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My friend's husband asked if people "spay" mares and we got to talking about how ...
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    Disease that causes skin to fall off

    My friend's husband asked if people "spay" mares and we got to talking about how it's expensive and evasive and only done if absolutely necessary. Then I said that some responsible horse owners will spay their mares if they have a genetic disease that can be passed on to their offspring so that if they ever sold the mare, she wouldn't be bred and contribute to ongoing problems such as HYPP and other diseases.

    This is when I remembered that there is some genetic disease that causes a horse's skin to fall off and for the life of me, I cannot think of it! I remember reading about it along time ago and I think it's most common in QH's. I believe it starts along the spine and the skin begins separating and sloughing off. The horse usually has to be put down. I even think it's something they can live with and never have it happen but most begin losing their skin at some time in their life. I want to say I remember reading something about someone who owned a horse positive for this and they were trying to find out how to manage it and prevent an outbreak.

    Am I crazy?!?! Can anyone think of what disease this is?
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    HERDA I believe.

    hereditary equine regional dermal asthenia (HERDA).
    When a horse has HC, there is lack of adhesion within the dermis, the deep layer of the skin, due to a collagen defect. Collagen serves a form of glue that holds the skin layers together. In horses with HERDA, the "glue" is inferior and the skin layers separate.
    In dramatic cases, the skin can split along the back and even roll down the sides, with the horse literally being skinned alive. Generally speaking, she says, the average lifespan for an HC horse is two to four years.



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    Quote Originally Posted by Jess! View Post
    HERDA I believe.
    LOL...I just found it. It was BIG back in the day, but I haven't heard much about it lately.
    Never argue with a fool; onlookers may not be able to tell the difference.

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    HERDA - traces to Poco Bueno. For it to present itself the foal must carry 2 copies (both sire and dam) but can be a carrier will never show any signs of the disease. (Sort of like how LWO is passed on.) One of our geldings carries Poco Bueno on both sides but as he is 13 y/o and no signs of the disease, I've never had him checked - gelding so "ain't a gonna" pass it on.

    There is a forum for/about HERDA at www.HERDA@yahoogroups.com

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    Quote Originally Posted by Kicks View Post
    HERDA - traces to Poco Bueno. For it to present itself the foal must carry 2 copies (both sire and dam) but can be a carrier will never show any signs of the disease. (Sort of like how LWO is passed on.) One of our geldings carries Poco Bueno on both sides but as he is 13 y/o and no signs of the disease, I've never had him checked - gelding so "ain't a gonna" pass it on.

    There is a forum for/about HERDA at www.HERDA@yahoogroups.com
    I was about to ask what LWO was but then it dawned on me. Which has now spurred another question. I was talking to someone who worked at a breeding barn that retired a BEAUTIFUL mare because she kept throwing lethal whites. I thought you could only have a lethal white if you bred two carriers (like you said above). I think she said it was a TB farm, so I don't think color was a goal. If the mare was as good as she says she was, wouldn't it make sense to keep he and only breed her to homozygous dark stallions? Lethal white isn't a genetic disease, but a bad combination of genes, right? Like almost any horse with a white gene if bred to another horse has a white gene, has some chance to have a lethal white baby. But horses w/more white genes have higher chances and shouldn't be bred together.
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    Senior Member Belladonna's Avatar
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    Quote Originally Posted by cowgirlnat View Post
    I was about to ask what LWO was but then it dawned on me. Which has now spurred another question. I was talking to someone who worked at a breeding barn that retired a BEAUTIFUL mare because she kept throwing lethal whites. I thought you could only have a lethal white if you bred two carriers (like you said above). I think she said it was a TB farm, so I don't think color was a goal. If the mare was as good as she says she was, wouldn't it make sense to keep he and only breed her to homozygous dark stallions? Lethal white isn't a genetic disease, but a bad combination of genes, right? Like almost any horse with a white gene if bred to another horse has a white gene, has some chance to have a lethal white baby. But horses w/more white genes have higher chances and shouldn't be bred together.
    Now that stuff about lethal interests me. Because lethal white is a genetic condition linked to horses that carry the overo gene. There is also some speculation (however no one is prepared to come outright and say it in a test result) that the overo gene itself IS the cause for lethal white foals.

    You're right about it being to do with the amount of genes. You see when a mare concieves and a zygot is formed 50% of the genes come from the mare and 50% from the stallion, these sets of genes "pair up" together to form the genetic structure of the foal. When a horse has two copies of a gene it's called homozygous, when an odd pair it's heterozygous. When a zygot is formed that is homozygous for the lethal white gene it is born lethal white. However when a horse is heterozygous it will live out it's life without ever showing any signs of ailment.

