Make a page for your border collie.

Share border collie rescue stories.

Know about these dogs? Click EasyEdit to add info anywhere on this page.

Short History of the Breed

The Border Collie is one of the most versatile of the dog breeds. Originally called 'working collies' the word "Border" was gradually introduced to reflect its use on the sheep country along the border of Scotland and England.
The exact origin of the Border Collie is not known; most contend that it was a mixture of various sheepdogs, including the Scotch Collie, the Bobtail Sheepdog, the Bearded Collie and the Harlequin Collie. There is even some suggestion that various setters may have been involved or the Springer Spaniel. The outstanding herding ability of this breed of dog was soon recognised and lead to its spread throughout the pastoral regions of England. In fact it was in Northumberland which later produced the strain now famous throughout the whole world. In 1893, Adam Telfer, a farmer living in Otterburn, bred a dog called Old Hemp, which might be regarded as the foundation sire of the breed as it is now. Indeed, Hemp was early recognised as the very quintessence of the working sheepdog., and his services were in great demand. Not only did he produce some two hundred puppies before he died in 1901, but he seems to have been capable of transmitting his own prepotency to his offspring; with the result that Border Collie pedigrees are about as clearly defined as any in the livestock world. And today practically every sheepdog pedigree of note, not only in Britain but in all other parts of the word, had its beginnings in either Isaac Herdsman's "Tommy" or Thomas Armstrong's "Sweep", both early descendants of Hemp and both, like their noted forebear, bred in Otterburn.

The next important step was the formation in 1906 of the International Sheepdog Society, which rapidly was to become the leading organisation of its kind in the world. Mr James Reid was the secretary of the ISDS between 1915 -1947 and instituted the first Stud Book in 1955 by tracing back to the earliest pedigrees. The first entry in Reid's Stud Book was Old Maid, whilst entry no. 6 was Old Hemp.

Each year the Society is responsible for the promotion of the International Sheepdog Championships -held in England, Scotland and Wales in turn - and which attract attention throughout the world. It also keeps an accurate register of all Border Collies bred on orthodox lines, and its recent series of stud books traces the pedigrees right back to the early days of Hemp and his contemporaries.

Most of the greatest trial dogs were descended from him and through Moss who was exported to Australia and continued the same bloodlines here.

The earliest record of sheepdog trials was in 1873, where the black and white sheepdog began to be noticed. Although not at this time known as Border Collies, it seems the names "Border Dogs" and "Working Collies" were frequently used, gradually changing to Border Collies over the years. The pedigrees of the dogs in Mr. Reid's Stud Book, instituted in 1955, did not contain the word "Border", but he added "Border" in brackets on application forms for registration with the Sheepdog Society. However, they must have been known as Border Collies prior to this, as they were being registered and shown in Australia as this breed in the late 1940's.

One of the first exhibitors was Mrs Molly Cleary from Unanderra. She was also among the group of people who formulated the first Standard for the breed in N.S.W.

In 1963 the Australian National Kennel Control approved and adopted a Standard for the breed although, prior to this, individual States and their own Standards and were issuing Challenge Certificates.

The breed was also established in New Zealand and the USA but it was not until 1976 that the Border Collies was recognised as a breed for show purposes in the UK.

However, they are now firmly established as a most versatile and adaptable breed and are being show in ever-increasing numbers, whilst their numbers are increasing in the Obedience field - where they show a natural ability for this type of work, several of them having spectacular wins to their credit.

Physical Description & Size:

Border Collies have no standard in the herding world. They are generally a medium sized dog (25 to 50 pounds), with a short to long coat (smooth, medium, or rough), and a bright, lively appearance. Border Collies come in a variety of colors, with the classic being a black dog with a white blaze, collar, and feet. The Border Collie is an athletic dog, built for sustained hill work.

