THE STAFFORDSHIRE BULL TERRIER


                                                        IS A ROBUST AND GENERALLY HEALTHY BREED OF DOG,

 

 

BUT LIKE ANY BREED, CAN SUFFER FROM HARMFUL AND DAMAGING DISEASES.

 

L2-HGA

L2-HGA(L-2-HYDROXYGLUTARIC ACIDURIA) IN STAFFORDSHIRE BULL TERRIERS IS A NEUROMETABOLIC DISORDER CHARACTERISED BY ELEVATED LEVELS OF L-2 HYDROXYGLUTARIC ACID IN THE URINE, PLASMA AND CEREBROSPINAL FLUID.
THIS HEREDITORY DISEASE AFFECTS THE CENTRAL NERVOUS SYSTEM, WITH CLINICAL SIGNS USUALLY APPARENT BETWEEN 6-12MONTHS (CAN APPEAR LATER). SYSTOMS INCLUDE EPILEPTIC SIEZURES,"WOBBLY" GAIT, TREMORS, MUSCLE STIFFNESS AS A RESULT OF EXERCISE OR EXERCISE AND ALTERED BEHAVIOUR.
THE MUTATION, OR CHANGE TO THE STRUCTURE OF THE GENE, PROBABLY OCCURED SPONTANEOUSLY IN A SINGLE DOG BUT ONCE IN THE POPULATION HAS BEEN INHEREDITED 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 FORM EACH PARENT) HAVE TO BE PRESENT FOR A DOG TO BE AFFECTED BY THE DISEASE.
INDIVIDUALS WOTH 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 APPENTLY HEALTHY CARRIERS ARE CROSSED, 25%(ON AVERAGE) OF THE OFFSPING WILL BE AFFECTED BY THE DISEASE, 25% WILL BE CLEAR AND THE REMAINING 50% WILL THEMSELVES BE CARRIERS.
THE ANIMAL HEALTH TRUST HAS RECENTLY IDENTIFIED  THE MUTATION RESPONSIBLE FOR THIS DISEASE AND HAS DEVELOPED  A DNA TEST WHICH DIOGNOSES DOGS THAT ARE AFFECTED WITH THIS DISEASE AND ALSO DOGS THAT ARE CARRIERS.
UNDER MOST CIRCUMSTANCES, THERE WILL BE A HIGHER NUMBER OF CARRIERS THAN THOSE THAT ARE AFFECTEDIN A POPULATION. IT IS IMPORTANT TO ELIMATE SUCH CARRIERS FROM A BREEDING POPULATION SINCE THEY REPRESENT A HIDDEN RESERVOIR OF THE DISEASE THAT CAN PRODUCE AFFECTED DOGS AT ANY TIME.
 

HEREDITORY CATERACTS

(ALSO CALLED JUVENILLE CATERACTS)

HEREDITORY CATERACTS IN STAFFORDSHIRE BULL TERRIERS HAS BEEN RECOGNISED AS AN INHERITED CONDITION SINCE THE LATE 1970'S.

HEREDITORY CATERACTS IS NOT CONGENITAL, SO THE LENSES ARE NORMAL AT BIRTH BUT CATERACTS APPEAR A FEW WEEKS TO MONTHS OF AGE, PROGRESSING TO TOTAL CATERACT(AND RESULTING BLINDNESS) BY 2-3 YEARS OF AGE. AFFECTED DOGS DEVELOPE CATERACTS IN BOTH EYES.

THE CHANGE, OR MUTATION TO THE STRUCTURE OF THE GENE, PROBABLY OCCURED SPONTANEOUSLY IN A SINGLE DOG BUT ONCE IN THE POPULATION, LIKE ANY OTHER GENE HAS BEEN INHERITED FROM GERATION TO GENERATION.

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.

INDIVIDUALS WITH ONE COPY OF THE DEFECTIVE GENE AND ONE COPY OF THE NORMAL GENE-CALLED CARRIERS- SHOW NO SYMTOMS BUT CAN PASS THE DEFECTIVE GENE ONTO THEIR OFFSPRING. WHEN TWO APPRENTLY HEALTHY CARRIERS ARE CROSSED, 25%(ON AVERAGE) OF THE OFFSPRING WILL BE AFFECTED BYT THE DISEASE, 25% WILL BE CLEAR AND THE REMAINING 50% WILL THEMSELVES BE CARRIERS.

