Health Bulletin No 9, July 2012
Further Assessment of the HC-HSF4 and L2-HGA Status in Show Staffords
A small study of the HC-HSF4 (the hereditary cataract gene) and L2-HGA status of dogs placed at Crufts this year showed that all of eighty four dogs studied were negative for HC and all but a couple we clear for L2 with no result being available for the two exceptions, although it was confidently expected that their status would be ascertained prior to breeding.
As Crufts might be seen to be biased towards the most responsible of owners, especially as dogs have to qualify, it was decided to study dogs at a breed club show to see if the findings from Crufts would be confirmed, or if the presence of dogs from a background perceived as not so ‘elitist’ yielded different results.
For the purpose of this study, the dogs entered in the catalogue of Morecambe Bay and Cumbria SBTC Championship Show at the beginning of May 2012 were assessed for their HC and L2 status using the Kennel Club’s Health Test Result Finder on their website. Overseas dogs were excluded as they, and their parents, will not be on the KC database, as were veterans as they may have been retired from breeding by the time the tests for the conditions came into general use.
A total of 188 dogs were available for study. Of those 170 (90%) were HC and L2 clear; 160 (85%) were hereditarily clear, seven had been laboratory tested and three were hereditarily clear for either HC or L2 and tested for the other. One dog was clear for HC but was an L2 carrier. Three, which were HC clear but apparently untested themselves for L2, had an L2 carrier parent while the other parent was clear. However personal communication suggests that the breeders had been totally responsible and tested them as puppies prior to KC registration, but this means results will not automatically be recorded on the registration forms or the database; this needs to be addressed.
Of the remainder, three were hereditarily clear for HC but L2 status was unknown; in all three cases, the dam was clear but the sire was untested. In five more cases, the sire was clear of both conditions but the dam was untested and there was one untested dog with one parent clear of HC but L2 unknown while the other parent was clear of L2 and HC unknown.. While it is disappointing that full testing had apparently not been carried out, none had the risk of producing affected puppies. More reprehensible was an untested dog with parents who were similarly untested, and thus had the risk of being affected with either condition; it is to be hoped that the owner does test fully should breeding be contemplated.
Of the four remaining dogs, none could be found on the KC database. With two, both parents could not be found either and in the case of the remaining couple, their sires were shown to be untested while there was no record of their dams. While unsatisfactory, there may be several reasons for this. The result finder service is very precise and if there is any error whatsoever when entering a dog’s name, then the search fail as no records will be found. Obviously errors in the catalogue simply compound the problem. Nevertheless it is surprising with these four dogs that details of all four dams and two of the sires could not be found on the database.
These results, although the percentage shown to be clear of both HC and L2 is slightly lower, are compatible with the small study conducted on the placed dogs at Crufts, confirming the satisfactory progress that has been made since testing was introduced. Finding that one dog was a carrier and three others could be is not a matter of concern, as their responsible breeders are clearly in the process of eliminating the L2 recessive from their stock. Although inevitable, finding dogs that are not appropriately tested is disappointing, especially the one that had no test history and was at risk
Health Bulletin No10. July 2012.
Analysis of L2-HGA Reports in Breed Records Supplement
Following discussion with the Animal Health Trust, as referred to in a previous bulletin, an analysis of L2-HGA reports in the Breeds Record Supplement has been undertaken. It is known that 90% of show dogs are clear of the recessive L2 gene and those that are not, are probably owned by breeders trying to eliminate carriers from their stock. When testing started, the carrier rate was shown to be about 15% but it is not known what it is currently in untested Staffords, or those where only one parent’s status is known.
All dogs with L2 tests reported in the Breed Records Supplement from the Summer 2010 issue to the Spring 2012 issue, covering the most recent two year period, were run on-line through the KC Test Result Finder to assess the status of their parents. This was to establish those whose parents had not been tested, although there is no way of knowing if any testing of earlier generations had taken place; this group could be taken as being comparable to Staffords in general before testing was introduced. The sex and status of the sire or dam was noted for dogs with only one tested parent. Any dog that had been tested prior to 2010 was omitted from the study.
One hundred and nineteen dogs from an untested background were found. One was clinically affected but it may be it was tested, not to establish L2 status, but for diagnostic purposes. Of the remaining 118, fifteen were found to be carriers. This give a carrier rate of 12.7% which is compatible with the rate of approximately 15% found in initial tests. This suggests that the carrier rate in untested Staffords has not declined significantly since testing was commenced about seven or eight years ago. Interestingly, a carrier rate of that found would produce about 1% affected dogs on random breeding, so finding one such dog should not be a surprise although the reason for testing is unknown.
One hundred and one dogs with one negative or clear (i.e. non-carrier) parent and one untested parent were found; 85 of the clear parents were sires and 16 dams. Five of the 101 dogs were found to be carriers. All five had clear sires and none were from clear dams, but this is just chance as the clear sire/dam ratio was so great. These figures show that at least five of the 101 untested parents were also carriers; this appears lower than the 12.7% rate reported above but as dogs born to clear x carrier parents have only 1:2 chance of being carriers themselves, it is probable that the carrier rate in the untested parents was twice that found, i.e. about 10/101, which is only slightly lower than the rate in untested dogs.. The disproportionate ratio of 85 dogs to only 16 bitches in the tested parents suggests that some breeders are adopting the policy of using clear stud dogs as there is no risk of any affected progeny, while not bothering to test their bitches.
Analysis of cases where known carriers were used is not so easy. Twenty dogs produced by carrier dams to clear sires were found; seven were carriers also, but the remaining 13 were clear. Included in this group were three litters; one had five clear puppies, another had three clear, while the remaining one had seven, five carriers and two clear. The breeders of these litters were acting responsibly in their efforts to ensure no affected dogs would be produced while trying to eliminate carriers from their stock but their inclusion means the figures for this group are not totally random. Totally reprehensible are those breeders who were found to have mated a carrier to an untested dog or bitch. Two cases of apparently untested bitches being mated to a carrier dog were found; one of the progeny was a carrier and the other clear. Last was a litter of five produced by a carrier dam to an untested dog resulting in three carriers and two clears. No cases of a carrier dog being used on a clear bitch were found, possibly supporting the idea that some breeders ensure they only use clear sires.
Interestingly, seventeen dogs with both parents L2 clear were found. It is not known if they were tested because their owners were being ultra-cautious or if they simply did not understand the genetics, but because these dogs were inevitably clear of L2 they were omitted from the study as their inclusion would distort the findings.
Although there is no way of knowing the colours of all the dogs reported, it would seem that significant numbers were blues on account of their names. While the blue issue is extremely emotive, it may be that the need for health testing is being increasingly recognised in these circles.
From the analysis of the last two year’s results, it is clear we must keep promoting L2 testing to all breeders. It would seem that testing is possibly becoming more routine outside of the show world to ensure affected dogs are not produced. However if some are achieving this by only using clear sires, even although this may achieve some reduction in the carrier rate in the long run, they perhaps ought to rethink, This policy may be penny-wise and pound-foolish. The money spent to have their bitches tested will reduce the need for future testing quicker as the numbers of their hereditarily clear dogs and bitches increases. It is evident the percentage of carriers in the general Stafford population has probably remained more of less the same since testing commenced, although this is no surprise. The situation needs to be monitored and repeating this analysis in about five years would be beneficial to assess any change.
Health Bulletin No11, July 2012
Death Survey (Preliminary Report)
Details of 578 dogs that had died from 1995 onwards were received. The information requested was Kennel Club registered or not, age when dying, cause of death, whether neutered or not, and whether put to sleep or died naturally.
The 578 dogs, of which 530 (92%) KC registered and 48 (8%) unregistered, comprised 226 (39%) dogs and 352 (61%) bitches; 52 (23%) of the dogs and been castrated and 257 (73%) of the bitches spayed at some stage, either for reproductive or medical reasons, and 441(76%) had been euthanized. The ages at death ranged from less than one year (10 months) to 18 years, the mean (average) age was 11.9 years and the median (middle of the whole age range of all in the study) was 12.5 years. The figure below gives the numbers dying by age. It shows a steep rise in dogs dying from nine years old onward with the onset of the aging process. A total of 137 (24%) dogs died prematurely which was considered to be less than ten years old although the death rate did increase a year earlier as noted. On the other hand 353 (61%) lived to twelve years or more.
Determining the causes of death with dogs is not easy as diagnoses are frequently vague and not supported by diagnostic tests in many instances. In this study 33% died basically of ‘old age’ and another 33% succumbed to one of the many types of cancer; heart problems were third with only 5.4%. The remainder died from a variety of causes, including trauma and poisoning. Many of those with cancer were elderly which is to be expected, as are other conditions associated with the aging process.
Of particular interest are those dying prematurely. As may be expected there were diverse causes for those dying under ten years old, including trauma, poisoning, and surgery associated deaths, plus a wide range of naturally occurring conditions. While nothing appears to be of particular significance on initial inspection, a detailed analysis will be conducted to see if there is any condition with a significantly higher prevalence.
Overall this brief initial assessment confirms that the Stafford is a pretty healthy breed with over three quarters living beyond ten years of age, having a realistic life expectancy of twelve to thirteen years. The next step is to analyse the various causes of death closely. For example, the overall cancer rate of 33% might sound rather high although probably about what might be expected when all factors are considered but it will be looked at by type and site, and in relation to age. In addition other factors, such as sex and the effect of procedures like neutering, need to be assessed. These studies will take some time and a full report of this survey, to which many have contributed, will be published at later date
Health Bulletin No12. Sept 2012
There is a lot going on with health currently so it has been a busy time – the first thing to be packed when going on holiday is the laptop! Sad, isn’t it! I am trying to get the general opinion of vets on what they regard as skin problems affecting the breed and when I get them collated I shall let you all know. However, the responses to the skin lump question in the ‘death survey’ have been analysed and a report prepared. I am sending it as a separate attachment along with this bulletin. Underneath is an abstract of the report, outline the salient points and this may be something you may wish to put on Club sites rather than the full report which will take up more space. The decision is yours and you can have it sent separately if you wish. The next step is to analyse the death survey in depth but as I pointed out last time this will be more time-consuming.