The AKC standard is the height at the withers varies from 19" to 22" for males, 18" to 21" for females. The body, from prosternum to point of buttocks, is slightly longer than the height at the withers with the length to height ratio being approximately 10:9. Bone must be strong, medium being correct but lighter bone is preferred over heavy. Overall balance between height, length, weight and bone is crucial and is more important than any absolute measurement. Dogs must be presented in hard working condition. Excess body weight is not to be mistaken for muscle or substance. Any single feature of size appearing out of proportion should be considered a fault.

Temperament:

In human terms, the Border Collie is an "A-type" personality; a dog who needs a job in order to be happy. A well bred Border Collie should have a stable temperament, when exercised and trained properly, will be a good canine companion.

Dog Care (exercise, grooming, diet):

Border Collies need an immense amount of exercise, both mental and physical. Daily walking (a few miles each day), running, ball playing, disc play, agility, flyball, or herding can exercise the body; trick training, obedience, and therapy work can exercise the mind. Be creative, a job can be almost anything you ask him to do!


Border Collie coats do not need specialized grooming; simply a good brushing once a week or so, and a bath when needed. No special trimming or shaping of the coat is called for, in fact, shaving the coat can cause the coat to never grow in properly thereafter.

A proper diet of a high quality kibble will help to keep a Border Collie happy and healthy.

Health Issues, Life Expectancy

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.


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%. Until very recently, the only way to know if a dog was a Carrier was for it to produce an Affected puppy. Since there are so many unknown Carriers, that meant there was no way to prevent inadvertantly producing Affected puppies. The ABCA, with support from other working Border Collie groups and owners, funded Dr Gregory Acland from the James A. Baker Institute for Animal Health, Cornell University, to develop a DNA test for CEA. That project was successful, and since the beginning of 2005 a test has been available which can determine whether a dog is Affected, a Carrier, or Clear. The test is being administered through OptiGen, LLC, and further details about it can be obtained on their website at www.optigen.com. The ABCA recommendations regarding CEA will shortly be updated in response to the availability of this new test and the statistical data so far gleaned from it.. In the meantime, the recommendations are as follows: --For owners of known Carriers (unaffected dogs that have produced a CEA affected puppy) - ABCA recommends that anyone who inquires about the dog's progeny or as a mate be told that it is a Carrier. It also recommends that people who have any of this dog's progeny be informed that all its offspring have at least a 50% chance of also being a Carrier even if the other parent is neither a Carrier nor Affected. -- For breeders of a litter in which one parent is a known Carrier - The ABCA recommends that all puppies in the litter have an ophthalmic examination by a DACVO by 12 weeks for accurate detection of "go normal" CEA. If this examination cannot be done, it is recommended that the puppy buyers be informed that they must determine from an ophthalmic examination that the dog is not affected with CEA before it is considered for breeding, as the progeny of affected dogs are not eligible for registration. --Do not breed two known Carriers together, as this will likely result in Affected puppies. --Do not breed CEA affected dogs. These dogs and their progeny are not eligible for registration with ABCA at this time.

Epilepsy 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 supporting research aimed at finding the gene(s) that may cause epilepsy in the breed. 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.

TNS Trapped Neutrophil Syndrome (also referred to as Hereditary Neutropenia) TNS is an inherited fatal immune disorder found in border collies. the Disease was first recognised by veterinarians, Frazer Allen and Boyd Jones in New Zealand, through assistance from breeder Judy Vos (Clan Abby). Although thought to have been around for a long time it is only recently that scientists have started to get a greater understanding of the way it works, it’s affects on the animal and mode of inheritance. The majority of this research has been done by Dr Alan Wilton and his team at the University of New South Wales in Australia.

Neutrophils are the precursors to white blood cells, produced in the bone marrow and, in a normal animal, released into the blood to fight infections. In a TNS affected animal these neutrophils cannot be released from the bone marrow so the animal is unable to mount an effective immune response to infection.

