All of our breeding dogs are health tested. Health testing is one of the tools that we use to help ensure that our puppies are the healthiest possible.
These are the tests that we do here at Kent Family Farms:
For Golden Retrievers:
Degenerative Myelopathy,
Dystrophic Epidermolysis Bullosa,
Ichthyosis,
Progressive Retinal Atrophy - Golden Retriever Type 1,
Progressive Retinal Atrophy - Golden Retriever Type 2,
Progressive Retinal Atrophy, Progressive Rod-Cone Degeneration,
Sensory Ataxic Neuropathy,
Hip Dysplasia,
Elbow Dysplasia,
and Heart Disease.
For Poodles:
Degenerative Myelopathy,
GM2 Gangliosidosis,
Neonatal Encephalopathy with Seizures,
Osteochondrodysplasia,
Progressive Retinal Atrophy,
Progressive Rod-Cone Degeneration,
Von Willebrand disease I,
Von Willebrand disease II,
Hip Dysplasia,
Elbow Dysplasia,
and Heart Disease.
For Goldendoodles:
Degenerative Myelopathy,
Ichthyosis,
Neonatal Encephalopathy with Seizures,
Progressive Retinal Atrophy - Golden Retriever Type 1,
Progressive Retinal Atrophy - Golden Retriever Type 2,
Progressive Retinal Atrophy, Progressive Rod-Cone Degeneration,
Von Willebrand disease I,
Von Willebrand disease II,
Hip Dysplasia,
Elbow Dysplasia,
and Heart Disease.
Note: DM, ICH, NEWS, PRA-1, PRA-2, PRA-PRCD, vWD I and II, OCD, GM2, SAN and DEB are all DNA tests, so we can know with assurance whether or not our puppies will be affected by any of these disorders. Hip Dysplasia, Elbow Dysplasia and Heart disease on the other hand are not as easy to eliminate from a breeding program. Hips and Elbows are checked by taking x-rays of their hips and having them evaluated by a professional, whether that be through Penn Hip, Dr. Wallace or OFA. These are very subjective tests, that can come out with different results depending on who takes the films. They are still useful to eliminate obvious hip issues, but are not the only tool that breeders to use to evaluate a dog hip wise. You can breed two Excellent rated dogs together and get a dysplastic puppy, this is why you should evaluate an entire pedigree for hips, not just the parents. All of our dogs will either have their hips rated and passed or will have atleast 4 generations of all Good and Excellent rated hips. Same goes for Elbows. It is important to know that only 25% of hip dysplasia is genetic, most often it is environmental. This is why it is so important to keep your dogs slim and not overweight! Also, all of our dogs have their heart checked at 8 weeks old and at minumum annually by our vet. This does not eliminate all aspects of heart disease, but it does eliminate any common irregularities.
Descriptions of these Diseases:
Degenerative Myelopathy
Degenerative myelopathy caused by Mutation of the SOD1 gene is an inherited neurologic disorder of dogs. This mutation is found in many breeds of dog, including the golden retriever. While it is not clear for some of the other breeds, golden retrievers are known to develop degenerative myelopathy associated with this mutation. The variable presentation between breeds suggests that there are environmental or other genetic factors responsible for modifying disease expression. The average age of onset for dogs with degenerative myelopathy is approximately nine years of age. The disease affects the White Matter tissue of the spinal cord and is considered the canine equivalent to amyotrophic lateral sclerosis (Lou Gehrig’s disease) found in humans. Affected dogs usually present in adulthood with gradual muscle Atrophy and loss of coordination typically beginning in the hind limbs due to degeneration of the nerves. The condition is not typically painful for the dog, but will progress until the dog is no longer able to walk. The gait of dogs affected with degenerative myelopathy can be difficult to distinguish from the gait of dogs with hip dysplasia, arthritis of other joints of the hind limbs, or intervertebral disc disease. Late in the progression of disease, dogs may lose fecal and urinary continence and the forelimbs may be affected. Affected dogs may fully lose the ability to walk 6 months to 2 years after the onset of symptoms. Affected medium to large breed dogs, such as the golden retriever, can be difficult to manage and owners often elect euthanasia when their dog can no longer support weight in the hind limbs.
