General

The Shetland Sheepdog, often known as the Sheltie, is a breed of herding dog. They are small to medium dogs, and come in a variety of colours, such as sable, tri-color, and blue merle. They are vocal, excitable, energetic dogs who are always willing to please and work hard. They are partly derived from dogs used in the Shetland Isles for herding and protecting sheep. The breed was formally recognized by The Kennel Club in 1909.

The Shetland Sheepdog's early history is not well known. Although of obscure origin, the sheltie is probably a descendant of small specimens of the Scottish Collie and the King Charles Spaniel. It was developed to tend the diminutive sheep of the Shetland Islands, whose rugged, stormy shores have produced other small-statured animals such as the Shetland pony.

Today it is raised as a farm dog and family pet. They were originally a small mixed-breed dog, 330 mm in height and it is thought that the original Shetland herding dogs were of Spitz type, and were crossed with collie-type sheepdogs from mainland Britain. In the early 20th century, James Loggie added a small Rough Collie to the breeding stock, and helped establish what would become the modern Shetland sheepdog. The original name of the breed was Shetland Collie, but this caused controversy among Rough Collie breeders at the time, so the breed's name was formally changed to Shetland Sheepdog.

Unlike many miniature breeds that resemble their larger counterparts, this breed was not developed simply by selectively breeding the Rough Collie for smaller and smaller size. The original sheepdog of Shetland was a Spitz-type dog, probably similar to the modern Icelandic Sheepdog. This dog was crossed with mainland working collies brought to the islands, and then after being brought to England, it was further extensively crossed with the Rough Collie, and other breeds including some or all of the extinct Greenland Yakki, the King Charles Spaniel (not the Cavalier), the Pomeranian, and possibly the Border Collie. The original Spitz-type working sheepdog of Shetland is now extinct, having been replaced for herding there by the Border Collie. The Shetland Sheepdog in its modern form has never been used as a working dog on Shetland, and ironically it is uncommon there.

When the breed was originally introduced breeders called them Shetland Collies, which upset Rough Collie breeders, so the name was changed to Shetland Sheepdog. During the early 20th century (up until the 1940s), additional crosses were made to Rough Collies to help retain the desired Rough Collie type – in fact, the first AKC Sheltie champion's dam was a purebred rough Collie.

The year 1909, marked the initial recognition of the Sheltie by the English Kennel Club, with the first registered Sheltie

being a female called Badenock Rose. The first Sheltie to be registered by the American Kennel Club was "Lord Scott" in 1911.

The general appearance of the Sheltie is that of a miniature Rough Collie. They are a small, double coated, working dog, agile and sturdy. Blue merle Shelties may have blue eyes or one brown and one blue eye, but all others have dark coloured eyes. Their expression should be that of alertness with a gentle and sometimes reserved nature. They are often very good with children. They carry their tail down low, only lifted when alert and never carried over the back. They are an intensely loyal breed, sometimes reserved with strangers but should not be too shy.

Shelties have a double coat, which means that they have two layers of fur that make up their coat. The long, rough guard hairs lie on top of a thick, soft undercoat. The guard hairs are water-repellent, while the undercoat provides relief from both high and low temperatures.

The English Kennel Club describes three different colours: tricolour, blue merle, and sable (ranging from golden through mahogany), marked with varying amounts of white and/or tan. Essentially, however, a blue merle dog is a genetically black dog, either black, white, and tan (tricolour). In the show ring, blue merles may have blue eyes; all other colours must have brown eyes.

Basic coat colours

Sable – Sable is dominant over other colours. May be pure for sable (two sable genes) or may be tri-factored or bi-

factored (carrying one sable gene and one tricolour or bicolour gene). Tri-factored sable and shaded sable are not

interchangeable terms.

Tricolour – black, white, and tan. Tricolour is dominant over bi-black. May be pure for tricolour (2 tri genes) or may be

bi-factored (carrying one tricolour gene and one bicolour gene).

Bi-black – black and white. Bi-black is recessive. A bi-black Sheltie carries 2 bi-black genes; thus, any dog of any other

colour with a bi-black parent is also bi-factored.

