Genetics the good the bad and the ugly...

[jaimiediamond]

So I admit to amusing myself on a slow day at work by reading posts and sometimes even seeing fit to comment.  I have heard back from a lot of great cattle people some with similar views and a lot with different views.  When it comes to any animal operation there will always be different opinions, feelings, and results in situations.  With that said I do feel there is one situation we all should if not agree on be fully aware of and educated about.  This situation is genetic defects.    I have listed a few that I am aware of and I would like to invite other cattle breeders to list ones that they know and I have missed and perhaps pictures .

Tibial Hemimelia commonly known as TH shows the  affected limbs are short and twisted, with fused joints.  Calves also have large abdominal hernias, an abnormally hairy coat, and deformed skulls.  If an affected calf survives birth, it is unable to stand to nurse and should be destroyed. This is a recessive defect which simply means that if a TH carrier is bred to another TH carrier there is a 50% chance that calf born will be a carrier 25% chance it will be free and 25% chance it will be the lethal fatal.  TH is now affecting not just Shorthorns but also Simmentals.  In the 1960s the Galloway breed eliminated this defect by mating suspected carriers together.

Pulmonary Hypoplasia with Anasarca commonly known as PHA is a lethal genetic condition caused by a recessive mutation. PHA-affected calves are born dead with underdeveloped lungs (Pulmonary Hypoplasia) and swelling caused by excessive fluid retention (Anasarca).  These calves are generally so large (over 200lbs) that a C Section is required to deliver them.  Again this is a recessive defect which simply means that if a PHA carrier is bred to another PHA carrier there is a 50% chance that calf born will be a carrier 25% chance it will be free and 25% chance it will be the lethal fatal. This defect affect multiple breeds at this time

Hypotrichosis or hairlessness occurs in several breeds of beef cattle. It expresses itself as complete or partial loss of hair. Calves are often born with no hair but will grow a short curly coat of hair with age. Affected individuals are prone to environmental stress and skin infections are more prevalent. Again this is a recessive gene.

Alopecia Anemiais a syndrome has recently been identified in the Polled Hereford breed. At the time of birth, alopecia anaemia may be mistaken for hairlessness. Affected calves are often small at birth, have a dirty-faced appearance, and have protruding tongue and eyes. Hair is wiry, tightly curled or absent while wrinkled skin gives the appearance of advanced aging. Calves are lethargic, cannot tolerate stress and are very prone to disease. Few survive past six months of age. Malfunction of the skeletal structure results in reduced red blood cell production (anaemia). Alopecia anaemia occurs in families but the exact mode of transmission is unknown.

Beta-mannosidosis  The result is the birth of calves that never get up and eventually die. The syndrome occurs in the Salers breed and a blood test is available for identifying carriers.The Beta-man disorder is due to a recessive gene that produces a defective enzyme.

 

[hntwhitetail]

Good post.

 

[BLRanch]

Nice post, very helpful.  (thumbsup)

 

[aj]

Do Trakehneres have any know genetic defects?

 

[OH Breeder]

Do Trakehneres have any know genetic defects?

Trakehner? Warmblood?
http://www.americantrakehner.com/Regulations/RegsP2.htm

Most of the stallions go through vigorous inspection. I use to ride dressage and encountered lots of the warmbloods and other european lines. AJ you taking up new sport?

 

[garybob]

What about water-head, curly-calf, fawn calf, snorter dwarf, long-nosed dwarf, mulefoot, and marble bone in Angus cattle?

Anybody listening? Hellooooo...............

GB

 

[aj]

Do Treckies like Trakehners?

 

[knabe]

What about water-head, curly-calf, fawn calf, snorter dwarf, long-nosed dwarf, mulefoot, and marble bone in Angus cattle?

Anybody listening? Hellooooo...............

GB

GB, didn't you get the memo?  angus are the defect free breed.

 

[Okotoks]

What about water-head, curly-calf, fawn calf, snorter dwarf, long-nosed dwarf, mulefoot, and marble bone in Angus cattle?

Anybody listening? Hellooooo...............

GB

GB, didn't you get the memo?  angus are the defect free breed.

