Fawn Calf

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phillse

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http://www.youtube.com/watch?v=PUt5fQ_3L20

Another possible genetic defect has showed up, and a picture of it is on youtube. The video was taken in NSW, Australia by Dr. Laurence Denholm in June of 2008.

I am not trying to stir the pot, I have never seen anything like this before.

I have a few guys/students who raise Angus cattle and am concerned about how this might affect them.

Is this going to be a problem in the US or is this isolated to Australia?

Anybody else seen this problem?

What do you guys think about it?
 

RD-Sam

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Looks pretty much identical to what I have been battling in breeding Chows. Causes of luxation at the patella joint are curved femors, which cause misalignment of the groove the patella rides in. Weak ligaments are another cause. Shallow patellar groove are another cause. It almost looked like there may have been a problem at the hip on that calf, but the video wasn't good enough to tell. Joint dysplasia is another problem I have been battling. Could be the calves whole problem is just weak ligaments, which will lead to degeneration of the joints.

It took decades of bad breeding practices to take it's toll on the Chow breed, but the breed is really taking a beating now, and it's hard to reverse all those bad years of breeding too.

What I want to know, is who is the suspect carrier that started the problem? You certainly would want to be careful of linebred animals from that carrier. I guess this is the downside to doing AI, if you never see the sire move, you never know for sure whether he is sound or not.
 

Brandonm22

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If you read the slides at the end of the movie, they say it comes from U.S. AI sires and can be traced to a cow in Indiana in 1976. I would like to have read more detail about which bloodlines have this. I have seen this before.
 

Brandonm22

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RD-Sam":18jocyb4 said:
I guess this is the downside to doing AI, if you never see the sire move, you never know for sure whether he is sound or not.

Actually, any sire that has passed a breeding soundness exam has been ruled "sound" by a vet.
 

brandonm_13

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Brandonm22":10ef80he said:
RD-Sam":10ef80he said:
I guess this is the downside to doing AI, if you never see the sire move, you never know for sure whether he is sound or not.

Actually, any sire that has passed a breeding soundness exam has been ruled "sound" by a vet.

Well, there are probably some vets that do not watch as closely as others. I've seen judges overlook animals because their handler was their friend. Of course the bull might not walk terribly bad in front of the vet. The bull might be keyed up in a high stress situation. If his body is tense, he will walk differently than when he is relaxed.
 

Brandonm22

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There can be room to disagree with a vet's judgement, and a "sound" bull may still have and pass on structural flaws to their progeny (and soundness has nothing to do with recessives a bull may or may not carry like AMC or fawn calf); but if a bull gets in any of the major AI stud's catalog a vet ruled him "sound".
 

RD-Sam

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I emailed them and asked what line or individuals they had naroowed it down to, if they respond I can let you know what they say if you want?
 

HerefordSire

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RD-Sam":1mclenq6 said:
I emailed them and asked what line or individuals they had naroowed it down to, if they respond I can let you know what they say if you want?

SMART! I would be interested in knowing. Thanks.
 

robert

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The word is that a genetic test for Fawn Calf Syndrome will be ready to go by the early part of March, DNA samples have been collected over the past several years since the Australians highlighted this defect. When the bulls / lines that carry this are announced it will be more devastating from a breeding point of view than AM (curly calf) because unlike the Precision cattle which were more terminally based (for a variety of reasons) the main sire that will be implicated in FCS has been very useful as a female sire, many AI bulls have him as a MGS, and a number of good breeding sons have also been in stud.

We observed a calf suffering from this defect several years ago and paternally (the dam was a commercial Angus cow) ties to the above cited bull.

There seems to still be some reluctance to accept the existence of FCS, partly because unlike AM it is a semi-lethal defect, meaning that calves that are able to nurse and grow stronger will eventually grow out though will still lack the substance and growth of unaffected herdmates.

The structural soundness / walking ability of a sire has zip to do with this defect, it appears from the Australian research to be a simply inherited recessive trait.

Naming the bull / bulls concerned at this point would likely invite a lawsuit, this was certainly the case when discussion of the potential sires involved was brought up on another chat site www.advantagecattle.com and there is a lot of information over there on this and other defects that folks might find useful.
 

sizmic

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I will also reitterate what Robert said about this being worse than AM. I also am not trying to stir the pot but this scares the heck out of me.

