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mjk05

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About mjk05

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    Western Australia
  1. We use our pet lambs as training sheep. We have about 20 of them now, yearlings up to 12 year olds- most of the ewes are out with mobs having lambs, and just come back to the house paddock later in the year, and the wethers hang out with our training sheep (cripples and random leftovers). So we have 30-50 sheep in the training paddock, and up to half of them can be ex-pets. Pet lambs go out with that mob as soon as they are off milk/milk replacement pellets, and we work them around with experienced dogs until they learn to stick with the other sheep. They make reasonable training sheep for young dogs- the only issue is their tendency to lean on legs, and lack of brakes when being pushed too hard.
  2. mjk05

    TNS

    Yes, we've had a few TNS carriers (have 3 at the moment aged between 12 and 5, and my parents' 10yo ex-working pet dog is a TNS carrier too), and no, none of them have ever had reactions to vaccinations or intermittent fevers or any issues with blood results. We don't do rabies vaccination, so I don't know about that, but our TNS-affected puppies did have minor vaccine reactions (localised swelling, mild malaise) to usual puppy vax. None of the carriers have shown any abnormalities.
  3. Orivet do an individual test for AU$75 but a full breed panel including CL, IGS for $150 (AU, so US$107). Compare that to CEA, which has a similar incidence of severe disease- AU$200 for a single test. Even in the past, TNS done individually by UniNSW was AU$55, and our small working sheepdog community negotiated a discounted price for group testing. I imagine a group like the ABCA would have significantly more bargaining power than 30 rural West Australian sheepdog triallers. Once many local breeders identified the majority of dogs that are clear, they rarely test unless using untested dogs. I don't think I see TNS where it isn't- I am open to the possibility that it's presenting without being identified. I still haven't seen any affected pups other than ours (although I have heard of them, in other working litters). Those pedigrees have well known working dogs on both sides, and it came from somewhere. The pedigrees don't have one easily identifiable common line. We don't know where it came from. So without testing, we don't know where it is going. If I were expending significant time and effort in breeding a litter, I would want to take the relatively simple step of DNA testing to make sure I knew where I stood on these easily avoidable diseases.
  4. Of course I assume you mean "a working dog... Or a working bred litter that was affected in the U.S." TNS is almost certainly underdiagnosed and poorly understood. The Israeli article I linked to earlier was very interesting for its mention of HOD as a concurrent diagnosis- that's what our later presenting TNS pup was provisionally diagnosed with (by a specialist vet centre with past experience with TNS). Osteomyelitis, gastroenteritis, respiratory tract infections, fading puppy syndrome- all potentially TNS-related. If they're fatal before extensive investigations are conducted, TNS could easily be missed.
  5. Some of the more successful and popular working border collies of recent years. Dogs that (rightfully) have a lot of first degree relatives being produced and producing around the working border collie world. Those don't have to be mutually exclusive, though, do they? We can breed with concern for maintaining genetic diversity AND perform cheap and simple genetic tests for known diseases.
  6. Yes, we're aware of EOD and keep it in mind when looking at dogs. If there was a simple cheap genetic test for EOD, then yes, absolutely we would test for it. Yes, we have tested for IGS since a cheap, simple test (like that for TNS) became available. Why wouldn't we? I have never met or heard of a local dog with IGS (or confirmed CEA in our state either, FWTW) but if the test is easily performed and affordable, it seems like a total no-brainer. If a test (such as gonioscopy or screening echo or BAER) was very expensive and logistically difficult (given we are a fair distance from the only city in our state with such facilities) AND the likely yield was not really high (ie those tests for conditions where mode/degree of inheritance is murky) then we would think hard and possibly elect not to do them. But a test like IGS or TNS these days? Of course. Because then (if I had the opportunity) I could confidently use a top dog like Llangwm Cap or one of those listed above (the Dewi Tweed offspring or Nij Vyas' young dog) to outcross to one of our dogs (lovely low COI!) and know that the pups would absolutely not be TNS affected. Wouldn't you?
  7. Did you look at those pedigrees linked to above, Mark?
  8. So that's fairly significant for an inevitably fatal disease, no? Much higher than rates of cystic fibrosis in the Caucasian population. If we compare to CEA, the Optigen website lists the rates (from eye testing in the 90s, presumably even lower that) of the severe manifestations of CEA/CH as 0.57% for coloboma, and 0.06% for retinal detachment. So similar to or lower than the quoted incidence of TNS (if we believe that). Obviously for breeders, CEA is more of a threat because it isn't fatal and genetically affected dogs can breed, significantly raising the allele frequency in the population beyond what is possible with TNS. But from a puppy buyers POV, there may be as much risk (or more) of getting a pup that dies of TNS as one that goes blind from CEA, if parents are untested. That's why it really surprises me that it isn't more publicised for working dog breeders. It isn't even mentioned on the ABCA website page on inherited disease. And so easily tested for! Check out the pedigrees listed above- various prominent, top working lines (honestly, look at them!), not heavily inbred. With international AI breeding so popular now, and top sires producing pups all over the world, the potential for TNS to crop up without awareness and testing must be increasing. Why is this still considered not really worth testing for? As far as the original question, re the word "widespread", I think its intended meaning was "spread across the population"- not necessarily common, but present in border collies around the world.
