The following educational articles are from The American Border Collie Website! To be considered a genetic disease, a health problem needs to have been demonstrated to be inheritable, that is, passed on through one or both parents. Some diseases have high heritability, which means if the genes are present, the individual will have the disease, and some diseases have low heritability, meaning both genetic and environmental factors are involved in whether the disease occurs. It is generally easier to control diseases with high heritability because all individuals with the genetic makeup for the disease can usually be identified. The term heritable disease should be distinguished from the term congenital disease, or problems that are present from birth, which may or may not be heritable.

 Border Collies are considered to be a generally healthy breed. However, as in all animals, there are some potential health problems. This information is presented to help both breeders and buyers to become more aware of some of the health and genetic issues in the breed at this time.

The primary genetic diseases currently thought to be a problem in the breed are as follows: Hip Dysplasia (HD) HD is by far the most prevalent known genetic disease that affects Border Collies. Factors that contribute to the development of HD ultimately cause the hip joint to be damaged. Joint damage called osteoarthritis, also known as degenerative joint disease (DJD) is manifested by cartilage and bone breakdown and irregular bony remodeling in response to stresses and inflammatory processes in the joint. DJD is, in effect, the identifiable result of factors that cause HD.

The standard for diagnosing HD at this time is still the front extended-leg view of the hips on x-ray such as that evaluated by The Orthopedic Foundation for Animals (OFA). OFA reports a 12.6% affected rate for Border Collies evaluated from 1974-2000. This HD incidence ranks them somewhere in the middle of the dog breeds. Pre-submission screening and selection for probable favorable OFA results by owners and their veterinarians very likely skews this percentage significantly to the low side. Therefore, the true incidence of HD is probably much higher, possibly as high as double the OFA figure. If true, this would mean, on average, one out of every four Border Collies has HD. 

Despite what some may claim, data from numerous scientific studies provide overwhelming evidence that HD is an inherited disease. It is thought to be caused by at least three and possibly as many as six primary genes. The number of genes involved, combined with the high incidence, means it's probable that most Border Collies are at least carriers of one or more of the genes that can contribute to the development of HD, even if they don't have the disease themselves. To confuse matters more, the expression of the disease is affected by environmental conditions such as the type and amount of food a dog gets at critical growth stages, as well as the type and amount of exercise and activity it gets. It must be remembered, however, that these environmental factors do not cause HD. They merely affect whether the HD genes present in that individual will be expressed to the fullest. Even if the expression of HD in a certain individual is suppressed by careful control of environmental factors, you have not changed the dog's genetic makeup. That dog will still pass on the genetic tendency for HD just as if it actually had the disease. Conversely, if a dog does not have the genes for HD, it won't develop the disease no matter how it's raised.

The possible incidence of one in four dogs may seem falsely high if the presence of HD is defined by dogs showing significant lameness.  The clinical symptoms of HD do not always correlate well with the severity of the disease as judged by radiological findings. Border Collies with HD that are fortunate enough to show few if any symptoms may have progeny that are not so fortunate.  The exact complex combination of genetic and environmental factors that contributed to an individual's lack of symptoms will not occur in its pups.  Therefore, it is important to remember that a high tolerance of an individual for the effects of HD does not mean that individual is suitable as a breeding prospect.

 The best way, at this time, to avoid producing puppies with a predisposition to develop HD is to test both parents and be aware of the hip status of other related dogs such as the parents' other progeny, the parents' parents, and the littermates and half siblings of the parents. The more tested, unaffected dogs there are in the pedigrees, the better the chances of producing unaffected pups. Unfortunately, even following the most stringent guidelines, puppies may still be produced that will develop HD. This does not mean there's no point in testing parents before breeding them. This line of false reasoning is akin to arguing that, because working parents will occasionally produce pups that won't work, there's no point in testing the working ability of breeding stock.