Skin Lumps in SBTs (Abstract)
In the ‘death survey’, 128 (22%) of 576 dogs were reported as having skin lumps during their lives; 27 had two different types at some stage giving a total of 155 reports. Of these 80(52%) were benign conditions, such as cysts, warts or fatty lumps; 51(33%) were cancers, and 24(15%) were not specified by the owner. Twenty three (45%) of the cancers were mast cell tumours, which varied from being relatively benign to extremely aggressive, eight were other forms of cancer, and the types of the remaining 20 (39%) were not specified. Almost half (49%) of the cancers were fatal or contributed to the dog’s death; with mast cell tumours it was 48% and for the unspecified group 55%.
Looking at the total 576 dogs in the study, in addition to 22% having lumps of some sort, 9% had skin cancer with 4% dying from it; for mast cell tumours, the most common cancer found, it is 4% and 2% respectively. The risk of a Stafford developing skin cancer was found to be 1:11 and for mast cell tumours 1:25. However the majority of those that died from skin cancers of any sort in the study were in late middle age or old age (over ten years) when the prevalence of all cancers increases.
The problems of the unspecified lumps and cancers are discussed as is lack of sufficient comparative data to determine if Staffords have a greater risk of skin cancers, especially mast cell tumours, than other breeds or dogs in general. As nearly a tenth of all Staffords may develop skin cancer at some stage, owners are advised to seek veterinary advice if their dog develops a skin lump to ensure early treatment, usually surgical removal, should it turn out to be malignant.
Health Bulletin No13. October 2012
At last I have been able to get some relevant SBT data from the KC/BVA eye testing scheme over and above the results that are routinely published in the Breed Records Supplement.
Litter testing for Persistent Hyperplastic Primary Vitreous (PHPV).
As most will know testing of whole litters for PHPV when about seven weeks old is recommended wherever possible, as it will ensure a puppy’s status will be known before going to a new home.
From 2008 to 2011 inclusive, 128 litters were examined. One or more affected puppies were found in six (4.7%) of those litters. Numbers affected in these litters varied from 1:8 to 5:6, and both in a litter of just two were positive. Overall eleven (35%) out of a total of 31 puppies in these litters were affected.
The total number of puppies actually tested over the 128 litters is unknown but as studies have shown that the average number of puppies per litter being registered is about 4.7, we can postulate the numbers of puppies tested is about 600. Thus the overall incidence of PHPV in the group tested is around 1.8%. This is compatible with PHPV cases reported in the BRS on routine eye testing.
As we all know the mode of transmission of PHPV has yet to be determined; despite no supporting evidence a dominant gene with variable expression was suggested many years ago although examination of the family trees of cases occurring at the time would have been equally compatible with a recessive gene being the cause. We simply do not know, but the ratios of affected puppies in these litters could be useful in pointing the way for the geneticists. The incidence of 35% affected is greater than the 25% to be expected on average if a recessive gene were involved. However the totals are comparatively small so finding a third affected rather than a quarter is not sufficient to rule out a recessive gene as the cause. It will be interesting to see what the genetic studies on PHPV in collaboration with the AHT eventually throw up. The grade of severity of PHPV in the affected puppies is unknown.
Persisent Polar Subcapsular Cataract (PPSC).
A major stumbling block with PPSC is that it is only on schedule B of the scheme so is not reported routinely in the BRS like the schedule A conditions. However of 784 dogs reported between 2009 and 2011, seven (0.9%) were found to have PPSC. Of these, four were aged between one and two years, while the remainder were three, five and eight years old respectively. These findings clearly demonstrate that PPSC is not a condition that develops mainly in older dogs as was suggested at one time; it is now known it can develop at any stage from six months old onwards. This comes from studies of the many other breeds in which it has been described and there is no reason to suspect that Staffords will differ in this respect, especially as four of the cases were one year olds. These findings have implications on eye testing policies and the frequency of examination.
The severity of the seven cases is unknown. Most cases of PPSC cause little, if any, visual impairment but one or two cases where the cataract has developed to affect sight have been found. Also unknown are the results of any previous eye tests in the three older affected dogs; negative results of any earlier test would help to pinpoint the age of development.
Health Bulletin No14, October 2012
Skin problems in Staffords – survey of vets
Although hard data would not be forthcoming, a survey of vets was conducted to ascertain their opinions of skin problems in Staffords. They were asked for:
- Estimate of proportion of dogs attending their surgeries were SBTs
- Estimate of proportion that was pure bred.
- Estimate of proportion that had skin problems
- Estimate of proportion that were blue or blue and white.
- Do they consider SBTs had more or less skin problems than other breeds
- What conditions they considered to be more prevalent.
- If they considered pure bred SBTs had more or less skin problems than crosses.
- If they perceived any relation between skin conditions and coat colour.
- If they had ever encountered coat dilution alopecia in blue SBTs.
The vets who work at the Dogs Trust gave a good response on dogs seen at the Trust and some in their practices.
- Proportion attending 6-10% (<1 to >10%) 6-10%
- Pure bred 51-75% 51-75%
- Proportion skin probs. 11-20% 11-20%
- Proportion Blues <10% (one thought >25%) <10%
- Other breeds Generally more than Generally more than
- Conditions Demodex. Atopy. Demodex, atopy
- Vis-s-vis crosses About the same. About the same
- Colour association White (2) White (1) blue (1)
- Seen CDA No (10) Yes (1,<5%) No
The Battersea vet also responded; his opinions were similar but thought over 20% had skin problems and was higher than in other breeds. He had not encountered any cases of CDA but thought that skin problems were more prevalent in whites.
A vet in private practice replied to the questionnaire. About 5% of dogs seen were ‘staffies’ of which half to three quarters were considered pure bred. Skin problems, mainly demodex and atopy, were considered to be greater than other breeds and ‘pure’ greater than ‘staffycrosses’. He considered there was no colour relation although the proportion of blue was <5% and no cases of CDA had been seen.
In addition, verbal information was received from breeders who had asked their own vets. Basically such responses were similar. Most saw few blues routinely, and none reported CDA. One specifically felt there were more problems with whites and that whites were becoming more fashionable.
On my experience of visiting dogs’ homes, I think some vets may over-estimate the proportion that are pure SBT’s, depending on how clients describe their dogs. However it would seem that in general, vets consider that Staffords have a higher incidence of skin problems than other breeds, with demodex and atopy being most prevalent. The proportion of dogs seen that are blue is very low and this is disproportionate to the numbers being registered, although regional factors need to be considered. Only one considered there was a relation of skin problems with blues, whereas several considered whites were at greater risk. Despite being specifically asked, only one reported as having ever seen CDA.
Health Bulletin No15, February 2013
The Assured Breeder Scheme and Staffords
Some breeders and owners seem to be uncertain about the requirements for Staffords under the Assured Breeder Scheme, so perhaps these should be specified to avoid further confusion:
- Hereditary catatact (HC-HSF4). It is a requirement that all dogs, being bred undergo the DNA test for this recessive gene prior to mating, unless hereditarily clear, to prevent two carriers being mated together.
- L-2-Hydroxuglutaric Aciduria (L-2-HGA). As with HC-HSF4, it is a requirement that all dogs, being bred undergo the DNA test for this recessive gene prior to mating, unless hereditarily clear, to prevent two carriers being mated together.
- Eye testing. It is a requirement that all sires and dams possess a current eye examination certificate i.e. tested within eighteen months prior to the birth of the litter. This will detect conditions like Persistent Hyperplastic Primary Vitreous (PHPV), Posterior Polar Subcapsular Cataract (PPSC) or any other eye condition that may be of a hereditary nature.
- Litter Testing. It is a recommendation, not a requirement, that litters are eye tested at six to seven weeks old. This will permit any cases of PHPV, which is congenital, to be detected at the earliest opportunity to the benefit of breeders, who will not unknowingly sell an affected puppy.
From a practical point of view, with show breeders/exhibitors co-operating since testing began and getting their stock DNA tested for HC-HSF4 and L-2-HGA, virtually all their stock, with only a few exceptions which are being adequately dealt with by responsible breeders, is now ‘hereditarily clear’ for these conditions rendering further testing unnecessary.
The frequency of eye testing is a bone of contention for some but again one must be sensible. Although the vets glibly say dogs should be tested annually, as far as the ABS is concerned a valid certificate is one issued within eighteen months prior to the birth of a litter. Thus if a dog is going to be used at stud, testing should be delayed until shortly before his first mating and, provided he is continuing to be used, about every seventeen or eighteen months thereafter. For bitches there is no point, under normal circumstances, to test until shortly before the first mating is due to take place, irrespective of age. In theory, one eye test could cover a bitch for two litters and, as the KC will only register a maximum of four litters from a bitch, two tests might be all that is required in her breeding years. Many show breeders only take one or two litters from a bitch so a couple of tests at most will be required depending on the time between litters.
As previously stated, litter testing enables breeders to determine the PHPV status prior to selling of puppies which gives protection against any potential acrimony or even litigation, should a dog be found to have the condition on a full eye test later. However as getting appointments for testing litters may be at a premium, breeders should book them as soon as possible, perhaps when the litter is about one to two weeks old. It is also advisable not to delay registering puppies with the KC and application should be made when a litter is about two weeks old to allow for any losses in the early post-natal period.
