TNS

[jdarling]

A while back, there was a thread about TNS being found in a "working" pedigree. I can't find it no matter how I search for it. Anyone remember what happened to it? I was interested in seeing that pedigree.

 

Thanks.

J

[juliepoudrier]

Jodi,

Are you sure that discussion wasn't about CL and not TNS? Try searching "trapped neutrophil" and you should find any threads that mention the disease, but I seem to remember the discussions about pedigrees being about CL.

 

J.

[jdarling]

Hmmm... thanks Julie. I tried that and it lead me to a dead link. I'm wondering if maybe the thread I'm thinking of deteriorated into ash.

 

Jodi

[2 Devils]

You may find what you want here

 

http://bordercolliehealth.com/TNSdatabase.html

 

You can also see results for CL and CEA

[Lenajo]

After much online debate, no pure working line has been determined to have TNS. There have been accusations, based on the pedigrees of the site above, but the defination of working pedigree is not the same as we would use here. A show dog bred to a herdingdoodle (combination show/work/and backyard genetics) does not a working cross make.

[Journey]

Actually, no matter how it is "defined" there has been no "non kennel club" pedigreed Border Collie confirmed with either TNS or CL.

 

Karen

[Janba]

After much online debate, no pure working line has been determined to have TNS. There have been accusations, based on the pedigrees of the site above, but the defination of working pedigree is not the same as we would use here. A show dog bred to a herdingdoodle (combination show/work/and backyard genetics) does not a working cross make.

 

 

TNS carriers have been found in ISDS registered dogs and it is in Australian working BCs (and remember our ANKC is a closed registry) and in dogs with no Australian blood. Even if those ISDS carriers are registered with a KC and don't herd they are still genetically ISDS BCs and the last I heard no show bred BC had been ROM to the ISDS. The figures you need to look at on the BC health site are the ones in the table on the first TNS page.

 

It first camt to light only 10 years ago in the BCs and if you look at the number of dogs that are carriers it has been around a lot longer than that. A population of approx 20% carriers doesn't appear in 10 years though this percentage will probably drop as more dogs are tested. The problem with TNS is that most pups who die from it do so at an early age and go undiagnosed. How many people who have had pups who have been small, haven't thrived and have died before they reach 8 weeks or about the time of their first vaccination? It is usually just put down as the pup being the runt etc and in most cases that will be right but you can't rule out TNS if you don't test for it.

 

How many ABCA dogs have been DNA tested for TNS? Unless you test you cannot say with any accuracy that TNS is not in the ABCA, especially with the number if ISDS dogs you import. By saying "it is not in my lines" are you hiding you heads in the sand? You might argue that by breeding for working ability only the incidence of TNS will stay the same and not be a problem, but only you need to get one or two very good carrier dogs who are used extensively to make the problem worse which is what happened with CL in the show borders here.

 

CL is a different matter. Last I heard there was one dog who supposedly died from it and was diagnosed by brain biopsy who had no Australian blood but as no one has seen the pedigree you can't say anything about this dog with any accuracy.

[Eileen Stein]

Jodi, could this have been the thread: http://www.bordercollie.org/boards/index.p...c=9768&st=0 ?

 

I won't repeat here what I said there.

 

ETA: But I will say that if someone has come up with a "20% carrier" figure, it is derived from a totally different population than working border collies. Some of us would say a different breed.

[Janba]

Actually, no matter how it is "defined" there has been no "non kennel club" pedigreed Border Collie confirmed with either TNS or CL.

 

Karen

 

I do have the pedigree of an ISDS registered dog, who is also KC registered, that contains nothing but ISDS dogs registered in the 8 generation pedigree I have and who is listed on several databases as a TNS carrier as well as the KCs carrier list and the pedigree contians some very good trialling dogs. I won't put the dogs name here on a public forum but will pm you the name if you want.

 

Although he doesn't fit into your "non kennel club" pedigreed Border Collie he has nothin but working lines that I can find going back to before the advent of KC registered dogs

[jdarling]

Thank you, Eileen. Yes, I think that was one of them. I think there was another one, but this one will work for the purpose I was looking for.

 

CL is a different matter. Last I heard there was one dog who supposedly died from it and was diagnosed by brain biopsy who had no Australian blood but as no one has seen the pedigree you can't say anything about this dog with any accuracy.

 

There are many people that stand on the "I heard ..." I always say "Show me." I'm still waiting. If someone can show me that not only is TNS or CL in the working lines, but enough to cause concern, I don't have a problem testing for it. I won't, however, waste the money on something that doesn't exist in my breed.