  9. Massive apologies for my massive overuse of the word "massive" in that last post. For those who are interested in the sorts of dogs that might have carriers in their lines (I know previously there's been some pedigree analysis to try to identify common ancestors), here's another pedigree of a really well bred dog tested as a carrier. And please do check out the pedigrees I linked above. I'm just so glad we have a simple, relatively cheap test that can prevent affected puppies being produced when such quality dogs are used extensively (as they should be).
  10. So, just to check because it's not my area, an allele frequency of 0.06 (which is what Wilton and Shearman reported in that study) would give a carrier frequency of about 12%, which is about what they've been quoted in other articles (Mason, Jepson, Maltman 2013). And a carrier frequency of 12% would be about 1 in 8.5 dogs? (edited to remove my erroneous comment about CEA- which apparently has an affected/incidence rate of 2.5%, so a carrier frequency of about 25%, but of course is not fatal, and many genetically affected dogs will have normal vision) Oh, I totally agree with you. They did try to reduce sample bias by eliminating dogs from known carrier parents, but I still really wonder where they got their samples. We did send in samples in 2006 (from dogs related to our TNS pups), and later on our sheepdog organisation did collections for (paid) testing at trials, and most people agreed to use of those samples for research, but I don't know if they were used for this study. And there were a significant number of dog owners who elected not to test, so it was somewhat skewed towards those with lines related to our affected pups. But I'm pretty sure there was no widespread sampling of Australian working dogs outside our isolated state. And anecdotally, I find it hard to believe that there is a TNS affected rate of 1 in 250, which I believe is what you'd expect from the allele frequency you've quoted above (correct me if I'm wrong, not my area). It is obviously poorly understood even now, and almost certainly frequently missed (interesting case from Israel Journal of Vet Medicine here, Gans 2015, where HOD was also diagnosed- that was the working diagnosis for one of our TNS pups also- "TNS is a relatively newly recognized disease entity, which has been identified in Britain and Australia since the 1990’s but relatively little has been published about it and its existence is not widely known in the practicing veterinary community. "). But 1 in 250 AFFECTED? Unless there is massively unrecognised in utero loss as a TNS presentation, I think that's got to be a massive overestimate. But it is almost certainly more common than anyone believed 10 years ago (when I was happily telling people it was a show dog disease, not found in working lines), or even 5 years ago. And when at least a couple of the ISDS International Supreme Champions in the past decade are either tested carriers, likely carriers or close relatives of carriers, I'm surprised that there isn't more widespread testing (or at least publicity about testing) in working dog circles. I'm massively saddened to still be hearing, just in this past year, of puppies bred by conscientious working dog breeders, taken home by experienced dog owners, no issues recognised, and later dying of TNS. It just shouldn't be happening with the available test. But, probably because of the lack of knowledge of the disease or the test among working dog breeders and their vets, and possibly because of that stigma and the persisting belief that this is mostly a disease of show dogs, it will keep happening.
  11. Which population studies are those, Mark? It doesn't seem that there is widespread testing yet, although obviously increasing. I definitely agree care needs to be taken, especially when carriers feature among such prominent dogs as recent IntSup Chs (which deserve to have a significant influence on the gene pool). Now the test is so cheap and easy and DNA testing for other conditions (like CEA) is being done by so many breeders worldwide, it seems irrelevant how widespread or not it is, why wouldn't we test?
  12. It's not really known how widespread it is, but in every population where testing is performed, it seems to be more common than predicted, and it certainly isn't limited just to show dogs. Testing is much cheaper now than it used to be, and I'd definitely be testing from any dogs I thought might be bred from. Getting either a clear or carrier result allows breeding without worrying about producing affected pups. There are some absolutely top shelf working lines with known carriers (Nat. and Int. Sup. Ch.s), so having information about your own lines can be really useful. Of course, there is still the stigma hanging over from past years (TNS = show dogs/poor breeding), and some breeders believe they'd definitely have noticed such a disease in their lines, so there's still reluctance to test or to even consider the issue, and that does make me sad. I heard recently about someone who bought a working-bred pup from a pretty experienced breeder with top dogs and a good reputation on the other side of the country (Australia) and lost it to TNS at about 4 months of age. Apparently it was a very healthy happy looking pup at the time of sale. A couple of interesting pedigrees to check out: Llangwm Cap, doesn't really need any introduction- advertised semen on the Come-Bye website, TNS carrier Dot, a Czech dog, all ISDS lines, TNS carrier- info here Jimmy- info here, TNS carrier Blaze and Bess - half siblings to Dot and to Jimmy's dam As testing is now cheaper and easier and becomes more common in working lines, I'm sure we'll have more information about its prevalence.
