In a 2004 mail survey, 87% of Minnesota horse owners reported their horses were pastured during the summer. In pastured Minnesota, Iowa and Wisconsin horses, we have increasingly recognized seasonal outbreaks of a muscle disease with greater than 90% mortality. It was originally assumed that horses died from consumption of the trematone toxin in the plant white snakeroot. However, in our 2004 study of 14 pastured horses that presented to the University of Minnesota Veterinary College or Diagnostic Laboratory with presumptive white snakeroot toxicity, no tremetone toxin was present. All horses had signs of muscle weakness and myoglobinuria which progressed to respiratory distress and death within a median of 16 hours. Frozen muscle sections had marked accumulation of intramuscular lipid. These horses became ill when pastured during cool wet autumns prior to snow cover or during a cool wet spring. Thus the term seasonal pasture myopathy (SPM) seemed appropriate for this condition. Dr Valberg’s Neuromuscular Diagnostic Laboratory at the College of Veterinary Medicine represents the only laboratory in North America that specializes in the clinical and histopathological diagnosis of muscular disorders in horses. Additional SPM cases were identified from lipid stains of muscle samples sent to our laboratory from horses in Appalachia and Georgia after a wet 2008 November, the Midwest during 2009, and Texas in 2010. A similar pasture-associated myopathy with high mortality rate has been witnessed as outbreaks in northern Europe and has been termed Atypical Myopathy. These outbreaks have been recognized with increasing frequency over the last decade. Seasonal Pasture Myopathy and Atypical Myopathy often go unrecognized because awareness is low, symptoms are easily confused with colic or founder, and diagnostic laboratories do not have the capacity to do lipid staining on frozen muscle tissue which has been the best means to diagnose SPM/AM.
Research at the University of Minnesota has expanded veterinarians’ diagnostic options and preventive measures that can be taken to avoid SPM. In the 2009 Midwest outbreak, we found that in addition to excessive lipid staining, horses with SPM had very high concentrations of plasma acylcarnitine and urine organic acids indicative of a lipid storage myopathy. Similar findings exist in horses with AM. In 2012, our lab identified the toxic etiology of SPM, hypoglycin A in box elder tree seeds, and developed a diagnostic test for metabolites of the toxin in blood and urine in conjunction with Baylor University. This test, once further validated, should provide an easy and accurate ante and post mortem diagnostic test for detecting exposure to hypoglycin A and SPM. Further analysis of box elder seeds from farms experiencing SPM as compared to farms that are not will help to delineate when seeds are most toxic and which environmental factors may put horses at highest risk for developing clinical disease.
Owners are devastated when horses die on pastures and they want immediate, research-based answers as to the cause of death, the risk to other horses, and when they can return horses to the affected pasture. We are more prepared than ever before to recognize and prevent SPM, but there are still questions to be answered. Through collaboration with referring veterinarians and horse owners, we will determine how to diagnose SPM cases earlier, which horses are most at risk for SPM, and which factors make for high risk pasture environments. The long-term benefits of full awareness and understanding of SPM include the ability to manage pastures to prevent SPM and the ability to intervene therapeutically earlier in disease to improve the odds of a favorable outcome.