Hi all, finally got  some more feedback re autopsy results .  External examination states the animal was in good body condition. There were abundant subcutaneous adipose tissue and the muscle bulk was well represented.  Carcase, skin no abnormality detected.    Muscular system no abnormality, Skeletal system no abnormality. detected.  Cardiovascular system no abnormality detected.    So far so good until we reach the nervous system, histopathological examination of the central nervous system identified lesions within segment of spinal cord (C5/C6) the lesions were localised bilaterally within the lower horns of the spinal cord grey matter involving axons and scattered neuronal bodies, which is consistent with clinical signs observed. Final studies are needed to identify the primary cause of  lesions in spinal cord,  Utz  had never shown neurological symptoms at all untill the day before he was PTS. My comment now, although the long wait was very upsetting for my husband & I  we are a little further with the answers but still do not know what caused the lesions, further tests are in progress. For our own peace of mind and after researching  rimadyl,  there is some evidence that rimadyl  can cause spinal lesions, but in our case yet to be proven. Will keep you all updated once I receive further results. For anyone not familiar with my story? it can be viewed in the rainbow bridge board, titled in memory of UTZjr my beautiful boy

sorry for your loss.

I hope you do get a final cause eventually even if it takes time

{{{{HUGS}}}}

Hi all, finally got final test results back, on Utz"s brain & spinal cord, pathology report states that Utz had a genetic disease called neuronal ceriod-lipofuscinosis,
(I had posted previously his preliminary autopsy results that lesions were found in C5-C6 of spinal cord) new evidence states that lesions were found in section L5-L6 of spinal cord, acute haemorrhages were observed in sub-leptomeningeal  layer in Cerebullum. Spongiotic degeneration of the axons of the vestibular, facial  trigeminal nerve were also observed, sorry for all the medical jargon, I am using the actual wording from todays report, After doing bit of research today I have found that this disease is more prevalent in other breeds of dogs, Dachshunds, Dalmatians, English Setters, Border Collies and Miniature Schnauzers. American bulldogs, Each breed has a variety of different symptoms which makes it difficult to recognize, especially in the early stages. Unfortunately, the prognosis of the disease is quite grave. A cure does not yet exist..
. For a dog to be affected by NCL, both it's sire and dam must be carriers of the NCL gene. In a litter of pups where both parents are carriers of the NCL gene, but not affected by the disease, about 25% of the pups will get the disease and have the gene, 50% will have the gene (and therefore be capable of passing it on to future generations), but not be affected by the disease, and 25% will be completely clear of the gene and the disease.  Dogs with NCL exhibit many changes in their gait and posture. Many breeds develop uncoordinated movement in their limbs in early stages of the disease, especially in the back legs. As the disease progresses, many dogs lose coordination in their front legs as well. Muscle twitching occurs throughout the course of the disease, even when sleeping. Also, some breeds develop a tremor and pronounced staggering. Aggression, Head tilts, seizures. Could this be the next time bomb genetic disease to affect our dogs.  As this disease is often misdiagnosed as other disease"s
Information I have taken from Pfizers information user guide leaflet for rimadyl PRECAUTIONS  NSAID therapy can unmask occult disease which has been previously been undiagnosed due to the absence of apparent of clinical signs.
NSAIDS inhibit prostaglandins that cause inflammation, they may also inhibit these prostaglandins which maintain maintain normal homeostatic function, these anti- prostaglandins effects can result in clinicly significant disease in patients with underlying or pre-existing disease more often than in healthly patients
 

This is a known inherited disease in Border Collies and their is a DNA test so affected pups should never be born as parents should be tested.

Not heard of this in dachsies "touch wood", hopefully it is only the odd case that has had the breed added to the list.

Is it the same gene causing the issue in all the breeds or like with PRA various forms caused by differing genes?

I have no idea Barbara and I am unsure if any research has been carried out into the gene in other breeds. Our DNA test was pushed for and funded by breeders in Australia.

In border collies and presumably other breeds this is a 'storage' disease, whereby toxins aren't removed from the body but build up and eventually kill the dog... a terrible illness which as stated above is testable for border collies thanks to the work of Alan Wilton in Australia... there is bizarrely very little in UK border collies but imported dogs from Australia/New Zealand need to be tested.  It was whilst trying to combat (prior to the DNA test) this in Australia that another fatal disease was discovered - TNS (fortunately a DNA test is also available for this).  It appears that the lines which were free of CL contained TNS :-(  TNS is around in UK dogs so worth testing for.

So sorry for you losing a dog in this way, but nothing you could do, there is no cure even if they knew what it was :-(

Hi all I am still in a state of shock regarding utz"s diagnosis of NCL, as he had never shown any symptoms at all until the day before he was put to sleep, apparently it normally occurs in younger dogs but onset can come on in older dogs age5-6, because of the nature of the hidden disease it is very difficult to know if your dog is affected until it manifests, the only way to eradicate it, is for all breeding dogs to be screened and if they have it they MUST not be used in breeding programmes,
Inheritance : AUTOSOMAL RECESSIVE trait
Sire     Dam     Offspring
            
Clear  x  Clear  >  100% Clear
            
clear  x  carrier  >  50%  Clear + 50% carriers
            
clear  x  affected  >  100% carriers
            
carrier  x  Clear  >  50%  Clear + 50% carriers
            
carrier  x  carrier  >  25% clear + 25% affected + 50% carriers
            
carrier  x  affected  >  50% carriers + 50% affected
            
affected  x  Clear  >  100%  carriers
            
affected  x  carrier  >  50% carriers + 50% affected
            
affected  x  affected  >  100% affected
so according to the chart utz would of been bred by at the very least 2 carriers, this is  very worrying for our breed, more research needs to be done, to see how widespread it is in rottweilers

That works fine if there is a DNA test available. 

Do we know that it is the same gene in your breed as in the breeds where a DNA test exists?

If it is then you need to get the breed club to ask members to DNA test dogs before breeding and get an official KC testing scheme set up so results go to KC and are included on dogs and progeny registration data.

When we got a DNA test for prcd-PRA in Oct 2008, it took until July 2009 for it to become official KC scheme (when the breed club asked for it) where the KC get all results.