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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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agree with you dee,
i was beginning to think the the eye problem situation was getting lost in this forum over the last few pages. i have to readily admit the coi argument is way over my head (although ive found it interesting reading and im sure i will look and learn about it) as im just the owner of a red setter dog with lopra who is just OUR ADORABLE PET.(the love of our life)
its true the only way forward is work together and for owners to have their dogs eyes tested(layla never showed any signs of been distressed at night due to night blindness.she may well have adapted to her disability long before it was diagnosed.the professor said shed had it for about 18 months) at regular intervals.we know too well if there is a problem such as lopra or the problem that you have in jas nothing can be done to help the dog ,but we can stop it from been passed on to future generations and this can only be done by eye testing and dna ing.yes the dogs adapt,its a painless disease but its heart breaking seeing such a beautiful dog restricted to what she can do just because shes blind and i dont want anybody to go through what im going through if something can be done to prevent it from happening in the first place
Sorry dee you are right the whole point of this forum is to find dogs that may be affected with CSNB, with the discussion swinging to COI 's which I admit I knew little about before. i just wanted to come upto speed so I could follow and understand the discussion better. Is there any way the kennel club could help with this problem or could the breed clubs possibly do a liitle more to encourage people to come forward?
From the ISAE website I understand there will be testing in shows. Last means numbers, so possibilities of dropping costs. As both LOPRA and CSNB is still relatively unknown, some help from visual media (BBC-Jemima?) could be of help - maybe you can interest sponsors that way.

Questionnaires - a clear possibility could be ISCN they send out those to all pedigreed IS, lineage mostly relevant. I don't believe asking sitemembers to test their setters in dark rooms will help much now in relevant cultures theres longer light and most sleep overnight.
"some help from visual media (BBC-Jemima?) could be of help"

Why?

Jemima Harrison is not formerly trained in genetics, she is not working in an area of genetics, she is not a dog breeder, and she is not a veterinarian. She has basically just taken some one-sided opinions expressed on an email list, found a handful of like-minded people, and a few sick purebred dogs (which may or may not have been bred by show breeders) and put them all on film.

Read more here: http://blogforshowdogs.blogspot.com/2009/03/abc-nightline-best-of-b...
I don't recall saying that COI's predicted anything, some may feel they do but that is a mistake. All that COI's indicate is relatedness within a pedigree, not health not potential health. And for 100 years breeders have been able to eyeball inbreeding just by looking at a pedigree, long before the days of computers and pedigree programs.

As for the comment genetic load ------------ genetic diversity:

All animals, dogs, people, etc. carry a genetic load of 4 - 5 defective genes. The idea behind a low COI is that by outcrossing there is less chance that two dogs (or people) carrying the same defective genes will pair up and produce offspring with that genetic problem. It works to some extent with people although we do still have genetic diseases cropping up in people. It works well in wild populations that are under the rigors of natural selection.

However, the model does not fit well over populations of purebred dogs. Purebred dogs are not subject to natural selection as wild popluations are. We spay/neuter thousands if not millions of perfectly healthy purebred dogs every year. Human and wild populations are not subjected to that kind of reduction to the genepool. If a person or wild animal survives to sexual maturity there is a good chance he/she will reproduce, not so for dogs.

In addition, most breeds of dogs are subject to a limited number of breed specific genetic diseases that are breed specific because they are prevalent in the breed, meaning the genes are widely distributed and highly frequent in the breed. I don't know how a low COI is going to help in instances of breed specific genetic diseases. And breed specific genetic diseases is what all breeds are up against, not the less frequent things that affect all dogs, both purebred and mixed breed.

Sure low COI's would work great for low frequency diseases but high frequency diseases just don't fit the model. That's why I wish people would focus less on COI's and more on promoting open databases and getting DNA samples in to the research studies. Because that is where the future lies, in hard cold DNA results, not some average probability and hoping your dog doesn't fall into the outlier zone. There are no studies on COI's in purebred dogs which look at health and breeding practises. Just because a dog has a high COI does not mean it is healthy. Just because a dog has a low COI doed not mean it is healthy/ It all depends on the genes inherited from it's parents. On average a low COI should increase the liklihood that defective genes are not matched up in a breeding but like I said with defective genes that are highly frequent in a breed, it just isn't going to work. You still need some way to identify carriers.

