Health

Hip Dysplasia

Hip Dysplasia is a terrible genetic disease because of the various degrees of arthritis (also called degenerative joint disease, arthrosis, osteoarthrosis) it can eventually produce, leading to pain and debilitation.

The very first step in the development of arthritis is articular cartilage (the type of cartilage lining the joint) damage due to the inherited bad biomechanics of an abnormally developed hip joint. Traumatic articular fracture through the joint surface is another way cartilage is damaged. With cartilage damage, lots of degradative enzymes are released into the joint. These enzymes degrade and decrease the synthesis of important constituent molecules that form hyaline cartilage called proteoglycans. This causes the cartilage to lose its thickness and elasticity, which are important in absorbing mechanical loads placed across the joint during movement. Eventually, more debris and enzymes spill into the joint fluid and destroy molecules called glycosaminoglycan and hyaluronate which are important precursors that form the cartilage proteoglycans. The joint's lubrication and ability to block inflammatory cells are lost and the debris-tainted joint fluid loses its ability to properly nourish the cartilage through impairment of nutrient-waste exchange across the joint cartilage cells. The damage then spreads to the synovial membrane lining the joint capsule and more degradative enzymes and inflammatory cells stream into the joint. Full thickness loss of cartilage allows the synovial fluid to contact nerve endings in the subchondral bone, resulting in pain. In an attempt to stabilize the joint to decrease the pain, the animal's body produces new bone at the edges of the joint surface, joint capsule, ligament and muscle attachments (bone spurs). The joint capsule also eventually thickens and the joint's range of motion decreases.

No one can predict when or even if a dysplastic dog will start showing clinical signs of lameness due to pain. There are multiple environmental factors such as caloric intake, level of exercise, and weather that can affect the severity of clinical signs and phenotypic expression (radiographic changes). There is no rhyme or reason to the severity of radiographic changes correlated with the clinical findings. There are a number of dysplastic dogs with severe arthritis that run, jump, and play as if nothing is wrong and some dogs with barely any arthritic radiographic changes that are severely lame.  (http://www.ofa.org/hd_info.html)


Elbow Dysplasia

Elbow dysplasia is a general term used to identify an inherited polygenic disease in the elbow of dogs. Three specific etiologies make up this disease and they can occur independently or in conjunction with one another. These etiologies include:
  1. Pathology involving the medial coronoid of the ulna (FCP)
  2. Osteochondritis of the medial humeral condyle in the elbow joint (OCD)
  3. Ununited anconeal process (UAP)

Studies have shown the inherited polygenic traits causing these etiologies are independent of one another. Clinical signs involve lameness which may remain subtle for long periods of time. No one can predict at what age lameness will occur in a dog due to a large number of genetic and environmental factors such as degree of severity of changes, rate of weight gain, amount of exercise, etc. Subtle changes in gait may be characterized by excessive inward deviation of the paw which raises the outside of the paw so that it receives less weight and distributes more mechanical weight on the outside (lateral) aspect of the elbow joint away from the lesions located on the inside of the joint. Range of motion in the elbow is also decreased.  (http://www.ofa.org/ed_types.html)


Exercise Induced Collapse (EIC)

Dogs affected with EIC can tolerate mild to moderate exercise, but 5 to 20 minutes of strenuous exercise with extreme excitement induces weakness and then collapse. Severely affected dogs may collapse whenever they are exercised to this extent – other dogs only exhibit collapse episodes sporadically.

The first thing noted during an episode is usually a rocking or forced gait. The rear limbs then become weak and unable to support weight. Many affected dogs will continue to run while dragging their back legs. Some of the dogs appear to be uncoordinated, especially in the rear limbs, with a wide-based, long, loose stride rather than the sort stiff strides typically associated with muscle weakness. In some dogs the rear limb collapse progresses to forelimb weakness and occasionally to a total inability to move. Some dogs appear to have a loss of balance and may fall over, particularly as they recover from complete collapse. Most collapsed dogs are totally conscious and alert, still trying to run and retrieve, but as many as 25% of affected dogs will appear stunned or disoriented during the episode.  (http://www.vdl.umn.edu/services-fees/canine-neuromuscular-eic/frequently-asked-questions)

Centronuclear Myopathy

Centronuclear Myopathy (CNM), previously known as HMLR, or Hereditary Myopathy, is an autosomal recessive mutation that causes insufficient muscle function in the Labrador Retriever breed. This is due to the centralisation of the nuclei in muscle fibers, caused by a missense insertion in the PTPLA gene.

Puppies are born apparently normal; however, it quickly becomes evident that there is a problem. The puppy will often not gain weight adequately due to decreased muscle tone in the esophagus. Within 2 to 5 months, the disease has usually progressed to display the full range of symptoms, including a loss of muscle tone and control, an awkward gait, and extreme exercise intolerance. This condition is exacerbated in cold conditions. 

Unfortunately, there is no cure for CNM, as the dog will never develop properly functioning muscle tissue. The dog usually has a normal life span but he will always be plagued with the symptoms of Centronuclear Myopathy.

Centronuclear myopathy is a recessive disorder, meaning that the dog must have two copies (CNM/CNM) of the defective gene to suffer from the disease. A dog can also be a carrier (CNM/n) of this disease, and will not display any symptoms. A carrier dog will pass on the mutation that causes CNM to 50% of it's offspring. If mated with another carrier dog, there is a 25% chance of producing an offspring affected by Centronuclear Myopathy.  (http://www.animalgenetics.us/Canine/Genetic_Disease/CNM.asp)

Genetic Eye Disease - CERF / OFA CAER

There are currently ten disorders for which there is an unequivocal recommendation against breeding in all breeds. These diagnoses are ineligible for OFA Eye Registry certifications.

These are conditions which frequently result in blindness and for which there is definite evidence of heritability in one or more breeds.

*Note: The prudent approach of these disorders is to assume they are hereditary except in cases specifically known to be associated with trauma, other causes of ocular inflammation, specific metabolic diseases or nutritional deficiencies.

  1. Keratoconjunctivitis sicca (KCS) - Breeding is not recommended for any animal demonstrating keratitis consistent with KCS. The prudent approach is to assume KCS to be hereditary except in cases suspected to be non-genetic in origin. See above note.
  2. Cataract - Breeding is not recommended for any animal demonstrating partial or complete opacity of the lens or its capsuleunless the examiner has also checked the space for “significance of above cataract unknown” or unless specified otherwise for the particular breedSee above note.
  3. Lens luxation or subluxation See above note.
  4. Glaucoma See above note.
  5. Persistent hyperplastic primary vitreous (PHPV)
  6. Retinal detachment See above note.
  7. Retinal dysplasia - geographic or detached forms See above note.
  8. Optic nerve coloboma
  9. Optic nerve hypoplasia
  10. Progressive Retinal Atrophy (PRA) - Breeding is not advised for any animal demonstrating bilaterally symmetric retinal degeneration (considered to be PRA unless proven otherwise.(http://www.offa.org/eye_eligibility.html)