IMPORTANT INFORMATION ON DM/PRA/VWD TYPE 1:
Many of you worry about DM and have asked questions about DM. I have researched and found this article. When speaking to an genetics testing lab person they advised me that yes an AT Risk/Affected Corgi has this gene but not always will they get this disease or have the symptoms. Please do not be afraid if your puppy is an At Risk/Affected puppy. In this article they found a very small percentage of Corgis are DM Clear, most are DM Carriers and AT Risk/Affected. DM is also found in other breeds too. This information is NOT to scare you, this is to inform you that even if you breed an AT Risk/Affected to an DM Clear, you still can get an DM Carrier. DM Clear is hard to find because not every breeder wants to take the time to test their stock because it is very pricey. Below are some facts why not to worry so much about having an AT Risk/Affected or a DM Carrier.
What percent get DM?
This question remains unanswered, but some information is available. Some At Risk corgis have lived into advanced years (14 and older) and their spinal cords donated for research, and no signs of DM have been found. For example, one corgi breeder had At Risk littermates, one of whom developed DM at age 13, the other was euthanized past 14 with no signs of DM. Other breeders have noted the same thing, that is, that being related and At Risk is not a predictor of developing DM or not. However, in 2014 the researchers published a paper in which they reported the results of an owner-survey. They had sent questionnaires to owners who had At Risk corgis tested by DNA before age 8, but whose corgis were now past age 10. This gave us the first rough measurement of what percent of at risk Pems would develop DM. Survey results were received from 17 Pembroke Welsh corgi owners. One GG (Clear) had, as expected, no clinical signs of DM. Six AG (Carrier) also had no clinical signs of DM. Of ten AA (At Risk) Pems, 7 had no clinical signs of DM and 3 had clinical signs of DM. This information suggests a rough 30% get DM, but that number should be used with caution for several reasons. It could be higher as more of the 7 now without DM could develop it as they age, or it could be lower, if owners with DM in their line were more likely to have tested or responded to the survey. Also, because the survey size is quite small, the room for error is large. However, it IS clear that it is not a small percent, but neither is it 100%. Cardigan Welsh Corgis were also included in the survey but only 1 Clear and 4 Carriers were included in the response, all of which were without any sign of DM (as expected.) Thanks to owners who have continued to donate blood and tissue samples from corgis, the researchers may be able to find a difference that will predict whether or not an At Risk corgi can develop DM.
How to breed away from DM remains a controversial issue. Statistics published by OFAare that 52% of tested Pembroke Welsh Corgis are At Risk (AA), 37% are Carrier (AG) and 11% are Clear (GG). These statistics have not improved much since the test was first available nearly five years ago and now represent the results from over 2000 Pems (mainly in the United States.) The extremely high incidence of the gene mutation means it is nowhere near as simple as eliminating all dogs with the mutation from a breeding program. Even in the US that would devastate the breed and likely create other problems. If all European test results were made public, we would have a better idea of the scope of the DM problem here in the USA. Ideally, all At Risk and Carrier Pems should be bred to Clear Pems. But with only 11% Clear, this, too, presents problems. A breeder with an At Risk or Carrier bitch may have a very hard time finding an appropriate Clear dog, and vice versa. Here are the possible breedings and their statistical results:
- At Risk to At Risk – all pups will be At Risk
- At Risk to Carrier – 50% At Risk, 50% Carrier
- At Risk to Clear – all pups will be Carrier
- Carrier to Carrier- 25% At Risk, 50% Carrier, 25% Clear
- Carrier to Clear- 50% Carrier, 50% Clear
- Clear to Clear- 100% Clear
- Clear puppy – cannot develop or pass on DM to Another Clear puppy
Currently, any breeding producing less than 50% At Risk is probably an acceptable one, including Carrier to Carrier. Carrier to Carrier can produce At Risk, but overall only at 25%, and can produce Clear at a higher percent (25%) than they are currently in the population. So for a breeder trying to improve the breed, but willing to take a chance of getting At Risk, Carrier to Carrier is an acceptable breeding. However, unless one parent is Clear, a breeding can produce At Risk pups. What would help with this problem would be for all breeders to test their breeding stock, and make any clear males publically known and available for breeding to acceptable quality Carrier and At Risk females. Finding those Clear males to sire litters is critical to being able to breed away from DM. In addition, if owners of Clear females would breed them to the best At Risk males, this would be a way to preserve great lines without producing At Risk puppies. It is also very important to make puppy buyers aware that a Carrier pup is a fine pet and will not get DM, and reserve any Clears that are breeding quality as breeding stock. If you, as a breeder, do not choose to breed a particular Clear who otherwise is perfectly decent, make it available to someone who needs it.
