Potential genetic defect in Shorthorn cattle

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knabe

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heres the cow side.

i noticed paramount in there, and a bull i would like semen on.

 

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sue

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DL said:
A number of cases (>5 and <10) of abnormalities of the distal leg/foot and dew claws in Shorthorn calves have been reported. These cases are not "classic" mule foot as the claws (toes) are not fused, typically the calf has inappropriately placed dew claws and may have some other slight curvature or deformity at the base of the leg that makes it somewhat difficult for them to mobilize. It is my understanding that the ASA is aware of these cases.

All cases have similar ancestors on one side of the pedigree. The DNA from these cases has been 50K genotyped and there is information to suspect that this abnormality has a genetic component. However there have been insufficient samples submitted to clearly determine if the abnormality is genetic or if there is another cause.

If you have a calf born with an abnormality of the distal leg/foot/dew claw contact the ASA and submit samples to Dr Beever. The attached pictures of newborn calves show what this abnormality may look like
Scotland here is a better discription of  potential defect.
 

DL

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scotland said:
i struggle to understand the comparison of apples and oranges (mulefort and crooked joint and dewclaws) . The link may be of interest to you all, states the facts and findings of mulefoot... Holsteins, Angus and a few Eurpeon breeds. http://vdi.sagepub.com/content/10/3/247.full.pdf


Don't struggle - there is no relationship between mule foot (where one or more toes are fused) and the deformities described in the distal hind limbs below the hock - the gene identified as responsible for mule foot (LRP4) is not involved in the distal  hind limb deformity of Shorthorn calves discussed here; several mutations have been identified for a variety of breeds of cattle, but some cases DO NOT involve the known mutations

There was apparently some confusion among breeders about the original description of the distal hind limb deformity -

Here is a review of syndactly that I originally posted under the disappearing thread - this is for information only this is NOT WHAT WE ARE TALKING ABOUT WITH THE DISTAL LEG ABNORMALITY IN SHORTHORN CALVES

SYNDACTLY (from Brian K. Whitlock, Lana Kaiser, and Herris S. Maxwell. "Heritable bovine fetal abnormalities" Theriogenology 70.3 (2008): 535-549.Theriogenology)

Syndactyly in cattle is also called ‘‘mulefoot’’ and refers to the fusion or non-division of the two functional digits of the bovine foot with synostotic (fusion of normally separate skeletal bones) phalanges. Phalanges are synostotic horizontally and by pairs; the second pair of phalanges is most fully synostotic, followed by the third, and then the first. This abnormality is often subject to a right-left and a front-rear gradient, being most often seen in the front and right feet. Proximal limb structures can also be affected in syndactylous animals, resulting in a reduced number of sesamoid bones. Synostotic phalanges can be detected as early as 37–40 d post-coitum in the bovine embryo.

Bovine syndactyly is an autosomal monogenic recessive trait with incomplete penetrance (_79% in Holstein cattle) and variable expression. Crossbreeding experiments between Holstein and Aberdeen-Angus have produced syndactylous progeny, suggesting a common locus responsible for the disorder in both breeds. The bovine syndactyly locus was localized to chromosome 15 in 1996 and is due tomutation in the low-density lipoprotein receptor-related protein 4 gene (LPR4). The occurrence of syndactylous cattle peaked in the 1970s as carrier animals were indirectly selected for superior production of milk and butterfat. The development of test mating and genetic testing greatly reduced the incidence of syndactyly.

Unfortunately, syndactylous animals are still occasionally observed in the Holstein population and some carrier animals are still being used for breeding. Eradication of syndactyly will require a precise method to detect the causal genetic mutation. Unfortunately there is extensive allelic heterogeneity in LPR4, with the six independent mutations described still not accounting for all analyzed cases. The two most frequent mutations are the Holstein-specific exon 33 mutation and the Angus-specific exon 37 mutation. Because not all causal mutations have been detected, genetic testing for the carrier status of single individuals remains difficult. Several labs offer testing for the known geneticmutations [Germany (http://www.tieraerztliches-institut.uni-goettingen. de/); Italy (http://www.lgscr.it/eng/index.htm); France (http://www.labogena.fr/); the Netherlands (http://www.vhlgenetics.com/vhl/index.html)]. Unfortunately, each laboratory utilizes different technologies and seldom analyze for the same genetic mutations.