"Modified" coat colours

Any of the above colours may also have a colour modification gene. The colour modification genes

are merling and white factoring. Merling dilutes the base colour (sable, tricolour, or bi-black) causing a black dog's

coat to show a mix of black, white, and gray hairs, often with black patches.

Blue merle—blue, white, and tan. A tricolour with the merling gene. May have blue eyes.

Bi-blue—blue and white. A bi-black with the merling gene. May have blue eyes.

Sable merle—faded or mottled sable and white. Often born with a mottled coat of darker brown over lighter brown, they usually present as a faded or lighter sable or can appear as a washed out blue-merle. Sable merles are shown in the breed ring as sables.

White factoring affects the amount of white on the dog. It is hard to tell, without actually breeding, whether a dog is white-factored or not, though dogs with white going up the stifle (the front of the hind leg) are usually assumed to be white-factored. Breeding two white-factored dogs can result in colour-headed whites—Shelties with coloured heads (sable, tricolor, bi-black, or blue or sable merle) and white bodies. For show dogs, dogs with more than 50% white are heavily penalized and thus are not shown in the breed ring; they are normal in every other way.

Double merles, a product of breeding two merle Shelties together, have a very high incidence of deafness and/or blindness.

There have been reports of a brindle Sheltie, but many Sheltie enthusiasts agree that a cross sometime in the ancestry of that specific Sheltie could have produced a brindle. Unacceptable colours in the show ring are a rustiness in a blue or black coat. Colours may not be faded, no conspicuous white spots, and the colour cannot be over 50% white.

Shelties normally weigh around 5–11 kilograms. In general, males are taller and heavier than females. Accepted height ranges may differ depending on country and standard used. KUSA specifies a male’s height as 37cm ± 2½ cm at the withers, and a female’s height as 36cm ± 2½ cm, however, some shelties can be found outside of these ranges but are not considered truly representative of the breed.

To conform to the breed standards, the Shelties' ears should bend slightly or "tip", this contributes to the "proper

Sheltie expression. The ear is to have the top third to a quarter of the ear tipped. Wide-set (too much distance between) ears are also not a desired trait, nor are ears which tip too low down.

Shelties have a double coat, and often shed a lot of the time, no matter the season. The top coat consists of long,

straight, water-repellent hair, which provides protection from cold and the elements. The undercoat is short, furry, and very dense and helps to keep the dog warm. Mats can be commonly found behind the ears, under the elbow on each front leg, and in the fluffy fur on the hind legs, as well as around the collar. The coat is usually shed twice a year. Females will also shed right before or right after giving birth. Male shelties technically shed less than females but fur still comes off constantly. Shaving these dogs is very bad for their skin and some do not regrow any significant amount of hair after being shaved, a condition known as alopecia. Spaying or neutering can alter coat texture, making it softer, more prone to matting and even more profuse. It should be noted that Shelties shed in clumps which can be pulled or brushed out of the main coat, rather than individual hair. This makes them much easier to groom and clean-up after than many smooth-haired dogs, which leave loose fur in their space.

Shelties have a high level of intelligence. According to Dr. Stanley Coren, an expert on animal intelligence, the Shetland sheepdog is one of the brightest dogs, ranking 6th out of 132 breeds tested.

Health

For the most part, Shelties are athletic and healthy. Like the Rough Collie, there is a tendency toward inherited

malformation and disease of the eyes. Each individual puppy should have his eyes examined by a qualified veterinary ophthalmologist. Some lines may be susceptible to hypothyroidism, epilepsy, hip dysplasia, or skin allergies.

Compared to other dogs, Shetland Sheepdogs have a four-fold increased risk of developing transitional cell carcinoma, a cancer of the bladder.

Dermatomyositis may occur at the age of 4 to 6 months, and is frequently misdiagnosed by general practice veterinarians as sarcoptic ordemodectic mange. The disease manifests itself as alopecia on the top of the head, supra- and suborbital area and forearms as well as the tip of the tail. If the disease progresses to its more damaging form, it could affect the autonomic nervous system and the dog may have to be euthanised. This disease is generation-skipping and genetically transmitted, with breeders having no clear methodology for screening except clear bloodline records. Deep tissue biopsies are required to definitively diagnose dermatomyositis.

