DCM
Dialated Cardiomyopathy
A Disease Affecting The Heart
Genetic Testing
Dialated Cardiomyopathy (DCM) Posted By Trinity Dobermans
Dr. Meurs at Washington State University
Has discovered "a" mutant gene
associated with DCM
Dr Meurs (Washington State University) has discovered a gene mutation that is consistent amongst all the dobes in her study group. This finding is huge - and hopefully it won't be the last discovery - Dr. Meurs has stated that she suspects there will be more than one gene that is a player on the DCM stage. But this first identification of a gene mutation is HUGE to our breed.
The Meurs DCM DNA Test is actually testing for PDK4 which is a specific mutated gene associated with DCM (Dilated Cardiomyopathy Mutation). It is believed that there is more than one gene associated with Dilated Cardiomyopathy in the Doberman. In humans there are over 100 genes associated with Cardiomyopathy. At this time we have the ability to test for just the one in Dobermans. PDK4 is a "regulator of the entrance of glucose into the heart's mitochondria." This is a quote from Dr. Meurs. In layman's terms, it helps regulate the energy used by the heart cells. When tested, there are 3 possible results: Negative, Positive Heterozygous, or Positive Homozygous.
This gene mutation is genetically autosominal dominant with Varied Penetrance. There is a DNA test available from WSU available available at this link http://www.vetmed.wsu.edu/deptsVCGL/Orders/doberman.aspx Test results will be one of the following.
Negative – no gene mutation
Positive/Heterozygous – 1 copy of the gene mutation
Positive/Homozygous – 2 copies of the gene mutation
According to Dr. Meurs, having a test result of Positive (either Heterozygous or Homozygous) is NOT predictive of "when" or even "If" your dog will get DCM - heart disease because of the varied penetrance of the mutated gene. Dr. Meurs did state that dogs that tested Pos-Homo did "appear" to manifest DCM earlier and have much worse symptoms once DCM was clinically apparent. Conversely, she also stated that dogs that came back Negative could not be guaranteed that they would NEVER get DCM.
So as exciting and important as this new discovery is it is also very frustrating as it is not one bit predictive of which dogs absolutely WILL or WILL NOT get DCM
This is because she suspects that it is highly likely that the mutant gene she found is probably not the ONLY gene that could cause the Negative dog to develop DCM. There are also other environmental causal agents like Diet, Virus and exercise that could "cause" DCM to manifest in a Negative dog. She also felt we could be dealing with two forms of DCM the enlarged heart and the fibrillation type of DCM disease.
So what are we left with - a test that gives us a very small but important piece in a very large complex DCM picture puzzle. I am going to test all my dogs - even the spayed retired ones - I think in order for this information to have any REAL decision making value - we need to have as much information from the test findings to even know how to process our own findings and make good breeding decisions.
Unless you know your dogs parents are both Negative I want to STRONGLY suggest everyone that can test there dog to test their dog - if you don't want to know the results then you can indicate that when you send the DNA brushes back in. But consider this - If I were to hazard a guess, I think the percentage of breeding dogs and show dogs are maybe 25% or less of the entire Doberman population. If most of the tests for this mutant gene come from that small portion of the breed the test results may be totally different than if the tests came from all segments (pets, companions, spayed, rescued) of our breed. In order for the test results to be really meaningful - those tests need to reflect the entire population of Dobermans.
I am much more encouraged and upbeat today than when this news first broke and we were left with so many questions - we still don't have all the answers, but we have a start.
I am also feeling better because even if I have Positive dogs in my lines – there has to be another causal agent or agents at work that affects the amount of pentrance in each dog.. Otherwise the current dogs and their ancestors would not have enjoyed the longevity validated by the Bred for Longevity and Longevity certifications in my pedigrees. I just don’t believe that those (like myself) who have studied pedigrees, bred with health and temperaments in mind and have demonstrated longevity have produced these dogs by accident, luck or incidence.
It is our duty to provide the healthiest pups we can. Every breeder lives in fear of getting the phone call to advise one of our pups is deathly ill - because your grief is our grief. In order to meet buyer expectation of us providing you with as healthy a puppy as possible, we are going to need to utilize EVERY dog that tests negative to help retain lines from those dogs that are positive Hetero so the resulting negative offspring can replace the positive parent. This process is not accomplished in one generation, Dr. Meur’s said it would likely take 3 generations.
Dr Meurs also strongly advised against whole scale culling of every positive dog out of the breeding pool – that would be disastrous. Breeders need to utilize the heterozygous dogs bred to negative dogs – create retain genetic diversity and increase the number of negative dogs.
Breeders will have to consider retaining the best negative puppies for their respective breeding programs, or place them in homes on breeding contracts to insure the gene pool stays as big as possible. Buyers will have to realize that responsible breeders may not be able to meet their own breeding program requirements and meet the buyers expectation of purchasing only negative pups.
If the majority of negative pups are placed in pet or companion homes and are spayed and neutered, breeders will not have the dogs needed to make improvements to the gene pool by increasing negative breeding stock and reducing the positive dogs. The doberman gene pool is already alarmingly small - we must retain as much diversity of good breeding lines as possible or we will allow other more deadly health issues to become prominent.
This test for DCM is just one ingredient in the recipe, I am blessed that my lines to date apparently have a very low or no penetrance for this disease because I have a tremendous amount of longevity in my blood lines. For me to have enjoyed demonstrated longevity in my dogs there must be a genetic factor braided into my dogs genetics, that so far has manifested a low to no penetrance of heart disease. What this genetic switch or faucet is remains UNKNOWN to us all, but hopefully as the research goes forward it, as another piece to this puzzle will be identified. I have to believe that there are companion genetics in the bloodlines that plays a dynamic role in allowing longevity to be expressed, no matter what the mutant test result is.
This is where the knowledge of pedigrees, cause of death, longevity and knowing the percentage of influence each ancestor brings to a planned litter is so important. In doing this type of research, breeders try and create a recipe that has enough longevity sweetness to over power and dominate the bitterness of DCM. We are going to have to go forward with these “older tools” in combination with the new test.
Dr Meurs said even a test result of Positive-Homozygous does not mean that your dog WILL get DCM or even DIE of DCM. And on the flip side having a Negative test result does not mean your dog will NOT get DCM through some other causal genetic or environmental factor. So lets be perfectly clear!!!! this test in not a bit predictive as to whether DCM is going to deliver a deadly blow to your beloved Doberman.
So now you know why breeding dogs is not for the faint of heart. For each puppy we sell we assume the responsibility for the length of life of our puppy and for each buyer’s individual happiness.
What a daunting task to assign breeders when there is no definitive predictor available to ensure if a dog we produce will get DCM. Nevertheless, undaunted, I am in this for the long haul, I will continue to be a guardian of the breed, research and study pedigrees, work towards matings that will allow demonstrated longevity to DOMINATE the co-efficient percentages in the planned litter’s pedigree and I will test my dogs so I know which dogs going forward not only had longevity first but if there is a correlation to the result of the initial DCM mutant gene test.
Breeding Strategies
#1 Best combination is Negative to Negative
100% of pups will be genetically Negative unaffected & clear of the gene mutation
#2 Second Best combination is Negative to Positive/Heterozygous
50% of puppies born will be Positive/Heterozygous -
50% of puppies born will be genetically unaffected & clear of this gene mutation
#3 Third combination is Positive/Heterozygous to Positive/Heterozygous
- 25% of puppies born Positive/Homozygous and genetically affected by this mutation
- 50% of puppies born Positive/Heterozygous or genetically affected by this mutation
- 25% of puppies born Negative or genetically unaffected by this genetic mutation
#4 Fourth combination is Negative to Positive/Homoozygous
100% of puppies born Positive/Heterozygous or genetically affected by this mutation
#5 Fifth combination is Positive/Homoozygous to Positive/Homoozygous
100% of puppies born carrying two copies of the gene and genetically affected by this mutation
I was one of the first in this breed, and am still one of only a very few that give a 6 year health guarantee, 2 years seems to be the hall mark for doberman breeders. I do not plan to change the length of my guarantee – I still have the absolute faith and confidence that my dogs can bear the weight of this guarantee as well as they have for the last 20 years – an almost 20 year track record of healthy dogs can’t be a coincidence or just plain luck – I will continue to stand behind the dogs and their past health record by keeping my guarantee at 6 years.
I will absolutely be mindful of this new genetic test as I make breeding decisions going forward, because if we can, over the next several generations reduce the number of dogs that are Positive Homozygous and increase the negative dogs that will absolutely be a huge benefit the breed. By reducing the number of Positive Homozygous dogs we reduce the highest risk for getting DCM – that should be the goal for all breeders.
Once I know the results of the tests on each of my dogs, I will develop a strategy for my family of dogs. I will work toward having a goal of having the dogs I breed be all negative of this single gene mutation over the next 5 to 10 years as suggested by Dr. Meurs. But even with an entire pack of negative dogs a dog breeder will still not be able to guarantee you that any puppy won't get DCM from some other mutant gene or causal agent. Just like your Pediatrician or even God can not guarantee that your child will not get cancer, heart disease or some other deadly disease - there are bad breeders out there. but the majority of us are just trying to do the best we can with the information we have today and praying for more and better information tomorrow.