Genetic Diversity has it's place and one of the best recommendations is to use more males in breeds and not only breeding to popular sires. We all know that leads to a glut of half brothers and sisters with no where to go for the next generation. There is a need to maintain distinct lines and to try to prevent lines from dying out due to lack of popularity. These are all important to breeds.

COI's matter but they are not everything. On the OrigCanGen list recently there were members asking for the COI of the recent Crufts winner as is that alone would be the sum of this dog and his quality. It's important not to put more emphasis on COI's than getting as much information as possible (including health testing) and taking all information into consideration when planning a breeding.

Wendy
Wendy from all scientists read bottom line is: lower coi means bigger chance for a healthy life.

Ofcourse it is important to collect as much health information as you can... But get your feet on the ground, breeds biggest tragedies (and for their humans!) did involve our topbreeders in USA and UK. It was huge inbreeding to their dogs providing high coi and a huge number of blind Irish setters.

The problem wasn't Kinvarra Kermit or Rheola Benedict (neither their coi), the problem was all Irish setters bred with umpteen times these dogs as their forebearers in extended pedigrees meaning both (often not always) huge coi and ditto tragedies.

Another problem was relevant information openly published for everyone in time. When the pattern for PRA was known in the UK and carriers as well, in the USA breeding suspect lines was continued.
No Henk, the PRA in Irish Setters was not about inbreeding. Inbreeding does not create defective genes but will bring them to the surface more quickly than outcrossing. The problem with PRA came about because dogs carrying the recessive unknowingly distributed the recessive gene throughout the US Irish Setter population at the time. Many of the breedings were outcrosses so it was well spread in the population as a result. If the issue was oe of inbreeding the genes would have stayed within the family being inbred on. Wide distribution of defective genes is an issue when trying to deal with defective genes by using low COI's, you spread the problem outwardly. As for the scientists recommending low COI's,the problem is that they are applying a wild popualtion model to domesticated populations with the assumption the populations are the same. They clearly are not as I pointed out earlier. Unfortunately scientists are not aware of how purebred dog populations are set up and the high frequency of breed specific genetic problem that are unique to each breed. A person who does understand both genetics and dog breeding for show is Dr. Malcolm B. Willis - he is both a geneticist and dog breeder. He does not see an issue with inbreeding when used by responsible breeders who know what they are doing. His recent article in Our Dogs made it quite clear that he disagreed with the KC's decision to refuse to register dogs from inbred breeding methods. He cited many studies that DO NOT indicate that inbreeding depression is occurring in various breeds. He says that inbreeding depression is not inevitatable. Inbreeding (COI > 25) comprise only 1 % of the registry and his studies have shown the average COI for the breeds he looked at fell around 5-6%, within low limits. Throw in that only 20% of registered dogs are coming from the "fancy" that leaves a whopping 80% coming from one-time breeders, backyard breeders, commercial kennels, and puppymills - folk who could care less about health or health testing and who in general have outcrossed pedigrees because they just breed to whatever dog they can find. And then there is the huge unregistered purebred market which don't even factor into the kennel club registries, but they are listed as their apparent breed on vet records all the same. It's ridiculous to be laying all the blame on show breeders for the health problems some breeds are experiencing. And plenty of sick dogs come from one-time breeders, backyard breeders, commercial kennels, and puppymills despite the low COI's and outcrossed pedigrees. There is some good stuff coming out of the genetic diversity discussions, most especially the recommendation of using more males in a breed rather than popular sires but purebred dog populations are more complex than most scientists would be aware. Purebred dog popultions are not random populations but split up into speciallized subgroups. Right now we don't even know where the problem dogs are coming from. Are the coming from the show breeders, one-time breeders, backyard breeders, commercial kennels, and puppymills, or the unregistered purebred breeders? All I know is that most show breeders, myself included, care very much about the health of our dogs and the breed and we health screen our breeding dogs. I absolutely resent having fingers pointed at me for being a show breeder who is responsible for the entire health of a breed. Show breeders comprise less than 20% of registered dogs. It's patently ridiculous to be pointing all fingers at us (and inbreeding methods).