[Eileen Stein]

Janba, if the dog "is listed on several databases as a TNS carrier as well as the KCs carrier list," what's the problem with naming it here? I looked through the UK dogs on that TNS test results site and couldn't find one meeting your description.

[Janba]

Janba, if the dog "is listed on several databases as a TNS carrier as well as the KCs carrier list," what's the problem with naming it here? I looked through the UK dogs on that TNS test results site and couldn't find one meeting your description.

 

He's not listed on the BC health database as that only lists dogs whose owners put them on there. The dog Is Henniker Spyro ISDS 259652

 

http://www.anadune.com/abcd/genetics.php?s...93&gene=tns

 

 

http://www.thekennelclub.org.uk/download/4...tnscarriers.pdf

 

also a 5 generation pedigree

 

http://www.anadune.com/abcd/pedigree.php?s...=5&export=1

[Janba]

A while back, there was a thread about TNS being found in a "working" pedigree. I can't find it no matter how I search for it. Anyone remember what happened to it? I was interested in seeing that pedigree.

 

Thanks.

J

 

 

Was this the thread?

 

http://www.bordercollie.org/boards/index.p...digree&st=0

[mjk05]

no matter how it is "defined" there has been no "non kennel club" pedigreed Border Collie confirmed with either TNS or CL.

We've had a completely working-bred litter with TNS. Non-kennel club pedigree.

 

I think our pups were the first non-show dogs ever confirmed with TNS. At the time they were sick and were put to sleep, we were told repeatedly by specialist vets and TNS researchers that it couldn't be TNS because they didn't have any identifiable link to Show-bred collies. The clinical picture also didn't match the documented cases (it was cyclical in nature, and while one of the pups had been a sickly runt, one of the pups looked "normal" and hadn't been sick as a young pup), and extensive testing on that "normal" pup was supposed to "exclude" TNS- he had plenty of functioning neutrophils in his lungs on lung lavage. But we were concerned that it was something inherited, even if it ddn't fit the TNS picture exactly, because two out of four pups were affected, and we had samples saved from the longest surviving affected pup (the one whose BAL "excluded" TNS). When the TNS DNA test became available, Alan Wilton agreed to test our sample (even though it was from non-show line dogs and nobody believed our pups had TNS) and we sent samples from the surviving littermates and their parents. The dead pup was "affected", the siblings and parents were "carriers".

 

There are no ANKC registered dogs in either parent's pedigree as far back as we can trace them (to the 1960s at least), they are both working bred with some ISDS ancestry. The parents are relatively unrelated, although they do share one ancestor in the 4th or 5th generation. A number of other Australian working dogs have been tested since and have been found to carry the gene.

 

It isn't just a "show dog disease". It might be an "Australian" disease that is more common here because our dogs (show and working) are relatively in-bred- presumably originating decades ago, before the show dogs were separated from the working lines (1960s, I think). But it is worth considering that our dogs are all descended from imported UK dogs, in many cases relatively recently. It may be that TNS comes from a mutation that occurred in an early Australian working dog, or it may be that it already existed in a UK dog that was brought over. Either way, it has probably increased in frequency in Australian dogs due to relative inbreeding, which has been worst in the Show BC because they originated from a small pool of Australian working border collies and don't have the numbers or the level of international outcrossing that our working dogs have.

 

I don't see how anyone can be 100% sure that it doesn't exist in UK working dogs. Until our dogs were tested (against veterinary advice), it had never been seen in Australian working dogs, either. We will be testing all our imported UK dogs where necessary.

[Janba]

We've had a completely working-bred litter with TNS. Non-kennel club pedigree.

 

I think our pups were the first non-show dogs ever confirmed with TNS.

 

I had wondered about that litter after a thread you had posted on another board.

[mjk05]

Janba, that is really interesting. For people not on Anadune, the pedigree can be seen on Border Collie Database

- search for Henniker Spyro, and click on the pedigree button.

 

No Australian dogs, no European or unknown ROM dogs (recently, anyway).

That suggests TNS is present in UK lines, if only rarely.

[Janba]

Janba, that is really interesting. For people not on Anadune, the pedigree can be seen on Border Collie Database

- search for Henniker Spyro, and click on the pedigree button.

 

No Australian dogs, no European or unknown ROM dogs (recently, anyway).

That suggests TNS is present in UK lines, if only rarely.

