Things are changing faster than a Doberman can run.
Read this important update on the current state of Doberman health testing
Canine genetic science is breaking new ground. The Doberman Diversity Project, which is partnered with Cornell University dog geneticists, intends to bring Doberman breeders and buyers cutting edge genetic testing to improve the genetic health and longevity of the breed. As a result, the DDP strongly advises puppy buyers and breeders to reconsider how they understand and utilize modern DNA testing.
Until recently, most breeders and buyers looked for "good" answers ("negative" or "clear", or at most "carrier" status for diseases that are recessive in nature) on DNA tests for specific genetic diseases. Most looked for a dog that tested "clear" on the PDK4 and DCM2 tests. But today we know more. Or more precisely, we know what we do not know. We now understand that taking such an approach may be indirectly causing an increase in genetic disease in the breed by removing "problem" dogs from the gene pool instead of using state of the art DNA analysis to match them properly so the puppies have a good chance at enjoying better genetic health than their parents.
New genetic testing technologies are focused not merely on the results from DNA tests for specific genetic problems (e.g., PDK4 aka DCM1, DCM2, etc.) but on the overall diversity of our dogs' genetics. We knew that the common Coefficient of Inbreeding (COI) pedigree calculators could not accurately predict levels of inbreeding because (1) they utilize too few generations in the calculation and (2) because the math assumes that the dogs in the oldest generation of dogs used in the calculation are unrelated -- which is FAR from accurate. But this pedigree formula was all that breeders had. Today things are different for the dogs tested through the Doberman Diversity Project. Each DDP tested dog has an actual Genetic COI calculated from the dogs' actual DNA. That number tells us what percentage of a dog's genes are inbred (each set of alleles is the same or heterozygous) or outbred (those pairs of alleles are diverse or heterozygous).
New DNA testing doesn't only permit us to calculate the Genetic COI in a dog. It also provides critical information on DLA haplotype, mitochondrial DNA, and more insight into meaningful genetic diversity. Geneticists now understand how this information is just as important (and possibly MORE important) to the genetic health of a dog than are the individual disease test results. It may be that a dog with strong genetic diversity (revealed through new DNA testing) is more likely to enjoy not only better health but also longevity than a dog that may be weak in terms of genetic diversity yet "negative" for DNA mutations for single diseases. But we don't yet know. What we do know is that relying solely on DNA disease tests, especially those related to Dilated Cardiomyopathy (e.g., PDK4 or DCM1 and DCM2) or solely on diversity testing (especially if based on a smaller number of genetic markers which can inadvertently speed the loss of genetic diversity) is likely an ineffective and potentially dangerous way to approach breeding where longevity and genetic diversity is important.
As such, The Doberman Diversity Project strongly advises that buyers and breeders consider disease-specific DNA tests in light of a dog's overall genetic diversity, conformation, temperament and pedigree/ancestral longevity. Doing so, and working with a reputable breeder who is transparent and open about the breed's genetic challenges, increases the odds that an individual dog or litter are stronger genetic contenders and better serves the BREED's health in the years to come, in ways we previously did not understand was possible.
Until recently, most breeders and buyers looked for "good" answers ("negative" or "clear", or at most "carrier" status for diseases that are recessive in nature) on DNA tests for specific genetic diseases. Most looked for a dog that tested "clear" on the PDK4 and DCM2 tests. But today we know more. Or more precisely, we know what we do not know. We now understand that taking such an approach may be indirectly causing an increase in genetic disease in the breed by removing "problem" dogs from the gene pool instead of using state of the art DNA analysis to match them properly so the puppies have a good chance at enjoying better genetic health than their parents.
New genetic testing technologies are focused not merely on the results from DNA tests for specific genetic problems (e.g., PDK4 aka DCM1, DCM2, etc.) but on the overall diversity of our dogs' genetics. We knew that the common Coefficient of Inbreeding (COI) pedigree calculators could not accurately predict levels of inbreeding because (1) they utilize too few generations in the calculation and (2) because the math assumes that the dogs in the oldest generation of dogs used in the calculation are unrelated -- which is FAR from accurate. But this pedigree formula was all that breeders had. Today things are different for the dogs tested through the Doberman Diversity Project. Each DDP tested dog has an actual Genetic COI calculated from the dogs' actual DNA. That number tells us what percentage of a dog's genes are inbred (each set of alleles is the same or heterozygous) or outbred (those pairs of alleles are diverse or heterozygous).
New DNA testing doesn't only permit us to calculate the Genetic COI in a dog. It also provides critical information on DLA haplotype, mitochondrial DNA, and more insight into meaningful genetic diversity. Geneticists now understand how this information is just as important (and possibly MORE important) to the genetic health of a dog than are the individual disease test results. It may be that a dog with strong genetic diversity (revealed through new DNA testing) is more likely to enjoy not only better health but also longevity than a dog that may be weak in terms of genetic diversity yet "negative" for DNA mutations for single diseases. But we don't yet know. What we do know is that relying solely on DNA disease tests, especially those related to Dilated Cardiomyopathy (e.g., PDK4 or DCM1 and DCM2) or solely on diversity testing (especially if based on a smaller number of genetic markers which can inadvertently speed the loss of genetic diversity) is likely an ineffective and potentially dangerous way to approach breeding where longevity and genetic diversity is important.
As such, The Doberman Diversity Project strongly advises that buyers and breeders consider disease-specific DNA tests in light of a dog's overall genetic diversity, conformation, temperament and pedigree/ancestral longevity. Doing so, and working with a reputable breeder who is transparent and open about the breed's genetic challenges, increases the odds that an individual dog or litter are stronger genetic contenders and better serves the BREED's health in the years to come, in ways we previously did not understand was possible.
Genetic Doberman Diseases.
What do we test for? What results might you see?
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Dilated Cardiomyopathy (DCM) -- Genetic (inherited)
Gene(s) Affected: PDK4 (Chromosome 11) and undisclosed genes identified asserted to be found by the DCM2 (NCSU) test.
Inheritance: Autosomal Dominant with Incomplete Penetrance
Mutation: Deletion
Genetic Tests: PDK4 (validated and OFA-approved). Included in the DDP/Embark panel. Note: Dogs who have tested "At Risk" for
this mutation (deletion) have lived long lives and dogs negative/clear for this test have died early from DCM.
DCM2 This test is currently a linkage test, and not a direct DCM2 test. A direct DCM2 test is anticipated in late 2019.
