TNS

[Rebecca, Irena Farm]

Look, I'm about to sound really callous here, especially since we have a member with personal experience. If the main symptom is puppies that fail to thrive, then yes I won't disagree that we could have it and not know.

 

But here's what happens when farmers get this sort of things happening. A puppy dies, they say, "Well, that happens. More milk for the others. Nature takes care of things." Two puppies die, they say, "Hmm, we'll have to watch that. Maybe the bitch doesn't have enough milk." Three puppies die, and he says, "That sucked. Bad bitch." And she is culled.

 

If TNS is recessive, that's the end of that carrier.

 

One factor is that it hasn't been common until recently among the working world, to go to extreme lengths to save puppies or keep lines going.

 

Sure, the sire keeps going on, but we are unlikely to cross his line back over itself for a long time. We tend to cross "style" rather than literal relatives.

 

As for the working dogs in Australia - you all are working from the same isolated gene pool ultimately. Most likely, if you compare Australian numbers to US working registry numbers, Aus numbers will fall far short.

 

I believe Eileen is right about the ISDS dog with TNS. He goes very quickly back to many very well proven lines. On the top, I've personally seen someone who line breeds the heck out of those dogs (JThomas) without health problems of significance (on the contrary, dogs from that line are locally famous for longevity and health). I can go right down the list and name many of the rest and say with confidence that they are not the culprits. I've seen Davy linebred for sure. Coon - oh yeah. The list goes on. They wouldn't be popular sires if females from those lines habitually produced failure to thrive puppies. Farmers aren't stupid. And they don't like low "production rates."

 

Maybe I'm missing something here?

[juliepoudrier]

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.

 

Okay, I'm pretty much ready to give up on this conversation. Ive spent a lot of time and effort here doing the exact opposite of what you claim. I haven't spent any energy saying that the genes don't exist in the working population. What I have said is that the gene doesn't seem to be often expressed in working dogs, and that's a big difference that seems to be lost on you. If you can't see that the conformation folks are doing exactly what you accuse the working dog folks of doing above (i.e., TNS and CL aren't their fault for concentrating deleterious genes through inbreeding and a small gene pool; instead it's a problem because the gene exists in the working dogs too--therefore the problem is somehow with the working bred dogs and not with breeding practices that concentrated deleterious genes mainly in a subpopulation of those dogs), then nothing I can say will change the conversation and I'm tired of trying. If you understood the Amish analogy then you wouldn't keep trying to hammer away at how TNS is a problem in the working border collie around the world. That's like saying the Cohen Syndrome is a problem for all people of Swiss or German descent and that's just patently untrue. Arguing otherwise won't make it true, no matter how hard you or anyone else tries. Does the average German worry about procreating with a fellow citizen because of a disease that is the result of inbreeding among one sect of Germans? No. Why ever not? Because for most Germans, there's not even a remote chance that the combining of their genes will produce a child with the genetic defect that causes Cohen Syndrome. Should the average Amish person who marries and procreates worry about the disease? Yes. Does the average Amish person try to tell all others of German or Swiss descent that they should be worried about Cohen Syndrome? No. Why? Because the Amish recognize that the intermarriage that is unavoidable in a closed genetic pool makes these problems inevitable (although they attribute it to God's will). They don't preach to the rest of us that it's somehow our fault that they have serious genetic diseases. Yep, the deleterious gene must have been carried by one or more of those original founding Amish, and certainly exists even by non-Amish Germans and Swiss. But the disease is recognized in the Amish because that's the population in which is has been expressed to a noticeable degree. That doesn't mean that two random Germans or Swiss couldn't have the bad luck of both carrying the gene and producing a child with Cohen Syndrome, but the chances are extremely slim. This is not about religion--it just so happens that a particular religious sect is a prime example of what happens with inbreeding and a small gene pool. If people who work with populations of dogs that have been inbred and have a limited gene pool can't make the connection, then I can't force them to.

 

I have said repeatedly that the genes probably do exist in working dogs. I have said repeatedly that breeding practices (i.e., inbreeding) is likely the major culprit for why the problem seems to appear at a greater frequency in one population of border collies vs. another. I know you'd apparently like me (and the rest of us) to "admit" that diseases like TNS are a problem in the working border collie population in places other than Australia, and so far I haven't seen any proof that's the case. Pointing out pedigrees with famous names really proves nothing. Those dogs were used a lot, and if they were somehow the absolute root cause of TNS in border collies, then certainly we'd be seeing more unexplained puppy deaths over the years in working breedings, and for some amazing reason that hasn't happened. But no doubt there are folks who would just argue that the working breeders are just engaged in a cover up. Big conspiracy theory and all that.

 

All I can say is that folks can choose to believe what they wish, but it won't change the fact that inbreeding and a closed gene pool are the most likely culprits for why odd genetic diseases pop up in a population of dogs (or humans). The fact that it's not running rampant through working lines would imply that the COI for working bred dogs is low enough to help prevent it from happening. That's not the same thing as sticking our heads in the sand and claiming that the genes don't exist in some dogs in working lines. It's saying that it's not a major problem in working bred dogs because apparently there is enough outcrossing and a large enough gene pool to prevent it from becoming one. You can nitpick all you want, but you won't change the facts.

 

J.

[Denise Wall]

I don't know why I'm bothering but I'll say this yet again. There are many mutations such as the ones for CL and TNS. Most if not all individuals be they humans, dogs, whatever, carry at least one or more deleterious genes such as these. They are normally recessive. They normally don't produce affected individuals in a naturally outcrossed population.

 

The most sensible strategy to avoid the expression of genetic disease and an increasing incidence of affecteds in a population is to avoid inbreeding.

[Janba]

Look, I'm about to sound really callous here, especially since we have a member with personal experience. If the main symptom is puppies that fail to thrive, then yes I won't disagree that we could have it and not know.

