Sunday, April 10, 2011
Researchers in Switzerland have their eye on clostridial toxins as the possible cause of Equine Atypical Myopathy (EAM), a seasonal, pasture-associated muscle disorder.
The disorder is characterised by a generalised complete degeneration of muscle fibres, which leads to sudden death due to collapse of the cardio-respiratory system in over 90 per cent of the cases.
Writing in the latest Gluck Equine Disease Quarterly, Dr Lucia Unger and Professor Vinzenz Gerber, from the Equine Clinic at the University of Berne, said the economic impact is often devastating.
Affected horses can either die quickly or show profuse sweating, muscle twitching, weakness, abnormal urine colour, reluctance to move, recumbency and difficulty breathing. Death can follow after 12 to 72 hours.
Since the cause is unknown, no effective protective treatment exists, and affected horses can only be treated for their symptoms.
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 new cases were reported to the Atypical Myopathy Alert Group, managed by Dominique Votion at the University of Liège in Belgium.
A very similar, if not the same, disease has also been observed in the United States and is called seasonal pasture myopathy.
From 1998 to 2005, 14 cases were described in Minnesota.
White snakeroot toxicosis (Ageratina spp., formerly Eupatorium spp., a perennial herb) was ruled out as a potential cause since its toxin (tremetone) was not found in liver or urine samples of affected horses.
Seasonal pasture myopathy is thought to be caused by the same agent as the European equivalent.
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 springtime and sporadic cases in winter.
Young horses kept full time at pasture without any food complementation are most frequently affected, highlighting the importance of contact with grass.
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).
Removing manure from pastures, providing clean drinking water and salt blocks, and bringing horses in from pasture during rough weather is advised.
Causes that have been discussed and investigated include ionophores, mycotoxins, and phytotoxins.
Recently, the development of the disease was associated with ingesting maple leaves (Acer pseudoplantanus) covered with European tar spot (Rhytisma acerinum).
Stress and metabolic imbalances within horses may be factors that predispose horses to developing the disease, the authors noted.
Over the last decades, the incidence of the disease, however variable from year to year, has increased, and demand is growing for the cause to be identified and effective treatments developed and preventive measures identified.
Identification of the causative agent is of paramount importance, Unger and Gerber said.
"Consequently, our current research at the Equine Clinic and the Institute of Bacteriology of the Vetsuisse-Faculty of the University of Berne is focused on clostridial toxins, specifically the lethal toxin of Clostridium sordellii," they wrote.
"This large clostridial cytoxin is able to induce severe muscular damage when injected intramuscularly into mice.
"Initially, we detected Clostridium sordellii DNA in faeces and intestinal contents of horses suffering from EAM but not in corresponding samples from healthy pasture mates.
"However, this finding was not reliably reproducible."
Subsequently, they found damage in muscle samples of affected horses, using light and electron transmission microscopy, to be very similar to Clostridium sordellii lethal toxin induced structural damage in the cytoskeleton of different cell lines.
"Most importantly, we were recently able to show that the lethal toxin of Clostridium sordellii is present in 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 from other EAM-affected horses."
Previously, 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 it may play a role as a trigger or even as the lethal factor in the cause of this disease.
Anecdotal evidence and the pair's most recent body-fluid 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," they said.
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