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Bill Fosher
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I realize that North...but I stated EACH pup had this chance set up ( 25/50/25). The luck of the draw is natures doing( or if you prefer the roll of the dice). LOL hence the reason I have 2 boys and one girl, SIL has 3 boys and other SIL has 1 boy. Since there are only 2 options in sexes if I was looking at the whole group of kids and applying that I should have 50/50. But we have 6boys to 1 girl and no where in math does that equal 50/50... But if you apply the 50/50 PER child then you have your 50/50 chance. So in that litter of pups, Yes all could be affected. However, EACH pup had a 25/50/25 CHANCE.

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. Of course the KC show people are likely to say that breeding only normals is the way to go and that good breeders will do that; they will say that regardless of the fact that the ABCA registers carriers. Of course some breeders will decide to breed only normals; they will do that regardless of the fact that the ABCA registers carriers. The fact that the ABCA's recommendations are against excluding carriers from breeding will cut no ice with them,

 

 

Actually the concensus of opinion here in the UK is that even if a dog /bitch is DNA 'd a carrier, provided the animal is worth breeding there is no reason not to bred back to a DNA normal. Why assume that all show breeders are going to be so blinkered as to exclude CEA carriers from the gene pool???

 

Interestingly the list of DNA results referred to is taken from results that have been published on lists I belong to of which the website owner is also a member.

 

I was also interested to see that out of over 100 dogs tested only one result was from the USA, how many dogs in the USA in the working fraternity been tested and are their results given anywhere. The testers in Europe have been very frank with their resuslts good or bad.

regards karin

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Would someone like to explain what CEA is (in non breeder terms). I am retired from the people medical field so I can handle medical terms and I am very interested in any medical conditions. I have a 5 month old BC and was owned by another for 11 years. I want to keep up with anything that may affect my dogs and do not mind doing research. thanks for any "lay", explanation you can provide. Joe Anne, Mirra, Sitka & Phoenix

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Bill, I'm away from home with such limited computer access under such wretched circumstances that I'm probably in an even worse position to give this full consideration than someone who's lambing.

 

Nevertheless, while I still disagree with you about the desirability of specifying that carriers are registerable, I think you have a point with regard to the rule barring affected dogs and their offspring. I still think it's too soon to consider changing the rule excluding affected dogs from registration (other than NB registration), but I think perhaps we should now change the rule barring registration of their offspring. I have to say that this is tentative thinking at this point, and I would need to do more thinking about it and consultation before I felt sure that was the way to go, but since we're now able to determine for sure whether the offspring of an affected is or is not affected, it makes sense to me that we should focus on the dog itself in deciding whether it's registerable or not, and not on the status of its parents. (BTW, I don't think the results of DNA tests will be applied retroactively to de-register dogs already registered who are now found by the DNA test to be affected. If I'm right about that, this is only an issue for the future.)

 

Tildy, dogs need to be DNA tested for CEA only once in their lives. Breeders who have their breeding stock examined every year or two are focusing on other eye diseases.

 

>

 

Karin, I didn't say that all would, I said it was likely that would be the position of show breeders generally. I based that conclusion on the attitude US show breeders have taken toward testing for genetic disorders in general up to now. Perhaps time will prove you right about the consensus you say is developing in Europe; if so, I will be pleasantly surprised.

 

I have no idea how many dogs in the USA working fraternity (or in the USA show fraternity, for that matter) have been tested so far -- I know there have been a few clinics, but it's early days yet as the test has only been available for a couple of months. I also have no idea whether there will ever be a website listing the test results of working dogs by name, since I don't really see the point of doing that.

 

Joe Anne, you can find a brief explanation of CEA as well as other health issues of border collies at http://www.americanbordercollie.org/Health...r%20Collies.htm . (Note that the CEA discussion there has not yet been updated to reflect the availability of the DNA test.) If no one has provided additional references for you by the time I get home, I will add a couple at that time.

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Hi JoeAnne

 

Here are a few more sites with info about CEA. The last one is from the company which has the genetic test, with an article by the researcher who led the development of the test.