Research in Degenerative Myelopathy with Special Emphasis on Corgis
By Bobbie Mayer PhD, USA
There is so much confusion about what is known in Degenerative Myelopathy (DM) and what is known is also changing fast, so I wanted to write this article to summarize current(2014) research on the disease in corgis specifically.
Background- DM has been known as a disease for over fifty years, and was first officiallycharacterized in German Shepherds, so many think of it as a disease of German Shepherds. However, it is actually more prevalent in other breeds, including corgis. It may be most prevalent in Pembroke Welsh Corgis, though some vets will not even know it is a possible diagnosis. It is also called chronic degenerative radiculomyelopathy, or CDRM.
In the nineties, Dr. Joan Coates at the University of Missouri, along with numerous colleagues, began a project to study DM in corgis and boxers. The research was sponsored by the AKC Canine Health Foundation and the Pembroke Welsh Corgi Club of America. Corgi and Boxer owners were asked to send in blood samples from dogs with DM and from dogs without DM, and eventually also to donate tissue samples, including spinal cords, from dogs that had died.
Breakthrough- the gene is found. In 2008 the researchers had a breakthrough -they found a gene associated with DM! Because DM is similar to Amyotrophic
Lateral Sclerosis, or ALS (Lou Gehrig’s disease), which affects humans, they had looked for a gene in the same region that one gene causing ALS had been found. They found that both Boxers and Pembroke welsh corgis with DM had two copies (AA) of a mutated gene for SOD1, the superoxide dismutase enzyme, which is responsible for destroying free radicals. Normal dogs (no DM) had either two non-mutated copies (GG) or one of each (AG), but also could have two copies (AA) and no DM. (Note: OFA labels the genes NN instead of GG and AN instead of AG.)
Although many dogs testing AA did not have DM, as the age of the dogs increased the likelihood that an AA dog would have DM also increased. The researchers developed a DNA test, which was initially available only from OFA, to test for the mutated genes. The test, which is now also available from other unlicensed labs, is a simple cheek swab, though a blood test can also be done.
What do the results of genetic testing mean? When you send in a sample to be tested, you receive one of three possible results.
Clear- GG /Carrier- AG /At Risk or Affected – AA
Clear means that that corgi does not carry the gene for DM and can be bred to any other dog and the offspring will not be able to get DM. Carrier means that the corgi can produce offspring with DM if mated to another carrier or an At Risk corgi, but will not itself get DM. (Although a very minute number of carriers with DM have been found in other breeds, none have been found in corgis, so the odds that a carrier could get DM are very, very low if not zero.) Initially there was some speculation that if a carrier lived long enough it might get DM, but at this writing, no carrier corgis with DM have been identified.
At Risk (Affected) means that the corgi has the potential to develop DM. Well discuss later how many At Risk corgis are likely to develop DM.
Further Research: The initial research publication left many questions unanswered.
- What percent of At Risk corgis get DM?
- What triggers the onset of DM?
- How can we breed to reduce DM without overly narrowing the gene pool?
- How can we prevent DM?
- How can we treat DM?
Some of these questions are on the way to being answered.