Possible Results: Negative (clear) or "At Risk" (one or both genes are defective)
Non-Genetic ProBNP: a simple blood test your vet can perform, that provides a quantitative assessment of a dog's heart
Tests: health by measuring the concentration of NTproBNP, which is released by cardiac myocytes in response to stretch and stress). Because it is a marker of heart muscle wall stress, it is likely to be high in Dobermans with abnormal echos and early DCM (levels are very high in Dobermans with heart failure and symptomatic DCM).
About the Disease: Dilated Cardiomyopathy is a genetic trait resulting in the inability of the heart to contract normally. This abnormal heart function, tells the dog's system that not enough blood is being pumped. To compensate for the heart's poor contractile ability, the heart dilates (grows larger) increasing the heart chamber size which, in the early stages of the disease, will improve output of the heart (stroke volume). At this time the disease is asymptomatic (the dog shows no sign of illness). As the disease progresses, further dilation of the heart no longer improves stroke volume but, in fact, leads to increasing pressure inside the heart. This, in turn, causes blood to back up in the blood vessels and lungs, which causes fluid to leak into the lungs. This fluid in the lungs causes difficulty breathing and, eventually, death.
Symptoms and progression vary widely. Some dogs will have no visible symptoms (they appear to be 100% healthy) and yet die without warning. This can happen in dogs as young as two or three years old. Rarely, puppies suddenly die from DCM. Other dogs will display heavy breathing, wheezing, coughing, loss of energy and appetite. Sadly, this deadly condition is not curable, although diuretics and other medications may provide some measure of comfort for the dog. Typical life expectancy for a Doberman, once diagnosed with this condition, is 6 additional months. Unfortunately, the most common sign of DCM is sudden death.
Recommended Testing Protocol for Cardiac Disease. Annual echocardiograms (an ultrasound of the heart), together with 24 hour Holter Monitoring, provides a snapshot of a dog's current heart health at that moment in time. Your vet can also perform a simple blood test that measures the concentration of NTproBNP in your dog's blood and is a good indicator of heart health. It is important to understand that test results can be normal one year and a dog can show signs of DCM the very next year. This is why breeders must perform ANNUAL heart screening. Two DNA genetic tests are available; they identify two mutations (PDK4) and DCM2) that are thought to be associated with DCM. The tests involves a simple cheek swab and don't necessitate a veterinary visit.
Genetic testing for cardio problems is, at present, an incomplete science. Geneticists do not yet have a firm understanding of what causes DCM in Dobermans. That said, there are two genetic tests for mutations known to be associated with DCM. Note that an association is not the same as causation or prediction. These two mutation tests are called PDK4 (sometimes referred to as DCM1) and DCM2. We believe that the DNA tests for the DCM1 and DCM2 genetic mutations, while not conclusive as to future health, are likely of some value. Two "negative" DNA test results (PDK4 and DCM2) in any dog may be the BEST result possible, but should not be considered to be a prediction or conclusive evidence that a 'clear' dog will not develop DCM. There is no such thing as "DCM Clear."
Gene(s) Affected: PDK4 (Chromosome 11) and undisclosed genes identified asserted to be found by the DCM2 (NCSU) test.
Inheritance: Autosomal Dominant with Incomplete Penetrance
Mutation: Deletion
Genetic Tests: PDK4 (validated and OFA-approved). Included in the DDP/Embark panel. Note: Dogs who have tested "At Risk" for
this mutation (deletion) have lived long lives and dogs negative/clear for this test have died early from DCM.
DCM2 This test is currently a linkage test, and not a direct DCM2 test. A direct DCM2 test is anticipated in late 2019.
Possible Results: Negative (clear) or "At Risk" (one or both genes are defective)
Non-Genetic ProBNP: a simple blood test your vet can perform, that provides a quantitative assessment of a dog's heart
Tests: health by measuring the concentration of NTproBNP, which is released by cardiac myocytes in response to stretch and stress). Because it is a marker of heart muscle wall stress, it is likely to be high in Dobermans with abnormal echos and early DCM (levels are very high in Dobermans with heart failure and symptomatic DCM).
About the Disease: Dilated Cardiomyopathy is a genetic trait resulting in the inability of the heart to contract normally. This abnormal heart function, tells the dog's system that not enough blood is being pumped. To compensate for the heart's poor contractile ability, the heart dilates (grows larger) increasing the heart chamber size which, in the early stages of the disease, will improve output of the heart (stroke volume). At this time the disease is asymptomatic (the dog shows no sign of illness). As the disease progresses, further dilation of the heart no longer improves stroke volume but, in fact, leads to increasing pressure inside the heart. This, in turn, causes blood to back up in the blood vessels and lungs, which causes fluid to leak into the lungs. This fluid in the lungs causes difficulty breathing and, eventually, death.
Symptoms and progression vary widely. Some dogs will have no visible symptoms (they appear to be 100% healthy) and yet die without warning. This can happen in dogs as young as two or three years old. Rarely, puppies suddenly die from DCM. Other dogs will display heavy breathing, wheezing, coughing, loss of energy and appetite. Sadly, this deadly condition is not curable, although diuretics and other medications may provide some measure of comfort for the dog. Typical life expectancy for a Doberman, once diagnosed with this condition, is 6 additional months. Unfortunately, the most common sign of DCM is sudden death.
Recommended Testing Protocol for Cardiac Disease. Annual echocardiograms (an ultrasound of the heart), together with 24 hour Holter Monitoring, provides a snapshot of a dog's current heart health at that moment in time. Your vet can also perform a simple blood test that measures the concentration of NTproBNP in your dog's blood and is a good indicator of heart health. It is important to understand that test results can be normal one year and a dog can show signs of DCM the very next year. This is why breeders must perform ANNUAL heart screening. Two DNA genetic tests are available; they identify two mutations (PDK4) and DCM2) that are thought to be associated with DCM. The tests involves a simple cheek swab and don't necessitate a veterinary visit.
Genetic testing for cardio problems is, at present, an incomplete science. Geneticists do not yet have a firm understanding of what causes DCM in Dobermans. That said, there are two genetic tests for mutations known to be associated with DCM. Note that an association is not the same as causation or prediction. These two mutation tests are called PDK4 (sometimes referred to as DCM1) and DCM2. We believe that the DNA tests for the DCM1 and DCM2 genetic mutations, while not conclusive as to future health, are likely of some value. Two "negative" DNA test results (PDK4 and DCM2) in any dog may be the BEST result possible, but should not be considered to be a prediction or conclusive evidence that a 'clear' dog will not develop DCM. There is no such thing as "DCM Clear."
