Versatile Hunting Dog Federation of Canada (VHDF-Canada) Feature Stories
This webpage was mounted on March 22, 2019 and last updated then by Sheila Schmutz
Pain for Dogs and Bane of Breeders
by Joe Schmutz
After five decades of coordinated selection against hip dysplasia worldwide, what is the beneficial practice today? While VHDF-Canada’s primary goal is to assist breeders and hunters in maximizing their dog's field ability, VHDF-Canada also aims to promote dog health for an all-round quality experience afield by hunter and dog.
Hip dysplasia, so it is said, is due to bone loss and an ever-wobblier fit of the all-important hip joints. When the dog’s body tries to compensate for the loss, tiny clusters of bone cells get misplaced contributing to an already uneven and painful joint surface. Some bone grains even get into the cartilage and feel like sandpaper (Fig. 1).1
It has always been assumed that a large gap in the joint, as from loose or weak tendons, cartilage and muscles, starts the bone decay. Logically therefore, early attempts at a solution examined the gap in the joint, also sometimes called laxity.
In a timeline of what steps were taken when, it is worth pointing out that hip dysplasia is not purely a dog problem. Hip dysplasia occurs in humans and has been described occasionally in horses and cattle. Even the Romans knew of its existence.1
1950s – 60s. Dog breeders teamed up with geneticists and veterinarians to combat hip dysplasia. Veterinary radiologists developed a diagnostic procedure based on hip x-rays and became trained and certified to evaluate hips radiographically. Known as the FCI-method in Europe with a similar approach in North America, it evaluates dogs at least 12 to 24 months old, depending on the service provider. Board-certified radiologists at the veterinary universities of Guelph and Saskatchewan offered this service, as did some smaller labs in Canada.2 In the U.S., the service continues to be provided by the Orthopedic Foundation for Animals (OFA).
When bone remodelling and arthritis could be seen on an x-ray, the bad news was clear. Was it possible though, one asked, to tell from joint x-rays how likely a dog was to develop hip dysplasia later. Radiographic screening is bound to help, but the method primarily describes the hip’s current health and makes no HD-free claim for the long term. Believing in joint looseness to be at least a partial cause of hip dysplasia, it seemed logical to use a ‘fulcrum’ to see whether excess joint sepapration could be achieved with pressure. This was later abandoned because the pressure itself could be a kind of trauma that could aggravate, if not cause, hip dysplasia. Also, if a dog’s skeleton or gait could compensate for some degree of looseness, then that in itself was a solution too.
1980s. A group of veterinarians started the University of Pennsylvania Hip Improvement Program known as PennHIP. This technique was modified from the former fulcrum technique and claims to detect a predisposition for hip dysplasia as early as 3 months. PennHIP promoters claimed that their method predicts hip health much better than the radiographic method could.3
In 2015, a team lead by Andrea Meyer-Lindenberg in the Department of Surgery and Small Animal Reproduction in Munich, Germany, compared the effectiveness of detecting a propensity for hip dysplasia between the radiographic and the PennHIP methods. Despite the claims by PennHIP promoters, the team found no evidence that the PennHIP method was more successful than the FCI method. Prof. Meyer-Lindenberg’s study included 248 dogs of 40 breeds. The researchers did say that the PennHIP method could provide a valuable second evaluation in borderline cases.4
Dogs are what they eat. Also in the 1980s, a completely different approach to hip dysplasia was promoted by Ian Billinghurst – diet (http://barfaustralia.com/ ). Billinghurst was raised on a ranch in the Australian Outback. When he became a veterinarian, he attended to diseases among the urban dogs that he saw rarely, if at all, among the outback ranch dogs. The ranch dogs were fed and scrounged a variety of foods. He rightly questioned the wisdom of the dog food companies, which enlisted animal scientists to formulate dog food. In those days, the animal scientists understood livestock nutrition well. They relied on pig nutrition studies to design dog food. Of course, there was a whole clash of cultures. Pigs are feed to grow fast to go to market young, and life span and working ability were unimportant. Pigs have a simple stomach more like dogs unlike the multi-chambered ruminant stomachs of cattle and sheep.
Dog food companies were understandably reluctant, but Billinghurst persisted and found allies among dog owners. His persistence and pulling no punches is evident in some of his book titles.5,6 Today, thanks in large part to Billinghurst and his allies, the major dog food companies have revamped their food design. Evidence is the range of dog foods available to dog owners today, notably the designs for slow growth of large breeds, in which hip dysplasia was most common.
Another way to explore whether hip dysplasia is largely a human made disease in dogs is to examine wild canids. Apparently, there is only one case of hip dysplasia in a wolf. Unfortunately this animal was kept in captivity and thus was fed a diet more similar to dogs than wolves.1 It is unfortunate that in North America, where so many coyotes are trapped or shot each year, no one seems to have examined the incidence of hip dysplasia in this species in the wild.
