Denise Wall

I finally got a chance to go through this video again trying to pay more attention to detail. Basically, my take on it is, as is obvious, it's not good to use high dose ivermectin (group 1). Lots of problems. In group 2, these dogs, different breeds and with their MDR1 status unknown, were already suspected of having retinal problems in association with regular heart worm meds alone or in association with other flea and tick products. Group 3 contains a "pure" group of dogs taking only regular dose HW meds but again, no info about the breeds or other info such as HDR1 status of the dogs. Group 3 also contains a control group that took no HW product and consequently showed little retinal toxicity.

So group 2 that would be most dogs as far as their mix of various HW, flea and tick products. But it's not exactly a pure group since they were already suspected to have retinal toxicity in association with HW/flea/tick products. As would be expected, this group did have various positive signs of retinal toxicity, some of it reversible once removed from the meds.

Group 3 (non control) was the most disturbing to me with about 21% of dogs showed retinal abnormalities. This is the group I don't know what to think about. This was just regular dose HW med.

I think there is evidence that there can be retinal problems with ivermectin/heart worm meds either alone or in combination with certain flea and tick products. Retinal problems may not be the only problems either. However, we really don't know much about which dogs, which breeds and whether the dogs had other problems contributing to these problems in this study at least. I suspect this could involve MDR1 as it's a likely suspect but more research is needed. There are genes that regulate production of the protein the MDR1 gene produces that could be a major factor for example. 

As someone who's been in the literature on this topic a fair amount lately I have to say it's amazing to me how little research has been done on this pretty important gene product in dogs. Especially given the number of breeds with high rates of mutation in this gene. Perhaps studies like the one in this video will lead the way to more sophisticated ones with more answers and better guidelines and better products.

So that's my follow up on the video. I hope I didn't miss anything. 

One main concern of mine from this presentation is the possibility that Comfortis and Trifexis (popular flea and tick preventatives) are inhibitors of p-glycoprotein, the protein produced by the MDR1 gene, and as such can increase ivermectin concentration 360%. See the slide at 59 seconds of the video. If true, this is concerning for all dogs on heart worm prevention. I think it's something that bears following.

I am working on this. It's a pretty complicated subject actually, and reading and properly evaluating the scientific literature as well as trying to find personal accounts in breeds other than border collies (where the incidence is extremely low) will take some time. Most of the dog forums and personal accounts revolve around heart worm medicine and other commonly used meds such as acepropazime. I'm just trying to be thorough because it's important. I'm sorry it's taking so long.

Rest in peace, Donald. You truly loved the working border collie.

No. I'v had white factored pups from two non white factored parents.

No problem Candy

I was actually trying to convey that many evaluations of and support for health and genetic disease problems are going on all the time over many years with the ABCA Health and Genetics Committee and ABCA Board, even if they aren't all apparent to the membership right away. Many of these situations for research are complicated and involve many factors and careful consideration. We're trying to play the "long game," although that's sometimes hard to understand and accept when one has an immediate problem.

Excellent news! I hope this is just the first of many steps forward in improving information and education about the health and genetics of our breed.

 

~ Gloria

I'm sure you probably didn't mean it this way, and believe me I'm not looking for personal thanks when I point this out, but as someone who's been on the ABCA Health and Genetics Committee for two decades, I hope people realize that this is not just the "first step" forward in improving information and education about the health and genetics of our breed. Many dedicated people have been involved for many years in this endeavor, even if their efforts haven't always been in the spotlight.

Not to hijack this topic but since this keeps coming up:

Pam and others, I'm not sure I agree 100 percent. The number of dogs that achieve high titles, have the structure, health and overall temperament to be outstanding representatives of their breed is what -- the top 5 percent? Top 2 percent? I would dearly like to buy my puppies from this select group any day of the week.
But if we only breed those, then our inbreeding will eventually produce a very limited gene pool with less desirable consequences. Every really spectacular working dog that has no "pedigree" probably has a breeder who thought that their not so great dog was worth breeding -- and I can accept that a bit better than breeding for bucks. But genetic diversity is not always achieved by breeding just the best to the best.
And I'm not a breeder and don't know how to square that circle in real life.

