HD & CsV
 

A statistique about HD results among CsV (1500 CsV), as a statistique it's not 100% accurate, nevertheless qualitatively informative:

A+B = 75,44%
C+D+E = 24,56%

Not better than GSD (19,1% for the OFA). I think it's time to think where the "wolf vigour" is gone.

I hope that a DNA-Test for HD will bring some improvement. But when I look at some matings it will only work when the FCI gives a general rule how to use it for breeding you definetly can´t rely on the breeders. The test is tested on the GSH-population at the moment and will be available for all breeds in some years.

But When you compare statistics you have to be very carfull, I don´t know who the OFA is but the German SV classifications differ from the usual ones, at least some years ago - and as far as I know till today - they have A1 for the normal A, A2 for the normal B and A3 for the normal C, what gives you a very high percentage of A´s.

Ina

I took GSD stats from the Orthopedic foundation for Animals: http://www.offa.org/hipstatbreed.html

Thank you for the link, it´s very interesting. There is a Hybrid in there with around 20%, if this is wolfhybrids it would be interesting which kind of and which generations.
And it also would be quite interesting to do some research on wild wolves, cause as far as I know there are only very few researches on captive ones. They don´t move that much and it is known that reducing the aktivity results in less HD so we don´t seem to know the real situation in wolves in itself.

Ina

I thought wild wolves were almost all HD free helped by natural selection. I saw only one publication: E. M. Douglass. Hip dysplasia in a timber wolf. Vet Med Small Anim Clin, 1981;401-3.

This is a theorie and a very likely one but not a proven one as far as I know.
Up to grade C the wolf won´t have any problems till the avarage age so I really have doubts that all wolves are A.

Interesting. This means we are indeed far from knowing about HD in wolves.

Other protective element:

"Hip dysplasia has not been reported in the wild undomesticated carnivorous animals, such as wolves and foxes. A study of their pattern of growth found that the pups were slow-growing and late maturing. The young pups were whelped in dens. As newborns, they received their nourishment by nursing during the first few weeks. When more food was required, the mother killed rodents and either brought them to the den or ate the animal where it was killed and then returned to the den where the ingested rodents were regurgitated for the young to eat.(61) Young carnivores were quite mature and 6 to 10 months old before they began to hunt. The amount of food available for the growing members of a litter was limited. This caused the young to mature slowly and remain thin and light for their body size. Such an environment favored the completion of ossification and developmental maturity of the joint before the hips could be subjected to possible injury, incongruity, or subluxation from excessive extrinsic forces (e.g., excessive body weight) (65,69)"

... but this protective way of living doesn't mean free HD-gene carrier.

That´s the point. There is no dog breed 100% free of HD and all dogs are descendents of wolf. It can be a mutation but the breeds developed on very different places.

Ina, do you know if this test is based on QTL or already on one or more genes ?

I think I read about examinations they made in the US on wolves (it might have been in Yellowstone National Park), which were killed (by cars) - and they found some wolves which had HD. It is a while ago, that I read it, so I do not know the source any more - but maybe I can find out.

Petra

Well, I will try to translate the few informations I have:
The test is able to verify the genomic HD-Breeding-Value. For that 17 marking-genes are selected out of the genom of a dog. The Probability of the occuring of HD and with that of the heritibility can be calculated out of the amount and kind of this markers.
This test has been developed by Prof. Dr. Ottmar Distl of the Institut für Tierzucht und Vererbungsforschung der TiHo Hannover it is available for GSH, it will be a model for other breeds in future. They are working at tests for ED, Cauda Equina, heart diseases and heriditary deapthness in Dalmatians and Epilepsi and heriditary Eyediseases.
The markertest can only be done together with x-rays at the moment. The genomic-breeding-value-estimating is only telling the propability of the occuring of HD and it´s heritibility. The succes of a genomic HD-selection has to be tested in future.
For joining the tests representativ amounts of EDTA-Blood of a breeding population are needed, together with the breeding-book-datas and informations about the anchestors of the breed. For breeds with smaller populations about 200-300 animals are needed. 50% of those animals have to be HD-free, 50% C to E. The time needed for this evaluation is 6-12 month. Interested breeding-clubs can get informed and register under:
www.tierzucht-hannover.de

At the moment there is a long waiting list and for CSW I would suggest to do it with an international population because we only have about 400 dogs here in Germany and won´t have enough dogs for the test but we will talk about it in our club and who is interested can contact me.

regards Ina

OFA answer:

"Most hybrid's are either Goldendoodles or Labradoodles.

