CURLY CALF SYNDROME in AAA

[Brandonm22]

8.4% is much smaller than I was thinking.

8.4% of the bulls tested doesnt come close to meaning 8.4% of the population. Future Direction and 1680 by themselves probably have more influence in the current Angus breed than the rest of the list. I would expect more in the 15-25% range for carriers in the whole breed.

Exactly, as I understand it it is 62 out of the 736 Angus bulls that have been used by the 5 major A.I. studs in the last 20? years. Most of them I have never heard of. Some are high impact sires. There are some people celebrating tonight and some people have whole tanks full of semen and are wondering what are they going to do with it now.

 

[alexfarms]

I have heard of this type of dead calf, as I understand CCS to be, being called other things that were not genetic in nature for YEARS. And i know for a FACT that all of these little calves have not been confined to the angus breed or angus cross cattle. Does anyone have information on whether CCS has been identified in breeds of cattle other than Angus?

 

[Brandonm22]

Folks on here "claim" that this has been found in four other breeds beside Angus. I think Simmental has told their people to keep an eye out for it....though they also register a lot of Simangus.

On the negative side, ABS is listing : 29AN1411 RITO 8E8 OF5H11 TRAVELER 11072078 AMC as a carrier. If his pedigree is correct, he has no Precision in him (a safe bet as he is two years older than 1680)
http://www.angus.org/common/epd_ped_dtl ... 42405C424A

If that is correct and I haven't bungled the search, then this thing is a LOT older than Precision and may trace back to Band 234 or Rito 9J9 making a lot more cattle suspect than we first thought.

 

[alexfarms]

I did a google on CCS and found this post:
http://www.steerplanet.com/bb/index.php ... 7#msg67337

I am referring to the post by "DL", reply #3 on september 06, 2008. The last sentence in the post is describing the syptoms of CCS and states: "It probably occurs in many Bos taurus breeds and has been reported in Angus, Charolais and Herefords since the 1970's." I suspect this is a genetic problem which will be shared by several US breeds and has not been recognized as genetic untill recently. So, Angus breeders take heart, you probably aren't alone.

 

[Brandonm22]

It is entirely possible, that this genetic condition exists in other breeds of cattle making using a known carrier in a commercial environment even more problematic. Dwarfism exists in both Herefords and Anguses and struck at about the same time even though both breeds are only distantly related. However breeds that have composites that include ANgus or have turned themselves Angus may have a higher concentration of carriers than the general population since 1680 was used so extraordinarily heavy in the 90s (5000++ reg Angus daughters alone entered production) when breeds were becoming black and composites were becoming fashionable.

 

[alexfarms]

It is entirely possible, that this genetic condition exists in other breeds of cattle making using a known carrier in a commercial environment even more problematic. Dwarfism exists in both Herefords and Anguses and struck at about the same time even though both breeds are only distantly related. However breeds that have composites that include ANgus or have turned themselves Angus may have a higher concentration of carriers than the general population since 1680 was used so extraordinarily heavy in the 90s (5000++ reg Angus daughters alone entered production) when breeds were becoming black and composites were becoming fashionable.

The pics of these dead calves look very familiar from 2 unrelated Hereford lines I worked with prior to getting my King Dominos. I sent them to Dr Steffen and he said at that time that if they were genetic abnormalities then they were a genetic abnormality that had not yet been identified. They were UGLY, cleft pallet, twisted, small. They were full term to 10 days late in gestation. The cows didn't freshen normally. I had to pull one of them, it was like the cow didn't dialate. I believe I had 5 of them over a 10 to 12 year period. The only thing Steffen could conclude at the time was "placental insufficiency". Which can be caused by lots of things, but this acted like a simple recessive genetic abnormality. 3 of the calves were from half sib matings. The other two were linebred within their lines. They were produced by 3 bulls in the one line. I sold all 3 of them because the calves were just too weird. Then I got 1 son of one of those 3 bulls that I could breed to anything and got no problems. That even made me more suspcious of a simple recessive that that bull didn't inherit. I concentrated on that bull until I had the chance to buy the King Dominos. The other line I got one dead calf out of was years ago using an AI bull. That calf was overdue also. Very ugly little calves. One story I was told at the time was that exposure to a virus at conception could cause some type of problem with development and cause those ugly dead little calves. There will be alot of questions asked from this CCS identification. Most likely the AHA will say nothing until after the genetic marker is discovered, then we'll probably be able to test our cattle and put a "FCCS" behind their names....or not.

 

[Aero]

On the negative side, ABS is listing : 29AN1411 RITO 8E8 OF5H11 TRAVELER 11072078 AMC as a carrier. If his pedigree is correct, he has no Precision in him (a safe bet as he is two years older than 1680)

8E8 is out of the 5H11 cow who is out of 9J9, a listed carrier. the 5H11 cow is in the pedigree of quite a few animals on the list and appears to be a carrier.

 

[Aero]

alexfarms,
as I understand it, the cause of the malformity stems from hydrocephalis (sp?) which is water buildup in the brain. this can be caused by many things environmental. early CCS cases were found after an outbreak of Curly Calf-like deaths were found. they removed the envronmental influence and still had a few of the same problems. this led them to think it might be genetic.

the researcher I talked to said this is what makes it so hard to identify CCS as a lone culprit.