Von Willebrands disease is an inherited bleeding disorder. In Shelties, affected dogs as a general rule are not viable and do not live long. The Sheltie carries type III of von Willebrands, which is the most severe of the three levels. There are DNA tests that were developed to find von Willebrands in Shelties. It can be done at any age, and it will give three results: affected, carrier and non-affected. Shelties may also suffer from hypothyroidism, which is the under-functioning thyroid gland. It is an Autoimmune disease where the immune system attacks the thyroid gland. Clinical symptoms include hair loss or lack of coat, over or under-weight, and listlessness.

Although small breed dogs are not usually plagued by hip dysplasia, it has been identified in Shelties. Hip dysplasia

occurs when the head of the femur and the acetabulum do not fit together correctly, frequently causing pain and/or lameness. Hip dysplasia is thought to be genetic. Many breeders will have their dogs' hips x-rayed and certified .

The two basic forms of inherited eye diseases/defects in Shelties are Collie eye anomaly (CEA) and progressive retinal atrophy (PRA).

Collie eye anomaly: An autosomal recessive inherited trait which results in incomplete closure of the embryonic fissure; seen almost exclusively in Collies, Border collies and Shetland sheepdogs. CEA can be detected in young puppies by a veterinary ophthalmologist. The disease involves the retina. It is always bilateral although the severity may be disparate (unequal) between eyes. Other accompanying defects (ophthalmic anomalies) may wrongly indicate a more severe manifestation of CEA. CEA is present at birth and although it cannot be cured, it doesn't progress. Signs of CEA in shelties are small, or deepset eyes. That is, the severity of the disease at birth will not change throughout the dog's life. CEA is scored similar to the way hips are.

CEA is genetic, inheritance is autosomal recessive, this means that even a dog that shows no phenotypic signs of the condition may be a carrier. Breeders should actively try to breed this disease out by only breeding with dogs that have "clear" eyes or very low scoring eyes. A CEA score considered too high to breed with may still be low enough not to affect the dog's life. These dogs live happy and healthy lives as pets but should be not used for breeding. The recent development of a DNA test for CEA makes control of this disease much more likely as more breeders take advantage of the test.

PRA can be detected at any time but usually does not show up until the dog is around two years of age. Breeding dogs should be tested for genotype for this condition before breeding and only animals found "clear" should be used for breeding. PRA can occur in most breeds of dog including mix breeds. In Most breeds it is also an autosomal

recessive condition, however it has been found in other breeds to be autosomal dominant and sex-linked in others. As the name suggests, it is a progressive disease which will eventually result in total blindness. Like CEA, an affected dog should not be bred with but these dogs can live happily as pets. Currently there is no treatment for either disease, but as both diseases (CEA and PRA) are hereditary it is possible to eliminate them using selective breeding.

MDR1 Gene Mutation - According to the College of Veterinary Medicine at Washington State University, the Shetland Sheepdog, and many other herding breeds, have a risk of being born with a MDR1 Gene Mutation, with about 15% of individuals affected. Cross-breeds are also affected. Dogs carrying Mdr1-1 share a common ancestor that experienced remarkable evolutionary success, having contributed genetically to at least nine distinct breeds of dog. Due to this genetic mutation, affected dogs may exhibit sensitivity or adverse reactions to many drugs. including Acepromazine, Butorphanol, Doxorubicin, Erythromycin, Ivermectin, Loperamide, Milbemycin, Moxidectin, Rifampin, Selamectin, Vinblastine, and Vincristine.

Work & Dog Sports

As the name suggests, Shelties can, and have been, used as sheepdogs and still participate in sheepdog trials to this day.

Herding dogs conduct livestock from one place to another by causing fear-flocking and flight behaviour. The instinct to herd is primarily a product of breeding. No amount of training can substitute this trait.

In their size group, the breed dominates dog Agility, Obedience, Conformation, Flyball, Tracking, and Herding.  