Dystrophic Epidermolysis Bullosa
Dystrophic epidermolysis bullosa (DEB) is a hereditary skin disease affecting Golden Retrievers. Clinical signs of DEB are present at birth. Affected dogs have fragile skin that is easily damaged from rubbing or trauma resulting in blisters, ulcers and scarring of the skin. Areas that are most prone to blisters are the face, foot pads, genital areas and ears. In addition, affected dogs will develop blisters and ulcers inside the mouth and in the esophagus. Ulcerations of the skin and mucous membranes are painful and can become infected. Blistering of the skin tends to cease at around 8 months of age however, ulcers of the mouth and esophagus persist into adulthood. Dogs with DEB are often smaller than littermates, likely due to difficulties eating.
Ichthyosis
Ichthyosis (Golden Retriever type) is an inherited condition of the skin affecting Golden Retrievers. The age of onset and severity of disease are highly variable, however most affected dogs present before one year of age with flaky skin and dull hair. Over time the skin develops a grayish color and appears thick and scaly, especially over the abdomen. The symptoms may progress to severe scaling all over the body, may improve with age, or may come and go over the dog’s lifetime. While the prognosis is generally good for affected dogs, they are at increased risk for skin infections.
GM2 Gangliosidosis
GM2 gangliosidosis is an inherited Lysosomal Storage Disorder affecting dogs. Affected dogs have insufficient activity of the Enzyme hexosaminidase B, which is responsible for breaking down specific carbohydrates in the cells. As a result, there is an accumulation of a glycoprotein, GM2 ganglioside, in cells, especially cells of the brain and nervous system. Affected dogs typically present with symptoms of neurologic disease around 9 to 12 months of age. Symptoms include vision loss, difficulties walking, loss of balance, head tremors and vomiting. Once an affected dog begins to show signs of the disease, the disease progression is rapid and dogs usually die between the ages of 18 and 23 months.
Neonatal Encephalopathy with Seizures
Neonatal encephalopathy with seizures is an inherited neurologic disease known to affect Standard Poodles. Affected puppies are smaller than littermates at birth, have difficulty nursing after a few days of life, and often die by 1 week of age. By 3 weeks of age, surviving puppies present with neurologic symptoms including muscle weakness, tremors, inability to walk, wide-based stance and frequent falling. The disease quickly progresses to severe seizures that become non-responsive to treatment. Affected dogs typically die or are euthanized by 7 weeks of age.
Osteochondrodysplasia
Osteochondrodysplasia is an inherited Musculoskeletal disease affecting Standard Poodles. Affected dogs typically present at about 3 weeks of age with stunted growth. Puppies often walk differently than unaffected littermates and stand with their feet turned out and hind legs splayed. Their legs are short and bent with enlarged joints and clubbed feet. They also have flatted rib cages and under bites, which can affect their ability to nurse and breathe. While affected dogs can survive for many years with supportive care, they will develop arthritis and will likely have breathing difficulty due to their deformed ribcages.
Progressive Retinal Atrophy - Golden Retriever Type 1
Progressive retinal Atrophy, golden retriever 1 (GR-PRA1) is a late-onset inherited eye disease affecting golden retrievers. Affected dogs begin showing clinical symptoms related to retinal degeneration between 6 to 7 years of age on average, though age of onset can vary. Initial clinical signs of progressive retinal atrophy involve changes in reflectivity and appearance of a structure behind the Retina called the Tapetum that can be observed on a veterinary eye exam. Progression of the disease leads to thinning of the retinal blood vessels, signifying decreased blood flow to the retina. Affected dogs initially have vision loss in dim light (night blindness) and loss of peripheral vision, eventually progressing to complete blindness in most affected dogs.
Progressive Retinal Atrophy - Golden Retriever Type 2
Progressive retinal Atrophy, golden retriever 2 (GR-PRA2) is a late-onset inherited eye disease affecting golden retrievers. Affected dogs begin showing clinical symptoms related to retinal degeneration at around 4 to 5 years of age on average, though age of onset can vary. Initial clinical signs of progressive retinal atrophy involve changes in reflectivity and appearance of a structure behind the Retina called the Tapetum that can be observed on a veterinary eye exam. Progression of the disease leads to thinning of the retinal blood vessels, signifying decreased blood flow to the retina. Affected dogs initially have vision loss in dim light (night blindness) and loss of peripheral vision, progressing to complete blindness in most affected dogs.
