Canine Multifocal Retinopathy

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Canine Multi-Focal Retinopathy  — CMR        Ron Hiskes, Ph.D.                                ACQ Spring 2007

 Retinal Dysplasia is well known in humans and dogs.  The retina is the nervous layer of the eye, and it normally lies flat against the back of the eye. The retina is responsible for collecting light impulses which are then transferred to the brain and interpreted as vision. When the retinas detach from their normal position, they cease to function and the patient becomes blind.

Tumors, fungal infections, severe trauma, inflammation, genetic predisposition, high blood pressure, or immunity problems can cause retinal detachment. Depending on what caused the detachment and how long the retina has been detached, in some cases the retinas can be reattached (medically or surgically) and vision restored. In many cases, however, the retina deteriorates and the prognosis for vision is poor

From the website of ACVO (American College of Veterinary Ophthalmologists:  The retina is the neurological structure in the back of the eye which receives light and converts it into an electrical signal. This electrical signal is transmitted to the brain by way of the optic nerve and is interpreted by the brain as vision. The embryological development of the retina is quite complex. It forms from a small part of the front of the primitive neural tube, the structure that becomes the nervous system (brain and spinal cord) of the adult. Malformations of the retina before birth are rare but can be due to either hereditary or environmental (in the uterus) influences. Retinal dysplasia is a type of retinal malformation. The word "dysplasia" simply means "a defective development of an organ or structure". Retinal dysplasia occurs when the 2 primitive layers of the retina do not form together properly. Mild dysplasia manifests as folds in the inner retinal layer. These are called "retinal folds". In "geographic" retinal dysplasia there are larger areas of defective retinal development. In the severe form of dysplasia, the 2 retinal layers do not come together at all and retinal detachment occurs.
Retinal dysplasia is not progressive. It is a congenital defect and animals are born with as severe a condition as they will ever get. Retinal dysplasia can be detected as early as 6-8 weeks on a CERF examination. However, because the size of the eye is small and young puppies are often wiggling during examination, a 6 month recheck is recommended in order for the ophthalmologist to better see the back of the eye.

The cause of retinal dysplasia in most breeds is genetic although prenatal infections with herpesvirus and parvovirus may also lead to it. Retinal dysplasia is reported in 25 of the 100 breeds of dogs listed in the 1996 edition of the CERF book Ocular Disorders Presumed to be Hereditary in Purebred Dogs. Twenty-four of these breeds had retinal folds reported, and 11 had
geographic areas of dysplasia and/or retinal detachment. Simple autosomal recessive inheritance has been suspected in Akitas, American Cocker Spaniels, Australian Shepherds, Bedlington Terriers, Beagles, Dobermans, English Springer Spaniels, Labradors, Rottweilers, Old English Sheepdogs, Sealyham Terriers, and Yorkshire Terriers. The means of inheritance has not been determined in many breeds. In Labradors and Samoyeds a combination of retinal dysplasia and skeletal defects has been described. This condition is known as oculoskeletal dysplasia.
In this condition an autosomal dominant gene is thought to be responsible for the genetic defects. Homozygous animals have skeletal changes and mild to severe retinal dysplasia while
heterozygous animals usually have mild retinal dysplasia.

Retinal folds rarely cause vision problems for the individual dog. They represent small blind spots which are probably not even noticed by the dog. However, large areas of dysplasia (geographic dysplasia) may lead to large deficits in the visual field and dogs with retinal detachments are completely blind.

There have been many questions recently about the certifiability of dogs with retinal folds. Retinal folds may be seen in many breeds and still pass a CERF examination and receive a CERF number. This is due to the fact that the condition is thought either not to be hereditary in the particular breed or has never been shown to be connected to serious (blinding) forms of dysplasia. In some breeds, particularly Labrador Retrievers, Samoyeds, and English Springer Spaniels, individuals with retinal folds are NOT given a CERF number. Since retinal dysplasia is common in these breeds and dogs and bitches with retinal folds can have puppies with blindness and/or skeletal problems the gene should not be perpetuated. In all breeds, individuals with geographic and retinal detachment forms of retinal dysplasia are NOT certifiable

