Reasons For Health Checks
Here at legend Golden Retrievers we believe that if you don't check a health concern in the breed then you really don't know if you have an issue or not. We check our golden moms and dads for the following Health concerns in the breed. Because the Golden is a popular breed, there is more research available on which things effect this wonderful breed.
We are currently testing our dogs for
HIPS, ELBOWS,HEARTS,EYES,PATELLA,DENTITION,3 types of DNA tests for PRA, ICH, MD. we will only breed normal to normal or normal to a carrier so that our puppies have the best chance possible for a normal non-effected life. there are still things that are out of our control which is why we stand behind our puppies, however we are doing our best to ensure that your puppy is healthy from the start.
Ichthyosis is an autosomal recessive genetic mutation that affects the skin of Golden Retrievers. The mutation prevents the outer layer of the epidermis from forming properly, resulting in skin that becomes darkened and thick and flakes excessively. The name "Ichthyosis" is derived from the Greek word for fish, which describes the skin's resemblance to fish scales. The most common symptom of ICH-A is excessive flaking of the skin. Other symptoms include areas of hardened skin and hyperpigmentation, which may make the skin appear dirty or blackened. Symptoms can be mild or severe. Evidence of the disease may be detected when the dog is still a puppy, but symptoms may take a year or more to develop. Additionally, symptoms can improve or worsen, depending on stress and hormonal cycles. Ichthyosis is generally not dangerous to a dog's health, but can be unsightly, and uncomfortable for the dog. ICH-A is frequently related to other health issues such as yeast overgrowth and fungal infections. An affected dog will usually require more care with special shampoos and treatments. ICH-A is unfortunately quite common in Golden Retrievers, but can be identified with a simple DNA test. An affected dog would need to inherit the mutation from both parents since the mutation is autosomal recessive. Asymptomatic carriers and affected dogs can be identified prior to breeding to avoid producing an affected pup.
Muscular Dystrophy Description:
GRMD is a mutation of the dystrophin gene that causes a deficiency of dystrophin proteins in Golden Retrievers. The lack of dystrophin proteins leads to the progressive degeneration of skeletal and cardiac muscles. The disease is similar to the human form of muscular dystrophy. Symptoms appear relatively quickly, at about six weeks to two months of age. An affected dog will exhibit muscle weakness, difficulty standing or walking normally, and difficulty swallowing, Symptoms can range from relatively mild to severe, but GRMD is generally fatal at about 6 months of age. The GRMD mutation is sex-linked and located on the X chromosome. So while both male and female dogs can be affected, GRMD is mostly a disease related to male Goldens. Females can be carriers of the mutation, however, and will not exhibit any symptoms. DNA testing to identify both male and female carriers is important to remove them from the breeding population.
Progressive Retinal Atrophy or PRA Description:
Progressive degeneration, or PRA-prcd, is a form of Progressive retinal Atrophy (PRA) in which the cells in the retina of a dog degenerate and die. PRA is the dog equivalent of retinitis pigmentosa in humans. Most affected dogs will not show signs of vision loss until 3-5 years of age. Complete blindness can occur in older dogs. Progressive Rod-Cone Degeneration is a form of PRA known to affect over 40 different breeds. The retina is a membrane located in the back of the eye that contains two types of cells known as photoreceptors. These cells take light coming into the eyes and relay it back to the brain as electrical impulses. These impulses are interpreted by the brain as vision. In dogs suffering from PRA-prcd, the photoreceptors begin to degenerate, causing an inability to interpret changes in light resulting in loss of vision. Rod cells, which are normally function in low-light, begin to degenerate first, leading to night-blindness. The cone cells, which normally function in bright-light or daytime conditions, will deteriorate next. This often leads to complete blindness over time. PRA-prcd is inherited as an autosomal recessive disorder. A dog must have two copies of the mutated gene to be affected by PRA. A dog can have one copy of the mutation and not experience any symptoms of the disease. Dogs with one copy of the mutation are known as carriers, meaning that they can pass on the mutation to potential offspring. If they breed with another carrier, there is a 25% chance that the offspring can inherit one copy of the mutated gene from each parent, and be affected by the disease.