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Von Willebrand's Disease -- Type 1 (vWD1) Genetic (inherited)
Gene(s) Affected: VWF.
Inheritance: Autosomal Recessive
Mutation: Point Mutation
Genetic Tests: vWD1 (included in the DDP/Embark Test Panel)
Possible Results: Negative or Carrier or At Risk
Von Willebrand's Disease (vWD) is an inherited bleeding disorder not unlike hemophilia in people. There is no cure for the disease which can be passed directly from one generation to the next, affecting offspring in varying degrees. While some dogs affected by vWD may have blood that seems to clot normally, when exposed to stress (physical, disease, drugs, and psychological), their blood can lose the ability to clot normally. The lesson? Don't assume that because a dog didn't bleed abnormally at tail docking and ear cropping time, they will not be affected by this disease later in life.
There are three possible results for the vWD1 test: (1) Negative, (2) Carrier, and (3) At Risk:
Gene(s) Affected: VWF.
Inheritance: Autosomal Recessive
Mutation: Point Mutation
Genetic Tests: vWD1 (included in the DDP/Embark Test Panel)
Possible Results: Negative or Carrier or At Risk
Von Willebrand's Disease (vWD) is an inherited bleeding disorder not unlike hemophilia in people. There is no cure for the disease which can be passed directly from one generation to the next, affecting offspring in varying degrees. While some dogs affected by vWD may have blood that seems to clot normally, when exposed to stress (physical, disease, drugs, and psychological), their blood can lose the ability to clot normally. The lesson? Don't assume that because a dog didn't bleed abnormally at tail docking and ear cropping time, they will not be affected by this disease later in life.
There are three possible results for the vWD1 test: (1) Negative, (2) Carrier, and (3) At Risk:
- NEGATIVE. A NEGATIVE (sometimes referred to as "clear") Doberman completely lacks the defective gene and, if bred with another NEGATIVE Doberman, will produce offspring which will be completely free of the disease. You may hear breeders refer to this as "clear by parentage." "At Risk" dogs are affected by the disease at different levels and must be diagnosed by a licensed Veterinarian.
- CARRIER. CARRIERS only carry the gene and are unlikely to experience symptoms. "Carriers" of the vWD gene are at little or no risk of bleeding from the disease but will transmit the gene to 50% of its offspring.
- AT RISK. AT RISK dogs may have blood that severely or entirely lacks the von Willebrand factor (vWF) (the protein that promotes blood clotting by increasing platelet cohesion. An AT RISK pup may bleed from its gums when teething, may have spontaneous nosebleeds, blood in its stool or urine, have excessive bleeding during estrus or after whelping, experience prolonged estrus, have blood in its gastrointestinal tract or it may display prolonged bleeding from small or superficial wounds which can lead to anemia, shock, or, if left untreated, even death. AT RISK dogs sometimes incur injuries and undergo surgery without ANY complications and never have a bleeding problem. Owners of AT RISK dogs should work closely with their vet to stay on top of the disease. AT RISK dogs should not be automatically euthanized because many, if not most, will live long, healthy lives with the proper attention to care.
Note: You may hear AT RISK dogs described as "affected" but that description can be quite inaccurate. Dogs with to mutated copies of this gene suffer from the disease in diverse ways. Only a veterinarian can properly determine whether an AT RISK dog is actually affected by this disease.
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Alanine Aminotransferase Activity (GPT) Genetic (inherited)
Gene(s) Affected: GA
Inheritance: Codominant
Mutation:
Genetic Tests: GPT (included in the DDP/Embark Test Panel)
Possible Results: Normal or Low Normal or At Risk
Known to be highly expressed in liver cells, activity levels of alanine aminotransferase, or ALT, is a common value on most blood chemistry panels and is known to be a sensitive measure of liver health. Dobermans with two ancestral G alleles show "normal" activity. Dogs that have one or two copies of the derived A allele on Chromosome 13 may have lower resting levels of ALT activity, known as "low normal". If your dog's result is "low normal" then when a blood chemistry panel is being interpreted the values that you and your veterinarian consider "normal" may need to be adjusted. Please note that neither a "normal" nor a "low normal" result for this predicts a disease state or increased risk for liver disease. Moreover, this mutation does not associate with increased levels of ALT: If your dog has high ALT levels, please consult your veterinarian.
CITATIONS: White et al 2016
Gene(s) Affected: GA
Inheritance: Codominant
Mutation:
Genetic Tests: GPT (included in the DDP/Embark Test Panel)
Possible Results: Normal or Low Normal or At Risk
Known to be highly expressed in liver cells, activity levels of alanine aminotransferase, or ALT, is a common value on most blood chemistry panels and is known to be a sensitive measure of liver health. Dobermans with two ancestral G alleles show "normal" activity. Dogs that have one or two copies of the derived A allele on Chromosome 13 may have lower resting levels of ALT activity, known as "low normal". If your dog's result is "low normal" then when a blood chemistry panel is being interpreted the values that you and your veterinarian consider "normal" may need to be adjusted. Please note that neither a "normal" nor a "low normal" result for this predicts a disease state or increased risk for liver disease. Moreover, this mutation does not associate with increased levels of ALT: If your dog has high ALT levels, please consult your veterinarian.
CITATIONS: White et al 2016
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Multidrug Sensitivity (MDR1) Genetic (inherited)
Gene(s) Affected: NN (Chromosome 14)
Inheritance: Codominant
Mutation:
Genetic Tests:
Possible Results: DD (Normal) or ND (???) or At Risk
Sensitivity to certain classes of drugs, notably the parasiticide ivermectin, as well as certain gastroprotectant and anti-cancer medications, occurs in dogs with mutations in the MDR1 gene. Symptoms can range from vomiting and diarrhea to lethargy, seizures, or coma. MDR1 mutations are particularly common in herding breeds including Australian Shepherds, Collies, and Border Collies, though many other dog breeds, including Dobermans, are affected.
To learn more about this condition, visit http://www.vetstreet.com/dr-marty-becker/multidrug-sensitivity-what-you-need-to-know.
