Degenerative Myelopathy (DM)
The canine degenerative myelopathy (DM) in dogs is a subject of heated discussion in Germany at the moment. Unfortunately, in the midst of this heated discussion, breeders may give credence to unfounded facts and statistics regarding research on degenerative myelopathy, paving the way for continued uncertainty in finding viable breeding options.
I have been able to observe this recently on a number of occasions.
This hysteria about DM already took its course in the US 3 years ago, and as with many things, it takes a bit of time before it swashes over the ocean to us in Europe.
When studies are carried out and a new gene test comes onto the market, the breeders are alarmed and unfortunately they overreact in some cases. Gene tests are meant to help us in breeding our dogs and they do, provided the results are dealt with properly!
What is degenerative myelopathy?
Degenerative myelopathy (DM) in dogs is a slowly progressive neurological disorder. The myelin (insulating sheath around the neurons) in the spinal cord is destroyed at the thoracic and lumbar vertebrae.
The disease leads to movement disorders. The affected dogs gradually develop uncoordinated movements in the hind legs and both dysfunctional self-perception as well as reflexes. As the disease progresses, the front limbs are also affected and eventually this results in paralysis. The diagnosis is generally made by eliminating other possible illnesses. Differential diagnoses such as a slipped disc, infarct of the spinal marrow, cauda equina syndrome and tumours have to be ruled out by means of appropriate examinations.
Compared to the other above-mentioned diseases, DM is not painful. Symptoms may occur in dogs eight years or older.
Some time ago, an American-Swedish research team discovered a genetic risk factor for degenerative myelopathy in Welsh Corgis and a few other dog breeds. It involves the mutation of the SOD1 gene which is considered the chief risk factor for this disease. Studies have shown, however, that other genetic risk factors have to be present, for example in the case of the Hovawart, before degenerative myelopathy develops.
This therefore means that the mutation of the SOD1 gene is a risk factor. But it is not solely responsible for the outbreak of the disease.
According to Prof. Tosso Leeb from the Institute for Genetics in Berne, this also affects the Rhodesian Ridgeback.
In cooperation with the universities in Berne and Uppsala (Prof. Kerstin Lindblad-Toh), the DM problem is to be solved in the Hovawart breed and the other genetic factors that increase the risk or protect the animal are to be identified. Only when the exact interaction of the SOD1 mutation with other genetic factors is understood is it possible to develop a gene test that can be practically applied for the breed.
In the meantime, Prof. Leeb has collected about 20 blood samples of dogs diagnosed with DM, but he requires at least 50 in order to carry out the study.
Prof. Leeb would also be prepared to include the Rhodesian Ridgeback breed in the study. He does, however, require blood samples from affected dogs that have been definitely diagnosed with DM. And here we draw attention to an important point: at present, we have no clinical data whatsoever concerning Ridgebacks that are afflicted with DM. This means that we know of no dogs that have been verified to have DM. If dogs are suspected to have DM, many other diverse disorders which frequently afflict older dogs and cause symptoms similar to DM have to be ruled out by an experienced veterinarian or even better, by a neurologist. Older, healthy dogs (>13 years) are well suited as control animals for the research.
According to RRCUS, 9 cases were documented in a five-year period between 1986 and 1991 in the US which testifies to a relatively low incidence if one considers the entire population of Ridgebacks in the US. In 2005 and 2006, 4 cases were confirmed.
In the meantime, a gene test can be carried out in Germany, too.
The following is a brief summary of the three genotypes (Source: Laboklin):
Genotype N/N – homozygous healthy
This dog does not carry the mutation and has an extremely low risk of developing DM. It cannot pass on the mutation to its offspring.
Genotype N/DM - heterozygous carrier
This dog carries a copy of the mutated gene. It has a very low risk of developing DM, but could pass on the mutation to its offspring with a probability of 50%. Such a dog should only be mated with a dog that carries no risk of a DM mutation.