Those of us who are keen readers of as many books on The Shetland Sheepdog as we can lay our hands on, must be aware of how the Sheltie has changed since it was the little dog, working in all weathers on the Islands to look after the sheep belonging to his Master and the Family. The climate of the Islands was cold and bleak in the long Scottish winters, so this dog although small, was strong because he had to withstand all extremes of weather and intelligent because of the work he must do. The early pictures show us a small, fairly long haired dog, with an almost Border Collie type head and some have been described as 'pommie' because of their rounded skulls, deep stop and short muzzles.

It is not really known exactly when the Sheltie has it origins, but in the very early 1800's they were thought to be a type of small working Collie which had been crossed (mostly by accident!) with the Icelandic Dog bought from Iceland on the fishing boats visiting the Shetland Islands. It has also been suggested that there may be some crossing with the Cavalier King Charles spaniel, but most of this information is sketchy and not actually proven. What is known however, is that a Mr. J Loggie who was one of the first Sheltie enthusiasts from the islands took the rather courageous step of introducing a small show Collie into the breed. This he did to establish a definite type, up until that time the little dog tended to appear as a variety of types, sometimes with a head which resembled a spitz type of dog, with pricked ears, or sometimes with a head of more rounded appearance, with a round eye to match! Apparently the actions of Mr. Loggie caused some concern amongst the Sheltie fanciers of that time, but it has since been acknowledged that it was probably one of the best things to happen.

Little was known on Mainland Britain of the Shetland Sheepdog until 1906 when the first Shelties were shown at Cruft's Dog show. Two years after that the Shetland Collie Club was founded in Lerwick, the capital of the Shetland Islands, then in 1909 the Club asked the Kennel Club for permission to change the name of the breed to Shetland Sheepdog, but this was refused. The breed was at this time, rather smaller than the present day - in 1909 the standard described them as "a Collie in miniature, height to be about 12 inches" and at this time there were two varieties, rough and smooth.

By 1909, the breed was becoming fairly popular both as a pet and a showdog and several societies were scheduling classes on the Mainland, although people were quite confused about the different types still to be seen in the ring.

1914 was a turning point for the breed with the formation of the English Shetland Sheepdog Club in January, then in August of the same year the Kennel Club gave the breed it's official recognition as a separate breed and gave it the name Shetland Sheepdog. The following year Challenge Certificates were offered and a year later the first breed champion emerged - Ch. Woodwold. Due to the World War which was raging during these important first years, little breeding and showing was done and by 1917 the breed was facing almost extinction. Miss Humphries of the Mountfort prefix, decided that it was time for another Collie cross as type seemed to be varied again, so the introduction of a small Collie bitch, Teena who was mated to a dog called Wallace seemed to set the foundations for the type which we know today. Miss Humphries made no secret of her Collie cross and most breeders accepted that in order to establish a definite type, this was necessary.

1924 saw the last of the necessary Collie crosses, this time a bitch, Chestnut Sweet Lady was mated to Chestnut Rainbow, a tricolour Sheltie and the result was eight puppies. This was to be one of the most important litters in the breeds modern day history, as one of the puppies, Chestnut Bud was sold to Jim Saunders of the Helensdale prefix and Bud was behind many of the famous Helensdales. Four puppies were sold to Dr. Margaret Todd of the Clerwood prefix, and the smallest puppy was bought by Mrs. E. Baker of the Houghton Hill prefix. This dog was the sire of Ch. Uam Var of Houghton Hill, one of the most important sires in those years leading up to the Second World War. Mrs. Sangster of the Exford prefix was the daughter of Mrs. Baker, so the Exfords had the good foundation of the Houghton Hills on which to build. The Exfords and a few years later, the Riverhills, were already established before the war, but were to become probably the most well known kennels of the post war years.

