Chondrodysplasia of Texel sheep û a new disease of suspected genetic aetiology (abstract)

Authors: Blair HT, Thompson KG, Linney LE, West DM
Publication: New Zealand Veterinary Journal, Volume 51, Issue 1, pp 45, Feb 2003
Publisher: Taylor and Francis

Animal type: Livestock, Production animal, Ruminant, Sheep
Subject Terms: Skeletal/bone/cartilage, Congenital disease, Genetics, Inherited disease/conditions, Locomotor, Pathology
Article class: Abstract

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Abstract: A chondrodysplasia characterised by dwarfism and varus deformity of the forelimbs has been recognised over four seasons in Texel and Texel-cross lambs on three related properties. Affected lambs appear normal at birth, but by 2 weeks of age have reduced growth rate, shortened neck and legs, varus forelimb deformities and a progressive reluctance to walk. Most die within the first 4 months of life. Some affected lambs have had normal co-twins.
Post mortem examination of two severely affected 3-month-old lambs revealed extensive loss of articular cartilage and exposure of subchondral bone on the weight-bearing surfaces of the proximal humeri and femurs. Articular and physeal cartilages were thicker than normal, suggesting delayed or impaired endochondral ossification. Histopathologically, there was disorganisation of chondrocytes in articular and physeal cartilage of all bones examined. In addition, there were multiple foci of chondrolysis, which coalesced in some areas to form large clefts. The chondroid matrix surrounding chondrocytes had an abnormal fibrillar appearance. One lamb that exhibited early signs of the disease died of an unrelated cause at 3 weeks of age, and although there was no erosion of articular cartilage, characteristic microscopic lesions were present in articular and physeal cartilage.
Although most of the affected lambs were born on a commercial property with a mix of different sheep breeds, all had Texel genes on both sire and dam sides of the pedigree. The farmer had been purchasing his Texel rams from the same flock for several seasons. Circumstantial evidence favours a genetic aetiology, characterised by either autosomal recessive inheritance or over dominance. Studies on the genetic and biochemical basis of the disease are continuing.

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