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National Bull Terrier Council (Australia)

Health Matters

Most breeds of pure bred dogs have some form of hereditary diseases which are passed on to their offspring through differing modes of inheritance. About 3000 hereditary diseases identified in humans, the total for dogs, we understand,is likely to be comparable but so far, 300 inherited canine diseases have been identified.

Part of every responsible breeder’s commitment to the breed, is to improve the health and lessen the incidence of genetic diseases.

The NBTC(A) have now designated the following as known hereditary health problems affecting the Bull Terrier breed :

Polycystic Kidney Disease
Hereditary Nephritis
Inherited Heart Disease
Deafness (Unilateral and Bilateral)
Luxating Patella
Primary Lens Luxation (Bull Terrier (Miniatures) only) This does not mean that these are the only hereditary health problems in the breed, it’s just that they are the ones being currently addressed.

Inherited Kidney Disease in Bull Terriers
By Dr Caroline O'Leary
University of Queensland

Inherited Kidney Disease (IKD) has been reported in many breeds of dogs including the Bull Terrier and Miniature Bull Terrier as well as in people.

There are many different types of kidney disease, inherited (or genetic) faults being only one cause. Infections, poisons, some drugs, non-genetic cancers, liver, pancreas, uterine, heart disease or many other diseases can all cause kidney diseases.

The inherited conditions in Bull Terriers can occur in very young (less than six months) middle-aged or very old animals. Some dogs can be 10 years old plus and have the faulty gene in their makeup, pass it on to some of their pups, and may appear normal to their owners. These animals may live to a ripe old age with no one suspecting they have the diseases or have passed it on to their pups.

Signs of kidney failure that are common to both types of IKD and to other causes of kidney failure include the following:

poor appetite
dullness or lethargy
weight loss or stunted growth
poor hair coat
vomiting/diarrhoea
foul breath and mouth ulcers
muscle twitching and convulsions
drinking excess water and passing too much urine – owners often notice an increase in the urine passed overnight.
Pale gums (anaemia)
Dehydration (sticky dry gums)

There seem to be two types of IKD in Bull Terriers.

The first type is polycystic kidneys where the kidneys contain fluid filled cysts (or balls of fluid) which can be seen by looking at the kidney, for example by using an ultrasound machine, as black "holes" inside the kidneys. At what age this commonly is first detectable is unknown. While it is possible to detect the defect in some dogs as puppies, it may be that in animals it is not obvious until the dog is much older. In this disease a urine test will not pick all affected dogs, so an ultrasound examination is ideal.

The second condition is nephritis where the kidneys may look fairly normal until a biopsy (or small piece of tissue taken from a live animal) is examined under a microscope. It is not possible to diagnose this disease on the basis of only an ultrasound examination. A urine test or kidney biopsy are the best tests for this disease.

Both conditions are thought to be inherited by an autosomal dominant fashion, which means that only one parent has to have the fault for half the litter to be affected. If both parents have the fault three-quarters or more of the pups may be affected.

Because of the way these conditions are inherited, there is no point in condemning whole kennels or blood lines. As an affected dog may produce many unaffected pups and these animals do not have the faulty gene/s, these animals are fine to breed with as long as they are regularly tested. They have the virtues present in the lines but without the ‘taint’ of the faulty gene/s.

Dogs that have either of these inherited problems SHOULD NOT be bred from.

There is no test available that can say for sure that dogs are unaffected below one year of age. It is possible some affected dogs are not detected until they are 3 or 4 years old. Even leaving the ethical problems out of deliberately breeding affected dogs that must be euthanised or given to homes with the knowledge that they are affected by a deadly genetic disease, these dogs cannot be reliably cleared until they are at least 1 year old and possibly 3-4 years old. These dogs would have to be kept until this age before being bred.

Dogs affected by both these conditions may have bloody urine on and off, and the vast majority of dogs with nephritis and some of the dogs with polycystic kidneys will have abnormal levels of protein in their urine (this is shown by a high U P/C or urine protein to creatinine ratio). Only a few who are late in the course of the disease will have abnormal blood results. In both these conditions, how fast the disease progresses and how severe it is varies from dog to dog.