The American Angus Association lists the status of several bulls and cows as carrier or free of the mutations responsible for syndactyly. However, this freedom from carrier status is based solely on progeny test information, and could be questioned in the context of the allelic heterogeneity of syndactyly in Holstein cattle.


 

DL

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scotland said:
i struggle to understand the comparison of apples and oranges (mulefort and crooked joint and dewclaws) . The link may be of interest to you all, states the facts and findings of mulefoot... Holsteins, Angus and a few Eurpeon breeds. http://vdi.sagepub.com/content/10/3/247.full.pdf

scotland - here is more info  on the abnormality noted in Shorthorn calves posted on the 27th and repeated here just for you  ;D

So let me reiterate what we know so far about this potential genetic defect in Shorthorn cattle

Seven cases of abnormalities of the distal leg/foot and dew claws of the hind limbs in Shorthorn calves have been reported

Hind limbs only affected, below the hock

These cases are not "classic" mule foot and the gene responsible for mule foot (LRP4) is not involved

The phenotype is variable, so one leg could be obviously affected and the other more subtly affected

Typically the calf has inappropriately placed dew claws and may have some other slight curvature or deformity at the base of the leg that makes it somewhat difficult for them to mobilize.

Most calves are born alive; severely affected calves are put down because they cannot walk; less severe can grow into it

If the calf survives it appears to "improve" as it ages (variable phenotype somewhat like like FCS)

Cases are from various geographic regions (again suggesting the abnormality has a genetic component)

All cases have similar ancestors on one side of the pedigree,  a popular AI sire or his sons

All 7 cases have been genotyped;  6 of 7 share a segment of 2.7 Mb for which they are homozygous, again suggesting that it may be genetic

Discussion of this potential genetic defect in Shorthorn cattle has led to increased breeder awareness and hopefully  submission of samples from potentially affected calves in the pasture or the freezer. If you have a calf with abnormal hind limbs below the hock do the right thing - submit samples
 
J

JTM

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Thank you DL for taking the time and putting in the effort to inform breeders of a "potential" genetic defect. I think that being able to discuss these things proactively will only help the breed. We got into cattle and Shorthorn cattle right in the middle of when TH was starting to get talked about and testing was underway. We were blessed to come out of the mess with only a couple of carrier cows to start the foundation of our herd. We have since only purchased or AI'd to thf or phaf cattle. I again want to say that I hope the ASA takes this on agressively in order to find a definitive answer quickly. That is what discussing things on a public forum will do, it will speed things up I believe. I will be contacting the ASA concerning this potential defect and encouraging them.
 

aj

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Seems amazing to me that they can pull samples out of meat. What if the locker plant does some switching of meat around.......that could be interesting.  ;D ;D ;D always trying to help.
 

KSUwildcat2009

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Holy cow this thing has exploded since I was last on... Can someone confirm this for me:  As far as I've seen, there is NOT obvious relation between the dams of affected calves and the sire in question, or there IS relation? 

Sorry, not going to lie, skipped a lot of the posts.
 

knabe

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theres a few that are in both pedigrees.

i think i missed a couple. didnt go way back on all of them on the spreadsheet links.

whats really stupid about the whole deal is that its free publicity and essentially free test development. anyone who complains is an IDIOT and cant see what a windfall this is.

1.  a defect is found and a test is made essentially cost free to the owner.
2.  a non genetic issue is found, free pub to the bull owners
3.  nothing is found and free pub to the owner.
4.  field rep might have some explaining to do.
5.  probably a few more.
 

trevorgreycattleco

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I call timeout on this madness. I have something to say that may have some importance. An amazing thing just happened to me. Not 5 minutes after I go on a rant about this crap, I get a call from Patrick Wahl. My wheels are a spinning folks. So i appologize if I have trouble getting on a screen how I feel.