The following is an article on one of the Angus genetic defects. Each breed seems to have one or more genetic defects or have had one and eliminated it. Probably makes sense that the Angus has so many as they have the biggest population.

Here is the link to The High Plains/Midwest Ag Journal article and a copy of the article
http://www.hpj.com/archives/2009/apr09/apr27/Anothergeneticdefectaffects.cfm
Angus breeders will have another management challenge for the coming breeding season, as another genetic defect has been identified among certain pedigrees.

On April 13, the American Angus Association released the identity of preliminary test results for Angus bulls to determine whether they are carriers or free of the mutation identified for severe hydrocephalus.

University of Illinois researcher Dr. Jon Beever and Dr. David Steffen of the University of Nebraska are now referring to the genetic defect as Neuropathic Hydrocephalus (NH).

With the increase in the number of abnormal calves being reported, Drs. Beever and Steffen have seen an increase in cases other than the previously discovered defects, which has led to the discovery of NH, as well as others.

"NH calves are born near-term and have 25 to 35 pound birth weights. The cranium is markedly enlarged--volleyball to basketball sized. The bones of the skull are malformed and appear as loosely organized bony plates that fall apart when the cavity is opened. The cranial cavity is filled with fluid and no recognizable brain tissue is evident. The spinal canal is also dilated and no observable spinal tissue is found," said Dr. Steffen.

Recessive disorder

NH is a recessive defect just as the previously identified disorder arthrogryposis multiplex (AM) is.

NH would be described in a similar way to how AM has been described by the Angus association. If an animal is homozygous for the normal variant (called an allele) they are referred to as NH-free (NHF), indicating that they have been tested for the causative mutation and been found "free" of the mutation.

If an individual is found to be heterozygous, or a "carrier" for the mutation--meaning they possess one normal allele and one mutant allele--they are referred to as an NH-carrier (NHC).

Although affected calves are rarely tested, they would be homozygous for the mutation and referred to as NH-affected (NHA). Using the known genetic information from two animals, a breeder can determine the chances of having an affected calf, according to Dr. Beever.

Tested list

After the release of the list of highly used A.I. (artificial insemination) sires who were tested for AM, the same group of A.I. companies requested that the Angus association provide to the membership the identity of and preliminary test results for Angus bulls tested by Dr. Beever to determine whether they were carriers of the NH mutation or were free of it.

The two lists have many of the same bulls on them but, after the release of the AM carriers and non-carriers, a couple hundred more bulls were added for testing, according to Dr. Beever.

While some bulls may show up positive for both AM and NH, the two defects are not linked at all.

"The genes are on different chromosomes, so they segregate independently. This means that from specific matings you might expect a predicted number of carriers for one, carriers for both, or carriers for neither," he said.

Dr. Beever explained if the normal NH gene is "A" and the defective gene is "a," mating a carrier bull with the genotype Aa for the NH gene to a carrier cow also with the genotype Aa for the NH gene will result in three calves that look normal at birth, but two of the three will be carriers for NH (Aa). The fourth calf will be born with NH (aa). Thus, mating two carriers gives a breeder a 25 percent chance of having an NH calf.

Mating a carrier bull or cow to a non-carrier cow or bull will result in 50 percent of the calves being NH carriers (Aa). A non-carrier would have the genotype AA.

More information

While there are other forms of hydrocephalus, this particular form of hydrocephalus only occurs in Angus-based cattle because the founder animal is Angus. Dr. Beever pointed out that other breeds have Angus genetics in them, so they may also be affected by NH.

"There are also other forms of hydrocephalus in other breeds, Shorthorn and Hereford specifically," he said. "However, it is important to remember that the genetic etiology is not going to be the same.

Since each genetic defect is a little different, the information he collects about each varies a well. "We estimate based on allele frequency and number of affected calves reported that there is a relatively high fetal mortality rate, potentially upwards of 70 percent," he explained. "This is consistent with the mouse data where 100 percent of homozygotes die before term."

Breeder cooperation

Dr. Beever and the Angus association would like breeders to continue to cooperate by submitting samples of calves showing any forms of genetic defects.