A major complaint from breeders has been the inability to get the results from litter tests recorded on the registration forms. The explanation from the vets is that they cannot specifically identify individual puppies, despite microchipping being a feasible option for many years now. However the KC is aware of this problem, which is not their fault, and steps that will hopefully rectify this unsatisfactory situation, are being taken. Any progress will be reported in due course.
Obviously the ABS requirements may change in the light of new developments but breeders will, of course, be kept fully informed.
As most will now be aware, microchipping of all dogs will become compulsory in 2016. Many do microchip their dogs routinely already so this will not affect them, and many may have been obliged to do so for health testing in some instances. It makes sense to get your dogs done sooner rather than later. Your vet will usually microchip and there are some independent trained ‘chippers’ who can do it for you. However it may be worth your while investigating what your local council offers. Many dog wardens will microchip the dogs of local residents free or at a reduced cost. Similarly, charities, such as the Dogs Trust, may offer free microchipping as part of campaigns promoting responsible ownership. It is just common sense to take advantage of such opportunities when they are available to save hassle at a later date.
As stated above, positive identification of puppies by microchipping would be advantageous if litters are being tested for a variety of conditions.
I am pleased to report that Cathryn Mellersh and her team at the Animal Health Trust have commenced their laboratory studies to hopefully identify the genetics of PHPV and develop a DNA test for the condition. Being a journey into the unknown, we do not know how long the work will take although we hope for a successful outcome. However you will be kept informed of how the research is progressing as necessary. As ever we are grateful to all the owners who have done their bit for the breed by submitting specimens from affected dogs and their relatives. (Please note, the incidence of PHPV in litters was discussed in Bulletin No13.)
Health Bulletin No16, May 2013
Since the last Bulletin in February, there are a few points to draw your attention to.
All should have received the completed full report which makes rather pleasant reading for those interested in the breed. In a nutshell, owners may reasonably expect their Staffords to live for 12-14years, eventually succumbing to old age or an age related condition. Inevitably some in the study died prematurely at under ten years of age as may happen with any species or breed but the good thing is that no peak of deaths at a young age was found. This occurs with some breeds when a greater than expected number die when, for example, six or seven years old, with those surviving past this age going on to a normal lifespan. This suggests some genetic condition is involved but fortunately Staffords do not seem to have anything of such a nature. The only conditions that we may need to watch are brain tumours and mast cell tumours. The latter was discussed in the skin lump survey published previously but more information is required on the former. Consequently a survey of dogs diagnosed with brain tumours is being undertaken and this is discussed below.
This has been undertaken and a preliminary report has been published to give some feedback to interested parties. A full analysis will take some time unfortunately but it would seem that demodex or allergies may each affect about ten per cent of Staffords at some stage in their lives. However, most cases usually appear to be well controlled by their owners. One specific aim was to assess any relationship of skin conditions with coat colour. Unfortunately it would seem initially that there are insufficient responses on blue and white dogs to allow meaningful comparison and once the full analysis is done, steps may be needed to look at these colours specifically as it is suggested that dogs of both colours may be at increased risk.
In conducting this survey, special thanks is due to the efforts of the folk from the SBTC who manned the Discover Dogs stall at Crufts and did a great job promoting the survey by a paper questionnaire which got many responses from pet owners, often with dogs that were not KC registered. Such thanks is due also to Ivor Keyes who conducted the survey on-line using ‘Surveymonkey’ and whose efforts have been invaluable in extracting the necessary data.
As you may know the AHT has started examining the specimens collected from affected Staffords and related dogs to see if the genetics of PHPV could be determined, possibly leading to a DNA test. At the last count, the specimens had been tested but the results had still to be analysed. Again this may take time and further information will be supplied when available.
Brain Tumour Survey
As mentioned above, the Mortality survey suggested that brain tumours in Staffords may need to be monitored as half of those reported as dying with a brain tumour were less than ten years old. This clearly requires further investigation of clinical signs, diagnosis, treatment and outcome. Consequently I would like owners, world-wide and not just British Isles, who have a Stafford currently diagnosed with a brain tumour or had a Stafford that died from a brain tumour after January 1st 2010 to contact me please, initially by email on firstname.lastname@example.org or by Facebook. A questionnaire has been prepared and can be sent out as required or completed over the telephone as getting all the necessary details is imperative. Good advice on the questions to include, was received from Dan O’Neill, the vet who is conducting the Royal Veterinary College’s VetCompass project which involves many veterinary practices on-line. Depending on the number of responses received and the information obtained, Dan can also put us in contact with his neurologist colleagues if further help and advice is required; such collaboration is imperative in improving the health of our dogs.
From the Mortality survey, I am not expecting to be overwhelmed by reports of dogs with brain tumours – I would be very alarmed if I were! However even if about thirty or so responses were received, it should give some idea of how brain tumours are dealt with and most importantly the ages at which they occur, to allow the way forward to be discussed with our veterinary colleagues.
Health Bulletin No17, July 2013
Epilepsy has been a topic of conversation in some quarters recently as it has been a matter of concern to some. By epilepsy we usually mean idiopathic epilepsy which has no known specific cause but epilepsy may be secondary to specific medical conditions such as head injury, brain tumour or certain metabolic disorders. As in humans, epileptic fits in dogs may be severe (grand mal) or comparatively mild (petit mal), and in the most severe cases, status epilepticus, where the fit is prolonged or there are two or more repeated fits without regaining consciousness between, may occur, resulting in the dog having to be put to sleep to relieve its suffering. Epilepsy of unknown origin usually commences when a dog is about one to three years old and there are several sites on-line which can provide full clinical information.
The big question is its prevalence. Most who have been in the breed for a few years will have heard of the odd case or two, perhaps even have bred one if they were unlucky. Of course if you have had an epileptic dog you become hypersensitive about it – you find cases in every nook and cranny and are forever worrying about how many cases are getting swept under the carpet. The inevitable outcome is that its prevalence is ‘talked up’.
However further light has been thrown recently on canine epilepsy of unknown origin thanks to the Royal Veterinary College’s Vetcompass project. Dan O’Neill the leader of the project has drawn my attention to the following paper:
Kearsley-Fleet, L., et al 2013 Prevalence and risk factors for canine epilepsy of unknown origin in the UK. Veterinary Record 172(13):338.
Abstract: Epidemiological evaluation of canine epilepsy is an under-researched area. The objectives of this study were to estimate prevalence and investigate risk factors for epilepsy of unknown origin (EUO) among dogs attending primary veterinary practices in the UK. The clinical data analysed spanned a two-year period and included all dogs attending 92 primary veterinary clinics participating in the VetCompass project. Five hundred and thirty-nine EUO cases were identified giving a prevalence of 0.62% (95% CI 0.57% to 0.67%). Males were over 1.5 times as likely to have EUO compared with females (95% CI 1.44 to 2.06; P<0.001). Of purebred dogs, the border terrier had 2.70 (95% CI 1.57 to 4.62; P<0.001) and the German shepherd dog had 1.90 (95% CI 1.28 to 2.80; P=0.001) times increased odds of EUO compared with crossbred dogs. In addition, the West Highland white terrier had reduced odds (OR 0.23; 95% CI 0.08 to 0.62; P=0.004) of EUO compared with crossbred dogs (likelihood ratio test P<0.0001). No association was found with neuter status, colour or weight. The current study highlights the clinical importance of epilepsy as a canine disorder in the UK. Increased awareness of sex and breed predispositions may assist clinicians with diagnosis. Further research is merited to evaluate the specific breed associations identified.
The prevalence in Staffords is not given in the paper but Dan has kindly dug out the data; there were 25 cases from 6796 SBTs giving a prevalence of 0.37% (less than the overall average which was 0.62%). Another publication which suggested that the prevalence in Staffords was greater than average is cited in the paper, but this one may not be totally reliable because of a case selection issue. Nevertheless one may conclude from the study that epilepsy is not as prevalent as one may imagine in dogs in general and in Staffords in particular, despite the fact that we do not know how many of the Staffords were ‘proper’ ones as the veterinary practices will record a dog’s breed usually on the owner’s say-so. It should also be noted that the study was on UK dogs so care is needed in extrapolating these results to populations in other countries. Dan also points out that dogs may die from fitting but this could just reflect age-related changes in the older brain including strokes, tumours etc and not genuine idiopathic epilepsy. In the previously published mortality survey, epilepsy was given as the cause of death in 1.9% of cases which appears considerably higher than the VetCompass paper. However the numbers in the mortality survey were less than six hundred compared with over six thousand in the VetCompass report so one should be careful about drawing any definitive conclusion.
There is the belief that epilepsy of unknown origin may be inherited and there are anecdotal reports of related dogs being affected, although it appears that non-inherited forms also exist. Clearly more detailed information would help. Despite the breed identification problems regarding Staffords, something which Dan O’Neill and his colleagues are aware of, VetCompass is likely to give us more reliable data simply because of the numbers involved. What we in the breed can do to help is perhaps by getting as much information as possible when apparently related cases should occur. This would require as much information as possible on parents, grandparents, siblings and half siblings of not just the affected cases but also those of these earlier generations, plus any clinical details available. The only persons likely to be able to collect such information are the breeders themselves as it would be an impossible task for any third party to undertake, being unfamiliar with the dogs and owners involved. If several family trees containing more than one dog with epilepsy of unknown origin were available, they could be passed to the geneticists for their opinions on whether there are any genetic relationships and possible modes of transmission.
The data available shows that epilepsy occurs at a low level in all dogs whether pure bred or not, just as it does in humans. On one hand we must not over-react, distressing though cases may be for their owners, but on the other it is not something to be swept under the carpet and needs to be monitored for any changes in the situation and hopefully gain a fuller understanding of the condition.
