Spider Lamb Syndrome
Ovine hereditary chondrodysplasia
What is the disease? How does it present? Is it lethal?
Because the disease is characterized as simple autosomal recessive and all lambs afflicted by the disease will never reach sexual/breeding maturity, the only way this disease can be passed on is if both ram and ewe are carriers. In other words, both parents may have a "normal" phenotype but if both have a heterozygous (Ss) genotype, there is a 1/4 (25%) offspring will be homozygous recessive (ss) with spider lamb syndrome phenotype.
1) Lambs are abnormal at birth, unlikely to ever stand; OR
2) Although lambs appear normal at birth, structural abnormalities gradually appear between 2-6 weeks.
- facial defects, e.g. roman nose
- humped/twisted spines
- abnormally long legs, often twisted or splayed (hence "spider legs")
- flattened ribs
- underdeveloped musculator
At this time there is no treatment. Individuals afflicted with this syndrome are homozygous recessive and rarely survive; therefore SLS lambs have no breeding value and are an economic liability. Due to the progressive malformation of the skeletal and musculatory systems, animals with SLS must eventually be destroyed.
Check out the video below for a heart-melting look at Gitta, the precocious spider lamb!
Is Spider Lamb Syndrome Preventable?
If genetic testing is not an option for breeders, breeding records (including progeny information) and pedigrees can be used to lessen the incidence of mating two carriers.
- Mutation probably first occured in the late 1960s and was proliferated in breeding stock that was popular for its production and show-ring performance.
- Structural abnormalities are thought to be the result of highly disorganized, nonparallel coumns of chondrocytes in the growth plates.
- Although suspected carriers are actively culled from flocks, frequency of SLS remains relatively high.
- Researchers are studying positional cloning of the gene responsible for SLS with the goal of fully eliminating the recessive allele.
- Not all lamb structural deformities are due to SLS. This is why it's important to perform postmordem evaluations and test breeding stock.
- SLS has a human chromosomal equivalent at the 4p16.3 location.
2) Suppose you had a flock of sheep and year after year a significant percentage of lambs are born with spider lamb syndrome. What steps would you need to take to prevent future instances of the disease?
3) Currently spider lamb syndrome has been observed in several breeds of sheep in the US, Canada and Australia--but not Europe. Is it possible for European shepards to prevent spider lamb syndrome from even occuring in their flocks? Why or why not? What steps would need to be taken?
N.E. Cockett, T.L. Shay, J.E. Beever, D. Nielsen, J. Albretsen, M. Georges, K. Peterson, A. Stephens, W. Vernon,O. Timofeevskaia, S. South, J. Mork, A. Maciulis, T.D. Bunch (1999)
Localization of the locus causing Spider Lamb Syndrome to the distal end of ovine Chromosome 6, Mammalian Genome, 10:1, 35-38
SJ O'Brien, M Menotti-Raymond, WJ Murphy, WG Nash, J Wienberg, R Stanyon, NG Copeland, NA Jenkins, JE Womack, JA Marshall Graves (1999) The Promise of Comparitive Genomies in Mammals, Science, New Series, 286:5439, 458-462 + 479-481
KG Thompson, HT Blair, LE Linney, DM West & T Byrne (2005) Inherited chondrodysplasia in Texel Sheep, New Zealand Veterinary Journal, 53:3, 208-212
Linked references available below: