Presented in part as an abstract at the 2011 American College of Internal Medicine Forum in Denver, CO
Equine Multiple Acyl-CoA Dehydrogenase Deficiency (MADD) Associated with Seasonal Pasture Myopathy in the Midwestern United States
Article first published online: 18 JUN 2012
Copyright © 2012 by the American College of Veterinary Internal Medicine
Journal of Veterinary Internal Medicine
Volume 26, Issue 4, pages 1012–1018, July-August 2012
How to Cite
Sponseller, B.T., Valberg, S.J., Schultz, N.E., Bedford, H., Wong, D.M., Kersh, K. and Shelton, G.D. (2012), Equine Multiple Acyl-CoA Dehydrogenase Deficiency (MADD) Associated with Seasonal Pasture Myopathy in the Midwestern United States. Journal of Veterinary Internal Medicine, 26: 1012–1018. doi: 10.1111/j.1939-1676.2012.00957.x
- Issue published online: 13 JUL 2012
- Article first published online: 18 JUN 2012
- Manuscript Accepted: 9 MAY 2012
- Manuscript Revised: 16 FEB 2012
- Manuscript Received: 15 DEC 2011
- Acute rhabdomyolysis;
- Lipid storage myopathy;
- Serum acylcarnitine profiles;
- Urine organic acid profiles
Seasonal pasture myopathy (SPM) is a highly fatal form of nonexertional rhabdomyolysis that occurs in pastured horses in the United States during autumn or spring. In Europe, a similar condition, atypical myopathy (AM), is common. Recently, a defect of lipid metabolism, multiple acyl-CoA dehydrogenase deficiency (MADD), has been identified in horses with AM.
To determine if SPM in the United States is caused by MADD.
Six horses diagnosed with SPM based on history, clinical signs, and serum creatine kinase activity, or postmortem findings.
Retrospective descriptive study. Submissions to the Neuromuscular Diagnostic Laboratory at the University of Minnesota were reviewed between April 2009 and January 2010 to identify cases of SPM. Inclusion criteria were pastured, presenting with acute nonexertional rhabdomyolysis, and serum, urine, or muscle samples available for analysis. Horses were evaluated for MADD by urine organic acids, serum acylcarnitines, muscle carnitine, or histopathology.
Six horses had clinical signs and, where performed (4/6 horses), postmortem findings consistent with SPM. Affected muscle (4/4) showed degeneration with intramyofiber lipid accumulation, decreased free carnitine concentration, and increased carnitine esters. Serum acylcarnitine profiles (3/3) showed increases in short- and medium-chain acylcarnitines and urinary organic acid profiles (3/3) revealed increased ethylmalonic and methylsuccinic acid levels, and glycine conjugates, consistent with equine MADD.
Conclusions and Clinical Importance
Similar to AM, the biochemical defect causing SPM is MADD, which causes defective muscular lipid metabolism and excessive myofiber lipid content. Diagnosis can be made by assessing serum acylcarnitine and urine organic acid profiles.