So I won't be culling or killing any Doberman pups that test positive - when this test is no more predictive of IF they will get DCM, or WHEN they will get DCM. A Positive puppy has as good a chance to live a long life just as the negative puppy does. The good news about the positive identification is that knowing which dogs they are, we can work toward reducing the number of positive dogs we produce going forward over the next 5 to 10 years,
To me this test is not an end at all but just the beginning, with the goal of greatly reducing the incidence of and hopefully at some point in the future eradicating DCM.
Today’s breeders have to deal with the hand they have been dealt by yesterdays breeders. Buyers need to remember that it really is not fair to hold today's breeders feet to the fire, making us be irresponsible for breeding decisions that we had no part in nor control over.
One last thought in closing. Dog breeders for some reason have been assigned the responsibility for guaranteeing the health of their pups far beyond any other domestic species breeder and I am not sure why this is, and I am not entirely sure it is a fair expectation.
Horses are vetted for that moment in time that the money changes hand. No horse breeder I know of would ever be expected to guarantee a horse would live X number of years and be free of genetic health issues. In fact as a horse buyer you hope he does not hurt himself in the trailer on the way home cause he was bought As-Is-where-is and you own him for better or worse no matter what happens. Horses also sell for hundreds and even millions of dollars.
Cats usually have a very limited guarantee and certainly none that I can find give more than a limited genetic health guarantee and I could find none offering anything past a year
Fish usually have a 7 day health guarantee
Avian health guarantees are from 72 hours to 10 days
I would like prospective puppy buyers to consider just how much power they think a canine breeder really has in being able to guarantee the puppy we sell.. As I explained to one of my puppy buyers about these latest developments with the new DCM Test, .... I would continue to stand behind the six year health guarantee,but just as before this new genetic discovery, I still could not guarantee genetics – he looked me right in the eye and said – "Don’t apologize for not being as powerful as God Gail, only the good Lord has any true power over life and death, I certainly don't expect you to play God". Kind of puts things in perspective doesn't it?
Breeders of today have to make decisions based on what we know today - breeders of tomorrow will have the benefit of knowing the past.
Dr. Meurs at Washington State University
Has discovered "a" mutant gene
associated with DCM
Dr Meurs (Washington State University) has discovered a gene mutation that is consistent amongst all the dobes in her study group. This finding is huge - and hopefully it won't be the last discovery - Dr. Meurs has stated that she suspects there will be more than one gene that is a player on the DCM stage. But this first identification of a gene mutation is HUGE to our breed.
The Meurs DCM DNA Test is actually testing for PDK4 which is a specific mutated gene associated with DCM (Dilated Cardiomyopathy Mutation). It is believed that there is more than one gene associated with Dilated Cardiomyopathy in the Doberman. In humans there are over 100 genes associated with Cardiomyopathy. At this time we have the ability to test for just the one in Dobermans. PDK4 is a "regulator of the entrance of glucose into the heart's mitochondria." This is a quote from Dr. Meurs. In layman's terms, it helps regulate the energy used by the heart cells. When tested, there are 3 possible results: Negative, Positive Heterozygous, or Positive Homozygous.
This gene mutation is genetically autosominal dominant with Varied Penetrance. There is a DNA test available from WSU available available at this link http://www.vetmed.wsu.edu/deptsVCGL/Orders/doberman.aspx Test results will be one of the following.
Negative – no gene mutation
Positive/Heterozygous – 1 copy of the gene mutation
Positive/Homozygous – 2 copies of the gene mutation
According to Dr. Meurs, having a test result of Positive (either Heterozygous or Homozygous) is NOT predictive of "when" or even "If" your dog will get DCM - heart disease because of the varied penetrance of the mutated gene. Dr. Meurs did state that dogs that tested Pos-Homo did "appear" to manifest DCM earlier and have much worse symptoms once DCM was clinically apparent. Conversely, she also stated that dogs that came back Negative could not be guaranteed that they would NEVER get DCM.
So as exciting and important as this new discovery is it is also very frustrating as it is not one bit predictive of which dogs absolutely WILL or WILL NOT get DCM
This is because she suspects that it is highly likely that the mutant gene she found is probably not the ONLY gene that could cause the Negative dog to develop DCM. There are also other environmental causal agents like Diet, Virus and exercise that could "cause" DCM to manifest in a Negative dog. She also felt we could be dealing with two forms of DCM the enlarged heart and the fibrillation type of DCM disease.
So what are we left with - a test that gives us a very small but important piece in a very large complex DCM picture puzzle. I am going to test all my dogs - even the spayed retired ones - I think in order for this information to have any REAL decision making value - we need to have as much information from the test findings to even know how to process our own findings and make good breeding decisions.
Unless you know your dogs parents are both Negative I want to STRONGLY suggest everyone that can test there dog to test their dog - if you don't want to know the results then you can indicate that when you send the DNA brushes back in. But consider this - If I were to hazard a guess, I think the percentage of breeding dogs and show dogs are maybe 25% or less of the entire Doberman population. If most of the tests for this mutant gene come from that small portion of the breed the test results may be totally different than if the tests came from all segments (pets, companions, spayed, rescued) of our breed. In order for the test results to be really meaningful - those tests need to reflect the entire population of Dobermans.
I am much more encouraged and upbeat today than when this news first broke and we were left with so many questions - we still don't have all the answers, but we have a start.
I am also feeling better because even if I have Positive dogs in my lines – there has to be another causal agent or agents at work that affects the amount of pentrance in each dog.. Otherwise the current dogs and their ancestors would not have enjoyed the longevity validated by the Bred for Longevity and Longevity certifications in my pedigrees. I just don’t believe that those (like myself) who have studied pedigrees, bred with health and temperaments in mind and have demonstrated longevity have produced these dogs by accident, luck or incidence.
It is our duty to provide the healthiest pups we can. Every breeder lives in fear of getting the phone call to advise one of our pups is deathly ill - because your grief is our grief. In order to meet buyer expectation of us providing you with as healthy a puppy as possible, we are going to need to utilize EVERY dog that tests negative to help retain lines from those dogs that are positive Hetero so the resulting negative offspring can replace the positive parent. This process is not accomplished in one generation, Dr. Meur’s said it would likely take 3 generations.
Dr Meurs also strongly advised against whole scale culling of every positive dog out of the breeding pool – that would be disastrous. Breeders need to utilize the heterozygous dogs bred to negative dogs – create retain genetic diversity and increase the number of negative dogs.
Breeders will have to consider retaining the best negative puppies for their respective breeding programs, or place them in homes on breeding contracts to insure the gene pool stays as big as possible. Buyers will have to realize that responsible breeders may not be able to meet their own breeding program requirements and meet the buyers expectation of purchasing only negative pups.
If the majority of negative pups are placed in pet or companion homes and are spayed and neutered, breeders will not have the dogs needed to make improvements to the gene pool by increasing negative breeding stock and reducing the positive dogs. The doberman gene pool is already alarmingly small - we must retain as much diversity of good breeding lines as possible or we will allow other more deadly health issues to become prominent.
This test for DCM is just one ingredient in the recipe, I am blessed that my lines to date apparently have a very low or no penetrance for this disease because I have a tremendous amount of longevity in my blood lines. For me to have enjoyed demonstrated longevity in my dogs there must be a genetic factor braided into my dogs genetics, that so far has manifested a low to no penetrance of heart disease. What this genetic switch or faucet is remains UNKNOWN to us all, but hopefully as the research goes forward it, as another piece to this puzzle will be identified. I have to believe that there are companion genetics in the bloodlines that plays a dynamic role in allowing longevity to be expressed, no matter what the mutant test result is.
This is where the knowledge of pedigrees, cause of death, longevity and knowing the percentage of influence each ancestor brings to a planned litter is so important. In doing this type of research, breeders try and create a recipe that has enough longevity sweetness to over power and dominate the bitterness of DCM. We are going to have to go forward with these “older tools” in combination with the new test.
Dr Meurs said even a test result of Positive-Homozygous does not mean that your dog WILL get DCM or even DIE of DCM. And on the flip side having a Negative test result does not mean your dog will NOT get DCM through some other causal genetic or environmental factor. So lets be perfectly clear!!!! this test in not a bit predictive as to whether DCM is going to deliver a deadly blow to your beloved Doberman.
So now you know why breeding dogs is not for the faint of heart. For each puppy we sell we assume the responsibility for the length of life of our puppy and for each buyer’s individual happiness.
What a daunting task to assign breeders when there is no definitive predictor available to ensure if a dog we produce will get DCM. Nevertheless, undaunted, I am in this for the long haul, I will continue to be a guardian of the breed, research and study pedigrees, work towards matings that will allow demonstrated longevity to DOMINATE the co-efficient percentages in the planned litter’s pedigree and I will test my dogs so I know which dogs going forward not only had longevity first but if there is a correlation to the result of the initial DCM mutant gene test.
