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Discussion starter · #41 ·
It very well could have been another form of PRA and until offspring are tested the world may never know.
Am I the only one with my head in hands wondering what the IQ level is on this thread?

Becky.....hellooooo? You are the one I quoted. You said the doctor diagnosed the dog as having prcd-PRA.
 
Am I the only one with my head in hands wondering what the IQ level is on this thread?

Becky.....hellooooo? You are the one I quoted. You said the doctor diagnosed the dog as having prcd-PRA.
Did I really say that? I said the diagnosis was made by a veterinary opthamologist. I did not specify prcd-PRA or if it was just PRA. I can tell you more in probably four weeks, maybe less.

As for the IQ on this thread, some might question one's IQ if their only line of reasoning that prcd-PRA exists is if we have a bunch blind dogs. Now before you all think I am picking on Melanie, prcd-PRA is a progressive eye disease that starts with diminished eye sight and eventually leads to blindness. Hey Melanie did you happen to breed any carrier to carrier litters? I see you posted several, I am just curious.
 
Yes, why do you ask?
Then why post other people's litters of potential carrier to carrier breedings asking how many offsping could potential be carriers. The pups from the litters you posted are relatively young and the affected offspring may not be symptomatic and how many owners from the litters actually know about prcd PRA testing?

Now the reason I asked if you bred a carrier to carrier litter is because you probably have accumulated your own data from that litter and I would suspect that they are probably over the age of five. Did the original punnett square percentages for breeding carrier to carrier hold out for your carrier to carrier breeding?
 
Melanie,

I am also curious as to why you mention other breedings and not your own. I have a Paws x Beau (AFC Topbrass Pawsability X FC AFC Emberain Beau Geste) puppy. As far as I know, 3 of the 6 puppies have been tested at this time, 2 are carriers (including one that I own) and 1 is clear. This litter was bred before anyone knew of prcd-PRA in Goldens.

Since the sire of my other dog is clear and the mother may be a carrier, I will have her tested if I decide to breed her. I will not breed carrier to carier -- WHY PLAY WITH FIRE?

BTW I have a graduate degree in biochemistry and I think that this discussion needs alot more data before there can be any conclusions.
 
Melanie,

BTW I have a graduate degree in biochemistry and I think that this discussion needs alot more data before there can be any conclusions.
I think this is why the original question was asked.

In all of these cases at least one clear ancestor appears in the gr-parent generation. In every case there is missing information on one of the gr-parents on the other side.
So are you saying it gets watered down? Jimmy is a carrier by process of elimination, cudos to who tested a female bred to him that produced a carrier, she was clear, and was tested at 12.There are so many possible carrier to carrier breedings due to just that and Push being a Carrier. Most done before the test.

Since the sire of my other dog is clear and the mother may be a carrier, I will have her tested if I decide to breed her. I will not breed carrier to carier -- WHY PLAY WITH FIRE
With one exception, I have not yet seen anyone who has said don't test.
Becky said
With selective breeding how many generations would it take to eliminate prcd-PRA carriers? My unscientific calculation would be several generations or even one generation if you only breed the clear pups from a carrier to clear breeding. Maybe I missed something here, I did not take a genetics class in college.
This to me is the problem, why do we want to eliminate something that we don't know is the root of the problem.Gene pool is already small enough. And it is obvious we have not eliminated carriers by being lucky, but a great example is Rugby, he is normal, Beau is a carrier. If we could only test all littermates, we would know more.

The dog Gerry talked about that was suspected PRA was tested, retested, owner told yes, finally went, had the blood test and then an extensive eye test found to have something else. In the meantime one of my dogs that I had bred to a close relative of this dog came back a carrier, Let's just say I sweated that out until her result came back normal.

There are 2 issues here-
PRA we do not have the answers that show why, how. who.

prcd-which had not been proven beyond a shadow of a doubt to cause the PRA disease when combined with another prcd. If a dog has high pressures, that can cause blindness, but that must be tested. Vets do see PRA, mine eye vet has not seen so much, and I would not go by what a regular vet says, but honestly, if a dog is blind, and you are a pet owner, that is all you know. I would not put my old dog through a ton of tests at my expense for research.

Finally, when does the prcd version strike? A couple of vets believe it is really late onset. Hell, Whistler sees what he wants to, and I just assume it is age (yes he has been tested, and we are best friends with his eye Dr) and I do not believe we have been that lucky, and there needs to be more funding. Optigen will not keep looking, as they are a testing money making facility, and can't even keep their information updated.I believe we need to keep looking, if we find more blind dogs.
If we don't we need to find the additional cause of those that do go blind.

