title: Role of thiamine status in sulphur induced polioencephalomalacia in sheep.
abstract: The effects of excess dietary sulphur were studied in sheep supplemented and unsupplemented with thiamine. The diets contained either 0.19 per cent sulphur (LS) or 0.63 per cent sulphur (HS) in combinations with 14 mg kg-1 thiamine (LB1) or 243 mg kg-1 thiamine (HB1). A total of 56 two-month-old lambs were used. Groups consisting of nine, nine, 22 and 16 lambs were fed LS-LB1, LS-HB1, HS-LB1 and HS-HB1 diets, respectively for 14 weeks. Out of 22 lambs fed the HS-LB1 diet, seven lambs developed neurological signs between the third and eighth week of the trial. Two of these lambs died, three that were in extremis were euthanased, and two recovered completely. All clinically affected animals had extensive malacic lesions in the cerebral cortex, midbrain and brainstem. None of the lambs from the LS groups or HS-HB1 group developed clinical signs. Several clinically normal lambs from the HS-LB1 group had necrotic lesions in their brains at gross and microscopic examination. Supplementation with dietary thiamine prevented development of clinical signs, but did not totally prevent development of microscopic brain lesions. Brain thiamine concentration, transketolase activity and thiamine pyrophosphate (TPP) effect were not different (P greater than 0.05) among groups. There was a strong effect (P less than 0.0001) of dietary thiamine supplementation on blood thiamine concentration and TPP effect. Blood thiamine concentration was higher whereas TPP effect was lower in the thiamine supplemented sheep. Blood and tissue thiamine concentrations in sheep exposed to high dietary sulphur did not indicate either systemic or local thiamine deficiency per se. Increased TPP effect in sheep fed the HS-LB1 diet indicated mild to moderate metabolic thiamine deficiency. Thiamine inadequacy may be an effect of an increased requirement for thiamine in animals exposed to excess dietary sulphur.
authors.affiliation: Department of Animal and Poultry Science, University of Saskatchewan, Saskatoon, Canada.
authors.forename: A A
authors.initials: AA
authors.lastname: Olkowski
authors.forename: S R
authors.initials: SR
authors.lastname: Gooneratne
authors.forename: C G
authors.initials: CG
authors.lastname: Rousseaux
authors.forename: D A
authors.initials: DA
authors.lastname: Christensen
mesh_terms: D000818:Animals; D001921:Brain / Q000201:enzymology / Q000473:pathology; D001923:Brain Chemistry; D004678:Encephalomalacia / Q000097:blood / Q000139:chemically induced / Q000188:drug therapy / Q000662:veterinary*; D004912:Erythrocytes / Q000201:enzymology; D005260:Female; D011897:Random Allocation; D012756:Sheep; D012757:Sheep Diseases / Q000097:blood / Q000139:chemically induced* / Q000188:drug therapy; D013455:Sulfur / Q000008:administration & dosage / Q000009:adverse effects*; D013831:Thiamine / Q000032:analysis* / Q000097:blood / Q000627:therapeutic use; D013835:Thiamine Pyrophosphate; D014174:Transketolase / Q000032:analysis / Q000097:blood
chemical_list: D013455:Sulfur; D014174:Transketolase; D013835:Thiamine Pyrophosphate; D013831:Thiamine