I think we can all be pleased that our puppy classes are so much better filled these days than they have been in recent years. If you want my personal opinion, I think that a lot of the 'bounce back' can be attributed to the fact that most breeders now taking a very sensible and pragmatic approach to the challenges of Juvenile Kidney Disease. I am certain that we went through a period when breeders were either too scared to breed at all, or when outcrossing at all cost appeared to be taking over. Bearing in mind how much hysteria was whipped up over the issue by folk who, quite frankly, should have known better, I'm not surprised that breeders responded in the way they did. However, my current take on it is that the vast majority of breeders now share the same view, that JKD is definitely something which we need to be mindful of but we should not completely over-react to it. There is absolutely no doubt that it has been with us since the breed was created and, dare I say, in the pre-internet age I'm sure that cases were conveniently swept under the carpet.
However, I do honestly believe that the incidence remains low and there are definitely other conditions which are far more detrimental to breed health as the last KC Breed Health Survey proved. I have said it before, and I will say it again, breeding dogs is like spinning plates. There are many variables that you need to be keeping an eye on and the knack is to balance out all of the competing issues when planning your matings. Unlike some folk who seem to spot dark ulterior motives everywhere (what kind of sad, paranoid world do they live in?).
I absolutely believe that the vast majority of Boxer breeders in this country are genuinely trying to breed the healthiest and most typey Boxers that they can. No breeder in their right mind wants their phone ringing with problems from past litters which could have been avoided and I find it hugely insulting when anyone suggests differently. However, very pleasingly, I see that the more hysterical internet contributions on the topic of JKD attract very little attention or comment these days. Boxer breeders in the UK are a down to earth group and they are certainly sensible enough to spot (and ignore) any troublemakers. Thankfully, there are very few (if any) troublemakers in the current population of exhibitors who are still actively involved in showing and breeding their Boxers in this country. I don't think any of us who are still living with the daily challenges of showing and breeding take very kindly to be lectured, hectored and sometimes abused by people who gave it up years ago. I know I don't.
I write at the request of the small international group of Boxer people (boxerjkd.com) who have dedicated much of their time over the last few years trying to understand and find a way through the inherited kidney disease problem that has come to attention in the breed. They are appalled by the disgraceful and demeaning comments directed at them by the Breed Notes correspondent who has also consistently sought to diminish and discredit the evidence on JKD from the start. We feel that a rebuttal that will put the whole problem into perspective is needed.
Nearly 40 years ago at a London and Home Counties Boxer Chatter event, a veterinary neurologist, Ian Griffiths, and I were describing an inherited progressive axonopathy (PA) that had emerged in Boxers when ago one famous Boxer breeder of the day stood up urging that PA was not so important and did not merit the attention it was being given. She was shouted down by the rest of the audience. This was at just one of a series of the open meetings on the subject organised by all the breed clubs around the country, not only to describe the disease and its inheritance but also to show explicit film of the affected dogs. Everyone was very hot on the subject. Ultimately a very tough breeding control scheme was adopted with extensive breeder input; it was a total success. We no longer have PA. This action started a movement to deal with other Boxer health issues that came to the fore. This took us through the heart conditions aortic stenosis (AS) and cardiomyopathy (CM or ARVC) with these also being reduced or eliminated from the show section of the breed. But here we are now with an inherited lethal kidney disease and the spirit of that breeder of 40 years ago rises again. How is it in the new era, when everyone is aware of genetics and inherited disease in dogs, there is still such a lack of understanding?
We are told all we need to do is be mindful of the situation. What on earth does this mean? The health committee and, I am afraid, Breed Council have advocated the pedigrees of affected cases should not be made public. So how is any one to be mindful? Were it not for the boxerjkd.com publication of JKD pedigrees, Boxer breeders would have had to rely on treacherous ringside gossip and the like. I think boxerjkd .com has done very well by the breed both in this country and overseas.