Read more at:

http://blogforshowdogs.blogspot.com/2009/03/malcolm-b.html
http://blogforshowdogs.blogspot.com/2009/03/bible-tells-me-so.html

Wendy
Because the episode in IRS history where extinction was close is apparently still not known into details and relevant for today’s happenings, here a reaction to Wendy’s post.

Wendy: Ch. Kinvarra Kermit had a COI of 4% and that is based on a pedigree database that goes back to Palmerston.

A no problem COI percentage, according to scientists.

Wendy: I don't have a full pedigree for Rheola Benedict.

I have so can compare both cases of outbreak of PRA. Benedicts parents Rheola Bryn and Rheola Mallie became main ancestors of show bred Irish setters in the UK. Inbreeding to that mating explains NUMBERS of blind Irish setters, nearly leading to extinction of IRS in the UK.

Wendy: Ch. Kinvarra Kermit was a son of English import Ch. Kinvarra Mollie of Gadeland. A brother and sister breeding of two of her puppies produced two blind puppies. The significance of this was not realized at the time. If it had, the spread of PRA could have been nipped in the bud.

Around the time of birth of these puppies in the USA, W.J. Rasbridge started in the UK breeding with a blind bitch from a brother/sister mating in Rheola-kennels, to chase a pattern. Kermit was more times related to source-animals spreading the gene.

Rasbridge had contact with the main USA breeder at the time Lee Schoen who himself was befriended with Kermits breeder Eldredge. Question is why UK information apparently did not reach USA-circles in time, that is before the tragedy happened….

Wendy: Kermit was a carrier of PRA and he was used widely. He was not inbred exclusively on but was bred to many different bloodlines and the recessive that causes PRA was unknowingly spread to many different lines. Eventually carriers were unknowingly bred to carriers and blind puppies started popping up everywhere. That Kermit carried for PRA had NOTHING to do with his COI (which was low) nor because of inbreeding. It was all about him being a carrier and being used as a sire. No doubt he was not the only carrier in the US at the time.

The NUMBER of blind Irish setters in the USA was caused by inbreeding to under more Kermit.

Wendy: It was basically a situation just waiting to happen. And one which has been completely rectified through the efforts of breeders who pursued test-matings which eventually led to the DNA test which has virtually eliminated PRA in Irish Setters worldwide.

At what price? Just how many Irish red setters have been suffering from blindness before the test was there? Or CLAD and the rest with a more complicated way of inheritance like (probably) epilepsy, bloat etc. What is your opinion on breeding concerned in this topic? Do you feel it is safe to continue this practice?


Both pedigrees concerned Kermit and Benedict. Note the related lines.
IRS going extinct? They were going blind, not extinct. They would have gone extinct had breeders discarded all blind and carrier animals and not engaged in any sort of test-mating approach to avoid the problem. But no, the breeders dug in and went through the brutal, heart-wrenching process of test-mating their breeding stock.

We need to establish a time line here, and I will when I get home this evening. The brother and sister breeding would have predated Kermit. Ted Eldredge started in the breed at 14 years of age and Lee Schoen was his mentor. When the blind pups came up Ted said in a later interview that he asked Lee about it and was advised not to worry about it because it would go away. And it did being lost in the predominantly PRA clear lines of Irish Setters in the breed at that time. This would have predated the test-mating that Rasbridge was doing. Let's not forget that the internet and blackberries and email were not around at that time and people still did a lot of letter writing back then. It would have taken time to see the significance of the problem (similar to what is happening with these three night-blindness cases) and to realize it was an inherited trait, etc.

Hindsight is 20/20. People did the best that they could at the time. Lee Schoen and Ted Eldredge and all the other breeders in that day would have had the best interests of the breed at heart. You don't voluntarily spend decades at something you don't care about. Nobody sets out to breed blind or unhealthy dogs if they care about the breed. You can sensationalize what happened with words like "tragic" and "suffering" all you like and trying to lay blame, but this is simply a genetic event that happened which breeders addressed and learned from. It's nothing more and nothing less.

