Aberdeen Angus cattle breeders are currently coming to terms with the presence of two genetic defects in some of our cattle. This page is my personal attempt to explain the defects and their effect in simple terms, while exploring some of the implications as I proceed.
Arthrogryposis Multiplex (AM), also sometimes referred to as Curly Calf Syndrome (CCS), is a recessive lethal genetic defect. Being recessive, an animal may carry the defect without any physical sign, because it will also have a (dominant) good copy of the gene. But when two carriers are mated together there is a 25% chance of both parents contributing the defective gene to the calf, leading to its malformation and death, generally before birth. Half of the offspring of such matings would be carriers which appear normal and one quarter would be free of the defect and therefore never able to pass it on to their own calves.
The earliest tested carrier of the defect is US bred Rito 9J9 OF B156 7T26. If that bull appears in the pedigree of any of your animals, and the descent from him to your animal is not broken by a tested Arthrogryposis Multiplex Free (AMF) animal, your animal is a potential carrier of the defect.
The NZ Angus Association eventually provided information on its website about AM and its response to the defect.
Many NZ Angus have been tested and their test results are available on the NZ Angus database.
If an animal has come from US stock and has "pedigree unavailable" on that database, its details may be found in the American Angus Association pedigree database.
Neuropathic Hydrocephalus (NH) is a recessive lethal genetic defect. Being recessive, an animal may carry the defect without any physical sign, but when two carriers are mated together there is a 25% chance of both parents contributing the defective gene to the calf, leading to its malformation and death before birth. Half of the offspring of such matings would be carriers which appear normal and one quarter would be free of the condition and therefore never able to pass it on to their own calves. It appears to have originated in the US Bull GAR Precision 1680 (both of his parents test clear of the defect), born in 1980. He, and his widely-used son, C A Future Direction are both carriers of AM and NH.
Animals with the above-mentioned bulls in their pedigrees may carry both defects, either, or none. AM and NH are inherited independently, so an AMF result tells you nothing about the NH status of an animal. Many AI sires have been tested for NH, but the test is not yet available in this country and the results for bulls which are already tested are not yet being listed on the breed databases.
In New Zealand there were over 70 registered stud herds with potential carriers of AM and/or NH, around 35% of the registered breeding members of the NZ Angus Association.1
A check on half of the largest herds in the three largest regional groups of NZAA members (just over 1000 animals born in 2006) showed that 15% are potential carriers of AM (having an AMC ancestor) and just under 7% were at risk of carrying NH.1
There were over 2800 progeny of AMC and/or NHC animals in the NZ register (progeny of GAR Precision 1680, or those of the next generation down). Those cattle were born from 2002 – 2008. Large numbers of those will have been bulls sold into commercial herds. (The number of potential carriers will gradually reduce as some of the primary ancestors are tested Free of the defects, but those of Carrier parents will require individual testing.)1
Responsible seed-stock breeders will eliminate carriers of genetic defects from their herds, or, if they choose to keep some carriers because of their superiority in other respects, they will test all off-spring and only sell those which are tested free of the defects.
By ceasing to sell carrier bulls into the commercial population, the frequency of carrier cattle will gradually decrease, although recessive genes can reside in the population for generations if no testing is done to expose them.
If as a commercial breeder using Angus cattle you suspect or know you have bought stock of the affected family lines, you may have carriers in your own herd. To avoid the possibility of producing affected calves, you must therefore ensure you always use tested defect-free bulls over your cows and heifers, or bulls from unaffected family lines. If you have a particular desire to ensure there are no carriers in your herd, testing is a simple matter of submitting a tail-hair sample to a laboratory which is licensed to perform the appropriate test/s. Collecting a sample involves pulling about thirty tail hairs from your animal, so the roots of the hairs are pulled out, and putting them into a clean envelope. The tests currently cost around $50 (+ GST) per test per animal.
The NZ Angus Association did little to limit the problems caused by the presence of these defects in the wider Angus population. There was very little publicity about them and a high probability that information was deliberately kept out of the public arena.
Distressingly, in several two-year-old bull sales after the information was released, several studs sold tested carrier (AMC or NHC) bulls.
My personal view is that the only responsible path to take when one has tested a bull as a carrier is to eliminate him from the breeding population. One AMC or NHC cow will contribute one potential carrier progeny to the population each year, but a bull potentially creates upwards of twenty times that many carrier progeny in a season under natural mating conditions.
The probability of commercially-produced carrier cattle being mated with other carriers increases every year as the carrier population spreads and ages. The possibility of there being numbers of deformed calves about to be born this season, with assistance needed in many cases (AM and NH affected calves are reported to cause difficulty during calving) should be of concern to the NZAA. There is an opportunity now to give warning of the possibility of problems to anyone who has mated carrier (or potential carrier) cattle together, so that the affected animals might be more closely monitored during calving. That opportunity will be lost as soon as any farmer loses a cow which usually calves easily, during a calving which required assistance but didn't get it early enough, in a case which the NZAA could have predicted carried a higher than normal risk of problems.
NZAA officials maintain that they have provided adequate information to their breeder members, but I contend that the quality of that information is inadequate and that the spread of clear information should be wider, to include breeders beyond the membership who potentially have carriers of both disorders in their herds. Not every commercial bull buyer pays attention to pedigrees and while commercial breeders may be less likely than some stud breeders to practice deliberate line breeding, the potential for the mating of carriers is not negligible.
Does this mean Angus are bad cattle? No. Genetic defects are present in all populations. There are known defects in all the mainstream cattle breeds in this country. The advantage of knowing about the defects is our ability to avoid them or to breed around them. So, ask any breeder from whom you wish to buy cattle what genetic defects are known in his or her breed and specifically ask if they have been tested for in the animals you are interested in purchasing. Not all cattle require testing, because not all defects are present in all family lines, but your breeder should be aware of the possibilities in their breed and willing to discuss them openly.
Please feel free to contact me with comments or questions about this page or the information it contains.
Ruth Renner, June 2009 (updated April 2012).