Primary Ciliary Dyskinesia (PCD)
For the sake of good order the dog related in this thread is the above mentioned OES and in no part of this thread am I referring to any other OES who may be called “Zorro”. The original thread seemingly lead to some confusion which I really do not understand, however since I find this is an important theme for all breeders I have decided to start this thread one more time. In late December we received our quarterly issue of the magazine “Old English Sheepdogs”, in this edition was an article written by Chris van Beirendonck-Lemprechts, in this article she went on to tell about an experience she had in 2006, since we also have a dog from Chris who was born in 2006 we read this article with interest. Unfortunately since no dogs were mentioned we were a little unsure if our OES “Fairbancks of Snowboot Bears” could be involved in this and if he possibly came from one of the affected litters. Due to the fact we were getting ready to mate our dogs we were now a little uncertain and I sent Chris an e-mail requesting more information, furthermore I also contacted the University of Liege, Belgium and spoke with a Dr. Frederik Billen whom I explained my suspicions to and this gentleman confirmed that the Sire from our dog was the dog involved. About a week later I had another telephone conversation with him and we were shocked to discover that our dog came from one of these litters. In addition to this bad news we were informed that the University would like a blood sample from “Zorro” but in no way could they give us reliable information as to his actual status, healthy – carrier – affected. In between times I had spoken to Chris and we have received valuable information regarding her experiences, please let me stress that in no way do we hold Chris responsible, then there is absolutely no way to detect a carrier dog and unfortunately she had two which allowed affected pups to be observed and monitored. With all this happening in a short period of time and with absolutely no warning we now had to make a quick decision regarding our breeding plans, since there was no way to be sure if he was a carrier and personally I do not think we need more genetic diseases in our breed we have decided not to breed with him. Although many people will disagree with me and a common comment in breeding circles is quote “ oh we can breed genetic diseases back out” unquote, I would like to know when are we going to start and if we have started then why do we still have HD, PRA, Cat, etc. etc. in our wonderful breed. In most cases when you read about genetic diseases it is mostly related to as a mathematical formula where the result is foreseeable, in this case the formula was completely wrong as in the first litter of nine pups 3 of them were affected which is 33% and in the second litter of five pups once again 3 on them were affected which is 60%. In the article Chris wrote she repeated the mating three times and observed no more sick pups. I think in this case we have to look and see if we have to have an additional condition to bring the illness out, e.g. atmospheric pressure, high humidity, excessive heat or maybe even through the food or water the mother has been digesting. I found this link which is about Irish Wolfhounds and I found it very interesting therefore I would like to share it with you http://www.irishwolfhoundstudy.com/pcd/casal.htm I would really like to start this thread again and if any of you have had experiences with this disease please share and tell me about it. |
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dairymaid wrote: In most cases when you read about genetic diseases it is mostly related to as a mathematical formula where the result is foreseeable, in this case the formula was completely wrong as in the first litter of nine pups 3 of them were affected which is 33% and in the second litter of five pups once again 3 on them were affected which is 60%. In the article Chris wrote she repeated the mating three times and observed no more sick pups.
Thanks for clarifying, Stewart. And, no, the statistical formula is not neceassarily wrong. With an autosomal recessive mode of inheritance, which Kerry suggested appears to be the case in other breeds so far - and your IW article link bears this out - you would only expect to approximate the rates of 25% clear, 50% carriers and 25% afffected produced in a mating between two carriers if the mating produced 100 puppies, which is clearly not practical (or desirable). So you can definitely have litters where all are affected, none are affected and anything else in between. Luck or lack thereof of the genetic draw. Taken cummulatively, you will approach the above numbers. It's a statistical concept that geneticists fully understand, but which is enough to drive breeders to pull their hair out in some cases 
If you had posted the number of the last litter, we would be able to calculate % of total puppies affected, which is more interesting than on a per litter basis, and it would be moving towards 25%, which is where you would expect it to converge the closer you get to 100 puppies. If all puppies born were affected, we would be closer to expecting an autosomal dominant mode of inheritance, which is clearly not the case. And if only male (or only female) puppies were affected (again we would need a significant sample number to say so with a high degree of confidence), we would suspect a sex-linked mode of inheritence. Presuming this is not the case <?