Akabane virus is well recognised for its ability to cause arthrogryposis often leading to dystocia problems. These calves are also commonly called ‘curly’ calves. A commercial Angus breeder in the Mudgee district noted one of these calves in 2006 and then again in the 2007 calving season he had 3 such calves in his 2 & 3 year-old heifers and first calvers which had all been mated to the same bull.
The following article outlines the investigation of this and a number of other similar cases around the Mudgee/Merriwa district over the previous 2 years. This led to the discovery that these arthrogrypotic calves were the result of a genetic disorder, rather than from the actions of a teratogen or an infectious insult.
Case 1: Mudgee commercial herd, August 2007: A suspect Akabane calf was necropsied by me and samples were submitted to the RVL Orange. It presented with severe scoliosis of the neck and spine, forelimbs fixed in a flexed state and the hind limbs extended and intertwined from a narrow rump. There were no significant pathological findings in the brain or cervical spinal cord and serum samples from the dam were negative for Pestivirus and Simbu group antibodies. An image of case 1 appears below.
Case 2: Mudgee commercial herd, June 2008: 2 arthrogrypotic calves from heifers were presented to Mudgee Veterinary Hospital for investigation from the same owner as in case 1. No evidence of Akabane or Pestivirus was found by the lab. A list of plant teratogens or manganese deficiency were suggested as possible causes.
Case 3: Mudgee commercial herd, July 2008: The owner of the above 2 cases delivered another arthrogrypotic calf direct to RVL Orange. At this stage he had 7 such calves all born to 2 & 3 year-old cows. The necropsy was conducted by Laurie Denholm and a detailed examination of brain and spinal cord was made. A domed head with low set ears was noted and the brain had evidence of dilation of the lateral ventricles with fluid and thinning of the cerebral cortex. Testing again proved negative for Simbu group and Pestivirus. A genetic cause was considered likely and samples were taken for further testing.
Case 4: Cassillis stud, August 2008: A Coolah practitioner submitted samples for pestivirus exclusion following the delivery of an arthrogrypotic calf by caesarean section on an ET recipient cow carrying an Angus embryo. Two similar cases including one with a domed head in the same herd were also reported. The sample from the calf was PACE test negative.
Case 5: Cassillis stud, September 2008: A stillborn Angus calf with severe arthrogryposis, torticollis and scoliosis was picked up from the owners and sent to RVL Orange. It proved negative to pestivirus AGID, bluetongue ELISA and Simbu group ELISA. IgG (AGID) levels were elevated suggesting a possible infectious cause. An image of case 5 appears below.
Case 6: Rylstone stud, September 2008: At the request of Laurie Denholm, blood was collected from 4 of 5 dams that had delivered curly calves since July to exclude possible viral causes. This herd was the source of the stud sire used in the Mudgee commercial herd. The stud breeder had also confided to me that he had experienced two similar cases and emailed photos. An image of one of these appears below.
Case 7: Rylstone stud, September 2008: A live suspect case was delivered direct to Laurie Denholm for a detailed necropsy. An image of this calf appears below.
Case 8: Mudgee commercial herd, September 2008: An eighth calf with ‘curly’ calf syndrome was delivered to me and was taken to Orange for necropsy by Laurie Denholm. The sire was Patawalla A38, the same sire as for several other cases. Distortion of the domed head with low set ears was noted. The calf exhibited the scoliosis, torticollis and arthrogryposis seen in other affected calves. A defect in the hard palate was also observed.
I reluctantly pursued the investigation of this syndrome initially as it did not appear to fit core business once Akabane and Pestivirus were excluded. However the persistence of the commercial breeder who was starting to accumulate unacceptable losses was rewarded. Suspicions of a possible heritable cause of the arthrogryposis were strengthened further by reference to Veterinary Medicine 9th Edition, where arthrogryposis is recorded as heritable in Corriedale sheep and in some breeds of cattle. I recalled an AABP list in January 2008 regarding an arthrogrypotic case in the US where infectious, toxic and genetic causes were all postulated as a cause. I sent off an email on the 20-7-08 to this list with photos attached. On the 21-7-08 a similar distribution was made to the QAAHL list.
A debate followed with a report of similar cases in the north of NSW that were suspected to have been caused by infectious agents. The North Americans had progressed investigations through the actions of geneticist Dr John Beever. He replied to my email as follows. ‘As far as genetic cause, the case here is pretty compelling. For example, one of the breeders that I am going to visit next week has had between 6% and 9% of his calves (out of 400 1st calf heifers each year) for 2005, 2006 and 2007 that are affected. Using the same population of females, he used Hereford bulls last year and this year only had 4 defective calves from clean-up bulls used the previous year.’ Laurie also became convinced of a genetic aetiology after detecting the cleft palate defect in case 8. This affliction has now been rapidly characterised as an autosomal recessive heritable defect and has been called Bovine Heritable Arthrogryposis Multiplex Congenita (BHAMC or AM for short). The popular sire, CA Future Direction 5321, has been identified as an influential carrier within the Angus breed.
Genetic testing for the carrier state is now available and it is being used through the Australian Angus breed society. A list of carrier sires has been produced both in the US and in Australia. When cases of curly calf or arthrogryposis are encountered, a genetic cause should be suspected alongside possible viral and teratogenic agents, especially in Angus cattle. Due to a reliance on artificial breeding and a shift away from line breeding within studs which acted as a progeny test, we can expect many more genetic diseases to appear in our beef cattle as they have done in Holsteins.
Over the past few years a number of genetic diseases have been identified in Angus cattle apart from BHAMC. These include: Osteogenesis imperfecta (brittle bone disease) - probably autosomal dominant and; Fawn calf syndrome - autosomal recessive.
James Mort, Erika Bunker, Patrick Staples, Sandy Yeates, Sam Allan, Lisa Willis, Laurie Denholm, Graham Bailey, David Brennan, Phil & Wendy Morton, Mudgee Veterinary Hospital, James Cleland, Lisa Nivison, Coolah Veterinary Clinic, Lisa Martin, Peter Windsor, Jonathon Beever, David Steffan and Mudgee-Merriwa RLPB directors.