D. Caroline Coile, Ph.D.
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2013 AKC Canine Health Foundation National Parent Club Conference

8/28/2013

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I was pleased to once again attend the AKC  Canine Health Foundation Parent Club Conference. Here's a synopsis of the  presentations: 

Bloat and  Multiple Organ Failure: Elizabeth Rozanski, Tufts
Management of bloat has advanced since the  early days when prognosis was grim and treatment options were basically passing  a tube or if possible, surgery. Survival increased with the introduction of  large volume of IV fluids and prompt surgical treatment (that is, going to  surgery within an hour of presentation---once fluids have taken effect--- rather  than waiting for the dog to stabilize or improve before surgery).   A huge improvement in long term survival came with the introduction of  various types of stomach tacking (gastropexy).  When promptly treated, 80-85% of dogs  survive. Much research has focused on what causes bloat, but mostly it has shown  that our initial ideas were probably wrong. It doesn't seem to matter if you  feed elevated, or twice versus once a day, or soaked kibble, or before or after  exercise. It does seem to matter what breed you have (large and deep-chested  dogs in general, but with exceptions), whether they have close family members  that bloated, and whether they tend to be nervous or stressed (as when traveling  or being boarded or shown).  It may help to feed large versus small food size, and it may help to avoid weather  extremes (sudden temperature changes). And exercise may be useful for promoting  gut motility. Using anti-gas pills won't hurt, and may help because one study  has shown that at least some of the gas in the bloated stomach is from fermented  food, not swallowed air.

 Cost of surgery ranges from about $2000 to  $8000, depending on area, time of day, and type of practice. Because of the high  cost, and the often pessimistic prognosis given by veterinarians, as many as 25%  of dogs with bloat are euthanized without surgery. It's often hard to decide  based on current diagnostic criteria which dogs have a poor prognosis. Lactate  levels are sometimes used to predict outcome but should not be used to decide  euthanasia versus surgery. Stomach tacking during surgery should always be
performed. 

Sometimes dogs survive the surgery but die  within days of other organ failure, mostly affecting the lungs, liver, kidney  and GI tract.  Blood clotting  abnormalities can be a confusing problem, as some dogs have a bleeding tendency  early on but others may clot too much following surgery. Although  counterintuitive, it may be beneficial to treat with heparin even early in the  course of therapy. Rozanski's group is studying the use of a clotting test  called the thromboelastograph (TEG) that can detect excessive clotting earlier  than conventional tests. 

Rozanski is a proponent of prophylactic gastropexy (tacking), even suggesting breeders of high-risk breeds may wish to  have pet puppies tacked before leaving for their new homes. She also wishes pet  insurance companies would provide a "bloat only" policy. 
 
Epilepsy:  William Thomas, University of  Tennessee
 About 1-2% of all dogs suffer from  epilepsy. Of these, about 60% suffer from status (seizures lasting over 5  minutes) or cluster (multiple seizures in short period) seizures. These dogs  have a significantly reduced average lifespan. Most dogs with epilepsy are diagnosed  between 1 and 5 years of age. Other causes, such as stroke, tumor, encephalitis and fungal infection can also cause seizures.

Epilepsy is more common in some  breeds, including Beagle, Belgian Shepherds, Bernese Mountain Dog, Dalmatian,  Golden Retriever, German Shepherd, Vizsla, Border Collie, English Springer  Spaniel, Irish Wolfhound, Keeshond, Labrador Retriever and Standard Poodle.  Different genes may be responsible for epilepsy in different breeds, as  supported by research in the Wirehair Dachshund, English Setter, Border Collie  and Lagotta Romagnolo.

Phenobarbital is the most commonly used drug in dogs, but  some newer human drugs such as zonisamide, levetiracetam, gabapentin and  pregabalin, or treatments such as vagus nerve stimulation, surgery and  acupuncture, may provide more effective seizure control with fewer side effects,  although some may be expensive.

Even with current treatment, a survey  showed that 95% of owners felt their  dogs had good quality of life, 48% felt seizure control was adequate, and 55%  felt the cost of advanced diagnostic testing was worth it. 
 
Inherited  Cardiomyopathies: Kathryn Meurs, North Carolina State University
Cardiomyopathies are diseases of the heart  muscle. The two most common types are Dilated and Arrhythmogenic, which together occur second only to valvular disease in dogs.