 

But here's what happens when farmers get this sort of things happening. A puppy dies, they say, "Well, that happens. More milk for the others. Nature takes care of things." Two puppies die, they say, "Hmm, we'll have to watch that. Maybe the bitch doesn't have enough milk." Three puppies die, and he says, "That sucked. Bad bitch." And she is culled.

 

If TNS is recessive, that's the end of that carrier.

 

In a TNS affected litter the most likely scenario in an affected litter is one or two pups who get sick and die, the carriers in the litter are as healthy as their clear littermates in regard to TNS symptons. When the pup dies at 8 weeks from an infection do they blame the bitch or just say it was the runt, these things happen?

 

The frequency of carriers of a lethal recessive gene tends to remain stable in a population under normal conditions if you don't actively select away from it and culling the odd bitch won't affect the frequency of the gene particularly if she has already produced a couple of "healthy" litters or the farmer blames the dog and breeds her a different dog next time and it doesn't remove her carrier relatives. If the frequency of carriers is 5% in the population now it will still be about 5% in 20 years under normal breeding conditions i.e. no increase in the rate of inbreeding or very predominant sires etc.

 

No one is saying go out and test everything or that it is a big problem, but it is the people who are saying that it is not in a true working pedigree and that it is only an Australian show dog disease that are the problem.

 

From what mkj05 has said I know someone whose very promising dog has a chance of being a carrier and another person whose good dogs are also closely related. Do I tell them so they can DNA test if they want to or just say chances of them being bred with a carrier are very slim so just let it slip?

 

Pointing out pedigrees with famous names really proves nothing

.

 

Nobody pointed to the famous names in that pedigree or said anything about them being carriers. It was just a pedigree of a carrier dog who had no Aus or comformation blood. If the pedigree had had no known dogs in it someone would have come on said it wasn't a "true working pedigree"

 

 

I also don't know why people keep bringing CL up. No one has said it is in anything but Australian show lines and even then the frequency of affected dogs was very small - less than 40 recorded litters with affected pups.

[mjk05]

Look, I'm about to sound really callous here, especially since we have a member with personal experience. If the main symptom is puppies that fail to thrive, then yes I won't disagree that we could have it and not know.

 

But here's what happens when farmers get this sort of things happening. A puppy dies, they say, "Well, that happens. More milk for the others. Nature takes care of things." Two puppies die, they say, "Hmm, we'll have to watch that. Maybe the bitch doesn't have enough milk." Three puppies die, and he says, "That sucked. Bad bitch." And she is culled.

 

If TNS is recessive, that's the end of that carrier.

That's not callous And we are farmers, if it matters.

 

But that's not what happens, Rebecca.

What happens is that 95% (or more) of dogs aren't carriers, so most of the time no pups are affected. In the rare circumstance where 2 carriers are bred together, one puppy in a litter dies (runt), and the rest are fine. The bitch gets bred again, probably to a non-carrier, so no pups die, and there are 8 healthy pups. But maybe the breeder repeats the first mating- 2 pups in that litter die (runts), the other 6 are fine. The bitch might get bred again, no pups die, or maybe 3 do, the other 6 are fine, and the bitch is culled. Result- 20 pups that have a 67% chance of being carriers, and a carrier sire still circulating.

 

The whole thing about TNS is: its not very common in working dogs. Not even Australian working dogs. Ours are STILL the only affected pups I've heard of, even from a breeder who routinely does son-mother type matings. And has TNS carriers in his lines. Lots of dogs in my area, all closely related to our dogs, many quite inbred, have been tested, and only a handful are carriers. If it weren't for me having come from a pet dog background, those pups being the first litter I'd been closely involved with, and me having more money than sense, they would have died/been PTS as tiny babies and I'd be saying "there's no evidence of TNS in working dogs" along with everyone else.

 

Its still pretty uncommon, and is probably very rare outside Australia.

 

As for the working dogs in Australia - you all are working from the same isolated gene pool ultimately.

No, we're not. Even my most inbred dog is very heavily bred on a dog that was imported from the UK after the Show BC split off. He's inbred, and his ancestry includes some of the same dogs the ShowBC is based on, but the gene pool for working dogs here is much much larger than the one the ShowBC is based on.

 

And we're not a closed gene pool, either, and have never been. Almost all our dogs have at least a couple of imported dogs in their 6 gen pedigree. We have 13 registered Australian working border collies here, 9 are current or potential breeding dogs. 4 of them are either imports or half-imported. We're not atypical among local farmers and working dog breeders.

 

Yeah, we do have less registered dogs over here, for what that's worth.

 

They wouldn't be popular sires if females from those lines habitually produced failure to thrive puppies. Farmers aren't stupid. And they don't like low "production rates."

No, they're not. But stupidity isn't required for TNS to be present in one's dogs. Our dogs are bred by farmers- people that make their living wholely from livestock, and keep and breed dogs for that primary purpose- as working dogs. And our dogs have TNS. Not at very high rates, and so there isn't habitual production of FTT puppies. But its there, nonetheless.

 

That's all. Nobody has to test for it. It's too rare to even worry about. But it has nothing to do with the mysterious L'Bleu or a spaniel called Nigger or breeding for conformation as opposed to work. It's a rare disease in border collies, brought to light because of inbreeding in the development of the Show BC. It is possible it may occur in working-bred border collies where a lot of inbreeding occurs, or very rarely for unfortunate others. That's all.

[mjk05]

I know you'd apparently like me (and the rest of us) to "admit" that diseases like TNS are a problem in the working border collie population in places other than Australia, and so far I haven't seen any proof that's the case.

No, I wouldn't. Not at all.

 

What I'd actually like is to know, as I suspect, that the rates of TNS carriers in the ISDS population are incredibly low, because we're going to continue using imported lines.

 

It isn't currently a "problem" in Australian working dogs, and I'd like to keep it that way.

