Search for the Cause of Equine Atypical Myopathy

Equine atypical myopathy (EAM), a seasonal, pasture-associated muscle disorder of unknown etiology (cause), presents a particular challenge to veterinarians. The disease is characterized by a generalized complete degeneration of muscle fibers, which leads to sudden death due to the collapse of the cardiorespiratory system in more than 90% of cases. The economic impact is often devastating.

Affected horses can either die peracutely (acutely) or show profuse sweating, muscle fasciculation (twitching), weakness, pigmenturia (urine discoloration), reluctance to move, recumbency (inability to stand), difficulty breathing, and death after 12-72 hours. Since the etiology is unknown, no effective prophylaxis (preventive treatment) exists and affected horses can only be treated symptomatically.

Large outbreaks have been reported since the 1980s in parts of Europe including the United Kingdom, France, Belgium, Germany, the Netherlands, Switzerland, Luxembourg, and Denmark. In 2010, 224 cases were communicated to the Atypical Myopathy Alert Group, managed by Dominique Votion, DVM, PhD, at the University of Liège in Blegium.

A very similar, if not the same, disease has also been observed in the United States and termed seasonal pasture myopathy. From 1998 to 2005, 14 cases were described in Minnesota. White snakeroot (a perennial herb) toxicosis was ruled out as a potential cause since its toxin was not found in liver or urine samples of affected horses. Seasonal pasture myopathy is thought to be caused by the same etiological agent as EAM.

Environmental factors such as regular access to pasture and certain weather conditions seem to influence the incidence of the disease, which occurs seasonally, mostly in autumn with lesser peaks in spring and sporadic cases in winter. Young horses kept fulltime at pasture without any food complementation are most frequently affected, highlighting the importance of contact with grass as a contributing factor in this disease. Further risk factors are adjacent streams and trees; dead leaves and branches in the pastures; and wet, windy, unpleasantly chilly weather conditions (but not severe frost). Veterinarians advise removing manure from pastures, providing clean drinking water and salt blocks, and bringing horses in from pasture during rough weather as preventive measures.

Causes of EAM that have been investigated include ionophores (an antimicrobial combound), mycotoxins (toxins from mold), and phytotoxins (toxins from plants). Recently, the development of EAM was associated with the ingestion of maple leaves covered with the fungus European tar spot. Stress and metabolic imbalances might predispose horses to develop the disease.

Over the last decades, the incidence of EAM, however variable from year to year, has increased, and demand is growing for effective treatment and prevention methods. Therefore, identification of the causative agent is of paramount importance. Current research at the Equine Clinic and the Institute of Bacteriology of the Vetsuisse-Faculty of the University of Berne in Switzerland is focused on clostridial toxins, specifically the lethal toxin of Clostridium sordellii, which is able to induce severe muscular damage when injected intramuscularly into mice.

Initially we (authors and researchers Lucia Unger, DVM, and Vinzenz Gerber, PD, DVM, PhD, Dipl. ACVIM, ECEIM, FVH) detected C. sordellii DNA in feces and intestinal contents of horses suffering from EAM but not in corresponding samples from healthy pasturemates. However, this finding was not reliably reproducible.

Subsequently, we found the ultrastructural damage of myofibers (muscle fibers) observed in muscle samples of affected horses by light and electron transmission microscopy to be very similar to the C. sordellii lethal toxin that induced structural damage in the cytoskeleton of different cell lines (i.e., structural damage to cells).

Most importantly, we were recently able to show that the lethal toxin of C. sordellii is present in the skeletal muscles of horses with EAM. Myofibers of affected horses reacted not only with an antibody specific for the lethal toxin, which failed to bind to the myofibers of either healthy horses or those with other myopathies, but also with sera (blood serum) from other EAM-affected horses.

Hitherto, C. sordellii-derived lethal toxin has been shown to cause gas gangrene syndrome in cattle and sheep, and toxic shock syndrome in humans. Its presence in the myofibers of horses suffering from EAM suggests that it might play a role as a trigger or even as the lethal factor in the etiology of the disease. anecdotal evidence and our most recent serological data suggest that naturally EAM-affected horses neither mount a protective immune response nor show a substantial increase in anti-lethal toxin antibodies, respectively, our findings may nonetheless suggest a rational approach for the development of a protective vaccine.

CONTACTS: Lucia Unger, DVM,, Equine Clinic, University of Berne, Berne, Switzerland
Vinzenz Gerber, PD, DVM, PhD, Dipl. ACVIM, ECEIM, FVH,, Equine Clinic, University of Berne, Berne, Switzerland

This is an excerpt from Equine Disease Quarterly, funded by underwriters at Lloyd's, London, brokers, and their Kentucky agents.

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Equine Disease Quarterly

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