Stafford Health Issues
Please find below some health issues that affect some Staffords, Bonnie has been tested for L2-HGA and is clear. She has also been tested for Hereditary Cataracts and is also clear. Crash and Summah are both clear by parentage as both their parents have been tested and are clear. These results will ensure that any pups bred from my kennels will be clear by parentage with a copy of their certificates supplied. Tilly and Kobi also hold certificates to be shown they are clear of these disease.
HEREDITARY DISEASES
The Staffordshire Bull Terrier, whilst a robust and generally healthy breed, can suffer from harmful and detrimental genetic diseases. Responsible breeders, with the support of the ANKC and other breeders, are attempting to selectively breed out these hereditary afflictions.
When purchasing a Staffordshire Bull Terrier from registered breeders (unfortunately not all breeders are registered with the ANKC, and generally refrain from health testing breeding stock, even some who are registered do not care for the idea of health screening) do not be afraid to ask the breeder about their stock, their breeding practices, nor be afraid to ask to see healthcertificates.
When purchasing a Staffordshire Bull Terrier from registered breeders (unfortunately not all breeders are registered with the ANKC, and generally refrain from health testing breeding stock, even some who are registered do not care for the idea of health screening) do not be afraid to ask the breeder about their stock, their breeding practices, nor be afraid to ask to see healthcertificates.
L2-Hga
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.
The test is available now and information on submitting samples is given below.
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. Courtesy AHT
Hereditary Cataracts (also called Juvenile Cataracts)
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.
The test is available now and information on submitting samples is given below.
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 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. Courtesy AHT
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.
The test is available now and information on submitting samples is given below.
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 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. Courtesy AHT
Distichiasis
Sometimes the condition is referred to as a double row of eyelashes, for extra hairs arise from the edge of the eyelid to rub against the corneal surface. The effects are variable and mild irritation to corneal ulceration will be seen. Treatment is extremely difficult and invariably involves surgery to remove the hair roots permanently. Plucking out the offending hairs is useful, but requires the maximum cooperation of the patient!
Of course it is followed by hair regrowth, and many surgical techniques have been invented to remove the roots. Even then success is difficult to achieve, and the dog may have to suffer this condition throughout its life. It is the most common eye defect found in the Stafford in .
Of course it is followed by hair regrowth, and many surgical techniques have been invented to remove the roots. Even then success is difficult to achieve, and the dog may have to suffer this condition throughout its life. It is the most common eye defect found in the Stafford in .
Entropian
Primarily an inherited condition. It is due to an excess of eyelid tissue, or a small eye, or both, the result being that a varying amount of hair-covered eyelid can turn in to rub directly against the cornea or conjunctiva, or both.
It is usually extremely painful, and the damage caused to the cornea can render the eye blind. Most dogs are affected by six months of age and in some the signs of the problem (excessive blinking and a wet face) may be seen within the first month of life.
Occasionally the condition is self-correcting as the puppy grows, but in the vast majority of affect dogs surgery is necessary to turn the eyelid away from the surface of the eye. Usually such surgery is successful, but it is much better that, as with the other inherited eyelid defects, breeders try to avoid producing this condition in their stock.
It is usually extremely painful, and the damage caused to the cornea can render the eye blind. Most dogs are affected by six months of age and in some the signs of the problem (excessive blinking and a wet face) may be seen within the first month of life.
Occasionally the condition is self-correcting as the puppy grows, but in the vast majority of affect dogs surgery is necessary to turn the eyelid away from the surface of the eye. Usually such surgery is successful, but it is much better that, as with the other inherited eyelid defects, breeders try to avoid producing this condition in their stock.
Hip Dysplasia
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. Courtesy OFA
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. Courtesy OFA
PHPV-- Persistent Hyperplastic Primary Vitreous
PHPV is a developmental abnormality of the eye which occurs in the puppy embryo at about 4-5 weeks of age after conception. Blood vessels which help develop the lens of the eye are not reabsorbed as they should be. This results in deposits on the lens which can result in mild vision impairment to severe (blindness) depending on the grade or severity of the condition.
The signs or symptoms are very difficult to pick, impaired vision in young puppies is difficult to pick up, but the condition in its severe form can be diagnosed by a veterinary ophthalmologist as early as 4 weeks of age, although it may be more readily detected when the puppy is older (8-12 weeks).
What treatment is available? This condition is not readily treatable. If the vision impairment is mild, the dog may live a good quality lifestyle by compensating with its acute sense of hearing and smell. Severely affected dogs can undergo specialist ophthalmological surgery but this is extremely delicate (and expensive) surgery with no guarantees of full recovery of vision.
PHPV is a developmental abnormality of the eye which occurs in the puppy embryo at about 4-5 weeks of age after conception. Blood vessels which help develop the lens of the eye are not reabsorbed as they should be. This results in deposits on the lens which can result in mild vision impairment to severe (blindness) depending on the grade or severity of the condition.
The signs or symptoms are very difficult to pick, impaired vision in young puppies is difficult to pick up, but the condition in its severe form can be diagnosed by a veterinary ophthalmologist as early as 4 weeks of age, although it may be more readily detected when the puppy is older (8-12 weeks).
What treatment is available? This condition is not readily treatable. If the vision impairment is mild, the dog may live a good quality lifestyle by compensating with its acute sense of hearing and smell. Severely affected dogs can undergo specialist ophthalmological surgery but this is extremely delicate (and expensive) surgery with no guarantees of full recovery of vision.