 In 2003, a condition thought to be Retinal Dysplasia was seen in the top winning show  Coton named Quincy.  It was an unusual form and was called “The Coton Form of Retinal Dysplasia”, consisting of tiny bubbles or lesions around the periphery of the retina.  It was not progressive and didn’t seem to impair sight.  This prompted an investigation by Dr. Grahn at the University of Saskatchewan to learn more about this condition.  ACVO asked ACC whether or not to classify this condition as “non-breedable”.  We replied that we were not experts and could not tell them what to do.  ACVO took the conservative approach and classified it as “non-breedable”.  Subsequently, an ACC member and Coton breeder, Caroline Brooke, had a couple of her Cotons CERFED with a similar condition.  She collaborated with researchers at the University of Pennsylvania and prevailed upon her friends and acquaintances to send blood samples for DNA research.  The researchers got lucky.  The defective gene was located at the same spot as in several other breeds they had been researching.   This resulted in a definitive DNA test to determine if a particular Coton was clear, a carrier or affected.  So far 10-20 Cotons have been tested and a few have been found to be carriers.  We ask each of you to help this research by contributing a blood sample to OptiGen, the organization that is conducting the tests.  We need at least a 100 Cotons tested to begin to  do the relevant statistics to know what percentage of Cotons are carriers.

Fairview Cottage and CMR Research at UPENN     Carolyn Brooke    ACQ March 2007

with thanks to researchers and all participants 

ACC member Carolyn Brooke is a retired breeder in Pennsylvania who has written previously for ACQ about her activities visiting shut-ins and rest homes with her Cotons. 

Looking back, it almost seems that we have always been working with "the eye project" for over 10 years since an essential ingredient of any Coton breeder's program is an annual CERF eye examination. (Canine Eye Registration Foundation). While the CERF eye examination is routine for breeding dogs, the reality of the examination is that, even for our dear Cotons, the exams can detect potential problems to be excluded or eliminated from a breeding program. 

And so for Fairview Cottage, our true realization of the impact of health tests began in January 1999.  Annie of Fairview Cottage (dob August  1996) was of the breeding age of 2 1/2 years.  While our thoughts of breeding her were still in the planning stage, we had begun our preparations by completing the health exam, OFA patella certification and  moved on to the eye exam.  And then in the darkened examining room of the ophthalmologist, Dr. Stephen Gross, I heard the words ..." um...this is very interesting".  Interesting is not what I wanted to hear!  Additional words "small areas of linear folds,"  "focal bullous retinal detachments," and "possibly the result of an earlier infection" meant nothing to me except that my dear Annie had a problem. 

Then, more concern kicked in and focused on the word infection; concern and worry for my other  "kids" surfaced.  Fortunately, veterinarians are special people for not only do they give their knowledge and love of animals to help "our kids" but they also understand and appreciate the anxious concerns of the kids' humans. Dr. Gross was no exception.  Despite the packed waiting room he allowed me to bring in my other 5 dogs for immediate exams to relieve my anxiety. . .. and all were fine. 

End of the "eye" story?  Well, if you had talked to me back then, I probably would have said yes.  What more could be said? This was an isolated case.  Annie had an eye problem.  She was spayed.  She has regular eye exams to monitor and insure her heath.  She is living happily ever after as Aunt Annie, the old maid.  

Soon I learned that Annie's condition may not have been an isolated incident.  Helga Lopatin, Past President of USACTC, issued an open letter (March 1999) to owners and breeders about Retinal Dysplasia (RD) in the Coton.  A copy of this letter can be found on the USACTC website under Health Information. Here too, you can find Dr. Grauwels' article on Ocular Hereditary Disease.  For a better appreciation and understanding of how far we've come, it is good to view the beginning research.  

As the number of  "kids"  increased at Fairivew Cottage, it became more practical, and perhaps comical as the herd of white fluffy dogs emerged from our motor home,  to attend CERF Eye Clinics for the examinations of our dogs. The ophthalmologist in our area who generally performs the examinations is Dr. Gustav Aquirre.  When we first met Dr. Aguirre, he was working at The Baker Institute, Cornell University in NY, but would come to suburban Philadelphia, PA (which is actually his home) on weekends and conduct CERF eye clinics.  

From the U of Penn website on the eye clinics comes the following description of his reputation. 