Thank you for your inquiry.

G.G. Keller, D.V.M., MS
Diplomate ACVR
Chief of Veterinary Services
Orthopedic Foundation for Animals"

:shock::shock:

I "googled" a lot but could not find anything about wolves and HD. Now I know why - thanks, Ina and Petra :)

I have also read about wolves whit HD, I think it was a Timber Wolf...

But I think it is very unusual, and it is also hard to know if this wolf had
food enough as a pup to develop a good bone structure...

But I´am no expert on this subject area, and do not know exactly how
much the food influence on the development of HD.

Is it possible to develop HD even if it is not inherit from the parents,
only by bad food or no food ???

Regards / Mikael

I know a link on the other direction, too much food => high growth rate => more risk for HD and ED.

Extracts from a French PhD published in 2005 (http://revmedvet.com/2005/RVM156_138_147.pdf), sorry if the translation is not accurate I used a translator:

“E - The food is not however the only factor in
cause. The genetics remains in spite of very dominating.

It is noted that the frequency and the gravity of the DCF are
all the more important as the parents are themselves
more reached. The crossing of unscathed parents of dysplasy
give subjects among which percentage of dysplasic
is weak. This percentage increases when them
parents are reached of light dysplasy; it is even more
raised if the parents present a severe dysplasy [23, 34].
The conditions of breeding, in particular the food, do not have
that an incomplete action and cannot thwart completely
effects of the genetics. Thus, LUST [22] showed
that if the control of the food could prevent the development
DCF in dogs resulting parents phénotypiquement
unscathed or affected of light dysplasy,
a food restriction cannot prevent the dysplasy
at products whose parents have a moderate dysplasy
with severe. “


“Control of the composition of food

After the introduced quantity, the second factor on which
an intervention is possible is the composition of food
proposed. This control relates in particular to greases which
mainly determine the energy density of food,
calcium and proteins, although an excess of these
last in the dog, unlike the other species,
do not involve effects prejudicial on the metabolism of
calcium or the development of the skeleton [31]. “


“If the food is suitable, a calcic complement
is not only useless but also prejudicial. One should not
not to transpose to the food of the dog this saying of
popular wisdom according to which “abundance of good cannot
not to harm”, considering that the calcium excess will be eliminated.
However, it was shown, in various species of which the dog,
that at the very young subjects, the absorption of calcium is
directly connected to the quantity present in the food
[13].

In short, for the dogs at the risk, it is recommended of
to choose a food whose characteristics are the following ones
[31]:
- Energy: 3,2 to 3,8 kcal/g (13,4 to 15,9 kj/g)
- Grease: not more than 12% ms
- Calcium: from 0,7 to 1,2% ms
- Proteins: from 22 to 32% ms "


“Zootechnical

If the food is an important risk factor, it
is that for the genotypes dysplasic and not for
others [5]. By the search for a slow growth rate or
at least adapted better to the race, the food is likely
to mask laxity, dysplasic expression of the genotype
: the animal will become a negative forgery [6, 16]. Admittedly one
will not mask all the dysplasies, but it will result from it
larger errors on the evaluation of the genetic statute
reproducers. “


“That brings moreover to raise another question: with
which period of the growth overfeeding is
more prejudicial as for the appearance of the DCF? All
period of growth, of the birth in 12 months is in fact
sensitive, but two periods appear particularly
important:
- the first 60 days according to HAZEWINKEL [13] but
also LUST [21] which highlighted it on pups born
by Caesarean.
- the period from 3 to 8 months as the many ones attest it
authors and in particular between 2nd and the 4th month,
when the process of ossification is with its maximum. “


“It is mainly the excess of energy contribution which is
prejudicial, especially if it is combined with excesses of contribution
calcic or with ionic imbalances of the ration. “