 

[alexfarms]

alexfarms,
as I understand it, the cause of the malformity stems from hydrocephalis (sp?) which is water buildup in the brain. this can be caused by many things environmental. early CCS cases were found after an outbreak of Curly Calf-like deaths were found. they removed the envronmental influence and still had a few of the same problems. this led them to think it might be genetic.

the researcher I talked to said this is what makes it so hard to identify CCS as a lone culprit.

hydrocephalis...would be "water head"? The calves I got were not water heads, that I am certain of. There is that genetic abnormality and it has been identified years ago. The calves I sent in were small, had multiple malformations. It was explained to me at the time that an infection by a virus at "organogenesis" could disrupt development of the calves and cause mutliple malformations. No sign of a virus could be found and Dr Steffen said usually the virus can only be detected for a short time after the infection. His only conclusion was "placental insufficiency", he said because that was the only thing that could definately be said. I had read that the CSU studies of several Hereford lines, years ago, had concluded that as inbreeding coefficient increases the incidence of placental insufficiency also increases, so I suspected that it may be a weakness in an inbred line brought on by inbreeding depression. If this CCS is similar to the affects of many "environmental influences" , then the DNA test is going to be a very powerfull tool to determine what is going on in these situations. I suspect this is a genetic abnormality that has been around a long time and it is just now being determined to be genetic, that is why it is so widespread and we are going to see alot of carriers identified. I have kept a small amount of semen on a bull that produced one of the ugly little things for me and when the test comes out I will get it checked. It really disgusted me at the time because I spoke to the herd manager where the linebred genetics originated from and he refused to even consider that there could be a genetic abnormality involved and I know he was getting some of the little things too. It may all have been environmental, I couldn't figure it out and only Dr Steffen was interested in helping me pursue it. It sure made me reluctant to get into that line too deep. Back in the 60's the Herefords were the big kid on the block and they took a lot of heat for the dwarfism outbreak, but other breeds had it too.

 

[HerefordSire]

8.4% is much smaller than I was thinking.

8.4% of the bulls tested doesnt come close to meaning 8.4% of the population. Future Direction and 1680 by themselves probably have more influence in the current Angus breed than the rest of the list. I would expect more in the 15-25% range for carriers in the whole breed.

If I read and understand the document correctly, the bull population was determined across a broad spectrum of Angus lines so as to calculate an error factor low enough to predict the probability of the issue exposure across the entire Angus population. Part of the reason for my post is to clearly understand the exposure by checking my logic in case I was in error. If 300,000 Angus animals (hearsay) are registered every year, about 25,000 would be carriers. I believe the main reason for the document and testing is to determine and publish the total exposure to the Angus population to prevent a cattle run, in panic. Initially I expected close to the numbers you are presenting. I think the document attempts to clearly scientificly lock in the 8.42% of the Angus population. Again, there are many assumptions and there are holes in the wording.

 

[Brandonm22]

It was explained to me at the time that an infection by a virus at "organogenesis" could disrupt development of the calves and cause mutliple malformations. No sign of a virus could be found and Dr Steffen said usually the virus can only be detected for a short time after the infection. His only conclusion was "placental insufficiency", he said because that was the only thing that could definately be said. I had read that the CSU studies of several Hereford lines, years ago, had concluded that as inbreeding coefficient increases the incidence of placental insufficiency also increases, so I suspected that it may be a weakness in an inbred line brought on by inbreeding depression. If this CCS is similar to the affects of many "environmental influences" , then the DNA test is going to be a very powerfull tool to determine what is going on in these situations. I suspect this is a genetic abnormality that has been around a long time and it is just now being determined to be genetic, that is why it is so widespread and we are going to see alot of carriers identified....... It really disgusted me at the time because I spoke to the herd manager where the linebred genetics originated from and he refused to even consider that there could be a genetic abnormality involved and I know he was getting some of the little things too. It may all have been environmental

That is why this is so hard to say for certain if we have seen this kind of thing before or not. A virus CAN cause deformed stillbirths, consumption of noxious plants can too, and a number of other pathogens or environmental influences like moldy hay can be responsible. Vaccines sometimes get blamed for stillborns too. I don't think this is as widespread as you suggest though because if there were a lot of carriers out there before Precision 1680 then when he was used on literally THOUSANDS upon thousands of cows (purebred Angus, commercial cows, and other pure breeds to create composites) we would have come across this before now and in much greater numbers. If half your herd were carriers and you used a carrier 12.5% of your calf crop would be stillborn plus whatever normal stillborns you have. A few herds like that and alarm bells would have gone off pretty early on in this. Dr. Steffan says he first saw it in 2002 in some sibling commercial blacks but didn't have the parental information to even begin to track it down. I am not doubting that you came across an unidentified lethal genetic defect (very, very possible); but it probably was not THIS one. I am wondering though if this thing has an environmental component that triggers the expression of the gene like the old stressor pigs (PSS). Good hogs; but if you popped on the rump or they had a bad truck ride that stress killed them dead and gone.

 

[Betty]

Some poison weeds(eg.lupine) can cause the joint problems seen in this syndrome.
A gentleman at the angus assoc. told me on the phone 3 days ago that hydrocephalus was sometimes part of this syndrome.
When I began whining about my baby bulls that I need to decide to cut or not SOON (or they are going to be too big to do safely in any sort of humane way)this gentleman told me he had 43 calves that were 1680 influenced and that he himself was in the same position.
I think that AA is doing a pretty great job trying to nail the thing down.

 

[donnaIL]

I haven't been checking angus.org as regular as I was, but did today and there is an update from 11/20 and 11/25 FAQ. They have adopted a new policy and related set of rules.

 

[blacksnake]

There is a 30-40 video on the AAA website by Dr. Jon Beever of UI that explains the CCS pretty well. It is very informative and worth viewing. He explains the odds of a CCS calf are very remote but also gives steps to eliminate it. Sounds like he is really on top of this. My vet said he knew a guy who had a calf with CCS. He has Salers.