A mini-course In Applied Genetics, the value of Health Tests and the genetic effects in the Miniature Bull Terrier.
A Mini-Course In Applied Genetics
Barbara J. Andrews, Publisher TheDogPlace.org
This applies to all breeds as do the fallacies of many health tests. By request, I have thus spent a day digging in old files to find something that most Mini-Bull breeders ignored and the realization of which drove us and other breeders out of the breed or at the least, out of breeding MBT. Don't let it happen in your breed!
MBT Breeders are no closer to getting a handle on health problems than they were twelve years ago. When I went to England and selected four dogs that we hoped would nick with the best lines here, I didn’t know that along with an exciting acceleration of breed type, health problems had also proliferated.
How can that be? Ok Ok, there are breeders that do seem to ignore a problem as long as its in someone else’s lap. Even so, we cannot blame all of the health problems on uncaring puppy producers.
If good breeders are conscientiously trying to solve genetic health problems, how can the health defects have reached such seemingly gigantic proportions? The equation is out of balance and that, in and of itself, may be a tip-off that we’re either not taking the right approach or the stats are misleading. If statistics have been incorrectly interpreted or inflated, then those numbers need to be corrected before any more people drop out of the breed rather than risk having their hearts broken. If the statistics are accurate, then our approach to solving the problem is faulty. Why is the MBT so disproportionately affected by three serious health problems? It isn’t like we have thousands of pups whelped yearly by hundreds of big producers as is the case in healthier breeds. Most Mini-Bull fanciers are dedicated, conscientious people trying to do the right thing.
I have rejected some of the more plausible explanations such as a dog that was dominant for heart defects permeated the breed with multiple heart problems. OK, then there must have also been a widely used dog dominant for kidney problems? Hmmm. Perhaps there was one dog capable of inundating the gene pool with both defects? Not likely – he would have quickly bred himself into extinction. So unless we also postulate that those one or two dogs were also dominant for lens luxation, you can throw such logical explanations out the window.
The examples are exaggerated but scientifically, I’m on solid ground. I don’t have letters after my name so it’s hard to state qualifications without sounding like a braggart. Bill and I have bred way over two hundred AKC champions from a lengthy but very limited breeding program. Over one hundred are Multi-Group, Specialty winners, and/or Register Of Merits. In fact, over half of all Akita Top Winners and Register Of Merit Sires and Dams are O’BJ bred. More important to us, Akitas O’BJ are known as the typiest, soundest, and healthiest in the world.
There are those who say “so what?” and who will try to belittle an accomplishment which they secretly envy. It doesn’t bother me because my ego is non-existent compared to the joy of having a living work of art that loves me back - and the satisfaction of having created it. The point here is that even if we were a jillion-dog puppy mill, we could not have achieved those records without a basic understanding of applied genetics.
That doesn’t mean throw the books away. It does mean having to backtrack, admit mistakes, study, earn the confidence of other top breeders and have sense enough to listen to them, and to be absolutely uncompromising about quality. It means a determination to breed complete dogs, not caricatures with numbers and letters but no brains or beauty. It also signifies a stubborn resolution not to be misled by popular but genetically unproven rhetoric, even when it comes from the hallowed pages of veterinary journals. Applying genetic theory so that you can reach certain pinnacles without falling on your face means you accept reality. It means you weigh new ideas on the scale of proven practicality.
First, Primary Lens Luxation. According to Professor Keith Barnard, Animal Health Trust (England), prominent and highly respected researcher, there have been no recorded cases of PLL (in England) in dogs under three years. On that basis, there is a sensible belief that there’s no need to check for PLL prior to three years of age. The Brits are a bit more in-the-know due to the small size of the country and fewer shows. It is harder to conceal problems and published critiques also help to promote a more open attitude about faults, something which has thankfully, filtered to the U.S. So unless there is conflicting documentation, I accept the British approach to lens luxation. There are other problems that can be identified earlier so this does not imply “don’t check,” it means simply that PLL has late onset. Put in perspective it could also mean that a dog may be lost to other age-related disease long before he luxates. Sort of like the new truth in prostate cancer. If you’re over seventy, forget surgery. You’ll die of old age or surgical complications before the cancer gets you.
