It takes two years before a dog can be vetted for breeding. Sometimes, an ethical breeder will invest in all the health testing recommended by the Breed Club and the dog fails one or more core areas and must be pulled from breeding stock. In addition, something may show up in a puppy in spite of complete health testing of the sire and/or dam and must also be pulled. This may happen to the best of us. There is no sure-fire way to guarantee we will come up with the perfect breeding dogs when we start out, and it can be devastating to an ethical breeder to have to pull one or more dogs, but this is so important when we commit to better the breed – the only reason to breed.
The OFA, working with the breed’s parent club, recommends the following basic health screening tests for all breeding stock. Dogs meeting these basic health screening requirements will be issued Canine Health Information Center (CHIC) numbers. For CHIC certification, all results do not need to be normal, but they must all be in the public domain so that responsible breeders can make more informed breeding decisions. For potential puppy buyers, CHIC certification is a good indicator the breeder responsibly factors good health into their selection criteria. The breed-specific list below represents the basic health screening recommendations. It is not all-encompassing. There may be other health screening tests appropriate for this breed. And, there may be other health concerns for which there is no commonly accepted screening protocol available.
No one can predict when or even if a dysplastic dog will start showing clinical signs of lameness due to pain. The severity of the disease can be affected by environmental factors, such as caloric intake or level of exercise. 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 x-ray evidence that are severely lame.
Elbow dysplasia is a general term used to identify an inherited polygenic disease in the elbow. Three specific etiologies make up this disease and they can occur independently or in conjunction with one another. These etiologies include:
Studies have shown the inherited polygenic traits causing these etiologies are independent of one another. Clinical signs involve lameness which may remain subtle for extended periods of time. No one can predict at what age lameness will occur in a dog due to many 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. The range of motion in the elbow is also decreased.
The procedure, which is conducted yearly, involves a careful and comprehensive examination of the eye. To start with, the dog’s pupils are dilated with eye drops. The examiner then illuminates the eye with a penlight to look for any key abnormality.
The eye is then examined in detail using a slit lamp bio-microscope to identify any diminutive anomalies in the lens, cornea, and anterior chamber. During this part of the exam anomalies such as distichia, cataracts, vitreal degenerations, and corneal dystrophy may be noticed.
Lastly, the retina is examined using an ophthalmoscope (usually an indirect ophthalmoscope). This exam provides the examiner with a lucid view of all the parts of the retina. The indirect ophthalmoscope device offers the veterinarian proper optics and a light source. Problems such as Progressive Retinal Atrophy, Retinal Dysplasia, optic nerve hypoplasia, choroidal hypoplasia may be revealed during this part of the examination.
If any problems are identified during these examinations, they are recorded in an official CERF form by the Ophthalmologist and sent to CERF for research record keeping and certification by the breeder or owner of the dog.
Congenital or advanced Cardiac Exam at 12 months or older, with an exam by a cardiologist.
Purpose: To gather data regarding heart diseases in dogs, and to identify dogs that are phenotypically normal prior to use in a breeding program. For the purposes of the registry, a phenotypically normal dog is defined as:
The OFA maintains two separate and distinct cardiac databases: The Congenital Cardiac Database and the Advanced Cardiac Database.
Congenital heart disease in dogs is a malformation of the heart or great vessels. The lesions characterizing congenital heart defects are present at birth 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. The most common congenital cardiovascular defects can be grouped into several anatomic categories. These anatomic diagnoses include:
Each dog is to be examined and classified by a veterinarian with expertise in the recognition of canine heart disease, in accordance with procedures outlined in The Cardiac Exam section.
Aliases: Canine degenerative myelopathy, DM
Degenerative Myelopathy caused by the Mutation of the SOD1 gene is an inherited neurologic disorder of dogs. This mutation is found in many breeds of dogs, 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 the 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.
Aliases: GR-PRA1, GR1-PRA
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 the 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.
Aliases: GR-PRA2, GR2-PRA
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 the 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.
Aliases: PRA-PRCD, PRCD
Progressive retinal Atrophy, progressive Rod-cone degeneration (PRA-prcd) is a late-onset, inherited eye disease affecting Golden Retrievers. PRA-prcd occurs because 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 the 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 like PRA-prcd. Genetic testing may help clarify if a dog is affected with PRA-prcd or another inherited condition of the eye.
The neuronal ceroid-lipofuscinoses (NCLs) are a class of inherited neurological disorders that have been diagnosed in dogs, humans, cats, sheep, goats, cynomolgus monkeys, cattle, horses, and lovebirds. Among dogs, NCL has been reported in many breeds, including English Setters, Tibetan Terriers, American Bulldogs, Dachshunds, Polish Lowland Sheepdogs, Border Collies, Dalmatians, Miniature Schnauzers, Australian Shepherds, Australian Cattle Dogs, Golden Retrievers, and other breeds. NCL is almost always inherited as an autosomal recessive trait.
All of the NCLs have two things in common: pathological degenerative changes occur in the central nervous system, and nerve cells accumulate material that is fluorescent when examined under blue or ultraviolet light. Although neurological signs are always present in canine NCL, these signs vary between breeds and can overlap with signs present in other neurological disorders. Until the gene defect responsible for NCL has been identified for a particular breed, a definitive diagnosis can only be made upon microscopic examination of nervous tissues at necropsy. Currently, we offer the DNA test for Lipofuscinoses in the American Bulldog (OFA Test Code LAM), the Golden Retriever (OFA Test Code CL5), and the Tibetan Terrier (OFA Test Code LTT).
Researchers at the University of Missouri-Columbia College of Veterinary Medicine are working to identify the mutation responsible for NCL in each breed where NCL occurs so that the disease can be diagnosed, and carriers can be identified based on a DNA-based test. The first step in identifying potentially affected dogs is for the owner or veterinarian to recognize signs that may be indicative of NCL and bring these dogs to our attention.
In Golden Retrievers this neurologic disease becomes apparent at approximately 13 months of age. Often the first sign of the disease is a subtle loss of coordination that is more apparent when the dog is excited. The extent of the incoordination gradually increases. The dog may begin pacing or circling when 15 months old and seizures often start before 18 months of age. Visual impairment and behavioral changes also start at that time. The neurologic deficiencies slowly but relentlessly increase and affected Golden Retrievers are often euthanized due to deteriorating quality of life when 30-to-35 months old.
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