Breeding Strategies
#1 Best combination is Negative to Negative
100% of pups will be genetically Negative unaffected & clear of the gene mutation
#2 Second Best combination is Negative to Positive/Heterozygous
50% of puppies born will be Positive/Heterozygous -
50% of puppies born will be genetically unaffected & clear of this gene mutation
#3 Third combination is Positive/Heterozygous to Positive/Heterozygous
- 25% of puppies born Positive/Homozygous and genetically affected by this mutation
- 50% of puppies born Positive/Heterozygous or genetically affected by this mutation
- 25% of puppies born Negative or genetically unaffected by this genetic mutation
#4 Fourth combination is Negative to Positive/Homoozygous
100% of puppies born Positive/Heterozygous or genetically affected by this mutation
#5 Fifth combination is Positive/Homoozygous to Positive/Homoozygous
100% of puppies born carrying two copies of the gene and genetically affected by this mutation
I was one of the first in this breed, and am still one of only a very few that give a 6 year health guarantee, 2 years seems to be the hall mark for doberman breeders. I do not plan to change the length of my guarantee – I still have the absolute faith and confidence that my dogs can bear the weight of this guarantee as well as they have for the last 20 years – an almost 20 year track record of healthy dogs can’t be a coincidence or just plain luck – I will continue to stand behind the dogs and their past health record by keeping my guarantee at 6 years.
I will absolutely be mindful of this new genetic test as I make breeding decisions going forward, because if we can, over the next several generations reduce the number of dogs that are Positive Homozygous and increase the negative dogs that will absolutely be a huge benefit the breed. By reducing the number of Positive Homozygous dogs we reduce the highest risk for getting DCM – that should be the goal for all breeders.
Once I know the results of the tests on each of my dogs, I will develop a strategy for my family of dogs. I will work toward having a goal of having the dogs I breed be all negative of this single gene mutation over the next 5 to 10 years as suggested by Dr. Meurs. But even with an entire pack of negative dogs a dog breeder will still not be able to guarantee you that any puppy won't get DCM from some other mutant gene or causal agent. Just like your Pediatrician or even God can not guarantee that your child will not get cancer, heart disease or some other deadly disease - there are bad breeders out there. but the majority of us are just trying to do the best we can with the information we have today and praying for more and better information tomorrow.
So I won't be culling or killing any Doberman pups that test positive - when this test is no more predictive of IF they will get DCM, or WHEN they will get DCM. A Positive puppy has as good a chance to live a long life just as the negative puppy does. The good news about the positive identification is that knowing which dogs they are, we can work toward reducing the number of positive dogs we produce going forward over the next 5 to 10 years,
To me this test is not an end at all but just the beginning, with the goal of greatly reducing the incidence of and hopefully at some point in the future eradicating DCM.
Today’s breeders have to deal with the hand they have been dealt by yesterdays breeders. Buyers need to remember that it really is not fair to hold today's breeders feet to the fire, making us be irresponsible for breeding decisions that we had no part in nor control over.
One last thought in closing. Dog breeders for some reason have been assigned the responsibility for guaranteeing the health of their pups far beyond any other domestic species breeder and I am not sure why this is, and I am not entirely sure it is a fair expectation.
Horses are vetted for that moment in time that the money changes hand. No horse breeder I know of would ever be expected to guarantee a horse would live X number of years and be free of genetic health issues. In fact as a horse buyer you hope he does not hurt himself in the trailer on the way home cause he was bought As-Is-where-is and you own him for better or worse no matter what happens. Horses also sell for hundreds and even millions of dollars.
Cats usually have a very limited guarantee and certainly none that I can find give more than a limited genetic health guarantee and I could find none offering anything past a year
Fish usually have a 7 day health guarantee
Avian health guarantees are from 72 hours to 10 days
I would like prospective puppy buyers to consider just how much power they think a canine breeder really has in being able to guarantee the puppy we sell.. As I explained to one of my puppy buyers about these latest developments with the new DCM Test, .... I would continue to stand behind the six year health guarantee,but just as before this new genetic discovery, I still could not guarantee genetics – he looked me right in the eye and said – "Don’t apologize for not being as powerful as God Gail, only the good Lord has any true power over life and death, I certainly don't expect you to play God". Kind of puts things in perspective doesn't it?
Breeders of today have to make decisions based on what we know today - breeders of tomorrow will have the benefit of knowing the past.
European Society of Veterinary Cardiology
screening guidelines for dilated cardiomyopathy in Doberman Pinschers.
Review article
Wess G, et al. J Vet Cardiol. 2017.
Show full citation
AbstractBACKGROUND: Dilated cardiomyopathy (DCM) is the most common cardiac disease in large breed dogs and is inherited in Doberman Pinschers with a high prevalence (58%).
OBJECTIVE: The European Society for Veterinary Cardiology convened a task force to formulate screening guidelines for DCM in Dobermans.
RECOMMENDATIONS: Screening for occult DCM in Dobermans should start at three years of age and use both Holter monitoring and echocardiography. Yearly screening over the life of the dog is recommended, as a one-time screening is not sufficient to rule out future development of DCM. The preferred echocardiographic method is the measurement of the left ventricular volume by Simpson's method of discs (SMOD). Less than 50 single ventricular premature complexes (VPCs) in 24 h are considered to be normal in Dobermans, although detection of any number of VPCs is cause for concern. Greater than 300 VPCs in 24 h or two subsequent recordings within a year showing between 50 and 300 VPCs in 24 h is considered diagnostic of occult DCM in Dobermans regardless of the concurrent echocardiographic findings. The guidelines also provide recommendations concerning ancillary tests, that are not included in the standard screening protocol, but which may have some utility when recommended tests are not available or financially untenable on an annual basis. These tests include assay of cardiac biomarkers (Troponin I and N-Terminal pro-B-type Natriuretic Peptide) as well as a 5-min resting electrocardiogram (ECG).
CONCLUSION: The current guidelines should help to establish an early diagnosis of DCM in Dobermans.
Crown Copyright © 2017. Published by Elsevier B.V. All rights reserved.
screening guidelines for dilated cardiomyopathy in Doberman Pinschers.
Review article
Wess G, et al. J Vet Cardiol. 2017.
Show full citation
AbstractBACKGROUND: Dilated cardiomyopathy (DCM) is the most common cardiac disease in large breed dogs and is inherited in Doberman Pinschers with a high prevalence (58%).
OBJECTIVE: The European Society for Veterinary Cardiology convened a task force to formulate screening guidelines for DCM in Dobermans.
RECOMMENDATIONS: Screening for occult DCM in Dobermans should start at three years of age and use both Holter monitoring and echocardiography. Yearly screening over the life of the dog is recommended, as a one-time screening is not sufficient to rule out future development of DCM. The preferred echocardiographic method is the measurement of the left ventricular volume by Simpson's method of discs (SMOD). Less than 50 single ventricular premature complexes (VPCs) in 24 h are considered to be normal in Dobermans, although detection of any number of VPCs is cause for concern. Greater than 300 VPCs in 24 h or two subsequent recordings within a year showing between 50 and 300 VPCs in 24 h is considered diagnostic of occult DCM in Dobermans regardless of the concurrent echocardiographic findings. The guidelines also provide recommendations concerning ancillary tests, that are not included in the standard screening protocol, but which may have some utility when recommended tests are not available or financially untenable on an annual basis. These tests include assay of cardiac biomarkers (Troponin I and N-Terminal pro-B-type Natriuretic Peptide) as well as a 5-min resting electrocardiogram (ECG).
CONCLUSION: The current guidelines should help to establish an early diagnosis of DCM in Dobermans.
Crown Copyright © 2017. Published by Elsevier B.V. All rights reserved.
Von Willebrands
A Bleeding Disorder
In 1926 a Finnish physician, Dr von Willebrand, discovered a clotting disorder. His primary research led to the discovery of a deficiency of a particular protein (the carrier protein for factor VIII), which was responsible for this clotting disorder. He discovered that though there seemed to be enough platelets, they were not ‘sticky’ enough to initiate clotting normally.
Von Willebrands is a bleeding disease. It is not sex linked, and is found in one form or another in over 30 breeds of dogs. It is not hemophilia but it’s the most commonly inherited bleeding disease of both people and animals. It is only one of many reasons that can cause abnormal bleeding in dogs. For many years it was a mystery why the disease was much milder in some breeds than in others (the Doberman an example of a mild form of the disease, the Scottish Terrier and example of the severe form of the disease). It is now understood that the mutation in the Von Willebrand’s factor gene in the Doberman causes faulty production 90 to 95% of the time, but 5 to 10% of the time the factor produced is normal and fully functional. As there are two genes for the factor, even with two of the mutant genes most Dobermans will produce 10-20% normal factor (and 80-90% non-functional factor). Under normal circumstances, this amount of factor is sufficient for normal clotting. In times of stress, or with major blood loss during surgery or as a result of trauma the disease may become clinically apparent with inability to clot. In other breeds such as the Scottish terrier, the mutation is more severe resulting in an almost complete absence of the factor, and in this breed a genetically affected dog is clinically affected as well.
In the past the ELISA test, which measures levels of the factor was the only diagnositic tool to differentiate between clear, carrier and affected Dobermans. This test was not very reliable, as there is much overlap in the amount of factor production between these groups of Dobermans. With great thanks to the research team headed by the University of Michigan geneticist Dr George Brewer, a joint effort between VetGen, Michigan State University and the University of Michigan developed a genetic test for this disease. Grant moneys donated from the DPCA, the Orthopedic Foundation of America, the Morris Animal Foundation, the DPFA, and the American Kennel Club made this possible. Now dogs may be definitively classified as clear, carriers, or affected by direct analysis for the actual genes.