The Urine Protein to Creatinine ratio (U P/C) is a very sensitive test and is valuable in detecting nephritis and some polycystic kidney disease before signs of kidney failure appear (so lengthening the dog’s good quality of life) and hopefully before the dog is bred. Using this test will hugely decrease the nephritis problem within one generation. This is especially so as it is possible to prevent popular affected stud dogs spreading the faulty gene/s widely by detecting them much earlier than was possible before with the BUN test.

Animals with a high U P/C need to have a full urinalysis completed to rule out other causes than inherited kidney disease. If the U P/C is high and there are no other obvious causes (e.g. reproductive problems, bladder problems) an ultrasound examination and possibly a kidney biopsy will give the full answer.

The U P/C is easy to use and relatively cheap, making it an ideal screening test for nephritis. We believe most of those affected Bull Terriers have a high U P/C result by the time they are about a year old. There are possibly occasional dogs that are affected, that only have a high U/PC once they are 3-4 years old, but there are no published records of this. Lifetime retesting is recommended at this stage.

A lot more work needs to be done to investigate both these diseases. The relationship between these two diseases needs to be looked at, the value of current testing procedures needs to be continually monitored and, hopefully, in the future a genetic test will be developed that can be done once in young pups to predict which ones have the faulty gene/s.

There is no effective cure for either condition. Prevention by breeding dogs free of these inherited faults is the best solution.

At this stage palliative treatment to maintain comfortable life for as long as possible is the usual treatment for IKF.

If the kidney failure is recognised early in its course the following can be tried:

constant access to fresh water.
controlled protein, phosphorous and salt diet (use only with care in growing dogs).
phosphate binders to bind phosphorous in the diet.
water soluble vitamins (especially B vitamins).
hormones for anaemia.
medication for nausea and stomach ulcers.
blood pressure medication if necessary.

Some of the reasons so little is known about inherited diseases include:

hard to detect carriers of faulty genes cheaply, accurately and early in life before dogs are sold or used for breeding.
Differences between dogs in the way the disease appears.
Need for commitment from the Breed Clubs to support research into the problem and develop strategies to breed soundly.

A certificate system to encourage breeding from unaffected dogs and a National Register appears to be the best solution.

Deafness

There are three deafness classifications,
Normal bilateral hearing
Unilateral deaf (deaf in one ear), and
Bilaterally deafness (deaf in both ears)

The only conclusive test for differentiating between normal and abnormal hearing is the BAER/BAEP test (Brainstem Auditory Evoked Response or Potential).

Testing can be done as early as 5 to 6 weeks of age. Only one test should be needed for verification of hearing status.

Deafness can occur in both white and coloured bull terriers.

Both unilaterally and bilaterally deaf dogs are genetically equilivant i.e breeding a unilateral is the same as breeding a totally deaf dog.

Mode of Inheritance:

The exact mode of inheritance is not yet known but it is believed to be recessive in nature and with probably more than one gene involved.

The first step in reducing deafness is to remove all unilaterals from the breeding population.

Luxating Patella (Slipping Patella)

Q. What is luxating patella? (Slipping patella)
A. It is the failure of the patella (kneecap) to remain in the groove provided for it in the front of the lower end of the thigh bone (femur),usually slipping to the inside, but rarely to the outside.

Q. Why does (can) it slip?
A. There are two reasons, and both are usually present in an affected dog.
1. The grove may be too shallow, or tilted to one side too much.
2. The thigh bone may be twisted and/or bent at the bottom or top, so that the thigh muscles pull the patella out of its groove.

Q. What causes these defects?
A. Shallowness of the grove is largely hereditary, though it is aggravated by faulty muscle pull. Twisting or bending of the thigh bone is partly hereditary and/or partly nutritional and/or partly due to use of or stress on the leg.

Q. What is the role of the thigh muscles in the trait and the resulting disease?
A. Muscles are under constant tension (tone) to retain their readiness for action and to help to stabilise normal joints. This tone is quite powerful and capable of bending , twisting and deforming bones which are not properly conformed in the first place. You have noticed the spinal deformities of hunchbacked people.... these are primarily due to the muscles’ pull on the bones only slightly misshapen to begin with. Bone is strengthened in normal structure by the muscle tone, but constant tension on misshapen bones greatly multiplies deformity.

