| Recently I received
an email from Sy Guth, in which she wrote, "You left out a Lab defect –
ectopic ureter. I bred Golden Retrievers and started a DNA project to find
the markers 2 years ago. We are still trying to get through the collection
of the samples and have not had any tested yet. You may find our website
of interest http://www.greudna.org.
I’ve consistently been told by a vet in Australia, 2 vets in the US, and
the head of an institution that breed both Labs and Goldens, that the defect
is more common in Labs than Goldens."
Ectopic Ureter is a
polygenetic condition in the Golden Retriever. It has occurred in other
breeds, including the Labrador Retriever, but with an exceedingly
low incidence. Breeding experiments carried out by Boyd Jones (Massey University,
NZ) in Golden Retrievers have indicated that it is an inherited condition
in the breed.
 Affected animals usually show up before one year of age, the majority by 6-8 weeks of age. The affected female puppies do not grow as rapidly nor are as active as other litter members, as they are very prone to bacterial infections. It is 8-9 times more common in females than in males since the prostate gland in males acts as a muscle sphincter, and therefore the dog may not have any dribbling of urine, but may show up at a later age, eg 5-6 years. Almost all females affected by ectopic ureter will show up at an early age although there have been a few cases without urinary incontinence (Osborne & Oliver, 1977; Jones 1980). . Click here to read more about the medical facts of Ectopic Ureter Defect: http://www.vetsurgerycentral.com/ectopic_ureter.htm . The polygenetic defect may go back to the 1930s or even further back and there is probably not a Golden Retriever in the world that will not have one or more of these early suspect carriers behind their pedigree. It seems likely that a pair of dogs from the 1930s in the UK, Ch Davie of Yelme (1931 out of Gilder & Sewardstone Tess) and Ch Dukeries Dancing Lady (1934 out of the Abbots kennels), were dominant carriers of the EU polygenetic condition. They may not have been the originators of the defective trait. It may go back even earlier than these two dogs. However, it gets a bit grey at this point and I’m not comfortable going back further. One thing is for sure – without locating the DNA markers involved and having DNA testing available we will never be able to predict the probability of the trait appearing from a mating. My question is: how
(and when) did this polygenetic defect come into Labrador Retrievers?
In LabradorNet's databases I was able to find 21 officially interbred dogs, born between 1916 and 1933. Four of them had a Flatcoat Retriever as a parent, two of them had a Chesapeak Bay Retriever as a parent, and in fifteen of them there was a parent which breed was unknown. All I know about these fifteen dogs (part of them may have had a Golden Retriever as their parent) that seven of them were black, a fact that would automatically lead to registration as a Labrador Retriever instead of a Golden Retriever. We know that between 1970 and 1990 several Golden Retrievers have been crossed into the Labrador Retriever, to improve the coats and the heads of certain lines, especially in Scandinavia, the United States, Australia, New Zealand and South Africa. This relative distance from the 'motherland' of the Golden and Labrador Retriever might explain why Ectopic Ureter defect isn't as common in Western Europe and the United Kingdom as it is elsewhere in the world. Could it be the
result of outcross?
After the 1930s the Labrador breeders in the U.K. had a relatively large population to pick from. This enabled them to be more selective and to eliminate certain defects. They could afford to stop breeding with a dog who produced puppies with Ectopic Ureter and choose dogs that didn't produce this defect. In Australia, New Zealand and America the English Labradors were far more unique and less replacable, so they weren't eliminated from the breeding process as easily. To be able to counter
the problem of Ectopic Ureter we need to know which lines are responsible
for passing on the defect to their progeny.
Jack Vanderwyk |