Symptoms can vary greatly, depending on which infections the pup happens to contract; it is because of this that the disease has been difficult to recognise in the past. There are still very few vets in the UK aware of this condition. Symptoms can be seen from as early as 2 weeks old. Affected pups are usually smaller than their siblings with slower growth rates and often appear to have a ‘weedy’ head and poorly conditioned coat. Other symptoms include vomiting and diarrhoea, inappetence, high temperatures/fever, swollen and painful joints and lameness.

Onset of symptoms frequently coincides with first vaccination since this is often the first challenge to a pups’ immune system. Live vaccines are designed to ‘mimic’ certain infections so that the pups’ immune system can produce antibodies against it and recognise it should it encounter the infection again in future. In a TNS affected pup of course this does not happen and the puppy will quickly develop the infection. It is important therefore that if a puppy is suspected of having the disease it does not receive any form of vaccination.

Up until recently diagnosis was difficult and involved invasive techniques. A pup displaying the clinical symptoms described above will usually be blood tested, a low neutrophil count would point to TNS but is not conclusive since other factors such as viral or bacterial infections may also cause this. A bone marrow biopsy is the best way to detect the disease, if the neutrophil levels in the bone marrow are higher than those in the blood it is an indication that these are trapped hence ‘trapped neutrophil syndrome’

Recently Dr Wilton and his team at UNSW announced a chromosome marker test for this disease; this test is able to detect the chromosome ‘carrying’ TNS in affected and carrier animals so it is now possible to obtain a diagnosis without using the invasive bone marrow biopsy technique. Research has shown that the mode of inheritance is recessive, so both parents must carry the gene to produce an affected pup. At this moment in time the marker test is only useful in suspected cases and close relatives of known affected/carrier animals. The research is ongoing to develop a full DNA test that can be used on ALL border collies so we can test all breeding stock and eradicate this disease from the gene pool.

If you think you may have an affected pup and would like to have it tested, please contact Dr Alan Wilton, he needs as many cases studies as possible to further his research.

The Border Collie Health Website now also contains a database of test results so far, as well as pedigrees of known affecteds. If your dog is related to any of these known carriers/affecteds you may be able to have it tested, please contact Dr Wilton for further information.

I also urge all those that have had dogs tested to PLEASE publish your results, good or bad; it’s only by sharing this information with each other that we can minimise the risks when planning matings and move towards eradicating this disease.

**Read Dr Wilton's latest Research Report **


Neuronal Ceroid Lipofuscinosis (NCL) NCL is often referred to as a disease that only impacts Australasian Border Collies. This is not true. We can only speculate that CL was believed to be associated with the Australasian Border Collies because CL was originally identified and diagnosed in Australia more than 25 years ago. However, since that time, in the United States, the Texas A&M University reported that it had diagnosed CL in several Border Collies located in Texas. Although the University never released the identity of those dogs, this occurred several years prior to the importation of any Australasian dogs to the United States. Therefore, these dogs had to be from American and/or British lines. Approximately 10 years ago, a Border Collie located in Great Britain died of CL. A post-mortem examination confirmed the diagnosis. Again, the identity of the dog was never released. However, the dog was known to be from 100% British lines. For more information and testing contact Dr. Alan Wilton.

The neuronal ceroid-lipofuscinoses (NCLs) are a class of inherited neurological disorders that have been diagnosed in dogs, humans, cats, sheep, goats, cynomolgus monkeys, cattle, horses, and lovebirds. Among dogs, NCL has been reported in many breeds, including English Setters, Tibetan Terriers, American Bulldogs, Dachshunds, Polish Lowland Sheepdogs, Border Collies, Dalmatians, Miniature Schnauzers, Australian Shepherds, Australian Cattle Dogs, Golden Retrievers, and other breeds. NCL is almost always inherited as an autosomal recessive trait. In humans, mutations in one of at least six different genes can lead to NCL. Mutations in several other genes have been found to be responsible for NCL in one or more animal species.

