Issues
If after careful veterinary examination and xrays, one of these conditions is found, it is recommended by veterinary surgeons that animals should not be used for breeding purposes. Canine Hip Dysplasia This is the most common cause of rear-end lameness in the dog. It occurs almost exclusively in the larger breeds – those weighing more than 35 pounds as adults. The problem lies in the structure of the hip joint. The head of the femur (thigh bone) should sit solidly in the acetabulum (Cup). In hip dysplasia loose ligaments allow the heqd to begin to work free. A shallow acetabulum also predisposes to joint laxity. Finally, the mass or tone of the muscles around the joint socket is an important factor. Tight ligaments, broad pelvis with a well-cupped acetabulum, and a good ration of muscle mass to size of bone, predispose to good hips. The reverse is true of dogs who are likely to develop the disease. Environmental factors, including weight and nutrition of the puppy and rearing practices figure into the final outcome. Hip dysplasia is an heritable condition. It is about twice as common among littermates having dysplastic parent. But even dogs with normal hips can produce dysplastic pups. Some dogs with x-ray evidence of sever hip dysplasia show no clinical signs and the disease goes entirely unsuspected until an x-ray is taken to check for it. Signs first appear during a time of rapid growth (four to nine months). A puppy might show pain in the hip, walk with a limp or swaying gait, bunny hop when he runs, and experience difficulty getting up. Pushing down on the rump often causes his pelvis to drop. If you roll him on his back, his rear legs may resist being spread into a frog-leg position. Canine hip dysplasia is graded under the KC. Hip Dysplasia scheme from the age of 12 months. This should always be undertaken prior to breeding your animals. There are two surgical procedures advocated in the treatment of hip dysplasia 1. Removal of the femoral head (s) and 2. Division of the pectineus muscle. These procedures may relieve pain and improve function in some individuals. It has been shown that repeated selection of normal dogs for breeding stock reduces the incidence of hip dysplasia in a susceptible bloodline. Slipping Kneecap (Patellar Dislocation) Dislocating kneecap can be inherited, or acquired through trauma. It occurs sporadically among Toy breed dogs, although of late has been found in larger breed as well. In dogs the kneecap is a small bone which protects the front of the stifle joint: it is the counterpart of the kneecap in man. It is anchored in place by ligaments, and slides in a groove in the femur. Conditions which predispose to dislocation of the patella are: a shallow groove; weak ligaments; and mal-alignment of the tendons and muscles that straighten the joint. The patella slips inward or outward. The signs of a slipped kneecap are difficulty straightening the knee; pain in the stifle; and a limp. The ti of the hock often points outward and the toes inward (the reverse of cow hocks). The diagnosis is confirmed by manipulating the stifle joint and pushing the kneecap in and out of position. The treatment to repair involves surgery to deepen the groove and/or realign the tendon. Popping Hock (Laxity of the Hock Joint) This condition, which may affect one or both hocks, is due to looseness of supporting structures around the joint. It is more common in large dogs with straight rear-end angulations. Usually it is not painful, but can impair the dog’s drive and agility. In late stages the joint can become arthritic. The diagnosis can be suspected by observing the dog in motion, at which time the hock will appear to give, causing an irregular gait. Manipulation of the joint reveals the lax ligaments. The hock slips out of place (either forward or to the side) when the joint is straightened. Treatment: Early immobilization by splints (or cage rest) may reversed the condition in some young pups. The disease is carried in certain bloodlines. It can be reduced by proper breeding practices. Elbow Dysplasia (Ununited Anconeal Process) The condition is caused by a faulty union of the anconeal process (one of the elbow bones) with ulna. It is of developmental origin. Again it is thought to be inherited. The loose fragment in the elbow acts as an irritant and abrasive arthritis is a common sequel. Pups begin to show lameness in the front leg at about six months of age. Some are unable to bear weight; others limp only when trotting. Characteristically, the elbow is held outward from the chest. Again the most effective treatment is surgical removal of the loose pieces of bone. Separation of Joint Cartilage (Osteochondritis dissecans) Osteochondritis dissecans affects dogs of the large rapidly growing breeds between the ages of four and twelve months. It usually is found in the shoulder joints, but rarely it can affect the hocks or stifles. It is due to a defects in the cartilage overlying the head of one of the long bones. A puppy who jumps down stairs might sustain such an injury. The tendency for cartilage to be easily damaged may be hereditary. Repeated stress to the joint perpetrates the condition. The signs are gradual lameness in a young dog of one of the larger breeds. Pain is present on flexing the joint. X-rays may show fragmentation of the joint cartilage, or a loose piece of cartilage in the joint. Treatment: The condition can be treated by confinement, or by surgical removal of the damaged cartilage. Pain tablets are contraindicated, as they are in most traumatic joint conditions, because they encourage the dog to exercise. Eyelid Rolled Inward (Entropion) This is the most common congenital defect of the eyelids. It may also be caused by injury or long-standing disease of the lids. Some cases are complicated by blepharospasm. Old English Sheepdogs are one of the