Technical name: Congenital Contractural Arachnodactyly


  • First Identified in Victoria Australia in 1998
  • Traced back to four bull studs from the United States, Freestate Barbara 871 was the first identified carrier
  • Semen from A bull in Indiana, Freestate Barbara 871, shipped to Australia

Symptoms & Diagnosis in Newborns:

  • Contracture of the front limbs with decreased range of motion
  • Appearance of kyphosis or scoliosis with a long body
  • Tall and skinny appearing calf in Angus cattle - poor muscling
  • eat normally IF they can get to their mother
  • Connective tissue poorly formed within the skeletal system

* Similar to Marfan Syndrome in Humans

  • Degree of severity among calves may vary
  • Subtle Phenotype
  • Hyperextension of the hind legs (distal limbs)
Fawn calf syndrome in angus calves

Prevention & cure:

  • It is preferred not to breed carriers of FCS
  • There is a registry through the American Angus Association for carriers of FCS
  • There is NO cure - calves born with FCS can grow up to live normal lives and reproduce
  • Culling

Challenges in Production:

  • Calves born with FCS have less muscling in adulthood
  • Cannot be registered with the American Angus Association as breeding stock
  • Calves with FCS tend to have larger frames as adults
  • Survival rate for calves with FCS is much lower due to their inability to move around normally - even with their interest in food and eating
  • Possible reduction in meat tenderness
  • Predisposed to degenerative Arthritis as the calves age


  • Haplotype marker recently discovered in Australia (according to Windsor 2011)
  • ™Autosomal recessive in Angus Cattle
  • A recessive mutation on a single chromosome
  • –Not sex linked
  • –Caused by the deletion of 38,000 base pairs™
  • CAC - CA Carrier, has been tested and carries the CA mutation.
  • CAF - CA Free, has been tested and does not carry the CA mutation.
  • CAP - CA Potential Carrier, animal that traces to one or more confirmed tested carrier animals in its pedigree that have no intervening ancestors that have been tested free of CA. (according to the American Angus Association)


Breeding a homozygous dominant bull with a heterozygous carrier cow:

  • –50% chance of homozygous dominant offspring (or CA Free)
  • –50% chance of a calf that is a heterozygous carrier


If two cows that are heterozygous carriers are bred:

  • –25% chance of CA Free offspring (or homozygous dominant)
  • –50% chance of a calf that is a heterozygous carrier
  • –25% chance of a calf that is only CA affected (homozygous recessive)


After learning more about this genetic mutation, do you think genetic modification is a tool that can and should be used to help breeders prevent this mutation? Why or why not?


1. "Contractural Arachnodactyly Information." American Angus Association. 2016. Web 3 May 2016. https://www.angus.org/pub/CA/CAInfo.aspx

2. "Contractural Arachnodactyly Fact Sheet." American Angus Association. Oct. 2013. Web 3 May 2016. https://www.angus.org/pub/CA/CAFactSheet.pdf

3. "™Fawn Calf Syndrome in Angus Calves." Dir. Laurence Denholm. Youtube.com. N.p., 20 June 2008. Web. 3 may 2016.

4. Lundeen, Tim. "Genetic defect causing CA in cattle identified." Feedstuffs 16 Aug. 2010: 10. Business Insights: Global. Web. 3 May 2016


5. "Managing Genetic Defects in Beef Cattle Herds." Progressive Cattleman. Jan. 2016. web. 3 May 2016. http://www.progressivecattle.com/topics/reproduction/7138-managing-genetic-defects-in-beef-cattle-herds

6. Van Arsdall, Dan. "Contractural Arachnodactyly (Fawn Calf Syndrome)." Apr. 2016. Web 3 May 2016. http://calfology.com/library/wiki/contractural-arachnodactyly-fawn-calf-syndrome

7. Whitlock, Brian K. "HERITABLE BIRTH DEFECTS IN CATTLE."Appliedreprostrategies.com. The University of Tennessee, Aug. 2010. Web. 3 May 2016. <http://www.appliedreprostrategies.com/2010/August/pdfs/3-1_Whitlock.pdf>.

8. Windsor, Kessell & Finney. "Neurological diseases of ruminant livestock in Australia. V: congenital neurogenetic disorders of cattle." Australian Veterinary Journal. Vol. 89:10. pp. 394-401. Oct. 2011.