shortstep

Do you know when the dam was xrayed? Was it any time around her heat, preg or when raising the pups?

It is not a meaningful indication of imporvement of hips in the breed. Only if you have maditory reporting of all dogs tested and enough dogs being tested would it be meaningful. When the current system has only a few dogs that are being screened, and it is owners choice to not report bad hips, then the numbers of this system will only reflect those dogs with normal hips that the owners (meaning breeders in most cases) selected to report. It is hard to find any expert on HD that will not double or even triple the affected rates of HD if it is a voluntary reporting system. What is the affected rate in Australian border collies? I would guess on the dogs reported it wil be next to none, however i would expect it to really be about 1 in 10 dogs as affected. If the animal rights folks get their way, then all hip xrays done at your local vets will be documented via the automatic data collection systems, even those xrays that are not sent for scores. I believe they then switch over to the affected or normal tabulation method. Only then we might have a better idea of how bad HD is in the breeds. BTW I was chating with some one just a few days who is reading xrays of border collie hips and then did not give the impression at all that everything was rosey. Back to the OP questions. There have been alot of studies done by OFA, PENN, by breed clubs, Unis, and as part of research on HD. The one thing you will find in almost all of the reports is which every one they want to promote will always seem to have the best results and the other methods will not have the best results. PENN is a prediction of HD not a DX of HD. So even if you PENN you still need to xray later to find out if the prediction came true. In some breeds it has a better chance of accurate predictions than in other breeds. PENNs potential real value would be to make early selection (at 12 weeks) for potential breeding dogs. But few people are using it for this. Edited to add. There are 2 major ideas on how to breed aganist HD. One is to look at only the parents and select the best scored parents you can fine, for example a 0-0 to a 0-0, you do not look at the larger family picture. This might give you the best chance of getting one pup with the 0_0 socre, however it does not seem to produced consistant hips across the litter and there can even be siblings with HDas not a rare even. The other method is to look at the exteneded families and a couple of generations. All siblings need to be screened of parents and grand parents litters and even half siblings can also be looked at. You look for dogs that come from families that did not have any HD, it is a mornal of affected way of judging the family history. This method does seem to have the best results for getting normal hips aross the whole litter in my opinion. Most of those in science feel that most of the improvment in hips seen over the past 20 years is attributied to the removal of affected parents for the gene pool. Secondly the change in ideas about feeding pups, keeping pups lean, slowing down growth and reduceing calcium in the diet are also proving to have very good results in reducing severity of disease. So much so that some in genetics are now concerned the good rearing methods could actually be so effective that we might be actually inhibiting the expression of poor hips (this can also account for reduced scores over all in a breed). To know if any of these systems will be really meaningfuly in breeding programs, you would have to select for hips as a #1 priority, in other words you actively go out and select only the dogs the very very best hips you can find and breed those dogs. Most people do not do that and nor should they as there is much more to a dog than good hips. Breeders would also have to be checking every pup they produced to have a true measure of how effective their methods were, this is seldom done by breeders. Most breeders only check the dogs hips they want to breed to see if fall in the nornal range.

I tried both links but cannot get either to work, it is just me??

Anything else nasty you would like to say about the Brazilians? Any comments or comparisons about the DNA testing at the Brazil sheepdog trials as compared the the DNA testing offered at the Australain sheepdog trails? DNA CEA or CL testing in Brazil can find them hosted by ISDS of Brazil registry. February 24, 2011 through March 12, 2011 - Brazilian 20/20 Clinic Blood collect for DNA CEA exam on ACOPAS 2011 1ª sheepdog trials, ISDS Registros on Brazil. Breed: Border Collie Location: Fazenda Quinzão - Sidrolândia - MS - BR Here is the CEA testing list, only those who wanted to list their dogs on the international disease register are on here. http://bordercolliehealth.com/Brazil.html Lots of the best show kennels in the world are mentioned on this list of dogs or their parents. Australian, New Zealand, America and Uk show kennels have not had a problem exporting to Brazil. I am glad to see that not all Australains feel the way PAZ does about the lovely people of Brazil. Anyway, back to Brazil. Did you know the Brazil is the second largest consumer of pet foods in the world? Dog dancing with a very a happy border collie. BTW PAX near the end of this video, the dog knocks over his handler and then makes a motion with his back feet, I think he would motion the same to your comments about Brazilians.