Characterizing the disease process
In 2010, Dr. Coates group published a paper which further characterized the disease. They established that the average age of onset in Pems is 10.9 years, and they reported that the median disease time (onset to euthanasia) in smaller dogs, such as corgis, who could be more easily cared for after becoming unable to walk, was 19 months. This does not mean that the corgi died of DM after 19 months, though, it means that was the average age at which, for whatever reason, euthanasia was elected. (A later report from Japan, where DM corgis are maintained even further through the disease, included corgis that survived as long as 48 months with DM.) As corgi owners who have had dogs with DM already knew, after the back legs were affected by DM eventually the trunk and front legs would also become involved, advancing eventually to quadriplegia and respiratory failure. Some of the Japanese corgis that were maintained late into the disease did have respiratory distress. In this paper, written for veterinarians, they also noted that other possible diseases that can mimic DM include cauda equine (lumbosacral disease), intervertebral disk disease (type II, non-acute), cancer of the spinal cord, and degenerative joint diseases. A diagnosis of DM cannot be confirmed without ruling out these other possible causes (ideally by MRI and not just X-rays.) This is an important point because when someone believes their corgi has DM, or even has a veterinarian;s diagnosis, but the dog is under eight years old or has Clear or Carrier status, it is most likely the dog has one of these other diseases, most of which are treatable. Several other published works describe the disease process at a cellular level and are beyond the scope of this discussion.
What triggers the onset of DM and how can we prevent it? Nobody knows – yet. It may be genetic, and a test may be developed for the factor that makes the difference. It may be environmental, or it may be a combination of reasons. Right now, we don’t know how to prevent it or how to predict which At Risk dogs will get it. Some things have been suggested as triggering signs of DM. One is anesthesia, another is neutering. However, it is extremely unlikely that these have anything to do with DM beyond coincidence. Humans – like all organisms- are genetically programmed to look for cause and effect in things. Our survival depends on it. Saber-toothed tiger bites someone, he dies. We conclude that we should avoid saber-toothed tigers. Wooly mammoth tramples someone, and we concluded that we should stay out of the way of stampeding mammoths. But although we are programmed to believe that if A precedes B, A caused B, it is not always – or even usually – true. There are many reasons it may not be true. A and B can be caused by the same thing, for example, or it can simply be coincidence.
In the case of anesthesia and DM, I think coincidence explains the cases where anesthesia seemed to hasten DM. In fact, DM starts before you see any visible signs of a problem. A breeder who is still showing- and gaiting- a corgi in competition may notice a subtle change in gait. An owner who is running a corgi in agility may notice slower times or ticking jumps. These signs can appear up to a year before the classic foot drag that usually signals the onset of DM. Only when enough nerve cells are affected will the obvious signs of DM appear. So a neuter or teeth cleaning done a few weeks before a foot drag is observed is, in fact, occurring long after DM has actually started its disease process. Some people have speculated that it is an environmental factor that “turns on” DM. Nobody knows. (Although a small percentage of ALS is known to be familial, 90% occurs without a known genetic predisposition, so is presumably environmental.) I do know of at least one case where littermates, both at risk, raised and living together for a lifetime, had different outcomes (one developed DM and one did not). In another case, the littermate that remained with the breeder and had good nutrition and was kept at a healthy weight with good vet care got DM, the overweight and less-well- cared-for sibling did not.
At this point the only known way to prevent DM is by not producing At Risk puppies.
There are only two proposed treatments for DM that have been published. The diet and supplements suggested by Dr. Clemmons has been widely publicized. Unfortunately, he never published any data that showed that it worked or had any effect on DM. He made the claim multiple times, but did not back it up with science. One set of researchers did attempt to find out if it worked, and found no effect, but the study had flaws. Only a few dogs were studied, and the only criterion was “time to euthanasia”, which is a decision of the owner and not objective. Some individuals claim the diet works, others have seen no effect, and likely this is based on individual differences in the rate at which dogs progress with DM and not on the diet itself. The other proposed treatment is canine rehabilitation therapy (physical therapy or physiotherapy.) Published work showed that the time to euthanasia was longer for dogs undergoing controlled therapy. Again, however, the study is flawed, as time to euthanasia is not a useful measurement. However, many owners have reported that keeping their dogs exercising and doing therapy helped them remain mobile (in or out of a cart) longer. It is almost certain to keep the dog healthier as the disease progresses. In the relatively near future tests may begin on possible pharmaceutical treatments for DM. While this is promising, it should be noted that no particularly useful drugs have been found for ALS.