 

http://va.essortment.com/collieseyeanom_rlpf.htm

 

http://www.upei.ca/~cidd/Diseases/ocular%2...e%20anomaly.htm

 

http://www.optigen.com

 

Some articles you will find talk about a high incidence ? that relates primarily to rough collies and Shelties. Incidence is much lower in Border Collies.

 

I have a little bitch who is mild CEA affected (choroidal hypoplasia but no colobomas) ? fortunately it doesn?t seem to affect her vision (although she may have more than usual difficulty working directly into the sun.) I have her looked at by a veterinary ophthalmologist every 12 months as a precaution. What was interesting at the last check (age 2.5 years) was that the defect was less obvious than it had been originally and at 1.5 years ? i.e. she seems to be a late ?go-normal? ? though she hasn?t gone quite normal. I knew she was CEA affected when I got her, but took her after a talk with the ophthalmologist, who reassured me that it should not be a problem for the activities I wanted to do with her.

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Karin,

 

My impression of the working fraternity in the US, generally, is that we aren't likley to advertise the eye status of our dogs -- good, bad, or indifferent. The breed statistics will be available through Optigen's database, and that's what really matters. We're not going to be going to a CEA database looking for potential studs or bitches for breeding. We will be going to farms, ranches, and trial fields, and when we spot a potential breeding partner, inquiries will be made as they always have been. The CEA status of both dogs will be discussed, in all likelihood, and the decision will be made.

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Barb,

 

I find it fascinating that you've noticed a slight disability also associated with the mild form of this disease. I was assured by the opthamologist who diagnosed Ben that his vision would not be affected, yet I have seen problems that I could only attribute to a difficulty with peripheral vision.

 

Some of the standard collie people I know say, "Yes, our breed has a lot of this disease, but it's not lifethreatening and it's largely not disabling." I've now started hearing this ("the disease is mild, why so much fuss about it?") from some of the people on the other extreme, the anti-testing crowd.

 

I think all of these should try to work one of these mildly affected dogs in extreme vision conditions before jumping to the conclusion that "mild" equals "irrelevant to working ability".

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Yes, Becca ? I must try to remember to ask the ophthalmologist about the looking into the sun thing specifically when Kirra has her next check-up ? to see if it?s more of a problem with CEA dogs than others. I don?t think she has any peripheral vision problem ? she?s pretty good at spotting sheep thinking about moving off the edges of a group! And she?s not experienced enough yet to do really big gathers on widely scattered sheep yet ? we have to walk into a paddock a ways so that I can set her up for success ? and by then the sheep have usually started to move ? so I haven?t had the chance to see if there are vision problems there.

 

I don?t in the least regret having taken her ? but probably would not have taken her if my livelihood depended on her.

 

I think the collie people?s attitude is largely influenced by the very high incidence of collie eye in their breed. In the case of Border Collies, the incidence of affecteds seems to be low enough that we have the luxury of taking affecteds out of the gene pool. I think the exciting thing about the new test is that it seems to mean that carriers and normals can be positively identified, and if they are important to the breed in terms of their contributions in working ability, can safely be bred.

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From what I have been hearing out and about....

 

I think that Bill has a valid point. ABCA coming out and embracing carriers and the creation of more carriers--- will go a long way towards keeping the general poplus from getting the wrong sque on how to make use of the new tests properly.

 

The goal needs to be focused on limiting affecteds NOT carriers. And I don't see it going that way right now and that worries me greatly.

 

We are going to get into the situation where people will refuse to purchase a puppy that is not guranteed to be clean-- and we don't need that.

 

This is going to go badly unless ABCA steps up and officially puts the breaks on it.

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Maybe I am not understanding something about CEA. I understand that "Normals" have no gene for CEA. "Carriers" have one recessive gene for CEA but have normal vision. "Affecteds" have two recessive genes for CEA but can range from eventual blindness through being affected to some degree to being only slightly affected.

 

Now, if this is just one gene, why do dogs with two copies of it, have a variety of phenotypes? Why are some virtually blind and others virtually non-detectable in terms of being affected? What other factors are influencing whether or not an Affected dog actually is functionally affected?