Nice music and the feel of Brazil while showing some excellent working dogs. Brazil is the worlds largest producer of beef and sheep are on the rise. They have an active interest in working border collies and have imported and now breed some of the best working dogs in the world. I mentioned recently the ISDS will now be accepting dogs registered in Australia Working Border Collie register into ISDS. This will make them internationally accepted, such as for the registry in Brazil. Most of the dogs in this video were bred in the UK. However Brailians have been very interested in investigating the Australian lines, which they will now be able to intergrate into their registry. Hope you enjoy. Adios!

I wrote what I thought you should do in my above post. What does your dog normally eat then? Is she always this fussy with her likes and dislikes?

Her first due date is Sun 20th and could be as late as 25th. The first xray you are looking at is way too early. I would not take the xray on Tuesday, that might be too early again. I would wait till Friday 18th. Then take it from there. You might just have some puppies it there! I would not fuss too much about here eating. She is a big dog and 3 pups will not take much nutrition from her normal diet to feed. As long her weight is normal and she is not losing weight, just let her decide. You might try adding some sardines if she would tolerate them, as they add good nutrients for the puppies neuro developement and usually thee like them and wil eat them. Get the ones packed in water. Not oil or tomato sauce.

Just me, but I would not enter into breeding a bitch knowing I needed to use drugs to try to get a bitch in whelp or if she needed them to hold on to a litter. The pups from her might inherit the same problem/s and it just sounds too risky for normal development of the pups. We want to breed for bitches the can breed and whelp freely. For some breeds 4 might be a bit old for a first litter, you would have to ask others in your breed. However I would not be totally sure this bitch is not preg, maybe one pup. She might not be as far along as you think. If the xray is showing something but not enough bone development for the age of the litter than that could mean that it is just too soon to take the xray, that your due date is wrong. The day you breed her and the day she actually conceived can be different by maybe 4 days. So from the very last breeding add another 4 days and then count forward 63 days, what is the due date then? If the xray was sooner than 5-6 day prior to this due date then it was likely too soon. Ultra sound will pick up hearts beating and some structures but you can miss them, on a big dog one pup can be tucked up under the ribs or behind something and be totally missed. Both on xray and ultrasound. I have had a 'Vet says they sure she is not preg' bitch go into labor and have a singleton pup. Opps forgot your first question, to join PM Troy and let him know.

You may be aware that Dr. Leigh Anne Clark of Clemson U. Genetics Lab has been working on megaesophagus research. I am writing this as a reminder to submit DNA cheek swab samples if you have a dog who was diagnosed at or before the age of one year (congenital megaesophagus). Info can be found here: http://www.pedigreedatabase.com/german_she...orum/95909.html Please share this with your other lists. All breeds are now qualified for DNA submissions.

Look at the labradodles, they rank the 7 most numerous 'breed' to be score for hips!!!!! That certainly puts their breeders in with the KC elite breeders who are actively screening for HD!! Wow I am very surprised at the very low number of dogs being scored. Even for breeds known to have real problems with HD. Also very surprised at how low some of the breed averges are. I would agree with your assesment and say you could double the average breed values, at least for some of the breeds I have worked with. I would also say a lot more breeders need to be screening their dogs and actually submit their less than perfect xrays for scoring. I really don't like these breed average system to reflect what is going on in the breed, even less for deciding what dogs to breed. Then factor in very poor compliance to testing and with reporting affected dogs so low. I think what is more helpful is to know the how many dogs are in each range of scores, affected, not affected and excellent hips (less than AVA 5 is usually used for this). For example if you have 20% in the excellent range, and say 4% affected, then the breed is in good shape. You should be selecting for normal hips but the pressure if off a bit and other areas of the breeding program can take a higher position in selection. However if you have 1% of dogs with excellent hips and 20% affected rate, then this breed is in big trouble and breeding for improvement in hips is a priority. You can also run these same numbers for your own breeding program or lines to help in breeding decsions.

