We use health testing to make sure we are producing the healthiest puppies possible. These is a list of tests that should be done when breeding Poodles and Doodles.
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.
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 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 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!
Descriptions of these Diseases: Degenerative Myelopathy Canine degenerative myelopathy, also known as chronic degenerative radiculomyelopathy, is an incurable, progressive disease of the canine spinal cord that is similar in many ways to amyotrophic lateral sclerosis (ALS). Onset is typically after the age of 7 years and it is seen most frequently in the German shepherd dog, Pembroke Welsh corgi, and boxer dog, though the disorder is strongly associated with a gene mutation in SOD1 that has been found in 43 breeds as of 2008, including the wire fox terrier, Chesapeake Bay retriever, Rhodesian ridgeback, and Cardigan Welsh corgi. Progressive weakness and incoordination of the rear limbs are often the first signs seen in affected dogs, with progression over time to complete paralysis. Myelin is an insulating sheath around neurons in the spinal cord. One proposed cause of degenerative myelopathy is that the immune system attacks this sheath, breaking it down. This results in a loss of communication between nerves in lower body of the animal and the brain. 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) syndrome is a group of immune-mediated sub-epidermal blistering skin diseases that result from defects in the dermal-epidermal attachment structures and characterized by flaccid bullae that soon rupture, leaving glistening, flat erosions. Although recognized in dogs for many years, until recently, these diseases were group into a category of bullous pemphigoid. In recent years, advanced diagnostic methods have allowed categorization based on immunohistochemistry developments. Epidermolysis bullosa is now categorized depending upon the level of intracutaneous cleavage into three major subgroups: simplex, junctional, and dystrophic epidermolysis bullosa, which contain more than 20 genetically and clinically distinct subtypes. These diseases are an immune-mediated disease directed against junctional basement-membrane laminin, triggered by autoantigens. Although the etiology of these diseases is unknown, a strong genetic predisposition in some breeds suggests a defect in autoantigen regulation. Affected dogs usually present with crusting, ulcerated lesions, alopecia and pigmentation on the face, trunk and extremities, together with dystrophic nails. Bilateral symmetrical erosions and ulcers are often seen affecting several mucous membranes in mucous membrane pemphigoid, the presence of characteristic eosinophil-rich sub-epidermal vesicles in bullous pemphigoid, and blisters and erosions affecting friction areas and footpads in epidermolysis bullosa acquisita. Diagnosis is usually based on histological examination of skin biopsy samples. A differential diagnosis would include dermatomyositis, cutaneous asthenia, ringworm and demodicosis. Successful treatment has been reported with the use of prednisolone, azathioprine, colchicine, intravenous infusion of immunoglobulins and doxycycline-niacinamide combinations[ 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 NEWS-is a recessive developmental brain disease. Affected pups exhibit extreme weakness, and those that survive the first week generally develop progressively worse ataxia, or inability to move properly. This is often accompanied by severe seizures. None have survived to 7 weeks of age. The mutation which causes this disease was identified by a research team at the University of Missouri led by Drs. Gary Johnson, and Dennis O'Brien. The test offered by Vetgen is based on their discovery. Animals with no copies of the mutation (clear), and those with only one copy (carriers) show no signs of the disease. This disease known to affect Standard Poodles. Affected puppies are smaller than litter mates 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. skeletal dysplasia is a general term for a disorder of the development (dysplasia) of bone ("osteo") and cartilage ("chondro"). Osteochondrodysplasias are rare diseases. About 1 in 5,000 babies are born with some type of skeletal dysplasia. Affected dogs typically present at about 3 weeks of age with stunted growth. Puppies often walk differently than unaffected litter mates 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 rib cages.
Progressive Retinal Atrophy – Golden Retriever Type 1 Progressive Retinal Atrophy (PRA) is an inherited disease of the retina (the “film in the camera”) in dogs, in which the rod cells in the retina are programmed to die. PRA occurs in both eyes simultaneously and is nonpainful. There are many different types of inherited retinal degenerative diseases in purebred dogs, and discussing these are beyond the scope of this article. PRA occurs in most breeds of dogs and also occurs in mixed breeds. It is recessively inherited in all breeds studied, with the following exceptions: PRA is dominantly inherited in Golden Retriever and Goldendoodle, and is sex-linked and found primarily in male dogs in Siberian Husky and Samoyed breeds. Because PRA makes rods die, and rods are responsible for vision in dim light (“night vision”), the first clinical signs that the owner often notices are night-blindness (poor vision in dim light) and that the pupils are dilated; owners often notice a “glow” and increased “eye shine” from the eyes. Clinical signs in dogs with PRA vary from the dog first becoming night blind in the early stage of PRA, to the entire visual field in all light levels becoming affected in advanced PRA. In the final stage of PRA, the dog is completely blind. The natural course of the disease, if specific daily antioxidant supplementation is not given, is that all dogs with PRA will become blind within one year of diagnosis. Sadly, some affected dogs are already completely blind by the time a veterinary ophthalmologist first examines them. PRA reduces vision in most affected dogs and cannot be cured, but in the opinion of many veterinary ophthalmologists, including Dr. McCalla, PRA is no longer a hopeless disease that always leads to complete blindness.