 

What I'm hoping doesn't happen is that the TNS discussion continues to imply that only dogs from dubious breeding can be carriers- ie dogs not really bred for work, or dogs with unknown ancestry, or mixed ShowBC-working-sports types. You aren't saying that, but participants in previous discussions here and elsewhere have certainly give that impression. What might happen then is that anyone who does suspect TNS in their working-bred dogs will brush it under the carpet- and now that we have a test for it, that's the only way there is any risk of it becoming a problem in working dogs.

[Lenajo]

Lets face it people...we got everything from the Chihuahua to the St Bernard from the same set of wolf genetics.

 

There is a possibility of every single canine genetic defect in every single dog out there.

 

A *possibility*.

 

You can spend your life running around looking for where the sky is going to fall and get nothing but a neck ache. You definately won't do anybody or any dog any good.

 

TNS is a disease of inviability. It is incompatible with life. Then there is the *working* Border Collie, who is bred and culled by viability. Farmers, shepherds, even trialers to borrow from Becca aren't stupid. Pups that don't grow to 8 weeks are noticed and a "bad" litter will either change the breeding program or cull the dam. Pups that are sold at 8 weeks and reported back as "dead at 6 months" are bad business. Nobody wants that name who has any reputation as a good breeder. Even the farmers who bought the $50 pups will bad mouth you if their pup costs money in vet bills and dies before a year.

 

Again everybody wants to blame inbreeding, but the true villian is *lack of culling*. When people spend 6k to find out why a puppy with failure to thrive is not thriving it is because they want to know how to breed that cross, or at least that female, again. My question, my farmer friend's question, every stockman out there's question should be "WHY?"

 

Would you breed a cow again that produced a 30 lb calf that died by 3 months? Heck no! She'd be sent to the sale yard. Well...she would be if she was a commercial animal being used to produce beef. Now..if she was a purebred registered cow with wins in the show ring...oooooh we'll have to save the wee calf if we can...cull the cow? you're kidding right? We paid a *lot* for that cow! She's a daughter of WhoHa He'sAProblem and out of a son of HeHawss SheDon'tMilkButGotAPrettyHoof

 

I think my point is clear here.

 

My other question is what farmer has 6K to put on a failing *puppy*? I want to farm what they are!

 

(I love my dogs, but that sort of money is hard to come by and would be reserved for time tested and proven dogs that had become members of the family. And even then I would have to think hard because of the debt it would ensue. Not to mention the fact that when you get to that level of money in a single health issue is there really hope for the dog anyway? usually we are dealing with human emotions at this point)

 

I recently looked at litter of pups from a gundog breed. The litter an outcross but only 2 pups of the 7 survived to weaning. Fading pups, weak pups, born too small pups, even a pup born with the intestines on the outside. To me that is a *bad* litter. Yet because the 2 remaining pups are of "show quality" they will be bred. And if they produce well, they will likely be inbred on to set "type" further. Of course the inbreeding will be blamed when that resulting litter fails. Too bad nobody could speak the truth and admit it was because they didn't cull the "bad" litter to begin with.

 

In that case one of the 2 pups died at 4 months with a virus he should have been susceptable too at that age and with that level of health care. The remaining pup is an agility/show dog and will now be raised and bred as the "savior" of that line.

 

Heaven help that breed if those genetics become a popular sire.

 

It's pretty easy to see how that gundog bred got into trouble - why is it so hard to see why the choices of breeders in this breed are the same?

 

The moment you _stop_ breeding for dogs that can be whelped, raised, and work their lifetime with only normal and reasonable husbandry then you start breeding for things like TNS.

 

I'm familiar with the line of dogs the "working" (aka agility dog first generation cross from ISDS lines) is from. It's produced some outstanding workers in several countries. I know quite a few of them that have been inbred on, and the pups are viable and useful.

 

I find it sad, and truth telling, that the first time problems pop up is when a cross is made based on something other than working quality.

[Janba]

I'm familiar with the line of dogs the "working" (aka agility dog first generation cross from ISDS lines) is from. It's produced some outstanding workers in several countries. I know quite a few of them that have been inbred on, and the pups are viable and useful.

 

I find it sad, and truth telling, that the first time problems pop up is when a cross is made based on something other than working quality.

 

So if they had bred the dam to a good working dog or a top trialling dog resulting pup would not have been a TNS carrier?

[Lenajo]

So if they had bred the dam to a good working dog or a top trialling dog resulting pup would not have been a TNS carrier?

 

Is, or not, frankly is highly unlikely too matter.

 

Why? Because when the next generation is bred again, for viability as a working dog, the chances are next to nothing of breeding to another carrier.

 

This has been proven many times over by the number of working crosses from these lines and others, both inbred and outcrossed, that are not producing affected TNS dogs.

 

You want us to worry about smoke in your house, when we've not had any fire in our houses...that is the majority (acutally none in most cases) of the genepool that is out there working at the top levels of the US, Canada, and the UK does not produce TNS pups.

 

And don't start with "people don't tell the truth, they won't tell you if their puppies died". The stockdog world is too small. If such happens, it gets out there pretty quickly. You know who's female isn't a producer, who lost a pup to this or that, etc. And again, the farmer mentality rules. Unproductive animals who's pups don't mature are culled from the breeding program. Popular lines produce hundreds of pups - again, random death of these pups is known.

[Janba]

No one is saying that you have a problem in your dogs or that you are producing a lot of TNS affected pups nor that you should run out and test UNLESS there is a problem with a close relative.

 

It is this statement that I had a problem with

 

I find it sad, and truth telling, that the first time problems pop up is when a cross is made based on something other than working quality.