When talking COI it is very important to list the number of generations, there is no standard number so it cannot be assumed. Now first hand in Australia from the Uni of Sydney, I was told that a COI-6 of 0.4% (in 6 generations) was not sufficent, that only 0% COI was acceptable but they never responded to my question of '0 % in how many generations'. I think they used 3 generation for their study of ANKC stud book COI for all the breeds (which BTW was this information ever released?). Now if they mean make a law about COI limits, then maybe that number would be higher than 0. I would think removing inbreeding to the level of daughter to grandfather or half brother to half sister or maybe even a little more than that, around 12% would be their starting point, but I an sure over time they would look to reduce that to around 2% max in 6 generations. Back to what you were told, 14% I am assuming that is in 3 or 4 generations is still pretty high. If it was 14% for the total life span of the breed, ( usually back to the early 1900's) that is still considered a high level of inbreeding by most experts in diveristy today. Usually they say about 6-7% for breed total COI and less than 1.5%-2% in 6 generations as being low inbreeding and what is called outcross (meaning in in purebreds). Edited Just wanted to add, in the KC that are now regulating COI, they usually look at each breeds total over all COI and then start from there to build a reduction plan. It may not be possible to restrict the COI too severely is a breed that is already highly inbreed. However that is when they move to ideas about cross breeding to get the level back to what is considered acceptable. In most breeds they set a limit, which is below the breed average and then every few generations try to lower that number again. They will also ban across the board high level inbreedings, usually meaning around grandsire to daughter level. The Uni here in OZ has sugested that COI be part of the EBV in the 10 point plan at the uni of sydney. Yes you would submit your planned breeding (hpefully several choices of studs) and they would run it though the EBV for that breed. It might set breeding values on any disease with out a DNA test or any of the multigene diseases such as hips elbows, heart disease, epi or any of the brain diseases and so forth. It might also track longevity. It would also look at COI and I suppose we are not far from needing maditory genetic diversity tests on all mateings. There is also talk of being able to take the health information from the Vets, tracked by microchip number and filter that for putting into EBV programs. For example say a dog had several pups that ended up needing treatment for skin allergies, then EBV could look for sire that have a very low incidence of producing pups with skin allergies. Or it could look for a dog that had the most possible genetic diversity in the immune section of a genetic diversity test. This is years away right now, but it could be possible if the government madates every dog have a chip, and if there is a feed of pedigrees by chip number from the ANKC to the uni and that every vet has a feed from their electronic records to the Uni using Dx codes for each vet visit, all the tecnology is here to do this it is a matter of having the system set up. Also just in case some do not know. Uni of Sydney has been assisiting the RSPCA UK, they are very much a part of the process going on in the UK. To your opening sugestion that perhaps this had more to do with promoting RSPCA dogs. Not a chance. This is a animal rights issue top to bottom, there is strong belief that purebred dogs, by their very nature of being purebred are an welfare issue. However more prominate right now, is the very very very strong belief that showing dogs is the crux of the most pressing animal welfare issues in pruebred dogs today and that showing dogs is driving and promoting animal cruelty in breeding practices in the kennel clubs.

