Congenital contractural arachnodactyly in cattle

Congenital contractural arachnodactyly (CA) is a non-lethal autosomal recessive genetic disorder in cattle.^[1] An autosomal recessive defect is a disease caused by the presence of two recessive mutant genes on an autosome.^[2] CA is classified as a heritable disorder of connective tissue, specifically a disorder of the endomysium and perimysium. The defect in the muscle connective tissue results in a reduced range of elastic extension. CA is also known as 'Fawn calf syndrome'. CA is predominately associated with Angus cattle, however it has also been detected in other Angus associated breeds such as Murray Greys. CA was first identified in Victoria, Australia in 1998. However, it has now been discovered in many other countries. CA calves are almost always born alive, most being able to walk and suckle on their mother's teat leading to their survival in the early stages, although around 20% of CA calves die soon after birth. Differences in phenotypes are not normally noticeable and the weight of new born CA calves are seen to be normal, this means that CA is not always recognised.^[1] CA is caused by a specific error in the DNA. This means it can be passed on from parents to offspring. Any cattle known to carry any category one genetic condition such as CA cannot be registered with cattle societies. The carriers of category 1 defects are all identifiable in the Australian Angus database. CA calves that survive are exposed to joint dislocation and early onset of arthritis. This is a result of their flexible joint laxity. Although CA is not as severe as other genetic diseases in cattle such as Mannosidosis (MA), Arthrogryposis multiplex (AM), CA is nonetheless a cause of calf deaths in herds where prevalence of the CA mutation in the herd is high and carrier sires are still being used.^[3] Diagnosis of CA can be made with a physical examination of new born calves. This should be done in the first 24 hours after birth, preferably done by a veterinarian or experienced breeder. Despite the variations between severe and non-severe cases, CA is easily diagnosed in a live new born calf. Both males and females can be affected. The following symptoms are observed: congenital proximal limb contracture, congenital distal limb hyperextension, congenital kyphosis and significant postnatal improvement in these clinical signs as the calf grows and matures. CA is not a difficult diagnosis however it requires careful physical examination of the calf followed by constant observation for improvement. Additional signs are present in the calves CA causes but can be more difficult to identify especially in mild cases. These include abnormal long leg bones resulting in a tall stature, loose jointedness, poor muscling and knee knocking . To prevent cattle being affected by CA, sires should be pedigree analysed to minimise the chance of the mutation. If CA is identified in a herd, other bloodlines which have tested negative for CA should be purchased. Some predominant Angus sires identified with CA are Rambo 465T of JRS, Te Mania Kelp K207, Bon View Bando 598, SAF 598 Bando 5175 and Boyd On Target 1083.^[3]

References

1. 1 2 Whitlock, Brian. "Heritable birth defects in cattle" (PDF). Department of Large Animals Clinical Sciences, University of Tennessee. Retrieved 2013-11-05. 
2. ↑ Charlier, Carole; Wouter Coppieters; Frédéric Rollin; Daniel Desmecht; Jorgen S Agerholm; Nadine Cambisano; et al. (2008). "Highly effective SNP - based association mapping and management of recessive defects in livestock". Nature Genetics. 40 (4): 449–454. doi:10.1038/ng.96. 
3. 1 2 1015, Prime facts. "Congenital contractural arachnodactyly in Angus cattle" (PDF). NSW Department of primary industries. Retrieved 1.11.13.  Check date values in: |access-date= (help)