 

The only reason the we know that there is TNS in that dogs lines is not from affected pups but because a healthy non affected dog was DNA tested and found to be a carrier. If you go back 4 generations in that dogs lines to before the breeding for agility at least one dog in that 4th generation was a carrier and that line will have produced carriers in the pure working population as well. The line may never have produced a TNS affected pup and may never produce one but they may be unlucky enough to breed a carrier to another carrier one day.

 

It is the idea that breeding for anything other than working ability increases your chances of TNS. It does if you introduce show lines, but if you stay away from KC lines the chances are no higher than in the working BC population where you can also see pedigrees of inbred and line bred dogs.

 

Culling of a carrier bitch that has been unlucky enough to be mated to a carrier dog will not lower the frequency of the gene in your population unless you also cull the sire and both their untested close relatives and do not breed from any of their untested offspring no matter how low the frequency is.

[Shoofly]

The moment you _stop_ breeding for dogs that can be whelped, raised, and work their lifetime with only normal and reasonable husbandry then you start breeding for things like TNS.

 

Wendy - I have to say i find your arguments pretty circular when it comes to inbreeding. You defend the working dogs as having a wide gene pool but then narrow it down to next to nothing by touting the benefits of inbreeding, which by nature limits the variety of genes available to be in offspring. You also say things like the above quote but still espouse inbreeding with heavy culling for problem pups and dogs. Surely it's obvious that even if you cull the "problem animals", you still retain "problem genes" in the healthy-appearing survivors?

 

Maybe i'm missing something here.

[Katelynn & Gang]

I spy a Obedience Champion in this dogs tenth generation. From that, I am going to assume that breeding for things other then working set in well before the fourth generation.

[Katelynn & Gang]

On a final note, Obedience Champion Patanne ISDS 14511 is the Dam of Crufts 1969 Obedience Champion, Blaze of Sealight. These were the foundation lines for some show/obedience lines in the UK which where found to produce TNS.

 

Check out the third and fourth pedigree down on the Border Collie Health site.

 

Katelynn

[Lenajo]

My point is that we have purebred dogs, therefore we have inbred dogs. The dogs for generations so far have been culled for viability - healthy working and the overall health that comes with that. They are, what we have chosen them to be. In this case of TNS we have a change in the breeding selection process - instead of chosing to mate 2 viable working dogs, the hallmark of the breed, the breeder chose to mate 2 unproven dogs from working lines based on a new selection process. Then they got a a "surprise" recessive and want the rest of us to be concerned even though we haven't change our own breeding selection process. We are still breeding working Border Collies...they are breeding Agility Collies based on foundations of our genetics.

 

Does the Chihuahua get to blame his open fontanel and luxating patellas on the Wolf he came from? Does he get to get on the Wolf Breed Boards and bash how we are not concerned with his genetic illness and how we obviously carry it?

 

Some want to blame it on inbreeding. I'm tired of hearing that excuse frankly. Inbreeding is nothing but a breeding method. The dogs in this case were not even inbred, they were just badly bred. Regardless of the fact that this was the "desirable" outcross type of breeding, no breeder worth their salt would breed from the resulting living pup knowing of such deathly ill littermates. So the recessive that popped from an ill planned breeding of unproven parents stops there. It gets buried in a common sense cull, and the parents if rebred to other dogs get the problem buried the vastness of the overall genetics out there in working BCs that don't carry it.

 

You can compound a problem by inbreeding on it and setting the genetics as homozygous. But again, you have to have the bad decision to breed unproven or poor quality dogs in the first place...

 

I showed that in the gundog and cattle example as well. Bad breeding, no culling, emotions/money/titles before common sense....

 

I am for heavy culling period. No matter what breeding problem/method you choose. (culling simply meaning removing from the genepool of breeding stock - spay/neuter or simply don't breed). I think far too many Border Collies are being bred that shouldn't be. If you aren't prepared to cull, then you shouldn't breed - period.

 

Surely it's obvious that even if you cull the "problem animals", you still retain "problem genes" in the healthy-appearing survivors?

 

Maybe i'm missing something here.

 

Yes you are. They *all* have problem genetics. All. of. Them. Those genetics have nicely stayed buried while we continued to breed and cull for work. We have that advantage in this breed. We have not lost the original work.

 

As for inbreeding in general, I think it's high time we look at it less emotionally. We are not above the KC dogs as far as we want to brag. We still have relatively closed genepools, with limited founder dogs. Our dogs are an inbred population. A relatively healthy one, if you base in on the results of the close inbreeding some breeders do that results in normal healthy working dogs.

 

Outcrossing and inbreeding are specks on the radar when it comes to keeping this breed what we love. That's going to involve maintaining the original purpose - if the government doesn't run all farmers out of business <sigh>

 

I'm too much of a livestock person to fear a breeding method. My greatest enemy is the same as every livestock and dog person before me: the ability to be objective about which animals should be culled.

 

Since you've asked me for clarification - I'll have to ask you: what is the solution here? We've got TNS from ISDS line dogs. Are you ready to start testing? Also, if we can ban close inbreeding, how would this help in this case? Where do you feel the problem occurred here? I'm interested...anyone got the answers?

[Rebecca, Irena Farm]

t least one dog in that 4th generation was a carrier and that line will have produced carriers in the pure working population as well. The line may never have produced a TNS affected pup and may never produce one but they may be unlucky enough to breed a carrier to another carrier one day.

 

I'm not following your point here. If we have carriers but no affecteds, what is your recommended point of action? Identify and cull carriers on purpose? That's never been a suitable course of action that I know of, for any genetic defect. We have a "bigger" problem with CEA but we are not culling carriers - it would be incredibly unwise.

[Janba]

I'm not following your point here. If we have carriers but no affecteds, what is your recommended point of action? Identify and cull carriers on purpose? That's never been a suitable course of action that I know of, for any genetic defect. We have a "bigger" problem with CEA but we are not culling carriers - it would be incredibly unwise.

