of diagnosis may take several days.[9]

First symptoms are usually muscular weakness, soreness and stiffness causing problems with walking and breathing. Within hours of first symptoms horse may be unable to stand and in 72 hours of the onset of signs mortalities may occur.[16][13][1] The mortality rate of atypical myopathy is high; only 30-40% of affected horses survive.[9]

EAM affected horse’s urine is dark red or brown. Sweating and muscle trembling can be observed while moving. Horses may hang their heads down and be apathetic. Symptoms resemble colic symptoms except that EAM affected horse doesn’t lose appetite. The body temperature, heart rate and respiratory rate may be normal in some cases.[9][3][1]

Prevention

As treatment is still unsuccessful in the majority of cases the main emphasis is on prevention.[17] Risk of atypical myopathy can be reduced by checking pasture for sycamore plants regularly and avoid letting horses graze in pastures where are sycamore trees. In case there are fallen sycamore leaves and seeds in pasture they should be cleaned from the ground. Fresh and clean water should be easily accessible all the time. Keeping the stock size appropriate reduces the risk as there is enough proper grazing for every horse. Taking care of regular vaccinations and anthelmintic treatments decreases the risk. The presence of HGA in pasture can be tested by submitting a sample to laboratory.[9][1]

Treatment

EAM affected horses are in need of intensive care. There is no antitoxin for HGA but some medications can be used to stop absorption of the toxin. Symptomatic treatment includes intravenous fluid therapy, supplementation of glucose and insulin as well as administration of carnitine, vitamin E, selenium and riboflavin. Anti-inflammatory medication is used to decrease the pain and possibly increase the chance to survive. Supportive therapy includes the regular emptying of the bladder. Affected horse should be kept warm.[18][1]

Horses usually recover completely if they survive the first days after being affected. Recovery may still take several months.[9]

References
  1. Votion DM, Serteyn D (November 2008). "Equine atypical myopathy: a review". Veterinary Journal. 178 (2): 185–90. doi:10.1016/j.tvjl.2008.02.004. PMID 18375157.
  2. Votion D (April 2010). "La myopathie atypique des équidés" (PDF). Archived from the original (PDF) on 2014-02-22.
  3. Van Galen G, Amory H, Busschers E, Cassart D, De Bruijn M, Gerber V, et al. (October 2010). "European outbreak of atypical myopathy in the autumn 2009". Journal of Veterinary Emergency and Critical Care. 20 (5): 528–32. doi:10.1111/j.1476-4431.2010.00574.x. PMID 20955305.
  4. González Medina S, Hyde C, Lovera I, Piercy RJ (2018-07-03). "Detection of equine atypical myopathy-associated hypoglycin A in plant material: Optimisation and validation of a novel LC-MS based method without derivatisation". PLOS ONE. 13 (7): e0199521. Bibcode:2018PLoSO..1399521G. doi:10.1371/journal.pone.0199521. PMC 6029767. PMID 29969503.
  5. Karlíková R, Široká J, Jahn P, Friedecký D, Gardlo A, Janečková H, et al. (October 2016). "Equine atypical myopathy: A metabolic study". Veterinary Journal. 216: 125–32. doi:10.1016/j.tvjl.2016.07.015. PMID 27687939.
  6. "Equine Atypical Myopathy Testing". Royal Veterinary College. 2017. Retrieved 2019-12-08.
  7. Żuraw A, Dietert K, Kühnel S, Sander J, Klopfleisch R (July 2016). "Equine atypical myopathy caused by hypoglycin A intoxication associated with ingestion of sycamore maple tree seeds". Equine Veterinary Journal. 48 (4): 418–21. doi:10.1111/evj.12460. PMID 25970235.
  8. Votion DM, van Galen G, Sweetman L, Boemer F, de Tullio P, Dopagne C, et al. (March 2014). "Identification of methylenecyclopropyl acetic acid in serum of European horses with atypical myopathy". Equine Veterinary Journal. 46 (2): 146–9. doi:10.1111/evj.12117. PMID 23773055.
  9. "Atypical myopathy (Sycamore poisoning)" (PDF). B&W Equine Vets.
  10. Boemer F, Detilleux J, Cello C, Amory H, Marcillaud-Pitel C, Richard E, et al. (August 2017). "Acylcarnitines profile best predicts survival in horses with atypical myopathy". PLOS ONE. 12 (8): e0182761. Bibcode:2017PLoSO..1282761B. doi:10.1371/journal.pone.0182761. PMC 5573150. PMID 28846683.
  11. Bochnia M, Ziegler J, Sander J, Uhlig A, Schaefer S, Vollstedt S, et al. (2015). "Hypoglycin A Content in Blood and Urine Discriminates Horses with Atypical Myopathy from Clinically Normal Horses Grazing on the Same Pasture". PLOS ONE. 10 (9): e0136785. Bibcode:2015PLoSO..1036785B. doi:10.1371/journal.pone.0136785. PMC 4574941. PMID 26378918.
  12. Lemieux H, Boemer F, van Galen G, Serteyn D, Amory H, Baise E, et al. (September 2016). "Mitochondrial function is altered in horse atypical myopathy". Mitochondrion. 30: 35–41. doi:10.1016/j.mito.2016.06.005. hdl:1854/LU-8507237. PMID 27374763.
  13. McKenzie RK, Hill FI, Habyarimana JA, Boemer F, Votion DM (May 2016). "Detection of hypoglycin A in the seeds of sycamore (Acer pseudoplatanus) and box elder (A. negundo) in New Zealand; the toxin associated with cases of equine atypical myopathy". New Zealand Veterinary Journal. 64 (3): 182–7. doi:10.1080/00480169.2015.1123123. PMID 26593855.
  14. Votion D, van Galen G, Marr CM (November 2009). "Equine atypical myopathy". The Veterinary Record. 165 (20): 605. doi:10.1136/vr.165.20.605-b. PMID 19915196.
  15. Votion DM (2018-01-01). "Analysing hypoglycin A, methylenecyclopropylacetic acid conjugates and acylcarnitines in blood to confirm the diagnosis and improve our understanding of atypical myopathy". Equine Veterinary Education. 30 (1): 29–30. doi:10.1111/eve.12617.
  16. Gonzalez-Medina S (February 2015). "Update on the cause of equine atypical myopathy". The Veterinary Record. 176 (6): 143–5. doi:10.1136/vr.h414. PMID 25655543.
  17. Votion DM (November 2012). "The story of equine atypical myopathy: a review from the beginning to a possible end". ISRN Veterinary Science. 2012: 281018. doi:10.5402/2012/281018. PMC 3671727. PMID 23762581.
  18. Fabius LS, Westermann CM (2018). "Evidence-based therapy for atypical myopathy in horses". Equine Veterinary Education. 30 (11): 616–622. doi:10.1111/eve.12734. ISSN 2042-3292.
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