 

I found that pedigree interesting especially as it has some well known dogs in it. I have managed to convert it to a jpeg

 

 

[juliepoudrier]

It might be an "Australian" disease that is more common here because our dogs (show and working) are relatively in-bred- presumably originating decades ago, before the show dogs were separated from the working lines (1960s, I think). But it is worth considering that our dogs are all descended from imported UK dogs, in many cases relatively recently. It may be that TNS comes from a mutation that occurred in an early Australian working dog, or it may be that it already existed in a UK dog that was brought over. Either way, it has probably increased in frequency in Australian dogs due to relative inbreeding, which has been worst in the Show BC because they originated from a small pool of Australian working border collies and don't have the numbers or the level of international outcrossing that our working dogs have.

 

MJK05,

I think the above statement is the point that many of us have tried to make in the past when this topic comes up. Certainly the genes originated somewhere, and since all border collies go back, sooner or later, to the dogs from the UK, it is entirely possible that working bred dogs carry some of these genes. I really believe, though, that there has been concentration of those deleterious genes, in places like Australia where show lines and working lines were intermingled extensively before being split, and especially in show lines because of the greater interbreeding (or perhaps popular sire effect) needed to fix the physical look of the show dogs. I don't think most of us would ever say that TNS or CL absolutely does not exist in working dogs, but that its incidence of occurrence is so low as to have negligible impact on the working-bred population as a whole.

 

I think it was in another old thread (maybe one of the ones linked to here) where Denise Wall brought up the possibility of the incidence of such diseases increasing in the breed as a whole as breeders proceeded to mix show and working line dogs. I agree with her that as such mingling of the two populations occurs we may indeed see an increased incidence in the working bred population (using the term working bred loosely, since I don't think most dyed-in-the-wool working breeders would deliberately breed to show or sport lines where this intermingling is most likely to occur). But I also think that people who are truly breeding to a work standard aren't going to repeat breedings where the pups all die early from an "unknown" cause or continue crosses that apparently produce sickly/unhealthy animals, since those dogs will not be successful for work. So in that regard, I see lethal genes as being somewhat self-limiting within the working-bred population--and that's probably the reason problems like TNS and CL aren't seen to a great extent outside of show lines or Australsian border collies.

 

I think where people get annoyed is when the show breeders cry "It's in the ISDS lines," as if it's the fault of the original dog carrying the mutation/deleterious gene when what they should be doing is looking at their own breeding practices and how those practices over time have contributed to the increase in the incidence of those genes in certain subpopulations of dogs within the breed as a whole.

 

J.

[Eileen Stein]

Thanks, Janba, for posting the dog. I don't know most of the dogs in the pedigree, but there is no apparent show dog or OZ/NZ dog on the 4-generation pedigree I was able to see. Do you know anything more about this dog? Since the dog is KC-registered and is included on Anadune, which I think of as a show site, I'm assuming he is basically at this point a Kennel Club dog, despite retaining his ISDS registration. Do you know whether he is mainly used for show, or sport, or work? How about his parents? Has he been bred, and if so, to whom?

 

Despite what I said earlier about not repeating myself, I guess I will repeat some of what I said in the earlier TNS thread that seems relevant here:

 

It's not impossible that there might be the odd British dog with no Oz/NZ in its background that carries this mutation. All dogs (and people, for that matter) have deleterious recessive alleles (gene variations) of one kind or another. These genes do not become expressed unless one carrier is bred to another, and this is unlikely in ISDS working lines.

 

Obviously, the Oz/NZ show breeders have concentrated this gene (whether it was a mutation that occurred after importation or before importation) in their dogs through inbreeding to "fix" physical traits that are desirable in the show ring. That is evident from the very high percentage of Oz/NZ breeding in the pedigrees of known afflicted and producing dogs. However, few if any working breeders breed like this.

 

It is pure sophistry for anyone to say "Look, that bitch has Wiston Cap and Bosworth Coon in her pedigree! We know how often they were used! That must mean TNS is all through working lines!" There is no reason whatsoever to think that Wiston Cap or Bosworth Coon carried the mutation. Actually, the very fact that they were used so often is very strong proof that they did NOT carry the mutation, or the disease would have shown up in their working-bred progeny by now. One of the little-known dogs among the 16 great great grandparents of this dog is far more likely to have been the carrier through which this allele descended, and for all we know the actual carrier may have no offspring surviving in working ISDS lines today.