Gene(s) Affected: NN (Chromosome 14)
Inheritance: Codominant
Mutation:
Genetic Tests:
Possible Results: DD (Normal) or ND (???) or At Risk
Sensitivity to certain classes of drugs, notably the parasiticide ivermectin, as well as certain gastroprotectant and anti-cancer medications, occurs in dogs with mutations in the MDR1 gene. Symptoms can range from vomiting and diarrhea to lethargy, seizures, or coma. MDR1 mutations are particularly common in herding breeds including Australian Shepherds, Collies, and Border Collies, though many other dog breeds, including Dobermans, are affected.
To learn more about this condition, visit http://www.vetstreet.com/dr-marty-becker/multidrug-sensitivity-what-you-need-to-know.
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Degenerative Myelopathy (DM) Genetic (inherited)
Gene(s) Affected: SOD1
Inheritance: Autosomal Recessive with Incomplete Penetrance
Mutation: Point Mutation
Genetic Tests: Embark Veterinary (Included in DDP Testing Panel)
Possible Results: N/A
Degenerative myelopathy is an inherited neurologic disorder caused by a mutation in the SOD1 gene known to be carried by Doberman pinschers. This mutation is found in many breeds of dog, though it is not clear for Doberman pinschers whether all dogs carrying two copies of the mutation will develop the disease. The variable presentation between breeds suggests that there are environmental or other genetic factors responsible for modifying disease expression. The average age of onset for dogs with degenerative myelopathy is approximately nine years of age. The disease affects the white matter tissue of the spinal cord and is considered the canine equivalent to amyotrophic lateral sclerosis (Lou Gehrig’s disease) found in humans. Affected dogs usually present in adulthood with gradual muscle atrophy and loss of coordination typically beginning in the hind limbs due to degeneration of the nerves. The condition is not typically painful for the dog, but will progress until the dog is no longer able to walk. The gait of dogs affected with degenerative myelopathy can be difficult to distinguish from the gait of dogs with hip dysplasia, arthritis of other joints of the hind limbs, or intervertebral disc disease. Late in the progression of disease, dogs may lose fecal and urinary continence and the forelimbs may be affected. Affected dogs may fully lose the ability to walk 6 months to 2 years after the onset of symptoms. Affected medium to large breed dogs, such as the Doberman, can be difficult to manage and owners often elect euthanasia when their dog can no longer support weight in the hind limbs.
The mutation of the SOD1 gene associated with degenerative myelopathy has been identified in Dobermans. The overall frequency of this disease in the breed and approximate age of disease onset are unreported for Doberman pinschers. However, in one study of 55 Doberman pinschers tested, 1.8% had two copies of the mutation and were at-risk.
Genetic testing of the SOD1 gene in Doberman pinschers will reliably determine whether a dog is a genetic "carrier" of degenerative myelopathy. Degenerative myelopathy is inherited in an autosomal recessive manner in dogs meaning that they must receive two copies of the mutated gene (one from each parent) to develop the disease. In general, carrier dogs do not have features of the disease but when bred with another carrier of the same mutation, there is a risk of having affected pups. Each pup that is born to this pairing has a 25% chance of inheriting the disease and a 50% chance of inheriting one copy and being a carrier of the SOD1 gene mutation. Reliable genetic testing is important for determining breeding practices. Because symptoms may not appear until adulthood and some at-risk/affected dogs do not develop the disease, genetic testing should be performed before breeding. Until the exact modifying environmental or genetic factor is determined, genetic testing remains the only reliable way to detect neurological disease associated with this mutation prior to death. In order to eliminate this mutation from breeding lines and to avoid the potential of producing affected pups, breeding of known carriers to each other is not recommended. Doberman Pinschers that are not carriers of the mutation have no increased risk of having affected pups.
Doberman Diseases in Validation Status with Embark/DDPWhen validated, these tests will be added to the Embark DNA Test Panel at no extra charge.
If you have a dog that is positive for any of these diseases, contact us about free testing opportunities. |
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Narcolepsy Genetic (inherited)
Gene(s) Affected: HCRTR2
Inheritance: Autosomal Recessive
Mutation: Insertion
Genetic Tests: Pending through Embark Veterinary (Currently in Validation Stage)
Possible Results: N/A
Non-Genetic Tests: N/A
Narcolepsy is an inherited disorder affecting Dobermans. Dogs with the inherited form of narcolepsy typically begin to show symptoms between one to six months of age. These puppies will be unable to stay awake for extended periods of time; episodes of collapse and sleep following positive stimulation such as play or food can occur. Affected dogs fall asleep faster than normal dogs and appear sleepy more frequently. During episodes of collapse dogs have a sudden loss of muscle tone and appear uncontrollably sleepy but may or may not completely fall asleep. Symptoms do not progress after one year of age and affected dogs do not appear to have other associated health problems.
Genetic testing of the HCRTR2 gene will reliably determine whether a dog is a genetic "carrier" of Narcolepsy (Doberman Pinscher type). Narcolepsy (Doberman Pinscher type) is inherited in an autosomal recessive manner [meaning that a puppy must receive two copies of the mutated gene (one from each parent) to actually develop the disease]. In general, carrier dogs do not have features of the disease but when bred with another carrier of the same genetic mutation, there is a risk of producing affected pups. Each pup that is born to this pairing has a 25% chance of inheriting the disease and a 50% chance of inheriting one copy and being a carrier of the HCRTR2 gene mutation. Reliable genetic testing is important for determining breeding practices. In order to eliminate this mutation from breeding lines and to avoid the potential of producing affected pups, breeding of known carriers to each other is not recommended. Dogs that are not carriers of the mutation have no increased risk of having affected pups.
Gene(s) Affected: HCRTR2
Inheritance: Autosomal Recessive
Mutation: Insertion
Genetic Tests: Pending through Embark Veterinary (Currently in Validation Stage)
Possible Results: N/A
Non-Genetic Tests: N/A
Narcolepsy is an inherited disorder affecting Dobermans. Dogs with the inherited form of narcolepsy typically begin to show symptoms between one to six months of age. These puppies will be unable to stay awake for extended periods of time; episodes of collapse and sleep following positive stimulation such as play or food can occur. Affected dogs fall asleep faster than normal dogs and appear sleepy more frequently. During episodes of collapse dogs have a sudden loss of muscle tone and appear uncontrollably sleepy but may or may not completely fall asleep. Symptoms do not progress after one year of age and affected dogs do not appear to have other associated health problems.