Selection for good hips will increase your chances of producing pups with good hips, but it's unrealistic to expect that puppies with HD will never be produced from tested, unaffected parents. Likewise, it is unrealistic to expect every dog who has ever produced a pup with HD to be banned from breeding. Since it's likely that most non HD-affected Border Collies are carriers of one or more of the genes for HD, most dogs will produce at least one pup with HD if bred enough times. Sooner or later, a cross with another carrier will produce the wrong combination of the HD genes and an affected pup will result. Given the incidence and complexities involved with HD in our breed, the recommendations at this time are to breed only hip tested, unaffected parents. Also, try to plan crosses having as many tested, unaffected dogs in the pedigrees of both parents as possible. If an affected puppy is produced from a cross of two unaffected parents, at the very least, don't repeat that particular cross because that affected puppy has proven that the two parents can together provide the right combinations of genes to create more puppies with HD.

The ABCA Health and Genetics Committee is investigating a promising new technique that measures several factors involved in the development of HD. This procedure involves taking hip x-rays on a sedated dog while the dog is in a kneeling position. This angle is favorable for identifying strengths and weaknesses in the hip joint in a more natural, weight-bearing position. This type of measurement is called a Dorsolateral Subluxation (DLS) measurement. ABCA is planning a study to evaluate this technique in 8-12 month old Border Collies.


Breed Rank Number of Evaluations Percent Excellent Percent Dysplastic

BORDER COLLIE 76 5726 11.4 11.3

BORDER COLLIE 60 597 98.8 0.8 0.5 0.2 0.2





http://www.offa.org/deafinfo.html p> http://www.offa.org/sainfo.html

CERF INFORMATION: http://www.offa.org/cerfdata.html THEIR WEBSITE: www.vmdb.org/cerf.html

NOTE THIS LINK: http://www.bordercollie.org/core.html


USBCC Newsletter, Summer 1994

A number of members have asked about the genetics of Hip Dysplasia. Should I refuse to breed my male dog to any bitch with less than Good or Excellent hips? How many dysplastic pups should I expect if one parent has bad hips? Should I breed a dog with severely dysplastic siblings? Does HD result from inbreeding? Unfortunately, the answer to all of these questions is "I don't know."

 As in most of genetics, breeding good hips is largely a matter of chance, or probability. Unlike more simple genetic traits, however, good (or bad) hips don't result from a single pair of genes. With a single pair, like the "red" genes I described in the last issue, the probability is easy to measure. We know exactly how many red pups, statistically, to expect from any combination. Hips, however, are affected by a large number of genes: some may be recessive like the b that causes red color; some may be dominant like the B that causes black. The problem is that we don't know how to identify any of them, and we have no idea how many there are. If we had hip measurements on all the members of hundreds of litters and their parents and offspring, we could make a start. We aren't even close.

The genetic situation goes something like this: there is some indication that HD might be caused by a combination of three different recessive pairs, call them aa, bb, and cc. Remember that every dog carries two copies of each gene and passes only one on to each pup. A dog that has the combination AaBbCc may pass on ABC, ABc, Abc AbC, aBC, aBc, or abc to any one pup. To form a single pair, again as in the case of the red dogs, the deleterious gene must be inherited from both parents. This would mean that mother and father would each carry at least one recessive copy of each of the three genes, and pass one of each to a particular puppy--that pup would then be dysplastic.

Other pups in the same litter might receive only one of each, or one a and one b and no c at all, or any of many, many combinations. The abc pup could pass all three to the next generation and produce dysplastic pups in turn if he is bred to another dog carrying all three recessives. The ab pup could never produce dysplastic pups because he doesn't have a copy of c. (He can only get one copy from each parent) All these genetic combinations, and others, could occur in the same litter. It is also possible, though, that the genes which in combination produce hip dysplasia are dominant--A, B, and C. In this case, only one copy of each is necessary, and each one would only have to come from one parent.

A dysplastic dog, AaBbCc, could easily pass all three to one or more puppies in a litter, with no genetic help from the other parent. We all know that two perfectly "normal" dogs can produce dysplastic pups. How is this possible? If the genes are recessive, this would be the common genetic condition, exactly as two black dogs can produce a red puppy. If they are dominant, one parent may carry, say, A and B; the other may carry only C. Neither parent has the combination that creates dysplasia. Together, they may pass on to one or more puppies the three dominant genes that make bad hips.