The entries of Shelties at shows during the late forties and fifties steadily increased, with more and more people finding the charms of the Sheltie hard to resist. Pictures of the Riverhills of this period show us the wonderfully balanced heads with flat skulls together the correct shape and placement of the eyes which makes the expression that is exclusive to the Sheltie. The Misses Rogers were very keen horsewomen and so construction and movement was a very important item on their breeding agenda as they knew the pitfalls of breeding animals with bad construction. The Exford Shelties were also very famous for their excellent construction and movement. They lived in the New Forest - a large area of natural forest in the South of England. They had the total freedom of the forest and used to accompany Mrs. Sangster when she rode her horses out on their daily exercise, so the Exfords had to be able to keep up with a galloping horse for many miles. 

The fifties and early sixties saw a huge increase in the popularity of the breed, not always a good thing because there is a danger of any breed becoming commercialised. The influence of the pre war kennels was, by this time, very important and the newer breeders who were keen to learn tended to attach themselves to the experienced people.

In the show ring during this period of time, very little importance was paid to temperament - the breed standard stated that the dog should be "reserved towards strangers" and I think this was taken literally. I can remember going to shows in the early sixties and watching some of these really beautiful dogs standing behind their owners legs while they were being judged, with the owners hardly noticing. Most of the championship show judges were breed specialists and were used to this kind of behaviour so paid very little attention.

The dog that turned this situation around (in my opinion) was Ch. Antoc Sealodge Spotlight. A most beautiful Sheltie to look at in profile, he had a lovely shape with a super neck and topline, well-balanced head with the neatest of ears which he never stopped using. He hadn't got the best front angulation in the world, but he was of outstanding quality and correct breed type. He was also a magnificent showman, totally in tune with his handler, and it was very obvious that he really enjoyed being a show off!! He took the eye of several all breeds judges, which previously a Sheltie had been unable to do (with the exception of Ch. Helensdale Ace). This then made the newer breeders sit up and take notice, realising that not only did they have to aim to produce Shelties of the right size, with correct heads and construction but they must also do something to improve the temperament.

It was quite an uphill struggle. So many of the larger kennels kept Shelties in vast numbers which meant they were unable to give the dogs the individual attention that they required to improve their temperaments. As the larger kennels also had the stud dogs which were influencing the breed at that time, it was difficult to plan a breeding programme when type, quality and now temperament was the consideration. Sadly Spotlight who was mainly Riverhill bred, was discovered to be infertile after siring just a few litters - his breeding and outstanding temperament would have been invaluable to many people, but it was not to be.

By the end of the sixties, Shelties were being bred by people who kept just a few dogs in the house, which meant that the dogs were very much part of the family, mixed with the children, saw all the visitors and were beginning to become much more sociable. However, with the increase in the number of Shelties being bred and shown, came a decline in the quality of the puppies being produced. People were taking less notice of the advice of the experienced breeders and were producing Shelties without thinking of the future generations. Temperament of course, was improving, but bad faults were creeping in, like straight shoulders and upper arms, also Shelties which were well over the size limit. Breeders were breeding from bitches of inferior quality and mating them to stud dogs who were popular and winning well at the time, without thinking whether or not the pedigrees of each were compatible.

Then came CEA!! Up until this time the only eye disease we had heard of was PRA and this didn't really affect the Sheltie. Then Dr. Keith Barnett who was the leading authority on animal eyes in this country visited America and came back with the disturbing news of this new disease which had been discovered in Shelties there. Everyone breeding Shelties was encouraged to have all their dogs tested. Some did and some decided it was best not to know, so without making testing compulsory it was very difficult to establish any kind of pattern of how the disease was, or was not progressing in the U.K. Most of the newer breeders tested, but the pre war people decided that it was best to leave well alone. 

By the mid seventies, more testing was being done and a pattern of affected lines was emerging, which meant some of the top stud dogs were no longer being used by so many people. This led to quite a variation in type and quality again, as breeders were tending to use clear dogs irrespective of their pedigree or suitability. Of course, much discussion followed on this subject, whether or not we should concentrate mainly on eradicating CEA or push CEA to the side and breed for the correct type.

During the eighties, the breed lost the influence of some of the top kennels, Riverhill, Shelert and Exford being the main ones. With their demise the breed had not only lost some outstanding Shelties, but the knowledge and experience of their breeders went with them. It is a well known fact that with age and experience comes wisdom and knowledge, so the breed had then to rely on those who had taken the trouble to learn and benefit from the teachings of these knowledgeable people.