 

Let me give an example of how this could be. Without naming names, there was a dog with Australian show ancestry on the topside of his pedigree (let's call him X) who was at some time in the past registered with the ABCA, because he had been accepted for registration by one of the sloppier US working registries, and at that time the ABCA was honoring all the registrations of that other US registry. A littermate of X, who was not registered with the ABCA, was later found to be a CL carrier. X was never tested, so he might or might not have been a carrier. X had about 14 offspring who were registered with the ABCA. But only 1 of that 14 had any offspring registered with the ABCA, and none of those offspring had any offspring who were registered with the ABCA. Why not? Presumably because the focus of the breeding in that line was on KC activities rather than on work, and so within two generations the owners of the pups were not bothering to register with the ABCA. So based on that one registration, it's possible that "CL was in the ABCA lines," but not in any way that had any significance for us (and not for long).

 

The show breeders make the point that vets were not aware of this disease until recently, and therefore it may be (and have been) much more prevalent than we realize. I agree that if one has had pups dying of infection or unknown causes before reaching the age of 4-6 months, then it's possible undiagnosed TNS might have been involved. But that is just something we are not seeing among working bred dogs in the US. If we're not seeing symptoms consistent with the disease, and the disease is one that produces drastic symptoms, doesn't it make sense to conclude that the disease is either non-existent or so rare that, as a practical matter, there is no need to test?

 

This is not denial on our part, as the show breeders like to claim. I would never deny, for example, that we have epilepsy present in our dogs, and some of it is almost certainly genetic. I think it makes sense to go all out to try to identify the genes involved and develop a DNA test for them, and use the test when it becomes available. Our registry (ABCA) was one of the principal contributers to CEA research and the development of the DNA test for CEA, because mild as CEA usually is, we knew we had it in our dogs. But I see no evidence that we have a TNS problem in our dogs, either from real life evidence or from the published pedigrees, so I see no need to test for it. All dogs carry a number of deleterious recessive genes. As work continues on the canine genome, a flood of tests are likely to become available for these defective genes. It certainly makes sense to make use of any particular test if there's a reasonable likelihood that the mutation the test identifies might be present in your dog. It doesn't make a lot of sense to test where there is little or no likelihood that the mutation would be present in your dog. What makes the least sense of all would be to test for every testable deleterious gene, and eliminate from breeding any dog who carries any one of them. Paradoxically, the likely result of doing so would be the concentration of other undesirable recessive genes, and the expression of diseases not previously seen, in a gene pool whose diversity has been much reduced.

[Liz P]

I don't know how often this happens in other countries, but I have seen it happen often enough in the USA... "Versatility" breeders often cross purely working, sport and show lines. Some are more focused on the working side than others and maintain ABCA registration on all their dogs. I have seen dogs who have show lines mixed in so far back that these dogs no longer appear on the ABCA papers. If you didn't think to look beyond the papers you would never know there were any show dogs in the pedigree. It can be impossible to tell sometimes if these dogs have short (classic) ABCA/ISDS names and come from lesser known versatility breeders.

 

As with others I am not outright denying the possibility of TNS in working lines, I was just providing a scenario for a purely show line problem entering the working dog gene pool.

[Janba]

I don't know how often this happens in other countries, but I have seen it happen often enough in the USA... "Versatility" breeders often cross purely working, sport and show lines. Some are more focused on the working side than others and maintain ABCA registration on all their dogs. I have seen dogs who have show lines mixed in so far back that these dogs no longer appear on the ABCA papers. If you didn't think to look beyond the papers you would never know there were any show dogs in the pedigree. It can be impossible to tell sometimes if these dogs have short (classic) ABCA/ISDS names and come from lesser known versatility breeders.

 

As with others I am not outright denying the possibility of TNS in working lines, I was just providing a scenario for a purely show line problem entering the working dog gene pool.

 

I have traced the pedigree I posted to before the BC was recognised as a show dog in the UK, or Aus for that matter and this is definitely pre dog sports as we know them, and could find no Australian blood.

 

I am not saying that you should all rush out and test you dogs, unless you have a problem litter like mjk05, but not discount the possibilty that it is there.