While Dr. Beever has developed a test for NH, it is not available commercially as of press time, he expects it to be available in the next few weeks.

To further the research on NH and other conditions, breeders are urged to report any suspected genetic defected calves immediately when they are detected, so that samples can be obtained on calves for study. Calves can be reported to Don Laughlin ([email protected] or 816-383-5140) at the American Angus Association, who will make arrangements for them to be shipped to Dr. David Steffen at the University of Nebraska for examination. DNA samples of the affected calves should go to Dr. Jon Beever at the University of Illinois.

For current information on all genetic defects affecting Angus cattle, visit www.angus.org.

Jennifer Bremer can be reached by phone at 515-833-2120 or by e-mail at [email protected]

 

[jaimiediamond]

Do Treckies like Trakehners?

Known carrier horses are listed online.   For example my QH mare she has her genetic test results as well as he parents genetic tests (she goes back to Impressive). So her papers state HYPP Negative. I think the horse people (this is all breeds) as Arabians do the same with there genetic defects as well as all of the Warmblood associations that make the information readily available. Which in turn has limited and basically solved the horse genetic problems. There are genetic defects but those involved don't breed to carrier sires or mares there are too many good animals to take such risks.  But Aj back on topic I was talking about cattle defects... Here is a link that could help people out, it has pictures and everything.  Excellent reference material just a note for those who don't like reading it is a few pages. http://www.appliedreprostrategies.com/pdfs/3-1_Whitlock.pdf

 

[Okotoks]

Here is an article on Curly Calf. It's important to note that by testing you can keep the good genetics and still elimante the problem and move on with clean bloodlines from the carrier animal. In the Belgium horse breed they had a genetic defect they had to manage carefully because of their small genetic base. It all comes down to management and being concerned about the implications.
Here is the link to the article from Beef Magazine Dec. 2008.
http://beefmagazine.com/genetics/1201-curly-calf-issue/

Listening to the rhetoric surrounding the September announcement that Arthrogryposis Multiplex (AM) — a lethal genetic defect also known as Curly Calf — had been discovered in Angus cattle and was likely tied to one of its most used sires, you'd have thought the end of the world was at hand.

“It created a hysteria I'd never seen before among some seedstock producers,” says Mark Gardiner of Gardiner Angus Ranch (GAR), Ashland, KS. Evidence indicates the genetic disorder stems from a bull the Gardiners bred and raised named GAR Precision 1680; actually it goes back to that bull's maternal grandsire 9J9.

According to Precision 1680's performance record from the American Angus Association (AAA), nearly 10,000 direct sons and daughters are part of the breed's genetic evaluation. Multiply that by a likely factor of 30 or 40 and you start to grasp the number of descendents this bull has spawned within the breed.

Precision 1680 was one of the first Angus sires to bend the genetic curve, providing low birth weight but superior weaning and yearling growth. Born in 1990 and deceased for a decade, his progeny continue to be favorites of seedstock and commercial producers. He's stacked five and six deep in some pedigrees.

Every breed, every species, every individual contains recessive genes. Those genes are seldom expressed, however, and thus rarely known about, except for the most abominable luck.

In the case of Precision 1680, it was inadvertent propagation. His genes were being multiplied and magnified because of his genetic merit; no one knew he also carried the recessive gene for AM. In other words, you're not likely to uncover problems in bulls used for a season or two and then discarded by the industry.

The initial emotional reaction was understandable, stoked by past episodes with genetic recessive disorders like Snorter Dwarfism, which decimated entire herds and lines of Angus and Hereford cattle in the 1960s, or Mule Foot in the late 1970s. In the last two decades, no fewer than six of the most heavily utilized breeds have had to contend with genetic recessive disorders.

In those days, the only way to determine if an animal possessed the recessive gene in question was to line-breed him and try to create problems. With the DNA test for AM, producers can identify noncarriers within the affected line of cattle and use them without fear of propagating the recessive gene.

DNA test near completion
In March 2007, AAA received notice of a handful of calves born dead with bent and twisted spines, the phenotypic expression of AM. Necropsies and some of the calves were sent, at AAA's request, to David Steffen, a University of Nebraska DVM and a longtime consultant to AAA. He was unable to determine the cause as environmental, genetic or due to viral infection.