Further information and useful links:
Progression of DM in video:
The dog in the video was a US Champion and an OTCH (obedience trial champion).
Corgis on Wheels book:
Information on DM and on the DNA test:
OFA link to buy the DNA test:
For DNA tests in Europe:
I hope this helps anyone out with this information and please not to be scared.
Love your Corgis like I do!!!
Canine Degenerative Myelopathy (DM)
OFA Accepted Degenerative Myelopathy (DM) is a progressive disease of the spinal cord in older dogs. The disease has an insidious onset typically between 8 and 14 years of age. It begins with a loss of coordination (ataxia) in the hind limbs. The affected dog will wobble when walking, knuckle over or drag the feet. This can first occur in one hind limb and then affect the other. As the disease progresses, the limbs become weak and the dog begins to buckle and has difficulty standing. The weakness gets progressively worse until the dog is unable to walk. The clinical course can range from 6 months to 1 year before dogs become paraplegic. If signs progress for a longer period of time, loss of urinary and fecal continence may occur and eventually weakness will develop in the front limbs. Another key feature of DM is that it is not a painful disease. Although any dog can be tested for DM, it is possible that the genetic background that predominates in some breeds prevents the development of symptoms even in dogs testing affected (at risk). At this time the required evidence of association between the genetic mutation and actual spinal cord evaluations has only been proven in the breeds listed.
Please see http://www.offa.org/dnatesting/dmexplanation.html and
http://www.caninegeneticdiseases.net/DM/ancmntDM.htm for additional information on DM diagnosis.
THESE ARE THE BREEDS THAT DM CAN AFFECT:
American Eskimo Dogs/Australian Shepherds/Bernese Mountain Dog/Borzoi/Boxers/Cardigan Welsh Corgi/Chesapeake Bay Retrievers/Coton De Tulear/German Shepherd Dog/Golden Retriever/Great Pyrenees/Irish Setters/Kerry Blue Terriers/Pembroke Welsh Corgis/ Poodle /Pug/Rhodesian Ridgeback/Shetland Sheepdog/Soft Coated Wheaten Terriers/Wire Fox Terrier
These dogs have two normal copies of DNA. Among the hundreds of dogs studied to date at the University of Missouri, only two dogs with test results of ‘CLEAR/NORMAL’ have been confirmed to have DM.
These dogs have one copy of the mutation and one normal copy of DNA. Carriers are far less likely to develop DM however; a few cases to date of DM have been confirmed in a small number of carrier dogs.
These dogs have two copies of the mutation and will likely develop DM during their lifetime. Although many dogs tested to date typed as ‘AT RISK/AFFECTED’ have been clinically confirmed DM, recent evidence suggest that there are other causes of DM in some breeds. In addition, not all dogs testing as ‘AT RISK/AFFECTED’ have shown clinical signs of DM. Research is ongoing to estimate what percentage of dogs testing as ‘AT RISK/AFFECTED’ will develop DM within their lifespan. At this point, the DM mutation can be interpreted as being ‘AT RISK’ of developing DM within the animal’s lifetime. For dogs showing clinical signs with a presumptive diagnosis of DM, ‘AT RISK/AFFECTED test results can be used as an additional tool to aid in the diagnosis of DM. I was researching and found this breeder who posted this very interesting article on DM, their information was passed on by a very respective Polish Breeder. We here at Precious Puppies Kennels s do DM testing on our PARENTS/FUTURE BREEDERS, however, this breeder does make sense. We here at Precious Puppies Kennels do believe in testing but we also believe in studies that NOT ALL AT Risk dogs will come down with this disease. Some do and some do not.