The probability of creating recessive combinations (aabbcc) is greater if there is a lot of inbreeding. Genes follow family lines and the same ones are simply more likely to be found in other members of the same lines. The chance of combining several independent genes (ABC), however, is greater in cases of outbreeding. No matter how many times you introduce into a pedigree a family line carrying A and B, dysplasia will not occur unless you outcross to a family carrying C.

Since we have no way of recognizing any of these until they come together, we can't know what lines to avoid crossing--until it happens. Certainly, if a particular pair of dogs produces a dysplastic puppy, we know the possibility is there; the combination shouldn't be repeated. Unfortunately, of course, we don't know until the puppy has grown up. In either case--and I stress that both are hypothetical and that the truth is probably more complicated than either--the severely dysplastic dog should not be bred.

I hear breeders say that a really good working dog should be used anyway, and the problem sorted out in later generations. It is exactly the really good dog with really bad hips that is the greatest danger. If he produces a lot of top quality trial dogs and enters the pedigrees and the major bloodlines of the breed, his dysplastic genes will be spread throughout the breed. Sooner or later, his descendants will begin to be bred back to each other. If the genes are recessive, we know what multiple linebreeding can do--that's why Wiston Cap has given us an increase in red dogs. If they are dominant, you have created a line in which all three dominant genes are rattling around. From time to time a descendant of our AaBbCc dysplastic dog carrying only A and C will be bred to a descendant carrying B or maybe A and B. This pair is going to produce some pups with bad hips. The more crosses there are in your pedigree back to this ABC dog, the higher the probability that the three genes will come together. Actually, for all the excuses we use for the high incidence of dysplasia (it's the pet/obedience owners; we're feeding them too much, etc) the usual cause for a high frequency of a detrimental gene in a breed is that it occurred in an extremely popular sire whose genes are now everywhere in the breed.  


Collie Eye Anomaly (CEA) CEA is a congenital disorder where the parts of the eye, particularly the retinal area, do not develop normally. The severity of the disease ranges from no visual impairment to blindness. It is not a progressive disease and affected dogs normally only have mildly impaired vision. Puppies should be tested before 12 weeks of age, if possible, by a Diplomate of the Association of Canine Veterinary Ophthalmologists (DACVO) because some dogs have a mild form of the disease called "go normal", where normal tissue grows over and covers up the diseased area as the dog matures. Identification of "go normals" is important, as these dogs are affected with CEA and will produce affected puppies just as if they had full blown expression of the disease.


This disease is much more straightforward than HD in both its inheritance patterns and in our ability to control it. CEA is an autosomal recessive disorder. Autosomal means it is passed on and expressed equally in males or females. Recessive means a dog may carry a bad CEA gene and pass it on to its offspring without having the disease itself. A dog is defined as Clear if it has no bad CEA genes. A dog is defined as a Carrier if it has one bad CEA gene and one normal gene. Both the Carrier and the Clear dogs will be unaffected and will test negative for CEA in the eye exam. A dog is defined as Affected if it eye tests positive for CEA. The outcomes of the different crosses of these dogs are as follows:


Clear X Clear = 100% CEA Clear puppies

Clear X Carrier = on average, 50% Clear, 50% Carriers

Clear X Affected = 100% Carriers

Carrier X Carrier = on average, 25% Clear, 50% Carriers, 25% Affected

Carrier X Affected = on average, 50% Affected, 50% Carriers

Affected X Affected = 100% Affected


The incidence of CEA in Border Collies in North America is about 2.5%. The carrier rate is probably ten times that figure, or 25%. The problem in controlling the disease at this time is that the only way to know if a dog is a Carrier is for it to produce an Affected puppy. Since there are many unknown Carriers out there, Affected puppies will inadvertently be produced until we have a better way to test for Carriers.  