No one is to blame. No breeding method is to blame. If anything, had the timing been more syncronized, inbreeding could have been the process for avoiding the entire problem. Had the UK PRA issues been known at the time that the two blind pups cropped up in the brother and sister breeding, two and two could have been put together and possibly nipped in the bud while the problem was still within family lines, and/or test-mating may have been started earlier. Inbreeding is highly effective for indentifying or disproving carriers and for bringing lurking defective genes to the surface. It provides a road map for identifying carriers and inheritable problems which outcross programs simply do not and cannot. If we had low frequency defective genes and sufficient population size, low COI's would work (though never as well as in wild population subject to the rigors of natural selection) but that is not what breeders are working with. Instead of a large population containing low frequency defective genes for 400+ illnesses, most purebred dog breeders are dealing with small population with high frequency defective genes for a a handful of known issues within the breed (give or take a few, some breeds are dealing with more than others). In Irish Setters the more prevalent problems are epilepsy, bloat, HOD, IBD for starters (PRA is not even on the radar screen anymore thanks to test-meting and DNA testing). Right now I would be at equal risk for epilepsy with breeding to any Irish Setter in the world since all the Irish Setter populations have issues with epilepsy. HOD is an issue in North America but does not seem to have cropped up in the UK. So I could take an Irish from a HOD prone line and breed to a UK Irish (low COI) and if HOD is a genetic condition (which many suspect it is) then I should get no HOD in that litter, and likely will have clears and carriers. If I am lucky and choose a clear pup, I could keep breeding to UK dogs and never see HOD again. Or if I am unlucky I could choose a carrier and breeding into UK lines will unknowingly put the defective gene into that population, and eventually it will pop up all over. (This is essentially what happned with Kermit in the US). I could take my clear US/Can ex UK pup and breed to a US/Can dog that never has produced HOD and might get clears or carriers, it all depends on whether that dog was a carrier or not. If I was unlucky and picked a US/Can ex UK pup that was a HOD carrier then breeding back into US/Can dogs could result in clears, carriers, or even affecteds if the dog being bred to was also a carrier. The problem is not knowing who the carriers are. The low COI approach on it's own is based on luck too, getting the clear one when you can't tell clear from carrier by looking at them.

Blaming anyone for the spread of defective genes is like blaming people for spreading a cold. Futile. There's no starting place and no ending place to germs/viruses or genes. The hard evidence is in the DNA research and test development. That's what people need to support with pedigrees and DNA samples - so simple and potentially productive. All this retrospective blame-laying is not only disheartening and discouraging but it directs attention away from the main issue, which at this point is the initial actions to realize the scope of the problem of the nightblindness, determine prevalence, and develop a plan of addressing the issue. Enough with blaming the breeders of the past. It's about as productive as wondering which one of my ancesters is responsible for my near-sightedness as if some how they must atone. I pop my contacts in every day and never give my eyesight another thought. Unfortunately there are some dogs going blind as a result of this problem. While there is nothing that can be done to reverse that, blaming won't fix it, people can come together to try to find a way to avoid any more dogs coming down with this. It's about being proactive and thinking positively, rather than wasting energy in blame and awfulizing the situation.

Wendy
Henk, one can improve the "chances" of producing healthy dogs with a thorough knowledge of the heath history and a concerted effort to breed away from known problems (if any) and problems that crop up (if any).

I would rather put my faith in the puppy from a conscientious breeder of 40 years than in an outcrossed pup of 0% COI with unknown health history.

I keep thinking back on a breeder on one of the online genetics lists describing two litters she had, one linebred, and the other outcrossed/low COI. The linebred litter lived to old age without any health problems and the low COI litter had several die at an early age due to severe health issues. Her comment was that the linebred litter was produced before she learned about the value of low COI's and genetic diversity and now she knew better. The irony of it all made me laugh in disbelief. Health problems arise from the combination of defective genes. She had healthy linebred dogs to breed from. The linebreeding did not bring any problems to the surface, suggesting that there were no defective genes common to the family line - they were healthy and free of defective genes within that family, clearly they were a breeder's dream. And yet she saw more value in the sick outcrossed litter by virtue of it's low COI. That defies common-sense.