 

If we removed all dogs that are identified as Affected from the gene pool, whether or not they are affected to a significant degree, might we not also be removing some characteristic from the gene pool that moderates or ameliorates the effect these genes have on dogs?

 

Wouldn't it make sense to remove from the gene pool only those dogs that are both DNA identified as Affected and also identified as Affected by actual examination or proof of significant vision impairment?

 

I am just trying to understand this issue better, and not trying to be contentious.

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I'm starting to kind of feel the same way as Bill and Karen. Put a finger in the teeny hole in the dam now or it will become a big hole later. I'm not thinking too clearly right now - what other precedent is there for the registry making positive statements about WHICH dogs should be bred from?

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We are going to get into the situation where people will refuse to purchase a puppy that is not guranteed to be clean-- and we don't need that.

 

This is going to go badly unless ABCA steps up and officially puts the breaks on it. >>

 

Karen, what has given the impression that things are going badly? It was certainly a big fear of the H&G committee that people might get the idea that only Normals (clear) should be bred, and so everything we did to publicize the test emphasized that it should NOT be used that way -- that preserving good working genetics was the primary concern, and the test was only a tool to do that, and that it would be a total mistake to exclude good working dogs from breeding just because they were Carriers. The explanations on the Optigen site emphasize that also. From all the discussions I've read on these boards, and on Sheepdog-L, and on the workingsheepdog list, I've been very pleasantly surprised at how receptive people are to this point of view. I really haven't seen more than one or two people opposing the continued breeding of Carriers, and many people have advocated the continued breeding of Affecteds. The few exceptions have been pretty effectively out-argued, I thought. I hope I'm not mistaken, but my impression is that a widespread consensus has already developed in favor of using the test as it should be used.

 

 

If we removed all dogs that are identified as Affected from the gene pool, whether or not they are affected to a significant degree, might we not also be removing some characteristic from the gene pool that moderates or ameliorates the effect these genes have on dogs? >>

 

Sue, I hope someone more knowledgeable than I am will respond to your question, but this is what I would say. There is a single gene at a single locus which determines whether the dog will be Normal, Affected, or a Carrier. That's what the DNA test can determine. But there are probably other, so-far-unidentified "modifier" genes that influence how severe the disease is in Affected dogs. I believe Dr. Acland is going to try to find and identify such genes in future research, but that will be a much harder task and there are unlikely to be results any time soon.

 

In KC Collies, where the vast majority of dogs are Affected, breeding the least-impaired ones together has been the only strategy they could take and still keep a purebred dog. It MAY be (nobody knows) that by doing so they have had the effect of selecting for the more benign of the modifier genes. But we do know that mildly Affected parents can and do produce severely Affected offspring, so it is probably not as simple as that.

 

In any case, I don't think that's a strategy that would be either effective or necessary for us. The reason I don't think it would be effective (and the biologists among you please correct me if I'm wrong) is that if we breed Affecteds, we would always be breeding to a Normal (since we are lucky enough to have such a higher percentage of Normals than the Collie people do, and we don't want to create offspring with the disease), and we have no way of knowing what the modifier genes that particular Normal is carrying are like, since the Normal has no CEA gene for them to modify. The resulting Carriers could end up carrying not only a CEA gene, but also modifiers of the type which would produce the most severe form of the disease.

 

But luckily, it will probably turn out (assuming the DNA test data confirms what the ophthalmological exams have previously indicated) that only 2% or so of border collies are Affected. That would permit us to avoid breeding Affecteds (with very, very rare exceptions) without having any impact on our working genetics.

 

What I personally would hope is that Affecteds are not bred unless they are truly extraordinary -- perhaps (for argument's sake) among the 20 best working dogs we have throughout the breed at any given time -- and preferably not bred frequently (i.e., not popular sires), and bred with the follow-through needed to reduce the CEA gene in subsequent generations. Figuring out how we could best bring about that result (given the widespread tendency for people to overestimate the excellence of their own dogs) is quite a challenge.

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