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  1. #81
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    Quote Originally Posted by rcloisonne View Post
    Yet although the test for SCID has been available since the 90's, less than 20% of Arabians of breeding age have been tested to date. I don't call that responsible, unless people are only breeding untested mares to tested stallions. Call me a pessimist, but somehow I doubt it.

    Unlike this ignorant QH/Paint breeder, SCID and the other Arab genetic problems are rarely evident at birth. These folks just bury their oopsies, nobody the wiser. In many cases they probably don’t even know why their foals got sick and died.

    Until the AHR mandates all PB foals be tested before registration papers are issued, affected foals will still be born (and die) on a regular basis. Given the low rate of testing, the majority aren’t going to do the right thing unless forced.
    I posted the question of how many people are breeding on ABN and I was somewhat surprised at the answers. I will have to admit that I was overly optimistic about how much testing was going on.

    Some have suggested that the testing be mandatory and on the horse's papers...given the current state of the membership's attitude about AHA, I doubt if that idea would fly.

    And a big ole thumbs down to the folks who are breeding without testing in every breed with known genetic problems!



  2. #82
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    Not too long ago I heard a "breeder" say that they would not try to breed HERDA out, because the HERDA gene makes a horse more flexible! If I understand it right, two HERDA genes makes the horse's skin slough off.

    And "Impressive syndrome" was known about for years, and mostly swept under the rug, until UC Davis (I think) forced it into the public eye!



  3. #83
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    May. 3, 2001
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    Default Unfortunate rule in place by WAHO

    Quote Originally Posted by oldernewbie View Post
    I posted the question of how many people are breeding on ABN and I was somewhat surprised at the answers. I will have to admit that I was overly optimistic about how much testing was going on.

    Some have suggested that the testing be mandatory and on the horse's papers...given the current state of the membership's attitude about AHA, I doubt if that idea would fly.

    And a big ole thumbs down to the folks who are breeding without testing in every breed with known genetic problems!
    Unfortunately, at the 2011 World Arabian Horse Organization (WAHO) meeting a rule was passed that prohibits having genetic test results put on registration papers or in stud books. Since AHA is a member of WAHO, the rule applies to AHA....though it's not like AHA had any interest in doing this before the WAHO rule was put into place.

    But FWIW!

    Beth



  4. #84
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    Quote Originally Posted by phanilah View Post
    Unfortunately, at the 2011 World Arabian Horse Organization (WAHO) meeting a rule was passed that prohibits having genetic test results put on registration papers or in stud books.
    What was the reason for this decision?



  5. #85
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    Quote Originally Posted by phanilah View Post
    Unfortunately, at the 2011 World Arabian Horse Organization (WAHO) meeting a rule was passed that prohibits having genetic test results put on registration papers or in stud books. Since AHA is a member of WAHO, the rule applies to AHA....though it's not like AHA had any interest in doing this before the WAHO rule was put into place.

    But FWIW!

    Beth
    Really? Why?

    People are so bizarre about this stuff. I swear, they treat the genetic stuff like it's voodoo - it's just a fact about the horse, not a curse.



  6. #86
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    Quote Originally Posted by NoDQhere View Post
    Not too long ago I heard a "breeder" say that they would not try to breed HERDA out, because the HERDA gene makes a horse more flexible! If I understand it right, two HERDA genes makes the horse's skin slough off.

    And "Impressive syndrome" was known about for years, and mostly swept under the rug, until UC Davis (I think) forced it into the public eye!
    FWIW - HERDA is considered an equine form of Ehlers Danlos Syndrome, which affects connective tissue (not just skin). EDS can allow for "hypermobility", such as the type of movement desirable in elite gymnasts, dancers, etc. So, there is a thought that the flexibility also carries over to horses in terms of any increased mobility being a benefit for performance events such as cutting.

    Not saying I'm an advocate for the justification, just an FYI for the discussion.

    Beth



  7. #87
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    Quote Originally Posted by Kerole View Post
    What was the reason for this decision?
    WAHO's concern was that "labeling" the horse's official record may result in discrimination against lines or demonization of horses, then leading to loss of lines and genetic diversity....that line of thinking can also be extended to loss of sales, breedings, etc.

    Now, a registry can still opt to mandate testing and run a list of test results separate from the official horse record (which some registries are doing).

    As far as AHA goes, it appears that the old AHRA philosophy of essentially "staying out of" testing has carried forward - which is unfortunate.

    Beth



  8. #88
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    As long as breed registries refuse to take these conditions seriously and do their best to eradicate them and/or educate owners, it is not surprising that uneducated breeders are unconcerned and don't bother to test.

    The lack of leadership shown by these organizations is inexcusable.