Arrhythmogenic Right Ventricular  Cardiomyopathy (ARVC) is common to Boxers and to a lesser extent, Bulldogs. The  heart muscle contracts well but microscopically, many of the muscle cells die  and are replaced with fat cells, leading to abnormal electrical conduction.  Affected dogs have an abnormal heart beat that may cause them to faint or die  suddenly. A genetic mutation has been found in a region of the genome involved in making a protein that sticks cardiac cells together. It seems to be inherited as an autosomal dominant; however, dogs with two copies of the mutation have more abnormal beats per day than with one copy. Usually. Actually, the mutation has about 72% penetrance, meaning that 72% of dogs with the gene will have  disease, but 28% of dogs with the same gene will not. 
 
Dilated cardiomyopathy (DCM) is most known  in the Doberman Pinscher, but also occurs in many large breeds. However, it may  be different kinds of DCM in different breeds. In humans, 24 different genetic  mutations can cause DCM. In Dobes, the cardiac mitochondria, which is involved  in cell metabolism, is abnormal. In at least some families of Dobes, dogs with a  mutation in a mitochondrial gene develop DCM. The gene is an autosomal dominant.  About 28% of Dobes with this gene develop DCM, suggesting that as with humans,  there may be different genetic causes even within one breed. 
 
DCM in Great Danes is again a different form, appearing to be caused by a sex-linked gene. This again suggests that you  can't generalize DCM genetic studies between breeds. You have to start fresh:  characterize the disease in your breed; characterize familial patterns; and  characterize molecular aspects of the disease. 
 
Realize that a gene test may not be as  helpful as you hoped, especially in cases where the mutation has incomplete  penetrance. Why do some dogs with the mutation show the disease and not others?  Is it diet, daily activities, genetic background? And if you have an unaffected  dog that has the mutation, how do you use that information to guide breeding decisions? Add to that the situation where you may have more than one mutation causing DCM in a breed, and you have another concern: Just because your dog  "passes" the one available DNA test for DCM, it doesn't mean he may not carry a  different gene for DCM. Meurs suggests dogs must still be phenotypically tested  with Holter monitors and cardiac ultrasounds. She does not suggest wide-scale  removal of dogs with the mutations, but balanced breeding to dogs not carrying  the same mutation. 

But---and this was not part of the  presentation--- some Boxer and Dobe breeders wonder how useful a DNA test is if  it essentially gives a large percentage of false positive and false negatives. 
 
Applying  Physical Therapy Techniques to Dogs: Janet Van Dyke, Canine Rehabilitation Institute
We've always been told to cage rest our  dogs following orthopedic surgery. But as anyone who has had such surgery  themselves knows, the current standard of treatment is to start physical therapy  immediately. Resting the affected area delays or even prevents return to use. In  humans, a raging debate continues about surgery versus PT for many conditions,  including knee injuries and lower back pain. There is good evidence that PT  produces equally good results. We are entering that debate with  dogs.
 
In a  study comparing two types of surgical treatment for cranial cruciate ligament repair with conservative treatment, no differences in success were found. None of the current surgical treatments for CCL repair can prevent osteoarthritis.  Conservative (non-surgical) treatment may give satisfactory results for many patients and even allow equal return to sporting activities.  Conservative treatment of CCL does not change the instability of the  joint, but may let the dog achieve a high level of function with an
unstable joint.  
 
In dogs with intervertebral disc disease, cage rest and surgery have long been the  standard of care. But as far back as 1961, a JAVMA article written by a human physical therapist outlined the success he had in treating 82 dogs with IVDD using only nursing care, muscle relaxants, thermotherapy, massage, exercises and stretching, electrical stimulation, and ultrasonic therapy.
 
Canine Rehabilitation also includes the  use of prosthetics. Currently, dogs needing any part of a limb, even a foot,  amputated end up having their entire limb amputation. But with newer prosthetics, dogs can use all four limbs. Van Dyke even gave an example of one  dog that had lost all four feet to frostbite, that was now running on his four prosthetic feet!
 
Rehabilitation is not necessarily cheaper than surgery, and certainly more work. But it can accomplish things surgery alone can't. Van Dyke showed the progress of a Lab puppy that had broken its  neck when hit by a car. Initially it could only move its rear feet. It required  stimulation, passive movement, walking fully suspended from a sling, walking on  a sling on an underwater treadmill, attaching elastic bands to its legs to assist it walking on the underwater treadmill, swimming in a pool, wearing orthotics that allowed a pre-dialed range of motion that was gradually increased, until two months later, "Lucky" was walking and even running!
 