In studies of healthy Dobermans, 35% are genetically affected (two copies of the mutant gene), 50% are carriers (one copy of the mutant gene) and 15% are clear (no copies of the mutant gene). Most Dobermans who are genetically affected will never have a bleeding problem. However, as times of stress or surgery may lead to bleeding problems, you may, as an educated Doberman Pinscher owner, opt to test your dog. One might request the vet keep desomepressin, and at times of scheduled surgery fresh frozen plasma, or cryoprecipitate (clotting factors) on hand, in case of emergency.
While most affected Dobermans may never show a sign of vWd, others may hemorrhage from the nose, gums, cuts, or genitals, etc… This usually comes after some minor type of injury. Some affected dogs go through protracted bruising/bleeding after a routine spay/neuter situation. Why some genetically affected Dobermans are clinically affected, while most are not, is not clear.
Cases of Dobermans having bled to death, due to von Willebrands, have been reported, although this usually occurs after some type of trauma. Most genetically affected Dobermans have injuries, and surgeries, without ANY complications. Some, years later have their first bleeding episode after a minor incident. Mostaffected Dobermans never have a bleeding problem. There are many other known, and some *unknown*, factors involved in bleeding situations. Stress is one, and there has also been some association between hypothyroidism and vWd bleeding episodes.
Many owners, and even some veterinarians become panicked at irregularities found in a Doberman, due to not being informed of the latest medical information. If a Doberman bleeds? Many will assume that it is automatically a vWd episode. So, this is why one would want to do the simple genetic test for vWd as soon as one obtains a Doberman. Knowledge is power.
A Doberman Pinscher who bleeds should NOT automatically be put down.
Some breeders will breed only clear to clear. However, our Doberman gene pool is already small and currently only 15% of the population tests clear. If we highly limited our accessible breeding stock, other problems will emerge as there are many genetic diseases affecting this, and other purebred breeds. vWD status is one of many factors considered when breeding. Further recommendations for use of vWD testing in breeding decisions can be found on the VetGen website.
WANT MORE INFO ON vWD?
VetGen website
General information on Doberman vWD
submitted by
Suzanne McDonald
edited by
Helayne Silver MD
DPCA Public Education Committee
Orthopedics
Conditions affecting the Joints
Hips
AN EXAMINATION OF HIP GRADING: The phenotypic evaluation of hips done by the Orthopedic Foundation for Animals falls into seven different categories. Those categories are Normal (Excellent, Good, Fair), Borderline, and Dysplastic (Mild, Moderate,Severe). Once each of the radiologists classifies the hip into one of the 7 phenotypes above, the final hip grade is decided by a consensus of the 3 independent outside evaluations. Examples would be:
ExcellentExcellent: this classification is assigned for superior conformation in comparison to other animals of the same age and breed. There is a deep seated ball (femoral head) which fits tightly into a well-formed socket (acetabulum) with minimal joint space. There is almost complete coverage of the socket over the ball.
GoodGood: slightly less than superior but a well-formed congruent hip joint is visualized. The ball fits well into the socket and good coverage is present.
FairFair: Assigned where minor irregularities in the hip joint exist. The hip joint is wider than a good hip phenotype. This is due to the ball slightly slipping out of the socket causing a minor degree of joint incongruency. There may also be slight inward deviation of the weight-bearing surface of the socket (dorsal acetabular rim) causing the socket to appear slightly shallow. This can be a normal finding in some breeds however, such as the Chinese Shar Pei, Chow Chow, and Poodle.
BorderlineBorderline: there is no clear cut consensus between the radiologists to place the hip into a given category of normal or dysplastic. There is usually more incongruency present than what occurs in the minor amount found in a fair but there are no arthritic changes present that definitively diagnose the hip joint being dysplastic. There also may be a bony projection present on any of the areas of the hip anatomy illustrated above that can not accurately be assessed as being an abnormal arthritic change or as a normal anatomic variant for that individual dog. To increase the accuracy of a correct diagnosis, it is recommended to repeat the radiographs at a later date (usually 6 months). This allows the radiologist to compare the initial film with the most recent film over a given time period and assess for progressive arthritic changes that would be expected if the dog was truly dysplastic. Most dogs with this grade (over 50%) show no change in hip conformation over time and receive a normal hip rating; usually a fair hip phenotype.
MildMild Hip Dysplasia: there is significant subluxation present where the ball is partially out of the socket causing an incongruent increased joint space. The socket is usually shallow only partially covering the ball. There are usually no arthritic changes present with this classification and if the dog is young (24 to 30 months of age), there is an option to resubmit an radiograph when the dog is older so it can be reevaluated a second time. Most dogs will remain dysplastic showing progression of the disease with early arthritic changes. Since HD is a chronic, progressive disease, the older the dog, the more accurate the diagnosis of HD (or lack of HD).
ModerateModerate Hip Dysplasia: there is significant subluxation present where the ball is barely seated into a shallow socket causing joint incongruency. There are secondary arthritic bone changes usually along the femoral neck and head (termed remodeling), acetabular rim changes (termed osteophytes or bone spurs) and various degrees of trabecular bone pattern changes called sclerosis. Once arthritis is reported, there is only continued progression of arthritis over time.
SevereSevere Hip Dysplasia: assigned where radiographic evidence of marked dysplasia exists. There is significant subluxation present where the ball is partly or completely out of a shallow socket. Like moderate HD, there are also large amounts of secondary arthritic bone changes along the femoral neck and head, acetabular rim changes and large amounts of abnormal bone pattern changes.
*********************
Elbows
ELBOW DYSPLASIA GRADES
Elbow dysplasia has multiple inherited etiologies which may occur singularly or in combination. These etiologies include fragmented medial coronoid (FCP) of the ulna, osteochondritis of the medial humeral condyle and ununited anconeal process (UAP). The most sensitive view used to diagnose secondary degenerative changes in the elbow joint is an extreme flexed medio-lateral view of the elbow which is required by the OFA and recommended by the International Elbow Working Group. The veterinary radiologists are most interested in the appearance of the anconeal process of the ulna.
When there is instability of the elbow joint due to elbow dysplasia, one of the most sensitive radiographic findings is new bone proliferation (osteophytes) on the anconeal process of the ulna associated with secondary developmental degenerative joint disease.
Bone proliferation can be very subtle to visualize in some dogs and may require the use of a special light source (hot light) rather than a traditional view box to diagnose it. Other arthritic findings such as sclerosis in the area of the trochlear notch of the ulna and bone spurs at joint edges are also reported. If fragmentation of the medial coronoid only involves the cartilage, it may not be seen radiographically but occasionally if the bone is also fragmented, it can be visualized as a separate calcific opacity superimposed over the radius.
Grading ElbowsFor elbow evaluations, there are no grades for a radiographically normal elbow. The only grades involved are for abnormal elbows with radiographic changes associated with secondary degenerative joint disease. Like the hip certification, the OFA will not certify a normal elbow until the dog is 2 years of age. The OFA also accepts preliminary elbow radiographs. To date, there are no long term studies for preliminary elbow examinations like there are for hips, however, preliminary screening for elbows along with hips can also provide valuable information to the breeder.
Von Willebrands is a bleeding disease. It is not sex linked, and is found in one form or another in over 30 breeds of dogs. It is not hemophilia but it’s the most commonly inherited bleeding disease of both people and animals. It is only one of many reasons that can cause abnormal bleeding in dogs. For many years it was a mystery why the disease was much milder in some breeds than in others (the Doberman an example of a mild form of the disease, the Scottish Terrier and example of the severe form of the disease). It is now understood that the mutation in the Von Willebrand’s factor gene in the Doberman causes faulty production 90 to 95% of the time, but 5 to 10% of the time the factor produced is normal and fully functional. As there are two genes for the factor, even with two of the mutant genes most Dobermans will produce 10-20% normal factor (and 80-90% non-functional factor). Under normal circumstances, this amount of factor is sufficient for normal clotting. In times of stress, or with major blood loss during surgery or as a result of trauma the disease may become clinically apparent with inability to clot. In other breeds such as the Scottish terrier, the mutation is more severe resulting in an almost complete absence of the factor, and in this breed a genetically affected dog is clinically affected as well.
In the past the ELISA test, which measures levels of the factor was the only diagnositic tool to differentiate between clear, carrier and affected Dobermans. This test was not very reliable, as there is much overlap in the amount of factor production between these groups of Dobermans. With great thanks to the research team headed by the University of Michigan geneticist Dr George Brewer, a joint effort between VetGen, Michigan State University and the University of Michigan developed a genetic test for this disease. Grant moneys donated from the DPCA, the Orthopedic Foundation of America, the Morris Animal Foundation, the DPFA, and the American Kennel Club made this possible. Now dogs may be definitively classified as clear, carriers, or affected by direct analysis for the actual genes.
In studies of healthy Dobermans, 35% are genetically affected (two copies of the mutant gene), 50% are carriers (one copy of the mutant gene) and 15% are clear (no copies of the mutant gene). Most Dobermans who are genetically affected will never have a bleeding problem. However, as times of stress or surgery may lead to bleeding problems, you may, as an educated Doberman Pinscher owner, opt to test your dog. One might request the vet keep desomepressin, and at times of scheduled surgery fresh frozen plasma, or cryoprecipitate (clotting factors) on hand, in case of emergency.
