Hyperkeratosis (Digital hyperkeratosis)
Also known as cracked pads, corny feet, hard pad disease, CF
Hyperkeratosis is most likely inherited by a single pair of recessive genes, one from each parent. The disease is not sex-linked. Parents usually show no symptoms, because if the individual just carries one defect allele, it cannot be seen from the outside. Having two similar defect alleles would mean that the disease displays in the invividual. Serious breeders do not breed from sick animals. The disease is so obvious that even a person who has no knowledge of dogs can see that a dog is ill only by looking at his paws.
In my opinion every breeder should be aware of the mechanisms, the statistics and the carrier lines unless you want to risk to breed it. This is a recessive illness and therefore it is impossible to root out completely.
Photo copyright: Jetta Tschokkinen, Sweden 1996. This dog was linebred to the original carrier, an English import. He also has a very untypical, thin, light, oily coat.
It is very common in the CF dogs.
False beliefs: ”It´s gone”
I bought my first Irish in 1983. I was told that there is a disease called corny feet in this breed. I was also told that the last cases were born about 30 years ago. It was a lie. About two years later I found out that the latest cases in Finland were born in 1980 and 1981 – not even 3 years ago. There were two litters with the same parents, i.e the latter was done although some individuals of the first already had proved to have hyperkeratosis. There was also a litter whose sire was the same, already proven to be a carrier, a Norwegian import. The mother had hyperkeratosis herself. This litter consisted of six puppies of which five got hyperkeratosis! The Norvegian male was the grandsire of my dog. This is why I became interested in the disease.
In Scandinavian countries all breeders knew already that the disease was inherited. It was also common knowledge among veterinarians. In past days many Irish Terriers had this disease. It was considered a minor cosmetic fault and it was not an obstacle for breeding. No wonder so many of our dogs in 1970´s had it. Luckily it has not reappeared in Finland – as far as I know, anyhow – and I have never bred a puppy with this disease.
”It came from the old lines”
I heard this often in the beginning. A breeder insisted that her male was clean, but the dam had given it to the puppies. How is that even possible? Even though I am not a biologist it sounded quite weird. The cases showed that the disease was inherited by a single pair of recessive genes, one from each parent. Her male was a carrier, and she was simply in denial – a condition not very rare in dog breeders.
”Lack of zinc”
Even as late as in 1984 the ITA (England) Year Book explored the theory of poor utilisation of zinc in the diet. This was again brought to life in 1996, when the breed representative in the newspaper Dog World, Lindsay Williamson, mentioned cracked pad in her column. Old-school breeders reminded her of the old theory. If this is true, how come no dog was ever cured by zinc treatment?
The Zurich research
There is study progressing in the Univerity of Zurich in Switzerland (supposedly now buried. -Author´s remark). It has been discovered that hyperkeratosis is inherited due to a recessive gene from each parent – both parents are carriers and do not necessarily display the condition. Hyperkeratosis is not sex-linked. The team is now trying to locate a marker gene for the disease. Once it is located, a simple blood or other cell test will establish whether or not a dog is a carrier.
In Bedlington Terriers they take a small amount of hair and the hair root cells from the dog´s cheek. These samples are easy to collect and keep. The only method currently available to confirm the non-carrier status of an animal is to do enough test breedings of a potential breeding animal with affected animal to statistically show that the genotype is clear.
With a disease like hyperkeratosis that does not display in a young puppy but in 4 to 6 months or an older puppy up to 12 months, this method causes several ethical problems. Is is right to intentionally produce sick animals? Where should a breeder keep the puppies until they are old enough? How many specimen does it take to be sure? (Using an affected to test an unknown, a resulting litter of 5 – with normal pads – is considered to be acceptable result. Using a carrier, a total of 12 puppies would be required. This means two or three litters. But then, the results may be wrong and the parents may be carriers anyway – the ratio is not necessarily visible in very small numbers).
The new genetic linkage test is to assist breeders of purebred dogs to evaluate the genetic status of their animals. The idea of the test is taking advantage of opportunities presented because particular canine diseases are due to genetic defects in which the same gene has been isolated (cloned) or a close-by marker is known in another species such as human or mouse. This knowledge about the gene in other species may allow the team to rather quickly develope a genetic test for the dog disease. In our case, there is no known counterpart in other species. The development of the Canine Molecular Genetic Resource (CMGR) allows for the systematic search for any canine disease gene and the development of a corresponding diagnostic test. The CMGR is a system of 500 DNA markers which are randomly distributed on the dog´s chromosomes. The first step in the test development is to determine which of the 500 markers is located close to the hyperkeratosis gene. To do this, DNA must be collected. To allow a linkage system to work, each of the markers must have certain important characteristics, one of the most important of which is a high level of genetic variability. This means that the genetic type of the marker in a pedigree has a good chance of showing variation, and that the marker type will likely be slightly different for dogs in the same litter. When this is true, the litter is useful and informative. What may cause problems is the availability of the background dogs. Especially samples from affected dogs should be useful. The Zurich project has had no progression for a long time as far as I know.
Pattern of inheritance
aa = affected
AA = clear
Test matings is presently the only way to differentiate between carrier and clear animals.
What breeders must know
A) When you have produced affected dogs
First of all, do not think it was your fault. But it is your fault if you keep on breeding from the dogs who produced this litter. Both the dam and the sire are carriers. It would be wise to spay or neuter both of these animals – because using them again, even with a non-carrier, will only increase the frequency of carriers in the population.
If you have already sold the affected dogs, try to keep in contact with the owners. We have the saying, ”Even a skinny peace is better than a fat fight”. Pay back some or all of the puppy price or tell the owners you will give them a healthy puppy for replacement. If you start argueing with them you will just ruin your reputation. Keeping it a secret will not work in the long run anyway.
If you want to go on breeding, you need a new bitch. Buy only from a reputable breeder. Ask the breeder if they have had this problem in their stock. Tell him/her about your problems.
It is not wise to breed from the siblings of the affected puppy. Even if there is only one sick animal in the litter, at least half of the others are carriers.
B) When you just want to avoid the disease
Do not inbreed. Selecting a stud who is a close relative of your bitch will just increase the number of genes that are homozygous (similar). It does not discriminate between good alleles and bad, and therefore you might be getting a litter with hyperkeratosis. Many breeders have the idea that outstanding animals can be produced by inbreeding – by doubling up the good alleles while somehow avoiding the bad.
Do not use over-popular studs. It will only cause that his alleles will be widely spread in the population. Later on, when you are looking for a stud for your bitch, you will find that most studs are her half-brothers. If you use one of them – or even breed back to the original stud – you will just cause more doubling of genes while you throw away a valuable set of other alleles.
Check the pedigrees. It is often fairly simple to find out where the disease came from. By examining the pedigrees of the affected animals you may find out which animals you should avoid in future. The accuracy of such analyses is directly affected by the number of relatives for which data exists – a stong argument for the open exchange of information between owners, breeders, veterinarians and researchers.
Keep in mind that breeders do not tell about their misfortune, so you can´t really trust them. Another important thing to keep in mind is that one might well get no affected pups in one litter and four in the next. To be sure, you need about 10 puppies from the same combination. In Irish Terriers this means 1-3 litters.
Just keep in mind that when working on his theory of recessive inheritance, monk Gregor Mendel (thus the laws of Mendelism) was working with flowers. He had fields full of pea flowers and he came to his conclusions by counting the different colours. A breeder can never have as many puppies, and even if we could, nature has its ways to prevent the defect individuals from being born.
Jetta Tschokkinen © 2000