Eyes are so much more complicated than this. Trust me, as I know more about Rod, glands, pressures, and changing vision. Glands that are blocked can cause vision problems, antibiotics can cause problems-and can be attributed to a lot of things.

I personally would not breed or consider a breeding where at least one is not clear. Notice one-I don't care about carrier status, just need to know if I do breed.Also ask. Ask why they have not tested. The general answer is oh we don't have that problem. There are a few that don't-
But there are many more that do.
 
I
Becky said


This to me is the problem, why do we want to eliminate something that we don't know is the root of the problem.Gene pool is already small enough. And it is obvious we have not eliminated carriers by being lucky, but a great example is Rugby, he is normal, Beau is a carrier. If we could only test all littermates, we would know more.

The dog Gerry talked about that was suspected PRA was tested, retested, owner told yes, finally went, had the blood test and then an extensive eye test found to have something else. In the meantime one of my dogs that I had bred to a close relative of this dog came back a carrier, Let's just say I sweated that out until her result came back normal.

There are 2 issues here-
PRA
prcd-which had not been proven beyond a shadow of a doubt to cause the PRA disease when combined with another prcd. If a dog has high pressures, that can cause blindness, but that must be tested. Vets do see PRA, mine eye vet has not seen so much, and I would not go by what a regular vet says, but honestly, if a dog is blind, and you are a pet owner, that is all you know. I would not put my old dog through a ton of tests at my expense for research.

Finally, when does the prcd version strike? A couple of vets believe it is really late onset. Hell, Whistler sees what he wants to, and I just assume it is age (yes he has been tested, and we are best friends with his eye Dr) and I do not believe we have been that lucky, and there needs to be more funding. Optigen will not keep looking, as they are a testing money making facility, and can't even keep their information updated.I believe we need to keep looking, if we find more blind dogs.
If we don't we need to find the additional cause of those that do go blind.

Eyes are so much more complicated than this. Trust me, as I know more about Rod, glands, pressures, and changing vision. Glands that are blocked can cause vision problems, antibiotics can cause problems-and can be attributed to a lot of things.

I personally would not breed or consider a breeding where at least one is not clear. Notice one-I don't care about carrier status, just need to know if I do breed.Also ask. Ask why they have not tested. The general answer is oh we don't have that problem. There are a few that don't-Mo was probably not a carrier, as almost anything close to him is clear.
But there are many more that do.
I do not have a problem with carriers, the point I was making was that through selective breeding and testing, it is possible to eliminate prcd-PRA. With the test, it should help prevent carrier to carrier breedings.
 
I do not have a problem with carriers, the point I was making was that through selective breeding and testing, it is possible to eliminate prcd-PRA. With the test, it should help prevent carrier to carrier breedings.
That is my point exactly. Why do you want to eliminate Prcd-PRA if it does not have an obvious impact that we can prove? I am NOT talking about PRA I am just talking about the prcd gene that must not be dominant or we would have a whole lot of blind dogs.

Carriers are not bad, we do not need to get rid of them. We do need to get rid of that mindset.
 
That is my point exactly. Why do you want to eliminate Prcd-PRA if it does not have an obvious impact that we can prove? I am NOT talking about PRA I am just talking about the prcd gene that must not be dominant or we would have a whole lot of blind dogs.

Carriers are not bad, we do not need to get rid of them. We do need to get rid of that mindset.
Even breeding carrier to carrier produces a low percentage of affected, so I am not sure why everyone anticipates that there are going to be tons of blind dogs around. Why keep something like prcd-PRA in the gene pool if it has the potential to produce a blind dog? If you can breed away from it, then why not?
 
Demi wrote:
Quote:
In all of these cases at least one clear ancestor appears in the gr-parent generation. In every case there is missing information on one of the gr-parents on the other side.

So are you saying it gets watered down? Jimmy is a carrier by process of elimination, cudos to who tested a female bred to him that produced a carrier, she was clear, and was tested at 12.There are so many possible carrier to carrier breedings due to just that and Push being a Carrier. Most done before the test.

Yes, in one generation the gene could disappear. Let us imagine we do not have a test, but do know the gene is recessive.