I read this first, which is included in a list of reasons why the AKC does not want the healthy Dals allowed in the register. http://www.thedogplace.org/Breeder/Genetic...-11031_Boyd.asp The Harvard geneticists who discovered the Dalmatian gene for high uric acid in 1938 made it a point to illustrate their article showing that low uric acid Dalmatians bred by backcross techniques displayed spotting patterns that did not approach that which is called for in the AKC standard of the breed. We have seen strong evidence of that finding in the majority of the Low Uric Acid Dalmatians of today…. 73 years later. The question then becomes “what else, less visible to the naked eye, came along with this mutated gene and what are the affects of these other things, if any, on the Dalmatian for now and in the future?” So to me they are saying a couple of things in the above paragraph. 1. That the white hairs found in the healthy dogs spots do not meet the breed standard. 2. That the non white hair spots of the Dalmatian are linked to the disease, but they might also be linked so some other unknown traits that might be lost if they breed out the disease. So then I went looking for the Harvard geneticists and found this http://www.dalmatianheritage.com/about/schaible_research.htm Dalmatian-type Spotting, Urinary Stones and Hives Dalmatians generally are born with pure white hair because those that do have patches of pigment (large spots like those of the English Pointer and Brittany Spaniel) are usually not retained for breeding. Many of the Dalmatian-type spots are present in the skin at birth but they do not appear in the hair coat until about two weeks of age. The spots become fully pigmented. Few, if any, white hairs are interspersed through the spots. Evidently almost all of the white hairs of the birth coat located within the spots are replace with pigmented hairs as the spots form in the coat. The Dalmatian-type spotting is found in many of the hunting breeds but is called “ticking”. Ticking and Dalmatian-type spotting are both believed to be determined by the same gene (Little, 1957). The tick spots of other breeds differ from Dalmatian-type spotting in that the spots are smaller and have white hairs interspersed throughout. Apparently, the white hairs of the birth coat of the other breeds are not replaced with pigmented ones during the formation of the spots. Trimble & Keeler (1938) observed that the absence of interspersed white hairs in Dalmatian-type spots was associated with a defect in the metabolism of uric acid, not only in the Dalmatian breed, but in the offspring resulting from Dalmatian-Collie hybrids being backcrossed to purebred Dalmatians. In the remainder of the backcross progeny, interspersed white hairs in Dalmatian-type spots were associated with normal metabolism of uric acid. In 1971 and 1972, I repeated Trimble & Keeler’s crosses and found that the same associations generally, but not always, occurred in the backcross progeny. Because the composition of the coats of Collies and Dalmatians differ so much it was possible that variation in the coats might have had the effect on the distribution of white hairs within the Dalmatian-type spots of the backcross progeny. The Collie was not the best choice of breed to use in genetic analysis. In 1973-1976, I repeated the breeding experiments again except that the Dalmatian was crossed to its nearest relative, the English Pointer, to minimize genetic differences except for the pair of genes controlling uric acid metabolism (Schaible 1976). The hybrid offspring had normal metabolism of uric acid and small tick spots containing interspersed white hairs (Fig. 1). When the hybrid animals were backcrossed to Dalmatians, 16 of the 36 offspring (nearly the expected 50%) had normal metabolism of uric acid. But 5 of the 16 were exceptions to Trimble & Keeler’s observations in that those 5 had few or no white hairs interspersed within the Dalmatian-type spots. The following conclusions are based on these results: (1) Absence of interspersed white hairs in Dalmatian-type spots is not an additional effect of the gene responsible for the defect in uric acid metabolism. (2) The absence of interspersed white hairs in Dalmatian-type spots is the effect of a separate recessive gene. (3) The locations (loci) of both genes are close together on the same chromosome (closely linked). (4) Absence of interspersed white hairs in Dalmatian-type spots and the defect in uric acid metabolism are associated in the Dalmatian breed because the gene for the uric acid defect, instead of its normal allele, just happened to be present with the gene for absence of interspersed white hairs in the primary progenitor of the breed. As selection for absence of interspersed white hairs made the responsible gene homozygous in all members of the breed, the gene for the uric acid defect was inadvertently made homozygous as well because of its close linkage on the same chromosome. The fourth point is speculative but the events are likely. Keeler (1940) attempted to locate Dalmatians that did not have the uric acid defect in Britain, as well as in the United States, but was unsuccessful. In the subsequent 40 years, Dalmatians have been used for demonstrations and research repeated in medical schools because their uric acid level in the urine is approximately the same as that of man. All of those Dalmatians have been found to have the typical elevated levels of uric acid in the urine. Unfortunately two serious health problems are positively correlated with the high uric acid levels resulting from homozygosity of the gene for the defect in uric acid metabolism. These are a unique form of dermatitis (hives) and the urate form of urinary calculi (bladder stones and kidney stones). There seems to be little doubt that both health problems are additional effects of the gene responsible for the defect in uric acid metabolism. Reduction of uric acid levels in the blood and urine by feeding allopurinol and meat-free diet relieves the symptoms of both stones and dermatitis. (Lowry et.al. 1973). Such a regimen of treatment is expected to be necessary for some Dalmatians and accepted as the usual way of life by most experienced breeders. However, the trouble and expense of maintaining the family pet in this manner are more than most families are willing to bear. Dalmatians with subclinical cases of urinary calculi and dermatitis contribute considerably to the propagation of the health problems. Kidney stones can be found on autopsy of some Dalmatians that are apparently health throughout their lives. A great hindrance to effective selection is that relatively late onset of both diseases in those animals that do develop symptoms. Most Dalmatians that develop symptoms do not do so until after one year of age. Breeders are reluctant to remove animals from their breeding programs once they have selected their best show prospects and raised them to maturity. Although the breeder may seriously consider removing the dog from the breeding program when it has an acute attack of either