Although I originally wrote this dart board analogy to describe what I *think* might happen when working breeds are lost, it applies to trying to imagine how to keep the working gene pool healthy. I am a breeder (or was at least) and it's a very difficult to circle that square in real life. Many here will be familiar with this analogy already:

Assume the border collie is the theoretical breed, where many strong workers existed in the original breeding pool and the need for their work was not lost or reduced over time but instead the dogs became less and less useful for it.

"What's recorded on the pedigrees and used for the UK database may not actually represent the true parentage. Sorry, but true. In one of my late dog's pedigrees there were three wrong UK sires listed that I know of. It happens here too. AKC once did a study of pedigrees versus the true parentage and found a shocking percentage of inaccuracies."

 

Denise, how did you find out about these inaccuracies?

 

Were they clerical errors or people lying in order to make the dogs' pedigrees look more impressive?

I've been in this a long time. I hear things and I know some things for sure. For example, in one case, a famous sire was tri. The dog's son off him was black and white. This black and white dog, also famous, was used *a lot* at stud. He never produced even one tri pup, not even when bred to tri bitches. When a dog sires 100 or 100s of pups, it starts to be outside the realm of genetic possibility that he is carrying the tri gene, which is recessive.

Other times, pedigree "inaccuracies" in the past are common knowledge overseas, even though no one will repeat them in writing. I've also heard that it's common practice overseas, or at least it used to be, to line a bitch with two studs just to make sure they catch. No big deal. One can only hear these things so many times before they start to seem like more than rumor. Not to piss anyone off, but it is what it is.

I have two points to add for interest.

What's recorded on the pedigrees and used for the UK database may not actually represent the true parentage. Sorry, but true. In one of my late dog's pedigrees there were three wrong UK sires listed that I know of. It happens here too. AKC once did a study of pedigrees versus the true parentage and found a shocking percentage of inaccuracies.

It doesn't matter if a dog was a popular sire (WRT passing on genetic disease through later line breeding) if no one breeds from the offspring. Sometimes that happens.

I just heard of this and add my absolute shock and sadness to that of her so many other friends who knew her personally and from the internet. We will miss you so much Hilary.

I can personally attest to the fact they really work. I've been using them on my 15 year old Mick for several months. He was having trouble on slick floors. I tried to put rugs everywhere I could, but he still found slick places to slip and fall. These toegrips have made a tremendous difference in his quality of life and my piece of mind. I would recommend them without reservation. Just get the right size and read the instructions.

ETA No, he doesn't chew them off. They actually stay on amazingly well.

Nobody started it yet so I guess I will.

Goodbye my sweet, wonderful boy. You were a brilliant working dog and taught me so much.

Stilhope Zeke (1999-2012):

TEC,

I'm a bit behind on this topic but wanted to have my say. One of the videos of a mild episode of BCC on this site is of my dog Zeke:

FWIW, I am a scientist with a PhD in biochemistry as well a clinical laboratory degree (BS MT(ASCP)) and experience in laboratory medicine. So even though I wasn't wearing a white lab coat, I have one Blood and other clinical parameters had been tested on this dog in the past and were all normal. Also, FWIW, I did not induce this episode. Sometimes, even after years of experience, it's difficult to tell what will precipitate an episode. In this instance, when I saw it had happened, I went to the house and got a camera. Fifteen minutes after the video he was completely recovered and perfectly normal. As has been said, this dog was functional enough to work and run big challenging Open courses such as Edgeworth with no problems. He retired at a normal age. It's a strange syndrome.

I've long been interested in this problem in border collies and have been a strong supporter in the research to discover the cause. I wanted to help others recognize these symptoms so I did the video. I believe all who contributed videos to this site had the experience with the condition in their dogs to know they were not at risk.

ETA I never saw this dog exhibit any symptoms until at least five minutes after he had stopped working.

