Genetically clear of L2-HGA og HC. These diseases are breed specific, affected dogs should therefore not be used in breeding programs.  L-2-HGA (L-2-hydroxyglutaric aciduria) in Staffordshire Bull Terriers is a neurometabolic disorder characterised by elevated levels of L-2-hydroxyglutaric acid in urine, plasma and cerebrospinal fluid. L-2-HGA affects the central nervous system, with clinical signs usually apparent between 6 months and one year (although they can appear later). Symptoms include epileptic seizures, "wobbly" gait, tremors, muscle stiffness as a result of exercise or excitement and altered behaviour. The mutation, or change to the structure of the gene, probably occurred spontaneously in a single dog but once in the population has been inherited from generation to generation like any other gene. The disorder shows an autosomal recessive mode of inheritance: two copies of the defective gene (one inherited from each parent) have to be present for a dog to be affected by the disease. Individuals with one copy of the defective gene and one copy of the normal gene - called carriers - show no symptoms but can pass the defective gene onto their offspring. When two apparently healthy carriers are crossed, 25% (on average) of the offspring will be affected by the disease, 25% will be clear and the remaining 50% will themselves be carriers. The mutation responsible for the disease has recently been identified at the Animal Health Trust. Using the information from this research, we have developed a DNA test for the disease. This test not only diagnoses dogs affected with this disease but can also detect those dogs which are carriers, displaying no symptoms of the disease but able to produce affected pups. Carriers could not be detected by the tests previously available, which involved either a blood or urine test detecting elevated levels of L-2-hydroxyglutarate or magnetic resonance imaging. Under most circumstances, there will be a much greater number of carriers than affected animals in a population. It is important to eliminate such carriers from a breeding population since they represent a hidden reservoir of the disease that can produce affected dogs at any time. Breeders will be sent results identifying their dog as belonging to one of three categories: CLEAR: the dog has 2 copies of the normal gene and will neither develop L-2-HGA, nor pass a copy of the L-2-HGA gene to any of its offspring. CARRIER: the dog has one copy of the normal gene and one copy of the mutant gene that causes L-2-HGA. It will not develop L-2-HGA but will pass on the L-2-HGA gene to 50% (on average) of its offspring. AFFECTED: the dog has two copies of the L-2-HGA mutation and is affected with L-2-HGA. It will develop L-2-HGA at some stage during its lifetime, assuming it lives to an appropriate age. Carriers can still be bred to clear dogs. On average, 50% of such a litter will be clear and 50% carriers; there can be no affecteds produced from such a mating. Pups which will be used for breeding can themselves be DNA tested to determine whether they are clear or carrier.  Hereditary Cataract in Staffordshire Bull Terriers has been recognised as an inherited condition since the late 1970’s. Affected dogs develop cataracts in both eyes at an early age. The condition is not congenital, so the lenses are normal at birth but cataracts appear at a few weeks to months in age, progressing to total cataract (and resulting blindness) by 2 to 3 years of age. The mutation, or change to the structure of the gene, probably occurred spontaneously in a single dog but once in the population has been inherited from generation to generation like any other gene. The disorder shows an autosomal recessive mode of inheritance: two copies of the defective gene (one inherited from each parent) have to be present for a dog to be affected by the disease. Individuals with one copy of the defective gene and one copy of the normal gene - called carriers - show no symptoms but can pass the defective gene onto their offspring. When two apparently healthy carriers are crossed, 25% (on average) of the offspring will be affected by the disease, 25% will be clear and the remaining 50% will themselves be carriers. The mutation responsible for the disease has recently been identified at the Animal Health Trust. Using the information from this research, we have developed a DNA test for the disease. This test not only diagnoses dogs affected with the disease but can also detect those dogs which are carriers, displaying no symptoms of the disease but able to produce affected pups. Under most circumstances, there will be a much greater number of carriers than affected animals in a population. It is important to eliminate such carriers from a breeding population since they represent a hidden reservoir of the disease that can produce affected dogs at any time. CLEAR: the dog has 2 copies of the normal gene and will neither develop Hereditary Cataract, nor pass a copy of the Hereditary Cataract gene to any of its offspring. CARRIER: the dog has one copy of the normal gene and one copy of the mutant gene that causes Hereditary Cataract. It will not develop Hereditary Cataract but will pass on the Hereditary Cataract gene to 50% (on average) of its offspring. AFFECTED: the dog has two copies of the Hereditary Cataract mutation and is affected with Hereditary Cataract. It will develop Hereditary Cataract at some stage during its lifetime, assuming it lives to an appropriate age. Carriers can still be bred to clear dogs. On average, 50% of such a litter will be clear and 50% carriers; there can be no affecteds produced from such a mating. Pups which will be used for breeding can themselves be DNA tested to determine whether they are clear or carrier.  This is another inherited cataract, although it is a much more complex condition and it is much more difficult to tell how it is inherited in pups. During a puppy's development, certain blood vessels are needed to help develop the eye. In 'normal' pups, these blood vessels disappear after they are no longer needed (usually within a few weeks during development) in puppies with PHPV the vessels don't disappear and can cause eye problems. PHPV is congenital (this means that it will be present at birth) and can be detected in puppies as young as 6 weeks old. The condition is not progressive – this means that once it's detected and manifests itself it will not get worse as the puppy grows older. Dogs can be affected very mildly or quite severely, and if it is present in a breeding dog, there is no way to know how badly pups will be affected in a litter. If the Dam or Sire has mild PHPV the pups could potentially have a much worse strain of the illness. This is why it is essential to ensure that all breeding dogs are screened for the illness along with HC and L2–HGA. Screened parents will have certificates and again pups can have a clear status added to their KC papers, if both adults are clear and are registered with the Kennel club.  