Compare Beau and Rugby. Beau is a carrier. If (we don't know that any are so far) an offspring of Beau were to turn up as affected, if we tried to go backward in the pedigree we might erroneously eliminate all Beau relatives. Rugby is a littermate to Beau and Rugby is clear. Without knowing the status of the individual dog, trying to go just by pedigree analysis, we could do a lot of damage to the gene pool.

By using the test we can play it safe by avoiding breeding carriers to carriers, while also gathering much-needed data to get a more definitive answers.

Demi wrote: prcd-which had not been proven beyond a shadow of a doubt to cause the PRA disease when combined with another prcd.

In other breeds, there have been enough physically affected dogs with double copies of the mutation to remove reasonable doubt. We need to locate more affected Goldens to achieve the same reasonable confidence for GRs.

Demi wrote: ... why do we want to eliminate something that we don't know is the root of the problem.

Dr. Aguirre's position, and one I can accept, the goal is to use the test to avoid producing affected dogs. He recommends NOT eliminating worthy breading candidates even if they are affected (because they can be bred to clear dogs without risk of producing affected offspring).

It just means that we must evaluate the other factors that go into our breeding choices as we have always done ... if there is a dog who has "fair" hips or higher PennHIP numbers, we have to weigh that against the performance traits we seek as well. Same thought concepts (in my mind, but I've been told I think weird before).

Demi wrote: I would not put my old dog through a ton of tests at my expense for research.

Understandably so. The dog mentioned was around 6 when this was happening. For the older progeny of carrierXcarrier breedings the basic eye clinic exam should be the first step. If they are affected the Optigen test is free, & that is a simple blood test.

Demi wrote: Eyes are so much more complicated than this.

Also there are some differences between the human eye & the canine eye. I don't know all the fine points, but dogs do not get "macular degeneration" (which humans do get) due to the differences between the species.

Demi wrote: Why do you want to eliminate Prcd-PRA if it does not have an obvious impact that we can prove?

The beauty of it is that we do not have to eliminate it if we can gather enough data to remove reasonable doubt that we can depend on the test. It would appear that the mutation is not pervasive in the breed, so we have leeway to work toward elimination (if we wish to do that) in a gradual way. People can make their own choices on how they wish to proceed. By sharing our information openly about DNA status it allows each individual to make their own personal choice.

As long as personal choices can be made, it is likely that there will be less constriction of the gene pool. Those who choose to breed carriers will remain a source of certain genes that might be eliminated by those who choose not to use carriers. This could be useful to either group for the long-run genetic health of the breed.

Becky wrote: Why keep something like prcd-PRA in the gene pool if it has the potential to produce a blind dog? If you can breed away from it, then why not?

We don't yet know how apparently unrelated traits may be connected on the DNA. We just have to note the "split" in any of the breeds between performance & conformation lines to see some examples of how the two groups might differ. There is evidence that the tameness in Siberian foxes was somehow tied into coat color, coat quality, and even drop ears.

We don't want to unwittingly discard genes that we need/want because we are lacking in knowledge of how they may be inter-related until it's too late.

Where are we? We know there is a mutated gene that occurs in the breed. We know that at least two individuals (within less than a year) were discovered to have duplicate copies of the mutation, and also have physical evidence of PRA. At least this is an "early alert" that this particular mutation exists in the breed. To learn more we need to gather data. It's simply in our hands to work on that.

Some may believe that Optigen or GRF should come up with the funding. Truthfully, I'd just as soon GRF devote serious funding to pigmentary uveitis and cancer research. That leaves this one in our hands.

What an incredible OPPORTUNITY to learn how to deal with the concept of genetic testing as a breeding tool with a disease that is not pervasive in the breed! Whether this test were to prove reliable for GRs or not, we will have learned how to assess each new genetic test we will face in the future. Questioning our thought processes is a good thing! We can learn so much from this!

I cannot read the CNM or EIC threads and imagine that GRs will not face similar challenges.
 
On this thread we have talked about age of onset of prcd-PRA (or any other form for that matter). Optigen says we could expect 4 to 6 years to see symptoms on an eye exam. I don't believe they specify the progression of the disease.

While the words "blind by 10" have been used in conversations, that does not indicate at what age the dog might begin to have vision deficiencies.

We do know that Daphne has continued to run in competitive agility till now at age 7, but there are definite deficiencies now that were not apparent 18 mos ago, or even a year ago.