Sizmic
 

RD-Sam

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I can see it turning into a real problem if people try and cover it up, and even worse if they breed affected cattle. I just read an article about it and they don't think it is anywhere near as prevalent as AM. I also just had a calf out of one of the suspected sires and she was linebred on him, she is a great little calf. Of course with that line breeding she could be a carrier, and I will get her tested once they have a test.
 

Brandonm22

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The big problem with this "defect" is it just looks like a small, puny, unthrifty calf. I would suspect a nutrition/mineral problem if we did not know that there was a genetic defect here.
 

RD-Sam

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Brandonm22":2w2dpwsc said:
The big problem with this "defect" is it just looks like a small, puny, unthrifty calf. I would suspect a nutrition/mineral problem if we did not know that there was a genetic defect here.

You obviously didn't read all the material I read, and watch the videos. There are some serious structural problems with those calves, they weren't just small and puny. If I had a calf that wobbled around like that I wouldn't breed it regardless of what it looked like when it grew up.
 
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phillse

phillse

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RD-Sam":10789cvj said:
Brandonm22":10789cvj said:
The big problem with this "defect" is it just looks like a small, puny, unthrifty calf. I would suspect a nutrition/mineral problem if we did not know that there was a genetic defect here.

You obviously didn't read all the material I read, and watch the videos. There are some serious structural problems with those calves, they weren't just small and puny. If I had a calf that wobbled around like that I wouldn't breed it regardless of what it looked like when it grew up.

I agree this calf goes beyond small, puny and mineral dificiencies. This apears to be serious. That calf has major issues and to say otherwise would be to say TH, PHA, Mulefoot, Dwarfism, and AM (curly calf) are not geentic disorders and not serious.
 
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phillse

phillse

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robert":228eowv0 said:
Naming the bull / bulls concerned at this point would likely invite a lawsuit, this was certainly the case when discussion of the potential sires involved was brought up on another chat site http://www.advantagecattle.com and there is a lot of information over there on this and other defects that folks might find useful.

I think this may be best advice given on this issue. We do not need to name animals, we do not need to jump to conclussions of what pedigree's might be involved until hard evidence is collected by the American Angus Association. I do think that by having a nice clean discussion, about it being a real problem that needs further investigation could be of value in bringing a resolution. In other words forward this information on to you neighbors, friends and family raising Angus so they can be more informed and be aware of the sign and symptoms. By doing this we can hope to increase the materiall tested and get a genetic test for this disorder sooner rather than later.
 

Brandonm22

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phillse":2t1laqs3 said:
I think this may be best advice given on this issue. We do not need to name animals, we do not need to jump to conclussions of what pedigree's might be involved until hard evidence is collected by the American Angus Association. I do think that by having a nice clean discussion, about it being a real problem that needs further investigation could be of value in bringing a resolution. In other words forward this information on to you neighbors, friends and family raising Angus so they can be more informed and be aware of the sign and symptoms. By doing this we can hope to increase the materiall tested and get a genetic test for this disorder sooner rather than later.

I agree with all of that. That said, if I were buying Angus genetics into a registered herd in the next 60 days I would be on the phone, email, and talking to people face to face if I had to to try to find out who do they suspect of being carriers.
 

LoveMoo11

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That is really interesting, nothing I've ever heard of or seen. I am guessing they call it Fawn syndrome because of the way the calf walks? Like a fawn? Correct me if I'm not right.
 

robert

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The calves, if they do manage to get on their feet, look like a fawn, conformation wise. The calf I mentioned, when I saw it first at about 2 months of age, the owner of the animal even questioned whether the thing was sired by a whitetail buck, the mannerisms of the calf, alert ears etc certainly fit the description! Sloped plates, hind leg structure and set added to the shelly, tight gutted phenotype only reinforced the 'Fawn' designation.
 

J+ Cattle

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OK, it has been over two years since this thread was started and I doubt there has been much progress made into identifying the FCS carriers. As a commercial cattle producer looking for a new Angus bull what am I to do? What bloodlines should I avoid? I would like to keep heifers as replacements and realizing that this is a large investment in time and money to grow and develop them I do not want them to also be carriers. How is the beef industry helping to be a better producer and not just a multiplier of genetic defects?

J+
 

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