I'm starting to think that the real mismatch in these discussions is not in terms of philosophy really, but in terms of thinking about populations/breeding practices vs individual dogs.

Further, because I think this is the heart of the matter. Have you (the general you) not noticed how working people on this board generally embrace rescue dogs and their owners, or dogs from puppy mills once the people have them and nothing can be done about it? What's done is done and people want the best for that individual. Ahead of time, promoting and supporting *breeding* other than for what the breed was meant to be is where the problem comes in for most of us.

I'm starting to think that the real mismatch in these discussion is not in terms of philosophy really, but in terms of thinking about populations/breeding practices vs individual dogs.

It always seems to happen like this.

A few random thoughts:

I trained and competed with horses over jumps in several areas (hunter, jumper, three day eventing) for decades. I don’t recall anything like ETS in horses. Poor style, or lack of ability or courage, of course, but not anything that showed up after an otherwise good start. The rider normally tries to control the striding distance so the horse jumps from the proper spot but horses are sometimes free jumped on a lunge line with no rider where they would have to pick their own distances. Has anyone ever heard of a horse developing something like this?

They already have and are developing genetic tests in dogs for things like the red gene and various structural features such as coat length and ear set. There will be genetic tests for the things people want them for if they can be developed, i.e., high heritability and not complex inheritance patterns. IOW there will be gene tests for lots of things that many others may not find important.

Once again, supposing ETS is a genetic problem, and the cost for the test reasonable, it *could* be treated just the same as any other preference in a working litter bred for the right reasons, instead of specifically bred for the preference. For example, one might like red dogs. Even without selection such as testing the parents for the red gene or selection by breeding red parents, red pups are born into working litters. One might take that pup because red is preferred, but this has not changed the standard for the breeding. This is selecting from the pups available, not selection for red pups by breeding reds dogs or testing the parents for the red gene. Therefore, one could find a working bred litter and test the pup you like for ETS before you buy it. No, this is not as efficient as testing the parents and selecting against this gene, but it will not change the gene pool. If you want to support working breeders, you can.

I’ve said this before but there’s pretty good evidence that in order to keep all the pieces balanced and working together correctly in a breed developed and selected for a high level of work performance, one must continue to stringently select for that purpose. Breeds can fall apart when only part of the traits are selected for and not balanced by those not selected for. The German Shepherd dog is a good example of this kind of failure, both mentally and physically.

So we’re back to the same philosophy – you can do the activity (I don't consider conformation an activity) you want with the dog you have. Or even pick what you want from those available pups on the ground. Just choose from pups bred for working ability from work-tested parents. You can still support the breed as it was meant to be and do what you want without harming the gene pool if it’s important enough to you.

If I go ahead and concede this is a real genetic issue with agility dogs, and does not appear to have any repercussions in any other activity or in a normal life for a dog, which I'm happy to do at this point. Testing and selecting parents based on their ETS DNA status officially marks for me the split of the breed into not only working border collies and conformation border collies, but into a third distinct group, sport collies.

If the test were used only on an individual to determine whether to purchase a pup as an agility prospect from an otherwise well-bred working litter from non tested ETS parents, it would be one thing. But my money's on selection against ETS for the agility market.

If your dog goes to water after exercise and drowns, it's certainly life threatening. That happened to quite a few water retrieving labs who had the similar disease, EIC. Sometimes it happened in the first episode so the handler would have no idea to be careful. It's quite possible BCC dogs could be pressed to death from inattention to the problem while working.

I own a dog with BCC and have seen many others over the years. It can definitely be a health risk in more situations than a dog's "career." It in no way compares to jumping too soon over an agility jump, if that's what ETS really is. ETS does not sound like a clinically significant problem IMO, while BCC is.