Here is the link of the article below for you.
The breeder goes on to say:
“The basics of it are simple. While we have long questioned the genetics behind the DM test currently offered in the US, now new evidence has been presented that not only is the genetic link behind the testing in question, but the science of the testing itself is not reliable!! Dropped Allelles can be misdiagnosed depending on the testing lab, or even based on the age of the dog. A puppy testing clear as a 10 day old, may not be really clear and may not test clear as an adult. (We ourselves have had this occur, and I have heard from reliable breeders that have also had this occur to them. One such breeder had three different test results on a female, from three different testing labs!) So why test if the genetic link is not clear, AND if the results may be flawed? We have made the decision to no longer test our puppies for DM. We will continue testing our adults extensively, and will upon request test a puppy from a litter if the new owner wishes. But we will no longer test complete litters. And we cannot guarantee the results outside insuring that the testing is as correct as we can possible make it.”
Now we here at Kocher’s Precious Puppies Kennels have not had this happen to us but it can. I want to make all my corgis owners aware of this. Stop being afraid of DM and love your babies. I myself had a boxer, we knew she would be prone to cancer or tumors and it did not stop us from giving her a life. Yes she was put to sleep at an old age due to tumors busting out of her skin but that did not stop me from taking care of her and loving her. I miss her but she had a good life. There is NO perfect dog and if that is what you are looking for then you should stop looking. Even us humans are NOT perfect. We here at Precious Puppies Kennels strive to make a healthy PET and that is what they are…..PETS. We are working on trying not to produce an AT Risk puppies but I do have 1 male and 3 females that I WILL NOT give up. They are my joy. Eventually we will have DM Carrier puppies and Clear puppies. My clears are at a higher price. There is no guarantee that mine will not produce an AT Risk, there is always a chance of that but again I am not afraid of it and we do raise beautiful corgis no matter what their outcome of DM. There is nothing wrong with having an AT Risk corgi! I love my AT Risk corgis.
INFORMATION ON EIC:
Exercise-induced collapse (EIC) is a genetic syndrome, predominantly occurring in mixed breed dogs related to several retriever breeds as well as purebred Labrador Retrievers but also seen in Chesapeake Bay Retrievers and Curly Coated Retrievers, Boykin Spaniels, Cocker spaniels, German wire-haired pointers, Old English Sheepdogs, Bouvier des Flandres, Pembroke Welsh Corgis and Clumber Spaniels (verified 2015 by Laboklin in the UK). The syndrome was first positively identified by DNA in Boykin Spaniels in 2010. Before this, EIC episodes may have been misdiagnosed as heat stroke. Affected dogs show signs of muscle weakness, loss of coordination, severe marked increase in body temperature and life threatening collapse when participating in strenuous exercise or activity. Affected dogs can tolerate mild to moderate exercise, but just 5 to 20 minutes of strenuous activity, or even extreme excitement such as that seen in field trials or hunt tests, can induce weakness or collapse. Dogs affected with EIC usually cannot continue with intense retriever training, but can live normal lives as house pets. A few affected dogs have died during exercise or while resting immediately after an episode of exercise-induced collapse so an affected dog’s exercise should be stopped at the first hint of in-coordination or wobbliness. EIC is being observed with increasing frequency, either from the genetics becoming more widespread or from previously misdiagnosed cases being correctly identified now that there is evidence in the form of a DNA test. Dogs that have EIC are prone to mild to severe collapse that can range from dragging of the hind legs to complete collapse. Most affected dogs have been from field-trial breedings. Signs become apparent in young dogs as they enter heavy training, which is usually between 5 months and 7 years of age as stated in the initial UMN study in 2007.  Dogs of either sex can be affected. Dogs with this condition are always normal at rest and are usually described as being extremely fit, prime athletic specimens of their breed. Nervous system, cardiovascular and musculoskeletal examinations are unremarkable as is routine blood analysis at rest and during an episode of collapse.  Through grants from the AKC CHF a patented DNA test was developed by the University of MN.  The Orthopedic Foundation for Animals provides a public database for those dogs that are DNA tested. The UMN VBS Genetics Lab is also investigating cases of quot;atypical collapsequot;  and also "Border Collie Collapse] quot;  where the dog is a carrier or clear of the disease on the DNA test, but continues to exhibit signs of the EIC disease.