Elbow dysplasia is the term for an elbow joint that is malformed on X-rays. The mechanism of the malformation is unclear but it may be due to differences in the growth rates of the three bones that make up the elbow joint, particularly the humerus and ulna. In mildly affected dogs the only consequence may be arthritis. In more severely affected dogs, osteochondritis dissecans (OCD), fragmented medial coronoid processes and united anconeal processes can result from the stress in the joint. Some vets think that these problems may not be secondary but may actually be the primary problems and that the bone changes occur as a result of them. It is difficult to be sure but there does appear to be measurable differences in bone growth in dogs that have elbow dysplasia. There are a number of changes visible on X-rays and the OFA does evaluate X-rays for evidence of elbow dysplasia. Due to the number of possible complications, it is hard to make predictions about how elbow dysplasia will affect a dog. If it can be identified at a young age before changes are severe, surgical correction has a reasonably good success rate. Once severe changes set in, it is much harder to prevent subsequent arthritic changes. Most dogs with this condition eventually become lame and the lameness can be very severe in some dogs, even to the point of disuse of one leg or severe difficult getting up and walking even short distances. Treatment consists of surgical correction of whatever complications are present, if possible. Medical management using aspirin or other anti-inflammatory medications is helpful. Weight control is very important over the long term for success of either surgical or medical management of this condition.  To understand hip dysplasia we must have a basic understanding of the joint that is being affected. The hip joint forms the attachment of the hind leg to the body and is a ball and socket joint. The ball portion is the head of the femur while the socket (acetabulum) is located on the pelvis. In a normal joint the ball rotates freely within the socket. To facilitate movement the bones are shaped to perfectly match each other; with the socket surrounding the ball. To strengthen the joint, the two bones are held together by a strong ligament. The ligament attaches the femoral head directly to the acetabulum. Also, the joint capsule, which is a very strong band of connective tissue, encircles the two bones adding further stability. The area where the bones actually touch each other is called the articular surface. It is perfectly smooth and cushioned with a layer of spongy cartilage. In addition, the joint contains a highly viscous fluid that lubricates the articular surfaces. In a dog with normal hips, all of these factors work together to cause the joint to function smoothly and with stability. Hip dysplasia is associated with abnormal joint structure and a laxity of the muscles, connective tissue, and ligaments that would normally support the joint. As joint laxity develops, the articular surfaces of the two bones lose contact with each other. This separation of the two bones within the joint is called a subluxation, and this causes a drastic change in the size and shape of the articular surfaces. Most dysplastic dogs are born with normal hips but due to their genetic make-up (and possibly other factors) the soft tissues that surround the joint develop abnormally causing the subluxation. It is this subluxation and the remodeling of the hip that leads to the symptoms we associate with this disease. Hip dysplasia may or may not be bilateral; affecting both the right and/or left hip. Dogs of all ages are subject to hip dysplasia and the resultant osteoarthritis. In severe cases, puppies as young as five months will begin to show pain and discomfort during and after exercise. The condition will worsen until even normal daily activities are painful. Without intervention, these dogs may eventually be unable to walk. In most cases, however, the symptoms do not begin to show until the middle or later years in the dog's life. The symptoms are similar to those seen with other causes of arthritis in the hip. Dogs often walk or run with an altered gait. They may resist movements that require full extension or flexion of the rear legs. Many times, they run with a 'bunny hopping' gait. They will show stiffness and pain in the rear legs after exercise or first thing in the morning. They may also have difficulty climbing stairs. In milder cases dogs will warm-up out of the stiffness with movement and exercise. Some dogs will limp and many will become less willing to participate in normal daily activities. Many owners attribute the changes to normal aging but after treatment is initiated, they are surprised to see a more normal and pain-free gait return. As the condition progresses, most dogs will lose muscle tone and may even need assistance in getting up.  A beautiful dog is a pleasure to the eye, but even more important is the knowledge that You are sharing Your everyday life with a dog that is harmonious and well-functioning. In DKK they are working to get a better insight in the dogs mental characteristics. One knows that the mentality of a dog is hereditary such as coat color, height and f.ex. positioning of the ears. The mental specification is therefore an important tool for the breeder who wants to know wich dog is best suited for breeding. The purpose of mental testing is - to give the special clubs a tool for working with breed profiling. - to give breeders a tool to pick right breeding dog. - to give dog owners better insight in their dogs characteristics. In DKKs mental description they use testmodels that in a large degree seperate the dogs congenital behaviour from the learned and trained. Dogs can be mentally tested from the age of ten months. All test results are registered, but only results from dogs in the age span 10 months to 24 months are entered in the calculation of different statistics for the breed in question. All breeds can be tested, as long as there is a profile made that describes which trades are desired. That means a profile that describes a dog that shows the ideal mentality for that breed. |
