Canine degenerative myelopathy (DM) is a progressively degenerative disease of the spinal cord which causes hind limb weakness, lameness and eventual paralysis. It appears to affect dogs between the ages of 8 - 12 and the prognosis for total paralysis is around 12-24 months. With this disease, the myelin sheaths that normally protect the spinal neurons disintegrate, exposing the underlying nerve fibers and disrupting the communication pathways between the brain and spinal cord. The precise cause of degenerative myelopathy is unknown.

You can use the chart below to determine the status of puppies from a breeding with each parent being either clear/carrier or affected.

CURRENT LIST OF TESTED DOGS AS PUBLISHED BY THE KC HERE

Dogs can be tested with a simple buccal cheek swab at home and sent to a Laboratory for example Laboklin.

Clear: Dog is negative for the Degenerative Myelopathy mutation.
Carrier: Dog carries one copy of the mutation associated with Degenerative Myelopathy, and could pass on the mutation to any offspring.
Affected - At Risk: Dog has a significantly higher risk of developing DM, and will always pass on a copy of the mutation to its offspring

UNIVERSITY OF MISSOURI DM HANDOUT (PDF DOCUMENT) DOWNLOAD HERE

My experience with DM by Julie Growcott
email: collielife1@gmail.com

The single nucleotide substitution in the gene called SOD1 that causes Degenerative Myelopathy is autosomal recessive with incomplete penetrance. This means that dogs that carry two copies of the mutation (homozygotes) are at increased risk of developing Degenerative Myelopathy during their lives. Dogs that carry a single copy of the mutation (also known as carriers or heterozygotes) are less likely to develop Degenerative Myelopathy as a result of the SOD1 mutation, but they will pass the mutation onto about half of any offspring they have. Breeding dogs that are less likely to develop Degenerative Myelopathy should be the breeder’s priority, with a reduction in mutation frequency within the whole breed being the secondary, longer-term target.

Carriers can be bred from safely, provided they are mated to a dog that has also been tested and is clear of the SOD1 mutation (i.e. carry no copies of the mutation). If a carrier is mated to a clear dog approximately half of the resulting puppies will also be carriers, so should be tested themselves prior to breeding. Breeding carriers to tested, clear dogs is safer, in terms of avoiding dogs affected with Degenerative Myelopathy, and will help to maintain the genetic diversity of a breed.

However the story of degenerative myelopathy is not that simple and the disease has been confirmed in some dogs with only one copy of the gene suggesting that there are other genetic or environment influences that determine whether a dog will develop the disease. One reference is –

 Zeng R, Coates JR, Johnson GC, et al. Breed distribution of SOD1 alleles previously associated with canine degenerative myelopathy. Journal of veterinary internal medicine / American College of Veterinary Internal Medicine 2014;28:515-521

 The University of Missouri recently found that an E40K missense mutation of superoxide dismutase-1 (SOD 1) is strongly associated with this disorder. SOD 1 is a gene that encodes an enzyme (superoxide dismutase) responsible for destroying free radicals in the body. Free radicals are reactive entities that are part of the natural defence mechanism; however they become harmful when they are produced in excessive quantities, causing cell death and a variety of degenerative diseases. The same gene mutation also can cause a form of human motor neuron disease called amyotrophic lateral sclerosis. However, the actual mechanism of the disease is still not clear.

 Crisp MJ, Beckett J, Coates JR, et al. Canine degenerative myelopathy: biochemical characterization of superoxide dismutase 1 in the first naturally occurring non-human amyotrophic lateral sclerosis model. Experimental neurology 2013;248:1-9.

 Awano T, Johnson GS, Wade CM, et al. Genome-wide association analysis reveals a SOD1 mutation in canine degenerative myelopathy that resembles amyotrophic lateral sclerosis. Proceedings of the National Academy of Sciences of the United States of America 2009;106:2794-2799

 DNA testing for the SOD-1 gene identifies dogs that are ‘clear’  i.e. the dog that has two normal copies of the gene and is extremely unlikely to develop DM; those who are ‘carriers’  i.e. dogs who have one normal copy of the gene and one mutated copy of the gene have less chance of developing DM [but may do so,, either because of other influences or because the recessive gene is switched on]. those who are ‘at risk’ i.e. dogs who have two mutated copies of the gene and are at risk of developing DM. However, the test does not identify dogs that are affected by the disorder, but only identifies dogs that are more at risk of developing clinical signs, but may not do so during their lifetime 

Degenerative myelopathy in the Collie breed: a retrospective immunohistochemical analysis of superoxide dismutase 1 in an affected Rough Collie, and a molecular epidemiological survey of the SOD1: c.118G>A mutation in Japan

Ultimately, a diagnosis of degenerative myelopathy is made by ruling out other diseases that cause progressive paralysis. Samples of cerebrospinal fluid can be taken and assessed for increased protein levels. Advanced imaging procedures can be performed to rule out other conditions.