                " Dr. Aguirre is an internationally recognized ophthalmologist whose  clinical and research work has been instrumental in controlling the major inherited eye diseases in dogs. He and  his research group have developed most of the  DNA-based tests that are currently available to specifically determine the affected, carrier or normal status of dogs with inherited eye diseases"  

Hopefully we do learn lessons from our experiences and do not take anything for granted. In this context it meant including our 13 month old Flossie in the group for annual CERF exams in 2002 rather than waiting until she was closer to breeding age.  Flossie's exam certainly stopped the steady flow of examinations at the clinic!  For me the emotional electricity in the darkened exam room became almost stifling; for Dr. Aguirre, ever the researcher, I think it was exhilarating.  He had detected a condition of interest - Multifocal Retinopathy.  Such a condition had been detected in the Great Pyrenees, but Dr. Aguirre had not seen it in the Coton. 

If I had been more in tune with the mind of a medical researcher, I probably would have, at the time, better appreciated Flossie's condition.  In retrospect, Flossie's diagnosis provided an opportunity to become part of valuable research in Coton eye health.  From the CERF screening, Flossie went to Dr. Gross, the ophthalmologist who had treated Annie, for medical workup and treatment. (Subsequently I learned that Dr. Gross had been one of Dr. Aguirre's students)   As with Annie, Flossie was spayed and continued her visits to Dr. Gross.  In April of 2003, Dr. Gross felt it would be of benefit for future studies to have Flossie visit him at U of Penn to photograph her fundus (the back portion of the eye).  Later that year Flossie again visited Dr. Aguirre, at a CERF clinic, to keep him advised of her status.  By this time I finally realized that the years of eye examinations, both at Dr. Gross' office and at Dr. Aguirre's CERF clinics, had the potential to produce a real benefit for the future health of Cotons. 

In 2004 Dr. Aguirre returned to University of Pennsylvania fulltime.  You may be interested in reading Susan Finklestein's article, "You Can Go Home Again: Dr. Gus Aguirre Returns to Penn"  in the Fall 2004 issue of The  Bellwether.  The web address for that article is:                http://www.vet.upenn.edu/schoolresources/communications/publications/bellwether/60/aguirre.html  

By 2005, plans for a project to investigate Canine Multi-focal Retinopathy were coming together. Dr. Karina Guziewicz became the lead researcher on "the Coton Study" project.  The aim was to find a DNA based test for the gene causing multifocal retinopathy in the Coton.  Since our Annie and Flossie had been diagnosed with the eye condition in 1999 and 2002 respectively, Fairview Cottage

became a source for research information. Many different bloodlines, which represent much of the Coton world, were in our immediate Fairview family of 15 dogs. The researchers presented me with their "wish list" for my part of the project. Dr. Aguirre's explanation for the "wish list" was "we ask for what we would like in hopes to get as much as we need [can get]".  In short form, the initial request was for blood samples, pedigree information, and copies of last eye exams for all 15 of our dogs at Fairview Cottage.  In increasing and differing degrees, the scope expanded to include any/all ancesters, offspring, siblings, anyone related and finally unrelated Cotons. 

For the first step of our part of the project, Fairview Cottage's veterinarian, Dr. Anna Edling, drew blood from our dogs. Vials of blood, pedigrees, eye exam data were delivered to the U of P researchers. Any dog that did not have a recent exam was taken to Penn for examination.  Additionally both parents of my oldest dog, Casey (dob 1993) and a sibling visited U of Penn for eye examinations and blood samples. For one line I secured samples from 5 generations.    We were well on our way to providing data for the investigation. 

After these first steps, it seemed almost impossible for me to continue.  How was I to secure blood samples from the dogs that did not live with me or in close enough proximity to transport them to my vet.  Fortunately Dr. Guziewicz came to my rescue.  Although more involved and time consuming on her part, she was able to extract the required DNA information from a cheek swab.  Now the project could move again.  My envelopes containing a  limited explanation and request for help, instruction sheets, and brushes for cheek swabs went out to our offspring.  Families we knew who had non-Fairview Cottage Cotons were also asked or offered to help.  Other breeders offered to contribute samples.  Our quest for data was moving along, although slowly.  

Eventually we were able to provide a substantial number of samples for the researchers to work with.  Since all the  breeding dogs had clear CERF examinations,  we could not provide the samples of the offspring of affected dogs. ( I almost wished we could find an affected dog who had produced a litter to actually see what the results would have been.) From Fairview Cottage's contributions, as well as the other samples,  we could only show if a dog was a carrier or non-carrier of the CMR gene. 