    What interests me about your case is that you said that this mare was a thoroughbred. Now while the overo gene is present in thoroughbreds it is extremely rare. And it's very surprising that she was breeding two overo thoroughbreds unless she was breeding the overo thoroughbred to another breed of horse. But yes, in short to your question, if she breed this mare to solid coloured horse that was negative for overo then there would be no risk of throwing a lethal white foal. However if she was a thoroughbred breeder she may not know all that much about colour genetics.

    Hope this helps clear some stuff up.
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    More Than Skin Deep?

    by: Les Sellnow


    It was two years ago--in April of 2004--that this magazine published the announcement that the Poco Bueno Quarter Horse sire line had been identified as carrying the recessive gene that causes hyperelastosis cutis (HC, also known as hereditary equine regional dermal asthenia or HERDA). This is an affliction involving the skin that very often carries with it a death sentence for the affected horse. During the past two years, a good deal more has been learned about HC, but at the same time, it remains an elusive entity as researchers seek to pinpoint its genetic location. This would be a major step in developing a DNA test that would identify carriers. (The gene is characterized as being autosomal recessive, which means that both parents must pass it on for their offspring to be affected.)
    University of California-Davis researchers have reported progress in their genetic investigations of this disease, but have not yet identified the specific gene. They have identified the chromosome on which the HC gene is located and have narrowed the field as to which gene might be involved, but have not reported identifying the gene itself.
    A new urine test can be administered to foals to determine if they are affected, but there is not yet a DNA test to determine which horses are carriers and can pass the condition to offspring. And, as knowledge expands, there is a growing concern that HC might involve more than just the skin of an affected horse.
    What is HC?
    When a horse has HC, there is a lack of cohesion within the dermis, the deep layer of skin, due to a collagen defect. Collagen is the protein constituent of bone, cartilage, tendon, and other connective tissue that in a manner of speaking, plays the role of glue in keeping the layers of skin together. However, when a horse has HC, the glue is inferior and the layers separate. When the horse is ridden or suffers trauma to the skin, the outer layer often splits or separates from the inner layer. It can also tear off completely. When the wound heals, there very often is a disfiguring scar. New damaged areas arise continuously, often without obvious trauma.
    Some affected horses have lived to old age, but for the most part, they have been the recipients of tender, loving care that prevented skin trauma. Sun damage is also a concern, and affected horses must be kept out of direct sunlight as much as possible.
    Ann Rashmir, DVM, MS, Dipl. ACVS, a researcher who heads up the HC research program at Mississippi State University, says that the affliction continues to strike with varying degrees of severity. With some, it is so bad that portions of the horse's skin literally fall off its body. With others, the horse is affected only mildly and can often be ridden in the performance ring if handled correctly, she says. However, one thing has not changed: There still is no cure for HC. For most horses, it is a death sentence, with the average life span being in the two- to four-year range.
    Much has been learned about handling affected horses, Rashmir says, with overall quality care and proper nutrition playing valuable roles.
    There normally are 24 affected horses in the herd at MSU that are being continually studied in an effort to learn more about HC and how to deal with affected horses. Unfortunately, says Rashmir, the often-virulent nature of the disease means that there is a fairly rapid turnover of animals in the herd. For example, two affected yearlings that had been donated didn't reach their 2-year-old years before progress of the disease and its side effects made it necessary that they be euthanatized.
    When a DNA test is developed, it could reveal if a sire or dam carry the recessive HC gene. The genetic law of averages indicates that if both parents are carriers, 50% percent of the offspring will be carriers, 25% will have HC, and 25% will be normal. When a horse with HC is crossed with a carrier, the odds go up. Under that scenario, the genetic law of averages indicates that 50% of the offspring will be carriers, and 50% will have the disease. When a horse with HC is crossed with a normal horse, 100% of the offspring will be carriers.
    Thus, one could reason, if the DNA test reveals that both stallion and mare have the HC gene, the wise thing is to avoid breeding them to each other. As a practical matter, however, that will not happen. Some of the HC gene carriers are talented stallions and mares in the cutting and performance horse arenas. Just being a carrier has no known negative effect on the horse's ability to perform.
    One breeder, who chooses to remain anonymous, says that he has bred three of his mares to a known carrier stallion that has a reputation for siring winning cutting horses. The mare owner does not know whether his mares are carriers, but says he was willing to "roll the dice," gambling that they are not. Even if they were known carriers, he says, he perhaps would have bred them to the stallion anyway, gambling that the offspring from the two carriers would be in the 50% group that were carriers or the 25% group that were normal.
    If one or more of the offspring from those matings fell within the 25% that were HC-affected, he would simply accept his loss, he says.
    New Test for Foals
    One of the more significant accomplishments to date at MSU involves development of the urine test mentioned earlier that can identify HC-affected horses when they are foals. There are changes in the horse's urine similar to what is seen in humans with Ehlers-Danlos type VI. (In this disease, tissue fragility and easy bruising are seen.)