I was curious what this might mean in terms of field work. Several people may know of the Jones' incredible website that compiles tons of statistics on Golden achievements in AKC events. (www.undeniablegoldens.com)

Here's what I found there:
Mean age for All Age achievement: 3.86 years (youngest1.14;oldest 9.9)
Mean Age for MH title: 5.2 years (youngest 1.42; oldest 13.29)
Mean Age for FC title: 5.44 years (youngest 2.17; oldest 10.36)
Mean Age for FC title: 5.76 years (youngest 2.65;oldest 9.9)

Some of the "youngest" in field trial achievements go back several years. Allowing for increasing difficulty of tests, those young ages may unfairly weight the mean age to the low side. (The website says the most recent update was July 2008)

My own "sense" had been that the FC/AFC titles would often be made "made" by around 6 or 7. All-Age somewhere between 2 and 5, and MH maybe around 3 to 5. Each of you who have actually achieved these titles may have your own "timetable" in mind.

I do not believe that Daphne is a field trial calibre dog, but if she were, she wouldn't be anymore at age 7. It is not likely she will still be competing in agility at age 8, while many other dogs are able to compete until age 10 or longer. As far as I know, the other affected dog is similarly afflicted at age 8. Don't know what visual deficiencies might have been noticed a year ago. Neither dog is totally blind yet.

What I see here is that it is worth striving to find the answers to questions raised, for better or for worse.
 
Gerry we are not disagreeing, just see it differently.
I do not belive it is as simple as it is being presented.
I do know that is a dog has high pressure, as in people, they go blind.
That it is inherited. People and dogs. Glaucoma, cateracts, rods, all are similar.
That there are vets "in the real world" that question if the prcd/prcd breedings indeed cause blindness. That there is another issue in most dogs cases. Not saying it is not true, but questioning.
Is there anything else in Daphne's background to hasten the process? Pressures? Lymes, any tick or auto immune disease?
I do not believe we will run into the EIC/CMN issues, as we retire and don't breed or run dogs that collapse-the labs are overall tougher and there are a lot more in those lines bred. In the "TRUE" field world the worst, which is bad enough, we have seen are seizures. And I personally don't know if a male FT dog who has those issues that is running now.There may be, but since I have heard so many other rumors, think that one would have surfaced by now. Don't pay any attention to the females. I am hoping the ones that had those issues are slowly leaving the gene pool.There are maybe 6-12 goldens? running regularly in the Open and Amature compared to 80 labs, but that is another debate. Not mine either:p Hunt tests are a different subject too.
Back to this-Carol L wrote about how unlucky she has been in the current GRNews, but also how lucky with no known affected. Then I have another friend who has NONE in her lines, except when she bred to two "new" dogs. So, while I would love to have a marker for Lymphoma, I also don't think we should just "trust the test" to make major decisions.
prcd-PRA has not disappeared, and made it down the lines to the major carriers we are finding now-it did not spontaneously appear.
We will never know if the dogs in the 70's and 80's had THIS PRA, just know they had PRA-

Where are we? We know there is a mutated gene that occurs in the breed. We know that at least two individuals (within less than a year) were discovered to have duplicate copies of the mutation, and also have physical evidence of PRA. At least this is an "early alert" that this particular mutation exists in the breed. To learn more we need to gather data. It's simply in our hands to work on that.

Some may believe that Optigen or GRF should come up with the funding. Truthfully, I'd just as soon GRF devote serious funding to pigmentary uveitis and cancer research. That leaves this one in our hands.

I am not sure how I feel about this. I agree we need to do more, but at 200 a test at a place that will do no more, I do not believe that is the answer. I am not sure the average person can do more, and I do believe out breed club needs to do more. Not all breeds are alike, as one breed the PRA is cause by an odd rod issue, and their club is investing millions to figure it out. Becomes a question of priorities.

Becky wrote: Why keep something like prcd-PRA in the gene pool if it has the potential to produce a blind dog? If you can breed away from it, then why not?

Because the dog may have something to offer-great temperament, pretty, marks like a dream, good hips,eyes, likes the water-how many dogs are out there that have those attributes. Let see, Push, Maverick, Beau, Paws, Snapper,Jimmy .....see what I mean. And they lived past 6. To me that makes a difference. So, yes, I will consider breeding to a carrier if the female is clear. And I hope by then it does not matter.
 
Gerry we are not disagreeing, just see it differently.

Actually, Demi, I don't even think we see it very differently :D
I think we both realize we can't ignore the whole thing. We both realize that we need to proceed with caution as we try to get better answers.