 

I would be doing what you are doing now but not repeat a mating that has produced a problem nor a similar mating with any close relatives unless you test. I have never been of the opinion that carriers should be ruthlessly culled unless you have a high frequency of a gene and no way of testing for it. I don't know what your rules there are for registering re CEA but I assume they are similar to the ISDS and that does not preclude registration of pups from carriers provided they are mated to a DNA clear dog or bitch. Similar rules could easily be applied to TNS or any disease that can be tested for. What I have been trying to say is that if you have a low frequency of a gene culling a bitch who has produced affected will have no affect on the % of dogs in your population that are carriers.

 

My ISDS dogs mother was a DNA CEA carrier but she was put to a clear dog and he is DNA tested clear. The bitch I almost bought instead was a DNA tested carrier but while she has probably turned out the better worker there were things in her temperament that didn't suit me. He has an obedience titled dog in his lines so maybe I had better castrate him now as he is not a "real working dog".

 

 

ETA Just out of interest have you found that the number of CEA affected dogs is dropping now that the DNA test is available?

[mjk05]

TNS is a disease of inviability. It is incompatible with life. Then there is the *working* Border Collie, who is bred and culled by viability.

Here we go again... "Yes, its possible, but not in real working dogs". (beats head against wall)

 

So- just to clarify, you're saying our dogs aren't *working* border collies?

 

Again everybody wants to blame inbreeding, but the true villian is *lack of culling*. When people spend 6k to find out why a puppy with failure to thrive is not thriving it is because they want to know how to breed that cross, or at least that female, again. My question, my farmer friend's question, every stockman out there's question should be "WHY?"

OK, since that's directed at me- that's rude, unnecessary and frankly rubbish.

 

I spent that amount of money on those pups for 3 reasons-

1) as I've said, they were the first pups I'd had so much to do with and I was really emotionally attached. The male pup, who had all the testing done, was the one I wanted to keep. I was soft and pathetic.

2) We were told a number of times, including by a large teaching vet centre with experience in TNS, that it was just that he'd had a bad start and had an infection (we had Kennel cough go through when they were 10 days old). Each presentation (starting at about 10 weeks, I think) was different. First he had a swollen joint and limp. Next time he had gastro. We had the smaller, runty puppy PTS earlier on. The boy appeared to recover from his first illness. I decided that if the boy got sick again we'd have him PTS too. When that happened, we took him to the large specialist vet centre to be PTS. The vet on duty in the emergency centre told me she thought he just had a chest infection and was an otherwise healthy pup, and I was being callous and uncaring (not quite in those words) to have him PTS. He was admitted to the hospital, where a consultant took over his care, and after lots of expensive investigations told me that he did NOT have TNS, but probably had a bone disease (hypertrophic osteodystrophy) he would grow out of. He recovered, we took him home. He got sick again, and we had him PTS. I think he was 16 weeks old.

3) I strongly suspected something genetic, and no, we did not hope to breed either parent again. But a number of our other dogs are closely related to those pup's sire- my OH's old dog is his full brother, and has been used a number of times at stud. A large proportion of the top trial dogs in my area are close relatives. I thought I was doing the responsible thing trying to get a diagnosis.

 

Both parents of this litter are now sterilised, as are the two surviving littermates (and they were before we even had a diagnosis). The bitch has one other litter of 6, all sterilised. Of course, now there's a DNA test that's not really necessary, but given the absolute horror experience we had, I think we can be forgiven for overreacting.

 

As far as them being from unhealthy stock, both the sire's parents worked on a commercial sheep farm (not like, a couple of hundred sheep) and trialled until their teens- in yard, utility and our 3sheep trials. I think both his parents represented our country or state at national events, and his father's littermates (also working farm dogs) also represented state and country and are still trialling at 13. As Janba said, there are some fairly handy dogs on the dam's side too.

 

ETA: none of them have ever produced any TNS affected pups. Or unhealthy pups of any sort, that I'm aware of. And some of them have been quite heavily inbred, as it happens.

 

My other question is what farmer has 6K to put on a failing *puppy*? I want to farm what they are!

I had the money (at least at the start of the whole hideous episode). Since you need to know all the details, apparenty, my OH is a farmer. I was working fulltime as a doctor, and even though it stretched things and got very difficult in the end, I felt a responsibility to those pups. My OH went along with it because a) he's a bit soft, too, b ) the vets kept telling us the pups would get better, c) I cried for half the day when the pups were sick and he's a typical bloke who just wanted to fix it. Is that enough personal information for you?

 

Now, of course, I'm living off the farm and have a young family, and if that happened again, we would put them to sleep and be done with it.

 

But obviously that is what we should have done, to have any credibility as *working* dog people. Knocked them on the head at birth or when they first got chesty, and then I could stand beside you and proudly proclaim "Yes, its possible, but not in real working dogs".

 

I certainly hope it never crops again in working dogs, but if it does, I'd definitely be advising the unfortunate breeders to shoot, shovel and shut up. Being honest gets you absolutely nowhere.

 

As far as "inviability" goes, I believe that about 30% of the population (in the US and Australia and the UK and I think most of Europe) carry the gene for cystic fibrosis. That, until recently, was a disease of "inviability". Affected people died young, and generally before they could have children. How many people with CF do you know? Even in a relatively non-inbred population (that legislates against close inbreeding), it is possible for an autosomal recessive "disease of inviability" to exist at high rates, and for affected individuals still to be fairly uncommon.

 

Its not unthinkable that TNS could exist in (gasp) *working* border collies at a rate of, say, 1 or 2%, and for you still not to have ever heard of affected pups (especially given its range of presentations and potential for misdiagnosis). And of course we won't have any idea what the rate is- how many *working* dogs have been tested?

 

As I've said ad nauseum, you don't need to care about it, you don't need to test for it. But it has the potential (however small) to be a problem where inbreeding or popular sires are used excessively. Its incorrect to think that breeding for *working* ability is protective. And its morally reprehensible to publicly ridicule and castigate anyone that admits to having had it.