Canine rehabilitation is becoming more popular, but watch out for people claiming to do rehab without credentials. Human physical therapists have a DPT degree that requires 4-5 year post-graduate  training. With additional training, some are now working in veterinary practices. The new American College of Veterinary Sports Medicine and Rehabilitation will drive additional research and progress in this area. 
  
Regenerative Medicine for Soft Tissue Injuries: Sherman Canapp, Veterinary Orthopedic and Sports Medicine  Group
Surgery and physical therapy don't always fix things. Tendons and ligaments are subjected to major stresses during physical activity, and if injured due to repeated microtrauma, heal very slowly because of poor vascularity. Tendon ruptures or avulsions are typically treated  by surgery, but core lesions---disruptions within the tendon---usually heal by fibrosis rather than regeneration. Fibrotic tissue is not as elastic and is thus more prone to re-injury. In horses, and now in dogs, use of stem cells or platelet rich plasma has been shown to heal and regenerate tendon core lesions, allowing return to activity without re-injury.

First, you must have a definitive diagnosis. You can't treat "front end lameness" without knowing what's causing it. Diagnostic procedures may include radiographs, MRI, ultrasound and arthroscopy. Not only do you need to know exactly where to put the stem cells, but you must be sure the lameness isn't due to cancer, because stem cells help  cancer cells multiple, too. 
 
Then you need stem cells. You can get them from bone marrow or adipose tissues, with the latter much easier, safer and are comfortable to harvest (basically a strip of fat tissue is taken from the area just behind the sternum while the dog is under anesthesia). The cells may be processed in-house or sent off. Be very picky about who does it. 
 
You could also use platelet rich plasma, which seems to hasten healing when applied directly at the site of injury  because of two growth factors within it. Plasma is derived as with any blood  draw, and then processed to make it rich in platelets. Again, the laboratory  that processes them is important.

The cells are then injected right into the  injured area using ultrasound to guide. You can't just inject them in the bloodstream or general area. 
 
Canapp presented case studies of dogs with longstanding injuries that had not responded to previous therapies.  The dogs were given combined stem cell and platelet rich plasma injection, followed by physical therapy. Results were apparent within weeks, with full return to function (even Border Collie agility!) within 6 months. 
  
Infection & Immunity: Adam Birkenheuer, North Carolina State University
Did you know 55,000 people die of rabies worldwide each year? With dogs the major source? And that while you can get exemption letters from your veterinarian saying your dog can't be vaccinated for medical reasons, if your dog bites somebody he will still be treated as an unvaccinated dog. 

Approximately 20 vaccines are now  available for dogs. The core vaccines (rabies, parvo, CAV-2 and distemper) should be given to all dogs; CAV-1, giardia and corona are NOT recommended; and the others (such as lepto) depend on your dog's particular circumstances. He also did not recommend the rattlesnake vaccine. 
 
We always hear about "new" strains of parvo. There are at least five known variants: CPV-1 (extinct); CPV-2, 2a, 2b and 2c.  CVP-2c, the newest, has been known for over a decade, but is said anecdotally to cause severe disease in vaccinated dogs. But controlled studies have shown cross-protection from existing parvo vaccine.  

Interference from maternal antibodies are  the most common reason for vaccine failure. But by age 12, and especially 16,  weeks about 99% of puppies respond to vaccination appropriately. 
  
In a study of vaccine reactions looking at  more than a million (!) dogs, the two main associations found were that the  lower the body weight, the more likely an adverse event; and the more vaccines given at once, the more likely an adverse event. 
  
What about vaccination and immune mediated blood problems?  One study showed that dogs with IMHA were more likely to have been vaccinated with one month prior, but this study has not been able to be replicated. 
  
Hemangiosarcoma:
Jaime Modiano, University of Minnesota
I should preface this by saying that Jaime  Modiano is the single most devoted researcher of canine hemangiosarcoma (HSA).  He works with a number of other researchers who also regularly report to CHF.  So most of the work here is highly collaborative. He and his collaborators also work on other canine and  human cancers, including osteosarcoma, lymphoma and melanoma--so first, the news on them:
 
Osteosarcoma:  They have recently identified molecular subtypes of osteosarcoma that will  enable better predictions of patient response to therapy.   One subgroup has a median survival time of 3 months, whereas the other has a median survival of 14 months. You cannot tell these groups apart by any physical features, only by their genetic microenvironment. Patents have been submitted to make this test, which would take a few days to get back results, available in clinical practice. 
 