I do not belive it is as simple as it is being presented.
I do know that is a dog has high pressure, as in people, they go blind.
That it is inherited. People and dogs. Glaucoma, cateracts, rods, all are similar.
That there are vets "in the real world" that question if the prcd/prcd breedings indeed cause blindness. That there is another issue in most dogs cases. Not saying it is not true, but questioning.

And I totally agree that we should make sure we are getting the best possible dx's. I think that most ACVOs want the same ... but it wouldn't be the first time I was naive.

Is there anything else in Daphne's background to hasten the process? Pressures? Lymes, any tick or auto immune disease?

Mardi would be best to answer this. I do remember that she had Lyme disease. But, then again, the tick diseases are probably now a way of life for our dogs :mad:

I do not believe we will run into the EIC/CMN issues, as we retire and don't breed or run dogs that collapse-the labs are overall tougher and there are a lot more in those lines bred. In the "TRUE" field world the worst, which is bad enough, we have seen are seizures.

I didn't mean to imply that the diseases we might face would be the same diseases that the Labs deal with. But if they come up with a DNA test for pigmentary uveitis that could impact a large portion of the conformation gene pool, and whatever we learn now will better prepare us for making decisions about a PU test (God willing they get one).

The more knowledge we gather, and the more our communication is enhanced with the internet, it is likely that we will become aware of more genetic diseases over time.

And I personally don't know if a male FT dog who has those issues that is running now.There may be, but since I have heard so many other rumors, think that one would have surfaced by now.

I no longer take anything for granted.

Don't pay any attention to the females. I am hoping the ones that had those issues are slowly leaving the gene pool.

It would be great if they are. From discussions I've had with others with experience with seizures & pedigree study on it, it's incredibly puzzling. Like studying pedigrees for cancer, sometimes you think you can predict it, but other times it seems "out of the blue".

Back to this-Carol L wrote about how unlucky she has been in the current GRNews, but also how lucky with no known affected. Then I have another friend who has NONE in her lines, except when she bred to two "new" dogs.

We want answers that can only become available from affected dogs. Finding those dogs, getting clearer answers to our questions will, perhaps, make it easier for us. We forget to downright rejoice that we don't have more blind dogs. It leaves us with more uncertainty in making our breeding decisions. For the dogs who are not blind, and never will be ... YIPPEE!

So, while I would love to have a marker for Lymphoma, I also don't think we should just "trust the test" to make major decisions.

Probably have to better define "major". Culling ever carrier would be major in my book. I simply would not do it or recommend it to anyone.

Culling one carrier here and there ... we cull all the time, deciding who's worth breeding and who's not.

prcd-PRA has not disappeared, and made it down the lines to the major carriers we are finding now-it did not spontaneously appear.

That's the way it looks.

We will never know if the dogs in the 70's and 80's had THIS PRA, just know they had PRA-

Absolutely true. However, if I find a prcd-carrier today, and I know of an ancestor who had PRA of unknown type, there would be reasonable suspicion that the ancestor also had prcd. However, it really doesn't matter ... it's really about starting where we are now & going forward.

I am not sure how I feel about this. I agree we need to do more, but at 200 a test at a place that will do no more, I do not believe that is the answer. I am not sure the average person can do more, and I do believe out breed club needs to do more.

It all starts at the grass roots. People with pigmentary uveitis might feel the breed club should do more for that. Others may feel that cancer deserves more attention.

There are ways to minimize the costs of the test, as with the clinic at the National this year. This is a trial balloon for Optigen, giving a larger discount for a larger clinic. GRF is providing blood draw and shipping at no charge. A 20-dog clinic brings the price down to about $146. A local club could, perhaps, underwrite the cost of the draw and shipping, especially at one of the club clinics where blood is also drawn for heartworm check or TBD. When I had my first test done, the vet drew one tube then split it, one for heartworm & one for Optigen.

Just plain old physical eye exams are the first line of defense. I encourage all my petowners to do that just as a wellness check. Affecteds that turn up get the test for free. If they are neutered pets, only the physical exam is of any importance.

Not all breeds are alike, as one breed the PRA is cause by an odd rod issue, and their club is investing millions to figure it out. Becomes a question of priorities.

From a reliable source, I was told that it cost at least over $2 million to come up with the original prcd marker test. When we talk of funding research, we often don't realize just how big those numbers can get.

