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.

Don't be fooled by the Backyard breeders that their Staffords don't suffer from these diseases as ANY Staffords can be affected by these mutant genes, not just show dogs.
Its certainly not worth the risk and its certainly not worth the heartache.  You should only buy from reputable breeders that test their dogs

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) do not be afraid to ask the breeder about their stock, their breeding practices, nor be afraid to ask to see health certificates.

 

L-2-HGA

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-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 carriersThe 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.

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.

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

---

Progressive retinal atrophy, or PRA as it is frequently termed, is a long recognized, hereditary, blinding disorder. It is inherited as a simple autosomal recessive in most breeds.PRA is a disease of the retina. This tissue, located inside the back of the eye, contains specialized cells called photoreceptors that absorb the light focused on them by the eye’s lens, and converts that light, through a series of chemical reactions into electrical nerve signals. The nerve signals from the retina are passed by the optic nerve to the brain where they are perceived as vision. The retinal photoreceptors are specialized into rods, for vision in dim light (night vision), and cones for vision in bright light (day and color vision). PRA usually affects the rods initially, and then cones in later stages of the disease. In human families, the diseases equivalent to PRA (in dogs) are termed retinitis pigmentosa.In all canine breeds PRA has certain common features. Early in the disease, affected dogs are nightblind, lacking the ability to adjust their vision to dim light; later their daytime vision also fails. As their vision deteriorates, affected dogs will adapt to their handicap as long as their environment remains constant, and they are not faced with situations requiring excellent vision. At the same time the pupils of their eyes become increasingly dilated, in a vain attempt to gather more light, causing a noticeable "shine" to their eyes; and the lens of their eyes may become cloudy, or opaque, resulting in a cataract.Diagnosis of PRA is normally made by ophthalmoscopic examination. This is undertaken using an instrument called an indirect ophthalmoscope, and requires dilatation of the dog’s pupil by application of eyedrops. Broadly speaking, all forms of PRA have the same sequence of ophthalmoscopic changes: increased reflectivity (shininess) of the fundus (the inside of the back of the eye, overlain by the retina); reduction in the diameter and branching pattern of the retina’s blood vessels; and shrinking of the optic nerve head (the nerve connecting the retina to the brain). These changes occur in all forms of PRA, but at different times in the different breed-specific forms. Usually by the time the affected dog has these changes there is already significant evidence of loss of vision.

 

---

Distichiasis