disease, his determination to do so usually wanes when the dog regains his health and again shows good potential of winning in the ring. Most of the breeders who cannot bring themselves to the decision to removed affected mature animals from the breeding program probably could make that decision if puppies that were likely to develop symptoms could be identified by 6 weeks of age. Although there is no method know for identifying all Dalmatian puppies that will eventually develop symptoms of urinary calculi and/or dermatitis, there is a relatively simple breeding program that will allow for the selection of puppies that will not develop symptoms. Such puppies could be produced and identified if the normal gene responsible for metabolism of uric acid to allantoin could be substituted for this defective allele in some individuals of the Dalmatian breed. This is now known to be possible. The production of 5 puppies having normal metabolism of uric acid and absence of interspersed white hairs in the Dalmatian-type spots in the backcrossing experiments, demonstrated that the gene for the defect in uric acid metabolism was not required to achieve the spotting pattern described in the standard. Furthermore, the normal allele for metabolism of uric acid to allantoin would eliminate the prevalent form of dermatitis and thus facilitate attainment of the coat that is described in the revision of the standard currently being considered by the Dalmatian Club of America. The proposed wording is “Sleek and glossy in appearance, the coat is in healthy condition, free from blemish.” In 1976 I advised the Board of Governors of the Dalmatian Club of America that I was going to attempt to breed dogs that would fit the standard as well as most show-quality Dalmatians but would also have normal metabolism of uric acid. From the 5 exceptional puppies produced by the backcross of the Dalmatian-English Pointer hybrid to Dalmatian, I selected the one that fit the standard best (Fig. 2) and backcrossed him to a registered Dalmatian. Fifty-percent of the resulting puppies had normal metabolsim of uric acid and consistently had Dalmatian-type spots without interspersed white hairs. The same procedure was continued for two more generations, through backcross four. The pedigree of the progeny of the fourth backcross shows the English Pointer as one of the 32 ancestors in the fifth generation, the other 31 being registered Dalmatians. Therefore, the offspring of the fourth backcross are 31/32 Dalmatian. The spotting pattern and overall type improved with each backcross to the point that the progeny of backcross four (Figs 3&4) are indistinguishable from purebred Dalmatians. Although 10 of the 12 pups were patched in the litter produced by the cross of the Dalmatian and English Pointer (Fig 1, see patch on side of head including ear), the portion of patching decreased to 1 of 13 puppies being patched in the litter resulting form backcross four. The latter frequency of patching is well within the normal range for the Dalmatian and is probably less than the average. The American Kennel Club is considering* registration of the dog and bitch shown in Figs 3 and 4 so that breeders will have an opportunity to select for Dalmatians that have normal metabolism of uric acid. Given that registered Dalmatians having normal uric acid become available, they may have to be proven in the show ring before the majority of breeders will be interested in them. I have been showing dogs for 33 years and will show Dalmatians with normal uric acid metabolism if registration of them is granted. Stud service and breeding stock will be available to other breeders at the usual price of registered Dalmatians. Many breeders, who are concerned about the health problems in Dalmatians, have already offered assistance in the backcross breeding program even though the dogs are not registered. If registration is granted, I am sure that a number of them will breed show-winning Dalmatians with normal uric acid metabolism and thus help to establish them in the breed. The British Kennel Club requires four backcrosses to registered animals of a given breed before the backcross progeny can be registered (Burns & Fraser 1966, p25). The American Kennel Club does not currently have such a policy but it seems to be warranted when (1) all members of the breed are homozygous for a gene that is responsible for health problems and contributes nothing desirable to the achievement of the breed standard. (2) the health problems can be resolved by backcrossing the normal allele of the defective gene into the breed. Initially, Dalmatians having normal metabolism of uric acid will all be produced from backcross mating and therefore will all be heterozygotes. They will comprise about 50 percent of the puppies in each backcross litter. They can be identified at 3 weeks of age when it becomes possible to obtain enough urine in a sample to conduct an assay for the ratio of uric acid to creatinine. Eventually, homozygous normal Dalmatians should be produced by breeding of heterozygotes together. When homozygous normal Dalmatians are bred to the current purebred type, all of the puppies will have normal metabolism and require no testing. It is unlikely that the gene for the uric acid defect will ever be purged completely from the Dalmatian breed even if all breeders should insist on using only dogs with normal metabolism for breeding. Progeny testing would have to be employed to detect carriers of the uric acid defect in the same manner as is required to eliminate any other undesirable recessive gene (Robinson 1972). Simply selecting normal dogs for breeding without progeny testing would insure that most Dalmatian puppies would be free of dermatitis and urinary calculi. That would be a definite improvement in the breed. So I am confused, not just about the spots, but the whole opposition. However, this breeding program has been going on for a long long time, the dogs are healthy and look great. I would think that the spots having some white hairs in some of the healthy dogs would not even be given a second thought. It seems that the patches can be well controlled and are no more frequent than in the sick dals. We also know that dals with patches are much less likely to be deaf, which is another big problem in the breed, so I am sure there are lots of folks who would not mind a patch. (which begs the question, do the healthy dals with white hair in their spots also have a lower rate of deafness?) I would think that the standard could proudly be changed to reflect this, that a few white hairs in spots is not a fault and in fact indicates what they have known since 1938, that white hairs in the spots means it is a healthy dog. I do not see any grounds for the other arguments presented in top link, which is that lack of hairs show linkage to the disesea, which clearly it can, so this means it could be linked to other desirable traits they want to preserve. But I won't go into this right now as I want to stay on subject of just the appearence of the spots and the standrad.

