HEALTH TESTING IS OUR TOP PRIORITY

OFA or PennHIP Evaluation

Hip Dysplasia typically develops because of an abnormally developed hip joint, but can also be caused by cartilage damage from a traumatic fracture. With cartilage damage or a hip joint that isn’t formed properly, over time the existing cartilage will lose its thickness and elasticity. This breakdown of the cartilage will eventually result in pain with any joint movement.

No one can predict when or even if a dysplastic dog will start showing clinical signs of lameness due to pain. 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.

OFA Evaluation

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:

• 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.

A CERF Eye Examination by a boarded ACVO Ophthalmologist annually for the dog's lifetime.

A CERF test is a distinctive eye screening exam that is carried out by Veterinary Ophthalmologists. These individuals are board certified by the American College of Veterinary Ophthalmologists (AVCO).

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 in the 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 a lucid view of all the parts of the retina. The indirect ophthalmoscope device offers the veterinarian with 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 exam by cardiologist.

Purpose: To gather data regarding heart diseases in dogs, and to identify dogs which are phenotypically normal prior to use in a breeding program. For the purposes of the registry, a phenotypically normal dog is defined as:

• One without a cardiac murmur.

• One with an innocent heart murmur that is found to be otherwise normal by virtue of an echocardiographic examination which includes Doppler studies.

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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:

• Malformation of the atrioventricular valves

• Malformation of the ventricular outflow leading to obstruction of blood flow

• Defects of the cardiac septa (shunts)

• Abnormal develop of the great vessels or other vascular structures

• Complex, multiple, or other congenital disorders of the heart, pericardium, or blood vessels

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Examination and Classification
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 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.

Ichthyosis 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.

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 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 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 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.

References

ofa.org and pawprintgenetics.com

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 substantially 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. At this time, 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 on the basis of 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 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.

Recently, an established group of canine skin disease researchers confirmed to the GRCA Health and Genetics committee (H&G) that a different gene can cause a recessive form of ichthyosis in Goldens and that this new ichthyosis causes more clinical signs than GR ICH1.

Clinical signs in affected dogs (those inheriting the gene from both sire and dam) reportedly can include more severe skin disease, chronic skin infections, and stunted growth. Some affected Goldens are euthanized.

Reference

GRCA