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Emerging Ataxia in the American Staffordshire Terrier

Natasha Olby

Updated January 11, 2004

Amstaff Ataxia FAQs

There has recently been some healthy debate on the topic of Amstaff ataxia and possible causes for this devastating problem. I thought it would be useful to address some of the frequently asked questions on the web site.

1. Is Amstaff ataxia a canine form of Mad Cow Disease?

   The answer to this question is NO. Here are the reasons why:

2. 1. Mad Cow disease, also called bovine spongieform encephalopathy, produces classic changes in the brain that can be seen when sections of the brain are examined with a microscope. The most obvious change is an appearance of holes within neurons, and indeed this is what gives the disease its scientific name of spongieform (sponge like) encephalopthy (brain disease). This appearance is the hall mark of the disease and is present in all forms of the disease (e.g. the human, feline and ovine). All of the diseases can be lumped together and called the "transmissable spongieform encephalopathies". If there are no "holes" in the neurons it is not a spongieform encephalopathy. In Amstaff ataxia there are no holes in the neurons.

   2. In Mad Cow disease the changes in the brain are found in several regions, but in particular in the gray matter of the cerebrum and cerebellum. In Amstaff ataxia, the changes are only found in the cerebellum, and even more specifically in the 3 outer layers of the cerebellum.

   3. We have shown statistically that this disease is inherited.

2. If Amstaff ataxia is inherited, why do we only see occasional affected dogs and why are several generations skipped sometimes?

3. 1. Based on our statistical analysis of pedigrees, we believe that this disease is a recessive disease. By this we mean that an animal must have 2 copies (one from each parent) of the abnormal (mutated) gene to cause signs of the disease. If they only have one copy of the gene they appear to be normal. As a result, apparently normal parents, each of which have one gene for the disease (making them hidden carriers of the disease) can produce a mix of affected and normal pups if bred with other carriers. This means that they can be bred over and over again without problem, it is only when they are crossed with another carrier that you can get affected offspring. Even then there is only a 25% chance that a dog will inherit copies of the abnormal gene from both parents.

   2. To add to this already confusing picture, affected dogs may not develop signs until they are over 8 years of age (most start to show signs between 4 and 6 years of age) and so the breeder may well not know that they have produced affected dogs as they can be so widely scattered by the time they show signs.

   3. Finally, the signs shown by dogs can vary in severity and because this is a new and relatively rare disease, it may not be recognized by the veterinarian. As there is no simple diagnostic test that confirms the disease at present, this makes diagnosis even more difficult.

   4. All of this factors conspire to make it difficult to know precisely which dogs in a litter are affected and make it difficult to be certain of the mode of inheritance. The only way to be 100% sure is to do test breedings between known affected dogs and keep all the offspring and watch them over at least 8 years: truly a slow and expensive process.

3. Does diet play a role in Amstaff ataxia?

   There has been a lot of discussion on the role of diet, and in particular on the role of raw diets in the pathogenesis of this disease. We did look at this quite carefully and even measured levels of vitamin E in the blood of affected dogs to see if there was a deficiency (a similar disease in people can be caused by vit E deficiency as a result of a mutation that causes abnormal processing of vit E). We found no evidence of diet playing role: the dogs we have seen are on a wide variety of different diets and had excellent blood levels of vitamin E.

4. Could the disease be caused by a toxin such as organophosphate toxicity?

   This is another possible cause that we looked at carefully. The pathology (changes) that we see in the brain of affected dogs are not consistent with a toxicity. Moreover, affected dogs come from all over the world so it is difficult to imagine that they have all been exposed to the same toxins, and in fact the only thing that they have in common is their lineage. There is always the possibility that the affected dogs have a genetic mutation that makes them more susceptible to a toxin that we have not identified as yet, but it seems unlikely.