DL, I respect what you have to say. Always have, always will. But like always, there is two sides to every story. This so called problem may not even be a defect. It could be a enviromental deal.  Its to early to tell. You cant call it a defect if you cant identify the problem. There is a problem. But as to say what is the cause is pure speculation. I fell victim to running my mouth when I didnt have all the facts. The most fascinating thing to me is I was the SECOND person who Patrick Wahl has talked to about this since the thread started. AND HE CALLED ME. As much as folks may not like aj, guess who the othe person was? Nobody has called him about this. NOBODY. call the Maine and Chi assoc and see what they have to say about this. ASA is working on this. They are the only assoc that is. Dont believe what you hear until it comes from the horses mouth. Put yourself in there shoes. What do they say when they dont have the answers. bad news rides a horse faster then Secretariat. This is what I know. This breed is at a crossroad once again. Lets do the right thing. ALL of us. This breed has sat on the sidelines way to far. Stop looking at the money and take 5 seconds and look at the big picture. There is plenty of room for LOTS of shorthorn breeders who do the right thing. How many black cows you seen lately? I personally think every animal will eventually test for a defect of some sort. it makes alot of money, so why stop testing?

I have badmouthed folks on here plenty and I apologize for that. I love this breed and Im not going anywhere. Lets relax, be patient, work through this and roll on. We got through Th and PHA. We can sure as hell get through this. This breed has to much to offer to let this stuff derail it. Just my 2 cents.

Brock Eagon
 

KSUwildcat2009

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knabe, I'm not sure I'm following what you are saying about "essentially free test development".  Are you complaining or saying it's a good thing?
 

DL

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KSUwildcat2009 said:
knabe, I'm not sure I'm following what you are saying about "essentially free test development".  Are you complaining or saying it's a good thing?


KSU - don't worry about it - many people don't follow knabe :(

trevor - I gather you have drank the koolaid  ;) you know I have heard everything you reported from you phone conversation before - with TH, PHA, AM, NH, FCS -t's deja vu all over again different defect, same song and dance - wanna polka??

The reason the title of this thread is POTENTIAL genetic defect in Shorthorn cattle is because ALTHOUGH THERE IS EVIDENCE THAT IT IS GENETIC we need more samples to prove it or disprove

[size=10pt]The data that suggests it is genetic is as follows
-involves the distal hind limbs below the hock - although the phenotype is somewhat variable (like FCS) there are many similarities
-abnormal calves from various geographic locations - again suggesting genetic not environmental
-a 2.7 MB region for which 6 of 7 reported calves are homozygous - again suggests it is genetic
-pedigree of affected calves sire is the same or son(s) of the same

The way to obtain more samples is to provide information to breeders - as far as I can tell NO breed association has provided members information about the potential genetic defect involving the distal hind limb


There is sufficient information to suggest this is a genetic issue in Shorthorn cattle and we need more samples - it is pretty simple

I will also note that several people have reported to me that they had calves with similar issues in 2010 - some have pictures - there may be some samples of sirloin in the freezer

and BTW trevor I stand by my statements and description of the issue, my information is accurate and I do not have a pony in the race

had this issue not come up under a different name in a hidden post chances are nothing would be happening

edited to make okotoks happy
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[/size]
 

Okotoks

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KSU - don't worry about it - many people don't follow knabe

trevor - I gather you have drank the koolaid  you know I have heard everything you reported from you phone conversation before - with TH, PHA, AM, NH, FCS -t's deja vu all over again different defect, same song and dance - wanna polka??

The reason the title of this thread is POTENTIAL genetic defect in Shorthorn cattle is because ALTHOUGH THERE IS EVIDENCE THAT IT IS GENETIC we need more samples to prove it


Well I suppose since I know before posting I'm going to get a caustic reply that is no reason not to post, seems it's DL's way of keeping other opinions to a minimum though.
The above statement to be scientific should have said we need more samples to prove or disprove it.
If you have an animal that matches the description you should send a sample in so they can find out what we are dealing with.
 