Who's 'us'? And what is 'that'? What is 'this' that it's a mistake not to believe in Australia? And why do you believe you have mind-reading skills? Us = people who read your post. That= that huge push to shut down purebred dog showing and even breeding if that is what takes to drive change which you are denying is happeing here in OZ Mind read = not hardly needed, anyone looking from can see it, more a smack in the head with a bat. Anyone who thinks that the vet checking a few breeds once a year at Crufts is going to make this all go away is blind. Blind to what they want, which is a total shift in how dogs in the kennel club are bred and the end of dog shows, which they believe drives the problems.

Well you keep telling the RSPCA that and the Uni of Sydney. Still waiting for that line of response to work and for them all to see it your way.

You keep telling us that. Like I said, anyone who believes this does not apply in OZ is sadly mistaken. I think you know that too. BTW how is the 10 point plan at syndey coming alone, and the Vet data base to track purebred dog vet visits and then there is the inbreeding study. So much going on there about purebred dogs and their welfare issues I can not even keep track.

You wrote Secondly, (and i know this is somewhat of a taboo subject), but is it safe for a mastiff to sire a litter (male dog)? Silly me for thinking you were asking the question, [is it safe for a mastiff to sire a litter. I spent a lot of time writing you a post to help to get your on your way to learning how to breed a mastiff safely. Ok I am now going to follow your directions and look up all your post and see what else you have said before so that I can fully know your inner soul....NOT.

So another words you are going to ignor all the health problems in your breed not to mention save your wallet, (a breed that you do not even know when it matures), and just collect the stud fee and dam the torpedos. And if anyone sugests differently then they are nuts coming out of the wood work.

Here are some of the health tests you need to do prior to breeding your mastiff. Your mastiff needs to be DNA tested for PRA. Certified eye exam for eye lid structure, lashes and glaucoma. 20% (2 out of 10) or more of Mastiffs have HD, your dog needs to be x-rayed and AVA scored in the normal range. Almost 2 out of every 10 also have ED which again must be x-rayed and AVA scored as normal prior to breeding. Heart disease is also a killer of Mastiff and your dogs should be cleared of heart disease. (see web site below) Mastiffs are also know to have epilepsy, this disease usually does not appear until 2-3 years of age. Cancer is also a heart breaking problem with most types found in mastiffs believed to be inherited http://www.mastiff.org/CANCER.htm This combined with a short life span of 6-10 years, needs to be taken into serious consideration. Most breeds with frequent cancers, epilepsy, cardiac disease, and shorten life spans, it is recommend male dogs be delayed in breeding until their middle to later years. This helps prevent breeding a young dog that will die of cancer or hearth failure or develope epilepsy in their younger years. Not sure what state you are in, but in some states now you can be guilty of breaking animal welfare laws if you breed a dog that passes on an inherited disease to it's pups, just something to keep in mind. You can read all about the different disorders that need to ruled out or tested for prior to breeding mastiffs here http://www.mastiff.org/MASTIFFHEALTH.htm Good luck, it is big finacial investment and huge repsonsiblity to breed the giant breeds.