In April 2008, another nine calves with a similar condition were reported. Based on Steffen's recommendation and growing belief the abnormality was genetic, AAA alerted members on Sept. 5 and requested they report any problems consistent with AM. By Sept. 15, AAA received verbal and written reports on another 48 calves.

AAA then issued notice that the cause was likely due to a lethal genetic defect, via a simple mode of inheritance, and likely stemmed from Precision 1680. Jonathan Beever, University of Illinois molecular geneticist, was also working with AAA and Steffen and has shouldered developing a DNA test to identify AM carriers.

The Gardiners first encountered AM in 1991. That was a potential diagnosis provided by renowned Kansas State University geneticist Horst Leipold, when the Gardiners brought a stillborn calf to him that had a bent and twisted spine.

Since then, the Gardiners have bred and raised about 27,000 calves. Eleven were stillborn and anatomically abnormal; six had no Precision in their pedigrees. The veterinarians and researchers consulted determined the likely cause was environmental or disease-related.

It wasn't until August 2008 that Beever told the Gardiners he believed the cause was AM and likely stemmed from Precision. The Gardiners quickly provided semen and DNA on Precision descendents. More analysis was done.

By Nov. 3, AAA provided members a list of AI sires and their AM genotypes. Beever also enlisted the help of bull studs to help validate the DNA test via the sires they represent. They understandably wanted to know as much as possible as soon as possible to inform their customers.

All told, 761 Angus sires were tested; 60 bulls turned up carriers, all directly related to Precision 1680 and 9J9. That 8% says nothing about the actual gene frequency within the breed. Anecdotally, however, it suggests the gene isn't nearly as pervasive as some may have feared.

By Nov. 3, confidence was running high that a commercial test would be available within 45 days.

“With DNA technology, we've gone from not having a test two months ago, to having the tool we need to manage this deleterious gene,” says Doug Frank, ABS global beef product manager.

Managing with Curly Calf
The simple mode of inheritance associated with AM thus far, and the test for it, mean the condition is easily managed, especially for commercial users.

Many are familiar with coat color in Angus as an example of how the simple mode of genetic inheritance works. Red is recessive and black is dominant. If a calf receives the gene for black from one or both parents, its coat color will be black. In order for the animal to be red, it must inherit the recessive gene (red), from both parents.

So it appears to be with AM: the animal must receive the recessive AM gene from both parents to be afflicted, though inheriting the recessive gene from one parent makes the calf an AM carrier (see “Curly Calf genetics”).

“If I'm a commercial producer and I haven't line-bred, my risk is essentially zero,” Gardiner says. In other words, the odds of mating a carrier bull to cows that are also carriers is extremely low. For commercial producers mating Angus bulls to cows of another breed, or vice versa, there is no risk, even if the Angus being used is a carrier.

For seedstock producers, it's a matter of knowing the AM status of their genetics and those they intend to use. It's also a matter of understanding AAA preliminary guidelines regarding registration of AM carriers and noncarriers.
Briefly, AAA won't suspend or revoke registrations of currently registered cattle based on their AM status. Calves born out of currently registered Angus cattle that are AM carriers must be tested to be eligible for registration; registration certificates will reflect their AM status.

Beginning Jan. 1, all calves born from currently registered Angus cattle that are AM carriers must be tested; only AM-free calves from those matings will be eligible for registration. AI-sired calves won't be eligible for registration if conceived more than 60 days after an AI sire is announced to be an AM carrier.

“ABS' desired policy is full testing, full disclosure and let the market decide. We certainly would not promote the use of carrier bulls but would encourage breeders to look at the total genetic merit of carrier bulls and females and how they fit into their breeding program,” Frank says, explaining how the industry has approached other breeds that have carried genetic recessives.

“After all, control is black and white and it's much easier using today's DNA technology to manage a simple recessive to have zero negative economic effect than it is to avoid the negative economic impact of other traits like reduced performance, excessive birth weight or poor feet and legs,” Frank says.