  13. This is a hard one to prove. There's undoubtedly been dingo-dog crossbreeding in the background of the kelpie, but I'm not convinced it fully explains ee red in our working dogs. Anecdotally, I do know of at least one dog with apparently all UK breeding that was ee red (owned by a local obedience/agility judge before she moved to Australia), but when you look back at the kelpie history records, some of these early dogs recently bred from imported working dogs looked like dingoes- it's often assumed that these "red" pups were brown/chocolate, but it seems far more logical that these were ee red. From the WKC website: The following description by Mr Phil Mylecharane gives an idea of what Brutus and Jenny looked like and their working ability. 'In 1870 I went out to Mr Allen, of Geraldra Station, to buy flock rams for Goldsborough Mort and Company. When I got there Mr Allen told me the rams were out in the paddock, but he would soon get them in for me. So saying he opened the yard gate, whistled up two smooth, prick-eared black and tan dogs, a male and a female, and sent them out into the paddock. In a very short time they were back with the rams, and put them into the yard. I never saw dogs work sheep like these two did, and noticing that the bitch had pups, made up my mind that I must have one. So after I bought the rams (I took a big lot of them) I asked Mr Allen where he got those dogs. His answer was that they had just imported them from Scotland from a wonderful working strain there; the dog's name was Brutus and the slut Jenny. I asked for a pup. He told me there was only one left, and he thought I wouldn't like its colour. We went around to see the pups, and he pointed mine out, a little red-coloured one, exactly like a dingo; the rest were black and tan. I thought that it was a dingo. Mr Allen assured me that this was impossible, as the pups were sired on board, and every care taken. He advised me to take the pup, and he would write home to the breeders and see about it. I took his advice and the pup. The latter turned out a splendid worker. After having him for two years he was stolen from me down at Coolagong, near Forbes. The next time I saw Mr Allen he told me that the breeders of Brutus and Jenny had written back to say that in nearly every litter they got a similar pup to mine and that they were great workers’. I don't think we'll ever know for sure.
  14. I think it must depend on the dogs. I was expecting all sorts of problems with my dogs and my kids, and haven't had any yet (touch wood!)- kids are now 5yo and 2yo, so babyhoods are almost over. None of our house dogs seem to have an issue with babies or our small kids, and in fact they mostly seem to really like them. The dog I was most worried about (a bit neurotic, not a fan of strange people, obsessed with me, slept on the bed) seemed to instantly recognise our children (especially the eldest) as part of me, and he'll follow them around like a nanny, lying down next to them if they stop to do something. The biggest issue we currently have with the kids and dogs is the dogs that are too enthusiastic with greetings or play, and knock small kids over, and one bitch who guards the kids against our other dogs. I haven't cracked down on this much because it's fairly subtle (body blocking etc) and has actually been handy to stop boisterous pups jumping into the pram etc, but in retrospect I think this was a mistake and I should have stopped it earlier. We have had our most recent puppy chasing and nipping at the kids when they run, but the kids seem to have largely dealt with this themselves and now she's 6 months she seems to have grown out of it. The other problem we've had has been with old dogs being hurt by the kids, and my eldest dog (a badly arthritic cattle dog) was wary of the baby when he started toddling. In my own experience, for what that's worth, some border collies are good with kids, some aren't. I'm sorry your dog hasn't taken to family life as you'd hoped, but kids grow quickly, and hopefully as you said, once they're old enough to engage with the dog in his favourite activities, they'll become good friends.
  15. The same with us (in Australia), Julie. We sell most of our lambs as soon as possible after weaning, mostly straight to abattoir. Less time here = less input costs like drenching, shearing, and more available pasture for the ewes, and available paddocks for cropping. Possibly if we had year-round pasture available we might keep them longer, but there would still be input for worm control/shearing etc, and really there's not much increase in value keeping them longer- they're pretty well-grown at weaning, definitely not 'baby' lambs. I guess that's about breed/trait selection for your farming system too- over here, if you need to keep lambs for much longer to get decent weights, you probably should be looking for another breed.
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