Combinations of linebreeding with outcrossing as has been practised by breeders for over a hundred years has not shown the degenerative changes that scientists would predict. Dr. Malcolm B. Willis did a followup study of another study of litter size in Bloodhounds, and over the 100 year period of the observations there was only a half pup in the difference. This is not indicative of inbreeding depression as would be predicted. As Willis stated, "inbreeding depression is not inevitable".

There are no identified levels at which point linebreeding becomes dangerous. Genetic diversity proponents will wave inbreeding studies of mice and wild animals at you as proof of the dangers. But pick through the examples and one soon realizes these are extreme examples that are not relative to how dogs are bred. Here are three examples typically used to support the agenda that breeders should not breed related dogs:

(1) Inbred mice are colonies based on 20 or more generations of brother and sister breeding. No one breeds dogs like that.

(2) Cheetahs are so inbred that they do not reject skin grafts from each other. They are estimated to have descended from one female and her cubs 10,000 years ago and the population held despite a high level of inbreeding until the past 100 years. They are now on the endangered list, but it is not because they are inbred but because of human encroachment on their habitat, farmers shooting them, and being unable to defend their young from lions which are so much bigger and stronger. The populations of Cheetahs sustained for 10,000 years but not the last 100 with human interference. They have also sustained despite exposure to contagious feline diseases and have developed immunity; the MHC is functioning despite the extreme inbreeding, and despite predictions that such a high level of inbreeding would damage the MHC and make it impossible to fight off infections.

(3) The latest example being flouted is the Isle Royale inbred population of wolves. The skeletal remains of wolves that have been found show that 58% of the wolves have transitional vertebare and some are calling for a genetic rescue of the wolves. And yet, the population has sustained for 50 years now, despite predictions of extinction within 20 years. The population is balanced with a 10% birth rate and 10% dealth rate. The wolves are bringing down strong bucking moose ten times their size. Clearly they are not hampered by the transitional vertebrae at this point in time *if* it is even present in the active population and was not just seen in the remians of unfit animals eliminated through natural selection. Transitional vertebrae are incidental findings on xrays in dogs and don't normally cause a loss of functioning in most cases, and rarely progress to equine cauda.

These are the current three examples used to demonstrate the dangers of inbreeding in purebred dogs. And even though these are extreme examples, all of these populations have sustained over long periods of time despite such intensive inbreeding, levels at which NO ONE breeds dogs. The reason extreme examples have to be used is because there are no studies showing degeneration of purebred dogs based on the level of linebreeding and outcrossing normally used by breeders.

So Henk, please don't discount the value of health histories and breeders' long-time knowledge of lines of dogs, in preference for low COI's. If one knows nothing about the pedigree then by all means they should outcross, but if one knows the potential in a pedigree, that knowledge can allow conscientious breeders to "hedge their bets", and push "chance" in their own direction, with more predictability than low COI's ever can. Of course it depends on knowledge and dedication on the part of breeder, but so does every breeding venture regardless of the breeding method used. There is a place for every breeding method available (linbreeding/outcrossing/occassional inbreeding) depending on the particular circumstances. It's way too simplistic to blame apparent problems in breeds on a single breeding method - how the method is applied is what matters. Most of the dogs that make up registered breeds (a good 80% of the AKC registrations) come from one-time breeders, backyard breeders, commercial kennels, and puppymills who do not health test and normally have very low COI pedigrees often with all unique individuals, and the dogs coming from these breeders are often far from healthy - and they don't even include the breeders of unregistered purebreds. And yet, it is show breeders who produce less than 20% of registered dogs, who do health checks, and mainly use line-breeding and outcrossing who are expected to shoulder the state of health of 100% of the breed.

Wendy
Wendy I know your website, your efforts to dive deep into health history, your writings in Canine Genetics, in a nutshell your version of the truth. It paints passion for our breed.

It is very healthy when people do not believe immediately "new" findings, even if -in the case of Canine Genetics- it is with a lot of collected wisdom.

We've had so called linebreeding as religion in dogpress since start of dogsports, so I don't think it will all change soon now scientists (not all) start preaching another religion.

Collecting as much information as possible, all sides in, is in my eyes the best attitude.

Analyzing most pedigrees of leading scenes in English speaking cultures, tells me old fashioned linebreeding-advocates and nowadays scientists would share one opinion: this is not linebreeding but inbreeding and has gone way too far.

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