Genetic testing of the HCRTR2 gene will reliably determine whether a dog is a genetic "carrier" of Narcolepsy (Doberman Pinscher type). Narcolepsy (Doberman Pinscher type) is inherited in an autosomal recessive manner [meaning that a puppy must receive two copies of the mutated gene (one from each parent) to actually develop the disease]. In general, carrier dogs do not have features of the disease but when bred with another carrier of the same genetic mutation, there is a risk of producing affected pups. Each pup that is born to this pairing has a 25% chance of inheriting the disease and a 50% chance of inheriting one copy and being a carrier of the HCRTR2 gene mutation. Reliable genetic testing is important for determining breeding practices. In order to eliminate this mutation from breeding lines and to avoid the potential of producing affected pups, breeding of known carriers to each other is not recommended. Dogs that are not carriers of the mutation have no increased risk of having affected pups.
Doberman Genetic Diseases not included in the DDP/Embark Test Panel.
Chronic Active Hepatitis (CAH) Genetic (inherited)
Gene(s) Affected: Unknown
Inheritance: Unknown
Mutation: Unknown
Genetic Tests: None
Possible Results: N/A
CAH is a progressive inflammation state that cause the liver to break down, and results in toxic levels of copper to be stored in the liver, and often leads to liver failure and death. No standard treatment yet exists, and the cause of CAH remains unknown. Females are more prone to the disease than males, and it can show up at any age. The average age however is middle aged, 4 to 6 years old. Researchers believe this is likely to be a genetically inherited disease. It is not an infection disease, it is hereditary. If the disease is in one of the parents, it may or may not be in the litter.
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Renal Dysplasia (RD) Genetic (inherited)
Gene(s) Affected:
Inheritance: Autosomal Dominant with Incomplete Penetrance
Mutation:
Genetic Tests:
Possible Results: Negative or At Risk
Renal dysplasia is a form of kidney diseases that affects Dobermans. Dysplasia is any abnormal growth or development of cells or organs. In the case of RD, the kidney fails to develop properly during embryogenesis in the womb. At birth, immature structures consisting of undifferentiated fetal cells or tissue types are found in the kidney, and are persistent throughout the life of the animal. Renal dysplasia can present with a wide range of symptoms and pathological findings. Definitive diagnosis of RD is done by a wedge biopsy of the kidney which reveals dysplastic lesions, including abnormal ducts, and glomeruli. Individuals with an abnormal biopsy can be asymptomatic (show no signs of the disease). On the other hand, the dog may present with classic signs of chronic end stage renal failure, or anywhere between these two extremes. Given this broad spectrum of symptoms, "affected" individuals often go undetected and remain in the breeding population.
RD is inherited as "dominant with incomplete penetrance." This means that animals with one or two copies of the mutation are at risk for developing the disease and/or passing this on to their progeny. Most AT RISK dogs are sub-clinical (they do not display signs of illness).
Gene(s) Affected: Unknown
Inheritance: Unknown
Mutation: Unknown
Genetic Tests: None
Possible Results: N/A
CAH is a progressive inflammation state that cause the liver to break down, and results in toxic levels of copper to be stored in the liver, and often leads to liver failure and death. No standard treatment yet exists, and the cause of CAH remains unknown. Females are more prone to the disease than males, and it can show up at any age. The average age however is middle aged, 4 to 6 years old. Researchers believe this is likely to be a genetically inherited disease. It is not an infection disease, it is hereditary. If the disease is in one of the parents, it may or may not be in the litter.
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Renal Dysplasia (RD) Genetic (inherited)
Gene(s) Affected:
Inheritance: Autosomal Dominant with Incomplete Penetrance
Mutation:
Genetic Tests:
Possible Results: Negative or At Risk
Renal dysplasia is a form of kidney diseases that affects Dobermans. Dysplasia is any abnormal growth or development of cells or organs. In the case of RD, the kidney fails to develop properly during embryogenesis in the womb. At birth, immature structures consisting of undifferentiated fetal cells or tissue types are found in the kidney, and are persistent throughout the life of the animal. Renal dysplasia can present with a wide range of symptoms and pathological findings. Definitive diagnosis of RD is done by a wedge biopsy of the kidney which reveals dysplastic lesions, including abnormal ducts, and glomeruli. Individuals with an abnormal biopsy can be asymptomatic (show no signs of the disease). On the other hand, the dog may present with classic signs of chronic end stage renal failure, or anywhere between these two extremes. Given this broad spectrum of symptoms, "affected" individuals often go undetected and remain in the breeding population.
RD is inherited as "dominant with incomplete penetrance." This means that animals with one or two copies of the mutation are at risk for developing the disease and/or passing this on to their progeny. Most AT RISK dogs are sub-clinical (they do not display signs of illness).
Inherited Doberman Diseases for which there is not yet a DNA Test
Head Bobbing Syndrome Genetic (inherited)
Gene(s) Affected: Unknown
Inheritance: Unknown
Mutation: Unknown
Genetic Tests: Not Yet Available
Possible Results: N/A
Head bobbing is characterized by episodes of head shaking or head trembling. This disease affects Dobermans and other breeds such as Boxers, French, and English Bulldogs. Head bobbing is a benign condition, which does not require any specific treatment. The time span between episodes of head shaking may last days or even months. The cause of head bobbing in the Doberman has not yet been identified. Head bobbing is not related to epilepsy, as once suspected.
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Wobbler's Syndrome (aka Cervical Vertebral Instability or CVI) Genetic (inherited)
Gene(s) Affected: Unknown
Inheritance: Unknown
Mutation: Unknown
Genetic Tests: Not Yet Available
Possible Results: N/A
The term Wobbler's disease is often used to describe CVI because of the distinctive gait displayed by dogs with CVI. This disease causes neck vertebrae (usually at the base of the neck in Dobermans, in or near vertebrae C5, C6, or C7) to become unstable and to shift, often resulting in pinching of the spinal cord. Although it is most commonly found in the neck, it can affect any part of the body. Unfortunately, this disease is often seen in Dobermans. The condition is generally not painful, at least not in its early stages. As the dog becomes more paralyzed, foot-dragging, stumbling, difficulty in getting up, and loss of urinary and bowel functions may occur. It rarely strikes until middle age (three or four years and older) and typically begins to cause pain and/or paralysis. Once the disease progresses, a dog's chances of recovery are almost non-existent.