The research conducted by Drs. Guziewicz and Aguirre with information gathered from many sources, including the efforts of Fairview Cottage,  research in Canada by Dr. Grahn, and research by Cornell's Dr. Acland (also associated with U of P's New Bolton Center), has enabled the development of the CMR Test (Canine Multifocal Retinopathy Test) for the Coton.  This year (2007) it was announced that the screening test for CMR is available through Optigen.  At present this test utilizes blood samples. As I view the test, the most important product of  this screening test is the detection of carriers of the CMR gene so that breeders can utilize this information to conduct their breeding program more effectively and with greater knowledge.  Responsible breeding is intelligent breeding.  Each scientific advance and discovery is a stepping stone...a building block for the next piece of knowledge.  The CMR test is one more tool that we now, in 2007, have available to us. Maybe it will also be one of the steps and tools to accurately detect other problems as well as remedies. 

As we (all Coton owners and breeders) continue living with our "kids" we  experience more conditions and challenges;  more opportunities become available to contribute to knowledge about the health of our breed.  One of the many benefits of our breed clubs is the ability to bring together people who share a common interest to work for the continued well being of a breed.  In the Coton world we are particularly fortunate to have breeders and breed clubs who are increasingly demonstrating a desire for real action to understand, protect and enhance our beloved Cotons.   

Editor’s note:  Over the years, Carolyn Brooke’s dogs have been known for their sound constitutions, beauty and sweet dispositions—model Cotons from a model breeder.

CMR Test —Canine Multi-focal Retinopathy             from the OptiGen web site        ACQ March 2007 

 At this writing, a peer reviewed research paper co-authored by researchers at U. of Pennsylvania, Cornell University and U. of Saskatchewan in press and expected to be released in the next couple of months.  In the meantime, Optigen has published the information contained in this article and asks for more samples.  There are still questions to be answered:  (1)  Is CMR a cause of Retinal Dysplasia?  (2)  Is PRA (progressive retinal atrophy) a particularly severe form of CMR?  (3)  What is the incidence of CMR in Cotons —  Dr. Grahn has stated it may be as high as 25%.  (4) At this time a blood test is most reliable.  Can a cheek swab test (much less intrusive and cheaper) be developed?   (5)  What is the best breeding strategy — will the DNA test affect ACVO’s decision to recommend “no breed” for this condition? 

Background:
The OptiGen^® CMR test is a DNA-based test that accurately diagnoses multi-focal retinopathy occurring in Mastiffs, Great Pyrenees and Coton de Tulear. The test also detects CARRIERS of this condition and clears dogs that are genetically NORMAL.

Canine Multi-focal Retinopathy (CMR) is a recently identified recessively inherited eye disease known so far to affect the Mastiffs (English, Bullmastiff, French mastiff or Dogue de Bordeaux), Great Pyrenees and Coton de Tulear. Early clinical studies in 1998 by Dr. Bruce Grahn at the University of Saskatchewan, Canada, first described CMR in the Great Pyrenees. The condition observed in each of the named breeds at an ophthalmologist’s exam includes numerous distinct (i.e. multi-focal), roughly circular patches of elevated retina with accumulation of material that produces gray-tan-pink colored lesions. These lesions, looking somewhat like blisters, vary in location and size, although typically they are present in both eyes of the affected dog.  Discrete areas of tapetal hyper-reflectivity might also be seen.  

The disease generally develops in young dogs before 4 months and might progress slowly, might appear to heal, or might even appear and then go away again. Some lesions disappear with no remaining sign, while some lesions leave a wrinkled area – a fold. Some leave the lasting lesion of a blister formation. Most dogs exhibit no noticeable problem with vision despite their abnormal appearing retinas. And in almost all cases, CMR does not progress significantly over time. The disease seems to have a consistent pattern among the breeds identified so far, although lesions in the Coton de Tulear are often more serious and seem to remain longer than in some of the other CMR-affected breeds. In rare severe cases, the clinical diagnosis could be confused with progressive retinal atrophy (PRA). The full range of clinical symptoms will learned as more dogs are tested for their genetic status.  

The clinical presentation and pathology of CMR closely resembles lesions of “Best vitelliform dystrophy”, a human disease with variable clinical expression but usually with serious affects on central vision. Identification of the gene mutation responsible for CMR was based on these similarities. A mutation in the human VMD2 gene – Vitelliform Macular Dystrophy 2 Gene – causes dominantly inherited human Best Disease. Analysis of the canine version of the VMD2 gene indicates that mutations in it cause CMR as a recessively inherited canine condition. The normal form of the VMD2 gene produces a protein named “bestrophin”. The bestrophin protein assembles, in the cells of the retinal pigment epithelium, in a group of four or five units that form a pore through which chloride ions pass.  

