Spider lamb syndrome, also known as spider syndrome [1] and more formally as ovine hereditary chondrodysplasia, [2] is a homozygous recessive disorder affecting the growth of cartilage and bone in sheep. The name derives from the limbs of afflicted animals being thin, elongated, and "spider-like". [3]
It is a semilethal trait, [4] which is thought to have been first observed in the 1970s, [5] and is most common in sheep of the Suffolk and Hampshire breeds. [6] These are both black-faced breeds of sheep; the syndrome has never been detected in white-faced breeds. [7]
The syndrome was an economically significant issue for sheep breeders in the 1980s, [8] but with strict testing and breeding programs it has become less common. [8]
The mutation which causes spider lamb syndrome is found on ovine chromosome 6, [9] and involves the inactivation of fibroblast growth factor receptor 3. [10] It has been compared to dwarfism in beef cattle. [7]
Afflicted animals may be visibly deformed at birth and unable to stand, or seemingly normal for the first 4 to 6 weeks of their lives. [4]
Symptoms have been observed on fetal lambs as early as by the completion of the second gestational trimester. [11] Under normal production circumstances, the lambs usually do not survive past the neonatal period. [12] For this reason, the disease is considered semi-lethal. [4] The disease typically affects the musculo-skeletal system. [12] The clinical signs can include: skeletal abnormalities, twisted or humped spines, facial defects, bent legs, abnormally long legs, flat ribs, and underdeveloped muscles. [4] Due to these symptoms, lambs cannot stand to nurse. [12]
Spider lamb syndrome is untreatable, and in almost all cases, the lambs must be euthanized. [11]
Spider lamb syndrome is caused by a mutation to the gene for fibroblast growth factor receptor 3 (FGFR3), on ovine chromosome 6. [12] FGFR3 is in the tyrosine kinase receptor family and its function is to restrict the proliferation of cartilage at the growth plates of the long bones: [12] regulating ossification (the conversion of cartilage into bone), limiting skeletal elongation, and thereby ensuring that the limbs are the right length. [12]
Spider lamb syndrome, also known as spider syndrome [1] and more formally as ovine hereditary chondrodysplasia, [2] is a homozygous recessive disorder affecting the growth of cartilage and bone in sheep. The name derives from the limbs of afflicted animals being thin, elongated, and "spider-like". [3]
It is a semilethal trait, [4] which is thought to have been first observed in the 1970s, [5] and is most common in sheep of the Suffolk and Hampshire breeds. [6] These are both black-faced breeds of sheep; the syndrome has never been detected in white-faced breeds. [7]
The syndrome was an economically significant issue for sheep breeders in the 1980s, [8] but with strict testing and breeding programs it has become less common. [8]
The mutation which causes spider lamb syndrome is found on ovine chromosome 6, [9] and involves the inactivation of fibroblast growth factor receptor 3. [10] It has been compared to dwarfism in beef cattle. [7]
Afflicted animals may be visibly deformed at birth and unable to stand, or seemingly normal for the first 4 to 6 weeks of their lives. [4]
Symptoms have been observed on fetal lambs as early as by the completion of the second gestational trimester. [11] Under normal production circumstances, the lambs usually do not survive past the neonatal period. [12] For this reason, the disease is considered semi-lethal. [4] The disease typically affects the musculo-skeletal system. [12] The clinical signs can include: skeletal abnormalities, twisted or humped spines, facial defects, bent legs, abnormally long legs, flat ribs, and underdeveloped muscles. [4] Due to these symptoms, lambs cannot stand to nurse. [12]
Spider lamb syndrome is untreatable, and in almost all cases, the lambs must be euthanized. [11]
Spider lamb syndrome is caused by a mutation to the gene for fibroblast growth factor receptor 3 (FGFR3), on ovine chromosome 6. [12] FGFR3 is in the tyrosine kinase receptor family and its function is to restrict the proliferation of cartilage at the growth plates of the long bones: [12] regulating ossification (the conversion of cartilage into bone), limiting skeletal elongation, and thereby ensuring that the limbs are the right length. [12]