While most affected Dobermans may never show a sign of vWd, others may hemorrhage from the nose, gums, cuts, or genitals, etc… This usually comes after some minor type of injury. Some affected dogs go through protracted bruising/bleeding after a routine spay/neuter situation. Why some genetically affected Dobermans are clinically affected, while most are not, is not clear.
Cases of Dobermans having bled to death, due to von Willebrands, have been reported, although this usually occurs after some type of trauma. Most genetically affected Dobermans have injuries, and surgeries, without ANY complications. Some, years later have their first bleeding episode after a minor incident. Mostaffected Dobermans never have a bleeding problem. There are many other known, and some *unknown*, factors involved in bleeding situations. Stress is one, and there has also been some association between hypothyroidism and vWd bleeding episodes.
Many owners, and even some veterinarians become panicked at irregularities found in a Doberman, due to not being informed of the latest medical information. If a Doberman bleeds? Many will assume that it is automatically a vWd episode. So, this is why one would want to do the simple genetic test for vWd as soon as one obtains a Doberman. Knowledge is power.
A Doberman Pinscher who bleeds should NOT automatically be put down.
Some breeders will breed only clear to clear. However, our Doberman gene pool is already small and currently only 15% of the population tests clear. If we highly limited our accessible breeding stock, other problems will emerge as there are many genetic diseases affecting this, and other purebred breeds. vWD status is one of many factors considered when breeding. Further recommendations for use of vWD testing in breeding decisions can be found on the VetGen website.
WANT MORE INFO ON vWD?
VetGen website
General information on Doberman vWD
submitted by
Suzanne McDonald
edited by
Helayne Silver MD
DPCA Public Education Committee
Orthopedics
Conditions affecting the Joints
Hips
AN EXAMINATION OF HIP GRADING: The phenotypic evaluation of hips done by the Orthopedic Foundation for Animals falls into seven different categories. Those categories are Normal (Excellent, Good, Fair), Borderline, and Dysplastic (Mild, Moderate,Severe). Once each of the radiologists classifies the hip into one of the 7 phenotypes above, the final hip grade is decided by a consensus of the 3 independent outside evaluations. Examples would be:
- Two radiologists reported Excellent, one Good—the final grade would be Excellent
- One radiologist reported Excellent, one Good, one Fair—the final grade would be Good
- One radiologist reported Fair, two radiologists reported Mild—the final grade would be Mild
ExcellentExcellent: this classification is assigned for superior conformation in comparison to other animals of the same age and breed. There is a deep seated ball (femoral head) which fits tightly into a well-formed socket (acetabulum) with minimal joint space. There is almost complete coverage of the socket over the ball.
GoodGood: slightly less than superior but a well-formed congruent hip joint is visualized. The ball fits well into the socket and good coverage is present.
FairFair: Assigned where minor irregularities in the hip joint exist. The hip joint is wider than a good hip phenotype. This is due to the ball slightly slipping out of the socket causing a minor degree of joint incongruency. There may also be slight inward deviation of the weight-bearing surface of the socket (dorsal acetabular rim) causing the socket to appear slightly shallow. This can be a normal finding in some breeds however, such as the Chinese Shar Pei, Chow Chow, and Poodle.
BorderlineBorderline: there is no clear cut consensus between the radiologists to place the hip into a given category of normal or dysplastic. There is usually more incongruency present than what occurs in the minor amount found in a fair but there are no arthritic changes present that definitively diagnose the hip joint being dysplastic. There also may be a bony projection present on any of the areas of the hip anatomy illustrated above that can not accurately be assessed as being an abnormal arthritic change or as a normal anatomic variant for that individual dog. To increase the accuracy of a correct diagnosis, it is recommended to repeat the radiographs at a later date (usually 6 months). This allows the radiologist to compare the initial film with the most recent film over a given time period and assess for progressive arthritic changes that would be expected if the dog was truly dysplastic. Most dogs with this grade (over 50%) show no change in hip conformation over time and receive a normal hip rating; usually a fair hip phenotype.
MildMild Hip Dysplasia: there is significant subluxation present where the ball is partially out of the socket causing an incongruent increased joint space. The socket is usually shallow only partially covering the ball. There are usually no arthritic changes present with this classification and if the dog is young (24 to 30 months of age), there is an option to resubmit an radiograph when the dog is older so it can be reevaluated a second time. Most dogs will remain dysplastic showing progression of the disease with early arthritic changes. Since HD is a chronic, progressive disease, the older the dog, the more accurate the diagnosis of HD (or lack of HD).
ModerateModerate Hip Dysplasia: there is significant subluxation present where the ball is barely seated into a shallow socket causing joint incongruency. There are secondary arthritic bone changes usually along the femoral neck and head (termed remodeling), acetabular rim changes (termed osteophytes or bone spurs) and various degrees of trabecular bone pattern changes called sclerosis. Once arthritis is reported, there is only continued progression of arthritis over time.
SevereSevere Hip Dysplasia: assigned where radiographic evidence of marked dysplasia exists. There is significant subluxation present where the ball is partly or completely out of a shallow socket. Like moderate HD, there are also large amounts of secondary arthritic bone changes along the femoral neck and head, acetabular rim changes and large amounts of abnormal bone pattern changes.
- © 2010 Orthopedic Foundation for Animals.
*********************
Elbows
ELBOW DYSPLASIA GRADES
Elbow dysplasia has multiple inherited etiologies which may occur singularly or in combination. These etiologies include fragmented medial coronoid (FCP) of the ulna, osteochondritis of the medial humeral condyle and ununited anconeal process (UAP). The most sensitive view used to diagnose secondary degenerative changes in the elbow joint is an extreme flexed medio-lateral view of the elbow which is required by the OFA and recommended by the International Elbow Working Group. The veterinary radiologists are most interested in the appearance of the anconeal process of the ulna.
When there is instability of the elbow joint due to elbow dysplasia, one of the most sensitive radiographic findings is new bone proliferation (osteophytes) on the anconeal process of the ulna associated with secondary developmental degenerative joint disease.
Bone proliferation can be very subtle to visualize in some dogs and may require the use of a special light source (hot light) rather than a traditional view box to diagnose it. Other arthritic findings such as sclerosis in the area of the trochlear notch of the ulna and bone spurs at joint edges are also reported. If fragmentation of the medial coronoid only involves the cartilage, it may not be seen radiographically but occasionally if the bone is also fragmented, it can be visualized as a separate calcific opacity superimposed over the radius.
Grading ElbowsFor elbow evaluations, there are no grades for a radiographically normal elbow. The only grades involved are for abnormal elbows with radiographic changes associated with secondary degenerative joint disease. Like the hip certification, the OFA will not certify a normal elbow until the dog is 2 years of age. The OFA also accepts preliminary elbow radiographs. To date, there are no long term studies for preliminary elbow examinations like there are for hips, however, preliminary screening for elbows along with hips can also provide valuable information to the breeder.
- Grade I Elbow Dysplasia: Minimal bone change along anconeal process of ulna (less than 3mm).
- Grade II Elbow Dysplasia: Additional bone proliferation along anconeal process (3-5 mm) and subchondral bone changes (trochlear notch sclerosis).
- Grade III Elbow Dysplasia: Well developed degenerative joint disease with bone proliferation along anconeal process being greater than than 5 mm.
Neurological Conditions
Wobblers Syndrome
Caudal Cerival Spondylomyelopathy
Other Names:
Wobbler Syndrome, Wobblers Syndrome, Audal Cervical Spondylomyelopathy, Cervical Vertebral Instability, Spondylolitheses
Caudal Cervical Spondylomyelopathy (Wobblers Syndrome): An Overview
Wobblers Syndrome is known by many names; caudal cervical spondylomyelopathy, cervical vertebral instability, and spondylolitheses, are just a few of them. No matter the name this syndrome can be devastating. In Wobblers Syndrome the vertebrae in the lower neck of the dog put pressure on the spinal cord. This pressure comes from either malformation of the vertebrae or can be caused by trauma or a ruptured disk. As pressure increases the nerves in the spinal cord become damaged. This causes them to be unable to send signals to the body. The result of this is that the dog appears to have a lack of coordination, hence the name Wobblers.
Although any breed of dog can develop Wobblers, large and giant breeds seem to be at a greater risk than others. Some breeds in which the disease may be genetically linked are Great Danes, Doberman Pinschers, Borzois, and Basset Hounds. In Great Danes Wobblers is normally seen in young dogs, however in other breeds the onset of Wobblers does not come until later in life.
Causes of Wobblers Syndrome
The cause of Wobblers Syndrome is not known but it is thought that genetics and diets are major contributors to the disease. In some cases the syndrome appears when large dogs grow very fast as puppies due to excessive nutrition. In other cases there is no clear evidence as to what brought on the syndrome, which supports the genetic theory. Each case is different and varies in terms of disease progression, clinical signs, and severity.
Prevention of Wobblers Syndrome
Without a genetic test for Wobblers Syndrome, the best prevention is careful monitoring of the dog's diet, so that the growth rate is kept to a normal, rather than a rapid, rate.
Symptoms of Wobblers Syndrome
As with most conditions, symptoms can vary but in wobblers syndrome you are most likely to notice motor function diminish. This can be seen as general instability of the dog, clumsiness, unnatural falling down, an unsteady gait, inability for the dog to raise its head, or paralysis in the forelimbs, hind limbs, or both. The severity of the case will determine the extent to which clinical signs are present. In some cases symptoms can come and go as pressure on the spinal cord increases and decreases.