Because the dog may have something to offer-great temperament, pretty, marks like a dream, good hips,eyes, likes the water-how many dogs are out there that have those attributes. Let see, Push, Maverick, Beau, Paws, Snapper,Jimmy .....see what I mean. And they lived past 6. To me that makes a difference. So, yes, I will consider breeding to a carrier if the female is clear. And I hope by then it does not matter.
See? We absolutely agree:D
 
Becky-

The goal should not be to eliminate the prcd-PRA gene but to control it. If you wish to find why, talk to any old-time breeder of Port. Water Dogs. They virtually eliminated one problem and got hit in spades with another.

Eric
 
Discussion starter · #55 ·
Regarding the discussion between Demi and Gerry about other issues that could cause "look alike" pra. Daphne has not had lyme (one of the few in my group that has not). She is healthy otherwise - even had her blood pressure checked. We do have a dog with some vision loss due to high blood pressure which is really a result of loss of kidney function.

I too will not throw away carriers nor will I reject the idea of breeding a carrier to a clear - but I am not taking any chances with my carrier bitch. I will only breed to a dog that is clear (if the stud owner will agree - i have had some say no) and I am willing to pay for it to make sure.
 
I am not sure where it was stated that I wanted to cull carriers or I had a problems with carriers, all I stated that it is possible to eliminate prcd-PRA through selective breeding and testing. I asked an honest question if you breed carrier to clear, how long would it take to breed away from the gene? I figured one generation if you only breed the clear from that litter but it might take several generations for the carriers.

Yes there are some great dogs out there that happen to be carriers but there are also some great dogs that are clear.
 
Interesting discussion overall. I have, at some point, also wondered why we are not seeing more affected dogs with so many carriers being bred. However and unfortunately, we are losing many of our dogs long before they hit 10 years of age, so the potential loss of sight issues may not be realized in many dogs.

My male Trooper is a carrier (half-brother to Steve Low's Cody) and I was initally devastated by it. After doing a lot more reading and research, I realized it was just something else to consider when breeding, like structure, biddability, temperment, desire and coat color (just kidding on the coat color, everyone knows red dogs rule). Carrier status should not eliminate a dog from the breeding pool, just be used as a tool for better breeding.
 
After doing a lot more reading and research, I realized it was just something else to consider when breeding,

Dawn, you hit the nail on the head!

This is not about doom and gloom, it's just about another breeding factor that we need to be aware of.

There were people, not so long ago, that didn't think we should bother to xray elbows on Goldens. Some Goldens have, over the past 10-or so years been disabled due to elbow dysplasia. You could say that the parents of those disabled dogs were "carriers"

Did we run out and neuter the parents? No. All their full siblings? No. But we realized that we ought to acknowledge the existence of the issue for Golden Retrievers.

like structure, biddability, temperment, desire and coat color (just kidding on the coat color, everyone knows red dogs rule). Carrier status should not eliminate a dog from the breeding pool, just be used as a tool for better breeding.
everyone knows red dogs rule

:eek: except for Ki, Barty, Cotton and a few others.
Still loving my blond kids ;)
 
Discussion starter · #59 ·
BEcky
I think you raise a good question about breeding it out of the line. I don't think it would take much if you are purposeful about doing the breeding of a carrier and intent on keeping the clear. Of course, keeping a clear dog doesn't guarantee the zillion other checks that have to be done. I didn't have a choice the first time as my "affected" bitch had been bred before her diagnosis and the bitch I kept from that litter is a carrier. I did breed her ( the carrier) and have kept a clear dog from that litter. Who knows if he will make it through all the other clearances - I sure hope so. But, in the meantime - I am still interested in breeding my carrier bitch again as I like what I see. All my pups went home tested so folks knew what they had and carriers went on limited registrations.
 
Well.......... I still think that "Knowledge is Power".And NOT a bunch of smoke. I love science and the advangements that are being made everyday.
I had Choctaw Deerwoods HellsBells tested a week ago today and am curiously waiting on the results as she will be 13 yrs in Dec.Last cerf. was 6/2002clear.
"Belle" is out of FC Gian Carlos of FoxCreek and Mioak's Deerwoods Blaze(Mo bitch).
Gotta love those old dogs that will tell. Also am debating on testing semen on FC Mioak's Chunk of Gold,SH.(very very small amt. of frozen semen),Buckshot's Beau's Bauer,MH (FC-AFC Pardner son)(again very small amt. of frozen semen)and Choctaw's Bark At The Moon,MH(still alive @ 10yrs. young -"Sprint" son) Ozzie and Beau's last cerfs were @ 8 yrs. young clear.
Will post on "Belle's" results when it is available.:)
Sue
 
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