Hereditary chondrodysplasia, or spider lamb syndrome, is an inherited, semilethal, musculoskeletal disease affecting lambs primarily of Suffolk or Hampshire breeds. Because the syndrome is a recessive genetic disorder, a lamb is afflicted only if both parents pass on the mutation. Thus, it is critical to identify carriers, which are structurally normal animals with only one copy of the mutation. The location of the locus causing spider lamb syndrome is along the distal end of ovine chromosome 6.
This mutation causes an inactivation of normal fibroblast growth factor receptor 3, which produces skeletal overgrowth in animals homozygous for the gene. Lambs have pronounced medial deviation of the carpus and hock and are unable to stand without distress. Pathologic changes in the skull reveal a rounding of the dorsal silhouette, producing a “Roman nose” appearance and a narrowed elongation of the occipital condyles. The thoracic and lumbar vertebrae are moderately kyphotic, which causes a dorsal rounding of the backline. The sternebrae are dorsally deviated, leading to a flattening of the sternum. The forelimbs have a medial deviation of the carpal joints with a bowed radius and ulna and irregular thickening of the growth plate cartilage. The hindlimbs have medially deviated hocks and bowed tibiae, which also have thickened, irregular growth plates. Muscle atrophy is also predominant. The regulation of liver insulin-like growth factor (IGF) and IGF-binding proteins may be involved in the physical manifestations of this disorder. It is suggested that the condition is inherited in a simple autosomal recessive pattern.