Ovine congenital progressive muscular dystrophy: clinical syndrome and distribution of lesions.
The distribution and severity of lesions in the skeletal muscles of 37 Merino sheep with congenital progressive muscular dystrophy (CPMD) are described. An explanation for the clinical signs is offered on the basis of functional defects in regional muscle groups. Lesions in the extensors of the hip, stifle and hock joints and flexors of the digits are primarily responsible for the progressive abnormality of hind limb gait that is characteristic of the clinical syndrome. Lesions in extensors of the elbow and flexors of the shoulder, carpus and digits affected fore limb function in advanced cases. The tendency for some affected sheep to develop ruminal tympany is probably caused by lesions in the diaphragmatic crus. Clinically affected sheep had higher resting and post-exercise concentrations of serum creatine phosphokinase and lactic dehydrogenase than unaffected control sheep. The rise in serum creatine phosphokinase after exercise was greater in affected sheep than in controls. Myotonia was not demonstrated in electromyographic studies in one sheep.
D000818:Animals; D001219:Aspartate Aminotransferases / Q000097:blood; D003402:Creatine Kinase / Q000097:blood; D005260:Female; D007064:L-Iditol 2-Dehydrogenase / Q000097:blood; D007770:L-Lactate Dehydrogenase / Q000097:blood; D008297:Male; D009137:Muscular Dystrophy, Animal / Q000151:congenital* / Q000201:enzymology / Q000473:pathology; D005082:Physical Exertion; D012756:Sheep; D012757:Sheep Diseases / Q000151:congenital* / Q000201:enzymology / Q000473:pathology
D007064:L-Iditol 2-Dehydrogenase; D007770:L-Lactate Dehydrogenase; D001219:Aspartate Aminotransferases; D003402:Creatine Kinase