[juliepoudrier]

Janba,

No one is discounting the possibility that it's there. As I stated in my previous post in this thread, as well as in other threads of this nature, all the various types of border collies (as well as some other, newer breeds) have the UK border collie as foundation stock and so it's likely that some gene defects can be traced back to those original dogs, and it's likely that the deleterious genes in question existed in the breed long before dogs were exported elsewhere or show lines were created. I'm sure there any number of rare genetic issues that would pop up if the breeding practices were such that the deleterious genes were concentrated (through inbreeding to fix a look for example, and wasn't that the exact point that the "Pedigree Dogs Exposed" program tried to make?). What everyone is saying is that in general breeding practices that produce the working border collie do not tend to concentrate such genes, hence we don't see a high enough incidence of them (in fact, many of us would say it's pretty much unheard of) in our specific working population of dogs today to consider it a breedwide problem or find it necessary to worry overmuch about or test for. Does that mean no strictly working-bred border collie will ever be found that has either CL or TNS? Of course not. It just means that it doesn't occur at a rate significant enough to be considered a problem in working-bred dogs because the breeding practices are such that deleterious genes generally aren't concentrated in the subpopulation of working dogs. (Notice that not once did I say "never;" it's all about probability.)

 

I don't understand why that's such a difficult concept for folks to grasp. It's like saying that just because the Amish here in the US exhibit certain genetic disorders that are basically nonexistent in the rest of the people in this country that we all (or at the very least, those of us who are of German or Swiss descent) should be in a panic over the possibility of our children developing something like Cohen Syndrome. There are probably many, many people of German or Swiss descent in this country who never, ever worry that their children will end up with some of the genetic diseases that Amish children face, even though the Amish come from Swiss-German stock as well. Why is that? This has been discussed here before, but I suppose it bears repeating, so I'll just quote from an older "60 Minutes" (a news show here in the US) program from 2005 titled "Genetic Disorders Hit Amish Hard":

The genetic problems come down to something called the "founder effect" because the nearly 150,000 Amish in America can trace their roots back to a few hundred German-Swiss settlers who brought the Amish and Mennonite faiths to the United States in the 18th century. Over generations of intermarriage, rare genetic flaws have shown up, flaws which most of us carry within our genetic makeup but which don't show up unless we marry someone else with the same rare genetic markers. [emphasis added]

 

So, yes, if any of us were to breed two dogs together who both happened to be carriers for TNS, we could have pups with TNS. But at least for now, the working border collie gene pool is large and diverse enough that the chances of that happening are relatively small. The working border collie is like the majority of people of Swiss or German descent--not likely to develop the rare genetic disorders that plague the smaller, more inbred subpopulation of those nationalities, the Amish (who would correlate with the more inbred subpopulation of border collies, the conformation-bred dog).

 

J.

[mjk05]

Eileen,

Spyro is a UK agility dog, which is why he's registered with the KC. His parents, I believe, are also agility dogs, but beyond that I believe they are ISDS-only dogs.

 

it is entirely possible that working bred dogs carry some of these genes.

Yes, it is. I'd say the pedigree Janba posted makes it extremely likely. And I know this is nitpicking, but working-bred dogs definitely do carry TNS, because our dogs are most definitely working-bred.

 

in places like Australia where show lines and working lines were intermingled extensively before being split,

Again, nitpicking- but the split in Australia happened so long ago that it was before "show-lines" really existed. Our working dogs haven't had "show-lines" mixed in, they had dogs selected out of them that became the show lines after many years of concentrated breeding. The working dogs have continued being bred for working ability, the way they have been since before the ISDS existed. I'd suspect we have a greater proportion of our "working-bred" dogs actually working for commercial farmers, on larger farms, than just about any other country in the world (possibly bar NZ). Some lines are significantly inbred (to "fix" working qualities, rather than appearance), but others aren't. As I said, our TNS litter had one common ancestor. And our separation from the show lines is more complete than just about anywhere, because our working dogs aren't accepted by the ANKC (+ working breeders don't use show dogs)- so we have no significant intermixing of show and working dogs.

 

Inbreeding to some extent, and especially the "common sire effect" is not limited to Show BCs. It's much more exaggerated there because of the very small gene pool they started with, but how many modern working-bred border collies don't go back to Wiston Cap? Presumably he didn't carry TNS or we'd know about it now, but there but for the grace of God...

 

But I also think that people who are truly breeding to a work standard aren't going to repeat breedings where the pups all die early from an "unknown" cause or continue crosses that apparently produce sickly/unhealthy animals,

I'm going to nitpick on that one, too. TNS is caused by an autosomal recessive gene. If you breed 2 carriers, each puppy will have a 75% chance of NOT having the disease. Its entirely possible that a litter will have no affected puppies, and more likely that one or two pups will be affected. The most unlikely scenario will be that all pups are sick and die. I expect most working breeders would repeat a breeding that had produced one or two pups that died at a few weeks old (and were runts anyway) and 6 or 7 pups that became healthy, fit, excellent working dogs.