Progressive Retinal Atrophy – Golden Retriever Type 2 Progressive retinal atrophy Golden Retriever type 2 (GR2-PRA) is one form of progressive retinal atrophy (PRA) affecting Golden Retrievers. Until now, in Golden Retrievers there have been identified three different forms of PRA caused by 3 different mutations. Progressive retinal atrophy (PRA) comprises autosomal recessively inherited diseases that lead to degeneration of retinal photoreceptor cells in dogs and other pets. There are more than 20 mutations responsible for specific forms of PRA, and some breeds, including Golden Retrievers, can be affected by more than only one form of PRA. Other than that, some forms of PRA are common to multiple dog breeds, while others are recognized in just a single breed. It has been identified in most dog breeds, but also in mixed breed dogs. In general, forms of PRA are characterized by disturbance of dark vision, visual field defects, and abnormalities in the electroretinogram. The electroretinogram (ERG) is a diagnostic test used to measure the electrical activity of cells in the retina in response to a light stimulation. PRA is a progressive disorder and can progress into blindness. It appears in both eyes simultaneously. The age of onset and rate of retinal degeneration varies between the different forms of the conditions. 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.
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’s disease (vWD) is a blood disease caused by a deficiency of von Willebrand Factor (vWF), an adhesive glycoprotein in the blood required for normal platelet binding (i.e., clotting) at the sites of small blood vessel injuries. In addition, vWF is a carrier protein for coagulation Factor VIII (necessary for blood to clot). A lack of vWF impairs platelet stickiness and clumping. Similar to hemophilia in humans, this condition can lead to excessive bleeding following an injury, due to the lack of clotting. VWF is an autosomal (non-sex-linked) trait, which both males and females express and transmit genetically and with equal frequency. The expression pattern of the severe forms (Types 2 and 3 vWD) is recessive while the milder form (Type 1 vWD) appears to be recessive or incompletely dominant. This is the most common hereditary blood clotting disorder in dogs, occurring with more frequency in some breeds, including, standard poodles, and golden retrievers.
Sensory Ataxic Neuropathy Sensory ataxic neuropathy is an autosomal-recessive geneticneurological disorder of Golden Retrievers. The disease is caused by a missense base-pair deletion mutation in the mt tRNATyr gene that results in mitochondrial dysfunction, specifically reduced ATP production in isolated muscle mitochondria. Affected dogs are usually young (under 6 months of age) and present with slowly progressive postural reaction deficits and reduced or absent spinal reflexes. Clinical pathology, radiography, and electrophysiology of motor systems are frequently within reference values. Electrophysiological examination usually reveals reduced conduction velocities of nerve impulses in sensory nerves. Histopathology of muscle tissues are usually unremarkable although histochemical staining for cytochrome c oxidase and succinate dehydrogenase shows marked reduction in their activity in affected dogs. A differential diagnosis would include ceroid lipofuscinosis and pyruvate dehydrogenase phosphatase 1 deficiency. There is no known treatment for this condition and approximately 50% of affected dogs are euthanized before three years of age.
In dogs, hip dysplasia is an abnormal formation of the hip socket that, in its more severe form, can eventually cause crippling lameness and painful arthritis of the joints. It is a genetic (polygenic) trait that is affected by environmental factors. It is common in many dog breeds, particularly the larger breeds, and is the most common single cause of arthritis of the hips.
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: Heart failure is a clinical syndrome that occurs secondary to severe, overwhelming cardiac disease. It occurs because the heart is no longer able to maintain normal venous/capillary pressures, cardiac output, and/or systemic blood pressure. It is most commonly caused by a chronic disease that results in a severe decrease in myocardial contractility, severe regurgitation or shunting, or severe diastolic dysfunction. However, it is common to have all three abnormalities present simultaneously (but with one predominating). By far, the most common clinical manifestations seen with heart failure are directly due to edema and effusion (congestive or backward heart failure). Much less commonly, animals present because of signs referable to a decrease in cardiac output (forward heart failure). Very rarely, they present in cardiogenic shock (low blood pressure due to decreased cardiac output). This occurs because the cardiovascular system operates under a system of priorities. Its three primary functions are to maintain a normal blood pressure and normal cardiac output, both at a normal venous/capillary pressure. When the system is overwhelmed, it allows venous/capillary pressure to increase first (and so allows edema or effusion to form) and then allows cardiac output to fall. Only after cardiac output has fallen remarkably does cardiogenic shock occur. In acute heart failure, before any compensation has occurred, cardiogenic shock may predominate, but even in this situation, acute chordal rupture is the most common cause of acute heart failure in animals and results in an increased left atrial pressure and thus pulmonary edema.
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