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The health of pedigree and mongrel dogs


In a recent interview of Nick Mays with Emma Milne she asserted that mixed breed dogs are healthier than purebreds. This is a common saying but seems unlikely since mongrels are mostly not carefully bred, they are products of the hazard, often badly raised, parents are mostly not selected and if so not expensively tested for inherited diseases. If breeds with different genetic diseases are crossed, the offspring will carry the disease genes of both parent breed. So better health in mongrels must be nonsense.


Pedigree v. mongrel
- when health issues are called into question may old arguments come into play
Photo by Alan V Walker

Now let us analyse this issue:

1) Traditional pedigree dog breeding is based on selecting the best breeding dogs according to the standard or/and working performance (if applicable.) In order to achieve rapid success particularly top studs are used as often as possible, at the expense of less qualified sires. The same holds true for bitches in principle but owing to the limitations set by nature to a much lesser degree.

2) Inbreeding and line breeding is used to concentrate the "good genes" even more. Thus the breeding goal is more rapidly achieved.

3) Every pedigree breed originated from a limited number of selected "founder animals".

These came from a regional variety, a "landrace", or were derived from crossing several such landraces to form the new breed.

Successful

Now what is the genetic result of this breeding system? At first, no doubt it was extremely successful and allowed to breed homogeneous stock of the desired traits. However, a price had to be paid that got higher and higher. Its name is emergence of genetic diseases and inbreeding depression.

The number of genetic defects is in the order of thousands. So many have been found in humans, so far about four hundred in dogs but this is just the figure of those scientifically described, in total there may be no less than in humans – and it is the mongrel populations carries probably about that number! Individual pedigree breeds, however, carry only much less, since the few founders only had a small portion of defect genes present in a big population. So again, mongrels must be more frequently affected by genetic diseases as they carry such a huge number of defects genes?

The problem in that reasoning is that, inversely, an enormous amount of diverse defect genes in a population is a quite natural thing and warrants a low rate of sick progeny! Animals get their genes twofold from their parents, one set each from father and mother. Most genetic diseases only pop up if a "bad" gene is transmitted by both parents. If a pup gets only one disease gene, most often it will stay healthy as mostly the "good" gene is dominant and suppresses the effect of the disease gene.

This was nature’s concept: allow for a constant reshuffling of genes and high genetic diversity by using two animals for each reproduction but keeping the inevitable toll of genetic diseases as low as possible – indeed, in such a big non-inbred population very rarely two disease genes will combine in the young animal, it will just be bad luck. It was nature’s trade-off between genetic diseases and the risk of defencelessness against the genetic "arms race" of developing parasites and disease germs.

This is why wild animals widely avoid mating with close relatives. In the dog’s ancestor, the wolf, it has been shown by DNA studies that against what was surmised the procreating lead pairs of wolf packs are mostly not related. That means that wolves run sometimes hundreds of miles to find a non-related partner for founding a new pack. With good reason: offspring of related parents would have a strongly impaired competitive and survival chance.

Now, if by our breeding practices we deplete the genetic variety (the amount of diverse genes – both good and bad ones!) the result is relatively few kinds but high rates of each kind of defect genes (alleles). Obviously, the risk of two defect genes of the same kind to meet in a pup is multiplied. This is an effect by in- and line breeding that strongly depletes the genetic diversity in the offspring, the result of the limited number of founders of the breed, and the over-use of popular sires. Every dog probably carries 2 to 6 different kinds of defect genes. These are now spread in the numerous litters of a much used top stud.

All his pups are half or full sibs and most of them carry now the same defect genes. Beginning in the second generation, when part of his get will be mutually mated, the disease is liable to emerge and hard if not impossible to eradicate, if no specific DNA test is available. The defect has become "a breed specific disposition". So, all the basic practices of purebred breeding, few founders and closed stud books, too few sires and too many litters from few top studs, inbreeding and line breeding tend to elicit an serious outbreak or, at least, a significant increase of genetic diseases. With time, dogs of a breed get increasingly related as the inbreeding coefficient (counted back from founders) raises, often up to the kinship level of half or even full sibs.

But sadly this is only half the story. Full vitality, resistance and viability needs genetic diversity too. With depleting of the gene pool the risk of inbreeding depression sets in, impairing the vital functions. When breeders observe these warning signs, they take recourse to outcrossing in order to regain what is called crossbreeding vigour, but is just the natural level of viability and stamina. Unfortunately, if the general inbreeding level in a breed is already too high, this effect cannot be produced any more. With the inevitable build-up of the general breed inbreeding coefficients there is less and less genetic diversity left in the breed to obtain the necessary crossbreeding vigour.

Confusingly, inbreeding depression does not always occur, so a breeder may not encounter the problem during his entire breeding life. He was lucky. This is the reason why lab mice or gold hamsters have survived decades in spite of being descendants of just a few or a single pair of animals. They are not very healthy animals, though. In the case of mice, in order to establish a sufficiently viable inbred line, a great number of pairs are inbred but perhaps 90% of lines derived will succumb at about eight to ten generations of inbreeding. The remaining may have had founding ancestors that carried no defect genes or the line has purged them during the process and survive.

