Margaret M Wheeler

Oh I can understand the reason for describing the test as one that identified carriers. I'll be the first one to agree that getting this test "out there" was a lot of complicated work and I think that in such situations things aren't going to workout 100% the way we would like them to. Optigen gave me their breeding recommendations in a private communication. I would advise that you to check with them if you have any doubts about my reliability. I thought you would have done that already. I don't mean that I would have but knowing you to be thorough and detail oriented I would expect you to know.

I didn't realize that the Optigen test was such a powerful diagnostic tool. The test was often presented as being a test "for carriers," and I was careless in the fact that I accepted this simplistic description as the complete diagnostic scope of the test. I assumed that the test was of a positive/negative nature. So it would be Yes the gene for CEA is present or No the gene is not present. I looked at the website again when my test results arrived and read the Optigen's own description of the test carefully for the first time. Only then did I understand that Optigen believes that it can accurately identify all three genotypes. I think it's important to note that one needs to understand this test, not just the phenomonon of go normal to come to the conclusion that the test accurately finds and measures not just the presence of absence of genetic information, but that it also gives information on the degree to which the gene is present. Also I think it should be noted that as it stands now, Optigen's recommendation is that mildly affected dogs(dogs that are genootype affected, but phenotype normal) "be bred only to normal(genotype normal and phenotype normal)." I am told by members of the ABCA's health and genetics committe that this recommendation is one that is given to rough collie breeders who have an extremely high incidence of CEA in their breed. The ABCA recommends that the relatively low incidence of CEA in the border collie makes it important to avoid producing more carriers by breeding mildly affected to normals.

As many of my fellow parents know, entire school systems are currently disallowing certain "food" substances like peanuts. Our town in NH (a state notorious for the failings of its public education system) has found within itself the resources to entirely ban peanuts from its elementary school even though it won't identify my son's moderate learning disability because it "can't justify the cost". The reason for the peanut ban? One little girl with an allergic response to peanuts. While most of the children in the school are not allergic to peanuts and some of the children in the school are mildly allergic to peanuts, this particular child according to her doctors, will certainly go into anaphillactic (sp?) shock if she comes in contact with the tiniest amount of peanut in any of its myriad forms. My point is that just as humans vary greatly between individuals with regard to allergies and immune responses, dogs' allergic/immune responses are probably to some extent species specific, but more importantly with regard to subsatances like onions the allergic/immune response varies greatly between individuals. So, it seems likely to me that one Jack Russell might die from an allergic response to a small amount of onions whereas another might scarf down a whole Vidalia with no negative effects. It might be of interest to folks that I knew a woman who had a terrier that demonstrated onion poisoning (as expressed by an attack of severe hemolytic anemia). Somehow the dog survived after thousands of dollars were spent on his veterinary care. It was generally made known that he had onion poisoning. Several years later, a young stud dog to whom I had bred two of my brood bitches died of hemolytic anemia. His owner made use of the most advanced medical techniques to save him but after the dog had for all intents and purposes "died" twice and been resucitated, the owner let him go after a third crash. This dog was a close relative of the dog who had survived "onion poisoning." Now, I don't necassarily discount onions as a contributing factor in hemolytic anemia, but I do believe that hemolytic anemia is very likely a medical cataclysm that is probably a result of an existing predisposition in individual lines of dogs. Vaccinations, tick born substances and microbes, parasite control agents and yes even onions seem to coalesce in the recent health history of dogs that have severe attacks of hemolytic anemia. I think the same is probably true of severe allergic responses to all sorts of substances.

Great News!!! Thanks!

Good Job Melanie! Solo is a very lucky dog to have a skilled and loving owner like you. Congratulations Solo! Thanks for providing Melanie with one of the only real challenge she has ever faced.* *Phd notwithstanding

I think it sounds like a lot of fun! Maybe you could have a premium jar for $10 with past winners and past national champions in there and have a regular $5 jar for the slightly less illustrious. Or would that cause hurt feelings?

Wow that run sounds very familiar! I'm still too full of stagefright to clearly remember the details like you, but: Nell did a good outrun to the left and did not get sucked in by a marshy dip on the way that brought some of the other youngsters in a bit tight. She lifted them well but then rushed at them a bit and was slow to take a lie down early on the fetch. I was able to keep her on the pressure for most of the fetch but I still got her too far up on the flank and they started to split as they neared the post. I got them round the post in a very ugly fashion (still happy to have kept them from bolting to the exhaust though). Andrea will not be surprised to hear that I did a repeat of my Canadian performance by making the panel in a decent fashion then popping them back through like an idiot. I didn't get my pen either. Honestly I have an unhappy memory of the sheep strung out against the fence behind the post but I can't remember if that was after the fetch or the drive. Lucky for me, we weren't the only team to annoy Bill's and Chris's nice sheep past the point where they would willingly pen, so we barely squeaked in for a prize.