Health Bulletin No 18, September 2013
PHPV Research Update
I have just received the report from the Animal Health Trust on the PHPV research and I have attached it at the bottom. As you will see they have been unsuccessful in identifying any recessive gene causing the condition, and suggest it may be a dominant, or co-dominant, gene being responsible or possibly a polygenic effect. This is, of course, disappointing but we must remember that research is a journey into the unknown and you are never sure of what you might find.
I shall naturally discuss the way forward with the AHT and those involved with health issues at the KC but planning our next steps may take a little time. If there is any more funding required, I would hope that the KC Charitable Trust would look favourably on any application but this would be done via the AHT.
From our point of view, it is thus still necessary to eye-test any breeding stock at some point prior to mating to ensure they are not affected with the condition. As everyone knows, testing whole litters about seven weeks old is encouraged and is a recommendation under the Assured Breeder Scheme. It is to be hoped as many as possible will do this.
Where breeders and owners can help is by ensuring mouth swabs are continued to be submitted to the AHT from any new cases plus parents and siblings if possible. If any affected puppies are found on litter screening, the situation is ideal to collect swabs easily from the whole litter and this is something the vets on the specialist panel really ought to be assisting with. Hopefully the BVA will encourage their vets to be more pro-active in this respect.
Thus if you are unfortunate enough to have a dog diagnosed with PHPV on have a litter with one or more affected, the best thing would be to contact Bryan at the AHT (details in report below) for swabs and advice. I hope overseas breeders and owners would help in this respect too but Bryan would need to be contacted on how this may be done with postal regulations of clinical specimens being an important issue
I would have loved to brought news of a ‘Eureka moment’ but scientific research is seldom like that. It can be along hard grind and as they say ‘you can’t win them all’! We can of course keep trying and shall do.
Canine Genetics Research Progress Report
Breed: Staffordshire Bull Terrier
Condition: Persistent hyperplastic primary vitreous (PHPV)
Date: August 2013
Funding: £5000 donated by the Staffordshire Bull Terrier Breed Council of GB & NI
£1200 donated by breed clubs, other organisations and individual donors
The research staff who are investigating persistent hyperplastic primary vitreous (PHPV) in the Staffordshire Bull Terrier are generously supported by the Animal Health Trust and by the Kennel Club, as part of the Kennel Club Genetics Centre at the Animal Health Trust, but resources such as consumables and laboratory materials are being funded solely by donations from funding organisations, breed clubs and individuals.
PHPV is a congenital eye condition caused by the retention of elements of the foetal vascular supply to the lens. The condition results in variable amounts of fibrovascular plaque on the posterior lens capsule and possible posterior cortical cataract. This is sometimes accompanied by bleeding into the back of the eye or into the lens. PHPV is inherited in Staffordshire Bull Terriers although the precise mode of inheritance is unknown.
We have recently conducted a whole genome scan using DNA samples from 24 dogs affected with PHPV – termed “cases”, and 23 unaffected dogs with clinically clear eyes – termed “controls”. Each of these dogs had been examined by a veterinary ophthalmologist – either as part of a recognised eye screening scheme or by a specialist in a clinical setting. We used a high-density scanning array to genotype around 174,000 markers spanning the
whole genome, in each of the 47 dogs in the study. The data we obtained was very good quality, with the DNA from each dog yielding high quality genotypes. We analysed the data for regions of the genome that were consistently shared between the cases but different in controls, which would indicate a position that harboured a mutation that played a role in the development of PHPV. Unfortunately, we did not identify any regions of the genome that were associated with PHPV at a statistically significant level, indicating that the disorder is unlikely to be caused by a single mutation with a recessive mode of inheritance. The most likely explanation therefore is that PHPV is either caused by a single mutation with a dominant or co-dominant mode of inheritance, or is a more complex condition with perhaps several genes involved.
We will preserve the current dataset and seek to collect an additional set of 24 cases and 24 controls which we can then examine using the same methods as above. We will then formally combine the two datasets to increase our power to identify mutation(s) associated with PHPV.
We encourage owners and breeders to continue sending us DNA samples from Staffordshire Bull Terriers that have been examined by a veterinary ophthalmologist, whether affected or unaffected by PHPV, along with a copy of their screening scheme certificate or clinical notes as applicable.
As always, we are grateful for any health updates you can give us on those dogs for which we currently hold DNA samples. For further information on how to submit a sample, or to send us updated health information, please email Bryan McLaughlin at email@example.com
We would like to thank all owners who have submitted samples and information from their dogs – without either of these we would be unable to make any progress with this project. We also thank all participating veterinary ophthalmologists for their continued support and advice.
Health Bulletin No 19, December 2013
Impact of DNA testing for HC-HSF4 and L-2-HGA
DNA testing for hereditary cataracts (HC-HSF4) and L-2-Hydroxyglutaric Aciduria (L-2-HGA) has been routinely available for eight years or so at the Animal Health Trust with results being published quarterly in the Breed Records Supplement. Results for individual dogs may be obtained on the Kennel Club’s web site by using the ‘test result finder’ for dogs bred in the UK. In previous bulletins it was shown that about 90% of British dogs in the show ring were hereditarily clear, as both parents were themselves clear, for both conditions. The percentage hereditarily clear for each condition separately was higher as some dogs may have been hereditarily clear for either HC-HSF4 or L-2-HGA but had had to be tested, or were awaiting testing, for the other one for various bona fide reasons. With the passage of time it was obvious that the numbers of hereditarily clear dogs should be ever increasing in the population but we had no idea of the numbers.
To provide answers, data on the numbers of ‘hereditarily clear’ dogs being registered from the start of 2012 to the start of December 2013 were obtained from the Kennel Club. The figures of those hereditarily clear only covered till mid November so will give a falsely low proportion for 2013 but only slightly so.
The data supplied was as follows:
Year Registrations HC-HSF4 clear L-2-HGA clear
2012 6339 2123 (33.4%) 2164 (34.1%)
2013 5378 1755 (32.0%) 1838 (33.5%)
2012-13 11826 3878 (32.8%) 4002 (33.8%)
Assuming the proportions of hereditarily clears were similar for the part of November where they had not yet been included, adjusting the figures to compensate would increase the percentages of clears for 2013 by about 1.6% for both HC-HSF4 and L-2-HGA to around 33.6% and 35.1% respectively.
These current figures indicate that a third of puppies being registered are hereditarily clear for each condition. The numbers that were hereditarily clear for both HC-HSF4 and L-2- HGA were not obtained, but as there was only a difference of 1% (32.8% v 33.8%) over the study period, it may be reasonably postulated that over 30% of puppies being registered are hereditarily clear for both conditions.
It was of course expected that the numbers of such clear dogs would increase as time passed since the introduction of the DNA tests, but this is the first time that an attempt has been made to measure the success of the testing programme. It may be possible sometime to look at earlier years to see there had been a continual improvement over the years. Much more important will be to repeat this in a couple of years to see if there has been an increase in the number of hereditarily clears being registered.
As we know, the vast majority of puppies produced by ‘show’ breeders are already hereditarily clear, but we do not know what proportion of all puppies being registered are bred by them. It would be disappointing if nearly all the hereditarily clears were being produced by them and few by breeders with no breed club contact; this would mean the message about the need for testing was not getting across to the non-show fraternity. On the other hand, if it were shown that, let’s say, half the clears were bred by non-show folk then it would show we are getting the message across to some at least. Interestingly, just under 30% of SBT Accredited Breeders (there are only about 120, of which a number of known ones seldom if ever breed) are not members of any breed club which suggests that a few at least see the benefits of testing, and being members of the scheme, even if perhaps only to boost their sales. Whether we should be pleased or disappointed to find that only a third of puppies being registered currently are hereditarily clear, and two thirds are not, is difficult to say. However, irrespective of how many of the so-called back street breeders test their stock, praise must be given to the show fraternity, including newcomers, for the way testing has been adopted assiduously to the benefit of our breed. To reach the desired point of having only hereditarily clear Staffords being registered may take many years, but the figures given above will at least provide a basis for monitoring future progress.
Health Bulletin No 19A, December 2013
Impact of DNA testing for HC-HSF4 and L-2-HGA
|Date||Number of Registrations||Number of HC-HSF4 Hereditary Clears||Number of L-2HGA Hereditary Clears|
|2004||12053||342 (2.8%)||342 (2.8%)|
|2005||13115||640 (4.9%)||627 (4.8%)|
|2006||12746||1250 (9.8%)||1324 (10.4%)|
|2007||12197||2109 (17.3%)||2192 (18.0%)|
|2008||10782||2121 (19.7%)||2222 (20.6%)|
|2009||8803||2361 (26.8%)||2477 (28.1%)|
|2010||8714||2599 (29.8%)||2637 (30.3%)|
|2011||7180||2197 (30.6%)||2297 (32.0%)|
|2012||6339||2123 (33.4%)||2164 (34.1%)|
Following on from the initial bulletin (No19) on the impact of DNA testing, data from earlier years has been supplied by the KC. Although some dogs registered prior to 2004 were hereditarily clear for HC-HSF4 and/or L-2-HGA, the numbers were erratic probably due to results being added retrospectively and not actually at the time of registration. These early results are of little use for assessing trends. The first year where a significant amount of testing seemed to have been undertaken was 2004, so the numbers of puppies that were hereditarily clear are presented in the table below, up to and including 2012, the last year where full results are available.
From 2004 onwards, there was a steady increase in the percentages of puppies that were hereditarily clear for both conditions up to 2009. From 2009 to 2012 the annual increases were not so marked suggesting that there may be a ‘flattening off’ or that any future increases are likely to be modest in comparison with earlier years. This is something that might have been expected.