Lymphoma: Treating dogs with lymphoma also gives widely varied results. Traditionally, veterinarians have classified the prognosis of B cell lymphomas as "bad" and T  cell lymphomas as "terrible."  But  really cell type is not predictive, as there are long and short term survivors in both groups. Using a four-gene signature test, veterinarians could predict which dogs will respond to treatment. Samples would initially require a biopsy,  but by next spring the technique should only require a fine needle aspirant.  (This test could potentially be combined with a new test developed by another CHF-funded researcher, Matthew Breen, that can determine best therapy for B-cell lymphomas). 
 
Hemangiosarcoma  (HSA):  Modiano terms it "the tumor from hell." By the time it's detected, it's too  late. HSA can occur in any breed at any age, but is more common in large breeds,  older (8-10 years) dogs and in certain breeds. First described in the 1950s, it  was only treated with surgery. By the 1980s, chemotherapy was also being used and considered helpful with surgery. 

Risk increases with age, but no age-related stratification by  breed. So whatever the breed disposition is, it's for the disease, not the age  at which it strikes. We still don't know the cause of HSA, but an hereditary  risk factor is assumed based on breed predilections, and has been confirmed at a genetic level in Goldens. A recently published paper citing environmental and lifestyle factors has significant biases and is based on anecdotal findings.  
  
HSA is classically described as a tumor of the endothelial  cells, but that's probably not correct. Perhaps it is instead a tumor of the  blood forming cells. It may be formed in the bone marrow and the tumor develops  wherever it happens to land, be it the spleen, heart or elsewhere. This means  removing the spleen to prevent splenic HSA won't help; it will just develop  elsewhere. 
 
Modiano's groups found a subgroup of endothelial precursor cells present in the blood of  Goldens with HSA. Modiano believes these cells are the same no matter the  breed, and no matter the site of the HSA tumor. This could provide a blood test  for HSA. 1) It could help decide whether a splenic tumor was a hemangiosarcoma  or a hemangioma without surgery. 2) It could provide early detection of HSA.  But still must decide how to deal with the possibility of false positives and  false negatives. See
http://cancer.landofpuregold.com/the-pdfs/cancerdiagnostics.pdf for a discussion of use and misuse of screening tests. A patent has been awarded but they still need a partner for distribution. A clinical trial is ongoing. 
 
Beyond  detection, how do we fight the tumor? One study has been published that used a  toxin to kill HSA stem cells. A clinical trial is ongoing but too soon to know results. 
 
They are  also looking at hereditary traits that may contribute to HSA in Golden Retrievers.  Information on  participating in trials or submitting DNA from any breed is available at  www.modianolab.org/studyInfo/studyInfo_index.shtml and
www.cvm.umn.edu/cic/home.html . 
 
Cytogenic  Landscape of Canine Cancer: Matthew Breen, North Carolina State  University
Cancer is the leading cause of death in pet dogs. Twenty five percent of dogs will develop cancer, and 50% of dog over age 10 will die of cancer. Many cancers have breed predispositions: 

LYMPHOMA: Old English Sheep dog, Boxer, Pointer, Golden Retriever, Rottweiler (Also evidence for Basset hound, St. Bernard, Scottish Terrier, Airedale and Bulldog.)
 
OSTEOSARCOMA: Large and giant breeds such as Irish Wolfhound, Scottish Deerhound, Great Dane, Bernese Mountain Dog, St. Bernard, Irish Setter, Golden Retriever, Doberman Pinscher, Rottweiler, Greyhound.

SOFT TISSUE TUMOURS: Larger dogs such as  Boxer, Bernese Mountain Dog, Airedale Terrier, Great Dane, Saint Bernard, Basset Hound, Golden Retriever --- all have twice as many as the general canine population.

HEMANGIOSARCOMA: German Shepherd, Bernese Mountain Dog, Golden Retriever, Flat Coated Retriever, Portuguese Water Dog, Labrador Retriever, Boxer, Skye  Terrier.

HISTIOCYTIC SARCOMA/MALIGNANT HISTIOCYTOSIS:
Bernese Mountain Dog, Flat Coated Retriever, Rottweiler, Golden
Retriever. 
 
In  humans, aberrations in the chromosomes of tumor cells have been shown to help identify cancers, assist in localizing cancer-associated genes and select best  treatment. Dogs appear to share many of these same cytogenomic changes. Breen's  lab is studying cytogenomic changes in canine lymphoma, leukemia, osteosarcoma,  histiocytic neoplasia, urogenital carcinoma, intracranial malignancies,  hemangiosarcoma and melanoma. 
 
