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I have been trying to think of a way to post this...I have been banging on, on this site, about breeders and owners, 'putting their hands up' to a ''new problem'' or even a problem that has been around for a while. So I am putting my ''hands up''
Some people will have see the Blog placed by Carol Gill (thank you Carol for posting this) called ''Crufts 2009'' in this blog it states that there is a leaflet supplied by ISAE with reference to a 'new eye problem' in Irish setters. It does not say which lines, or who own the dogs, this problem has been found in..Carol asked me if I knew!! (all three people involved have stated that ''If asked we would not lie'' we would say who we were).
I have one of the 3 ''affected'' dogs, 3 doesn't sound much but when you think that only 7dogs have been tested then this number is quite high.
The dogs have what we think is akin to or is CSNB (Congenital Stationary Night Blindness) which is found in Breards only, at the moment, THIS IS NOT PRA.
The dogs in question have the problem in varying degrees Jas being the worst one affected, she is clinically blind at night.
People have already said that they feel that this comes down a particular line, and named the dog...
PLEASE LETS NOT START SLINGING MUD AT DIFFERENT DOGS, OR ABOUT DIFFERENT BREEDERS. although my bitch and her sister (the other affected bitch) do have many famous dogs, in there lines the THIRD dog has a very different male line, so NO MUD SLINGING PLEASE I am putting this on this site, to get a conversation going, and to see if there are people who have noticed a problem, which I have to say is VERY difficult to see, I have heard of people with totally blind animals that didn't know their dogs were blind, if it happens slowly the dogs adapt to their surroundings, and these, affected dogs, CAN see during the day...
I must reiterate that a breeder CAN NOT legislate against something that they do not know about, and this comes from very diverse lines. If you feel that your dog has any kind of vision problem please ask, where ever you are, this could be a very widespread problem.
Lets now discuss this and see if we can get to the bottom of it ASAP....lets not let it linger and spread through this lovely breed, it isn't PRA, or something painful like Bloat, but it must be very distressing for the animal and I know that it is distressing for the owner involved. We all love this breed or we wouldn't be on this site, and this site is so good to ''get the word out'' and lets see if you can get this eradicated.

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Well said, Dee!
Low COI's are not the answer. It doesn't matter what the COI is of a litter is. If the parents of the litter both carry for the same defective genes there will be puppies in the litter that have that genetic problem that was inherited from the parents, high or low COI, makes no difference. If the parents do not carry for the same defective genes, you can inbreed brother to sister without problem. Inbreeding and linebreeding DO NOT create defective genes, they only increase the chance of homozygosity (the liklihood of two defective genes coming together in a breeding) of defective genes carried with in family line coming together. With certain genetic conditions that are fairly widespread in a breed population even using low COI's exclusively won't help much. Defective genes that are high in frequency in a population are likely to match up regardless of how closely or loosely you breed in some situations. What matters more is gene combination and expression, not the COI. COI is just one piece of information to consider. What will evolutionalize breeding in the future will be DNA tests - they will go a lot farther in helping breeders avoid doubling up on defective genes than low COI's ever could.

You can read more on this at: Blog For Show Dogs (http://blogforshowdogs.blogspot.com/)\\

Specifically these entries:


The Voice of Reason: Dr. Malcolm B. Willis http://blogforshowdogs.blogspot.com/2009/03/malcolm-b.html

ABC's NIGHTLINE: Best of Breed? Pedigree Dogs Face... http://blogforshowdogs.blogspot.com/2009/03/abc-nightline-best-of-b...

The Bible Tells Me So ...
http://blogforshowdogs.blogspot.com/2009/03/bible-tells-me-so.html

Wendy
Actually, Wendy I believe up-to-date scientists are nowadays convinced that a low COI is definitely at least part of the answer.

Removing all animals who may be carriers is not the answer either... this would lead to new bottlenecks and would cause us to loose even more genetic diversity due to the COI becoming higher yet again...

From what I have read, dogs (and humans) are capable of coping with all kinds of influences due to something known as homeostasis which enables the body to cope with all kinds of influences, ie combat disease, influence aging processes, influence fertility and so on. A high level of COI is shown to be detrimental to homeostasis.

I think it is more or less accepted that GDV (bloat) a) has a genetic component and runs in families and b) is very likely to a a poligenetic problem rather than just monogenetic as a simple recessive gene.
Same probably goes for epilepsy in our breed, although there are some breeds with a certain type of epilepsy that has been linked to a recessive gene. I fear in most cases it is more complex. Same obviously goes for HD.

We are not just talking of individual detrimental recessive or dominant genes, there is unfortunately much more to 'this genetic business' than is comprehensible to most of us, myself included!
Some people are putting way too much stock into COI's. They are but one piece of information. What matters is what defective genes are carried and whether they are being combined in a mating. COI's tell you relatedness in a pedigree, they do not indicate the presence of defective genes. Unfortunately COI's have been touted as "the answer" like some kind of miracle cure, they are not. People are being misled by a lot of jargon and one-sided information.