Your vet can diagnose this disease via myelogram -- a fairly invasive procedure that you and your vet must decide upon together. Use only a very experienced veterinarian for this procedure. Adverse effects of poorly performed myelograms can be devastating and, in some cases, worse than the original disease. A less invasive alternative diagnostic tool, Magnetic Resonance Imaging (MRI), is now available through most specialty vet practices. While there is no cure for CVI, surgical intervention can stabilize the affected area but it must be done at the first onset of the disease. Surgery for this condition is rarely viable. It is expensive, has a three to ten month recuperation period, and does not appear to reverse existing damage. Short-term relief may be provided by corticosteroid medications, which help to relieve the pressure.
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Hip Dysplasia Genetic (inherited)
Gene(s) Affected: Unknown
Inheritance: Unknown
Mutation: Unknown
Genetic Tests: Not Yet Available
Possible Results: N/A
Non Genetic Tests: X-Ray Testing and Grading
Hip dysphasia (improper growth of the hip) is both polygenetic (some researchers speculate that there may be as many as 13 genes involved) and multifactorial (influenced by many non-genetic factors). It is more common in large breeds and results in a hip socket (acetabulum) that is too shallow to properly seat the femoral ball (at the top of the leg where it joins to the hip) or in a femoral ball or femoral neck which is deformed or small causing excessive movement at the hip joint. This condition causes gradual loss of cartilage, bone spurs and the joint to eventually become inflamed and weakened. Dogs with hip dysphasia appear to be born with normal hips and then to develop the disease later. The hip joint is not the only area of the dog which can be affected. Knee, shoulder and spinal joints can also show evidence of dysplasia.
The degree to which dogs exhibit symptoms depends upon many factors such as the strength of the muscle and ligament which help hold the joint in place. It can vary in severity from mild to completely debilitating. Other factors include rapid growth and weight gain which can stress the young joint -- very compelling reasons to follow your veterinarian's guidance as to feeding and exercise as your puppy is growing.
Studies have proven that dysplastic puppies whose diet is controlled in order to slow growth and weight gain may display no outward sign of the condition and may remain functional despite severe dysphasia. This approach allows the muscles and ligaments to develop enough to compensate for bone failure. Some people believe that they can cause dysplasia in their dog by too much exercise however, most vets agree that this is not the case. In other words, how you raise your puppy won't determine whether or not your puppy is dysplastic, but it can affect when and, perhaps whether, he begins to develop symptoms as well as their severity. Some factors which may hasten or worsen symptoms include rough play, jumping, climbing stairs, slick floors, excess weight gain or rapid growth and calcium supplementation which may increase bone remodeling.
Available Testing for Hip Dysplasia.
PennHIP testing requires multiple x-ray views of your dog's hips, which are sent to veterinary radiologists to be quantitatively analyzed. Studies show that PennHIP is a much more sensitive test for hip dysplasia than OFA grading, which means that PennHIP scores more accurately diagnose hip dysplasia than OFA scores. PennHIP testing can also be performed in puppies as young as 16 weeks of age, allowing breeders to make decisions about their breeding stock earlier.
OFA hip testing requires a "hip-extended" x-ray view, which can be done at 2 years of age and sent to the Orthopedic Foundation for Animals (OFA) for qualitative analysis by three veterinary radiologists for grading (excellent, good or fair). The results can be registered on that site (OFFA.org). OFA (hips) test results should be considered standard once the dog has reached two years of age. The results for a dog tested at or beyond two years of age are lasting -- that is, the dog doesn't need to have its hips checked annually.
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Hypothyroidism (low thyroid function) Genetic (inherited)
Gene(s) Affected: Unknown
Inheritance: Unknown
Mutation: Unknown
Genetic Tests: Not Yet Available
Possible Results: N/A
Non-Genetic Tests: Thyroid Panel
Antibodies are proteins designed to defend the body from foreign organisms such as bacteria and viruses. In autoimmune hypothyroidism, antibodies attack and destroy thyroid gland cells preventing the gland from being able to release normal amounts of thyroid hormone. The term hypothyroidism has been loosely applied to describe all stages of this disease process whereas, strictly speaking, it should be reserved for the end-stages when the animal’s thyroid gland is no longer capable of producing sufficient hormones to sustain clinical health. Symptoms of hypothyroidism may include droopy eyes, a "tragic" facial expression, muscle wasting of head and/or body, lethargy, fatigue, weight gain, thinning of hair along the back ("razor back"), disruption of reproductive seasons, females failing to impregnate and/or carry to term and temperament changes. It is also frequently linked to adrenal insufficiency, allergies, hives, dry skin, vomiting and intolerance to cold or heat. Hyperactivity (overactive thyroid), weight loss and aggression can occur with hyperthyroidism.
Hypothyroidism develops in genetically susceptible animals and is characterized by the presence of anti-thyroid antibodies in the blood or tissues. In most cases, it starts around puberty and gradually progress through mid-life and old age to become clinically expressed hypothyroidism once the thyroid glandular reserves have been depleted. During the progression of the disease, the animal becomes more susceptible to other diseases (like von Willebrand’s). Fortunately, this disease is easy and inexpensive to treat.
Testing for Thyroid Disease: Thyroid screening is unlikely to be meaningful before puberty. Therefore, testing should commence once healthy dogs have reached sexual maturity (usually between 9 and 14 months in males and following the first estrus cycles in females). Thyroid titers should be done by your vet every 18 to 24 months throughout a dog’s life.
"Genetic testing for inherited hypothyroidism (autoimmune thyroiditis) is based on the presence of thyroglobulinauto antibodies. A dog with normal TgAA levels on two tests at least two years apart between two and six years of age is phenotypically normal. However, TgAA levels should not be measured within 2-3 months post-vaccination, as a transient iatrogenic rise can occur during this period."
Popular-Sire Syndrome: Keeping watch over health and quality issues in purebreds By Jerold S Bell, DVM, Tufts Cummings School of Veterinary Medicine.
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Inherited Eye Defects Genetic (inherited)
Gene(s) Affected: Unknown
Inheritance: Unknown
Mutation: Unknown
Genetic Tests: Not Yet Available
Possible Results: N/A
Non-Genetic Tests: An OFA Eye Certification Registry Exam are conducted by Canine Opthamologists. LINK
Dogs can inherit a variety of eye disorders. Before breeding, dogs should have their eyes examined and evaluated (known as an OFA Eye Certification Registry Exam) for a wide variety of diseases by a certified canine opthalmologist. Fortunately, dobermans are fairly free of inherited eye disease with the most common being cataracts (which occur prior to 2 years of age and have not been conclusively shown to be an inherited trait) as well as microopthalmia (very small eyes) and persistent pupillary membrane, all of which are rare. Nonetheless, pre-breeding and periodic eye examinations are highly recommended.