As mongrels are overwhelmingly not inbred and no popular sires exist, defect genes are neither concentrating and nor will occur any inbreeding depression. So the expectation is a higher level of overall health, less genetic diseases and longer lives. So far the (well founded) theory. But in reality?

Today a considerable number of comparative studies have been published. The problem is if they truly represent the population of both purebreds and mongrels. The latter may be on average less frequently presented to the vet, or conversely be more often in a surgery because they are worse kept and thus get more often sick. At any rate, the overwhelming majority of studies show higher mean longevity and less than average morbidity in mongrels. In this case, you will find the mongrel ranked amid the more longlived small breeds.

However, this does not yet give the true picture. Most investigations compare individual breeds with mongrels all lumped together. Since small dogs live far longer than large ones, so do small purebreds and mongrels compared to large ones. If however, as in one extensive study, mongrels and purebreds are compared on a weight categories basis, mongrels of each weight class lived one to two years longer than the respective purebreds, as was to be expected. This shows the general inbreeding depression of purebreds.

Planning

Since mongrel populations, as shown above, have much more defect genes but no defect gene accumulation, someone planning to breed mongrels would have no or less reason to test them for genetic disease carriers, except when crossing breeds with high risk of the same genetic disease caused by the same defect gene (there are often different defect genes responsible for the same disease in different breeds!) But - no doubt, there are mongrel-specific genetic disease risks too – and these are also the risks of outcrossing within the breed. It may occur when polygenic diseases are present, i.e. those that are caused by more than two alleles (genes), like HD. These are manifested as soon as a certain threshold (majority of the specific defect genes) is exceeded.

Now it may be that one breed (or a line) is entirely healthy because it is carrying an insufficient number of these defect alleles, and equally a second one an also insufficient number of those alleles that by hazard lack in the other. When those lines or breeds are crossed, the allele sets get supplemented and arrive at the emergence threshold, so sick pups will occur.

This is why many breeders are reluctant to outcross. So some maintain outcrossing is bad in principle as defects alleles are spread and you wish to keep your line "clean". This is basically right, but mostly this spreading is harmless if the newly spread defect alleles are not accumulated successively by inbreeding etc. In breed populations too, a high number of kinds of defect genes with low rates of each is far better than few kinds but in high amounts present. At any rate, without outcrossing it is not possible to overcome the basic problem of purebred health, depleted genetic diversity, and what is more, scientific counselled breeding advice (genetic management) will be necessary in future.

This may well firsthand appear as bad news for the sake of the pedigree dog, but no, it is good news and prospective. The better health of the often badly bred and raised mongrels shows clearly the great potential there is to breed pedigree breeds with better health than the mongrel! The more so since there is evidence that pedigree dogs with inbreeding coefficients below 6% through ten generations show comparable longevity to mongrels (which regrettably may be hard to find as yet or impossible in some breeds.)

So, to save some breeds, even planned outcrossing to closely related breeds may be necessary, as in several occasions in the past. The experiments of the geneticist Dr. Cattanach with Boxers and Pembrokes to breed a bobtail Boxer has shown that this is even possible with strongly diverse breeds.

Pedigree breeding badly needs genetic management at the breed level to boost up genetic diversity to original standards while maintaining breed homogeneity by skilled selection. No doubt concessions will have to be made. In- and line breeding will have to be cut down just as sire limits should be introduced, such as already applied by a growing number of Scandinavian breed clubs. In other words, the mongrel is not the goal for the new millennium but the genetically diverse pedigree dog.

So much is to be gained: less suffering and emotions in dogs and people, better image of the pedigree dog in the media, less vet expenditure and breeding risk, more conformity to ethical standards, overcoming the mongrel competition. The skill of the knowledgeable breeders will again get more benefit, image and response from a genetically diverse, thus high-quality low-health-risk pedigree stock. This however, will require KC assistance as being initiated by the Dutch and the Swedish KC which discuss a new role by assumption of their responsibility for the health and welfare of their dog breeds, in cooperation with the breed clubs.

© Hellmuth Wachtel

References

B.N. Bonnett, A. Eigenvall, P. Olson, Å. Hedhammar, Mortality in Swedish dogs: rates and causes of death in various breeds, The Veterinary Record, 12/7/1997, S. 40 - 44)

A. Egenvall et al., Gender, age, breed and distribution of morbidity and mortality in insured dogs in Sweden during 1995 and1996, The Veterinary Record, April 29, 2000, S. 519-525

A. R. Michell, Longevity of British breeds of dog and its relationship with sex, size, cardiovascular variables and disease, Vet. Rec., 27 Nov. 1999, S. 625-629

G.J. Patronek, D.J. Walters, L.T. Glickman, Comparative Longevity of Pet Dogs and Humans: Implications for Gerontology Research, J. Geront., Biological Sciences, 1997, Vol 52A,No.3, B171-B178