>, we can probably rule that out as well. If it is indeed an autosomal recessive mode of inheritance that is, in the grand scheme of things, good news, as diseases inherited this way tend to be easier to predict and therefore avoid producing. Please understand, however, that all dogs (and people and so on) carry some usually unspecified lethal recessives. ALL dogs. In the case of Zorro's sire and dam, we happen to know what one of them is and that is very valuable information. But just because a given dog (or bitch) doesn't (or hasn't yet) produce anything, does not mean the dog does not carry any "bad" genes. Rest assured that every dog every one of us owns carries something deterimental. We are only aware of the potential for a limited number of them - whether or not someone some day will produce something depends partly on the frequency of the deleterious genes in the population as well as a touch of luck, bad luck we would normally say - and we can test for even fewer. The fact that Chris experienced this and shared her experiences with the breed is a critical first step for controlling this particular disease. But no breeder should draw a sigh of relief and presume their dog is clear of all things and that we'll ever be able to breed with zero risk, because chances are we never will. To believe otherwise would be detrimentally naive. Yet as breeders we tend to only believe what we see and that if we can't see it our dogs must be healthy (which is measurable and may be the case) and only capable of producing disease-free offspring, which, in combination with the "right" mate, is not necessarily the case. A much used sire produced a litter of puppies with some kind of renal disease. Time and time again he was used and never produced this. In combination with one particular bitch, he did. Proving that he was a carrier (exact mode of inheritance not known to the best of my knowledge, but I don't believe it suggested a dominant mode of inheritance). Because he was bred to so many bitches and produced so many puppies and only produced this in one case, this suggests that the spread of that gene (or those genes, if polygenic) in the OES population, or at least a given OES population, was probably fairly low. However, here's the kicker, he was widely used, potentially spreading those genes throughout the breed as his get and puppies thereof have been and continue to be widely used, enabling further spread. In fact, all of my younger dogs go back to a full brother of his, whose status was not known. We may not know the full effect, if any, of an event like this on the breed for decades. But it does speak strongly against falling into the popular sire trap. Not because he wasn't a nice dog - he was - or shouldn't have been used - he deserved to be used. Just not by everyone and their grandmother. Time and time again we do this, and this is one of the most detrimental things we can do as breeders for the sake of the breed as a whole. Yes, Stewart - I know I'm speaking to the choir
In cases like Zorro's - who has affected littermates, so presuming we are indeed dealing with something that has an autosomal recessive mode of inheritance, he would have a 67% chance of being a carrier himself - we can come to understand the particular risk for a particular disease. Similarly, we know that any dog his sire produced with bitches who have no known carrier risk themselves would have a 50% chance of being a carrier under this mode of inheritance. I.e in some cases risk is measurable. In the case of the dog above, gone for a number of years now, by the time he produced a particular form of renal disease he had already been widely used, and his get were already being bred. Do we retroactively stop breeding everything that goes back to him? We would be taking out a significant portion of the gene pool, and not just in the US at this point. Without even knowing the mode of inheritance or which of his get are not carriers of the disease by genetic luck. But since we don't know this, we toddle on, hopefully at least aware of the risk that is back there, but often probably not unless people are willing to speak up and can do so without fear of retribution. What we're going to discover as more information on genetic disease becomes available to us is that we are all indeed breeding carriers of SOMETHING as long as we breed at all. And the more something we know, the more impossible it will become to ever declare any dog completely clear of all things (recall that they are not now, we just don't know what they are carriers of). So breeding decisions are only going to become harder and harder as we go along as more and more of what has always been the case becomes apparent to us. Of course, information is a good thing, because ignorance is NOT bliss for our dogs or the people who love them. But the increased knowledge will also force us to understand that we will be making more and more decisions based on relative risk analysis and "lesser evils". Not because our gene pool has become more "polluted", though certainly we have the ability to cause that and probably have in our ignorance shifted it towards an increase in some diseases and a decrease in others, but because we will finally understand what geneticist already know: There are no genetically perfect dogs. None. The best we can do is understand carrier risk (which can only happen when people share information) in order to avoid producing affected dogs, as well as minimizing producing more carriers, all the while supporting research into the most common and dehabiliting disease in our breed. Which reminds me. Health survey. Have you filled it out yet? (I know Stewart has - thank you, Stewart!) http://www.keysurvey.com/survey/211252/2567/ Kicking the soapbox aside and hoping my car will start in this deepfreeze. So tedious. Hope it's warmer your way, Stewart. 
Kristine |
to you both! |
| To you both as well. If all breeders were willing to concentrate on the health of the dogs, and not just the popularity contests, we could have a much healthier dog. It is encouraging to see breeders share the good and bad info.
Yes, I have filled out the health survey for all of my OES that apply to the time period listed. Everyone should!!! |
| Thank you for the very in-depth explanations. This certainly offers illumination to the phrase "it's all a genetic crap shoot". |
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