It is interesting that while total registrations have halved between 2006/7 and 2012, the actual numbers of hereditarily clears have remained on the whole pretty constant at over the 2000 mark, without any pro rata decrease. A possible explanation is that the vast majority of hereditarily clear puppies are bred by ‘show’ breeders who, as we know, have been very successful in eliminating both recessive genes from their stock to nearly the 100% level. If the show fraternity continued to breed at similar, or only slightly lower, levels from 2007 onwards to what they did in earlier years then the number of puppies, which will be virtually all hereditarily clear, will remain reasonably constant from year to year. It is thus possible that the decline in total registrations is largely due to decreased activity by ‘puppy farmers’ and ‘backyard’ breeders. Alternatively, if the numbers of puppies bred by show breeders declined over the period this would be accompanied by a similar decline in the number of hereditarily clear puppies. Thus the fact these have not declined similarly may suggest that there has been an increase in ‘non-show’ breeders testing their dogs routinely, but determining what is actually the case is very difficult, if not impossible.
Monitoring registrations in the years to come will be required to determine further increases in the proportions that are hereditarily clear but, irrespective of the success achieved so far, especially among the show and breed club fraternity, there is still the problem of stressing to all breeders the need for proper control of these conditions for which there are DNA tests; unfortunately many will not want to know but some may be convinced of the benefits of testing which is now second nature to all responsible breeders.
Health Bulletin No 20, January 2014
Further observations on the impact of DNA testing.
In Bulletin 19A, the impact of DNA testing for HC-HSF4 and L-2-HGA was discussed. It was shown that over the nine year period from 2004-2012, the proportion of dogs being registered which were hereditarily clear for these conditions rose steadily, By 2012 approximately a third were clear for each. Previous studies have shown that virtually 100% of dogs produced by show breeders and those associated with the clubs are ‘clears’ but the impact of this on the overall figures is difficult, if not impossible, to assess. Do ‘show’ breeders account for all the clear puppies being produced or is testing being adopted by ‘backyard’ breeders to any extent? It is impossible to assess this from registrations listed in the Breed Records supplement although analysis of DNA test results in the BRS suggested that some non-show breeders were ensuring either the sire or dam of a litter were clear to so that there would be no risk of affected puppies being born. However as we are not aware of any ‘show’ breeders deliberately breeding for blues, analysis of the status of blues being registered may serve as an indication of testing by non-show breeders. Of course blue puppies are occasionally produced by show breeders but their numbers are small and would not have a major impact on the figures especially as many all blue litters from two blues parents are registered currently. Registration figures, plus hereditarily clear status, for blues were thus obtained from the Kennel Club and compared with the data for all registrations and also ‘non-blues’.
The total number of registrations, divided into all other colours (i.e. non-blues) and blues of all variations from 2004 to 2013 are given in table 1.
Year Total ‘Non-blues’ Blues
2004 12053 11767 (97.6%) 286 (2.4%)
2005 13115 12520 (95.5%) 595 (4.5%)
2006 12746 11616 (91.1%) 1130 (8.9%)
2007 12197 10351 (84.9%) 1846 (15.1%)
2008 10782 8518 (79.0%) 2264 (21.0%)
2009 8803 6206 (70.5%) 2597 (29.5%)
2010 8714 5626 (64.6%) 3088 (35.4%)
2011 7180 3717 (51.8%) 3463 (48.2%)
2012 6339 2873 (45.3%) 3466 (54.7%)
2013 5601 2170 (38.7%) 3431 (61.3%)
Table 1 Numbers of blue and non-blue puppies registered from 2004-2013.
While incidental to the main objectives of this study, these figures do not make good reading showing that over three fifths of registrations in 2013 were some variant of blue such as blue, blue brindle, blue fawn, all with or without white. Although no figures were sought, a quick look at any edition of the BRS will show many all blue litters being produced by mating two blue variants together. Many mixed litters containing both blues and other colours are registered too but it is not known how many of these are the result of matings designed to produce some blues e.g. a blue being mated to a known carrier of the colour, or being produced by the chance mating of two non-blues that were carriers unknown to the breeder. Despite spread of the blue gene(s) into ‘show’ stock, where it has been previously low, would seem inevitable, we can assume that the majority of ‘show bred’ puppies are in the non-blue category. It is impossible, however, to say how many ‘non-blues’ are bred by active exhibitors and club members or by casual or ‘backyard’ breeders.
The overall incidence of hereditarily clear puppies for both HC-HSF4 and L-2-HGA are presented in table 2 which is an updated version of that published in Bulletin 19A. Tables 3 and 4 present the numbers of ‘clears’ for ‘blues’ and ‘non-blues; respectively.
Year Total HC-HSF4 Clear L-2-HGA Clear
2004 12053 342 (2.8%) 342 (2.8%)
2005 13115 640 (4.9%) 627 (4.8%)
2006 12746 1250 (9.8%) 1324 (10.4%)
2007 12197 2109 (17.3%) 2192 (18.0%)
2008 10782 2121 (19.7%) 2222 (20.6%)
2009 8803 2361 (26.8%) 2477 (28.1%)
2010 8714 2599 (29.8%) 2637 (30.3%)
2011 7180 2197 (30.6%) 2297 (32.0%)
2012 6339 2123 (33.4%) 2164 (34.1%)
2013 5601 1788 (31.9%) 1871 (33.4%)
Table 2. Numbers and percentages of hereditarily clears registered 2004-2013
Year Total HC-HSF4 Clear L-2-HGA Clear
2004 286 7 (2.4%) 7 (2.4%)
2005 595 20 (3.4%) 25 (4.2%)
2006 1130 57 (5.0%) 66 (5.8%)
2007 1846 223 (12.1%) 219 (11.9%)
2008 2264 314 (13.9%) 377 (16.7%)
2009 2597 563 (21.7%) 611 (23.5%)
2010 3088 759 (24.6%) 800 (25.9%)
2011 3463 860 (24.8%) 904 (26.1%)
2012 3466 878 (24.3%) 920 (26.5%)
2013 3431 937 (27.3%) 987 (28.8%)
Table 3. Numbers and percentages of hereditarily clear ‘blues’ registered 2004-2013
Year Total HC-HSF4 Clear L-2-HGA Clear
2004 11797 335 (2.8%) 335 (2.8%)
2005 12520 620 (5.0%) 602 (4.8%)
2006 11616 1193 (10.3%) 1258 (10.4%)
2007 10351 1796 (17.4%) 1973 (19.1%)
2008 8518 1897 (22.3%) 1845 (21.6%)
2009 6206 1798 (29.0%) 1866 (30.1%)
2010 5626 1840 (32.7%) 1837 (32.7%)
2011 3717 1337 (36.0%) 1393 (37.5%)
2012 2873 1245 (43.3%) 1244 (43.3%)
2013 2170 851 (39.2%) 884 (40.7%)
Table 4 Numbers and percentages of hereditarily clear ‘non-blues’ registered 2004-2013
From table 2, we can see that there has been a slight drop in the incidence of hereditarily clear dogs being registered during 2013 for both conditions; this will be discussed further below. Of greater interest are the findings in the blue population (Table 3) which may reasonably be taken as representative of dogs bred by those not associated with the show scene or the clubs. Although they are lagging behind the overall average, approximately 28% as opposed to 33%, one can conclude that DNA testing has been adopted by a proportion of such breeders at least, with the proportion of clear puppies increasing from year to year. It would probably be reasonable to assume that some ‘non-show’ breeders of other colours are also embracing DNA testing. Even if some backyard breeders only ensure either the sire or dam of a litter is clear, this will, in time, lead to a reduction of the recessive genes in the population and thus an increase in hereditarily clear levels although more slowly than if a more vigorous testing policy was adopted.
As might be expected the levels of hereditarily clears were greater, around the 40% mark in ‘non-blues’ (Table 4). This is almost certainly due to the inclusion of show stock which is nearly 100% clear of both recessive genes and thus boosting the overall figures. There was a slight drop in the percentages of hereditarily clears for all colours combined and this is clearly due to the similar drop in those of the ‘non-blues’. Why this has occurred is difficult to say, principally because we do not know what proportions of ‘non-blues’ are produced by show/club and ‘backyard’ breeders respectively. A significant drop in puppies produced by show breeders, and thus clear stock, is a possible explanation. Alternatively a surge, even a comparatively small one, in litters from untested backgrounds being registered might account for this drop. This slight drop might just be a ‘blip’ of no significance but continual monitoring is essential.
Despite the inherent difficulties in identifying which breeders or groups of breeders may or may not be testing for HC-HSF4 and L-2-HGA, it would appear that some breeders not associated with the clubs are DNA testing. Whether this shows real concern about such health issues or whether it is down to commercial concerns is irrelevant, the desired result is being achieved. Naturally it is hope that, despite the small downturn in 2013, the proportions of hereditarily clear puppies being produced annually will increase in future years. This will be comparative easy to monitor, but nevertheless the promotion of appropriate DNA testing must remain a priority for all involved.
Our thanks is due to Bonnie-Marie Abhayaratne of the Kennel Club Health Department for supplying the relevant data.
Health Bulletin No 21, April 2014.
There has been much discussion recently about persistent hyperplastic primary vitreous (PHPV) regarding incidence and whether mildly affected cases may be used for breeding, although the standard advice from the geneticists and ophthalmologists has always been not to breed from affected dogs irrespective of how mild their condition may be. This bulletin will therefore try to give an update on its incidence and current trends.
Results of routine testing.
These are based on dogs tested under the KC/BVA eye testing scheme and were kindly supplied by both the KC and BVA, and reported in the KC’s Breed Records Supplement. Although eye testing was becoming routine after the issue of PHPV arose in the 1980’s, early figures are perhaps inconsistent so the data is presented below from the start of 1994 to the end of 2013 in two ten year periods.