Heart defects. It would be utopia if we knew for sure what is genetic and what isn’t. But since researchers don’t know yet if certain conditions are acquired or inherited, we’re going to have to wait. We just had a youngster diagnosed as “most likely a form of tricuspid valve dysplasia.... possibly congenital.” Italics are mine because I find such reports insulting. Bill could easily hear the whooshing, could see the gaping on doppler, and quickly spotted the enlargement on thoracic radiographs. So why mince words? She has serious heart defects, has already fainted once. The breeder said “put her to sleep” but we will keep her and love her for as long as she lives. What troubles us is that even the most obvious problems are couched in the same deliberately obtuse, incomprehensible, CYA terms as are tests that reveal nothing! We don’t know if increased flow rates are “normal” in Minis. We don’t know if it indicates a serious potential or future problem. Sadly, neither do cardiologists!
I will happily provide copies of reports on our dogs. They all say “nothing showed up but...” or “appeared normal at this time” etc etc. There will always be instances when a definitive report is impossible but only the tester can benefit from a speculative essay riddled with self protecting loopholes based on personal interpretation. We are learning that many (most?) echocardiograms present a gray area filled in only by the experience of the cardiologist. Even more frustrating for all concerned, the doppler is often contradicted by no auditory evidence of abnormality or vice versa!
We know of instances wherein dogs were found normal on doppler and very soon thereafter they died from “massive heart problems” per autopsy reports. We can cite other dogs who didn’t do well on a doppler but who lived long active lives with no symptoms of any problem whatsoever. So the bottom line as we see it at this time: Definitive diagnosis by doppler is possible only when glaring abnormalities are present. Incidence Statistics in all three areas could be flawed. There exists confusion as to which defects are proven hereditary and which are the result of trauma, virus, illness, test compromises, or external influence. Readings are subjective. It is not like x-raying your tooth and being able to point out a cavity that is certain to enlarge. OFA was forced to raise the minimum certification age from twelve to twenty four months because the readings were so often wrong. They still are and now Penn Hip has joined the fray of critical comments. In fact, there is growing evidence that what some outspoken breeders have said for decades may be the only truth in dysplasia – hip x-ray is a great diagnostic tool but is not necessarily predictive!
We are expecting too much of cardiologists at this time. We are so demanding of “answers” that we have frightened some vets into a new way of writing reports. Perhaps the unexpected (and therefore infinitely more traumatic) deaths of dogs believed to be heart-sound accounts for increasingly ambiguous written reports. In one recent episode involving four dogs, we received oral summaries at the time of exam, followed by written reports, followed by totally rewritten and contradictory reports after the cardiologist conferred with another vet “more familiar” with Mini-Bulls.
I suggest that we continue to use every means at our disposal to foresee and avoid genetic problems but that we not run about like the Mad Hatter when a vet refuses to give an unconditional “all clear” on your dog. The sky probably isn’t falling. It is our expectations that should be lowered until such time as definitive lab testing and/or DNA analysis is available for eye, heart, and kidney problems.
Do not ever refer to this article as a reason to “not bother” with health tests and periodic evaluations. Just put things in perspective. Remember that eggs were bad for us. Now they aren’t. Butter was sure to clog our arteries, now we’re told its better than margarine due to trans-fatty acids. Remember how many ulcer patients suffered horrible emotional, physical, and financial hardship because doctors refused to listen to one small voice in Australia kept saying “uh excuse me guys, but its really only an easily treatable bug called pylori bacteria.....”
Please test. Please disclose. Please help. Please keep your priorities and perspective in balance. And please urge your parent club to provide meaningful and accurate information. (Our offer to fund another simpler, re-worded survey is still on the table.) Most of all, PLEASE put aside personalities in order to work together for that little guy who follows every step you make. He will do anything for you. We just need to be worthy of that kind of unconditional love and trust.
Excerpted from A Little Bull, Summer 1999
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