----------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------
Doberman Vestibular Deafness (DINGS) Genetic (inherited)
Gene(s) Affected: Unknown
Inheritance: Unknown
Mutation: Unknown
Genetic Tests: Not Yet Available
Possible Results: N/A
Non-Genetic Tests: N/A
Affected puppies can exhibit clinical signs of vestibular defects (head tilt and possible loss of balance) as early as one to two weeks of age, though the presentation is commonly mild at a young age and becomes more pronounced as the dog ages. The affected dog can appear normal by a routine physical examination, however a neurological examination often reveals signs of bilateral vestibular disease and auditory testing (BAER exam) is critical to identify deafness. Pathological findings reveal degeneration with the cochlear portion of the inner ear. This disease was first reported in the Doberman Pinscher breed in the early 1980’s, and later clinically characterized in 1992. More recently the genetic basis of this recessively inherited disorder was resolved through the successful collaboration efforts of Dr. Mark Neff, Head of the Laboratory of Canine Genetics & Genomics at the Van Andel Research Institute, in Grand Rapids, MI, and Dr. Aubrey Webb of the CullenWebb Animal Neurology & Ophthalmology Center in NB, Canada. A causative genetic mutation was identified enabling the development of the now available DNA test. As the disorder is an autosomal recessive disease, breeders can now judiciously choose to reduce the prevalence of the disease by only crossing known heterozygous ("carrier" dogs) to known "unaffected" dogs or choose to only mate "unaffected" dogs.
Gene(s) Affected: Unknown
Inheritance: Unknown
Mutation: Unknown
Genetic Tests: Not Yet Available
Possible Results: N/A
Head bobbing is characterized by episodes of head shaking or head trembling. This disease affects Dobermans and other breeds such as Boxers, French, and English Bulldogs. Head bobbing is a benign condition, which does not require any specific treatment. The time span between episodes of head shaking may last days or even months. The cause of head bobbing in the Doberman has not yet been identified. Head bobbing is not related to epilepsy, as once suspected.
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Wobbler's Syndrome (aka Cervical Vertebral Instability or CVI) Genetic (inherited)
Gene(s) Affected: Unknown
Inheritance: Unknown
Mutation: Unknown
Genetic Tests: Not Yet Available
Possible Results: N/A
The term Wobbler's disease is often used to describe CVI because of the distinctive gait displayed by dogs with CVI. This disease causes neck vertebrae (usually at the base of the neck in Dobermans, in or near vertebrae C5, C6, or C7) to become unstable and to shift, often resulting in pinching of the spinal cord. Although it is most commonly found in the neck, it can affect any part of the body. Unfortunately, this disease is often seen in Dobermans. The condition is generally not painful, at least not in its early stages. As the dog becomes more paralyzed, foot-dragging, stumbling, difficulty in getting up, and loss of urinary and bowel functions may occur. It rarely strikes until middle age (three or four years and older) and typically begins to cause pain and/or paralysis. Once the disease progresses, a dog's chances of recovery are almost non-existent.
Your vet can diagnose this disease via myelogram -- a fairly invasive procedure that you and your vet must decide upon together. Use only a very experienced veterinarian for this procedure. Adverse effects of poorly performed myelograms can be devastating and, in some cases, worse than the original disease. A less invasive alternative diagnostic tool, Magnetic Resonance Imaging (MRI), is now available through most specialty vet practices. While there is no cure for CVI, surgical intervention can stabilize the affected area but it must be done at the first onset of the disease. Surgery for this condition is rarely viable. It is expensive, has a three to ten month recuperation period, and does not appear to reverse existing damage. Short-term relief may be provided by corticosteroid medications, which help to relieve the pressure.
------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------
Hip Dysplasia Genetic (inherited)
Gene(s) Affected: Unknown
Inheritance: Unknown
Mutation: Unknown
Genetic Tests: Not Yet Available
Possible Results: N/A
Non Genetic Tests: X-Ray Testing and Grading
Hip dysphasia (improper growth of the hip) is both polygenetic (some researchers speculate that there may be as many as 13 genes involved) and multifactorial (influenced by many non-genetic factors). It is more common in large breeds and results in a hip socket (acetabulum) that is too shallow to properly seat the femoral ball (at the top of the leg where it joins to the hip) or in a femoral ball or femoral neck which is deformed or small causing excessive movement at the hip joint. This condition causes gradual loss of cartilage, bone spurs and the joint to eventually become inflamed and weakened. Dogs with hip dysphasia appear to be born with normal hips and then to develop the disease later. The hip joint is not the only area of the dog which can be affected. Knee, shoulder and spinal joints can also show evidence of dysplasia.
The degree to which dogs exhibit symptoms depends upon many factors such as the strength of the muscle and ligament which help hold the joint in place. It can vary in severity from mild to completely debilitating. Other factors include rapid growth and weight gain which can stress the young joint -- very compelling reasons to follow your veterinarian's guidance as to feeding and exercise as your puppy is growing.
Studies have proven that dysplastic puppies whose diet is controlled in order to slow growth and weight gain may display no outward sign of the condition and may remain functional despite severe dysphasia. This approach allows the muscles and ligaments to develop enough to compensate for bone failure. Some people believe that they can cause dysplasia in their dog by too much exercise however, most vets agree that this is not the case. In other words, how you raise your puppy won't determine whether or not your puppy is dysplastic, but it can affect when and, perhaps whether, he begins to develop symptoms as well as their severity. Some factors which may hasten or worsen symptoms include rough play, jumping, climbing stairs, slick floors, excess weight gain or rapid growth and calcium supplementation which may increase bone remodeling.
Available Testing for Hip Dysplasia.
PennHIP testing requires multiple x-ray views of your dog's hips, which are sent to veterinary radiologists to be quantitatively analyzed. Studies show that PennHIP is a much more sensitive test for hip dysplasia than OFA grading, which means that PennHIP scores more accurately diagnose hip dysplasia than OFA scores. PennHIP testing can also be performed in puppies as young as 16 weeks of age, allowing breeders to make decisions about their breeding stock earlier.
