23 Cases of Atypical Myopathy Diagnosed in Spring 2012

Twenty-three cases of equine atypical myopathy (EAM) have been reported this spring to the University of Liège, in Belgium, and the RESPE (Réseau d'Epidémio-Surveillance en Pathologie Equine, or the Epidemiological Surveillance Network for Equine Diseases), according to a May 2 notice from the Atypical Myopathy Alert Group.

According to the alert, 18 cases have been identified in France, four in Great Britain, and one in New Zealand.

Atypical myopathy, a seasonal, pasture-associated muscle disorder, 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 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.

Researchers at the University of Berne's Equine Clinic, in Switzerland, recently evaluated whether the lethal clostridial toxin of Clostridium sordellii, which is able to induce severe muscular damage when injected intramuscularly into mice, could play a role in EAM development.

In a 2011 Equine Disease Quarterly article researchers Lucia Unger, DVM, and Vinzenz Gerber, PD, DVM, PhD, Dipl. ACVIM, ECEIM, FVH, explained some of their research:

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.

Research into the etiology of EAM is ongoing.

About the Author

Erica Larson, News Editor

Erica Larson, news editor, holds a degree in journalism with an external specialty in equine science from Michigan State University in East Lansing. A Massachusetts native, she grew up in the saddle and has dabbled in a variety of disciplines including foxhunting, saddle seat, and mounted games. Currently, Erica competes in eventing with her OTTB, Dorado.

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