Diagnosing Wobblers Syndrome
Diagnosing wobblers is initially done using x-rays. An x-ray can show a veterinarian if the vertebrae are formed incorrectly or are in a position which is putting pressure on the spinal cord. To determine exactly the extent of the pressure being put on the spinal cord, a myelogram is usually performed. In a myelogram a contrasting material, or dye, is injected around the spinal cord. This dye allows veterinarians to view the more exactly the amount of damage being done to the spinal cord. In addition to the x-ray and myelogram, CT scans and an MRI can also be performed to aid in the diagnosis.
Treating Wobblers Syndrome
With cases which are slow to progress and mild, treatment normally starts with steroids, such as prednisone, to reduce inflammation and swelling. This along with a lifestyle consisting of very minimal activity can help keep symptoms from worsening. In more sever cases a neck brace may be required to help stabilize the neck. Surgery is also an option. Surgery will be performed to remove the pressure on the spinal cord, along with fusing the unstable vertebrae. There are many ways which this can be performed with none being more successful than another. Surgery is considered to be more helpful in sudden onset cases as opposed to chronic, slowly progressing cases. Treatment will vary depending on severity and on the dog itself and is best determined on a case by case basis.
Care for dogs with Wobblers Syndrome
If your dog has been diagnosed with Wobblers Syndrome there are certain steps which you can take to make your dog more comfortable. As always following your veterinarian's instructions is a must. In addition to this limit your dog's activity. Any high energy activity can increase the pressure on the spinal cord and cause symptoms to worsen. When walking your dog a harness is recommended. This decreases the amount of pressure put on the dog's neck and is more comfortable for them than a collar is. For more information on wobblers syndrome and care contact your local veterinarian.
- American Kennel Club Canine Health Foundation, Inc.
- P.O. Box 900061
- Raleigh, NC 27675-9061
******************************************************
Other Conditions To Be Aware Of
Preventing Bloat
What is the recommendation for feeding and exercising a dog - especially for deep-chested breeds that are prone to bloat? Is it better to walk a dog first thing in the morning and then wait and hour and feed him/her or feed first, wait an hour and then exercise?
For those who aren't aware, let me describe what is commonly called "bloat" in dogs. The proper medical name is gastric dilatation and volvulus, or GDV. In this condition the stomach twists, either rotating along it's axis or flipping 180 degrees. In either case, the inflow and outflow of the stomach are closed off resulting in gasses building up inside the stomach. This can cause difficulty breathing as the stomach balloons against the diaphragm, but more importantly pressure against the wall of the stomach can cut off the blood supply and lead to a rupture. As can be imagined, this is a critical condition and dogs can die quickly once it begins.
Dogs that bloat most commonly act and look like they swallowed a large beach ball. Their abdomen becomes large and tense, their gums can become pale, they will become suddenly lethargic, and will usually act like they are gagging or retching. If you see your dog act like this with a bloated belly, consider this a life-or-death emergency and see a vet immediately.
Though this can theoretically happen in any dog, there are definitely certain breeds that are more prone to GDV. These breeds include English bulldogs, Weimaraners, Rottweilers, German shepherds, Great Danes, and any other large, deep-chested breed. Though it seems like it's a genetic breed tendency, it's really more a factor of the anatomy of these breeds based on their size and shape. Studies have looked at how to prevent it, and there is really only one thing that has been shown to significantly increase the risk--exercise after filling the stomach with food or water. So take a dog of the right size and breed, fill their stomach with food or water, then let them run around a lot. That's a formula for bloat.
Here are precautions to take to help prevent this deadly condition:
* Wait at least one hour after eating or drinking before allowing exercise. This is the main factor shown to prevent bloat.
* Don't encourage your dog to roll over. Though a low risk, the twisting action has been shown to lead to bloat. In fact, some veterinarians do not rotate a dog over their back while anesthetized due to this risk.
* Feed 2-3 meals during the day rather than one large meal. However, be sure that you're taking the measured amount of daily food and dividing it into the meals rather than giving the once daily amount two or three times.
* Don't allow excessive water drinking immediately before or after a meal. Abnormal amounts of water have the potential to delay breakdown of food and lead to gas production.
* DO NOT raise the food bowl. While this was at one time thought to prevent bloat, a study in 2000 showed that this can actually increase the risk.
* Dogs who have had episodes of GDV are at risk for further occurrences. A surgery can be performed to attach the outside lining of the stomach to the body wall (gastropexy). While this doesn't completely prevent the stomach from rotating, it does lower the risk. Some advocate having this surgery performed routinely on high-risk breeds, but personally I disagree. Even in breeds that are prone to bloat most will never have this happen, and I don't think the benefits of the procedure (since it's not a guarantee that it will never happen) outweigh the risks. Remember, this is only in cases of preventative surgery. I certainly do think that it should be done in a dog who has bloated once since they show a personal tendency.
What is the recommendation for feeding and exercising a dog - especially for deep-chested breeds that are prone to bloat? Is it better to walk a dog first thing in the morning and then wait and hour and feed him/her or feed first, wait an hour and then exercise?
For those who aren't aware, let me describe what is commonly called "bloat" in dogs. The proper medical name is gastric dilatation and volvulus, or GDV. In this condition the stomach twists, either rotating along it's axis or flipping 180 degrees. In either case, the inflow and outflow of the stomach are closed off resulting in gasses building up inside the stomach. This can cause difficulty breathing as the stomach balloons against the diaphragm, but more importantly pressure against the wall of the stomach can cut off the blood supply and lead to a rupture. As can be imagined, this is a critical condition and dogs can die quickly once it begins.
Dogs that bloat most commonly act and look like they swallowed a large beach ball. Their abdomen becomes large and tense, their gums can become pale, they will become suddenly lethargic, and will usually act like they are gagging or retching. If you see your dog act like this with a bloated belly, consider this a life-or-death emergency and see a vet immediately.
Though this can theoretically happen in any dog, there are definitely certain breeds that are more prone to GDV. These breeds include English bulldogs, Weimaraners, Rottweilers, German shepherds, Great Danes, and any other large, deep-chested breed. Though it seems like it's a genetic breed tendency, it's really more a factor of the anatomy of these breeds based on their size and shape. Studies have looked at how to prevent it, and there is really only one thing that has been shown to significantly increase the risk--exercise after filling the stomach with food or water. So take a dog of the right size and breed, fill their stomach with food or water, then let them run around a lot. That's a formula for bloat.
Here are precautions to take to help prevent this deadly condition:
* Wait at least one hour after eating or drinking before allowing exercise. This is the main factor shown to prevent bloat.
* Don't encourage your dog to roll over. Though a low risk, the twisting action has been shown to lead to bloat. In fact, some veterinarians do not rotate a dog over their back while anesthetized due to this risk.
* Feed 2-3 meals during the day rather than one large meal. However, be sure that you're taking the measured amount of daily food and dividing it into the meals rather than giving the once daily amount two or three times.
* Don't allow excessive water drinking immediately before or after a meal. Abnormal amounts of water have the potential to delay breakdown of food and lead to gas production.
* DO NOT raise the food bowl. While this was at one time thought to prevent bloat, a study in 2000 showed that this can actually increase the risk.
* Dogs who have had episodes of GDV are at risk for further occurrences. A surgery can be performed to attach the outside lining of the stomach to the body wall (gastropexy). While this doesn't completely prevent the stomach from rotating, it does lower the risk. Some advocate having this surgery performed routinely on high-risk breeds, but personally I disagree. Even in breeds that are prone to bloat most will never have this happen, and I don't think the benefits of the procedure (since it's not a guarantee that it will never happen) outweigh the risks. Remember, this is only in cases of preventative surgery. I certainly do think that it should be done in a dog who has bloated once since they show a personal tendency.
Critical Periods in Puppy Development
Neonatal Period (0-12 Days): The puppy responds only to warmth, touch, and smell. He cannot regulate body functions such as temperature and elimination.
Transition Period (13 - 20 Days): Eyes and ears are open, but sight and hearing are limited. Tail wagging begins and the puppy begins to control body functions.
Awareness Period (21 - 28 Days): Sight and hearing functions well. The puppy is learning that he is a dog and has a great deal of need for a stable environment.
Canine Socialization Period (21 - 49 Days): Interacting with his mother and littermates, the pup learns various canine behaviors. He is now aware of the differences between canine and human societies.
Human Socialization Period (7 to 12 Weeks): The pup has the brain wave of and adult dog. The best time for going to a new home. He now has the ability to learn respect, simple behavioral responses: sit, stay, come. Housebreaking begins. He now learns by association. The permanent man/dog bonding begins, and he is able to accept gentle discipline and establish confidence.
Fear Impact Period (8 - 11 Weeks): Try to avoid frightening the puppy during this time, since traumatic experiences can have an effect during this period. As you can see, this period overlaps that of the previous definition and children or animal should not be allowed to hurt or scare the puppy -- either maliciously or inadvertently. It is very important now to introduce other humans, but he must be closely supervised to minimize adverse conditioning. Learning at this age is permanent.
This is the stage where you wonder if your dog is going to be a woosy butt all his life. Also introducing your puppy to other dogs at this time will help him become more socialized. If available in your area, a doggy day care is great for this.