INFORMATION ON PRA:
Progressive retinal Atrophy, Rod-cone dysplasia 3 is an inherited eye disease affecting dogs. Progressive retinal atrophy, Rod-cone dysplasia 3 occurs as a result of degeneration of both rod and cone type Photoreceptor Cells of the Retina, which are important for vision in dim and bright light, respectively. Affected dogs have abnormal thinning and degeneration of the retina beginning around 4 weeks of age. Signs of progressive retinal atrophy including changes in reflectivity and appearance of a structure behind the retina called the Tapetum that can be observed on a veterinary eye exam by 6 to 16 weeks of age. Rod photoreceptor cells degenerate first resulting in loss of peripheral vision and night vision. As the disease progresses, cone photoreceptor cells also degenerate resulting in complete blindness. Most affected dogs are completely blind by 1 year of age, but some may retain limited sight until 3 to 4 years of age.
Genetic testing of the PDE6A gene will reliably determine whether a dog is a genetic Carrier of Progressive retinal Atrophy, Rod-cone dysplasia 3. Progressive retinal atrophy, Rod-cone dysplasia 3 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 being a carrier of the PDE6A 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. However, because there are multiple types of PRA caused by mutations in other genes, a normal result in PDE6A does not exclude PRA in a pedigree.
** Abbreviation is PRA. We test our adult breeders for this and the results are posted as we receive them from Gensol. If our breeder’s parents are CLEARS the offspring we keep as breeders are not re tested. Our tests are done by Gensol. The information was provided by Paw Print Genetics, another company that we have used.
- CLEAR/CLEAR IS A CLEAR
- CLEAR/CARRIER IS A CLEAR OR A CARRIER
- CARRIER/CARRIER IS A CARRIER OR AN AT RISK
- AT RISK/AT RISK IS A AT RISK
VWD TYPE 1:
von Willebrand disease, also called vWD, is the most common inherited blood clotting disorder in dogs. It’s the result of an insufficient amount of von Willebrand factor (vWF), which is a plasma protein that helps blood to clot. vWD can result in excessive, serious bleeding from even a minor skin wound. There are three types of von Willebrand’s. The most common is Type 1, which is the mildest form of the disorder. Types 2 and 3 are much more serious. Symptoms of the disease typically occur only in more serious cases, and include bleeding from the mouth or nose for no apparent reason, bleeding in the GI tract evidenced by bloody or dark tarry stools, blood in the urine, anemia, and excessive bleeding that accompanies everything from loss of baby teeth to major surgery.
Diagnosis of von Willebrand’s disease is done through blood and bleeding time tests, as well as a DNA test that identifies symptomatic dogs and those who are carrying the disease but haven’t yet shown symptoms. Caring for a dog with vWD means managing the disease and its symptoms, since there is no cure. The goal is to control bleeding, reduce the number of bleeding events, and correct any underlying conditions that might be contributors to the disorder.
By Dr. Becker: von Willebrand disease is also called vWD and is the most common inherited blood clotting disorder in pet dogs. Dogs with the condition have an insufficient amount of von Willebrand factor, called vWF, which is a plasma protein. This protein is needed in order for the blood to clot properly. The disease inhibits normal clotting function and causes excessive bleeding even for minor skin wounds. For this reason, it can be a serious and even deadly bleeding disorder. von Willebrand is caused by a genetic mutation and is equally common in both male and female dogs, though the severity of the condition varies.