Our current understanding is that CMR is inherited in an autosomal recessive pattern. This means the gene mutation responsible for CMR is located on an autosome (that is, a chromosome that is not a sex chromosome) and CMR disease results when the gene mutation is passed to the offspring by both the mother and the father. It should be noted that the human disease that mirrors CMR in dogs is an autosomal dominant disease with incomplete penetrance. This means that sometimes, but not always, only one copy of the disease gene needs to be present in order for the disease to be observed clinically. At this point CMR in dogs is NOT considered to be an autosomal dominant disease however as more animals are characterized genetically with the CMR test, it is possible that we will find a similar form of inheritance as is seen in humans. 

There is complete concordance of the mutation with the disease among affected dogs in the Mastiffs, Great Pyrenees and Coton de Tulear. However, retinal dysplasia described in other breeds, for example in Labradors, Samoyeds or English Springer Spaniels, is very distinct in comparison to CMR and these conditions are not caused by the CMR mutation.

Due to the abnormal appearance of the CMR-affected retina, CERF, ACVO, ECVO and other ophthalmologist’s eye exam reports typically record these multi-focal lesions as “retinal dysplasia” or “retinal folds”, to denote a defect in formation of the retina. Such findings might disqualify the dog from breeding. Presently CERF doesn’t list CMR as a specific condition, but does fail a dog for “retinal dysplasia/retinopathy – folds, detached.”  

The genetic test for CMR is valuable for identifying the cause of a retinal deformation. Given the exact genetic diagnosis, the owner can be reassured that there probably will be little or no vision loss due to this condition. All the same, future cases of the condition can be prevented using the CMR test as an information tool for breeding  

Genetic Testing:

An exact diagnosis of this eye condition can be difficult. Definitive clinical diagnosis might even change due to the changing appearance of the retina as the dog ages. The CMR genetic test solves this problem immediately since presence of the CMR gene mutation is detected by testing a DNA sample. This result gives the owner immediate diagnostic information and aides in making decisions for the affected dog and for breeding strategies.  

· The OptiGen CMR test can be done reliably at any age – even in young pups, and the result will be the same at any age, and will be the same whenever it is repeated.

· The exact frequency of this disease, and of the gene mutation causing it, are not known as yet. Data accumulated through genetic testing will help to provide that information.

· Tallies of test results are updated and provided quarterly to national breed clubs. 

Breeding Strategies using the CMR Test:
This table highlights all the desirable breedings that include at least one Normal/Clear parent. All other breedings are at high risk of producing Affected pups. All dogs can be bred safely following the recommended schemes. It isn't necessary - or even desirable - to remove clinically healthy dogs from the breeding population. But when choosing pups to retain as potential future breeding stock, it is important to select for Normal/Clear dogs and select against Carrier dogs.

Benefits & Limits to All Genetic Testing:

The benefits of genetic disease testing are clear. With informed breeding practices, breeders immediately can avoid producing CMR affected pups, yet use any healthy dog in their program regardless of genetic status. And since genetic testing can be done at any age, each dog’s genetic status can be known even before clinical disease signs are recognized. Over several generations of selection away from the disease gene, breeders can eliminate a disease gene completely from their line.

BUT, there are basic limits for any and all DNA genetic tests. Whether a test is mutation-based or marker-based, it identifies only the specific mutation being tested or the association between a specific marker set and the disease. For example, a mutation test detects one specific mutation in one specific gene. If there are several different mutations or several different genes that can cause the same condition, one must discover and then test for each mutation and each gene. It can be difficult or even impossible to know how many mutations or how many marker sets exist in all the members of a specific breed. As more and more dogs are tested, previously unknown variations may come to light.  

Ordering the CMR Testing:

The CMR test is done on a small sample of blood obtained by your veterinarian. This allows the lowest risk of contamination of the sample and added assurance of a match of the sample with the identified dog. Please read the paragraphs below, and then read “Instructions and Information” to learn about ordering a test, shipping a sample and prices.  

