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Health:
Sbt health:
L-2-Hydroxyglutaric aciduria 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-hydroxyglutarate is normally metabolised to a-ketoglutarate but in affected dogs it is not, and builds up in the body with devastating results. 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 behavior.
Hereditary Cataract Hereditary cataract in the Staffordshire bull terrier was first reported in the United Kingdom in 1976. The condition is not congenital, so puppies are born with normal eyes, but cataracts begin to appear at a few weeks to months in age, progressing to total cataracts by 2 to 3 years of age. This cataract is always bilateral, symmetrical in the two eyes, and progressive until total with resultant blindness.
Autosomal Recessive Disease Both HC and L-2-HGA are autosomal recessive conditions. This type of disease is caused by a mutation within a single gene located on one of the 38 pairs of autosomes. Mutations causing recessive diseases can be small (for example a single incorrect nucleotide, or the insertion or deletion of a small number of nucleotides) or large (such as the deletion of a large number of nucleotides). Because the mutations are within genes located on the autosomes both males and females suffer from the disease with equal frequency. A dog has to have a mutation in each copy of the gene (i.e. the copy on each of its chromosomes) before it will actually develop symptoms of the disease. This is known as being homozygous for the disease allele. If it has one mutated copy of the gene and one normal copy it will be a carrier of the disease but will never actually develop symptoms. It can, however, pass the mutation onto future generations. For a dog to be affected with an autosomal recessive disease, both its parents have to be either carriers or affected. If two carriers are mated together on average one in four of their offspring will be affected, one in four will be genetically clear and half will be carriers.
Hip Dysplasia
Hip Dysplasia can be common in some larger breeds of dogs, especially Labradors. It is a condition that is often attempted to be bred out of the dogs by responsible dog breeders. Hip Dysplasia usually presents in older dogs, although younger dogs can be affected by this condition as well. There are several options to treat and even try to cure Hip Dysplasia in dogs that may work in some cases. For the most part, this is a deteriorating condition that leads to arthritis as the malformed hips grind against the cartilage and gradually wear it down, causing the inflammation of the hip joints.
Causes
This is an inherited condition that affects certain breeds of dogs more than others. Larger dogs are more prone to this condition than smaller dogs. Despite the fact that since it was first discovered in 1930 breeders have been trying to breed out the condition, it still remains a problem with certain breeds, especially larger hunting dogs such as the Labrador. Dogs with tighter hips have less of a chance of hip dysplasia than dogs with looser hips.
Symptoms
Dog owners may assume that the dog is suffering from arthritis or some other ailment while not suspecting the truth. It is important to have a dog that is exhibiting any signs of hip dysplasia examined by a qualified vet. Some of the symptoms are as follows:
-Unsteady gait -Trouble walking up the stairs -Trouble getting up from a resting position -Limping and whining
A vet will want to do a physical examination of the dog as well as x-rays to check for hip dysplasia. If the condition is found, then the vet will be able to recommend a series of treatments. In some cases, surgery is an option. In others, it is not. Surgery depends on the severity of the situation as well as the age of the dog.
Treatment
Treatment of hip dysplasia in dogs includes some exercise, such as swimming, chiropractic care and also acupuncture. In some rare cases, a hip transplant can be an option when it comes to treating this condition. Anti-inflammatory drugs are also administered for dogs with this condition that can ease the pain.
Prevention
The best prevention for hip dysplasia in dogs is to look for puppies and dogs that do not have loose hips. Purchase your dog from a responsible breeder who is aware of the genetic component of the disease and has bred it out of their litters.
Because dog obesity can also be a factor in hip dysplasia, owners of dogs should make sure that their dogs get a proper diet and the right amount of exercise. Swimming is one of the best exercises for dogs that are prone to this condition because it exercises the joints. Making sure that a dog has adequate rest and is comfortable is also recommended for this condition.
Through proper breeding techniques as well as good diet and exercise, hip dysplasia can be prevented. Those who are interested in purchasing a dog that may be prone to this condition should take a look at the parents of the puppies before they commit to buying the dog. If the condition becomes known after the owner has the dog, exercises and other treatments should be considered. In some cases, a replacement of the hip with an artificial joint may be recommended by the vet.
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Elbow Dysplasia
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Elbow dysplasia is an inherited disease which primarily affects intermediate and large breed dogs. A high incidence of occurrence has been noted in the Bernese Mountain Dog, German Shepherd, Rottweiler, Golden Retriever, and Labrador Retriever. Other breeds affected are the Newfoundland, Saint Bernard, Mastiff, Springer Spaniel, Australian Shepherd , Chow Chow, Shar-Pei, Shetland Sheepdog, and some Terrier breeds. Typically, both elbows are affected. However, unilateral elbow dysplasia is also recognized.
