Scientists found increased levels of cyanide in certain tissues from fetuses and foals killed by MRLS earlier this year, and many believe it is linked to the leaves of wild black cherry trees. Tobin said the research represents the first attempt at defining normal levels of cyanide in the horse in Kentucky.
Cyanide has been identified as a potential risk or contributing factor in two illnesses that have dominated the Thoroughbred industry headlines this year.Scientists at the University of Kentucky's Maxwell H. Gluck Equine Research Center have been examining the role of cyanide in the mare reproductive loss syndrome and will incorporate what they learn from cyanide's potential involvement in the syndrome to factors associated with the development of grass sickness.Dr. Thomas Tobin, a veterinary pharmacologist/toxicologist at the Gluck Center, is working on the basic toxicology of cyanide in horses. The information should help to couple the research areas.The project to determine the cause of grass sickness, and possible preventive measures, is already under way. It combines the work of research groups in Dubai, Northern Europe, and in Lexington.Grass sickness can be acute or chronic, involving the partial or complete paralysis of the gastrointestinal tract, rendering it unable to digest. The disease is usually fatal and could be linked to a neurotoxin produced by anaerobic bacteria of the Clostridium botulinum family, members of which are associated with botulism in the horse.Horses can contract botulism by ingestion of the toxin through contaminated feed or water; through the entrance of C. botulinumin a wound; or in foals, by the entrance of the organism through the necrotic (dead) tissue of the umbilical stump. Grass sickness was first described in Europe about 100 years ago, and it isn't clear why few or no cases have been found in the U.S.Tobin explained why cyanide is being targeted in the fight against grass sickness. "There is some evidence to support suggestions that if you have exposure to higher levels of cyanide, there may be an alteration of glut flora which encourages or allows certain bacterial species to proliferate," he said. "In this model, the pathogenesis of grass sickness would be a two step mechanism -- the effects of the cyanide, and then the effects of Clostridial proliferation."Tobin also will be looking at what might trigger the increased concentration of cyanide levels in the pasture. White clover is under investigation for harboring levels of cyanide.