DL

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Okotoks said:
KSU - don't worry about it - many people don't follow knabe

trevor - I gather you have drank the koolaid   you know I have heard everything you reported from you phone conversation before - with TH, PHA, AM, NH, FCS -t's deja vu all over again different defect, same song and dance - wanna polka??

The reason the title of this thread is POTENTIAL genetic defect in Shorthorn cattle is because ALTHOUGH THERE IS EVIDENCE THAT IT IS GENETIC we need more samples to prove it


Well I suppose since I know before posting I'm going to get a caustic reply that is no reason not to post, seems it's DL's way of keeping other opinions to a minimum though.
The above statement to be scientific should have said we need more samples to prove or disprove it.
If you have an animal that matches the description you should send a sample in so they can find out what we are dealing with.


wow are you touchy - seems that the opposite of prove is disprove and seems obvious and redundant to me - but to make you happy I have edited it in the above post - are you smiling now?
 

Okotoks

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DL said:
Okotoks said:
KSU - don't worry about it - many people don't follow knabe

trevor - I gather you have drank the koolaid   you know I have heard everything you reported from you phone conversation before - with TH, PHA, AM, NH, FCS -t's deja vu all over again different defect, same song and dance - wanna polka??

The reason the title of this thread is POTENTIAL genetic defect in Shorthorn cattle is because ALTHOUGH THERE IS EVIDENCE THAT IT IS GENETIC we need more samples to prove it


Well I suppose since I know before posting I'm going to get a caustic reply that is no reason not to post, seems it's DL's way of keeping other opinions to a minimum though.
The above statement to be scientific should have said we need more samples to prove or disprove it.
If you have an animal that matches the description you should send a sample in so they can find out what we are dealing with.


wow are you touchy - seems that the opposite of prove is disprove and seems obvious and redundant to me - but to make you happy I have edited it in the above post - are you smiling now?
;D Nothing better than a theorem proved!
 

knabe

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KSUwildcat2009 said:
knabe, I'm not sure I'm following what you are saying about "essentially free test development".  Are you complaining or saying it's a good thing?

im saying its a good thing and over and over people cant figure it out that finding these defects and having tests for them is a good thing.

they dont have to pay for squat to develop the test, complain the test costs too much and complain they cant control barn talk which would ruin their reputation as a potential honest cattleperson.

really the whole defect phenomenum is the best thing that happened to the cattle industry.

these tests allow cheaper linebreeding without having to test breed so many individuals. course the complainers would never think of test breeding, tooooo expensive, and what if something shows up, the current philosophy apparently is dont tell anyone. what a joke. its mind boggling that in this day and age, any real cattle breeder doesnt understand simple recessives and free test development. you would think a simple thank you would be in order rather than nasty phone calls.

think about when spastic pareisis and monkey mouth tests come out, pretty soon there will be a defect panel that will be a lot cheaper. but no, lets go ahead and complain some more.
 

Okotoks

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knabe said:
KSUwildcat2009 said:
knabe, I'm not sure I'm following what you are saying about "essentially free test development".  Are you complaining or saying it's a good thing?

im saying its a good thing and over and over people cant figure it out that finding these defects and having tests for them is a good thing.

they dont have to pay for squat to develop the test, complain the test costs too much and complain they cant control barn talk which would ruin their reputation as a potential honest cattleperson.

really the whole defect phenomenum is the best thing that happened to the cattle industry.

these tests allow cheaper linebreeding without having to test breed so many individuals. course the complainers would never think of test breeding, tooooo expensive, and what if something shows up, the current philosophy apparently is dont tell anyone. what a joke. its mind boggling that in this day and age, any real cattle breeder doesnt understand simple recessives and free test development. you would think a simple thank you would be in order rather than nasty phone calls.

think about when spastic pareisis and monkey mouth tests come out, pretty soon there will be a defect panel that will be a lot cheaper. but no, lets go ahead and complain some more.

Do they know how these two defects are inherited? I take it that it is not a simple recessive. How often does it occur and have they identified some of the carriers through linebreeding?
 

knabe

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there are two bulls that carry these defects, cunia, and another bull called cunia.

by the way, i like your ulysses bull. good pick.
 
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