Optigen charges $95 for a blood test to determine CMR.  To determine if there is a link between the gene responsible for CMR and the condition of PRA (progressive retinal atrophy—which inevitably causes blindness), Optigen request blood samples along with 4 generation pedigrees from any Coton diagnosed with PRA.  Because this program is still in the research phase the testing is free.  Breed clubs may sponsor genetic disease registries, and ACC is working with OptiGen on this.  You may contact OptiGen to send samples at www.optigen.com and by phone at 607-257-0301. 

Editor’s note:  The more we know and the more we share, the better off we all are—this is the real work of our breed club. 

Mongo, who lives with Ron and Susan Hiskes, was one of the Cotons used in developing the test for CMR.  He is a CMR carrier .  So is his daughter, “J”, a beautiful pet.  All the other dogs at Maison des Cotons are clear, and all, including Mongo, have passed CERF tests.  Mongo is now retired from our breeding program and spends his days intimidating Cesar.

New information from OptiGen as of May 21, 2007 --  A cheek swab DNA test has proved to be effective which makes testing much easier.  Owners can now collect DNA by swabbing the cheek with a foam swab and sending to OptiGen instead of having blood drawn at the vet.

New information from Sue Pearce-Kelling of Optigen as of December 7, 2007. 

Dear Ron,
    In conversations with Dr. Aguirre, I think the most important message that he would want to relay to the Coton community is to warn people to not exclude a good dog from a breeding program based solely on its CMR genotyping.  It is not at all uncommon to see a breed community that is dealing for the first time with definitive DNA test results (especially for health tests) to initially respond by excluding all Carriers and Affected animals from any breeding strategies.  In a relatively rare breed like the Coton, such a dramatic restriction in the gene pool can have (and in other breeds has caused) other undesirable, or more serious disease-causing, recessive traits to arise. The DNA test information should instead be looked at as providing information as just one of the factors a breeder considers when choosing a mate for their dog.  Although the disease associated with CMR is typically mild in the Cotons, it would still be advisable for people to choose breeding pairs that will result in no Affected pups (i.e. any Carriers or Affected dogs should only be bred to genetically Normal dogs.)
    I've just tallied the current testing results and this is how things stand as of December 2007:
Total number of Cotons tested (worldwide) =304.  Of these, 107 are from the USA
Total number of CMR Affected = 5 (all in the US)
Total number of CMR Carriers = 69 (38 from USA)

So this results in the following percentages:

List of CMR Tested Cotons

Although CMR is genetic and inherited, it is a general condition which may manifest differing degrees of
severity.  It is fine to breed carriers as long as the DNA of offspring is monitored.  Often it is not serious - that is,
it may be detectable by a CERF examination but may not progress or cause any loss of vision.  The DNA test is useful
because it can determine which Cotons are carriers.  Carriers exhibit no symptoms and in fact do not have CMR. 
They just have the potential to pass the genes on to their offspring.  If two carriers are bred, they may produce affected
offspring.  The DNA test is useful to breeders because it allows selection of a clear mate to a carrier, ensuring that
the condition is not passed on.  Continued responsible testing with breedable offspring ensures that CMR will not be
a significant problem in the breed.

The heroes and heroines of the Coton Community are those who test and make the information available.  Because
the DNA test and the information is available, no one needs to have any concern if any carriers or affected Cotons
appear in their Coton's pedigree.

The testing company, Optigen, reports that as of 12/7/07 304 Cotons have been tested with a few more in progress.
Five are CMR affected and 69 are carriers.  There is a range of expression of the disease.  In other breeds it has been
found that even though affecteds may not exhibit clinical signs (pass a CERF exam), offspring who are affected may
have more severe forms of the disease.

The following table lists only those dogs whose owners have submitted their results to ACC.  Optigen maintains an
anonymous database to protect the owners as is customary with research data.  This is why the total number of Cotons
tested is larger than appears here.  Some owners don't want to make the information about their dogs public.

We stress that carriers do not have and will never have the disease, they only carry the potential to pass it on. 
With the DNA test available, there is no need to be concerned and no need to remove either carriers or affected Cotons
from the gene pool.  Carriers can be bred to clear to produce clear offspring to carry on the lines.  Even affecteds
can be bred to clear.  Although their offspring are carriers, they can be bred to clear to produce clear Cotons to
carry on exceptional lines.

200 total as of 7/8/08     25 carriers = 13% carriers       0 affected   (these numbers only reflect dogs submitted
to this web site, not the total number of dogs tested nor the complete results tabulated by Optigen)

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