Years Dogs tested PHPV affected % affected
1994-2003 1877 20 1.07%
2004-2013 3027 17 0.56%
Totals 4904 37 0.75%
The apparent reduction between the two decades has to be treated with caution. Firstly we do not know how many re-tests are included either for dogs owned by Assured Breeders who are obliged to have a current eye certificate for their dogs or those owned by non-ABS breeders who nevertheless follow the guidelines as it is ‘the right thing to do’. Re-tests could account for 10% of tests in recent years with some dogs being tested three or four times. Secondly litter testing has increased and affected puppies are almost certainly never going to be bred. Hence, they are most unlikely to have an adult eye test, thus removing them from the system. Detecting even a very small number of affecteds as puppies instead of adults could have a considerable effect in reducing the percentage affected of dogs tested as adults. Unfortunately, unlike continental Europe where cases of PHPV are graded 1-6 according to severity, there is no such system in place routinely in the UK so we have no idea what proportion of the 37 affected cases were mild or severe.
To enable some comparison, data has been obtained from Norway and Finland. In Norway, 1657 Staffords were examined between 2006-2013. Of those 53 (3.2%) were affected with PHPV; 45 (2.7%) were grade 1 and thus mildly affected, three (0.2%) were probably grade 1 but unconfirmed, while five (0.3% of all dogs tested or 9.4% of those with PHPV) were grades 2-6 and thus more severely affected. In Finland, from 2009 to 2013, 651 dogs were examined; thirteen (2.0%) were affected with PHPV, twelve were grade 1 and only one was grade 2-6.
How important these differences between countries are, is difficult to say. As numbers are comparatively low, it would only take a couple of litters with, let’s say, four or five affected dogs out of seven or eight puppies, to skew the figures if all found their way into the testing system. A more likely answer is the use of grade 1 affected dogs for breeding as the current European advice suggests that grade1 dogs may be used but not grades 2-6, in contrast to the advice given to British breeders of not using even dogs only mildly affected in their breeding programmes. Gathering data on litters where one of the parents is affected with PHPV is under way but will take some time and beyond the scope of this report.
Parental history of affected cases
The eye test status of the parents of the affected dogs reported under the KC/BVA scheme from 1994-2013, plus a single case from 1993, were investigated using the KC’s test result finder service. However one of the later affected dogs was foreign bred so no parental tests are available and is thus omitted, although still leaving a total of 37 affected dogs the results for which are given below.
Both parents unaffected. 17 (45.9%)
Both parents untested under KC/BVA scheme. 11 (29.7%)
One parent unaffected and one parent untested. 8 (21.6%)
One parent AFFECTED and one parent untested. 1 (2.7%)
Perhaps of greatest interest is the case with one affected parent. This is a bitch with an affected dam which is also included on the list of affected dogs. Interestingly the daughter was tested before the mother, suggesting the latter’s test was only undertaken on discovery of the affected offspring. This finding is consistent with inheritance of the condition but the fact that seventeen affected dogs had unaffected parents must also be considered, suggesting that the mode of inheritance may not be a simple one.
About eighteen months ago, the results of litter testing 2008-2011 was reported in a previous bulletin; 128 litters had been tested during these four years and six (4.7%) had been found to contain one or more affected puppies. Of the combined total of 31 puppies in these litters, eleven (35.5%) were affected. Following on from these, during 2012-2013 a further 131 litters have been tested; 50 in 2012 and 81 in 2013, showing an increasing uptake by breeders.
Of these 131 litters, six (4.6%) were found to contain one or more puppies affected with PHPV; five of the litters had two affected out of four to seven puppies while the remaining litter was one out of three. Thus of a combined total of 31 puppies in the six litters, eleven (35.5%) were affected. Apart from a couple of extra litters tested and minor differences in the numbers in those with affected puppies, the results for these litters from 2012-2013 are, co-incidentally, identical to the previous four years.
If we combine these results to cover the six year period from 2008 to 2013, 259 litters have been tested and twelve were found to contain one or more affected puppies with numbers ranging from 1:8 to 5:6. These litters had a combined total of 62 puppies with 22 (35.5%) affected. The number of puppies tested in those litters with none affected is unknown but if we assume the average number of puppies in all litters examined to be five (in previous bulletin it was taken as 4.7 based on other studies but further research suggests that it may be nearer five), this means that around 1300 puppies have been examined and 22 (1.7%) were affected. Despite being a bit greater than the percentage affected on routine testing over the past decade, for which there are several reasons as discussed previously, it is nevertheless compatible with routine findings both here and in Europe. A major problem is that the results of litter tests are not published in the BRS, their parentage is thus unknown and not only is one unable to ascertain the eye test status of the sire and dam but it is also unknown if there is any common factor, such as same sire, between any affected litters.
It is probably important that the PHPV cases found are concentrated in a comparatively small number of litters. This supports the belief that there is a genetic cause for PHPV and it is thus hereditary although the mode of inheritance is still unknown. If it were a random occurrence that ‘just happened’, a wider scatter through a larger number of litters would be expected.
It is hoped that litter test results will be reported routinely in the near future thus allowing them to be analysed in greater depth. It would also be beneficial if some grading system of severity was put into place, as it is in Europe; this might enable greater understanding of why severity varies and whether mild cases can indeed produce more severely affected ones if used for breeding. Currently information is being sought on litters being bred where sire or dam (or even both) are PHPV affected and it is hoped this may be presented in the near future.
Thanks are due to Catrine Arntzen and Cvetka Bogovcic for their invaluable assistance in supplying the European figures included.
Health Bulletin No 22, May 2014
Previously in Bulletin No13, the number of cases of posterior polar sub-capsular cataract (PPSC) diagnosed from 2009 to 2011 was reported. Initially only six cases were reported by the BVA at that time but this has now been amended to seven. Over 2012-2013 a further two cases have been reported so these will be combined with previous figures.
Thus from 2009 to 2013, nine cases of PPSC have been reported from a total of 1262 adult eye tests giving an incidence of 0.7%; we do not know exactly how many of the total dogs are retests, nor if any cases were detected in dogs being retested, but as retests have been estimated to be perhaps about 10% of the total, we can be confident that the incidence among dogs being tested is less that 1.0%. Data from Finland indicates that six cases were found among 651 dogs tested between the same years, 2009-2013, giving a similar incidence of 0.9%.
Of the nine UK cases, six were one year olds when diagnosed, and the remaining three were 3yo, 5yo and 8yo respectively. The one year old dogs would almost certainly be diagnosed at their first adult eye examination. The same may be true for the dog aged three if testing was delayed until being bred for the first time, and even the five year old. As for the eight year old dog, one would have expected it to have had its eyes tested on a previous occasion especially if its owner was a show breeder, although it is possible that the dog was undergoing a full eye examination for another reason and finding PPSC was co-incidental.
Initial thoughts were that PPSC tended to develop mainly in older dogs but this is clearly refuted by finding two thirds of these cases in dogs aged less than two years. PPSC has been found in numerous breeds and may be there from six months of age upwards although it is considered it may develop at any age. It was always considered that dogs with PPSC suffer little, if any, visual impairment but there have been a few reports of it progressing to affect sight although we do not know in what breeds nor how often this has actually occurred.
Labrador Retrievers are one of the main breeds associated with PPSC. On one relevant site, no information is given on its incidence although considered to be the most common type of cataract in that breed and may usually be diagnosed from about 12m old. It would also appear that PPSC may progress in less than 5% of affected Labradors. Extrapolating data from one breed to another requires the greatest caution, but if the risk of progression was the same it would mean that the chance of a Stafford having sight problems with PPSC is approximately only 1:2000 We are aware, anecdotally, of one case being found in a 5yo SBT which had had a couple of previous clear eye tests, but there would appear to be no reports of any PPSC affected Stafford developing visual impairment as a consequence.
These figures suggest PPSC is not common in SBTs although determining its incidence accurately would require the examination of a large number of older dogs perhaps aged ten or more to see how many have actually developed it and if it had caused any sight problems. Clearly they have implications for future eye testing policies but this is a matter to be discussed by the Clubs.
Health Bulletin No 24, March 2015.
Discussion about blues and the numbers being registered is seldom off the various social internet sites. Like everyone else, I deprecate the actions of those who breed blue Staffords (or French Bulldogs etc.) purely for money without due regard for the quality of their dogs, whether in relation to the Standard or to their health. The topic has become so emotive that clear thinking has become very cloudy in many instances. As one who simply wants the scientific truth in this matter (and all other such topics) I have sought the comments of the academic experts, as well as trying to get reliable information on any associated problems.
I will assume that readers will understand the workings of the ‘D’ (dilution) gene and its recessive ‘d’, of which there are at least two alleles or variants, one of which is more common in dogs in general and is the only one to be found in some breeds; it is not known if both are present in Staffords or not. It is ‘d’ when homozygous, i.e. a dog carries two copies, one from each of its parents, that produces ‘blue’ by causing the eumelanin (black) pigment in hairs to clump rather than be evenly distributed throughout.
Firstly a question – ‘Is there any difference, in respect to ‘d’(assuming it is the more common allele involved), between a blue dog produced by two brindles that carry it or one which is the result of blue to blue matings over several generations?’ The answer is simply ‘No’! If you tested each dog, either by DNA sequencing or by the DNA tests for ‘d’ offered by some companies, you would get exactly the same result, which in turn means that the expression of ‘d’ in both would also be the same. In the course of correspondence regarding blue to blue matings, Prof Schmutz of Saskatchewan University, who is regarded as the queen of colour genetics, simply stated that you can’t get “more homozygous” by the process and did not see why it would matter, thus supporting what has been pointed out above. Prof Tosso Leeb of Bern University, whom I also consulted, responded in a similar vein seeing ‘no rational reason for a ban on blue x blue matings’
Some confusion may have arisen by using the term ‘dilution’ for the gene which in scientific literature is now referred to as the MLPH gene in accordance with its function at the molecular level. It was the American geneticist, Clarence Little, the father of coat colour genetics, who coined ‘D for dilution’ in the 1940s on account of its recessive ‘d’ ‘diluting’ black to blue (actually a slate grey) as he put it and nothing more. Some however may have the impression that when you mate two blues or dilutes together you are then ‘diluting’ further and further with each generation, which is simply untrue. Once the initial ‘dilution’ has occurred to produce the blue dog which is homozygous ‘d/d’, then that is the dilution process complete!