I didn't say anything about removing carriers. In many instances they can be safely bred to clear dogs, but they have to be identified. There are some strong proponents of genetic diversity that are advocating breeding any dog with any condition provided it is outcrossed to keep the COI low. There are some conditions that severly impact on a dog's qulaity of life and I seriously question the advisability of keeping these dogs in the gene pool. There will always be a need to remove affected (carrier) dogs from gene pools. Unaffected carriers, however, quite often can be cautiously used and eventually replaced with non-carrier offspring.



Do you mean homozygosity? Malcolm B. Willis said "honozygosity is not a disease". Unless homozygosity involves two defective genes, there is no genetic problem as such. Inbreeding brother and sister for 20 generations or more in mice will lead to immune issues among other things but there is no one breeding brother to sister in dogs for 20 years. There is no determined COI "safe range". High COI's of 25% or more comprise only about 1% of registered purebred dogs and studies done by Malcolm B. Willis for a number of breeds found breed average COI's ranging around the 5 to 6% range, which is the same or lower than first-cousin pairings in humans which are acceptable in may countries. Willis recent paper also pointed out studies on litter size for a number of registerd breeds over a 100 year period and virtually there was no change in litter size. As he said "inbreeding depression is not inevitable". If it was, there would be oodles and oodles of evidence of the effects of inbreeding depression in registered breeds, but really there is not much of anything to find.



It's familial, no doubt about it. How much is genetic, environment, common practise (following what the breeder recommends)?



There may be several modes of epilepsy inheritance in the breed. I do think they will find the genes responsible in time.



Apparently an HD gene has been found. See: http://blogforshowdogs.blogspot.com/2009/03/breakthrough-discovery-...



Genetics are complicated which is why I emphasize not relying solely on something as simple as just lowering COI's in the faint hope of insuring health. Breeders still need to learn as much as they can about the health history behind their dogs by talking to the breeders behind the pedigrees, using DNA and phentypic heath screenings, and using healthy dogs free of structural prpblems and chronic problems like allergies, etc. The selection bar needs to be held very high.

Wendy
You obviously haven't looked at Jas's pedigree....Her grandfather, on her father's side, is her mothers brother, When you have a high COI you are doubling up on genes, good and bad, and if you have a problem then it is going to emphasise it, likewise it will give you what you want in the way of size and looks etc, but it is this doubling of bad genes that is the problem here, and Susan I agree with you as far as Bloat/Epilepsy is concerned, I was trying to put it in it most simplest terms.
You are right that it is much more complicated, you also have other things like stress and in some cases feeding and exercise but this is not the only reason for the problem, and of cause these dogs have a predisposition to Bloat just because of their shape....the thing that I had a hard time getting my head around was it was the NARROW spring of ribs that were more prone to it that the LARGER more roomy spring of ribs.
When you have a high COI you are doubling up on genes, good and bad,

"When you have a high COI you are doubling up on genes, good and bad" - Only *if* the two dogs being bred carry for the same defective genes. A high COI does not mean there are more bad genes compared with a dog with a low COI nor do high COI's create bad genes. Theer are perfectly healthy, long-lived dogs with high COI's that never produced any problems in their offspring either. There are also low COI dogs with problem. Like I said, low COI's are no guarantee of health in and of themselves. A high COI does mean that *if* there is a particular defective gene(s) with a family line, there will be an increased liklihood of the defective genes pairing when breeding related dogs. The expression of those defective genes will alert a conscientious breeder to the problem and that both parents are carriers. This information can be used to work away from problems. There are no simple fixes, lowering COI's is no guarantee of a healthy dog and if certain breed-specific genetic diseases are widely spread (high frequency) within a breed to rely solely on low COI's is like playing Russian Roulette. Until we have DNA tests for every conceivable problem thorough health histories are vital, especially when used in conjunction with DNA and phenotypic tests.


Wendy
Wendy,
Do you have ANY understanding of genetics, besides the simple Mendelian stuff, ably written down by Dr. Willis in his book?
There has been some progress in genetics since Dr. Willis, you know, and I’m afraid he is not the most notable reference these days. Some of his fellow geneticists think he rather talks the breeder’s talk.
There is this OrigCanGen list started by the late Dr Armstrong, you probably know about?
High COI and loss of genetic diversity and it’s consequences are discussed there, leaving no room for interpretation.
You seem to count on the knowhow of the geneticists when it comes to DNA tests that could clean up our problems.
What do we have so far? CLAD and PRA DNA tests, both autosomal recessive inherited diseases, the simple stuff, so to speak. But there is no predisposition-to-HD or bloat or epilepsy gene, these are far more complex.
Scientists warn us about the loss of genetic diversity but we seem deaf!!
What none of us here should do is try to explain, by hobby genetics, the very complex issues discussed here. There is no room in this for assumptions or gossip. Straight facts, supported by scientific evidence, no less.

Leen
Dee I've analysed pedigrees concerned again, lets cross fingers, your problem and two others is hopefully an incident because otherwise we are facing a new tragedy... Not for 99%, but predominantly near to all over the world.