breeds that is now looked at under the KC BVA Eye Scheme. Most commonly it affects the lower eyelid. The hair on the lower part of the eyelid turns in and rubs against the eye making it red, and sore. The dogs eyes tend to run and you can see the dog rubbing his head along walls and fences to try to stop the irritation. Entropion can be found in the upper lid as well. The condition requires surgical correction. Eye Irritation from Hairs Distichiasis/Ectopic cilia. This is a congenital condition in which an extra row or bunch of lashes grow from the lid margins and rub against the cornea. The irritation may not be severe enough to cause symptoms until the dog is mature. The hairs will need to be burned out with an electric needle or removed by surgery. Again this condition is now being looked at under the ECVO Eye Scheme. As with all eye conditions dogs with this problem should not be used for stud work or bitches used for breeding. Progressive retinal atrophis (PRA) P.R.A. is a common hereditary eye complaint amongst dogs but not so widespread in this breed. However a few cases have been reported and confirmed. The disease is sometimes known as night blindness as this is one of the first symptoms. It is progressive so that the disease will get worse until total blindness occurs. If suspected, cases should be reported toyour veterinarian. Treatment is seldom successful, once detected and confirmed it is necessary to have all your stock tested. Confirmed cases must never be bred from. Primary Ciliary Dyskinesia is a relatively new disease found amongst some OES (approx 15 - 20%). There has been some DNA research done into this disease by Professor Anne Merveille in Belgium. Cerebellar Abiotrophy in OES To understand the diagnosis of cerebellar abiotrophy (CA) in the Old English Sheepdog, you must understand the condition. CA causes a progressive loss of muscular co-ordination. It is not a painful condition, does not cause muscular weakness, and does not affect the mind of the dog. CA is a simple autosomal recessive genetic disorder. This means that for a dog to be affected, both parents have to be a carrier of the defective gene. Carriers do not show signs of the condition, and do not differ from other normal dogs except for their ability to pass the defective gene to approximately half of their offspring. The cerebellum controls muscular co-ordination in the body. CA causes a specific cell, called Purkinje cell, to die off in the cerebellum. The Purkinje cell acts as a connector between several other cells in the cerebellum to control a process called proprioception. This process allows the mind to recognize where your limbs and body are "in space". Because of this process, you close your eyes and touch your nose, because you "know" where your nose and hand are. This process is progressively lost in CA. CA manifests itself as an over and under modulation in muscle activity. Affected dogs cannot smoothly control the rate, force, and range of their movements. This can cause an over-reaching and high stepping gait. When going up and down stairs, they can float their front legs out, because they don't know where their leg is in relationship to the stair. This is a very specific movement for CA. It has caused some owners to question whether their dog may have a problem with vision, which is normal. Affected dogs also often stumble or miss a step with their hind paws. There can also be abnormal body movements of the trunk, with swaying of the pelvic limbs and a characteristic bounce of the hind end. There can also be a mild disturbance of balance in CA, where affected dogs can fall over, but then get right up. All four limbs are affected with CA. The severity of clinical signs is symmetrical between the left and right sides of the body, although the forelimbs or hind limbs may be more significantly affected. There is a great range of severity of affected Old English Sheepdogs. Some can progress in their severity to the point that they fall all the time, while others can remain mildly affected and only show limited signs of in-coordination. Some dogs plateau and their clinical signs can remain static for long periods of time, while others can slowly progress over months to years. CA is a constant condition. Affected dogs always have the disability, though it may not be evident with all motion. Clinical signs of CA are most evident when observing complex movements, such as running and stair walking. Such complex manoeuvres are more than most CA affected dogs can deal with through their ability to concentrate. Some Old English Sheepdogs affected with CA can compensate for the lack of proprioceptive control by watching where they place their feet, and consciously "learning" everyday movements that would be automatic for any other dog. Some dogs that have a specific set of stairs that they use every day, can learn to place one foot at a time and get up and down cleanly. For those dogs, their clinical signs become more evident when they are tired or excited (and can't concentrate as well). For this reason the classical signs of CA may be most evident when running and chasing a ball or doing a "new" set of stairs that the dog may not be used to. Because of the ability for some CA affected dogs to compensate, their clinical signs of in-coordination may appear episodic, rather than constant. If an owner only sees the signs when the dog is running, they may think that the running causes the onset of signs. Together with Dr. Natasha Olby (North Carolina State University) and Dr. Alexander de Lahunta (retired, Cornell University) we have been studying cerebellar abiotrophy in several animals' species and several breeds of dogs. Each breed with CA has the same pathological cause; that being the degeneration of the Purkinje cells of the cerebellum. The dog breeds with the most similar CA presentations