Progressive Retinal Atrophy - Progressive Rod-Cone Degeneration
Progressive retinal Atrophy, progressive Rod-cone degeneration (PRA-prcd) is a late onset, inherited eye disease affecting Golden Retrievers. PRA-prcd occurs as a result of degeneration of both rod and cone type Photoreceptor Cells of the Retina, which are important for vision in dim and bright light, respectively. Evidence of retinal disease in affected dogs can first be seen on an Electroretinogram around 1.5 years of age for most breeds, but most affected Golden Retrievers will not show signs of vision loss until 5 to 6 years of age or later. The rod type cells are affected first and affected dogs will initially have vision deficits in dim light (night blindness) and loss of peripheral vision. Over time affected dogs continue to lose night vision and begin to show visual deficits in bright light. Other signs of progressive retinal atrophy involve changes in reflectivity and appearance of a structure behind the retina called the Tapetum that can be observed on a veterinary eye exam. Although there is individual and breed variation in the age of onset and the rate of disease progression, the disease eventually progresses to complete blindness in most dogs. Other inherited disorders of the eye can appear similar to PRA-prcd. Genetic testing may help clarify if a dog is affected with PRA-prcd or another inherited condition of the eye.
Von Willebrand disease I
Von Willebrand disease I (VWDI) is an inherited bleeding disorder affecting Standard Poodles. Dogs affected with VWDI have less than half of the normal level of von Willebrand coagulation factor (vWf), which is an essential protein needed for normal blood clotting. There is variability in the amount of vWf such that not all dogs with two copies of the Mutation are equally affected. Dogs that have less than 35% of the normal amount of vWf generally have mild to moderate signs of a bleeding disorder. Affected dogs may bruise easily, have frequent nosebleeds, bleed from the mouth when juvenile teeth are lost, and experience prolonged bleeding after surgery or trauma. Less often, the bleeding may be severe enough to cause death. Due to the variable severity of the disorder, affected dogs may not be identified until a surgery is performed or trauma occurs at which time excessive bleeding is noted. Veterinarians performing surgery on known affected dogs should have ready access to blood banked for transfusions. Most dogs will have a normal lifespan with this condition despite increased blood clotting times.
Von Willebrand disease II
Von Willebrand disease type II (VWDII) is an inherited bleeding disorder affecting dogs. Dogs affected with VWDII have decreased levels and abnormal function of von Willebrand coagulation factor (vWf), which is an essential protein needed for normal blood clotting. Affected dogs generally have moderate to severe signs of a bleeding disorder. Affected dogs may bruise easily, have frequent nosebleeds, bleed from the mouth when juvenile teeth are lost and experience prolonged bleeding after surgery or trauma. The bleeding may be severe enough to cause death. Due to variable severity of the disorder, affected dogs may not be identified until a surgery is performed or trauma occurs at which time excessive bleeding is noted. Veterinarians performing surgery on known affected dogs should have ready access to blood banked for transfusions. Dogs can have a normal lifespan with this condition although they are susceptible to life-threatening bleeding with an accidental injury or any surgical procedure.
Sensory Ataxic Neuropathy
Sensory ataxic neuropathy is an inherited neurologic condition affecting Golden Retrievers. Affected dogs typically present between 2 to 8 months of age with signs of neurologic disease. Symptoms include a lack of muscle coordination, abnormal gait and difficulty balancing especially affecting the hind limbs. Muscle mass appears normal and the condition does not appear to be painful. Although the disease progresses slowly, dogs are often humanely euthanized before three years of age.
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.
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:
Pathology involving the medial coronoid of the ulna (FCP)
Osteochondritis of the medial humeral condyle in the elbow joint (OCD)
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.
Heart Disease:
Congenital heart disease in dogs are malformations of the heart or great vessels. The lesions characterizing congenital heart defects are present at brith and may develop more fully during perinatal and growth periods. Many congenital heart defects are thought to be genetically transmitted from parents to offspring; however, the exact modes of inheritance have not been precisely determined for all cardiovascular malformations. All of our breeding dogs are checked for Heart Murmurs prior to breeding by our veterinarian. We do not breed dogs with Heart murmurs, not even an innocent heart murmur as there is too much unknown about inheritance of cardiac disease.
Health Testing
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