All of the NCLs have two things in common: pathological degenerative changes occur in the central nervous system, and nerve cells accumulate material that is fluorescent when examined under blue or ultraviolet light. Although neurological signs are always present in canine NCL, these signs vary substantially between breeds and can overlap with signs present in other neurological disorders. Until the gene defect responsible for NCL has been identified for a particular breed, a definitive diagnosis can only be made upon microscopic examination of nervous tissues at necropsy.

Our goal is to identify the mutation responsible for NCL in each breed where NCL occurs so that the disease can be diagnosed and carriers can be identified on the basis of a DNA-based test. To achieve this goal, we will first need to identify dogs from each breed in which NCL has been definitively diagnosed based on presently available criteria. The first step in identifying potentially affected dogs is for the owner or veterinarian to recognize signs that may be indicative of NCL and bring these dogs to our attention. Toward this end, we list below the signs of NCL that have been reported in the literature or observed in dogs we have examined in our clinics for each breed. Care should be used in relying only on the listed disease signs as these may be based on very few cases and incomplete information. In addition, more than one form of NCL can exist within a particular breed, as appears to be the case among Dachshunds.

Some progress has been made toward the above-stated goal. A mutation in CLN8 is responsible for NCL in English Setters (Katz et al 2005); a mutation in CLN5 is responsible for NCL in Border Collies (Melville et al 2005); and a mutation in CTSD is responsible for NCL in American Bulldogs (Awano et al, 2006). In addition, we recently discovered the mutation for a form of NCL in Longhaired Dachshunds (Awano et al., submitted for publication, 2006). The clinical onset of this Dachshund NCL is much earlier than the Dachshund NCL described in 1980 by Vandevelde and Fatzer, and the ultrastructural appearance of the storage bodies is different, indicating that the Dachshund NCL we studied is a distinct disease. We will publicize the identity of the mutant Dachshund gene as soon as a report of this discovery is accepted for publication in the scientific literature. DNA tests to identify affected, non-symptomatic carriers, and normal dogs are available for these breeds (see below). We are interested in samples from possible affected dogs in the other breeds listed below, or dogs of any breed suspected to have NCL. Please contact us if you suspect you may have an affected dog.

Registration

American Border Collie Association (ABCA)
American Kennel Club (AKC)

Genetics

Border Collie Coat Colors

Additional Resources
Border Collie - Online Community

www.mabcr.org

What is Rescue?

by Sarah Ruckelshaus
Executive Director and President of Mid-Atlantic Border Collie Rescue

What is Rescue??
res-cue v. to free from danger n. and act of deliverance. Rescuer n. (syn) liberate, release, deliver, deliverance, liberation.
That is Mr. Webster's definition and his synonyms. And, that pretty much describes what we do here in rescue.
In today's society, dogs (and cats) tend to be viewed as possessions, things that one acquires in order to fill a particular need. Once that need is filled (by marriage, children etc) that possession can be gotten rid of or forgotten as easily as it was acquired. That is where our work becomes necessary.
As rescuers, most of our job entails taking a neglected dog from his current situation, putting some TLC and training into him and then placing him into a permanent, loving home. We strive to educate the public about our charges before they are a 'problem' but often times we are too late as people tend to contact us only when they are at their wit's end with a dog and not before they have gotten that cute puppy who they 'just had to have'.

• We assess and pull dogs from shelters.
• We assess and pull dogs from homes where they are no longer wanted.
• We provide medical care for those dogs.
• We provide food and shelter for those dogs.
• We provide training and LOVE for those dogs.
• We provide education to the public.
• We provide education to prospective adopters.
• We find new homes for those dogs.
• We start over again.
• 
  

Border Collies on Wikifido

• Maddie, the Belgian Sheepdog/Border Collie Mix
• Spunky

• Tuxcitto
  

• David Duchovny and Blue
• Kingsley the Border Collie