So Mark, Tell me about your run! Nell and I went into PN last weekend and she got a purty orange ribbon in spite of my best efforts to ruin the run entirely! Marg

Hey gals, Welcome home Sam! Thanks for replying. Just got home from my lesson with Carol and now on the run to kids' soccer practices. I have a couple of questions that will have to wait til tonight or they won't make any sense. Course there's no guarantee that I'll make sense later but I'll have more time to try.

Sheepdog-L has an open membership, meaning you don't need approval from the moderator to join, but I don't know if you can read there without a membership. I'll send you an email with the post in it. http://groups.yahoo.com/group/Sheepdog-L/

I've been oblivious! I pulled about 6 off my poor pups head and neck tonight after a couple of walks in the woods. Cool weather and some rain brought the lil bassages back en masse.

Hi Caroline, Thanks for replying. Is your friend aware of the post on Sheepdog-L regarding this issue?

J and T*, Thanks! *Hey Terry, I always nap before crafts. This week it's an early start on Christmas coasters, (the unusable yarn weaving plastic canvas kind). For those I had to nap before AND after.

I?m interested in deafness, in part because I trained as a teacher of the deaf and in part because of the occurrence of deafness in Jack Russell terriers, a breed that I have had some experience with. Because deafness is such an important issue with regard to stockdog work, I wanted to share my thoughts and raise a couple of questions that seem important to me. Also, at the end of my post I have linked to Dr. George Strain's website, a site that seems to be an excellent resource on deafness in dogs. Scamper, my 12 year old Jack Russell terrier, BAER tested normal at around two years of age, but she has become almost completely deaf in the last couple of years. It?s important to note that she might not be deaf due to a sensorineural hearing loss. A BAER test could help me know the cause of her hearing loss because the test bypasses the structures of the ear canal and the middle ear and tests the ability of the inner ear to detect(for lack of a better word) sound. So, if I BAER tested Scamper tomorrow, and she BAER tested normal, I would have good reason to believe that her deafness was a result of some problem that did not involve the inner ear. It might be that, for one reason or another she has a fairly common form of mechanical hearing loss i.e. the tiny bones in her middle ear are no longer vibrating as they should in response to sound and so are not transmitting those vibrations to the inner ear via the eardrum. I think it is safe to say that most deafness found in newborn puppies is a direct consequence of an inherited defect for sensorineural hearing loss. On the other hand, it is much more difficult to be certain of the causes of age-related deafness (presbycusis), even deafness that is known to sensorineural. Disease, trauma, dangerous noise levels, toxic substances can all contribute to sensorineural hearing loss in an adult dog. Certainly, the structures of the inner ear often become less and less functional with age (at least in dogs and humans), and it has been established that general physical aging has a genetic component. Still I believe that some degree of sensorineural hearing loss in older dogs should not be considered to be pathological. So for me some of the important and interesting questions with regard to hearing loss and the selection of breeding animals for stockdog work are: With what frequency do we see adult onset deafness in border collies? At what age do we consider adult hearing loss to be a defect in the dog? What degree of hearing loss would we deem ?pathological? in adult dogs? Below, I have pasted a paragraph from an article that Dr. George Strain. This article is just one of many useful resources offered on Dr. Strain's website. http://www.lsu.edu/deafness/deaf.htm ...sensorineural deafness can be primary or secondary. Primary deafness results from destruction of hair cells in the cochlea without antecedent events. This occurs in hereditary deafness in Doberman pinchers, some forms of ototoxicity, and presbycusis. Secondary deafness occurs when hair cells die as a consequence of other damage in the cochlea, most commonly to the stria vascularis. This occurs in pigment-associated hereditary deafness and some forms of ototoxicity. Degeneration of the stria vascularis eliminates the high K+ levels in the fluids surrounding the hair cells, resulting in death of the hair cells and deafness. In pigment-associated hereditary deafness, the strial degeneration and hair cell death usually occur 2-4 weeks after birth. George M. Strain, Hereditary Deafness in Dogs and Cats: Causes, Prevalence, and Current Research. Tufts' Canine & Feline Breeding and Genetics Conference, October 2-4, 2003,Sturbridge, MA

I can't seem to find anything that tells me who the judges were. I know it's probably hiding in plain sight, but could somebody point at it for me or even better, tell me who judged the open finals? I know the nursery judges, but for some reason I have it in my head that nursery and open have different judges... I figure since I've already asked one really dopey question about the nursery scores that I might as well ask another one about open.