DM causes insidious and progressive lack of muscle coordination, called ataxia. The hind limbs usually are affected first by weakness and slight or incomplete paralysis (paresis). Owners will notice some or all of the following symptoms on affected dogs:

Three dog breeds have a particular heightened risk of developing or passing on the gene mutation that causes canine degenerative myelopathy, and these are the German Shepherd, Boxer dog and Pembroke Welsh Corgi. Overall, however, 43 different breeds of dog have been identified as having the propensity to develop and pass on the gene mutation, but most commonly include the Boxer, Chesapeake Bay Retriever, German Shepherd, Pembroke Welsh Corgi, Cardigan Welsh Corgi, Rhodesian Ridgeback, Poodle, Wire Fox Terrier, and Labrador Retriever. The mean age of affected dogs is 9 years. Males and females are equally affected. Younger dogs also can be affected, but this is uncommon.

Any dog can get DM. Being homozygous for the gene makes it more likely that a dog will get clinical DM, but a clear or carrier does not mean they will not get DM, clear and carrier dogs have been confirmed with DM on autopsy, DM cannot be diagnosed without an autopsy. DM is a disease that looks like other diseases, and many other diseases can look like DM. DM is a specific disorder, it is not a back problem, where a dog loses control of its back legs, limps or has progressive paralysis. It is not the only nerve disorder and it is not the only thing that makes dogs lose rear function. Dogs can “go down” because of disc disease, a whole load of muscle diseases, other nervous disorders, vestibular issues, a huge range of injuries, and even the simple muscle atrophy of old age. Any one of these can mimic DM.

Exercise and other forms of physical therapy are very important to help delay the onset of disuse muscle atrophy associated with DM and to help affected dogs maintain mobility and strength in their pelvic limbs. This commonly involves what are called “range of motion” exercises (passive stretching and flexing of the rear legs by hand in a regular pattern). Activity seems to slow the progression of the disease, and as a result with regular physical therapy affected dogs are able to maintain strength, balance and the ability to walk for a longer period of time. Recently, hydrotherapy also has proven to be beneficial for dogs with this disease. This involves swimming exercises, underwater treadmill use and other techniques that help the dog exercise and use its muscles.

A viable management option for dogs that have lost mobility in their pelvic limbs is the use of a wheel cart – essentially, a wheelchair for dogs. As long as the dog is able to use its front legs normally, a wheel cart will keep it comfortable and mobile. Once the front limbs are severely affected, a wheel cart cannot be used. Your veterinarian can help you find a wheel cart suited to your particular dog.

No drug has proven effective in slowing or stopping the progression of canine DM. Vitamins and omega-3 fatty acid supplementation have been advocated as potential therapies but are not yet proven. Vitamin E, vitamin B complex and vitamin C are under investigation as possible useful supplements for managing this disease. Their efficacy also is unknown. Other chemical therapies are being studied, including administration of aminocaproic acid and the potent antioxidant, acetylcysteine. These experimental treatments have some adverse side effects, are expensive and may require long-term use. Still, if no other treatment protocol helps a particular dog, these unproven “treatments” may be considered. Of course, a veterinarian is the only one able to assess and decide upon the right treatment regimen for an affected dog. The suspected diagnosis of degenerative myelopathy is based on clinical signs, breed, and age and supported by the absence of other clinical diseases.

HEALTH TESTING RESULTS AS PUBLISHED BY THE KC PLEASE NOTE THAT THIS IS NOT UP TO DATE AS THE KC
ONLY UPDATE TWICE A YEAR AND A LOT OF BREEDERS CHOOSE NOT TO PUBLISH THEIR RESULTS PUBLICLY
DOWNLOAD HERE

I have undertaken a lot of work on the Pedigree database and added all known Health Test results
to each dog HERE

MORE ON DM HERE

YOU CAN READ MORE ABOUT THE RESEARCH INTO DM HERE

DM IN THE ROUGH COLLIE
by Stephen Webb

Sources
Veterinary Centers of America
American College of Veterinary Surgeons
UC Davis
Washington State University
American College of Veterinary Surgeons
Petmd.com
vetinfo.com
vetnutrition.edu
vetnutrition.tufts.edu
prime.vetmed.wsu.edu
noahcommpendium.co.uk
Dogs Naturally
Dr Conor Brady

This information is not meant to be a substitute for veterinary care. Always follow the advice provided by your veterinarian.