OFA hip testing requires a "hip-extended" x-ray view, which can be done at 2 years of age and sent to the Orthopedic Foundation for Animals (OFA) for qualitative analysis by three veterinary radiologists for grading (excellent, good or fair). The results can be registered on that site (OFFA.org). OFA (hips) test results should be considered standard once the dog has reached two years of age. The results for a dog tested at or beyond two years of age are lasting -- that is, the dog doesn't need to have its hips checked annually.
-----------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------
Hypothyroidism (low thyroid function) Genetic (inherited)
Gene(s) Affected: Unknown
Inheritance: Unknown
Mutation: Unknown
Genetic Tests: Not Yet Available
Possible Results: N/A
Non-Genetic Tests: Thyroid Panel
Antibodies are proteins designed to defend the body from foreign organisms such as bacteria and viruses. In autoimmune hypothyroidism, antibodies attack and destroy thyroid gland cells preventing the gland from being able to release normal amounts of thyroid hormone. The term hypothyroidism has been loosely applied to describe all stages of this disease process whereas, strictly speaking, it should be reserved for the end-stages when the animal’s thyroid gland is no longer capable of producing sufficient hormones to sustain clinical health. Symptoms of hypothyroidism may include droopy eyes, a "tragic" facial expression, muscle wasting of head and/or body, lethargy, fatigue, weight gain, thinning of hair along the back ("razor back"), disruption of reproductive seasons, females failing to impregnate and/or carry to term and temperament changes. It is also frequently linked to adrenal insufficiency, allergies, hives, dry skin, vomiting and intolerance to cold or heat. Hyperactivity (overactive thyroid), weight loss and aggression can occur with hyperthyroidism.
Hypothyroidism develops in genetically susceptible animals and is characterized by the presence of anti-thyroid antibodies in the blood or tissues. In most cases, it starts around puberty and gradually progress through mid-life and old age to become clinically expressed hypothyroidism once the thyroid glandular reserves have been depleted. During the progression of the disease, the animal becomes more susceptible to other diseases (like von Willebrand’s). Fortunately, this disease is easy and inexpensive to treat.
Testing for Thyroid Disease: Thyroid screening is unlikely to be meaningful before puberty. Therefore, testing should commence once healthy dogs have reached sexual maturity (usually between 9 and 14 months in males and following the first estrus cycles in females). Thyroid titers should be done by your vet every 18 to 24 months throughout a dog’s life.
"Genetic testing for inherited hypothyroidism (autoimmune thyroiditis) is based on the presence of thyroglobulinauto antibodies. A dog with normal TgAA levels on two tests at least two years apart between two and six years of age is phenotypically normal. However, TgAA levels should not be measured within 2-3 months post-vaccination, as a transient iatrogenic rise can occur during this period."
Popular-Sire Syndrome: Keeping watch over health and quality issues in purebreds By Jerold S Bell, DVM, Tufts Cummings School of Veterinary Medicine.
----------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------
Inherited Eye Defects Genetic (inherited)
Gene(s) Affected: Unknown
Inheritance: Unknown
Mutation: Unknown
Genetic Tests: Not Yet Available
Possible Results: N/A
Non-Genetic Tests: An OFA Eye Certification Registry Exam are conducted by Canine Opthamologists. LINK
Dogs can inherit a variety of eye disorders. Before breeding, dogs should have their eyes examined and evaluated (known as an OFA Eye Certification Registry Exam) for a wide variety of diseases by a certified canine opthalmologist. Fortunately, dobermans are fairly free of inherited eye disease with the most common being cataracts (which occur prior to 2 years of age and have not been conclusively shown to be an inherited trait) as well as microopthalmia (very small eyes) and persistent pupillary membrane, all of which are rare. Nonetheless, pre-breeding and periodic eye examinations are highly recommended.
----------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------
Doberman Vestibular Deafness (DINGS) Genetic (inherited)
Gene(s) Affected: Unknown
Inheritance: Unknown
Mutation: Unknown
Genetic Tests: Not Yet Available
Possible Results: N/A
Non-Genetic Tests: N/A
Affected puppies can exhibit clinical signs of vestibular defects (head tilt and possible loss of balance) as early as one to two weeks of age, though the presentation is commonly mild at a young age and becomes more pronounced as the dog ages. The affected dog can appear normal by a routine physical examination, however a neurological examination often reveals signs of bilateral vestibular disease and auditory testing (BAER exam) is critical to identify deafness. Pathological findings reveal degeneration with the cochlear portion of the inner ear. This disease was first reported in the Doberman Pinscher breed in the early 1980’s, and later clinically characterized in 1992. More recently the genetic basis of this recessively inherited disorder was resolved through the successful collaboration efforts of Dr. Mark Neff, Head of the Laboratory of Canine Genetics & Genomics at the Van Andel Research Institute, in Grand Rapids, MI, and Dr. Aubrey Webb of the CullenWebb Animal Neurology & Ophthalmology Center in NB, Canada. A causative genetic mutation was identified enabling the development of the now available DNA test. As the disorder is an autosomal recessive disease, breeders can now judiciously choose to reduce the prevalence of the disease by only crossing known heterozygous ("carrier" dogs) to known "unaffected" dogs or choose to only mate "unaffected" dogs.
OFA-Cardiac Update
The NEW OFA-ACVIM Congenital Cardiac Database has implemented a new Two-tiered cardiac disease clearance system which screens for: (1) congenital, and (2) adult onset cardiac disease. Why?
The Bottom Line:
- Improved statistical data regarding prevalence and progression of canine cardiac disease,
- Exams are now limited to ACVIM/ECVIM Cardiology Diplomates (not any veterinarian's examination meets the requirements),
- Results meet all CHIC cardiac criteria, and
- No changes to OFA submission procedures.
The Bottom Line:
- Dogs must now be a minimum of twelve (12) months to test,
- OFA Ratings/Certificates will be one of three varieties:
(1) “This dog has been found to be free of congenital cardiac disease" (valid for the dog's lifetime),”
(2) “This dog has been found to be free of adult onset cardiac disease” (valid for only one year), or
(3) “This dog has been found to be free of congenital and adult onset cardiac disease.” - To maintain OFA Cardiac Rating for Adult Onset Cardiac Disease, dogs must be tested annually.
- OFA will not certify ECHO without a Holter Monitor performed within 90 days.
- Your regular vet may no longer interpret Holter test UNLESS he/she is a boarded veterinary cardiologists with Diplomate status in either the ACVIM or the ECVIM.
- Read More