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More on Fawn Calf Syndrome

katrina

Well-known member
High Plains said:
Old Timer, in my opinion you are blowing a whole bunch of hot air on this one. You act as if a whole slew of Angus breeders, the Angus board of directors and association staff are really operating with criminal intent. Yeah, they all have a lot to gain by perpetuating problems in the breed. :shock: Your slanderous remarks are pitiful. The Connealy family that bred the "All Around" bull are good people. These are the people that you're trying to discredit here. What axe do you have to grind with them? Based on your comments, I'd say you've never even met them. But you're quick to unload both barrells. :roll: Do you think they've been successful due to dishonest practices? I don't see too many ranchers flocking to do business with dishonest people. :roll: They may not raise your kind of Angus cattle but they've raised some awfully good ones and they will continue. You probably blame them for what you call "ruining your cows" with the "bigger, better, faster" genetics that seem to have caused you trouble in the past. Well guess what, you're the one that turned the bulls out and nobody else. So get over it and take your own path if you didn't like the results. But since you're out picking fights with good people that are doing good things with the breed, I can't help but call you out on it. It makes no sense that they would actually want to have FCS or anything else in their genetics or their customers'. They wouldn't want to perpetuate it for one minute!! Take a step back and get some reality working for you. They'll handle their issues and move forward doing as good a job as they possibly can.

Crawl down off of your throne, oh King of Cattle. :roll:

:agree:
 
A

Anonymous

Guest
Well whats coming out is that the Australians, Australian Vets, and Australian Angus Association has been investigating some of these defects as far back as the 90's- as well as reporting it- and the suspected sires- to the AAA- the producers of those sires- and the bull studs....And some of the carriers they've found trace back to the 1970's...

The rumors have also ran rampant about genetic defects in some of these sires ( Future Direction comes to mind first) for years- altho noone knew what genetic defect as they knew nothing of these AM, NH, Fawn Calf.....Then 2-3 years ago some of the Australians started making public on the internet and chat sites these defects- altho still nothing came from AAA or the studs/producers....

Little of this really became public until a major Administrative change took place in the AAA...And Dr. Beever is working now and apparently very close to isolating the genetic marker for this defect too...

When were you first informed by the AAA or a major stud/producer of even the possibility of these defects... :???:

Was there a coverup by the AAA, bull studs, producers - its up to you to decide :???:

But to me it sure smells of what has taken over much of this countries business/corporate world-- GREED over ETHICS and MORAL responsibilty... :(

But some would rather stick their head in the sand and pretend these defects aren't occurring either-- if that better fits their agenda.... :roll:
 
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Anonymous

Guest
PATB said:
ABS did the right thing by anouncing that onward is suspected of producing possible FCS challenged calves. The AAA could take a more active roll investigating reported abnormal black angus calves and educating breeders of possible genetic challenges to keep a look out for.

For info--The AAA- besides listing all carriers- has started marking all pedigrees of those testing positive for AM or NH right by the registration number- (AMC/NHC) - and is putting the following statement on the registration of all those that have a positive ancestor in their pedigree and are potential carriers:

This animal has one or more ancestors known to carry a mutation that can result in calves with a genetic defect known as Arthrogryposis Multiplex (AM), or if applicable, Neuropathic Hydrocephalus (NH). The American Angus Association recommends DNA testing at an approved laboratory to confirm the absence or presence of the mutation.

This can not be removed until the animal is tested free of the defect...

I would imagine that as soon as they get the final test perfected for this Fawn Calf Syndrome, they will probably do the same.....
 
A

Anonymous

Guest
Another article by Dr. Denholm....

FAWN CALF SYNDROME (FCS) and FRAME SCORE

Frame score is a relevant issue in any discussion of FCS - simply because FCS affected cattle have a higher frame score than their unaffected siblings.

