HIP DISPLASIA

NORMAL **************************** HIP DISPLASIA

MANY BREEDERS X-RAY THEIR SIRES AND DAMS IN AN ATTEMPT TO CONVIENCE THEIR CUSTOMERS THAT THE PUPS THEY ARE PRODUCING ARE SAFE FROM HIP DISPLASIA. NOTHING COULD BE FURTHER FROM THE TRUTH!

Research shows that as little as 15% of hip dysplasia is inherited and up to 85% is caused by environmental factors. Decades of selective breeding has made very little impact on the problem.

See the research posted below or click on the link to read the complete study.

The Institute of Canine Biology 

https://www.instituteofcaninebiology.org/blog/the-10-most-important-things-to-know-about-canine-hip-dysplasia

3) Environmental factors are also important

Although there is a genetic influence on hip dysplasia, the heritability of the trait is rather low. Many studies have shown that genetic variation accounts for only a modest fraction of the variation in hip scores, usually 15-40%. This means that some fraction of the variation in the quality of the hips is the result of non-genetic, or “environmental” influences. This is one reason why decades of strong selection has resulted in only modest reductions in hip dysplasia in some breeds. At the current rate of progress and selecting only by phenotype, it could take decades to achieve a meaningful reduction in the incidence of hip dysplasia (Lewis et al 2013). ​The top three environmental factors that have been found to play a significant role in the develop of dysplastic hips are: a) joint laxity, b) weight, and c) exercise.

10) We can dramatically reduce hip dysplasia now

Genetic selection should continue to produce modest progress in the reduction of hip dysplasia. But a significant and immediate reduction in the number of afflicted animals could be achieved by better control of non-genetic, environmental factors. Weight management, appropriate exercise, proper nutrition, and early intervention at the first sign of lameness are simple steps we can take that will dramatically reduce the pain and suffering caused by hip dysplasia. The research will surely continue, but we already have the information we need to tackle this problem. 

DEGENERATIVE MYELOPATHY

Breeding Carriers and Keeping the Gene Pool Stable 

Breeding Carriers – DNA Testing in Breeding Program – AnimaLabs©

The only way to be sure of your dog’s genetic heritage is DNA testing. Responsible breeders are aware of the importance of such tests and get their dogs tested in order to maintain or improve the quality of their dogs. On the other side, often when the results show that their dog is a carrier for certain autosomal recessive disorder, owners appear confused or disappointed. Considering centuries of inbreeding among pure breed dogs, the appearance of carriers is not unusual. Additionally, some breeders appear discouraged from using their carrier dogs in the breeding program. Although the dog carries one copy of the causative mutation, other copy of the allele is healthy, and the carrier dogs will be completely healthy dogs considering a specific disorder. When breeding carrier with a clear dog, there is 50% chance that puppies will be clear and 50% chance that puppies will be carriers, but ALL PUPPIES WILL BE HEALTHY. On the other side, excluding carrier completely from the breeding program will reduce the gene pool for this dog’s genetic material. Carrying out this practice throughout years would cause dramatic shrinkage in the gene pool, which in turn, can lead to appearing of some new, until now unknown or extremely rare disorders. 

Degenerative Myelopathy – A Brief Description

Degenerative myelopathy (DM) is a fatal, chronic, progressive, degenerative disease of the spinal cord of several breeds of dog, including the German Shepherd dog (GSD). There is no treatment for this disease and in time it leads to complete paralysis in all limbs (tetraparesis). Euthanasia is usually opted for before the disease progresses to this stage.

In DM there is a slow, progressive degeneration of an outer layer of tissue of the spinal cord (the white matter) in the thoracic (chest) section of the spine with loss of myelin and axons (Shell 2008). This degeneration appears to be due to the presence of excessive amounts of damaging reactive oxygen species molecules (ROS): biochemicals that react with and damage the components of cells, causing oxidative or free radical injury. High numbers of ROS occur with this condition, due to a mutation in the gene which codes for the production of the superoxide dismutase-1 (SOD1) enzyme, which is produced by cells to help break down ROS and limit any damage they might cause (Awano et al 2009).

The first signs of DM are classically seen at around 8 to 9 years of age and involve hindlimb ataxia (swaying when moving). As the disease progresses, hindlimb weakness occurs, leading to an inability to stand and then complete hindlimb paralysis. Most owners elect for euthanasia, once significant paralysis or paraplegia has occurred; however, if allowed to progress, the disease will ascend up the spinal cord to affect the forelegs leading to tetraplegia (inability to use all four limbs) (Awano et al 2009).

There is currently no effective treatment for this disease or its effects, though physiotherapy can help some dogs stay mobile for longer.