THE ANIMAL HEALTH TRUST HAS RECENTLY IDENTIFIED THE MUTATION RESPOSIBLE FOR THIS DISEASE AND USING THIS INFORMATION HAS DEVELOPED A DNA TEST WHICH DIOGNOSES THAT ARE AFFECTED THE BY THE DISEASE BUT ALSO DOGS THAT ARE CARRIERS.

UNDER MOST CIRCUMSTANCES, THERE WILL BE A MUSH GREATER NUMBER OF CARRIERS THAN AFFECTED 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 PUPS

 

 

PERSISTENT HYPERPLASTIC PRIMARY VITREOUS (PHPV)

PHPV IS A CONGENTAL CONDITION IN WHICH THERE IS A DEVELOPMENTAL DEFECT IN THE NORMAL REGRESSION OF SOME OF THE INTRAOCULAR STRUCTURES OF THE EYE AND IS PRESENT FROM BIRTH. THIS CAN RANGE FROM VERY MILD TO SEVERE ABNORMALITIES WHICH MAY LEAD TO BLINDLESS.

THE PRESENCE OF MILD ABNORMALITIES ARE USUALLY SEEN AS SMALL PIGMENTED DOTS ON THE POSTERIOR LENS CAPSULE. PREVIOUSLY THE LITERATURE INDICATED THAT THIS WAS ALWAYS OBSERVED AS A BILATERAL PHENOMENON BUT RECENTLY IT HAS BEEN STATED THAT AFFECTED DOGS MAY SHOW UNILATERAL INVOLVEMENT, ALTHOUGH THIS IS LESS COMMON.

THE PRESENT KNOWLEDGE OF THE MODE OF INHERITANCE OF THIS DISEASE IS THOUGHT TO BE AN AUTOSOMAL IRREGULAR DOMINANT WITH VARIABLE EXPRESSION. SUE TO PHPV SLEDOM RESULTING IN SECONDARY CATERACTS IN THE STAFFORD, THOSE THAT ARE MILDLY AFFLICTED WILL SELDOM SHOW ANY FORM OF VISUAL IMPAIRMANT DURING THE COURSE OF THEIR LIFE. EVEN THOSE THAT ARE MORE SEVERELY AFFLICTED, MAY BE CAPABLE OF ADAPTING BY USING PERIPHERAL TO COMPENSATE.

STAFFORD BREEDERS SHOULD THEREFORE NOT ASSUME THAT THE PROBLEM IS ABSENT SIMPLY BECAUSE THEY HAVE NOT ENCOUNTED BLATANT SIGNS OF VISUAL IMPAIRMENT, INSTEAD DISCERNING BREEDERS SHOULD ENSURE THAT ALL THEIR STAFFORDS ARE TESTED THROUGH THE NATIONAL EYE SCHEME.

 

DISTICHIASIS  

SOMETIMES THIS CONDITION IS REFERRED TO AS A DOUBLE ROW OF EYELASHES, FOR EXTRA HAIRS ARISE FROM THE EDGE OF THE EYELID AND RUB AGAINST THE CORNEAL SURFACE. THE EFFECTS ARE VARIABLE AND MILD IRRITATION TO CORNEAL ULCERATION WILL BE SEEN. TREATMENT IS VERY DIFFICULT AND INVOLVES SURGERY TO REMOVE THE HAIR ROOTS PERMANTLY. PLUCKING OUT THE OFFENDING HAIRS IS USEFUL, BUT REQUIRES THE UPMOST 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. 

 

 TESTING OF THESE DISEASES ARE NOW AVAILABLE IN AUSTRALIA THROUGH GENETIC TECHNOLOGY.

 

CHEEK SWABS CAN BE TAKEN BY A VET OR AN AUTHORISED COLLECTOR. A LIST OF NAMES FOR EACH STATE IS AVAILABLE ON THE GENETIC TECHNOLOGY WEBISTE

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