[Eileen Stein]

mjk05, I understand your frustration, but I just want to address one point you made:

 

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).

 

Julie was certainly not saying, "See what religion does." She was saying, "See what inbreeding does." Except for Lenajo, I think all the "working dog people" who posted here were pointing to inbreeding as the problem. But the reason these affected dogs are found more often among the conformation population is that breeders for conformation inbreed (or have inbred) to a very high degree, and in general (at least in this country) working breeders don't. I don't agree with you that you can inbreed for working ability with anything like the effectiveness of inbreeding for physical characteristics like color, coat, ear set, etc. Working characteristics simply cannot be "fixed" the way physical characteristics can. Working traits are much more interactive and fluid/unstable. We very often want something in moderation -- not too much eye and not too little eye, for example -- rather than in the extreme. We want traits in balance -- a lot of eye needs a lot of push to avoid stickiness, for example. And most working breeders are simply mistrustful of high levels of inbreeding. Of course Lenajo is right that when you are crossing members of a registered breed you are necessarily "inbreeding," in a way that you are not if you breed randomly throughout the species. But it's a matter of degree, and in general -- there are certainly some exceptions -- working dog breeders simply don't breed anything like as closely as conformation breeders do.

 

I also don't perceive that what's going on here is that working breeders are bringing the subject of TNS or CL up to bash conformation breeders -- to say, "You have it and we don't." It's far more frequently the KC breeders who bring the subject up and say, "You have your head in the sand. You've got it in your dogs. You should be testing for it. You have irresponsibly produced an unhealthy breed, and we responsible breeders are fixing it." You spoke of working dog people "making all sorts of claims that 'it doesn't exist in working dogs' because they can't find any evidence that it does." That strikes me as an odd charge because, well, why wouldn't your working assumption be that it doesn't exist in working dogs if you can't find any evidence that it does? Isn't it reasonable to base one's conclusions on the existing evidence? I think it was only natural for your vets to discount the possibility that TNS was the issue with your pups, if they had never encountered TNS in the working population. Once they found evidence of it, they wouldn't say that any more, although they might justifiably continue to say it's exceedingly rare. I know of no evidence that TNS exists in working border collies in the US. I wouldn't be surprised if there are carriers of the TNS allele in US working border collies (although it's certainly possible there are none), but I almost never hear of a working border collie litter with fading puppies, so I can't see the actual disease as a problem, and therefore can't see any reason to test dogs for it. And if I'm understanding you correctly, I guess we are in agreement on that point.

[mjk05]

mjk05, I understand your frustration, but I just want to address one point you made:

Julie was certainly not saying, "See what religion does." She was saying, "See what inbreeding does." Except for Lenajo, I think all the "working dog people" who posted here were pointing to inbreeding as the problem.

Yes, you're right, she was saying that.

But other people in this (and previous) discussions on this topic have spent a lot of time trying to find a "non-working" dog in carrier pedigrees- eg the L'Bleu discussion. I get very frustrated when discussions on TNS are based around trying to prove no working dogs are affected, or that Australian working dogs are just the same gene pool as the ShowBC (they aren't) or whatever. Why not just say, "we have a bigger gene pool, we don't inbreed much, so the odd carrier dog isn't a problem, and let's keep it that way".

 

And the other thing that Julie implied, and that other people (like Katelynn) have referred to, is that somehow breeding for "working ability" as opposed to conformation or sports ability is protective against these diseases. It isn't. If the gene exists in a population (no matter how rarely) and you breed two carriers, you can get affected pups. That might be because of inbreeding, or it might just be very unlucky chance. If you inbreed for working ability, you increase your risk of producing pups with recessive conditions like TNS, and increasing the gene's frequency in the population. If sports breeders outcross as much as working breeders do, they won't have any more problem with TNS than working breeders do.

 

Our two carriers were relatively unrelated. The dam's parents were brought here from 4000 km away. The sire was from very inbred local lines that have never produced TNS (that anyone knows of). His father had earlier been used over his own mother- big, healthy litter, some of which are still working and trialling at 11yo. And even in those inbred lines, in which quite a few dogs have now been tested, the rate of TNS carriers isn't that high. We didn't get TNS in this litter because we were inbreeding (we thought we were outcrossing, actually), we didn't get TNS because we were breeding for conformation or agility or anything other than working farm and trial dogs- we were just unlucky.

 

Probably there is a higher rate of TNS in Australian working dogs, because of relative inbreeding. But that doesn't mean it can't exist in a less inbred population, and that people can't get unlucky there too.

 

Because TNS affects very young pups, and because it is autosomal recessive, it isn't something like CL or epilepsy or hip dysplasia that is likely to be weeded out by selecting for good working dogs. When we look at the top UK trial dogs generations back in pedigrees, do we know how many pups there were in their litter and if any were runts that didn't make it? Or, more to the point, if their littermates that didn't make top trial dogs ever had one litter where one pup got gastro and died at 4 weeks?

 

Its not a common gene (although we have no idea how uncommon), so as an actual disease it must be downright rare. Even over here. Given that UK pedigree it, probably does exist in ISDS dogs. Rarely.

 

I don't agree with you that you can inbreed for working ability with anything like the effectiveness of inbreeding for physical characteristics like color, coat, ear set, etc.

You're probably right. I wasn't really saying that you can inbreed for working ability. I was just saying that people do. I'm new to working dogs, and even newer to breeding dogs. I don't know whether inbreeding is an effective technique or not. But people here and elsewhere do it, aiming to produce working ability. Probably more so in my area, which has some breeders who have had a lot of success with inbreeding working dogs, but as per Lenajo, there are some working breeders elsewhere who have used inbreeding to produce working dogs. There is an interesting chapter on inbreeding for setting working traits in Tully Williams' book. Definitely worth a read- even if I know a lot of people here disagree with him.