Around 2000, several research groups around the world began to pursue the hip dysplasia holy grail in earnest. They looked for the smoking gun, the gene. So far, this search has failed. It is possible that a genetic mechanism exists, but that the mechanism is so complex that it is beyond the reach of research focused on a single gene. Our high school and much of university education in genetics is based on the laudable single-gene insights provided by Gregor Mendel 150 years ago. However, the single-gene mantra inherent on the usual Punnett square describes only a fraction of real world genetic mechanisms and leaves us woefully unprepared to understand the true complexities. The hip dysplasia mechanism could, for example, include: i) an environmental trigger that occurs only some of the time, ii) it could involve not one or even two but many genes acting together, and iii) it could be of an only recently recognized epigenetic nature.
One breed club's experience. The Large Munsterlander Association of Canada (LMAC; http://lmcanada.net ), formerly the Large Munsterlander Club of North America (www.lmcna.org ), began in the 1970s to fight hip dysplasia. LMAC relied on institutional guidance of the Animal Pedigree Act of Canada as a state-of-the-art tool for breeders. From 1977 to 2017, Large Munsterlander breeders and hunters have had over 200 LMs x-rayed for hip dysplasia.
The data showed convincingly that three sires in the LM gene pool were responsible for a disproportionate number of offspring that developed hip dysplasia. These sires might have helped to provide a clue for the genetic mechanism but they were never used for research.
Figure 2. Hip-dysplasia ratings of Large Munsterlanders (vertical axis) in relation to the average rating of their two parents (horizontal axis). Squares indicate the average hip rating, the vertical line shows the range of ratings, and numbers show how many dogs were x-rayed in that category. The dysplastic parents had developed hip dysplasia later in life, after they had already sired offspring. Parents with both had hips rated Excellent showed the best results in their offspring. Surprisingly, parents with hips rated Fair or Good but still HD-free and parents actually developing hip dysplasia later had similar proportions of dysplastic and HD-free offspring.
The results of screening and breeding only HD-free sires and dams are shown in Fig. 2 (above), which suggests three things for breeders. First, the graph shows on the right side of the panel that even a dog that was dysplastic and accidentally mated to a HD-free dam still had more HD-free than dysplastic offspring. Second, various matings of HD-free dogs in the “Good” hip conformation range still produced some dysplastic offspring. Finally, only HD-free dogs with both mates rated “Excellent” produced no dysplastic offspring.
These results, on the surface, suggest a solution: apply intense selection pressure and only breed dogs with hips rated excellent on radiographs. Unfortunately, it is not that simple. Even within the single breed, the Large Munsterlander, the data suggest that excellent hips occur primarily in the fine-boned and lightly built specimens that occupy the lower end, or even fall outside the breed standard. This would mean that some of the larger versatile breeds are in trouble. Their characteristic medium-sized bodies could not be maintained.
The trend for a higher incidence of hip dysplasia in large breeds of dogs has long been known.1 A former Canadian Kennel Club judge, genetics professor and breeder of St. Bernard and Clumber Spaniels also reached that conclusion. Taking the hard-line time and again in selecting his breeding stock, Prof. Roy Crawford managed to significantly reduce the incidence of hip dysplasia in both breeds over time. However, he said, the dogs’ appearance changed. They became finer boned, lighter in weight. Eventually few breeders and owners were interested in his dogs because they no longer looked like St. Bernard and Clumbers in or outside the show ring.
One breeders’ experience with hip dysplasia. After 40 years of breeding Sunnynook Large Munsterlanders, and always in full support of the Large Munsterlander Association of Canada’s goals to select against hip dysplasia, Sheila and I reached our own conclusions and are encouraged by our results. Our ratio of HD-free Sunnynook dogs over the first 20 years, then the next 10 and the last 10 years of breeding were: 69% of 36, 95% of 20 and 100% of 5 dogs x-rayed. Over this same period the breed’s founding breed club in Germany and other North American breeders practiced equal diligence wehereby we could collaborate and complement one another’s efforts. We feel it would be unwise not to x-ray, and to breed dysplastic or even hip-status-unknown hunting dogs. We like it when our Sunnynook dogs have excellent hips but we also bred dogs whose hips are ranked Good, and two with merely Fair hips. Beyond x-rays, we take several steps in our kennel:
In our discussion with other responsible and experienced breeders, we find that others have come to similar integrated and broadly based approaches to breeding. Breeding dogs responsibly and finding a suitable home has been as challenging as most anything we have experienced in our lives. We have learned much in the process of breeding hunting dogs for four decades. We will continue with our approach and proceed with eyes open.
Breeding quality hunting dogs is a community effort. It can be done best in collaboration with other breeders and owners that are diligent (Fig. 3). The community of hunting dog owners with similar goals provides us with enhanced breeding choices that we could not have on our own. The successes are shared by all and are seen at the end of a good day in the field. Breeders can tackle their bane and the dogs can have less pain.
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