    The prime researchers involved in developing the test were Rashmir; Cyprianna Swiderski, DVM, PhD, assistant professor in the department of clinical sciences at Mississippi State; and Marzia Pasquali, PhD, associate professor of pathology and director of the Biochemical Genetics and Supplemental Newborn Screen at ARUP Laboratories at the University of Utah.
    The test, says Rashmir, leaves some questions unanswered, even though it identifies affected foals. "It does tell you that this is a horse you will have to worry about because it has HC," she says, "but it doesn't tell you how seriously the horse is affected. You don't know whether it will turn out to be a mild case or one that is so severe that it results in the horse being unusable."
    More Than Skin Deep?
    There are other unanswered questions concerning HC. A number of stallions with HC are cryptorchids, Rashmir says. Is it merely the result of continued inbreeding, or did HC play a role?
    A number of HC foals also suffer what sometimes develops into a life-threatening infection. This appears to be happening with too much frequency to be coincidence, she says.
    Does this mean that HC horses are different from other horses in more ways than just defective collagen involving the skin? Nena Winand, PhD, a geneticist at Cornell University who has been researching HC, thinks that might be the case. "This is not just a skin disease," she says. "There is an impact on other tissues that needs to be studied."
    Winand says, for example, that she has seen evidence that HC might have an orthopedic impact. Her investigation into that possibility is continuing.
    There also is the question of whether there is a connection between vision problems and HC. MSU researchers are working on this and suspect that there might be, Rashmir says, but as yet do not have definitive answers.
    Interestingly, the two researchers who authored the first paper on HC in 1978 also mentioned that one of the two affected horses studied had a reported vision problem. The two researchers were Dana J. Lerner, DVM, MS, an equine veterinarian in Monticello, Ill., and Malcolm McCracken, DVM, PhD, a professor in the College of Veterinary Medicine at the University of Tennessee.
    The two horses featured in that first paper were brought to the clinic at the University of Illinois in 1976 and ultimately were diagnosed as being afflicted with HC, according to the researchers' published report in the Journal of Equine Medicine and Surgery. In the report, they described what had been found in a 2-year-old Quarter Horse colt and a 5-year-old Quarter Horse mare. The researchers suspected that genetics might be involved because both horses had the same grandsire. The grandsire was not identified.
    What the two researchers reported after examining the two affected horses would be repeated over and over in the future as more and more cases came to light. Here, in part, is what they had to say about the colt: "A black colt was presented in late February with an 18-month history of abnormal skin. The horse had recently been put into a training program when several abnormal areas in the saddle path appeared to be unusually sensitive. Previous treatment for this had included oral griseofulvin, which was ineffective. Skin lesions were present on the left foreleg below the elbow and on the left lateral thorax at the level of the 18th rib. These areas appeared dry and were hairless. They varied in diameter between 4 and 6 centimeters. Additional skin lesions were noted over the back, between the 13th and 18th ribs (two in number) and one on the right rump over the gluteal musculature. Each of the latter areas was very hyperelastic. With tension, the center of each lesion was readily elevated 3 to 5 centimeters off the body. No resentment was evidenced by the animal. Immediately after the tension was released the skin returned to the original site. Extreme thinness was readily appreciated..."
    With that horse, the researchers reported, there was no evidence of abnormalities within the muscoskeletal or ocular systems. However, with the second horse examined-the 5-year-old mare--the owner had reported a vision problem.
    The concern among horse owners and researchers alike is that the HC problem is continuing to grow because of continued inbreeding that concentrates the gene pool. Horses carrying Poco Bueno blood, in many cases, are prized for their athletic ability and, in the minds of some breeders, if a little Poco Bueno blood is good, a lot is better.
    There has been some speculation that many of the cutting horses carrying Poco Bueno blood have skin that is more sensitive and flexible and, as a result, are more apt to be affected than their counterparts who are not cutting horses.
    As of a couple of months ago, according to Rashmir, the number of horses positively identified as HC carriers stood at 465, an increase of about 300 over the known number of carriers two years ago.
    There can be little doubt that the 465 horses identified as HC carriers represent the tip of the iceberg. So, one might wonder, how will this all play out? Will a definitive DNA test in the future result in fewer carriers being mated to carriers, or will breeders knowingly continue to "roll the dice?" Where does responsibility lie in identifying carriers? Many of the horses offered for sale at the prestigious auctions during the NCHA Cutting Horse Futurity have the potential to be carriers. Are sale companies responsible for alerting the public as to a horse's HC status?
    No, says Rashmir to the last question. "A sales company's job is to sell horses, not guarantee their health status. It comes down to the owners. We can hope that someone will guarantee a horse to be a not a carrier or not affected and, as a result, will get more money for it. That would encourage others to test their horses (when a DNA test for carriers becomes available) or test the foals with the urine test to guarantee that they are not affected." At least one case involving a breeding that resulted in a pair of HC foals via embryo transfer has been in the court system, and the result of that suit might also have a bearing on how the industry handles disclosure of HC carrier status.
    ejforrest-