The ABCA, with support from other working Border Collie groups and owners, has funded Dr Gregory Acland from the James A. Baker Institute for Animal Health, Cornell University, to develop a DNA test for CEA. This test will identify the CEA clear dogs (those with no bad CEA genes). The test is now available!

Epilepsy is a disease characterized by seizures or "fits" as they are sometimes called. Although it's clear Border Collies can be affected with epilepsy, the incidence and heritability in our breed are unknown. The ABCA is conducting a health survey to determine the extent of this problem in the breed. Please help us in this effort, whether you have an affected dog or not, by responding to the health survey on ABCA's web page listed below. Since there can be many causes, determining why a dog has seizures is a complex process. The diagnosis of primary epilepsy is made based on negative results for other causes of seizures. Therefore, it is a diagnosis made by exclusion rather than by a specific test. Since we have little breed-specific information to go on, ABCA breeding recommendations concerning this disease are based on those for other affected breeds in which the disease is more well-defined. Recommendations are: Do not breed affected dogs. If two unaffected dogs produce an affected puppy, do not repeat that cross.
Genetic diseases not considered to be a significant problem in the breed at this time!


If you are interested in this study, please reply to this message and I will
send you an official letter and a form which should be included with the
bloodwork. These documents were sent to me by Alison Ruhe from UC Davis.

The files are also on that YahooGroups file section (you must have a YahooID
to log in on the web): http://groups.yahoo.com/group/BCSA_Announce/files/

Genetics of Idiopathic Epilepsy in Border Collies

Idiopathic epilepsy is a complex disease that defies simple inheritance. The
underlying genetic defect does not appear to determine the disease, but
rather to predispose dogs to recurrent seizuring. Thus, some dogs with the
genetic defect might never show clinical signs of seizures.

The complexity of epilepsy in dogs necessitates a unique approach, one that
emphasizes distantly related dogs that are definitively affected. If a
sequence of DNA is shared identical by descent among all affected dogs, but
is present at a much lower frequency among unaffected control dogs, then the
DNA is likely to harbor the defect causing epilepsy.

To discover such a region, our laboratory is currently collecting blood
samples from as many Border Collies as possible. We have collected blood
from both affected and unaffected dogs, but additional samples are needed to
improve the statistical power and the mapping resolution. Toward this end,
we invite breeders and owners to participate by contributing a blood sample
from any registered Border Collie. As with all academic research, complete
confidentiality is strictly maintained.

To include a dog in our study, we must obtain at least 3 mls of blood. This
can be shipped directly to our laboratory at our expense using the Federal
Express account number and address provided below.

Please direct any inquiries to Dr. Mark Neff at (530) 752-1381.

Federal Express Account # 2527-7516-1 (Please send STANDARD overnight)

Most veterinarians have been most helpful and are willing to waive blood
draw charges for a research project, but if payment is necessary please
contact us we may be able to reimburse up to $15/draw.