Lymphoma:  Breen developed a predictive test for response to certain therapies for dogswith lymphomas several years ago, but is still trying to get it on the market.  
 
Mast cell tumors: Generally graded 1, 2 and 3, with grade 1  being good news, grade 3 bad news, and grade 2 who knows? Now a test can give  more guidance as o whether a grade 2 tumor will act like a grade 1 versus a  grade 3. If you have a dog with a grade 2 mast cell tumor in the last three  years, its biopsy specimen may still be available at the testing facility.  Please contact the Breen lab (
info@breenlab.org)  as they would like access to it, especially if you have updated information on  the tumor's grade.   
 
Hemangiosarcoma: HSA ells are hard to work with because the  cells are usually mixed in with normal cells. But analyses show three different  clusters of cytogenonic changes in dogs with HSA. Different breeds have  different cytogenomic changes; for example, Australian Shepherds have 5983 genes that are aberrant in HSA---but by comparing five different breeds (Aussies,  Berners, GSDs, Flat Coats and Goldens) they found "only" 396 genes shared by all  five breeds. T reduce that number further, they're now looking at Dachshunds,  PWDs and Briards---but if your breed has high incidence of HSA, please send  samples! All samples and information will be merged with the data from the  Modiano lab.  
 
Other tests forthcoming will 1) predict with 95% accuracy how  long your dog with lymphoma will respond to doxorubicin or CHOP treatment; 2)  whether it will respond very well or very poorly to single agent doxorubicin; 3)  separate lymphoma from histiocytic malignancy in breeds with both; and 4)  identify the presence of urogenital carcinoma cells in dog urine.  
 
"Without all the money and resources, none of this work can be
done without samples from your dogs---even though it is often difficult at such a grief-stricken time." --Breen.
 
Other talks: Cytokines and nutrition, focus areas in GI  research, modeling biomechanical forces after CCL surgery, genetics primer,  breeding and genetics discussion panel and canine cognition. 
  
The  Canine Cognition talk by Brian Hare was of course the most interesting. Do dogs imitate? Navigate?  intentionally deceive? take short cuts? know what you can and cannot see? know  what you do and do not know? understand causal properties like gravity? understand symbols, like children do?  think about others' thinking? Do breeds differ?
 
It's not interesting that dogs can learn a lot of words, says  Hare. What's interesting is that at least some can use the exclusionary  principle to learn them. In other words, tell a dog to find the "blablah" and if  a new toy is among other toys all of which he already knows, if he can bring you  the new one, and ID it as he blahblah, then he's used this exclusionary logic to  deduce the name of the new toy. Some dogs, and human infants, can do this. No  other species.

Dogs can follow pointing and gaze directions. Chimps can't.  Foxes and wolves can, but only if hand raised.

Hare is working on a battery of tests that can predict working  (guide or military) dog success, or help better place shelter dogs.  Some dogs look for help when they can't reach a goal, others don't. One  subtype is better for certain jobs than others. For trainers, test results  could help diagnose why a dog has a harder time learning a particular task; maybe scores low in memory, or gesture interpretation, or high in cunning. 
 
You can test your dog at
www.dognition.com (for a fee, although  a couple of sample tests are available for free). Tests are based upon  scientifically verified protocols. Not only will you receive a report based on  your dogs test scores for memory, empathy, cunning, communication and reason  categories, but your dog's data will be entered into a huge database (more than  68,000 so far!) dogs that will enable breed differences to possibly emerge. 
 
I have just signed up Pepe. I'll let you know how it goes...If I  can get him to come.

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Spots, Stones, Pointers and Dals---and the AKC

11/8/2011

9 Comments

 
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We live in exciting times---at least, those of us interested in canine health do. And at its October Board meeting, the AKC stirred the excitement (and controvery) a little more with a couple of announcements. I'll talk about just one of them today, the procedure involved in registering Dalmatians with a Pointer ancestor.

Wait a minute---isn't the whole point of AKC "papers" that the dog is purebred? Historically, yep. But a few other things can occasionally trump pure breeding, even in a purebred dog registry. One of those is health, and that brings us back to exciting times. The AKC is opening its eyes and on occasion, its studbook, to situations in which allowing a leak in purity might plug a flood of health problems. 