Q. What is the effect on my dog?
A. The effect varies from none to severe lameness.

Q. What determines how bad it will be?
A. The degree of inheritance from each parent, the amount of bone deformity and/or groove deficiency, the activity of the dog (especially its acrobatic tendencies), and its age (older is worse).

Q. When can I tell ?
A. If all dogs are examined by an experienced veterinary orthopaedist at 4-6 months, the presence and the degree of the trait can be detected. At this time, a projection of the possible severity can be graded:
Grade 1 - Patella is found in its groove, can be manually shifted out of its groove, but returns at once spontaneously and never displaces (slips) spontaneously.
Grade 2 - Patella is found in its groove, can be manually shifted out of its groove, but does not immediately spontaneously return and will stay displaced for few steps or moments.
Grade 3 - Patella is found out of its groove, but can be replaced in the groove manually.
Grade 4 - Patella is found out of its groove and cannot be replaced in the groove manually.

Q. How does it affect the dog?
A. All Grade 3 and Grade 4 and some Grade 2 will become arthritic in the stifle (knee) at maturity or later, due to the cartilage damage to the patella and edge of the groove resulting from use and wear in the displaced (slipped) configuration. Some dogs will be affected more than others.

Q. Can it be treated?
A. Grades 2 and 3 can be helped by orthopaedic surgical procedure to improve the groove and/or straighten the thigh bone, and/or redirect the pull of the muscles. While this may make the individual dog more comfortable, it doesn’t cure the genetic defect, which can only be managed by not breeding from animals in Grade 2, 3 or 4 and selecting mates which are free from the trait for Grade 1 in animals.

Q. How can I tell if a Bull Terrier has Slipping Patella?
A. Only a qualified examination is accurate. You can’t tell by looking. Hind leg lameness and hitching can be caused by dozens of different things, many of them temporary, such as a cut pad or a pulled muscle. Straight stifles, bowed out stifle joints, or overbent stifles do not necessarily have the combination of defects which cause slipping patella.

Q. What can I do to reduce the increasing incidence of this painful inherited defect in Bull Terriers?
A. 1. Have your dog examined by a qualified veterinarian, preferably one who specialises in orthopaedics.
2. If your dog is affected, send a copy of the report to the breeder of your dog.
3. The incidence of slipping patella in Bull Terriers can be reduced dramatically if affected animals are not used for breeding.
4. Owners of stud dogs are encouraged to have their dogs examined by a qualified veterinarian and provide a certificate of the results of that examination if the bitch owner asks for it.
5. Brood bitch owners are encouraged to have their bitches examined and to provide a certificate of the results if the stud dog owner asks for it.

Q. Do these certificates guarantee that I will have no Slipping Patellas in my litter?
A. No. What it does guarantee is that it will dramatically reduce your chances of getting puppies with slipping patella’s in your litter.

Due to the fact that slipping patella is caused by a combination of inherited defects, it is difficult to completely eliminate it from ever happening. However, breeding animals together who already have the defects in combination increases the chances of having it in your puppies, as does linebreeding to common ancestors who were affected with slipping patella.

Q. How can I make a difference when other people don’t seem to care?
A. Every decision not to breed an animal with slipping patellas takes one more potential producer of this painful affliction out of circulation. The number of concerned breeders is on the increase and with a concerted effort the incidence of slipping patella’s in Bull Terriers can be reduced by an enormous percentage.
1. You can personally educate other Bull Terrier owners (all of whom are potential breeders) who may not be aware of the problem by giving them a copy of this brochure.
2. You can ask for proof of examination from the owner of the Bull Terrier which you are mating to your dog.
3. You can raise the consciousness of other owners that you meet elsewhere.
4. You can contact a Club Committee member if you have any suggestions or comments.

You can make all the difference in your own breeding program and, with enough responsible breeders, the breed will benefit a thousandfold. You will make a difference.

Reference/Acknowledgement: Bull Terrier Club of America’s information handout.

Primary Lens Luxation

The term luxation means the displacement or dislocation of the lens from its normal position in the eye (i.e. behind the iris and on the line of vision) There are several causes of lens displacement,for example ocular diseases such as glaucoma or cataract. However, the most common form of the condition in the United Kingdom is inherited and is called primary lens luxation. It is seen principally in the terrier breeds, may affect either sex and arises spontaneously in middle age (3 - 7 years). Sometimes both eyes are affected at the same time but usually there is an interval of weeks or months in between. Once one eye is affected the other will invariably follow sooner or later.