 

From my experience, I don't think TNS is well understood as a disease. We spent $6000 trying to get a diagnosis on one of our pups, unsuccessfully- the only thing they could assure us was that he (the one later tested) did NOT have TNS. There were other explanations, and if we'd followed vet advice early on we would have accepted that at least one of them had just been an unlucky runt with a novice mother, had them PTS and left it at that.

 

So in that regard, I see lethal genes as being somewhat self-limiting within the working-bred population--and that's probably the reason problems like TNS and CL aren't seen to a great extent outside of show lines or Australsian border collies.

So what is the explanation for TNS in the Australian working border collie? It hasn't been self-limiting in our dogs, who, I would argue, are "bred for work" as much as any. And possibly more.

 

The thing about TNS is that it usually affects young pups, they die of infections, and if one pup in a litter dies in the whelping box of unknown causes or even at 16 weeks from gastro or pneumonia, it isn't going to have as much impact as, say, CEA or CL, which can affect older trained dogs that have potentially bred. TNS-affected pups are easily misdiagnosed or just notched up to being "failure to thrive" or whatever.

 

I think where people get annoyed is when the show breeders cry "It's in the ISDS lines," as if it's the fault of the original dog carrying the mutation/deleterious gene when what they should be doing is looking at their own breeding practices and how those practices over time have contributed to the increase in the incidence of those genes in certain subpopulations of dogs within the breed as a whole.

I don't see that at all. I see the opposite, that working dog people are using diseases like TNS and CL to disparage the Show BC (unnecessary given there's so much else wrong with conformation breeding), making all sorts of claims that "it doesn't exist in working dogs" because they can't find any evidence that it does. Granted, the Show BC people are desperately wanting them to be in the working lines because it makes them feel better. But some arguments I've heard from some working collie people about why TNS is purely a ShowBC disease are ridiculous, and frankly sound like they have their fingers in their ears, humming madly.

 

I agree with you about the Show BCs' level of inbreeding having consolidated the gene and dramatically increased its incidence, and yes, that's an argument for not increasing its incidence in working lines by continuing to allow mixing of ABCA and AKC lines. But it also sounds like a great justification for ShowBC breeders to continue using working-bred dogs for outcrossing

 

I personally think the only practice to "blame" for the rates of TNS is inbreeding. Breeding "for work" isn't protective.

 

I don't think working breeders need to spend money getting tested, given the possibly low rates of carriage in that population. It would be useful for research purposes, and to try ot establish rates in US/UK working dogs, but not essential for individual breeders. But it is worth being aware that it exists, it probably exists (at a low rate) in your dog population, and just keeping it in the back of your mind.

[mjk05]

Just to add: as far as CL goes, that hasn't yet been found in working-bred dogs in Australia, either, and as far as I'm aware all the carriers and affected dogs have been Show BCs.

 

I used to dismiss the chance of a working-bred dog (from anywhere) having CL, in part because of the impact it would have on those lines as working dogs. Now I'm quite open to the possibility that working dogs may carry it. Alan Wilton told us he thought it was unlikely, and not really worth testing for in our dogs, but he tested some of them anyway at our request. We won't be bothering any more, but I'm not going to suggest its just a show dog disease.

[mjk05]

Julie, I really appreciated the Amish analogy. I think that's a really accurate comparison, and we're basically in agreement on this topic.

 

But there is the added issue with the dogs of "breeding for conformation" as opposed to "breeding for work".

 

Working dog people seem to be pointing to the Amish and their genetic diseases saying, "See what religion does!". Its not the religion, its not the breeding for conformation that is responsible for the rates of Cohen disease and TNS- its the inbreeding. You can inbreed for working ability very effectively (some of our dogs come from a working breeder who uses extreme inbreeding, and I know of other breeders who do). The risks and benefits of inbreeding for working ability are just the same as they are for conformation, perhaps with the small advantage that culling on working ability will more effectively remove health problems than culling on showring conformation. One argument for inbreeding is that at least in the TNS affected inbred lines TNS has been found and can be addressed, while in the wider population of border collies who knows which dogs may carry it? If just one popular and successful stud dog in the UK or US is an unknown carrier, the situation in working border collies could change significantly.

 

The problem I have with discussions of TNS in border collies is that so much time and effort seem to be expended by working dog people on proving that all TNS affected dogs are not "real", verified working border collies so that we can continue to say that TNS has never been found in working lines. There's no compelling reason for working dog breeders to start testing their dogs for TNS, but its pointless for people to keep insisting that it doesn't exist in "real" working dogs.

 

Now I'll shut up for a while