 

I also don't perceive that what's going on here is that working breeders are bringing the subject of TNS or CL up to bash conformation breeders -- to say, "You have it and we don't." It's far more frequently the KC breeders who bring the subject up and say, "You have your head in the sand. You've got it in your dogs. .... I know of no evidence that TNS exists in working border collies in the US. I wouldn't be surprised if there are carriers of the TNS allele in US working border collies (although it's certainly possible there are none), but I almost never hear of a working border collie litter with fading puppies, so I can't see the actual disease as a problem, and therefore can't see any reason to test dogs for it. And if I'm understanding you correctly, I guess we are in agreement on that point.

Yes, we are in agreement. Totally. I'm mostly in agreement with the majority of other people in this discussion, too.

 

I'm seriously regretting mentioning our litter, frankly- and I think I regret even testing our dogs now. Ignorance was bliss and I was a lot richer. We would probably never have bred those dogs again, and would never have had a problem. All the other dogs we've had tested are non-carriers. I brought it up because I thought it was interesting, that it had relevance to the assumption that "breeding for work" was a factor in the low rates (or "nonexistance") in working dogs, and also just to point out that TNS isn't always obvious clinically, even to specialist vets with experience with the disease in ShowBCs. It isn't about entire litters of "ferret-like", fluffy sickly pups- it might be one pup in 100 litters from carrier-line dogs that dies of ?gastro or a chest infection or who-knows-what as a tiny baby. It isn't a problem for working dogs by any means, and I hope it stays that way.

[Katelynn & Gang]

And the other thing that Julie implied, and that other people (like Katelynn) have referred to, is that somehow breeding for "working ability" as opposed to conformation or sports ability is protective against these diseases.

 

Whoooa. Excuse me! I must have missed my reply where I even so much as implied that breeding for working ability as opposed to conformation or anything else protects the working gene pool from diseases like CL or TNS.

 

I simply looked at the pedigrees of two dogs and stated "well theses lines here are the same lines there." Big deal, its obvious to anyone who has a clue to what a pedigree is used for that CL and TNS affected and carriers pretty much all come from or have at least one or two lines in common.

 

Do I believe that breeding for working ability rather then breeding for other things is safer? You are damn right I do. I don't think its a sure thing, as nothing in life it is BUT so far, its proven the safest route in breeding healthy sound dogs.

 

Katelynn

[mjk05]

Do I believe that breeding for working agility rather then breeding for other things is safer?

Freudian slip, there, hey?

You are damn right I do. I don't think its a sure thing, as nothing in life it is BUT so far, its proven the safest route in breeding healthy sound dogs.

Regardless of the level of inbreeding?

 

Katelynn, yes, that's correct. Selecting dogs on working ability (and the working ability of their offspring) is the best way of selecting the healthiest dogs- and that is definitely helpful in reducing rates of diseases like hip dysplasia, and probably epilepsy and symptomatic genetic eye diseases. It isn't really helpful in reducing rates of TNS, where the only evidence a dog is a carrier may be that one of it's mother's cousins once had one pup that died in the whelping box.

 

ETA: I do take Eileen and Julie's point that in practice, breeders of working dogs are much less likely to use extreme inbreeding than conformation breeders. But that's not always a given, and the popular sire effect has been an issue in working bred dogs. I stand by my point that its not "breeding for work" that protects the working dog against TNS, its outcrossing and large gene pool.

[Katelynn & Gang]

I'd be interested in seeing the pedigree of the litter you had which was TNS affected. What was the degree of inbreeding? And were any of the lines related to the lines of the other TNS producers, carriers and affected like this other dog who you've posted about?

 

I do find it interesting that it seems there are common denominators in all the pedigrees.

 

I stand by my point that its not "breeding for work" that protects the working dog against TNS, its outcrossing and large gene pool.

 

It is the breeding for work that gives us such a large gene pool in which to outcross, in return minimizing the chances of things such as TNS to show up.

 

 

Katelynn

[mjk05]

I'd be interested in seeing the pedigree of the litter you had which was TNS affected. What was the degree of inbreeding? And were any of the lines related to the lines of the other TNS producers, carriers and affected like this other dog who you've posted about?

 

I do find it interesting that it seems there are common denominators in all the pedigrees.

It is the breeding for work that gives us such a large gene pool in which to outcross, in return minimizing the chances of things such as TNS to show up.

Katelynn

 

And heeere we go again...

Why, Katelynn?

You won't know any of the dogs. You won't find them on Anadune or the other databases. You won't find any ShowBCs or obedience titled dogs in there. You eventually will go back (if you have access to the written state WSDA studbooks, which you don't) to some ISDS dogs, some unregistered farm dogs (just like many ISDS pedigrees, because our WSDAs are open registries), and some dogs that were imported from the UK before the ISDS even existed. No, none of them have any common relatives with the ShowBC affected lines in recent years- that I can find anyway.

 

There are probably common denominators in the pedigrees, way way back. Just like there are common denominators in most ISDS or ABCA pedigrees, if you go back far enough.

 

I've told you that the sire is super-inbred. He has relatives who are even more inbred- and don't carry TNS.

 

No, breeding for work does not = outcrossing. Ask Lenajo. They might tend to go together, but one is not synonymous with the other. Our dogs are bred for work. My dogs (and their parents and grandparents and so on) have probably worked more sheep than yours will see in their lifetime. Feel free to argue that point, but my dogs are working bred. Inbred, in many cases, but working bred.

 

What the heck is the point of this? So you can "prove" that, ah ha, there is an unregistered dog behind these dogs. It must be a well-bred black Field Spaniel! (rolls eyes).