Congenital Cardiac Disease and the OFA
Congenital heart diseases in dogs are malformations 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. Developmental Inherited Cardiac Diseases (SAS and Cardiomyopathy) At this time inherited, developmental cardiac diseases like subaortic stenosis and cardiomyopathies are difficult to monitor since there is no clear cut distinction between normal and abnormal. The OFA will modify the congenital cardiac database when a proven diagnostic modality and normal parameters by breed are established. However at this time, the OFA cardiac database should not be considered as a screening tool for these diseases. Purpose of the OFA Cardiac Database To gather data regarding congenital heart diseases in dogs and to identify dogs which are phenotypically normal prior to use in a breeding program. For the purposes of the database, a phenotypically normal dog is defined as: 1. One without a cardiac murmur -or- 2.One with an innocent heart murmur that is found to be otherwise normal by virtue of an echocardiographic examination which includes Doppler echocardiography
Types The Three Faces of 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.
Eye Certification Registry
Overview An eye examination The purpose of the OFA Eye Certification Registry (CAER) is to provide breeders with information regarding canine eye diseases so that they may make informed breeding decisions in an effort to produce healthier dogs. CAER certifications will be performed by board certified (ACVO) veterinary ophthalmologists. Regardless of whether owners submit their CAER exam forms to the OFA for “certification,” all CAER exam data is collected for aggregate statistical purposes to provide information on trends in eye disease and breed susceptibility. Clinicians and students of ophthalmology as well as interested breed clubs and individual breeders and owners of specific breeds will find this useful. Portions of the material above have been reprinted with permission of the American College of Veterinary Ophthalmologists from the publication “Ocular Conditions Presumed to be Inherited in Purebred Dogs”, 5th Edition, 2010, produced by the Genetics Committee of the American College of Veterinary Ophthalmologists, © American College of Veterinary Ophthalmologists.
Severe Hip DysplasiaHip 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.
The patella, or kneecap, is part of the stifle joint (knee). In patellar luxation, the kneecap luxates, or pops out of place, either in a medial or lateral position.
Bilateral involvement is most common, but unilateral is not uncommon. Animals can be affected by the time they are 8 weeks of age. The most notable finding is a knock-knee (genu valgum) stance. The patella is usually reducible, and laxity of the medial collateral ligament may be evident. The medial retinacular tissues of the stifle joint are often thickened, and the foot can be seen to twist laterally as weight is placed on the limb.
Also called genu valgum, this condition is usually seen in the large and giant breeds. A genetic pattern has been noted, with Great Danes, St. Bernards, and Irish Wolfhounds being the most commonly affected. Components of hip dysplasia, such as coxa valga (increased angle of inclination of the femoral neck) and increased anteversion of the femoral neck, are related to lateral patellar luxation. These deformities cause internal rotation of the femur with lateral torsion and valgus deformity of the distal femur, which displaces the quadriceps mechanism and patella laterally.
Bilateral involvement is most common. Animals appear to be affected by the time they are 5 to 6 months of age. The most notable finding is a knock-knee (genu valgum) stance. The patella is usually reducible, and laxity of the medial collateral ligament may be evident. The medial retinacular tissues of the stifle joint are often thickened, and the foot can often be seen to twist laterally as weight is placed on the limb.
Idiopathic Hypothyroidism (Thyroid)
Chow ChowAutoimmune thyroiditis is the most common cause of primary hypothyroidism in dogs. The disease has variable onset, but tends to clinically manifest itself at 2 to 5 years of age. Dogs may be clinically normal for years, only to become hypothyroid at a later date. The marker for autoimmune thyroiditis, thyroglobulin autoantibody formation, usually occurs prior to the occurrence of clinical signs. Therefore, periodic retesting is recommended.
The majority of dogs that develop autoantibodies have them by 3 to 4 years of age. Development of autoantibodies to any time in the dog’s life is an indication that the dog, most likely, has the genetic form of the disease. Using today's technology only a small fraction of false positive tests occur.
As a result of the variable onset of the presence of autoantibodies, periodic testing will be necessary. Dogs that are negative at 1 year of age may become positive at 6 years of age. Dogs should be tested every year or two in order to be certain they have not developed the condition. Since the majority of affected dogs will have autoantibodies by 4 years of age, annual testing for the first 4 years is recommended. After that, testing every other year should suffice. Unfortunately, a negative at any one time will not guarantee that the dog will not develop thyroiditis.
The registry data can be used by breeders in determining which dogs are best for their breeding program. Knowing the status of the dog and the status of the dogs lineage, breeders and genetic counselors can decide which matings are most appropriate for reducing the incidence of autoimmune thyroiditis in the offspring.