Seniority Classification Period (13 - 16 Weeks): This critical period is also known as the "Age of Cutting" - cutting teeth and cutting apron strings. At this age, the puppy begins testing dominance and leadership. Biting behavior is absolutely discouraged from thirteen weeks on. Praise for the correct behavior response is the most effective tool. Meaningful praise is highly important to shape positive attitude.
Flight Instinct Period (4 to 8 Months): During this period puppies test their wings- they will turn a deaf ear when called. This period lasts from a few days to several weeks. It is critical to praise the positive and minimize the negative behavior during this time. However, you must learn how to achieve the correct response. This period corresponds to teething periods, and behavioral problems become compounded by physiological development chewing.
Second Fear impact period (6 - 14 Months): Also called, "The fear of situations period", usually corresponds to growths spurts. This critical age may depend on the size of the dog. Small dogs tend to experience these periods earlier than large dogs. Great care must be taken not to reinforce negative behavior. Force can frighten the dog, and soothing tones serve to encourage his fear. His fear should be handled with patience and kindness, and training during this period puts the dog in a position of success, while allowing him to work things out while building self-confidence.
Maturity (1 - 4 years) : Many breeds' especially giant breeds continue to grow and physically change well beyond four years of age. The average dog develops to full maturity between 1-1 1/2 years and three years of age. This period is often marked by an increase in aggression and by a renewed testing for leadership. During this time, while testing for leadership, the dog should be handled firmly. Regulars training throughout this testing period, praise him for the proper response. Giving him no inroads to affirm his leadership will remind him that this issue has already been settled.
http://www.puppyculture.com/exercise-chart.html
The Total Doberman! Factors To Consider To Preserve The Breed
PRIORITIZE FOR SUCCESS
A Manifesto for the New
TOTAL DOBERMAN
By Vic Monteleon
There is an insidious, lethal disease running rampant in Dobermans, which, if left unchecked, has the potential to destroy our breed. It has been around for awhile, camouflaging the enormity of its damage beneath glossy advertising, behind self-promoting rhetoric designed to protect individual kennel names and reputations, and by a desire to safeguard the enormous financial investments made in campaigning top conformation show dogs.
However, because of the information revolution, the consequences of the disease are becoming evident and hard to ignore.
Unfortunately, it is not a disease that the Doberman Pinscher Foundation of America can throw funding at. It isn't one with a genetic basis. It's a disease in the minds of Doberman fanciers and breeders. It is a disease of PRIORITIES! It is a mindset that states that: THE ONLY VALID MEASURE OF A BREEDING PROGRAM ARE WINS IN A SHOWRING!... It is the belief that breed type, as defined in the Doberman Standard, is the only important goal of a breeding program, and that show wins (especially Breed, Group, and BIS) are the single measure of success.
Back in the early 70's, I coined the term "The Total Doberman" in an article I wrote for Top Dobe Magazine. Then, I said that the Total Doberman was a dog who had a championship, one or more obedience titles, and had passed a temperament test, In retrospect, 25 odd years later, I admit I WAS WRONG! I didn't go far enough. not nearly far enough. I've done some self examination over the years, and have reset my priorities. If I can encourage just a few of you to look at yours, then this article will have served its purpose.
In any event, these are my priorities, and they are in order of importance:
1. TEMPERAMENT
2. HEALTH and LONGEVITY
3. FUNCTIONAL STRUCTURE
4. BREED TYPE
My rationale for ordering the priorities and a discussion of each will form the remainder of this article.
TEMPERAMENT: Temperament is still one of the most misused words in dog vocabulary. It is defined as the "totality of traits manifested on one's behavior or thinking". in short, an umbrella term. It is analogous to the term "conformation". which is the totality of physical / structural traits of an organism. For a specific breed, temperament is defined by favorable possession of those traits. Thus, the DPCA's WAE evaluates a critically necessary subset of the traits required of a good Doberman. but truly good temperament goes beyond even a WAC. Good temperament goes beyond even our Standard's description.
Our breed standard calls for a dog that is "energetic, watchful, determined, alert, fearless, loyal, and obedient. without a trace of shyness of viciousness". This is an excellent description, but it doesn't go far enough. In terms of the "preserve and protect" charter of DPCA, I' add the
following: Intense and focused prey drive. This is a primary characteristic of a great working dog. It is the foundation for training in many dog sports, from fly ball to schutzhund to agility..in fact, any sport in which the dog is motivated to move fast, chase, or run. It is an essential ingredient for search and rescue dogs and police dogs.
Calm and relaxed manner when not engaged in work This is very important, and relates to livability in an urban environment. It is also very important for police dogs or service dogs. A dog who's constantly wound up, is hyperactive, or can't / won't relax will either tend to be nervy and over reactive (we call them "nerve bags") or be exhausted from the stress when actually needed to work. A good patrol / police dog can just hang out all day, in relaxed manner in the back of a patrol car, yet be instantly "up"
and ready to work when required. More dogs wash out of training because they are nervy than any other single cause. and not just Dobermans.
Moderate threat stress threshold. A Doberman is a watchdog / guard dog / protection dog. A low threat stress is always seeing threats. where there are none. This is the dog who'll hackle and inappropriately growl and bark at everything. The high threat stress dog won't see a threat until he's practically being beaten. A good protection dog is alert but calm until threatening behavior is evident, then reacts appropriately.
A Dobe can meet the behavioral portion of our standard, yet have none of the three traits described above. Among the working elite, the Doberman is generally getting an AWFUL reputation! Many of the agility dogs lack speed and confidence. Many of our sport / protection dogs lack focus, drive, and confidence. Many are too soft to be trained for anything, but will bait and show just fine in a breed ring. Many are just too easily stressed, and when stressed, don't have quick recovery.
For the "temperamentally" serious out there, there are tools to help us. The DPCA has the Working Aptitude Evaluation, which has all but been ignored by most breeders of show dogs. Roughly 10% of dogs evaluated at any given time are Champions. The United Doberman Club has an even more ambitious set of tools. They have the Youth Temperament Test, the Adult Temperament Test, and the Sport Dog Temperament Test for conformation dogs to pass *before* they're allowed to get a UDC Championship, and last year, they implemented a "Fit for Breeding" (FFB) test as well as the German ZTP which are both a combination of a temperament test and conformation critique in which breed type *and* functional structure are evaluated. The UDC goes a step further with these tests than the Europeans do inasmuch as the club requires a full set of health tests before they'll award the FFB or ZTP titles.
We live in an incredibly litigious society. That society requires us to be ever vigilant to breed specific legislation. NOTHING will cause our breed grief faster than bad temperament. All it takes is a notionally reported incident, and our breed could be legislated into oblivion. Of all the breeds, only the Doberman comes with a ton of negative baggage. Whether deserved or not, the mention of Doberman to the general public is still met with fear and loathing. Had the three dogs that had gotten loose and killed that schoolboy been Dobermans instead of Rottweilers, we'd be in a hole right now that all the Best in Shows in the world couldn't get us out of.
When it comes to temperament, our attitude ought to be ZERO BEHAVIORAL DEFECTS. We mustn't breed nervy, gun-shy, sight sensitive, skittish, people shy Dobermans. No dogs with questionable temperaments. period! My first priority!
HEALTH AND LONGEVITY: The degree to which many of our "serious" breeders are ignoring health and longevity is shocking! Health should be a major factor in planning a breeding and we owe it to those who buy our puppies to do all that's humanly possible to insure that the pups we produce live long, vigorous, healthy lives. Health and longevity are not synonymous. A dog can be long lived, yet still have health problems. Dysplasia, late onset cardiomyopathy, thyroid immune problems, vWD may not cause a dog to be short lived, but they are still health concerns to that dog. I've known dogs of other breeds that get crippling arthritis. and live on Ascriptin, or now Rimadyl. They are long lived thanks to drugs, but they're not healthy, nor do they have the quality of life of a healthy dog.
This is my number two priority because NOT paying attention to it can have disastrous consequences. By the time something is so well established in a breed that it is recognized as a severe problem, it can be too late to be eliminated without a severe reduction in our gene pool. Reduction of a gene pool is almost a "Catch-22' SITUATION. By working to eliminate a single bad trait, we can unknowingly also lose good traits. So it behooves all of us as serious breeders to eliminate problems early. as soon as we know how. Or at least we should try to before the problem is widespread. But you might wonder, "How can we proceed when we don't know the mode of transmission of the problem?" Well, the worst case scenario is to assume, in the absence of knowledge, that the mode of transmission is that of an autosomal dominant gene. Evidence is mounting, for example, the Dilated Cardiomyopathy (DCM) follows this pattern. At its best, breeding for health is like waking a tightrope. at it worst, there's no safety net under the rope. If someone isn't willing to take that risk. they shouldn't breed!
Consider the following:
A well-known breeder commented to me at ringside, that he'd "rather have a pretty dog for five years than an ugly one for thirteen." By what twisted logic does such a person pass off health / longevity and beauty as mutually exclusive characteristics?
A well-known stud dog dies suddenly at a young age, and the show folk are there with excuses. "Oh. it was just a heart attack". or "a stroke". or it "was due to stress in the life of a show dog". Was an autopsy done? No. Do many breeders care? No! All this DESPITE the fact that dogs don't suffer heart attacks as humans do. Dogs are carnivores. They don't get atherosclerosis, coronary artery disease, or occlusion / myocardial infarcts which cause human hart attacks. If a dog has a heart problem. it's most likely a congenital valve problem, a secondary result of infection such as abscessed teeth or a bacterial / viral infection, or dilated cardiomyopathy.
