title: A familial degenerative neuromuscular disease of Gelbvieh cattle.
abstract: A degenerative skeletal muscle disease with vascular, neurologic, and renal lesions and a probable familial distribution was identified in 4-20-month-old purebred Gelbvieh cattle. Thirteen affected animals were confirmed from 6 separate beef herds, with a mortality rate of 100%. Clinical signs in affected animals consisted of ataxia, weakness, and terminal recumbency. Gross and histologic muscle lesions were indicative of nutritional myopathy of ruminants, with a lack of myocardial lesions in most cases and only rare myocardial changes in a few animals. Acute to chronic lesions in most large skeletal muscle groups consisted of degeneration, necrosis, regeneration, fibrosis, and atrophy. Fibrinoid necrosis of arterioles was a common feature in multiple tissues. Lesions in the spinal cord white matter and peripheral nerves consisted of degeneration of the dorsal columns and axons, respectively. Changes in the kidneys consisted of chronic interstitial nephritis with fibrosis, hyaline droplet change and tubular epithelial vacuolar change and were most severe in the older calves. Intracytoplasmic myoglobin and iron were demonstrated within the hyaline droplets in degenerate renal cortical tubular epithelial cells. Vitamin E levels were deficient in most (6/7) of the animals tested. Investigation of the pedigree of affected animals revealed a common ancestry for all but 1 of the animals whose parentage could be traced. This investigation suggests that a hereditary metabolic defect, possibly involving antioxidant metabolism, could be responsible for this condition. Renal disease, possibly secondary to myoglobinuria, may be unique to this bovine condition.
authors.affiliation: Rollins Animal Disease Diagnostic Laboratory, North Carolina Department of Agriculture, Raleigh, USA.
authors.forename: Peter G
authors.initials: PG
authors.lastname: Moisan
authors.forename: David J
authors.initials: DJ
authors.lastname: Steffen
authors.forename: Michael W
authors.initials: MW
authors.lastname: Sanderson
authors.forename: Jerome C
authors.initials: JC
authors.lastname: Nietfeld
authors.forename: Melissa R
authors.initials: MR
authors.lastname: Finley
authors.forename: Dale M
authors.initials: DM
authors.lastname: Grotelueschen
authors.forename: Gordon A
authors.initials: GA
authors.lastname: Andrews
authors.forename: Gayle
authors.initials: G
authors.lastname: Johnson
authors.forename: Lisa
authors.initials: L
authors.lastname: Williamson
authors.forename: Steven D
authors.initials: SD
authors.lastname: Rushton
authors.forename: D Greg
authors.initials: DG
authors.lastname: Hall
authors.forename: Barry G
authors.initials: BG
authors.lastname: Harmon
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000378:metabolism; D001259:Ataxia / Q000209:etiology / Q000662:veterinary; D002417:Cattle; D002418:Cattle Diseases / Q000235:genetics* / Q000473:pathology; D017809:Fatal Outcome; D005260:Female; D007674:Kidney Diseases / Q000209:etiology / Q000473:pathology / Q000662:veterinary; D008297:Male; D008659:Metabolic Diseases / Q000235:genetics / Q000662:veterinary; D018908:Muscle Weakness / Q000662:veterinary; D009468:Neuromuscular Diseases / Q000235:genetics* / Q000662:veterinary*; D010375:Pedigree; D014810:Vitamin E / Q000378:metabolism
chemical_list: D000975:Antioxidants; D014810:Vitamin E