Dalmatians have become the poster breed for the battle of purity versus health---and health won.  Dalmatians have the higher incidence of a type of urinary stones called urate stones of any breed. Some estimates place it as high as 34% of all Dals, although that estimate is probably too high because of methods in sampling. Nonetheless, it's a problem. The high percentage is related to the fact that all purebred AKC Dalmatians have a metabolic abnormality that causes high levels of uric acid in their urine. The high levels often lead to crystallization of uric acid salts or to urinary stone formation, which in turn can cause urinary blockage, especially in males. In some cases, surgery is needed to relieve the condition; in others, euthanasia is the only solution. Dalmatian owners may need to feed their dogs a special diet, along with providing lots of water and plenty of opportunities to urinate, to combat the condition. The one thing they can't do is find a puppy not at risk for it. That's because every purebred AKC Dalmatian is homozygous for (that is, has two copies of) the autosomal recessive SLC2A9 gene responsible for high uric acid.  
                  
Dalmatians aren't the only breed with the mutated SLC2A9 gene. It (along with urinary stones) is found in Black Russian Terriers and Bulldogs, among others, at high frequencies. But these breeds also have the normal version of the gene causing low uric acid. Their breeders can DNA test their dogs and avoid producing homozygous recessive dogs. Dalmatian breeders can DNA test their dogs all they want, but the outcome will always be the same: homozygous for the mutant high uric acid gene. Selecting against the gene is thus not an option for them.  
                 
How did this aberrant gene become so widespread? A 1940 survey of Dalmatian urine showed every Dalmatian tested had high uric acid. The high levels were initially thought to be a trait associated with the Dal's spots. Dalmatian spots are actually not like big spots you see on many breeds, but a type of ticking you more often see in other breeds as little spots with intermingled white hairs. Initial studies using Dalmatian crosses suggested that ticking (spots) without white hairs in them were always indicative of high uric acid.

But in 1973, Robert Schaible, Ph.D., a medical geneticist and Dalmatian breeder, crossed a Dalmatian with a champion Pointer and produced (among others) five puppies that had both clear spotting and low uric acid, leading him to conclude that the gene for Dalmatian ticking was very close to the gene for high uric acid on the same chromosome; that is, they were closely linked. Early breeders had inadvertently selected for the mutated gene when they selected for the clear ticking. More importantly, Schaible surmised that descendents from these clear-spotted low uric acid (LUA) puppies could introduce the normal gene back into the Dalmatian population without losing breed type. His plan was to breed the LUA dogs that best fit the Dalmatian standard in each generation back to AKC Dalmatians. He apprised the Dalmatian Club of America (DCA) of his
project in 1976. 

 In 1981, with approval from the DCA, the AKC approved the recognition of two dogs from his fifth generation LUA Dalmatians. But soon afterward feelings within the DCA changed, leading to a contentious few years within the club, and ultimately, to the AKC rescinding the right for the LUA dogs' offspring to be registered. The LUA project continued without DCA support, with a few litters a years. LUA Dalmatians competed successfully in United Kennel Club shows, and in obedience and other performance events, but they were still banned from AKC registration.  
                 
Then, in 2006,  the DCA opened the matter again and voted to support the breeding and testing of the LUA Dalmatians, with a vote on registration to follow in 2008. The AKC generally defers to parent breed clubs, such as the DCA, on matters of opening registration to non-AKC registered dogs, but it has on occasion registered dogs descended from crosses to other breeds, or dogs from a breed's native land, if the parent club can show a good reason, such as one related to health. The club must then vote, with 2/3 of those voting in favor of registration, for the AKC to consider opening the registry. The 2008 DCA vote had less than half voting to allow the LUA Dalmatians' registration.   
               
The AKC Health and Welfare Advisory Committee looked into the matter, issuing a report in Fall, 2010. They concluded that the LUA Dalmatians are essentially purebred and that their inclusion in the Dalmatian gene pool would be good for the breed's health as long as not everyone rushed to breed to them (which would potentially create a genetic bottleneck and cause their genes to be overrepresented in the next generations).  
                 
By now, the backcross project has dogs that are 11 to 15 generations down from the Pointer cross. In an 11 generation pedigree, there are 4095 dogs, of which only one is a Pointer, and of which only 10 to 15 are LUA Dalmatians. The dogs are considered to be more than 99.5% Dalmatian on average.                    
              
The AKC Health and Welfare Committee stated: "Because the introduction of the low uric acid dogs into the AKC registry gives Dalmatian breeders a scientifically sound method of voluntarily reducing the incidence of the condition, this committee strongly recommends some controlled program of acceptance of these dogs.  Where the strict health and welfare of the breed is the over-riding concern, no other argument can be made. Individual breeders can be free to make their own
decisions about incorporating the normal gene.  However, it would be a disservice to the health and welfare of the Dalmatian breed to not allow the normal gene to be reintroduced." 