  9. #89
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    Quote Originally Posted by Laurierace View Post
    With the information we have about the disease and it's cause is there any "excuse" for having a lethal white foal born today? I don't have any experience with color breeds but even I know enough to look into the possibility when breeding colored horses. There was a colt born today on Marestare and I was wondering if that is something that can still happen by accident or were they either too lazy to look into it before breeding or too uninformed to be color breeders? Your opinion?
    There is a genetic test for it...so for anyone breeding as a business they should know better and there should be no accidents breeding known frame overo horses. Uninformed mare owners that are breeding their trail horse and know nothing about genetics may truly be uninformed enough to get a poor Olw foal. The really sneaky ones are the solid colored horses....mostly unmarked paints or quarter horses but even the rare odd bloodlines of thoroughbreds, that don't think their horse is overo and don't think to test for it.


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  10. #90
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    Can you please educate me - how can you tell the difference between an overo frame and a regular paint?

    I've been looking at pictures... most of those labelled "frame" have solid color on the back and down their spine and the white is below that. Whereas a regular paint can have white blotching anywhere, including their back? Is that the correct way to tell the difference?

    I wonder how long it will take this to show up in the warmblood population, since there are individuals who are trying to breed the paint type coloring in the warmbloods.

    Is the gene only found in paint/overos? What about dilutes who are solid buckskin or palomino or what about cremello/perlino?
    http://www.mariposasporthorses.com/

    Practice! Patience! Persistence!



  11. #91
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    Quote Originally Posted by rodawn View Post
    Can you please educate me - how can you tell the difference between an overo frame and a regular paint?

    I've been looking at pictures... most of those labelled "frame" have solid color on the back and down their spine and the white is below that. Whereas a regular paint can have white blotching anywhere, including their back? Is that the correct way to tell the difference?
    Frame does not at all like to put white over the spine between withers and tail, so that's one clue. It tends to "frame" the body in the darker color, putting white inside that frame, including the upper legs, when it's working in a more maximal form. It tends to look like it's moving down the horse top to bottom.

    If you see a horse with lots of leg white that looks like it started at the feet and worked its way up, that's not Frame, but if you see a horse with lots of body white and lots of leg white and, say, one leg that's solid, or has a really low white, you might strongly suspect Frame is there, trying to keep white off that leg.

    Frame tends to really like jagged edges, so if you see a horse who really looks Tobiano, but has jagged edges, think that Frame might be there (Tobi, along with Splash really love smooth edges).

    But remember too that NONE of the Overo patterns, including the homozygous deadly Frame, have to make their presence known. An absolutely solid horse can be a Frame carrier

    I wonder how long it will take this to show up in the warmblood population, since there are individuals who are trying to breed the paint type coloring in the warmbloods.
    I'm sure it's already there, since I'm sure there are a few horses from the Letter of Marque/Remarquez TB Frame line who have been bred with WBs. Profile In Style is a Frame TB in Australia. Ellusive Look is a Frame TB stallion that Gwen at Gestut Falkenhorst bought and took to Germany, and she is opening his breeding to WB mares. Ellusive Look as a Frame sister, Quit Starring, who could also be bred to WB stallions.

    Is the gene only found in paint/overos?
    Frame is a subset of Overo, so one needs to be very careful how those terms are used The rampant misuse of Overo for Frame in the APHA world has led to such confusion about what's what, and makes some people really wiggy about the whole term "overo" when it's only one of those genes that is the worry

    Frame is found in most breeds that carry pinto patterns. Minis, TBs, Paints, QH's, Appies, and more. But not all pinto pattern carrying breeds carry frame - Arabians have Dominant White, Splash, and Sabino, but do not carry Tobiano or Frame.

    What about dilutes who are solid buckskin or palomino or what about cremello/perlino?
    The dilution genetics are 100% separate from any Overo genetics, so yes, anything solid but dilute, either single or double, can also carry Frame if they are of the right breeding/breed.
    ______________________________
    The CoTH CYA - please consult w/your veterinarian under any and all circumstances. - ET


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  12. #92
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    I think it is time people took seriously the possibilities of genetic flaws in their breeding. This lethal white has been around a long time. If there is a way to test for it then there ought to be noted on the registration papers if the horse is carrying that gene. Then breeders should be aware of what can happen if they choose to breed anyway to the stud that aslo carries that gene. It is playing Russian Roulette for the foals. Some very close breeding practices have brought out many bad things in Arabians and Quarter Horses and to continue breeding horses known to be carriers of the genetic flaws is not being responsible. You can not " Breed it out" of any horse mare or stallion if the gene is there. You can outcross to a different line of the breed but then the foals still are carriers. Yes you do intensify good genes by line breeding or inbreeding but then you also intensify the bad genes too. I have seen far too many horses with genetic flaws that never should have been born. Extra teeth, swayed backs, bad legs, and lack of intelligence. Backyard breeders seldom do the research to void stallions that carry bad genes. This is a case in point with the Lethal White syndrome. Breeders will sell off mares that are genetically flawed but they seldom mention the problems theyare disposing of. Genetic testing is one way to catch problems. If the mares carry bad genes then they should be spayed. Stallions should be gelded. There has to be a definite attempt to stop the bad genes. JMHO