Can someone explain to me about the spots on the health uric acid dogs. How do the spots look different on the healthy normal uric acid level dogs as compared to the spots on the affected high level uric acid dogs? I know they have some white hairs in the spots, is that it? How visable are these white hairs? Do the spots also make patches, are patches unacceptable in dals? I was told the healthy low uric acid spots do not meet the standard. How do the healthy dogs spot not meet the standard? Would a dog with the healthy low uric acid spots not look like a dal? Has there ever been any consideration to changing the standard for the spots so breeders would select for the dogs healthy low uric acid spots?

Thanks, that is the same inheritance pattern as for border collies. Border collies can and are also bred smooth to rough. Well every where in the world except in the Australain kennel club. They decided to bred out the dominate, perfectly heatlhy and far more suitable for Australian working ocndtions, smooth coated genes from the show dogs. Smooth coated dogs make up about half of the population of border collies world wide. Many people not only prefer the ease of care of smooth coats on their working dogs but also prefer the sleek and stealth apperance of a smooth coated dog when at work.

Sorry. I tried to make it understandable. You know with basic genetics it always take 2. So each trait/gene has two parts, one from each parent. Dominate traits are capital letters. Recessive traits are lower case. So each dog will have 2 letters, that shows what their coat is and also what possible coats they can pass on. Each parent can give only one of their 2 traits (letters) to each pup. So for example an SS dog has two dominate traits for smooth coat. He must be smooth coated. He can only give a S trait on to his pup, and therefore can only produce smooth coated dogs. rr is a rough coated dog, he is rough coated because there is no dominate S traits present. He can only give r recessive rough coated gene to his pups. It does not tell you what coat the pup will have as it is only one part of the pups 2 traits and r is recessive, but we do know at least his pup will be recessive for rough. When a dog is Sr, it means that have the dominate S traits so will be smooth coated, but they are recessive for rough. They can pass on either a r or a S trait to their pups. Is it sort of making sense now? In border collies a dog can be one of three types SS smooth coated and can only pass on a dominate smooth coat rr rough coated and can only pass on a recessive rough coat trait Sr Smooth coated but recessive for rough, can pass on either a recessive rough or a dominate smooth. To figure a litter between 2 dogs you just select the parents from above and pull out all the possible combinations. Problem is a smooth coated dogs could be dominate for smooth SS or they could be Sr smooth and recessive for rough. One smooth SS can only have smooth pups, the other Smooth Sr can have both smooth and rough pups.

Interesting, so smooth collies always recessive for rough? It is not that way in border collies, then can be SS and will never produce rough pups nomatter what coat type they are bred to.

Sorry about your dogs lamness and the worry. As others have said it could be many things. Agree with above, only xrays and read by vet trained to read them (not just your general vet) can Dx elbow dysplasia. So before you get too concerned about ED, good xrays and a proper reading are needed. According to OFA Orthopedic Foundation for Animals http://www.offa.org/stats.html#breed (scan down to table 'Search for Statistics by Breed', select Golden Retriever and then click Show Stats) Approx 1 in 10 goldens have elbow dysplasia which is considered very inheritable. Goldens are more prone to hip dysplasia at approx 2 out of 10 dogs affected. One concern I would want to rule out is that the dog does not have poor hips and this has lead to using the front end more, leading to the lameness in front. (just like when you sprain your left ankle and few days later your right hip or knee starts to hurt because you are using that leg differently). Have seen this happen a few times.

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Allergies are the result of a mal functioning immune system and they are a big health problem. Most believe that immune system disorders such as a tendency towards allergies is inherited. Dog breeders need to actively and aggressively breed against allergies or any other indication of a mal functioning immune system in dogs. Now how to breed away from immune system disorders is another story.