In June 2011, the Dalmatian Club of America members voted by a 55 to 45 percent margin to register the LUA dogs. In July, 2011, the AKC agreed to open its studbook to them. The registration numbers of these dogs and their descendents will contain a letter that designates their Pointer ancestry so that breeders can make informed decisions about integrating them into their bloodlines. 

Now, at its October Board meeting, the AKC has published the exact guidelines for registration, below. It's a lot of reading, but the gist is that only descendents of this original Dal X Pointer cross are included in the open registration, and only those descendents that have at least one copy of the normal gene. Whether this is enough to effectively combat the health situation in Dals in debatable; probably not, since it would create a bottleneck of breeding to this one line. But perhaps with success a peption can be made to create a second unrelated LUA line. It is clear the AKC (and the Dalmatian Club of America) don't wish to create a situation where everyone can run out and cross their dal witha Pointer and register the offspring. So it's a compromise...but it's a step.  

What are your thoughts? Leave a comment.


Dalmatian Registration Procedures

 Following a motion by Dr. Davies, seconded by Dr. Battaglia, it was VOTED (unanimously) to adopt the following procedures to be used for registration of
Dalmatians descended from “Stocklore Stipples” known as LUA (low uric acid) Dalmatians, effective November 1, 2011.

REGISTRATION PROCEDURES
1) An Open Registration application is required:

 a) Include pedigree for the dog. While application only calls for a three generation pedigree, the pedigree in this case must go back to and to document that the dog in questions is a descendent of Stocklore Stipples,
NS 601000. All dogs in the pedigree must be AKC registered or AKC registrable.

 b) Include photographs of the dog, as required as part of the Open Registration process.

 2) Application is reviewed and pedigree researched by AKC staff.

 3) The dog must be tested for the normal SLC2A9
gene.

 4) Only dogs tested as homozygous or heterozygous for the normal SLC2A9 gene will be registered under this program (see 6 below). The test results will be recorded by OFA, with OFA covering the cost of this recording
for one year, and the DCA covering the next two years. The results must accompany the Open Registration application.

 5) Applicants that qualify will be registered with an “NY”
prefix. The same “NY” would also appear as a registration prefix for all of their descendants.

 6) Any descendants of Stocklore Stipples that do not test as homozygous or heterozygous for the normal SLC2A9 gene would not be eligible under this program to receive the “NY” prefix directly as the whole purpose
of the Open Registration was to introduce the normal gene into breeding programs at the option of the breeders. Such dogs, which only carry the same mutated gene as in presently registered Dalmatians, would be eligible to apply for AKC registration, which would include the NY designation, provided both parents are AKC registered dogs, at least one of which carries the NY designation. Such registration of these dogs during the Open Registration period can only be accomplished as a member of a registrable litter.

 7) If it comes to AKC’s attention that any imported dog is a descendent of Stocklore Stipples, that dog would receive the “NY” prefix. Each application is researched and handled on a case-by-case basis.

 8) The Open Registration period will be for three years (November 1, 2011 through November 1, 2014). However, the policy on imported dog will remain in effect indefinitely.

 9) Frozen Semen may be registered only if the dog that produced it is deceased, and if it meets the requirements above. Any living dog must meet the Open Registration procedure, after which its frozen semen may be used to produce an AKC registrable litter.

 10) Once a dog is registered under this procedure, any
descendants may be registered under regular AKC registration procedures. This would include any litter whelped prior to the dog’s registration. As prior
registrations of such litters was previously prohibited by AKC, any late penalty would be waived.


 
9 Comments

A Designer Dog Book? Really?

11/5/2011

6 Comments

 
Picture

OK, out with it: The designer dog--er--elephant in the room. Or on the website. Yes, I wrote a book about designer dogs. "But how, Caroline, how could you write about those overpriced mutts that are helping bring down apple pie, dog shows and the American Kennel Club?"

It took some soul searching (and a glance at my bank statement). When I was first approached by Weldon Owen, a book packager (and we can talk the differences between book packagers and publishers in a future entry) to write it, I sighed and regretted I'd be turning them down.  I've been an AKC participant for most of my life, and I enjoy the perks my AKC dogs allow me. Writing about designer dogs seemed so traitorous.