DCM is far and away the most common of Doberman heart problems.
An article in the Winter issue of the Quarterly downplayed the existence of a vWD problem in our breed and ridiculed those for whom it was both a concern and issue. The disease if FACT. The genetic test for the mutant gene which is necessary to cause the disease is FACT! That Dobermans are bleeding and some are dying from lack of vWF is FACT! Yet many are taking the position that the disease doesn't exist. claiming that it is some trumped up VetGen conspiracy. or claiming that, because they haven't personally seen it, it can't be a problem. Others think that it's only a pet" disease, and that our show dogs are somehow immune to getting it. This isn't the case. I have first hand knowledge of two dogs that've had vWD related bleeding episodes, and know of at least fifteen others where the ONLY identifiable factor was lack of circulation vWF! One of the two was owned by a member of our Doberman club. The other was a Doberman who was in our boarding kennel.
What on Earth would I personally have to gain by making this stuff up?
A person whose Doberman died after a spay as a result of post surgical complications due solely to vWD sent me an email, a portion of which I'll reproduce here:
"I don't know where to start or what to say. I'm angry, I'm hurt; I feel frustrated and bewildered and furious all at the same time. I feel dismissed, patronized, insulted - labeled a somehow either overly impressionable, an emotional anthropomorphic sufferer, or just plain not too bright because I think that vWD is worthy of consideration when planning a breeding. HOW MANY of us. people who've had direct incidences with vWD clinically affected dogs - how many must trot out our stories, our "proof", our facts, figures, and anecdotal experiences before some of these long time breeder (and BOY do I use this term loosely now!) of Dobermans HEAR us?"
This was written to me in response to the aforementioned article in DQ. You think it's not a problem when people lose dogs and are devastated? Can you feel her frustration and pain?
Just a few years ago, people were clamoring for a definitive test for vWD.
Now that we have it, suddenly it appears that people think that vWD's not an issue. and many are saying that they're not testing because cardio is really the big problem! How will breeders react when that test is finally available? Will they not use it. citing cost, or "cause "actually CVI is the biggest problem"? It's all about priorities, folks.
FUNCTIONAL STRUCTURE. or DYNAMIC CONFORMATION: This is NOT synonymous with breed type. It has to do with the ability of a dog to functionally perform work. It is. a head that has the power to bite, a body that can do a double suspension gallop, a front that can withstand the repeated shock of jumping.
an agility that allows a dog to twist6, turn, and pivot with ease. Static conformation is what you see when a dog is stacked in the ring. You can't tell anything about the do's ability to use his muscles, tendons and ligaments to articulate that static structure. and the gaiting required in the show ring won't show it to you either.
The Doberman is a double suspension galloper. In order to do this, the dogs must have flexion of the spine. The backbone must be convex when the dog's legs are under him, and concave when the dog is stretched out. You just CAN'T see this in a trot. The dog has to gallop. A Dobe must be agile, and while his legitimate work doesn't require the hair-trigger changes of direction required of a herding dog, he still must be agile and supple. not rigid. You can't evaluate this in the breed ring, but you CAN on an agility course. A Doberman must be able to absorb shock. That means that on landing after jumping, the front assembly has to have some "give". the pasterns must flex, the feet must splay slightly. the shoulder / upper arm assemble must flex. You CAN'T see this in the breed ring. but you CAN in an obedience ring, or on an agility course, or on a Schutzhund field. A Doberman must have the facial and jaw structure to bite and hold. A Dobe must have sufficient depth of cheek, sufficient fill beneath the eyes, and sufficient facial musculature for a good solid bite on a sleeve. You CAN see this in the breed ring. A Doberman must have a strong, well muscled, dry neck.
Otherwise, the neck will be the primary injury site when doing a long bite, or when absorbing shock from jumping. You CAN see this in the breed ring.
The exaggeration of breed type we often see judges putting up in the breed ring can actually hurt functional structure. A top line that looks rock solid in a stack and in a trot may also be too rigid to allow for efficient galloping. How do you know without observing that gallop, and making it a priority? A set of ramrod straight pasterns and very tight cat feet may not possess the necessary flexion for proper shock absorption. Overdone fronts without sufficient musculature in the rear to counterbalance it will bring the dog's center of gravity too far forward, with disastrous consequences to a jumping dog. And if a judge thinks aardvark heads on swan necks are somehow "prettier", he Is mortgaging away our noble breed's birthright as a protection dog supreme!
Having participated n a variety of do activities over a Doberman career spanning three decades, I'm always amazed at the "know it all" arrogance of some of the closed-minded breed ring only types. I speak here, not only as a Doberman person, but as an ex-handler of many other breeds as well. Few have considered what it means for a dog to be truly athletic. not just standing, and trotting "pretty". Even fewer have worked dogs in disciplines that would allow them to see the consequences of breed type run amuck! Quite a few conformation judges fall into this category. As a result many breeds are split along show and working lines. and many people incorrectly assume that the major differences are only behavioral. They are NOT. they are also structural.
Field Labradors, with their length of leg and hard, muscular bodies scarcely resemble their squat, endomorphic, heavily coated cousins in the breed ring.
Working Dobermans have strong, well muscled, dry necks. not swan-like. They have strong, well filled out fronts. not pigeon breasted with a chest that sticks out so far forward that the dog's center of gravity is between his front legs. A good working dog will be heavily muscled from the rear. Those hamstrings are what propel the dog forward in a gallop.
Limits should be set on breed type by function, and we should strive not to go beyond those limits. You judges out there. wake up! Don't sacrifice function to some exaggerated notions of style.
BREED TYPE: Only when I have paid attention to temperament, health / longevity, and functional structure. only then do I shift my focus to typiness. Please don't misinterpret what I'm saying. Breed type is important. Without it, our Dobermans would lose the characteristic "look"
that makes our breed the envy of all of dogdom. That noble outline and that "look of eagles" would disappear. The breed ring is what keeps that look alive.
Make no mistake about it. I want type. I want my dogs to do well in the breed ring. I want Champions as much as the next guy. I want type in my breeding program validated. BUT I won't do it at the expense of temperament.
I won't do it at the expense of heath and longevity. And I won't do it at the expense of the dog's physical ability to work. I will not mortgage away by my Doberman Breed's future merely to chase ribbons. But breed type shouldn't be the primary. It should be the icing on the cake. It's up to us as breeders to make damn sure that there's a cake under all that frosting.
There's strong indication that we're not doing that, and it's time to look at our priorities. Socrates said that "the examined life isn't worth living". This is the time to examine our priorities, se our courses, and do what we have to do to ensure the future of our great breed.
Temperament, health and longevity, functional structure, and breed type.
those are my choices. those are my priorities. A Dobe who has all of the above is now my definition of a "Total Doberman". Anything less is an incomplete package. Look around you. How may complete packages do you see?
Very few? I thought so! Do you or should you care? It should be a resounding YES! Are you willing to take responsibility for and a leadership role to "preserve and protect the Doberman Pinscher and to do all possible to bring its natural qualities to perfection" as stated in the DPCA's charter? The choice is yours.
A Bit About Breeding
Inbreeding Line-breeding and Out Crossing
INBREEDING:
Matings involving parents and siblings.
Brother/Sister (the closest form)
Father/Daughter
Mother/Son
Half-Brother/Half-Sister
LINEBREEDING:
Matings involving relatives other than parents and siblings.
Cousins (have one or two Grandparents in common)
Nephew/Aunt
Niece/Uncle
G. Granddaughter/G. Grandson
Grandson/Granddaughter
Grandfather/Granddaughter
Grandmother/Grandson
Linebreeding past the 4th generation has little effect
OUTCROSSING: The breeding of unrelated animals.
(Matings involve unrelated animals.)
DEFINITION: For a dog to be linebred there must be an ancestor in the pedigree that is common to both the sire and the dam. Figure 2 illustrates this concept. Kelly is linebred because the dog, Brahms, appears twice in the sire’s side and once in the dam’s side of the pedigree.
COMMON MISCONCEPTION: A pedigree may show either the sire and/or the dam to be linebred but no ancestor common to both the sire and dam. This is outcrossing, not line-breeding
Matings involving parents and siblings.
Brother/Sister (the closest form)
Father/Daughter
Mother/Son
Half-Brother/Half-Sister
LINEBREEDING:
Matings involving relatives other than parents and siblings.
Cousins (have one or two Grandparents in common)
Nephew/Aunt
Niece/Uncle
G. Granddaughter/G. Grandson
Grandson/Granddaughter
Grandfather/Granddaughter
Grandmother/Grandson
Linebreeding past the 4th generation has little effect
OUTCROSSING: The breeding of unrelated animals.
(Matings involve unrelated animals.)
DEFINITION: For a dog to be linebred there must be an ancestor in the pedigree that is common to both the sire and the dam. Figure 2 illustrates this concept. Kelly is linebred because the dog, Brahms, appears twice in the sire’s side and once in the dam’s side of the pedigree.
COMMON MISCONCEPTION: A pedigree may show either the sire and/or the dam to be linebred but no ancestor common to both the sire and dam. This is outcrossing, not line-breeding