 

Oh, you know what, the sire's pedigree goes back to an ISDS dog called Glen II 48637, who you should be able to find some background on, because he won some stuff- you might find he has a common ancestor with that Henniker dog. I'm sure that will prove something useful.

 

Yep, you've certainly got a great grasp of the issues here. Nothing more to say, really.

 

Because you'll get so much joy from it, the sire's pedigree is the same as the one here:. I haven't got the bitch's pedigree up on the net, and the pedigree software is on the other computer. I might post it later, but I suspect I will have given up hope long before that. The only common ancestor is Dodge's Gem, who is the bitch's grandmother.

 

Off to help unbog tractor from field...

[Katelynn & Gang]

No, breeding for work does not = outcrossing.

 

No it does not and nor did I imply any such thing.

 

I did imply that because of breeding for working ability only, that we have secured a large enough gene pool to keep our breed alive and healthy if we so choose to do so. No one needs to exercise their right to use that large gene pool but for those who choose to do so, the tools are there.

 

What the heck is the point of this?

 

The point is I am curious as to what the pedigree looks like, just as I am sure others here are too. Just as we all were of Spyro's pedigree who you so willing posted. I by far wasn't bashing the dog nor his breeding, as he has a very nice pedigree if you really look into it (as Eileen, I did not recognize most of the dogs in the first four generations). I was just clearly making a point of a connection I saw between his pedigree and other TNS producing pedigrees.

 

Seems all the TNS dogs are somehow related by lines which were/are used for breeding in things other then working ability rather they are ISDS registered or not. There are people who believe those lines are working bred because they have a registry behind their names which promotes breeding for working ability but as we all know to well here in American, letters don't mean a thing.

 

I guess if I had produced a litter of working bred dogs affected with TNS, I'd also take things personally when people claim that it doesn't exist in such lines. Which I am sorry you feel that way but as of now, there is no real proof that TNS affects the bloodlines of working bred Border Collies in North America. So you cannot really expect any of us to run out and test all our breeding stock or even say that it exists. The very best you'll probably get is that there is a possibility that it could be in our lines but with the hundreds of dogs being bred here, I think we've had had at least one person open enough to come forward and say so.

 

Katelynn

[mjk05]

Well, Katelynn, your relentless quest to prove any TNS-carrier isn't really working-bred says otherwise.

 

because of breeding for working ability only, that we have secured a large enough gene pool to keep our breed alive and healthy if we so choose to do so.

"We"?!

The reason "we" have such a large gene pool to choose from is because there used to be a lot of working dogs needed for work on farms. That's still the case in Australia and NZ. We don't have anywhere near the number of registered dogs, but I'd imagine that we probably have more actual working-for-a-living-on-commercial-farms-dogs than the US does. The gene pool is big in large part because it started big. It's probably stayed big because of how great collies are as sheepdogs (so they've spread across the world), because they are such versatile dogs so different lines have been supported and continued for different jobs, because of the exporting and importing of dogs from different lines, because of the rise of hobbyists to match the decline in actual working farms and perhaps because, as Eileen said, modern sheepdog breeders avoid inbreeding for either cultural or scientific reasons.

 

Some factors in modern day sheepdogs have probably acted to reduce the gene pool (the popular sire effect can be more broad-reaching with modern transport and technology) and others have acted to increase it- exporting and importing of dogs, travelling greater distances to trials etc.

 

Back at the origin of the breed, there were probably quite high levels of inbreeding in places. That is how the "breed" was established. Farmers and shepherds probably wouldn't have travelled so far, they would have just bred to the best dogs that were readily available. Unlike some of us, a shepherd in the 1800s wouldn't have sat down and looked up pedigrees to the 10th generation on Anadune- they would have just picked the best dog, and if that was his neighbour's dog, with the same grandfather as his bitch, he would have used it.

 

Just as we all were of Spyro's pedigree who you so willing posted.

I didn't post it.

 

Seems all the TNS dogs are somehow related by lines which were/are used for breeding in things other then working ability rather they are ISDS registered or not.

So- what exactly is the link between my dogs and dogs used "for thing other than working ability"? Can you identify it?

Because, if we can't prove it, it's probably unlikely. Or at least miniscule. Isn't that the way things work?

 

there is no real proof that TNS affects the bloodlines of working bred Border Collies in North America.

Eileen, Julie- when I referred to the fact that the TNS discussion always seems to be about proving that "our dogs don't have it", this is the sort of thing I meant. First it was "it doesn't exist in working dogs" or it was "it doesn't exist in dogs without any Australian-NZ ancestry". Then it was "it doesn't exist in working bred dogs in North America".

 

"It doesn't exist" is so pointless. You can only keep saying until it does appear, and then you have to either try to hide it, or disassociate yourself from it.

 

It probably does exist, its just so rare you don't have to worry about it. Thank God for big gene pools and outcrossing. Although frankly, if I had to choose between TNS and say, epilepsy in my gene pool, I'd pick TNS every bloody time. We have a gene test, we have a known mode of inheritance, and it only tops puppies in infancy, so I'm not risking losing my good trained dog.

 

So you cannot really expect any of us to run out and test all our breeding stock or even say that it exists.

Where did I suggest that anyone did that? I presume you've read the rest of the thread, Katelynn, so you'll have seen multiple comments from me that you don't need to worry about it, you don't need to test for it.

 

The very best you'll probably get is that there is a possibility that it could be in our lines but with the hundreds of dogs being bred here, I think we've had had at least one person open enough to come forward and say so.

What, so they can get the 3rd degree from you, the way I have? So you can spend a couple of hours on the databases and come up with a station-bred dog in the 10th generation, or, heaven forbid, an obedience titled dog somewhere there, and "prove" that their dogs aren't really "working bred"?

 

And how many people on this board are actually breeders? How many of the farmers in the UK and the US and anywhere else who breed working dogs spend time on this board? It is hardly a wide and thorough sample.