I thought some more. I studied my bank account some more. And, as I try to do every decade or two, I opened my mind. Not everybody wants to compete. Not everybody wants one of the 150 or so AKC breeds, or even the 450 or so breeds registered elsewhere. And this IS America, home of the free, and home of the freedom to choose an AKC dog, a mutt or even a designer dog.  Withholding information is never the answer, and I'm egotistical enough to think I'm the best source of that information. Who better to present the truth about designer dogs? Who better to say we can't subtitle it "Better than  purebreds" or some other unsubstantiated claim? So I agreed. Well, yeah, I did try to convince them I should write under a pseudonym, but that was a no. Apparently my name has value. How inconvenient.

So, here's the truth about designer dogs: In some cases, they work. Look at the huskies running the Iditarod; most are mixes.  Look at the lurchers (sighthound x non-sighthound mixes) favored for poaching in Britain. The longdogs (sighthound X sighthound mixes) so successful at coyote and jackrabbit hunting in the western United States. Want to succeed at flyball? Get a BorderJack or BorderStaff or one of the other crosses bordering on insanity. Breeds, like cultures, evolve. We strive to hang on to cultural artifacts and antiques, but that doesn't mean we don't stop inventing. Every pure breed we now have was once a novel invention---perhaps even sneered at in  its infancy. 

But let's be truthful: Most designer dog breeders aren't out to make a better hunter or worker. They're out to make a better companion, and their main claim that these dogs are better (besides the fact that most are cute as h**l) is that they're healthier. 

Here's an excerpt from the book: 

When kennel clubs began registering purebreds, they allowed any dog of that general family type to be registered as the breed. At some point, registration closed, leaving a fixed number of potential sires and dams. What wasn't known at the time was that all of us, dog or human, carry from five to seven recessive genes that, if we carried two copies of any one of them, would
result in some type of hereditary disease. Because humans are a bunch of mixed breeds, we don't often end up with a mate who carries the same bad recessive gene
as we do, so it's unusual to produce an affected child. Because those early canine sires and dams carried some random bad recessives, and because all present-day purebred dogs descend from them, there's a fair chance that dogs carrying that same recessive gene might mate, creating a puppy with the disorder caused by that gene. 

The solution? Widen the breeding options, deepen the gene pools to create crossbreeds that don't share the same bad recessives. That's one argument for breeding dogs by design. The trouble is that idea works only within limits. Cross two breeds that share the same disorders and it doesn't work at all. Cross two hybrids again after the initial cross, and you're right back where you started---maybe even worse off: those hybrids will stand a good chance of carrying recessive genes and producing pups with two of the recessives and thus
two disorders. A designer dog should never be just a random mating to "see what happens." Instead, the best mixes blend breeds that can reasonably be expected
to produce desirable physical and behavioral traits.

I can't stress this enough: Just as with a purebred, your source is critical. Most of the designer dog breeders I interviewed left much to be desired in their knowledge of health or genetics. One memorable one had a clearly hydrocephalic designer dog puppy that was being touted as their poster puppy for good health; another had a puppy with a leg I swear was attached backwards! Well, it WAS a novel design...

Too many internet breeders jumped at the chance to produce puppies they could charge twice as much for as they could puppies from same-breed matings. To be fair, many purebred breeders are equally naive and money-motivated. Cave canem, buyer beware and all that. 
 
As for the book, it turned out to be one of the most beautiful  books I've been associated with--and fun. The folks at Weldon Owen were a dream to work with, my editor, Peter Cieply, made me look smart, the photography by Anna Kuperburg was stunning, the models captivating, the owners thrilled and the text gave me a chance to be both fanciful and factful (Is that a
word?). And I got to meet some pretty cool dogs!

For example, there's the Chesador, whose profile begins with:  Attaboy--shake it out! This sportsman loves a good dousing, be it from splashing along in the surf or dog-paddling around the lake. If you share the  Chesador's enthusiasm for all things active, you'll get along swimmingly...

The Jack Chi: All saunter and swagger, the Jack Chi acts like he's the biggest deal on the block. But despite his bold braggadocio and bad-boy image, he's a trickster and a charmer. And though he's happy to be scrappy, he
also craves a cuddle...

 ...And 34 other breeds, all represented by dogs who are very special to someone, and just as cherished and deserving as any purebred. 



6 Comments

    Caroline Coile

    Dog writer, science geek, Saluki savant and communicator of all things dog. I'm concerned about hereditary health problems,  the decline of purebred dogs and the changing climate of dog ownership. I compete with my Salukis in conformation, agility, lure coursing and obedience. I write about science, breeds, health and competitions---and I don't believe in blindly folllowing the accepted dogma of the dog world.

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