And then there is criticism of hysteria about JKD on Facebook. There was no Facebook 40 years ago but with PA there were masses of very upset people. But they were mainly show breeders, because the non-show section did not follow the dog papers or club news and so would barely have heard of the disease and they had no way of discussing it either. Odd cases of PA would have remained odd cases. Whether these folk knew it or not their fate was in the hands of show breeders and this was to prove well-placed. But now we have a turn around with non-show people having the larger voice, on Facebook, and once the kidney disease was mentioned there, everybody was aware. New cases were reported in this medium, and so the movement for action took off with some show people leading the way. And, through Facebook, which is the only medium that is not tightly controlled, JKD quickly became recognised as a major international problem despite the lack of concern expressed in the dog press and the absence of any open meetings. Was this hysteria? It was real. We could not wish it away. Something had to be done and the only group to take it up were the boxerjkd.com members, greatly aided by this public support and also by many concerned show breeders. Cases were reported and pedigrees published along with carefully-assessed breeding guidelines. But do we have support from the Breed Notes correspondent? No, we are considered merely as trouble makers. Are we now back to the ignorance and poor thinking of 40 years ago?
But why the turn-around in thinking about inherited disease? My answer, based on genetical issues rather than political, is that with PA there was a neat recessive inheritance where on average 25% of puppies in affected litters suffered the disease. Everyone could understand this. But now with JKD, as also also with ARVC, there is the problem that only a small proportion of the genetically affected cases actually develop the disease and this leads to disbelief in the severity of the problem. So is JKD really a major breed problem? Is it worth bothering about? Yes it is, because it is not just the incidence of affected pups that we have to think about, horrible as the disease is (photos) but the far greater incidence of carriers and undetectably affected dogs. These will greatly increase in frequency if we continue to breed from JKD-producing animals. This is how JKD is to be found everywhere in the world; it is an international problem for the breed. I suggest the lack of perception of JKD in earlier days was not necessarily a hide-it-under-the-carpet thing’; the kidney disease was simply not recognised as inherited – until mass inbreeding in the UK and over-use of certain dogs brought it to light.
So the bottom line is that the only means at our disposal for dealing with JKD is NOT to breed further from animals that have produced it (and widen the stud dog options). To do otherwise only propagates the disease gene. Such selective breeding is aided by the JKD pedigrees published by boxerjkd.com, but probably limited by the withholding of other pedigrees by the Health Committee.
The breeding recommendation was made by boxerjkd.com, and do not forget that members of the group have successful breeding and showing experience with Boxers here or abroad, and have many years’ experience on health committees. Moreover, three of us are professional research geneticists. And, for my part and blowing my own trumpet, I have probably worked with more new mutations and totally novel inheritances than anyone else on the planet. Furthermore, none of us is linked to any breeder group that could be deemed to risk personal bias, and indeed I felt I had to drop all Boxer breeding to deal with what I saw as the emerging huge JKD problem.
There is, as everyone knows a last ditch effort to find the location of the gene for JKD. This attempt uses a very different approach from all other methods and has had enormous backing from Boxer breeders around the world. It is funded by the former Council of Docked Breeds and notably also by The Kennel Club. I pray that it has success, but believe me, if it does there could then be serious panic notably in the UK where I expect the incidence of carriers in UK populations might be frighteningly high. So, again, it would be wise to apply some simple selective breeding now to reduce the incidence of carriers as much as possible before any gene test comes into play.
What is needed in effect is an end to all this opposition and unwarranted criticism but instead full support from all, including our Breed Council, both for the efforts of boxerjkd.com to help breeders, and the research to find the location of the gene.