There are of course anecdotal reports of blue to blue matings producing coat and other problems, plus comments that many blues are different from other colours in build and appearance. Should this be considered so, it is almost certainly a question of ‘bad’ breeding rather than ‘blue’ breeding. If you breed for one particular aspect, in this case a colour, without regard for the whole dog (or other animal) then you are asking for trouble. This is something that has been seen in other species, for example in cattle where breeding for milk production solely has had serious adverse effects on cows’ health.
The big problem is a virtual total lack of data, i.e. peer-reviewed papers in scientific journals, and there would need to be several to ensure that any finding was corroborated. I am aware of some papers of a histological or molecular nature but none on the incidence of coat colour-related conditions in dogs in general or in specific breeds. (If anyone comes across any, please let me know.) Hearsay and anecdote have been the basis for so many opinions when firm data is essential. In fact a vet I was talking to very recently at a seminar highlighted this lack of facts and figures.
In Staffords we must be very aware that perceived coat problems may not be confined to blues. I know we are again forced to rely on anecdotal opinion, but if one goes back thirty years or so you may have heard of certain stud dogs being associated with progeny with poor coats and I do recall seeing brindle dogs, supposedly from a certain popular line, with ‘spectacles’ of hair loss round their eyes. Some may recall I asked vets from a large canine charity (Health Bulletin 14), plus others along the way, for their thoughts and clearly the body of opinion was that blues were no more affected with skin and coat conditions than other colours, in fact some vets consider that whites may be at greater risk.
Currently the greatest hope of getting meaningful data is the VetCompass project which receives information, including coat colour as well as the usual parameters, from many veterinary practices on all ‘patients’ being seen. I have spoken to Dr Dan O’Neill the veterinary epidemiologist in charge about our concerns. At the moment no data has been extracted in relation to coat colour but, having asked the right questions, it is on the ‘to do’ list. However, even if health conditions were found to be more prevalent in blues (or any other colour), thus showing a correlation, that would not be the end of the matter. Correlation does not equal causation! Further studies would be necessary see if the colour genes were actually involved and to rule out co-incidental findings such as inadvertently selecting genes for other conditions.
To appreciate why great care is needed with ‘correlation’ we only have to look at the hereditary cataract cases that emerged in the late ‘nineties’. There was a correlation with the red breeding, with a few saying to keep away from the ‘reds’, but no one with the least understanding ever claimed it had anything to do with their coat colour or the genes that produced it. It was just chance that it came to the fore in reds.
The one condition that is associated with blue dogs is colour dilution alopecia (CDA) where the blue hairs become fragile and break off. It can vary in severity and may lead to extensive bald areas where the skin may be affected by dryness and infection requiring long term topical treatment. White areas, if present, are not affected and in blue fawns CDA is likely to be much milder simply because of there being much more phaeomelanin (red) than eumelanin (black) in their hairs. However many blues (of many breeds where the genes are the same, as well as Staffords) have good, even excellent, coats with no problems so one cannot say that, although only blue hair is affected, the d/d genotype is specifically the cause. Expert opinion now considers that some other, as yet undescribed, genetic factors are involved; these will also be carried by non-blues but have no effect because of the different coat colours. There have been attempts to understand CDA but sadly very little progress has been made and there would seem to be no current research. Prof Leeb does have a call online for case reports plus specimens; I have no idea what the response has been but one suspects it has not been overwhelming. This may simply reflect a low incidence of CDA but perhaps VetCompass will shed light in due course. In addition, only one of the vets surveyed from the large canine charity referred to above reported seeing a case of CDA. Furthermore if a blue dog does have hair loss, all other possible diagnoses, such as demodex, allergy, etc., must be eliminated before considering CDA and if there is reasonable recovery, CDA can almost certainly be excluded. In the course of discussions, it was suggested that if breeders of blues were concerned about the possibility of CDA or similar coat and skin problems, then they ought to ensure they used only dogs with visibly good coats. This of course is common sense and constitutes ‘good’ breeding.
Of course the absolute way to eliminate all risk of CDA would be to discourage or prohibit breeding for blues as the colour is essential for the expression of those genes that may be the real cause. As far as we in UK are concerned, this would mean changing the Standard by deeming blue to be ‘highly undesirable’ along with liver and black and tan.. In fact some years ago I wrote an article to this effect pointing out the anomaly of permitting blue but not liver or black and tan, bearing in mind that black and tan is a perfectly normal coat colour and liver is produced by black eumelanin being replaced with the brown variety, without any hair abnormality, which the eumelanin clumping in blues undoubtedly is.
As many know, there was no mention of ‘blue’ in the original 1935 Standard, being only added in the 1948 review. There is no documented evidence of why this was done to my knowledge. It may be that blues pre-1948, were included with brindles and fawns but added after the genetics had been described by Little as mentioned above. Thus if a change in the Standard to discouraging blues, because of perceived health issues, were to be proposed, the inevitable question is why has it taken well over sixty years to be raised? And more importantly, where is the evidence, in the form of peer reviewed papers, which will withstand scientific scrutiny?
Even if the KC were persuaded to implement such a change, the greater threat of legal action is a possibility. A commercial breeder, all above board and licensed with the local council, might sue the KC (or other KC’s or similar bodies that have implanted colour breeding restrictions for registration) as their business might be adversely affected. Unless I am greatly mistaken (the legal experts will correct me I’m sure) the KC would back down rapidly as they would know that it was a lost cause.
Health Bulletin No26, March 2015
KC Update on Health Testing
The 2014 Dog Health Group Report has now been published and with it the KC have supplied data on health testing over a fifteen year period and for 2014 up to November 1st. Rather than simply put up the relevant tables, I thought it better to present only the Stafford data to save folk the bother of going through all the breeds listed.
Test/Period Number tested Clear Carrier Affected Hereditarily Clear
HC-HSF4: 15 year 2206 2131 75 0 19789
HC-HSF4: 2014 75 73 2 0 1916
L-2-HGA: 15 year 2451 2223 224 4 20406
L-2-HGA: 2014 85 83 2 0 1984
The numbers coming through as hereditarily clear on registration demonstrates the success of the testing scheme. However it should be noted that the numbers of hereditarily clears and those tested do not equal the total registrations. While we are at the stage that virtually all show bred litters are clear, it is evident that this is not the case with ‘non show’ stock. Many non-show bred dogs are hereditarily clear, but others are the produce of breeders who ensure at least one parent is clear so that no affected puppies are produced, and it is also evident that an unknown number of breeders are producing litters with no regard to their health test status, running the risk of producing affected puppies.
This is over the 15 year period only.
Total tested Clear Total Affected PHPV Affected HC Affected
4456 4420 36 28 8
It should be noted that we do not know how many of the total are re-tests so total dogs tested may a bit less. The numbers of PHPV affected dogs does not include any detected on litter testing so cannot be used to determine the incidence accurately. In addition those with hereditary cataract may not all be of the juvenile HC-HSF4 variety. Rather contentiously some vets have deemed the odd dog to have a different type hereditary cataract when tested and although efforts have been made to clear the situation, they may still appear under this heading. The test numbers again are only a fraction of the numbers registered but this is to be expected as few, if any, pet Staffords will ever be tested under the KC/BVA scheme if there are no sight problems.
During the 15 year period, 43 Staffords were hip scored under the scheme with only one being tested in 2014. The mean (average) score was 13.58, the median (midpoint of the dogs tested) was 11 and the overall range was 0-53. The mean for the last five years was reported as 17.27 and the median as 12, but the relevance of this must be dubious as the numbers are very small compared with other breeds. As hip scoring is not required or recommended for Staffords under the Assured Breeder Scheme nor by the clubs, we have no idea why these dogs were tested. Some may have been tested because of a clinical problem so the limited data presented may not be representative of the breed as a whole.
To see the full report go to:
Health Bulletin No 28 May 2016
I was just turning things over in my mind when I asked myself the question ‘Is there any difference in the co-efficient of inbreeding (COI) between the blues and non-blues?’ This was prompted by several issues. Firstly there is the concern about the apparently large numbers of blues being bred, secondly there seems to be several popular blue sires producing more litters per year than the most popular of non-blue sires especially any on the show scene, and thirdly some of these blue sires have, themselves, extremely high COIs well in excess of 30%, or, to put it another way, they are more closely inbred than father x daughter, or brother x sister, progeny. To help answer the question Dr Tom Lewis, who is now the geneticist on the Kennel Club Health Team, very kindly dug out all the relevant data and some is surprisingly interesting.
Fig 1, Registrations of blues and non-blues on a yearly basis from 2000 to 2014.