In an affected eye, the lens usually moves forward, coming to lie behind the cornea. Occasionally it may pass backwards into the vitreous body. Sometimes it may move between the two sites. An anteriorly luxated lens causes an opacity (cloudiness) of the central cornea where it touches. If left untreated, the dislocated lens will lead to a pressure rise in the eye (glaucoma) which in time causes redness, pain and clouding of the cornea and sometimes swelling of the eyeball (hydrophthalmos) with total blindness.

Q. What are the signs I look for?
A.
Primary lens luxation rarely occurs before 3 years of age and may develop much later; before it happens the eyes appear quite normal to the owner. Most cases only become obvious when the lens has moved (luxated) out of its normal position, usually into the front part of the eye behind the cornea. There maybe irritation and pain at this stage but often the owner simply observes that the eye has an unusual glassy appearance or appears bluish. If not treated promptly the eye may quickly become red and painful, with loss of vision. It is important to recognise that the second eye will also become affected, if not at the same time then within weeks or months of the first. It is vital to observe the second eye frequently and carefully, particularly if the first eye has been lost!

Q. How can I tell if my dog is affected?
A.
Until the lens begins to luxate there is no reliable way of telling whether a dog is affected. However, veterinary surgeons specialising in ophthalmology may be able to recognise the first signs of the luxation weeks or months before any change is apparent to the owner.

Q. What affect will lens luxation have on my eye?
A.
If the condition is left untreated it is almost certain that, sooner or later, the outcome will be total blindness. Usually this happens because the pressure within the eye rises, causing pain as well as loss of vision. Occasionally a lens which moves backwards into the eye causes little problem, but this is exceptional.

Q. Is there any form of treatment?
A.
Yes. If the case is examined early enough it is possible to remove the lens surgically. The veterinary surgeon may decide to operate on the second eye at the same time, even though signs may not be apparent to the owner. If the operation is successful the dog will have good guidance vision. In a limited number of cases, usually when the lens has passed backwards into the eye, it may be preferable to treat with drugs rather than surgery.

Q. Is there any way of stopping my dog becoming affected?
A. No.
The condition is certainly inherited in the Tibetan Terrier and probably also in the true terrier breeds. If the dog carries the gene, or genes, responsible than it will sooner or later become affected.

Q. Can the condition be caused by a blow to the eye?
A.
Only very rarely will a lens become dislocated following this type of trauma in a normal eye. However, in a potentially affected eye, trauma or even boisterous behaviour, may hasten the onset of this condition.

Q. Can anything else cause it?
A.
Lenses may become dislocated in some other disease conditions of the eye, for example, cataract or glaucoma. Usually the cause and effect relationship is obvious, and other signs are apparent in the eye. It sometimes happens that lens luxation occurs in terrier breeds as a consequence and not a cause of glaucoma.

Q. If my dog is affected is it fair to keep him?
A.
If surgical treatment has been successful there is no reason why your dog should not lead a happy healthy life. Even when the outcome has been successful and vision has deteriorated the dog may still be able to adjust satisfactory provided the eye is not painful; however, each case must be judged on the individual circumstances in consultation with your veterinary surgeon.

Q. Can I get a certificate to prove my dog is clear?
A. No.
As yet there is no recognised scheme for the control of lens luxation. However, if the condition is found during an examination under the British Veterinary Association/Kennel Club Scheme, mention of it would be made on the certificate.

Q. Can I breed from my dog?
A.
No. Affected dog should be bred from under any circumstances. Also the parents and progeny (which are likely to be carriers) should not be used for breeding.

Q. Is there any other action I can take?
A.
The control of lens luxation lies in the hands of the relevant breed club or society. The Tibetan Terrier Association has set an example by publishing (with owner’s permission) the identities of known affected dogs and promoting freedom of discussion within the breed.

Reference/Acknowledgement: Hereditary Eye Abnormalities in the dog - a guide for owner and breeder by Animal Health Trust Publication. Second edition.

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