Send blood sample to:
c/o Katy Robertson
DNA Collection
Center for Veterinary Genetics
UC Davis School of Veterinary Medicine
Davis, CA 95616-8744
Please refer to the BCSA web site, for permanent club information: http://www.bordercolliesociety.com/
PROGRESSIVE RETINAL ATROPHY (PRA)! PRA is a progressive disease where tissue in the retina of the eye is destroyed. It may initially be noticed as decreased ability of the dog to see at night, and may eventually progress to total blindness. Despite the persisting impression that this genetic disease is prevalent in the breed, extensive investigation has shown the incidence of PRA in Border Collies in North America to be extremely low to non existent. Therefore, the American Border Collie Association does not currently consider it a major health concern. Elbow dysplasia is a general term used for what is essentially three different types of degenerative elbow disease. These diseases may occur singly or together and are thought to be caused by several different genes. More and more owners are having their Border Collies' elbows evaluated each year. However, OFA reports a 0% incidence of elbow dysplasia for 210 Border Collies tested from January 1974-December 1999. ABCA does not consider elbow dysplasia a significant health problem in the breed at this time.
Common diseases with questionable heritable causes
OSTEOCHONDRITIS DISSECANS (OCD) OCD is a condition that occurs primarily in puppies between the ages of 4-9 months, but can also be found in older puppies. It is considered to be a common disease in rapidly growing dogs of large breeds. However, medium breeds such as the Border Collie can also have a high incidence of this disease. It is seen twice as often in males as in females. The shoulder joint is the most commonly affected site but it can be seen in stifles, elbows, hocks or other joints. The diagnosis is usually confirmed by x-ray of the involved joints.  In approximately one third of the cases of OCD, the disease is bilateral (in both joints). Occasionally, it is present in several different joints in the same individual. OCD is thought to be caused by a problem in the growth rate of the joint cartilage relative to the underlying subchondral bone. Although the factors that cause OCD are not completely understood, direct factors considered to be involved in the development of OCD are rapid growth and trauma to the joint. Indirect factors affecting rapid growth include nutrition, hormones, and genetic predisposition to rapid growth and large size. Indirect influences that may lead to increased trauma to the joint include conformation and behavior, which are also influenced by heredity. Therefore, the genetic link for most types of OCD is considered to be indirect, that is, an inherited tendency. Certain sites for OCD lesions, such as the elbow, appear to have a greater direct genetic contribution and a higher heritability than other sites, such as the shoulder. The most important contributing factor in OCD of the shoulder, the most common site, is thought to be trauma. OCD can best be prevented in growing puppies by controlling the main precipitating factors, overnutrition and activities that could result in injury to the joints. Because factors involved in the heritability of OCD are considered to be indirect, and therefore not easily controlled by selection, ABCA has no breeding recommendations for OCD at this time.




CANINE EPILEPSY - ... Kidney disorders; Liver disorders; Infections such as canine distemper; Tumors; Toxins, like antifreeze, lead, or chocolate; ... Types of seizures. ... http://www.swiftwaterfarms.com/swiftwater/p21epilepsy.htm Canine Epilepsy - ... Canine Epilepsy By Pam Bethurum, ASCA Educational Coordinator. Canine epilepsy is characterized by "fits" or seizures. Seizures are not always hereditary. ... http://www.asca.org/Education/Advanced/epilepsy.htm brain diseases - ... Canine seizures. This brief ... Acrobat Reader. Please note that this document covers canine seizures in all breeds of dog, not just Dalmations. ... http://vetgate.ac.uk/browse/cabi/c35ef09d22a7dbeee24cfc11f5fb3068.html Dr. Barbara G. Licht - ... Current work in our lab includes the development of a system to classify canine seizures. Classification of seizures is important ... http://www.psy.fsu.edu/faculty/blicht.dp.html Seizure Disorders - ... Affiliated with the Veterinary School at the University of Missouri at Columbia, this site reviews canine seizure disorders, treatment, history and more. ... http://www.marvistavet.com/html/body_seizure_disorder.html Wauu.DE: Health: Animal: Pets: Dogs: Conditions and Diseases ... - ... Canine Epilepsy - Diagnosis and Treatment Learn about canine epilepsy, canine seizures, and medications to contol seizures in dogs. ... http://www.wauu.de/Health/Animal/Pets/Dogs/Conditions_and_Diseases/Epilepsy/ Canine Epilepsy - ... Since only 0.5 to 5.7 percent of the general canine population has seizures in their lifetime, these results strongly suggest the epilepsy in the offspring of ... http://clubs.akc.org/nntc/health/epilepsy.html http://www.sailormoonworld.ru/phenobarbital/in/treating/canine/pituitary/tumor/seizures/ Diseases or defects in Dogs - Chinaroad Lowchens of Australia - - ... Clinical & Genetic Advances - Canine Epilepsy. Canine Seizures. Commonly Asked Questions Regarding Epilepsy & Treatment. Idiopathic Canine Epilepsy. ... http://www.lowchensaustralia.com/health/diseases.htm The Natural Canine: Epilepsy - Epilepsy is not a single disease. It is intermittent, repeated seizures with an unknown cause. ... Seizures can occur in dogs of all ages. ... http://www.naturalcanine.com/Merchant2/merchant.mv?Screen