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    Quote Originally Posted by cowgirlnat View Post
    I was about to ask what LWO was but then it dawned on me. Which has now spurred another question. I was talking to someone who worked at a breeding barn that retired a BEAUTIFUL mare because she kept throwing lethal whites. I thought you could only have a lethal white if you bred two carriers (like you said above). I think she said it was a TB farm, so I don't think color was a goal. If the mare was as good as she says she was, wouldn't it make sense to keep he and only breed her to homozygous dark stallions? Lethal white isn't a genetic disease, but a bad combination of genes, right? Like almost any horse with a white gene if bred to another horse has a white gene, has some chance to have a lethal white baby. But horses w/more white genes have higher chances and shouldn't be bred together.
    TB's DO carry LWO and should be tested for it if you are ever going to breed them, the same goes for QH's as well as paint horses. LWO is homozygous lethal only, it causes a problem with the colon I believe. I would not worry about the horses with alot of white genes as much as horses that are solid, the solid ones are where you could get a LWO because you would never suspect a solid horse to carry the gene, while you should probably assume one with a lot of white patterns does for safety's sake. It is just easiest to get them tested and know for sure. I really wonder if the TB farm was having max white sabinos or true lethal whites and really wonder why they did not get those horses tested and stop breeding them to each other.
    I have also compiled a list in the making of horses and pony breeds with frame (LWO) http://equine-color.info/phpBB3/view...php?f=3&t=1330
    Quote Originally Posted by Belladonna View Post
    There is also some speculation (however no one is prepared to come outright and say it in a test result) that the overo gene itself IS the cause for lethal white foals.
    What do you mean speculation? I have never heard anyone that said that frame did not cause lethal white foals, it is pretty well known that it causes lethals.

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    Quote Originally Posted by CMhorses View Post
    TB's DO carry LWO and should be tested for it if you are ever going to breed them, the same goes for QH's as well as paint horses. LWO is homozygous lethal only, it causes a problem with the colon I believe. I would not worry about the horses with alot of white genes as much as horses that are solid, the solid ones are where you could get a LWO because you would never suspect a solid horse to carry the gene, while you should probably assume one with a lot of white patterns does for safety's sake. It is just easiest to get them tested and know for sure. I really wonder if the TB farm was having max white sabinos or true lethal whites and really wonder why they did not get those horses tested and stop breeding them to each other.
    I have also compiled a list in the making of horses and pony breeds with frame (LWO) http://equine-color.info/phpBB3/view...php?f=3&t=1330
    I agree on testing the solid's for overo as well. I tested my homozygous black stallion who appears brown and only has a star. Everyone thought I was nuts BUT he is a QH, from an appendix sire, and has had some interest from Paint mare owners so I just went ahead and tested. I'd rather be absolutely safe than sorry. To me it just shows responsible breeding even if I was almost positive he definitely wasn't carrying an overo gene in any way shape or form.


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    What do you mean speculation? I have never heard anyone that said that frame did not cause lethal white foals, it is pretty well known that it causes lethals.
    While it's accepted that frame overo is the cause of lethal white foals it's speculated that all overo patterns may have the ability to cause LWO. How true it is or not I have no idea.

    I agree on testing the solid's for overo as well. I tested my homozygous black stallion who appears brown and only has a star. Everyone thought I was nuts BUT he is a QH, from an appendix sire, and has had some interest from Paint mare owners so I just went ahead and tested. I'd rather be absolutely safe than sorry. To me it just shows responsible breeding even if I was almost positive he definitely wasn't carrying an overo gene in any way shape or form.
    I agree, better to be safe then sorry. Any breeding stock I was planning on breeding that had overo patterning or had blood lines of breeds that were known to have had overo, I'd get tested if only for my own peace of mind.
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