Types of von Willebrand Disease:
There are three types of vWD. Type 1 usually causes mild to moderate symptoms. Fortunately, it’s the most common form of the disease. Breeds prone to Type 1 von Willebrand’s include Dobermans, Golden Retrievers, Standard Poodles, Manchester Terriers, the Akita, the Pembroke Welsh Corgi, and the Miniature Schnauzer.
Type 2 causes severe symptoms and occurs primarily in German Wirehaired and Shorthaired Pointers.
Type 3 von Willebrand’s is also a very severe form. It is seen most commonly in Chesapeake Bay Retrievers, Scottish Terriers, Shelties, and less commonly in other breeds.
Dogs with hypothyroidism may also be at greater risk of bleeding disorders. von Willebrand occurs in both male and female dogs and has been reported in more than 50 breeds.
Symptoms and Diagnosis:
Fortunately, most dogs with the disorder have few if any symptoms, and symptoms tend to improve as a dog matures. In fact, dogs with Type 1 vWD are often not diagnosed for years until surgery or an acute injury points to a problem with a blood clotting issue. More severe symptoms of the disorder are usually obvious by the time a dog reaches one year of age. These can include bleeding from the mouth or nose for no apparent reason, bleeding in the GI tract evidenced by bloody or dark tarry stools, blood in the urine, anemia, excessive bleeding from the loss of baby teeth, tail docking, or ear cropping. Sometimes dewclaw removal can cause excessive bleeding. So can simple basic wounds, surgical incisions from spaying or neutering, heat cycles or whelping (giving birth) in females, and even as a result of a basic nail trim. Mild injuries that occur during play can cause bleeding to the joints and result in lameness in young dogs. von Willebrand disease can be diagnosed by a blood test and bleeding time test that measures the length of time it takes the bleeding to stop from a tiny incision in the inside of a dog’s gum. The blood test for von Willebrand measures the level of vWF in the dog’s bloodstream. There is also a DNA test available that identifies both symptomatic dogs and those carrying the disorder. It is the most accurate diagnostic test for this particular disease.
Caring for Dogs with vWD:
Unfortunately, von Willebrand disease can’t be cured. But it can be managed. The treatment goals are to control bleeding, reduce the number of bleeding events, and correct any underlying conditions that might be contributors to the disorder. Dogs with von Willebrand’s may require blood transfusions during surgical procedures to restore levels of vWF to allow normal blood clotting to occur. Several transfusions can be required for dogs with the severe form of this disease. Steps can be taken to increase a vWD dog’s blood clotting ability in order to reduce surgical risks. These include giving IV clotting factors and medications prior to a procedure. Bleeding caused by external wounds can be controlled by bandages, pressure wraps, sutures, or skin glue. Dogs with this disease should be prevented from rough play with each other or with people, as even minor injuries to their joints or body can be pretty risky. Hard bones and treats or hard toys that may cause bleeding from the gums should also be avoided. Since von Willebrand dogs tend to also develop hypothyroidism, I think it’s a really good idea to have an annual thyroid test for dogs with the condition. There are certain drugs that should not be given to dogs with vWD, including NSAIDs and medications that involve any type of anticoagulant or anti-platelet activity. And there are also a few supplements that should not be given in high doses, including vitamins C and E, the proanthocyanidins such as grape seed extract and pine bark, as well as high doses of omega-3 fatty acids. We test our adult breeders for this and the results are posted as we receive them from Gensol. If our breeder’s parents are CLEARS the offspring we keep as breeders are not re tested. Our tests are done by Gensol. The information was provided by Paw Print Genetics, another company that we have used.
- CLEAR/CLEAR IS A CLEAR
- CLEAR/CARRIER IS A CLEAR OR A CARRIER
- CARRIER/CARRIER IS A CARRIER OR AN AT RISK
- AT RISK/AT RISK IS A AT RISK
Kocher’s Precious Puppies Kennels/ breeder Diann Kocher has the right to modify, edit, delete or change terms, conditions, and/or prices at given time with or without notice.