Skeletal deformities associated with nutritional congenital rickets in newborn lambs

Abstract

CASE HISTORY: A group of 545 pregnant rising 2-year-old Coopdale ewes on a Southland sheep farm were grazed over winter on a fodder beet (Beta vulgaris) crop. Subsequently, 45 out of approximately 750 lambs were born with a variety of skeletal deformities, including shortened limbs, varus and valgus angular limb deformities, palmar grade stance and cranial bowing of the carpus. Analysis of the crop showed the fodder beet contained a low percentage of phosphorus. In addition, 60 out of 460 rising 2-year-old ewes that had been grazed on the fodder beet crop as 1-year-olds had incisor abnormalities and malocclusion.

PATHOLOGICAL FINDINGS: Two affected lambs (1-day-old and 3-days-old) with representative clinical signs examined postmortem were found to have markedly enlarged costochondral junctions, and noticeably enlarged long bone metaphyses. In addition, one lamb had a dense band of metaphyseal sclerosis beneath the physes of all long bones examined. Histopathological findings included small islands and columns of chondrocytes and eosinophilic cartilage matrix present in the metaphysis. Metaphyseal trabeculae were disorganised and often lined by accumulations of pale pink osteoid; similar pale pink osteoid was also present in the cortices. Unerupted molar teeth in the affected lambs lacked a layer of enamel, and the dentine was irregular with globular basophilia.

DIAGNOSIS: The gross and histopathological lesions were consistent with a diagnosis of rickets.

CLINICAL RELEVANCE: Nutritional congenital rickets has not been previously diagnosed in sheep, but is a recognised disease of human infants with vitamin D deficient mothers. The rickets in affected lambs was most likely associated with phosphorus deficiency as a result of the pregnant ewes grazing fodder beet during gestation. While vitamin D deficiency was not definitively ruled out in these cases, practitioners are alerted to the possible effects of feeding phosphorus-deficient fodder beet to ewes for long periods during gestation and to 1-year-old sheep during important growth periods.     

Involvement of ATP‐sensitive K+ channels in the peripheral antinociceptive effect induced by ketamine

ObjectiveTo investigate the contribution of K⁺ channels on peripheral antinociception induced by ketamine.Study designProspective experimental study.Animals110 male Wistar rats weighing 160–200 g.MethodsThe paw pressure required to elicit limb flexion was designated as the nociceptive threshold. Hyperalgesia was induced by intraplantar injection of prostaglandin E₂. All drugs were administered locally into the right hind paw of rats. Ketamine was administered into the right hind paw 2 hours and 55 minutes after local injection of PGE₂. Tetraethylammonium was administered 30 minutes prior to ketamine and the other K⁺ channel blockers, glibenclamide, dequalinium and paxilline, were administered 5 minutes prior to ketamine.ResultsProstaglandin E₂ (2 μg per paw) induced hyperalgesia. Ketamine (10, 20, 40 and 80 μg per paw) elicited a local peripheral antinociceptive effect that was antagonized by a specific blocker of ATP‐sensitive K⁺ channels, glibenclamide (20, 40 and 80 μg per paw). In another experiment, the non‐selective voltage‐dependent K⁺ channel blocker tetraethylammonium (30 μg per paw) and small and large conductance blockers of Ca²⁺‐activated K⁺ channels, dequalinium (50 μg per paw) and paxilline (20 μg per paw), were ineffective at blocking the effect of a local ketamine injection.Conclusions and clinical relevanceAnalysis of these results provides evidence that ketamine, may in part, induce peripheral antinociceptive effects by ATP‐sensitive K⁺ channel pathway activation.