Before we look at any COIs, it is worth looking at Fig 1 which shows the number of registrations, by year of birth, of blues (i.e. all dogs where blue is mentioned in registration) and non-blues (i.e. all other colours) annually from 2000-2014 (certain 2015 data are not yet available at time of writing). This is based on the colours being registered and does not differentiate blues from all blue litters from mixed litters of different colours or the odd unexpected blue from ‘out of the blue’, but this does not distort the overall picture. From this we can see that non-blue registrations peaked at over 12,000 in 2005 after which there was a steady, and rather remarkably sharp, decline to less than 2000 in 2014. On the other hand the number of blues being registered was very small until 2004 after which they increased steadily until peaking at less than 4000 in 2013. It is claimed that non-blues are being swamped by the increasing number of blues being bred but this graph clearly shows that there is only partial truth in this at most, and certainly not the whole story. It may be that the increase in blues has resulted from some breeders, who are not associated with the Clubs or the show scene, switching colours from brindle or red etc. to blue, but this does not account for the massive decrease in non-blue. Any switching of colour preference can only account for less than 4000 dogs of the total decline at most, but this leaves about 6-7000 registrations (in the region of 1000-1500 litters per annum) to be accounted for when comparing with peak numbers. Thus over half the decline in the numbers of non-blues being bred is simply due to there being fewer breeders, breeders having fewer litters or a combination of both. Unfortunately we tend to look at colour ratios on a comparative percentage basis, so if one goes up as a percentage then another must go down, but in this instance the basic totals of each present a truer picture. Thus, despite the increase in totals of blues, the major problem is the numbers of brindles and reds etc. that are not being bred! A contributory factor to this may be breeders being made to feel guilty through the repeated claims of more and more dogs in rescue (and I mean all rescues including the large national charities) or feeling they may be called ‘puppy farmers’ if they have more than the occasional litter.
Fig 2 Mean (average) COI for blues and non-blues by year of birth
Fig 3 Median COIs for blues and non-blues by year of birth.
Figs 2 and 3 give the mean (average) and median (value of dog in the middle of the whole range) COIs, respectively, by year for blues and non-blues. Firstly may I point out that the COI values at the left hand side (y axis, to be technical) are given as a proportion and not percentage so 0.02 equates to 2%, 0.04 to 4% and so forth, plus the values on each graph are not identical. The error bars should also be ignored but more importantly we should also ignore any data given for blues prior to 2005 when their numbers really started to increase. Prior to that time their totals were very low hence results tend to be erratic from year to year.
Whether it is the mean or median values that are being considered, it is clear that the COIs of both blues and non-blues increased between 2006 and 2014, although the median values possibly give a better picture overall. The mean values may be affected by dogs with extremely high COIs which increase the average to a greater or lesser degree. There are also the frequently used blue stud dogs with COIs of over 30% and each will almost certainly have siblings with the same COI, hence it is easy to see how they might affect the average. Of course it is possible to have non-blues with high COIs but any of over 30%, as with blues, do not seem to occur often, if at all. On the other hand any shift in the median value shows that the group as a whole has shifted and is unaffected by dogs with high values well outside the main range. It is also clear that the mean and median COIs of blues show a greater increase over the period than that of non-blues.
Fig 4, Histogram covering three five year periods, 2000-2004 top, 2005-2009 middle, and 2010-2014 bottom, giving proportion of dogs on left and COI values increasing from left to right on bottom
Fig 4 is interesting as it shows changes from a slightly different perspective covering three time periods: 2000-2004 in the top two graphs, 2005-2009 in the middle two and 2010-2014 in the bottom ones. The left hand side (y axis) gives the proportions of registrations and as before 0.1 equals 10% etc. and the bottom line (x axis) gives the COI value and again 0.2 equals 20% and so forth. Looking at the first two time periods, 2000 to 2004 and 2005 to 2009, the column denoting the COI value of the greatest proportion of dogs in each group (this is technically known as the modal value or simply modal) shows that almost 40% or greater of dogs born, blue and non-blue, in the period had low COIs of 3-4%. Of course there were some with greater COIs mainly in the region of 5-10% and, perhaps inevitably there were odd ones with very high COIs but these may just be blips as you move to the right of the graphs. However if you look at the bottom two graphs, covering 2010 to 2014, it will be seen that the modal for non-blues was still 3-4% but had decreased from almost 40% of registrations in the period to about 30%. With blues the proportion in the 3-4% group had dropped from about 50% during 2005-2009 to just over 20%, and modal for the group was now 5-6%. It is also evident that the columns representing COIs greater than the modal in the region of 7-20% had increased. This shift to the right in the graph denotes a general increase in COIs and is consistent with the increasing mean and median COIs shown in Figs 2&3.
One might wonder of the increase in the average COI of non-blues was related to the dramatic decrease in litters and thus births. This is not illogical, asking if the lesser numbers being bred led to greater inbreeding and perhaps gene loss. This however conflicts with the position in blues where the increase in average COI has occurred in association with an increase in numbers. The most likely explanation, according to Tom Lewis, is the popular sire effect, which may be more obvious in blues as there are several sires in this group whose use at stud far exceeds that of any current non-blue sire.
The effective population size (Ne, as it is usually expressed) must be considered along with the COI. The Ne is the theoretical number of ancestral individuals that are contributing to the current generations of a breed. It has no relation to the actual population size, hence a breed may be numerous with thousands being born annually but have a very small Ne and vice versa. (I am sorry if I have difficulty in explaining this briefly but complicated mathematics are involved which I would not attempt to understand). The Ne for SBTs is 98, which means that all the dogs being bred are the equivalent of 98 dogs breeding randomly from a genetic perspective. If a breed has a Ne of over 100 then it should be able to manage its genetic diversity and a balance between selective and inbreeding; between 50 and 100 could mean genetic diversity is being lost or previously high inbreeding has stabilised; and below 50 a breed could be heading for serious trouble. (Please see attached KC literature for a fuller explanation.) With a Ne of 98, the Stafford is on the borderline but this should not cause any real problems if breeders are sensible.
So what is the way forward? The good news is that the Stafford does not have the problems that some breeds face, such as those with high average COIs considerably greater than that of grandfather x granddaughter matings but with no sources of ‘new blood’ to go to. With non-blues while the average COI has increased over the past few years it is not very high and there are still sufficient non-blues being bred to make this sustainable. With blues, the COI has risen a bit quicker than non-blues but is still within sustainable limits although the various popular blue studs with COIs greater than 30% suggests that some extremely inbred litters are being produced with possible adverse effects in the long term. In this discussion I have treated blues and non-blues as basically two sub-populations despite any crossover and common ancestry, but while the Ne for the breed as a whole is 98 as stated above, this could in theory vary a little between such sub-populations.
From a practical point of view, the one thing we must try to avoid is doing anything that might damage the gene pool, while at the same time we ought not to be obsessed with COIs, as some in a few other breeds may be. Common sense should prevail. If your bitch has a significantly higher than average COI, let’s say 15-20% or over, then it is obvious one needs to choose a dog that will give a litter with a COI that is around the average or lower, and not a closely related one that might produce even greater COIs in the litter. On the other hand if a proposed mating would produce puppies with a COI that is greater than that of a dam (or sire too) with a low COI, that is not sufficient reason not to go ahead but with the knowledge care may be required with the next generation. It is a case of balancing selective versus in-breeding, by selective we mean choosing a partner that will enhance the virtues and correct any faults or weaknesses but with no specific regard to pedigree. When I started in Staffords over thirty years ago, we were told the best breeding practice was ‘in’ for two generations and then ‘out’ on the third. I have mentioned this to several of the geneticists and, guess what, they all thought this might not be a bad way to go! And now, unlike these ‘olden’ days, we have Mate Select on the Kennel Club’s web site so it is easy to find out not only what any dog’s COI is, but also the COI of litters resulting from any proposed matings.
We do not know what the future may hold and while we would all hope that we are not faced with problems associated with too much inbreeding, we can never be totally sure that we will never need to look for ‘fresh blood’. If such problems did emerge whether in non-blues or in blues, then the answer may be to cross one with the other, should the two apparent sub-populations still exist. I have no doubt a population of brindles, reds etc. will be to the fore in the future but the comparative popularity for blues could easily decline. There have been suggestions for some time that ‘white’ could be the ‘new blue’ but this has not yet come to pass. I realise all too well that such suggestions are anathema to many who would never contemplate using a blue stud or, more likely, allow their dog to mate a blue bitch, but I am simply pointing out the possibility although it is taken for granted the quality of the dogs would be paramount if going down this route. It would be a ‘get out of jail’ card in time of need.
It may have been noticed I have not mentioned overseas dogs so far. The reason is that, on this occasion, you cannot extrapolate the data based on UK dogs to those in other countries with substantial numbers of SBTs, notably South Africa, Australia, New Zealand or Northern America. Of course Staffords in such countries did originate from British dogs initially but inevitably the breeding of subsequent generations would lead to inadvertent gene selection that could differ from back in Britain. In addition a number of stud dogs, which were widely used and had a significant effect on local populations, have been exported over the years, thus their genes are lost to the British pool but could persist at comparatively high levels in the local pools or regional sub-populations.
I have not mentioned Europe either in this respect but here too we could find the existence of sub-populations although defining these is not so easy with pet passports and increasing ease of travel. This makes it so much easier not only for our European friends to use stud dogs in the UK but also for British bitches to be taken to some of the top class dogs now gracing the European show rings. A further bonus is that it may be easier to import dogs from overseas through Europe as British quarantine regulations do not apply. And lastly, but far from least, is the comparative ease we now have in storing and exporting or importing semen which may enable fresh ‘blood’ to be introduced should the need arise.
Thus as far as the Stafford is concerned, we are nowhere near any crisis point regarding inbreeding, the mean COI or effective population size. But we cannot be complacent. If the average COI for the breed continues to show an upward drift or if the currently borderline Ne declines then action may be required. Fortunately we do have somewhere to go, unlike some breeds that are extremely inbred. With the Stafford now being popular all over the world, the option of using of using unrelated dogs or bitches by importing or exporting stock, or semen, is always available. Breeders do need to exercise care to ensure they do not inbreed excessively but perhaps sticking to ‘in for two and out on the third’ might suffice.