Genotype DM/DM – homozygous affected
This dog carries two copies of the mutated gene and has a very high risk of developing DM. It will pass on the mutation to its offspring 100% and should only be mated with a dog that is absolutely free of the DM mutation.
The American study
The Orthopedic Foundation For Animals (OFA) is carrying out a study in which 1711 Ridgebacks have been tested up to now (Status: August 2011). The Rhodesian Ridgeback is therefore the breed that has been most frequently tested in the course of this study.
911 Ridgebacks were unaffected which is equivalent to 53%.
688 (40%) were carriers and 112 (7%) were dogs at risk meaning these dogs carry two copies of the mutated gene.
As a comparison to the status in November 2010: 1425 tested Ridgebacks, of which 749 (53%) Ridgebacks were unaffected, 577 (40%) carriers and 99 (7%) dogs at risk.
As we can see, the percentages have not changed during this period.
Here are further statistics prepared by the OFA (Status: November 18, 2010):
1045 Chesapeake Bay Retrievers were tested. 46% are unaffected, 43% carriers and 12% dogs at risk.
In the case of the Pembroke Welsh Corgi, 1017 dogs were tested and only 8% were unaffected, 39% carriers and 52% were at risk.
1016 Boxers were tested, of which 43% are dogs at risk, 39% carriers and only 18% unaffected.
In the case of 808 German Shepherds, 50% were unaffected, 30% carriers and 20% at risk.
You will find the current test findings of the OFA at: http://www.offa.org/dna_teststats.html
From most of the remaining other breeds, fewer than 100 dogs were tested, in some cases only one or two, which does not lead to conclusive results. The statistics are, however, being constantly updated and the values may change.
As mentioned, this study simply contains proof of the mutation of the SOD1 gene, but is not a clinical study. It is not known whether one of the Ridgebacks that tested positive is even sick.
Impact of the OFA study in America
The OFA study has already had a huge impact on breeding practices in America. Some breeders have immediately removed dogs, which have tested positive, from breeding and had them castrated.
The OFA recommends incorporating the results of the test into the breeding strategy which is definitely a good idea. This means that carriers should only be mated with unaffected dogs. In light of the present knowledge on the topic, geneticists feel carriers should not be excluded from breeding, since this restriction of the gene pool inevitably leads to other problems.
If we were to exclude the dogs identified by the OFA statistics as carriers from breeding, we would lose 50% of our breeding potential. Unthinkable and deadly – for all breeds! Gene tests are becoming increasingly important in dog breeding and more and more tests will be available to us in the next years. This is a development which breeders have to live with.
But what happens if we do not handle the results carefully and a radical blow is dealt to whole races of dogs by defaming them, and people stop breeding their dogs with these races? Generalized premature judgments about whole bloodlines inevitably result in exclusion from breeding. Breeders purchase bitches from other races and the stud dogs belonging to these races are not used anymore. Where does that lead us? Away from the variety of genes that we have painstakingly established in years and decades of breeding experience, towards extreme inbreeding and line breeding.
What happens if we only breed with these other races and in a few years truly serious clinical problems appear through inbreeding and line breeding, and we are no longer allowed to breed with these dogs because of illnesses? What do we fall back on if we have removed those dogs from breeding that show no clinical symptoms whatsoever, but simply have a genetic predisposition towards a disease in theory? Particularly then when we already know that a test is not (yet) really conclusive as in the case of DM.
What will happen when the next gene test is developed? If the statistics are similar, then 50% of our dogs will again be excluded from breeding, etc. etc.... Within a short time, we would no longer have any dogs left for breeding purposes. It is as simple as that. An absolutely disastrous development which is not our goal and is not permitted to be so!
As mentioned at the beginning, gene tests are meant to render support to breeders. Careful evaluation of the results of these gene tests is the responsibility of the breeders and all those involved with the breeding process.
(Reproduction including excerpts, only with permission of the author)