Spider lamb syndrome

Overview

Spider lamb syndrome (SLS), also known as hereditary chondrodysplasia, is a genetic disorder that affects sheep, particularly those of the Suffolk and Hampshire breeds. It is characterized by skeletal deformities that give the affected lambs a spider-like appearance due to abnormally long, thin, and crooked legs. The condition is congenital, meaning it is present at birth, and it often results in severe physical abnormalities that are incompatible with survival.

Spider lamb syndrome has significant implications for animal welfare and livestock management. Affected lambs often die shortly after birth or are euthanized due to severe malformations and inability to stand or nurse properly. The syndrome is caused by a mutation in a gene that affects bone and cartilage development and follows an autosomal recessive inheritance pattern.

Causes

Spider lamb syndrome is caused by a genetic mutation in the FGFR3 (fibroblast growth factor receptor 3) gene, which plays a critical role in regulating bone growth and development. The mutation leads to uncontrolled cartilage growth and improper bone formation during fetal development.

The condition is inherited in an autosomal recessive manner, meaning that a lamb must inherit two copies of the defective gene (one from each parent) to develop the disorder. Sheep that carry only one copy of the mutated gene are asymptomatic carriers and can pass the gene to their offspring. Breeding two carriers increases the likelihood of producing affected lambs.

Symptoms

Lambs with spider lamb syndrome display a variety of skeletal and physical abnormalities, most of which are apparent at birth. Common symptoms include:

• Abnormally long, thin legs resembling spider limbs

• Flexural limb deformities (twisted or bent legs)

• Scoliosis (curvature of the spine)

• Kyphosis (hunched back)

• Facial deformities, such as a Roman nose or elongated facial bones

• Abnormal rib cage and sternum formation

• Inability to stand, walk, or nurse properly

The severity of the deformities can vary, but most affected lambs are weak, immobile, and unable to survive without intensive care. Many die within days of birth due to complications such as starvation, exposure, or respiratory distress.

Diagnosis

Diagnosis of spider lamb syndrome is typically made through clinical examination based on the characteristic physical features observed at birth. Additional diagnostic steps may include:

• Necropsy: Postmortem examination of affected lambs can confirm internal skeletal abnormalities and rule out other conditions.

• Genetic testing: DNA testing can identify carriers of the FGFR3 mutation, allowing breeders to make informed decisions and avoid carrier-to-carrier mating.

• Breeding history analysis: Reviewing pedigrees can help identify patterns of inheritance and track the presence of the mutation within a flock.

Because the syndrome is often lethal, early diagnosis and genetic testing are important tools in managing and preventing the condition within breeding programs.

Treatment

There is no cure or effective treatment for spider lamb syndrome. Management focuses on prevention through selective breeding and humane handling of affected animals. Key strategies include:

Supportive Care

• Humane euthanasia: Severely affected lambs are typically euthanized to prevent suffering, as most cannot stand, feed, or breathe effectively.

• Assisted feeding: In rare cases with milder deformities, bottle-feeding and supportive care may be attempted, although long-term survival is unlikely.

Preventive Measures

• Genetic testing: Identifying and excluding carrier animals from breeding programs is the most effective way to prevent the syndrome.

• Responsible breeding: Avoiding mating between known or suspected carriers eliminates the risk of producing affected lambs.

• Educational programs: Informing breeders and veterinarians about the risks and management of the syndrome helps reduce its prevalence in affected breeds.

Prognosis

The prognosis for lambs born with spider lamb syndrome is extremely poor. Due to the severity of their skeletal deformities, most affected lambs either die shortly after birth or are euthanized. There is currently no known therapy that can correct the underlying genetic defect or reverse the physical abnormalities.

However, the long-term outlook for controlling and reducing the incidence of the syndrome in flocks is promising with the use of genetic screening and informed breeding practices. By eliminating carrier animals from breeding programs, livestock producers can effectively prevent the occurrence of this debilitating condition in future generations.