At birth, FCS affected calves have longer than normal leg bones (the technical terms are “dolichostenomelia” and “arachnodactyly”), as demonstrated in Australia by measurements taken on radiographic images of the long bones in whole body CATScans of newborn FCS affected calves and their normal siblings. This greater than normal length of long bones in newborn FCS calves is maintained until maturity, as shown by more recent frame score measurements taken on the same animals now that they are mature adults.

It is quite possible that at some time in the past, selection for higher frame score was a significant factor in increasing the prevalence of the genetic mutation that causes this recessive genetic defect in the Angus breed. Although FCS calves that are severely affected at birth have a very undesirable phenotype as adults (tall and poorly muscled with weak foot and leg conformation), there is a bit of variation in the clinical severity between cases, as newborns and as adults. At least some of the calves with less severe signs of FCS at birth end up as adults that look reasonably normal to the untrained eye.

In my own small FCS research herd, it appears that the calves that were most severely affected at birth have become the tallest adults. Moreover, whilst the two tallest FCS animals are always “hard doers” that can be distinguished from their unaffected siblings at any time of year and would be very unattractive animals in any breeding program, the other two FCS cows are less severely affected and, when they are in fat condition, it can be difficult to distinguish them from their adult siblings that were normal at birth, unless they are standing side-by-side. These latter two FCS cows are however still a bit taller than their normal siblings and readily distinguished from them at the end of winter.

My conclusion from these observations is that at least some less severely affected FCS cases amongst a group of potential replacement heifers could appear to be acceptable as future breeders, particularly if selection is done at a time of year when all the heifers are in good body condition. With subcutaneous fat masking their poor muscling, a breeder seeking to increase frame score might even prefer some of the better looking FCS cases over the smaller normal heifers. Moreover, many less severely affected FCS cases may not be recognised at birth, even though clinical signs are always most pronounced at birth. In less severe cases, there is often a significant reduction in the severity of kyphosis (upwards arching of the spine) and joint laxity in the lower limbs within a few days of birth. Some FCS affected calves can appear relatively normal by 10 days of age, with no more than residual contractures in the hindlegs. Very few FCS cases are still “down on their pasterns” after the first 10 days. If these less severely affected FCS calves are not first observed until for a few days after birth they may not be classified as abnormal.

Until there is a test available to distinguish between non-carriers and heterozygous FCS carriers, there will also remain the possibility that the apparently normal heterozygous carriers are a little taller than their non-carriers siblings. If this is the case, selection for frame score in any population in which the mutation is present would likely result in an increasing prevalence of the FCS mutation in that population.

Frame score is a relevant consideration in FCS and vice versa.

It is true that FCS is a less severe defect in the individual newborn calf than a defect such as AM or NH. However, this does not mean that FCS is less important. The more insidious nature of FCS has probably allowed the mutation to become much more widespread in the Angus breed than other mutations that cause lethal defects.

The FCS phenotype is not just “different” or just “framier”. The FCS phenotype is commercially quite undesirable. In addition to the increased calf mortality under commercial field conditions, from weak calves that cannot get up and suckle quickly after birth, the persistent loose-jointedness in adult FCS cows predisposes them to the premature onset of degenerative arthritis and resulting early culling. Some FCS cases have had very severe osteoarthritis by six years of age.

Although the issue of unacceptable meat quality (lack of tenderness, not necessarily poor taste) is based on anecdotal reports and hence is speculative at this stage, this issue is something that requires investigation given that the basic biochemical defect in FCS appears to be in the connective tissue surrounding individual muscle cells. Some change in biomechanical properties of the meat would not be entirely unexpected in a syndrome like FCS where there appears to be a defect in the elasticity of muscle tissue at birth.

Although FCS may be a relatively “mild” phenotype defect and many FCS cases can survive to maturity and breed successfully, no sensible Angus breeder would want the FCS phenotype to become so common in the Angus breed that it was perceived as a normal Angus “type” by the wider cattle industry. These are not the type of cattle we want to breed, but they may become the cattle we do breed if some action in not taken.

The sooner we have a test available to clean up the FCS affected bloodlines the better.
 

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