Elbow dysplasia is characterized by varying degrees of elbow incongruity, bony fragments (bone chips), and ultimately, severe arthritic change. The term was introduced to describe generalized osteoarthritis (arthritis) of the elbow joint in which the anconeal process may be ununited, the medial coronoid of the ulna may be fragmented, and osteochondrosis of the humeral condyle may be present. Clinically, the symptoms range from an intermittent lameness in some affected dogs to severe, crippling disease in others.
Development
The elbow joint is composed of three bones (radius, ulna, and humerus) which must all grow together and fit perfectly. The radius is the main weightbearing bone. The ulna serves more as a lever arm for the extensor muscles of the elbow joint. The normal elbow joint is characterized by a smooth transition from the ulnar joint surface to the radius joint surface. The medial coronoid process of the ulna sits level with or slightly below the surface of the radius.
In a dysplastic elbow, the medial coronoid process and the edge of the ulnar surface lie above the level of the adjoining radius, creating a step between the radius and ulna and causing incongruity of the joint. This incongruity alone is often a source of pain and lameness. The height of the step may vary from barely noticeable to a distance of four millimeters. When this occurs, the weightbearing force on the ulna is increased, resulting in excessive pressure on the medial coronoid process. This leads to fragmentation of the coronoid. This usually occurs when the dog is between five and seven months of age. The fragments are often the size of a rice grain or larger. Incomplete fragmentation in the form of cracks or fissures can also occur. A superficial to deeply grooved "kissing lesion" is often present on the humeral articular surface opposite the fragment. A cartilage flap or OCD (osteochondritis dissecans) lesion may also be present. Secondary arthritis becomes evident at six to seven months of age. Compensatory adjustments during growth may occur in some dogs, tending to minimize unequal growth rates between the three bones and moving the ulna distally to better conform to the radius. However, excessive force is then placed on the anconeal process at the top of the ulnar articular surface. This force will cause a failure of ossification and lead to an ununited anconeal process.
The onset of pain usually occurs between four and six months of age and corresponds with the fragmentation of the coronoid, the development of OCD, and/or failure of ossification of the anconeal process. Joint fluid entering through fissures and cracks in the cartilage causes marked pain. The fragments are a constant irritant, causing more pain, a more severe lameness, and more rapid progression of arthritis.
Clinical Signs
Affected dogs are frequently lame or have an abnormal gait. The gait is often characterized by excessive paddling or flipping of the front feet. The animal may either hold the elbows out or tucked in and often stands with the feet rotated outward. Many sit or lie down much of the time or play for shorter periods of time than other dogs of comparable age. They are often described as quiet or even lazy. Frequently, they are stiff when rising and tire easily. Exercise typically makes the lameness worse. In dogs with bilateral elbow dysplasia, the lameness may seem intermittent or shift from one front leg to the other. When both front legs hurt, dogs do not limp constantly. Rather, they shift weight off their elbows by altering their gait and stance. These dogs will only limp when one elbow is more painful than the other. On examination, manipulation of the elbow is often resisted. Swelling and crepitus (grating) may be palpated. The swelling may be worse after exercise. In some cases, the joint will be thickened. Muscle atrophy may also be present.
The diagnosis of elbow dysplasia is made from a combination of clinical signs, palpation of the joints, and radiographs (x-rays). Correct radiograph technique is critical for making the diagnosis. Radiographs will reveal the incongruity of the joint. Sclerosis (increased bone density) of the ulnar notch is evident. OCD lesions and ununited anconeal processes are often evident. While the fragments of the coronoid process cannot readily be seen on x-ray, the coronoid process will be missing. Arthritis is often present and can be mild to severe.
Treatment of elbow dysplasia is often a combination of medical and surgical management. The objectives of therapy are to relieve pain and maintain limb function as well as to keep the dog at as normal an activity level as possible. Surgical removal of the fragments is recommended before the development of severe arthritis occurs. While the choice of surgical technique (arthroscopy or traditional surgery) may vary, the results are similar. Unfortunately, this disease is progressive. Improvement is expected, but not normality. Medical therapy consists of weight control, moderate exercise, and antiinflammatory medications. Each case is evaluated for the degree of discomfort and arthritic change before a final treatment choice is selected.
All immature dogs with fragmentation of the coronoid, OCD, or an ununited anconeal process are surgical candidates. Recent studies suggest that, if an ununited anconeal process is detected early enough, an ulnar osteotomy (cutting the ulna) to relieve the stress may allow the process to unite in a normal fashion. Dogs with mild to moderate incongruity and minimal arthritis have the best prognosis. Even dogs with marked incongruity and large lesions benefit from surgery due to the decrease in pain. Dogs that have a combination of an ununited anconeal process and a fragmented coronoid have a poor prognosis.
Mature dogs with mild to moderate arthritis may also be considered for surgery. The objective is to slow the progression of the arthritic change.
Reference: Wind, A.P., Elbow Dysplasia, Textbook of Small Animal Surgery, pgs. 1964-1975. |
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