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| Department of Dairy Science University of Wisconsin-Madison |
National Association of Animal Breeders |
Don’t Fear Genetic Defects like CVM . . . Manage Them!
It seems like every time we turn around there’s another genetic defect to worry about. In Holsteins, we’ve confronted Mule Foot, BLAD, and several lesser defects over the years. Now we’re faced with CVM, an undesirable genetic recessive discovered by Danish scientists that seems to cause stillborn calves, abortions, and early embryonic losses.
Why does it seem like we’re finding these genes at an ever increasing rate? The main reason is that advances in molecular biology have allowed scientists to identify a genetic basis for many problems that were previously attributed to bad luck or poor management. For example, we learned a decade ago that BLAD was responsible for the deaths of some calves shortly after birth, and we’re now finding that CVM seems to be responsible for some of our embryonic losses, abortions, and stillbirths.
Just as we’re better equipped to identify genetic defects today, we’re also better equipped to control them. The strategy for controlling such disorders is two-pronged. First, we need to limit the economic impact of CVM on the farm by avoiding matings of known carriers, and second, we need to reduce the frequency of the CVM gene within the breed by aggressively testing DNA samples from proven bulls, young sires, and donor dams.
First, let’s concentrate on controlling economic losses due to CVM on the farm. It’s a lethal recessive, so in matings of two carrier animals, one-quarter of the offspring will be affected by CVM, one-half will be CVM carriers, and one-quarter will be non-carriers. Among the quarter of pregnancies that are affected by CVM, only a small proportion will result in full-term stillborn calves with deformities. Many will be lost early during the gestation period (such that the cow will simply return to estrus) and some will be aborted later during the gestation period. Fortunately, accurate genetic testing can easily distinguish bulls that carry the CVM gene from those who don’t. Because all of the major AI studs are currently testing the bulls in their lineup for CVM, farmers will be able to obtain a list of the carriers and non-carriers from each organization. Most producers will not spend the time and money to test individual cows for CVM, and it’s not really necessary anyway. It’s easy to identify cows that are likely to be carriers by checking to see if their sires and/or maternal grandsires are known carriers. Then it’s simply a matter of avoiding service bulls that are known carriers when selecting mates of cows that are likely to be carriers as well. Managers of small herds can just inspect the pedigrees of individual cows and their potential mates, but managers of large herds may need to develop a spreadsheet program to identify problem matings or encourage their semen supplier to provide a mating program that considers CVM status. This strategy can greatly reduce the incidence of CVM on your farm. The following table shows the expected number of CVM-affected pregnancies, according to the percentage of cows in your herd that are CVM carriers, if you don’t make any effort to control CVM.
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Expected Number of Embryonic Deaths, Abortions, and Stillbirths due to CVM In Herds That Don't Make a Special Effort to Avoid the Mating of Carrier Animals | |
| Percent of Cows
in the Herd That are CVM Carriers |
Number of CVM Cases
Per 1000 Pregnancies |
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5% |
0.6 |
| 10% | 2.5 |
| 15% | 5.6 |
| 20% | 10.0 |
| 25% | 15.6 |
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Expected Number of Embryonic Deaths, Abortions, and Stillbirths due to CVM In Herds That Examine Pedigrees to Avoid the Mating of Known or Suspected Carriers | ||
| Number of CVM Cases Per 1000 Pregnancies | ||
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Percent of Cows in the Herd That are CVM Carriers |
Check if Cow's Sire is a Carrier |
Check if Cow's Sire or Maternal Grandsire is a Carrier |
| 5% | 0.3 | 0.2 |
| 10% | 1.3 | 0.6 |
| 15% | 2.8 | 1.4 |
| 20% | 5.0 | 2.5 |
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25% |
7.8 |
3.9 |
As shown in the table, if you avoid mating service bulls that are CVM carriers to cows whose sires are known carriers, you can cut the frequency of affected pregnancies in half. You can again halve this frequency by checking whether or not the maternal grandsires of your cows are carriers. But don’t plan on avoiding CVM by switching to natural service bulls. These bulls are rarely tested for CVM or any other genetic defect, and heavy use of one or two carrier bulls in your herd could generate quite a few carriers and affected pregnancies.
Why not just avoid all bulls that carry the CVM gene? The main reason is that there is an opportunity cost in eliminating many of the breed’s top sire families from your breeding program. These bulls may carry many other beneficial genes that will help you achieve your breeding goal. So don’t panic, you’ve been using bulls that carry CVM and other “yet to be discovered” defects for years, and now you have a chance to control the impact of one of these genes through DNA testing. Besides, in just a few years, the number of AI bulls that carry the CVM gene will be minimal, as explained in the next paragraph, so don’t worry too much about creating a few more cows that are carriers of the defect.
Now, let’s review the role that AI studs can play in managing CVM and other undesirable genetic recessives. Every young bull that enters an AI stud is subjected to a battery of genetic tests, and young bulls that are recognized as carriers of a defect are typically culled prior to distribution of their semen to progeny test herds. However, the financial investment is quite large once a bull has been sampled, and very few AI studs will cull “sires in waiting” or elite proven sires. This means that the frequency of CVM among proven bulls will decrease rather slowly over the next three years. But once the young bulls that have been screened for CVM enter the proven lineup, the frequency of carriers will decrease dramatically. Then it’s only a matter of time until the frequency of CVM in the cow population also decreases to a negligible level. The following graph shows how the frequency of BLAD declined among US AI sires during the first few years after it was discovered.
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As shown in the graph, there were more than 150 BLAD carrier bulls born in 1988, but by 1991, only a handful remained. The pattern for CVM will likely be similar.
In summary, here are the key points regarding the control of CVM in your herd.
1) Don’t panic. Keep in mind that CVM is not new (it’s been around and undiscovered for decades), only the DNA test is new. Every animal carries some undesirable genes; we just haven’t found all of them yet. You’ve made good genetic progress in the past, in spite of genes like CVM, and you’ll do even better in the future as modern genetic tools allow us to identify and eliminate these defects from the breed.
2) The key to limiting the impact of CVM in your herd is to avoid mating service bulls that are known carriers to cows whose sires or maternal grandsires are also carriers. If you don’t routinely record sire identification in your herd, this is yet another good reason to start doing so immediately. And remember that natural service bulls are not usually tested for any genetic defects, so you’re much better off using AI bulls that have been thoroughly screened for such disorders.
3) The key to eliminating genetic defects like CVM is widespread testing of young bull calves when they enter AI progeny testing programs, and this testing is already underway. In just a few years, this strategy will decrease the frequency of CVM in the Holstein breed to a negligible level.
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National Association of Animal Breeders PO Box 1033 Columbia, Missouri 65205 |
Tel: (573) 445-4406 Fax: (573) 446-2279 Email: naab-css@naab-css.org |