Winston, an 8-year-old Thoroughbred gelding, was settled in what seemed a perfectly healthy lifestyle typical for many American horses. His owner of five years worked him under saddle most mornings, either on trail rides or in low-level dressage work, then turned him out to spend the remainder of the day grazing in a small pasture with other horses at the boarding facility. At sunset, he was brought in to spend the night in his own stall, where he received 15 pounds of hay and four pounds of sweet feed per morning and evening feeding. Yet for some time, the gelding had not been 100 percent. Even though Winston got plenty of work and free exercise, the muscles of his topline and hindquarters were poorly developed, almost to the point of looking atrophied. He moved stiffly and had an odd hind-end “hitch” at all gaits, and he resisted the farrier’s attempts to work on his hind feet. Despite his ample ration, Winston had been losing weight, and his owner became quite concerned with the most recent development: His urine intermittently took on a brownish hue.
Watching Winton’s owner struggle with the changes in her horse, a fellow boarder, the owner of a big Belgian named Buddy, stepped forward to suggest a possible cause. She recognized in Winston’s signs a pattern similar to equine polysaccharide storage myopathy (EPSM), a muscle abnormality common in, but not exclusive to, the draft breeds. Buddy, a retiree from a theme-park hitch, had never shown signs of the disabling condition, but he received a special diet as a preventive measure. After learning of the irreversible muscle damage produced by the metabolic abnormality, Buddy’s owner decided to take preemptive action by managing the horse’s energy intake. Otherwise, she might discover his problem the hard way–by finding the horse down and unable to rise, suddenly immobilized by the excruciating pain of exertional rhabdomyolysis (tying up) or, like Winston, exhibiting a more generalized decline.
The Metabolic Error
Veterinary pathologist Beth Valentine, DVM, PhD, of Oregon State University’s College of Veterinary Medicine in Corvallis, observes that muscle pathology consistent with EPSM has been recognized in horses for a century or longer. Traditionally called Monday morning disease because draft horses were often stricken when resuming work after their weekly day of rest, the condition was considered primarily a disease of mismanagement. The triggering factor seemed to be giving the horses full grain feeds during their days off from work. Then, in research published in 1992, Stephanie Valberg, DVM, PhD, of the University of Minnesota’s Department of Clinical and Population Sciences, identified an underlying metabolic error in the muscles of a group of Quarter Horses afflicted with recurrent tying up. Since that seminal study, EPSM has been identified in individuals from many breeds who exhibit a variety of signs related to muscle malfunction. More than half of all draft horses and draft crosses are believed to have the potential for developing EPSM, given the “right” environmental conditions. Valentine finds that draft ponies, including Norwegian Fjords and Haflingers, draft mules and warmbloods are equally susceptible, and she sees the disorder often in Appaloosas, Arabians, Paints, Quarter Horses, Standardbreds and Thoroughbreds. American miniatures, Andalusians, Morgans, Paso Finos, Saddlebreds, Tennessee Walking Horses and Welsh ponies/Welsh crosses may also be affected.
EPSM is thought to arise from the individual’s inability to properly utilize the soluble carbohydrates consumed as sugars and starches in the grains and sweet feeds typically fed to American horses. A roughage-only diet of hay and pasture is sufficient for maintaining horses up to moderate work levels, but the demands on harder-worked horses are usually met by feeding some sort of concentrated energy source. But horses affected by EPSM are unable to efficiently metabolize the soluble carbohydrates provided by most concentrates. Instead of converting carbohydrates to “burnable” glycogen, these horses produce polysaccharides that end up clogging the muscle cells with molecules that can’t be converted to energy. As a result, EPSM horses can eventually become energy deficient despite an adequate ration, and their muscle cells break down, leading to stiffness, cramping, muscle wasting and even death.
According to Valentine, the list of EPSM signs includes symmetric loss of muscling, especially of the rump, shoulders and topline, weakness, usually in the hindquarters, trembling, often after exercise, difficulty in backing/reluctance to back, poor performance, lack of energy, stumbling, reluctance to pick up the feet for farriery work, a slightly stiff, awkward or short-strided gait in one or both hind limbs, “locking” stifles or “shivers,” in which a hind leg hikes up and out and possibly the tail also rises and quivers, episodic colic-like signs, especially after exercise, tying up, inability to rise from recumbency.
Because of EPSM’s broad range of locomotor manifestations, it is commonly confused with neurological conditions, particularly equine protozoal myeloencephalitis (EPM), and with infectious diseases, such as Lyme disease, that produce generalized debility. Affected horses are frequently dismissed as being “poor movers” or mistakenly diagnosed with hock problems, arthritis, anemia, back soreness, tying up and colic. The most reliable EPSM diagnostic is a muscle biopsy that can be examined for both cell abnormalities, indicating associated muscle damage, and the presence of stored polysaccharides. The biopsy procedure requires care in gathering, preserving, shipping and handling to provide a good laboratory specimen, but it is a relatively noninvasive on-farm practice that can be performed with the horse sedated and the sampling site numbed with local anesthetic.
Part Two – Dietary Controls for EPSM
Elsewhere on the Web:EPSM article by Dr. Beth Valentine
This article originally appeared in the September 2002 issue of EQUUS magazine.