Pearse, I think we are in general agreement in that we both feel the dog must be extraordinary to make the breeding worth it. All dogs can contribute something to the gene pool that no other dog can because they are all individuals. Whether what they can contribute is good enough is another argument. There is no "all other things being equal" scenario because the genetics and expression of working traits is so complex. If the unique combination a dog can contribute is of enough value to the breed, the progeny can be carefully selected and bred on to lose the gene in two generations. (I realize you know all of this but let's just look at it anyway.) For example, assuming there's one main EOD gene, when a carrier is bred to a DNA clear, statistically, there will be 50% carriers. If all one cares about is EOD, the pups can be tested and a DNA clear one kept, assuming there are enough of them for a clear and statistics bear out. The rest of the pups that are carriers can be neutered. Then, if the clear selected pup is breedworthy in other ways, the line can continue without the EOD gene. The same thing can be accomplished when breeding an affected dog, except all of the first generation would be carrier. A limited number, say one that trained out the best, could be kept intact and bred to a DNA clear mate. Then the same process as with the carrier x clear mating above is carried out. Just because the other dogs produced are not being bred it doesn't decrease their usefulness or value as working dogs in their lifetimes and no affected pups would be produced.

Alternately, in the first example, If a carrier is bred to a clear, the pups could all be followed and the best one chosen for breeding, neutering the others. If the best worker tests out to be a carrier, the process can be repeated until the result is a DNA clear to carry on the good and unique characteristics of that line. The problem has been bred through while retaining the good traits. It's not so different from breeding the affected dog. Either way, it must be done knowledgeably and responsibly with regard to the number of times the dog is bred and how the progeny are chosen and bred on.

However, the biggest argument I can think of for why we should go to all this trouble to keep these various individuals and their unique combination of characteristics in the gene pool despite genetic diseases is just look back and think of all the outstanding dogs and lines we *wouldn't* have if they hadn't been accidentally bred, not knowing their problem(s). I believe every dog I've had for the last two decades goes back to a dog that might be excluded if their DNA status had been known for various genetic diseases in the breed. Though there were affected dogs produced along the way, there were also many that resulted, mostly accidentally, as successful "breed throughs" of the problem. Now we can refine that. Why not do it with care and knowledge?

I think it's appropriate to evaluate the specifics of each genetic disease in the specific breed before making sweeping breeding recommendations or restrictions. In this case, it would be important to obtain reliable data on the affected and carrier rate within the population. Once the DNA test is out, and the incidence of the gene is known, then breeding recommendations could be considered based on the prevalence, severity of the problem as a health concern (i.e., I would not consider EOD as severe a problem as idiopathic epilepsy), the value of the particular dog otherwise in the gene pool, and the ability to control breeding of progeny so the incidence of the gene is not significantly increased in the overall gene pool (i.e., a worthy affected dog is bred carefully, to a limited number of appropriate mates and the progeny tested and followed).

I'm not talking about a broad recommendation to breed an affected dog as much as you want as long as it's bred to a DNA clear dog. I'm talking about careful breeding to keep valuable genetics in the breed. As in the approach for CEA, "breeding through the problem" in order to not lose the valuable contribution of certain dogs or lines.

In Jamie's defense, it was mostly Diane touting her dogs' bloodlines.

...we live in ARIZONA...

So how far have you traveled for conformation shows?

And on another topic, in case you think we working stockdog people don't care about our dogs' health, please peruse the Health and Genetics section of this board for starters.

Chaosstockdodgs,

I wish you would stay and at least keep reading. Most of what you post is the parroting of AKC party line. Perhaps if you stayed and read some you might be surprised to learn that we know more about our world than you do

While I agree that USBCHA especially at the open level is the ultimate test for this breed, just because my dogs arent there yet doesnt make them any less of nice dog. They have been genetically tested and are clean and they have the working ability to back it up. As I read on another forum you can breed two open working dogs and have puppies in that litter that just wont stack up as a good working dog. We can only do the best we can when it comes to breeding and Im making decisions that I feel are correct.

Since you seem to feel that "you can breed two open working dogs and have puppies in that litter that just wont stack up as a good working dog" and as we all know, even two parents who are OFA excellent can produce dysplastic pups, then why do you bother to hip test your dogs? What am I missing in your reasoning?

It's all about odds.