as the Old English Sheepdog include the Gordon Setter, Scottish Terrier, American Staffordshire Terrier and Spinone Italiano. All of these breeds show a later onset, slowly progressive form of CA. Each breed has its own specific characteristics of the disorder. In the Gordon Setter, the onset of CA is 4 to 12 months of age, with most owners recognizing the in-coordination by 1 to 3 years of age. The American Staffordshire Terrier has a much later age of onset usually recognized between 3 to 5 years of age. There are Scottish Terriers with CA whose owners believe that they first recognized clinical signs at 5 to 10 weeks of age and some with very mildly affected dogs that did not recognize the clinical signs until 3 - 5 years of age. In the Old English Sheepdog, the clinical signs can be mild and are usually recognized between 1 - 5 years of age. The most definitive diagnosis of CA is through a pathological examination of the brain and cerebellum after death. The degeneration of the Purkinje cells (with the secondary changes that occur due to this degeneration) confirms the pathological diagnosis. Because of the size of the Purkinje cells, their cellular processes (axons and dendrites) and the stimulation of the cells that they connect to, there is a gross reduction in size weight of the cerebellum compared to the rest of the brain in CA affected dogs. The reduction in size of the cerebellum can be measured by magnetic resonance imaging (MRI) in a live dog, and has been used as another diagnostic parameter in CA affected dogs. This was documented in South African CA affected Scottish Terriers in a veterinary journal article. However, at this time, the extent of degeneration that is necessary to cause a measurable gross reduction in the size of the cerebellum has not been established. Because of this an MRI may not be able to diagnose CA in dogs who are young, whose disease process is not longstanding, or whose clinical signs (and therefore the amount of Purkinje cell degeneration) are mild. The criteria for MRI diagnosis in CA affected dogs with different degrees of severity are one aspect of the ongoing CA research. As most Old English Sheepdogs with CA are expected to live a normal lifespan, the majority of CA affected Old English Sheepdogs will receive a clinical diagnosis of the disorder. It would be unfair and wrong to euthanize these special dogs simply to establish a pathological diagnosis. A clinical diagnosis of CA requires documentation of the specific clinical history, progression and neurological signs that are consistent with the condition and that rule out other causes. This can be a confusing process to an owner that does not understand the differences in movement between a dog affected with CA and other dogs whose movement disorders can be due to other causes. Other disorders that can cause clinical signs of an abnormal gait include brain infrctions (encephalitis), toxins, injury, spinal cord disorders, luxating patella's, and other musculoskeletal abnormalities. CA affects all four limbs. The signs are always symmetrical between the left and right sides of the body, although either the forelimbs or the hind limbs may be more severely affected in each dog. This differentiation eliminates most musculoskeletal abnormalities. Spinal cord abnormalities (including "Wobblers" and intervertebral disc disease) cause pain and weakness, as well as either a sinking or stilted gait (depending on the location of the lesion in the spinal cord). Encephalitis and toxins will cause more injury in the brain than just the Purkinje cells and this will be evident in the clinical examination. There are no toxins found to selectively affect just the cerebellar Purkinje cells. Infections and toxins will also present with an acute onset and more rapid progression than seen with CA. These same differences will be evident with a brain injury. The cerebellum is in a protected area of the skull. If this area of the brain were injured, the clinical signs would be representative of more than a pure Purkinje cell degeneration. In addition, all of these conditions are likely to present with asymmetrical clinical signs. A clinical diagnosis of cerebellar abiotrophy is best obtained through a neurological examination by an ACVIM board-certified neurologist, in consultation with Dr.Olby. I also offer a videotape review of dogs suspected of being affected with CA with Dr de Lahunta. In order to make a clinical diagnosis based on videotape. The classical movements that would separate CA from other disorders during a neurological examination need to be present. The clinical history and progression of the clinical signs must also be compatible with CA. Please contact me (Jerold.bell@tufts.edu) if you feel that your dog may be showing signs of CA. The specific neurological movement of CA that must be present on a video tape for clinical diagnosis are best shown when stair walking, and running or chasing a toy off lead. There are several owners who have submitted videotapes of the Old English Sheepdogs that probably have CA. However, a clinical diagnosis has not been offered in these dogs because the confirming and ruling out movements are not present in the video. In these cases, we recommend that the dog be examined by a neurologist. CA is not the most prevalent or most important hereditary condition affecting Old English Sheepdogs. However, it is a condition that is being diagnosed worldwide in the Old English Sheepdog, has a simple autosomal recessive mode of inheritance and has a wide pedigree base that does not preclude any Old English Sheepdog from being affected. With the cooperative efforts of the breeders, owners and researchers we should be able to deal with CA and thus improve this particular health aspect for the Old English Sheepdog Breed. |
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