  13. #93
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    Quote Originally Posted by sadlmakr View Post
    If there is a way to test for it then there ought to be noted on the registration papers if the horse is carrying that gene.
    This assumes registration which, sadly, is low in priority for many folks breeding
    ______________________________
    The CoTH CYA - please consult w/your veterinarian under any and all circumstances. - ET



  14. #94
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    Quote Originally Posted by JB View Post
    But HERDA carriers are unaffected in the hetero state, and sure, there can be an argument to allow them to breed to non-carriers, but still - why? In this case, it's a QH thing, diversity is not an issue, why not disallow registration of all carriers and just get rid of the disease? well, "get rid of" as best we can, as there will always be unregistred crossbred carriers There isn't any benefit, aesthetic or otherwise, to allow carriers to remain around, not like Frame/LWO

    Because, in selecting *against* a known gene, one is selecting *for* other unknowns.

    At least with recessive genetically transmitted defects for which testing is available, one can avoid producing an affected individual.

    And who's to say "there isn't any benefit aesthetic or otherwise"? It is highly likely that there *is*, else that defective gene wouldn't have been amplified in the population in the first place. It could be an entirely unrelated trait that just happens to reside near the defective gene in question.
    "It's like a Russian nesting doll of train wrecks."--CaitlinandTheBay

    ...just settin' on the Group W bench.



  15. #95
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    Quote Originally Posted by wcporter View Post
    Sorry, if this is a gruesome question, but what about the LWO gene causes the actual fatality? The foal is born alive and then dies? From what?

    I am involved in Federal genomics policy, and this stuff (as sad as it is) fascinates me.
    Intestinal agangliosis.
    The innervation of the GI tract is buggered, so there is a lack of motility.
    "It's like a Russian nesting doll of train wrecks."--CaitlinandTheBay

    ...just settin' on the Group W bench.



  16. #96
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    I'm sorry but there is just no excuse for having a LW foal.

    I've been to that site and this is not the first lethal white to have foaled out on camera.......In my opinion they try to swept it under the rug rather then step up and try and educate people so I believe they are a part of the problem.

    Dalemma


    2 members found this post helpful.

  17. #97
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    Cocolalla Creek Sport Horses has frame in their warmbloods. From a paint source but its there

    http://www.cocolallacreeksporthorses.com/
    Check out my Equine Genetics Blog! Updated April 25th with Splashed White!!!
    http://equinegenetics.blogspot.com/



  18. #98
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    Quote Originally Posted by Ghazzu View Post

    And who's to say "there isn't any benefit aesthetic or otherwise"? It is highly likely that there *is*, else that defective gene wouldn't have been amplified in the population in the first place. It could be an entirely unrelated trait that just happens to reside near the defective gene in question.
    Sort of like malaria resistance in sickle cell carriers.



  19. #99
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    Quote Originally Posted by Ghazzu View Post
    Because, in selecting *against* a known gene, one is selecting *for* other unknowns.

    At least with recessive genetically transmitted defects for which testing is available, one can avoid producing an affected individual.

    And who's to say "there isn't any benefit aesthetic or otherwise"? It is highly likely that there *is*, else that defective gene wouldn't have been amplified in the population in the first place. It could be an entirely unrelated trait that just happens to reside near the defective gene in question.
    The only thing positive this trait that it's linked to is the paint frame coloring, which has been selected by humans. It's a huge problem when people who don't understand that we are putting animals under selective pressure that isn't necessarily good for the animals, and instead assume that because a trait occurs it must be associated with a desirable traite. These traites aren't usually associated with positive traites, they simply carried because breeders are inbreeding horses and not culling horses who care bad genes because often this horses have positive traites as well (this does not mean the two traites HAVE to be link, it only means they are both present in the parent). This does NOT have to be the case. It's not an issue where the traites are tied to good traites. The mutation is tied to a developmental issue which creates incorrect development, incorrect development is what causes the pretty pattern that humans like. If both versions of the gene are incorrect one can't compensate from the problem in the other so you see a damaging condition. One gene compensating for the lack of function in an other typically isn't going to be a positive thing. Sickle cell is a very rare cause where this is positive since it is harder for the parasite to infect, this is NOT the normal case with carriers. In LW it's actually unusual in the sense that carriers have what humans consider a positive traite. In most cause the traite is simple not bad in carries because one copy of the gene can compensate for the problem in the other gene NOT because there is something good about being a carrier.

    It's very very important to remember that humans are selecting for traites, these traites can be bad or good. Because they occur does not mean they are somehow associated with positive traites! More often then not they are breeding mistakes.

    Here's a good paper about LW. http://hmg.oxfordjournals.org/content/7/6/1047.full.pdf



  20. #100
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    Quote Originally Posted by FayeHanoverian View Post
    It's very very important to remember that humans are selecting for traites, these traites can be bad or good. Because they occur does not mean they are somehow associated with positive traites!
    In this case the pretty color is the positive trait. That is why people breed for it. I can't think of anyone who intentionally breeds specifically for undesirable traits.



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