As for bloat, you come up with new info (for me) that underlines a good survey into facts (pedigrees) could help prevend a lot of misery. Because I see a lot of pedigrees in the Lena site with more and more same names of Irish setters dying from bloat....

What puzzles me, is who tied your hands????? Is it a conflict of interests? Near to all publications on our beloved breed are hypocrit, full of hiding and half truths. Maybe thats where the real problem is....
Henk I would love to give you the third pedigree, it would give you the info. that you need to say that this IS probably a world wide problem, (in my opinion) the third dog has as his sire a dog that at first glance has NO connection with the girls (Jas and her Sister) until you look much further back. I and one of the other owners, have pedigrees coming out of our ears...of cause we are no experts, (but are heading that way with modern pedigrees).
Perhaps we will soon be able to let everyone know the third pedigree very soon, I do hope so.
As far as my hands being tied. First the Professor had thought that it may just be a familial thing, (just one of those things), so we couldn't say anything then. BUT when the third dog was confirmed as affected with this ''thing'' it was no longer just a familial thing. Then we had to wait until everyone concerned was informed...then we had to wait until the breed club was informed, and it was eventually made public. At the moment we are, out of respect for the stud dogs owner/breeder not able to say anything as to the third pedigree until she has her dog tested. As I have said before, if this is a recessive gene, he will at best only be a carrier, at worst affected. We need to respect her for this, having her dog tested so quickly, there are at present, a few more dogs waiting to be tested. These dogs are related to all the dogs concerned.
This third pedigree will be important to all this. So please be patient. Please keep your fingers crossed, but I don't think it will help, I am not usually pessimistic, but in this case......my glass is half empty....
I have informed Leen about my dogs, but I forgot to mention the ones that died of Bloat, I must do so....information is important. The more information the better we can 'see' where these problems are coming from.
Thanks for your openness, again Dee. What I miss in relevant official information is a statement like two affected Irish setters are inbred to currently leading showlines in most of the world. Between diagnosis and real openness a lot of puppies are born....

As for the health report ISCN: near to always breeding in the Netherlands was predominantly from UK showlines. The quick scan was on 2000, not 2008. Mention was made of the vet Wim van Gemert, I hugely respect him for his decision to stop breeding from a genepole providing many cases of epilepsy. We need more of these people....
Henk I am of the opinion (and this is only my observations) that Epilepsy is connected with Bloat, I don't know how, or even if it actually is...it seems to me that the litters that have Bloat in them seem to have a high percentage of Epilepsy or Encephalitis (as you know this has the same symptoms as Epilepsy) I think breeding from these lines is a mistake. This is why I lost all my lines in the 80's I couldn't perpetuate this dreadful problem, and bring pain to any puppy owners of mine.
Yes these two girls do have a very high inbreeding to currently leading showlines in most of the world. The third dog has, as his sire, yet another line that is in a lot of show dogs, again all over the world...and you are very rite (unfortunately) there has been many many puppies produced between diagnosis and real openness, but we are now discussing it and this has to be a step in the rite direction. We will I hope soon have the third pedigree, and all the implications of that to discuss.
In my experience Bloat is caused by many different things and Irish Setters certainly seem to have a predisposition to it but I do not neccessarily believe it is solely heriditary & therefore unfortunately I doubt we will ever have a DNA test for it.

The cases I have personally know are these;-

A male who was always a fussy eater, one day decided he liked a certain food & I in my excitement allowed him to have as much as he wanted, within hours he was at the vets being operated on. He never had bloat again & died of old age. None of his very few offspring to my knowledge have been bred on.

A bitch, not of my breeding but loosely related, started to bloat for the 1st time when she was in whelp, she was "managed" by lifting her rearend & massaging her until the gases escaped - so no torsion. This happened several times but stopped whilst she was rearing her puppies. Unfortunately she bloated again 3 more times, usually around her seasons, each time needing veterinary treatment & we thought the kindest thing was to put her to sleep. Again none of her puppies have been bred.

Next a dog I bred but did not own, was wormed & his son was also wormed, within hours of each other they both bloated!!

Whether it was coincodience or due to genetics his sister, my bitch, also bloated sometime later. She had been wormed a few days before.

The dogs had been dosed with Drontrel + but mine was with Panacur liquid, has anyone else noticed a link with worming?

My bitch had already had one litter & as far as I am aware there has been no problems & obviously she wasn't mated again after the bloat.

On the eye problem is anyone keeping a record of the dogs who have been tested using the method described in the ISAE leaflet. All my dogs had an enjoyable time running around in the dark, even the 9 1/2 year old managed perfectly well. Of course 4 of them are under 4 years so I mustn't be complacent & will test again in the coming years.

On blind dogs & how they cope, we had a Shih Tzu who had glaucoma & ended up having both eyes removed - so definately no vision. He managed perfectly well even when we moved house with him at about 12 years old, being a small dog he was happy to be in just the house & garden & soon found his way around. When we spoke to him he would look straight at us & you would swear he could see!!

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