When I gave some opinions on JKD in a recent column I almost ended my remarks by saying that I fully expected to be immediately pilloried and screamed at as a result. I see that, entirely predictably, this has now happened yet again. It really does bother me that we have some folk in our midst who simply cannot abide anything other than complete, unquestioned agreement with their theories on this topic. In the latest outburst I even see that some poor un-named person from 40 years ago is still being attacked for holding a different opinion on a previous health issue. With the topic being made so toxic, it is hardly surprising that very few people are actually prepared to express their own views on JKD since they know that they will be immediately attacked for doing so. I also find it very depressing that the very vocal actions of a tiny minority make it seem to the outside world that Boxer people are at war. I don't think anything could be further from the truth. My experience is that the overwhelming majority of Boxer exhibitors in this country actually rub along with each other pretty well and very sociably. The atmosphere at shows is really good and there is usually a good exchange of views, conducted in a civilised manner at the ringside. We don't all agree with each other but we can respect each other's opinions. The keyboard warriors don't ever take part in that since we seldom, if ever, actually see them at shows. Having now 'dangerously' expressed some more opinions (which I think I am perfectly entitled to do after more than 30 years in this breed) I shall now set my watch and wait for the next onslaught but in the meantime I will continue to enjoy the shows and the many friendships that are an integral part of that enjoyment.
It seems that our attempts have failed to convince the Boxer Breed Notes correspondent that a few hundred Boxer deaths from Juvenile Kidney Disease (JKD) do mean something. He would still deny us opportunity to present the scientific evidence simply because it does not agree with his preferred opinions and beliefs, these based on his lack of understanding of the genetics and development of the disease. This should not really matter but for his almost total control over the UK Boxer media and the influence that this has. So let us try again.
The main issue seems to be the low incidence of the disease relative to what might be expected with a recessive gene inheritance. He does not seem to understand that the kidney damage is variable and there has to be almost total kidney failure before the symptoms appear. A low incidence of dogs affected with this disease is therefore to be expected, but this does not mean the disease is not inherited. Perhaps also part of the problem is that some of the JKD pedigrees that we (boxerjkd.com) have published don’t show enough information to illustrate the inheritance fully. So let us a try a mini-step further with an example of an annotated pedigree giving more information on the disease transmission. The pedigree shown is a real pedigree, if without dogs’ names, but it indicates more forcefully the capacity of key dogs to transmit the gene. The transmission criterion used is three or more progeny that ‘have produced affected cases to different partners’, whether or not the key dogs have produced cases themselves. Parents that have produced JKD are routinely shown in blue. The previously empty pedigree is now filled with evidence of JKD. This can be done for all the published pedigrees.
Boxerjkdf.com is not peddling myths and beliefs to be debated, but presents actual genetic evidence, and we continue this with the new molecular studies. The Cambridge work, funded by the Council for Docked Breeds and The Kennel Club has received the support of Boxer breeders and owners around the world with the result that:
- over 1000 swabs for making DNA have been obtained;
- a survey of microsatellite markers (anonymous bits of DNA) has shown many to be highly variable, with numbers of different forms, which makes them ideal for gene screens ;
- the very first screen has indicated one particular chromosome as the location of the gene for JKD. Two markers on this chromosome appear to be significantly co-inherited with the disease phenotype, this incidentally supporting the inheritance of the disease;
- consistent with this, a dog suspected of being homozygous for JKD (two doses of the gene) was found to be homozygous for the marker (two doses of the same microsatellite form);
- it has further been found that Boxers of different national origins can have different forms of the microsatellite marker associated with JKD. The co-inheritance is therefore loose. Better/closer markers are therefore being sought.
So, as of now, everything fits perfectly and in a single step we have got as far attained with the heart disease cardiomyopathy (ARVC) with its loosely co-inherited striatin marker; we know the chromosome on which the gene for JKD is located. As with ARVC we have still to identify the gene itself; but with JKD there are several candidate genes in the region. Finding the actual gene will be the hardest part of this work, and everything to date has to be checked and double-checked, but these findings represent a major step forward in understanding and resolving the very real JKD problem of Boxers.
Bruce Cattanach, on behalf of boxerjkd.com