 HISTORY
Condensed from the
report Dana [Russe] compiled for all VIB’s in Oct. of 1995.
** Several Veterinarians/ Geneticists that have been consulted regarding this litter felt that at least a percentage of progeny should be “effected” * *IF* * there was any true genetic cause for these anomalies. 2) Captain was bred to Lizzy- one of those puppies born 4/10/94, Cooper, went lame in the hind-end. He was 9 months old. The veterinarian diagnosed “traumatic fracture of the transverse process of L1 with instability and bony proliferation of T13-L1 .” This was causing spinal cord compression and his paraparesis. Cooper’s surgery was a modified dorsal laminectomy to stabilize T13-L1 and relieve the compression. Siskiyou was treated by a national recognized surgeon--Cooper was treated at a university Both vets determined that the dogs’ condition was the result of an injury. No ONE was aware of the similarity between the two injuries. Please note that this area, T13-L1, is one of the areas of the back most susceptible to injury. 3) Jimmy- Captain/Lizzy second litter whelped 1/24/95, came down with sudden paralysis of his rear quarters and he was put to sleep. It was at this point that Tina and Wendy decided to do some researching. A conversation with Bev and Penny enlightened us about the similarity of the problem with Siskiyou and Cooper. We spoke with Ellen Grandner, Lizzy’s owner who told me that Jimmy’s problem was due to an injury. She said that all of this had been researched by her vet before and there were no similarities between the accidents of the three dogs. She did forward a copy of Jimmy’s report from Cornell which revealed that extradural compression of the spinal cord at T13-L1 was identified as the source of his paralysis. Jimmy’s diagnosis was moderate trabecular osteoptrosis with the comment that perhaps there had been insufficient vertebral body remodeling during growth. * Jimmy DID NOT have a FRACTURE or BONY GROWTH between the vertebrae. It was further instructed by the Cornell vet that Jimmy be neutered at six months of age due to the “possible heritability of his vertebral anomaly”. This letter from Cornell was dated June 27, 1995. None of the information contained in the letter, especially the part about possible heritability, was made available to the club, Tina, or Wendy, until I received a copy of the letter in October. 4) Just a few weeks ago, Jimmy’s brother Titan and sister Annie, were taken to their vets with similar symptoms- sudden onset of paralysis or ataxia in the hind-end. Annie had compression at the spinal cord, the same as Jimmy. She has been put down and her body donated to Cornell. The surgeon, neurologist and pathologist are in the process of performing a necropsy on her- including decalcifying her vertebrae. This process reveals the bone, layer by layer, and will indicate the amount of calcium in her bones. We ore awaiting the results of the necropsy.* Titan is being seen by a University veterinarian who is conferring with the Cornell veterinarian that treated Jimmy. *UPDATE! Unfortunately those results were inconclusive. But through the MRI, AND FURTHER TESTING ON TITAN, Dr. McDonnell of Tufts University was able to detect SPECIFIC **LESIONS**!! **THIS WAS WONDERFUL NEWS FOR THE OWNERS OF THIS LINE, BECAUSE NOW WE COULD DETERMINE **IF * * A PROBLEM EXISTED, WITHOUT WAITING FOR symptoms. Dana’s conclusion 10/95 as presented to her by Dr Mc Donnell: I spoke with Titan’s vet, Dr. McDonnell, at some length. He advised me that the problems these six dogs have experienced with their backs is symptomatically related, and that there seems to be a familial tendency which indicates a genetic involvement. He explained that what we have is a malarticulation of the vertebrae. Apparently, the cartilage does not fit together properly which causes instability in that area of the back and allows too much movement which in turn causes torsion injuries and spinal cord compression. This malarticulation is seen in Thoroughbred horses, but these vets have not seen it in dogs before. In theory, this disease is something like OCD, most commonly found in the elbow joints, but which also plays a role in Wobblers Syndrome. But so far, this is just theory and there seems to be no commonly known disease we can name that produces the symptoms these dogs have experienced. UPDATE (from Tina) Although in Dana’s article she discussed the various modes of transmission, in the event this could reflect a “genetic” influence—We can almost assuredly eliminate the possibility of a POLYGENETIC THRESHOLD TRAIT. NO OTHER DOGS- CARRYING ANY OF THESE SAME GENES (as Captain/Lizzy) WHEN INBRED/OUTCROSSED/LINEBRED etc. - - - IN ANY OTHER COMBINATIONS HAVE SHOWN ANY SUCH PROBLEM!! ** IF you have questions regarding the “POCA” line (Lizzy’s Dam) please call JUDY VANEMAN ….
Another theory that was investigated: And there’s always the mutant gene:
There is a very
famous Quarterhorse, “Impressive”, who was a World Champion and became a
World Champion Sire. He has 55,000 descendants of which at least 14,000 are
known to have a particular disorder called HYPP which makes the horse have
tremors, convulsions, fail down, and sometimes die. Only his descendants
have the disease, ft has not been seen anywhere else in the horse world, so
it has been termed “Impressive Syndrome”. It has taken researchers 10 years
to prove that Impressive Syndrome is a genetic disease determined by an
autosomal dominant mutant gene. This was a big deal - 55,000 horses - and it
still took 10 years and gosh knows how much money. REPRINT OF TINA’S LETTER TO THE VIB’S WRITTEN 9/95 Dear VIB’s…. Dana has presented as factually clear a case as we are able to do at this time. Unfortunately, we do not have all of the answers yet, and may not be sure of anything definite for years to come. Since any slack in control could possibly lead to major disasters down the road, we have to take some strong precautions now: 1) Captain has been x ‘d (Breed Warning). This means that NO INBREEDING OR LINE BREEDING can be done on him. If you have a grandson or granddaughter of his, you MUST study the pedigree of every dog you plan to breed to, to insure that Captain does not appear in their pedigree for at least 5 generations!! This will protect us from the infiltration of a possible lethal gene. 2) We will continue to monitor all of the Captain lines very closely. We presently have a total of 54 Captain grandkids on the ground with 2 more litters due soon. This will tell us a lot over the next 12 months! If none of these approximately 70+ pups show any signs of problems, we will be able to “breathe a lot easier.
3) We will continue to research the problem, looking into the orthopedic, neurological, genetic nature of these symptoms as well as environmental and nutritional influence.
Even though we do not have all of the answers, we have ways to protect the future of our breed through our strict ISSR rules!! As breeders, we cannot ignore problems like this or ‘pretend’ they are somebody else’s!! We must all unite in taking aggressive action into researching and eliminating such “traps" from our gene pools!!
Our hearts go out to
those people who have been directly affected by this problem. We ARE aware
how tough it is to have a dog with a problem like this. Our responsibility
to Shiloh owners and to the breed is to work hard to identify and eliminate
ANY AND ALL problems that affect the health, temperament or beauty of the
Shiloh Shepherds. Please be aware that while we are not claiming that our
breed is now perfect - Shiloh Shepherds have historically FAR FEWER health
problems than other purebred breeds. This is because of my dedication to the
ideal of the perfect dog, which means that I have spent many years breeding
and culling - hardening my heart - to eradicate health and temperament
problems. And I will not quit!! We will continue to keep you informed of any future developments, Tina.
The above letter (except for the *UPDATES*) has been copied word for word as printed in the VIB REPORT 10/95. UPDATES were from December 1996.
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