title: Hepatic failure and hemochromatosis of Salers and Salers-cross cattle.
abstract: Hemochromatosis is rare in domestic mammals. Five clinical cases and one preclinical case of hemochromatosis were diagnosed in Salers and Salers-cross cattle. Clinical disease developed between 9 and 22 months of age. Animals were healthy until weaning but then lost weight, developed rough hair coats, and lost incisor teeth. In two animals, hemochromatosis was identified by liver biopsy, biochemical evidence of hepatic injury, and/or elevated transferrin saturation values. At necropsy, carcasses were thin, with firm dark brown livers and lymph nodes, soft bones, and brown-colored small bowel. The principal histologic changes were hepatocellular siderosis and periportal, bridging, and perivenular fibrosis. Siderocalcinosis involved collagen, elastin, reticulin, and basement membrane components in liver, lymph nodes, spleen, duodenum, and kidney. Hepatic iron concentrations in clinically affected cattle were 1,500-10,500 microg/g wet weight (reference range for cattle = <300 microg/ g). Ultrastructurally, the heaviest intrahepatic deposition was in hepatocytes, which contained large intracytoplasmic siderosomes. Iron deposition in bone was associated with osteopenia. Genetic analysis indicated a common ancestral bull in the pedigrees of five of six affected cattle; no pedigree was available for the remaining animal. Four dams of five affected animals were phenotypically normal and had histologically normal livers. Test mating of four cows to the ancestral bull resulted in a female calf that developed clinicopathologic and histologic evidence of preclinical hemochromatosis by 40 days of age. It was not possible to establish the pattern of inheritance because of the small number of pedigrees from affected cattle.
authors.affiliation: Department of Veterinary Sciences, University of Wyoming, Laramie 82070, USA. DOT@uwyo.edu
authors.forename: D
authors.initials: D
authors.lastname: O'Toole
authors.forename: E J
authors.initials: EJ
authors.lastname: Kelly
authors.forename: M M
authors.initials: MM
authors.lastname: McAllister
authors.forename: A W
authors.initials: AW
authors.lastname: Layton
authors.forename: R W
authors.initials: RW
authors.lastname: Norrdin
authors.forename: W C
authors.initials: WC
authors.lastname: Russell
authors.forename: K
authors.initials: K
authors.lastname: Saeb-Parsy
authors.forename: A P
authors.initials: AP
authors.lastname: Walker
mesh_terms: D000818:Animals; D015139:Blotting, Southern / Q000662:veterinary; D002417:Cattle; D002418:Cattle Diseases / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D003300:Copper / Q000378:metabolism; D003433:Crosses, Genetic; D004386:Duodenum / Q000473:pathology; D005260:Female; D006680:HLA Antigens / Q000235:genetics; D006432:Hemochromatosis / Q000235:genetics / Q000378:metabolism / Q000473:pathology / Q000662:veterinary*; D015395:Histocompatibility Antigens Class I / Q000235:genetics; D006651:Histocytochemistry / Q000662:veterinary; D007501:Iron / Q000097:blood / Q000378:metabolism; D008099:Liver / Q000378:metabolism / Q000473:pathology / Q000648:ultrastructure; D008107:Liver Diseases / Q000235:genetics / Q000378:metabolism / Q000473:pathology / Q000662:veterinary*; D008198:Lymph Nodes / Q000473:pathology / Q000648:ultrastructure; D008297:Male; D008565:Membrane Proteins; D008854:Microscopy, Electron / Q000662:veterinary; D010375:Pedigree
chemical_list: D006680:HLA Antigens; D015395:Histocompatibility Antigens Class I; D008565:Membrane Proteins; D003300:Copper; D007501:Iron