A new model

In an industry often driven as much by emotion as market logic, the Gardiners' most recent sale serves as a refreshing example of the common sense being leveled at AM and the line of cattle it apparently stems from. The Gardiners' fall bull sale was Sept. 29, when AM emotion was running hot. They sold 214, 18-month-old bulls for an average of $4,620 — $500 more than the previous year.

The Gardiners did provide the carrier probability of each bull. But the success likely had more to do with the relationship they've developed with customers and their reputation for standing behind their cattle.

Such commonsense buying also has plenty to do with the confidence spawned by the rapid and transparent response of AAA, its members and the Gardiners to attacking the problem.

In fact, the response of the breeder, the breed and science to AM provides a new model for the industry to use in addressing future genetic recessive issues.

 

[Show Heifer]

Did beef mag get that article from the aaa? Seems they missed a few very good details.... sun shining on crap is still crap.

 

[jaimiediamond]

Did beef mag get that article from the aaa? Seems they missed a few very good details.... sun shining on crap is still crap.

Perhaps if it is crap you should enlighten us.  I opened this thread to find out more about genetic defects out of curiosity and I am sure others would like to hear what you know

 

[Okotoks]

Did beef mag get that article from the aaa? Seems they missed a few very good details.... sun shining on crap is still crap.

Actually it seems like you are the one missing a " a few very good details......". When you post something like that without details you imply wrong doing but don't really substantiate or even indicate why you have this knowledge that you don't want to share.
So are you talking cow crap or donkey dung................

 

[Show Heifer]

gardiners are famous for linebreeding... have done it for decades.  This has been discussed and cussed many times before... do some research if your interested. So instead of me spoon feeding the information, I think its kinda fun to "seek and find", don't you? ..... crap is crap, even if the sun is shining on it!  <beer>

 

[Torch]

May be a dumb question but is line breeding bad?

 

[Okotoks]

gardiners are famous for linebreeding... have done it for decades.  This has been discussed and cussed many times before... do some research if your interested. So instead of me spoon feeding the information, I think its kinda fun to "seek and find", don't you? ..... crap is crap, even if the sun is shining on it!  <beer>

Well the article did state that the bull showed up many times in some pedigrees. It also said the diagnosis at first was not genetic! I have had that experience myself when I took a calf in that was TH,this was before I had ever heard of it and the diagnosis was developmental.I guess I don't understand why some people on here want to dump all over people because they have not done their research. Some one on one thread was asking about calves out of Boardwalk and got dumped on because the bull wasn't old enough to have calves. Well why not just post that? I spend too much time on here as it is, I certainly don't have time to research every thread or breeding program especially if it's not my breed. I come on here to learn ,to share and hopefully have a laugh while doing it!
<beer>

 

[Okotoks]

May be a dumb question but is line breeding bad?

That's actually a good question that will get you many different answers! I like to linebreed to fix a type but if there is a recessive gene that is bad you will get it expressing itself.(bad could include a recessive lethal or just a trait you don't want) If you select the good ones and discard the poor ones you can fix some of the traits you want. Before genetic testing linebreeding was the only way to eliminate recessive lethals. Breeders would breed a bull back to a group of his daughters to ensure he was not a carrier. When you think of the time that would take genetic testing is a pretty inexpensive option.
When the Shorthorn breed was getting started the Collings linebred to fix type as did Bates, Booth, Cruikshank and a lot of other early breeders. When linebreeding ran into trouble is when others would only breed their Bates to Bates or Cruickshank to Cruikshank. They never actually took the time to see that those early breeders did introduce outcrosses.

 

[justintime]

Linebreeding is not bad, if you are willing to accept the fact that you may get some cattle that will have to be discarded because of the reasons Okotoks gave. The cattle you like from a linebreeding situation should be animals that will breed a truer type and more consistent calf crops. Whether you will ever get a premium for going to all this work is another question. It seems to be working somewhat with some of the Trump lines, but it gets cussed as much as it gets praised.. depending on who sees them. Cattle that are intensely line bred usually work very well with an outcross bloodline when it is introduced.

 

[advocate]

Linebreeding is why tim ohlde is famous