Some new names have emerged in the late eighties and nineties, some have fallen by the wayside, others have proved to be beneficial to the breed by breeding for correct type and quality. Sadly type is still varied, but this is bound to happen when so many people are breeding, and do not have the experience to know exactly what is meant by the correct type. It is the responsibility of every breeder and judge to concentrate on this true Sheltie type and as we go into the next century we can only hope that everyone understands the importance of doing this, thus keeping the Sheltie as our standard describes it "a small long haired working dog of great beauty"

It is true to say that over the years there have been changes in the appearance of the Sheltie, but the last forty years have seen the improvement of the temperament which has to be an asset. We now have to safeguard the breed and not allow it to become a tool for ambitious people who are looking for a quick way to the top and who care nothing for the well being and future preservation of the correct type.

Collie Eye Anomaly (CEA)

 Collies share Collie Eye Anomaly (CEA) with several other breeds ie the Sheltie. CEA is more technically known as Choroidal Hypoplasia (CH). It is a recessively inherited eye disorder that causes abnormal development of the choroid - an important layer of tissue under the retina of the eye.

Since the choroid layer does not develop normally from the start, the primary abnormality can be diagnosed at a very young age. Regrettably, there is no treatment or cure for CEA.

 The primary problem is choroidal hypoplasia (CH). There is under-development (hypoplasia) of the eye tissue layer called the choroid. The choroid appears pale and thin, almost transparent, and the blood vessels of the choroid can easily be recognized in those “thin” areas. The ophthalmologist, looking at the back of the eye (the fundus) with an ophthalmoscope, typically will see an area of choroidal thinning that appears like a “window” to the underlying vessels and sclera.

 MILD disease: Mild disease is very common in Shelties. It is easily recognizable on careful ophthalmologic examination as early as 5 to 8 weeks of age. Once the retina changes to its adult colour around 3 months of age, the normal pigment sometimes masks the changes in the choroid (so-called “go normal”). In mildly affected dogs, choroidal thinning is the only detectable abnormality and the dog retains normal vision throughout life. However, dogs with mild disease can produce severely affected offspring.

 SEVERE disease: Colobomas are seen at and near the optic nerve head as outpouchings or “pits” in the eye tissue layers. Colobomas can lead to secondary complications such as partial or complete retinal detachments and/or growth of new but abnormal blood vessels with haemorrhage – bleeding inside the eye. This can affect either one or both eyes. Complications of severe disease can lead to vision loss, although this disorder only rarely threatens total blindness.

 CEA/CH is not progressive in the usual sense. The essential features, choroidal hypoplasia and coloboma, are congenital – the abnormalities develop as the eye develops. These features are also stationary once ocular development is complete around 8-12 weeks. Retinal detachments and/or aberrant vessel formation can be congenital or develop later, in general only in eyes with colobomas.

BOTH the mild and severe forms of CEA/CH disease now are proven to result from the exact same gene and mutation in ALL of the affected breeds.

Multiple Drug Resistance (MDR1)

MDR1 is a mutant gene that occurs in some breeds which affects the canine's ability to pump certain systemic drugs out of the brain. Without this ability, drugs can reach toxic levels causing neurological symptoms. Sometimes these symptoms are mild and other times the symptoms are severe enough to lead to coma and death. 

Your dog may start showing drooling, irritability, ataxia… things you would not immediately think of as a drug reaction.

Drugs that can cause reactions

Acepromazine

Butorphanol

Emodepside

Erythromycin

Ivermectin

Loperamide

Selamectin

Milbemycin

Moxidectin

Vincristine

Vinblastine

Doxorubicin

Progressive Retinal Atrophy (PRA)

Researchers from Norwegian University of Life Sciences have identified a novel mutation in CNGA1 gene that causes early onset PRA in Shetland Sheepdogs . 

PRA in Shelties is clinically indistinguishable from PRA in other breeds. As in other forms of PRA, it is characterized by visual impairment due to degeneration of the photoreceptors in the retina, eventually leading to blindness. Often the first sign of PRA apparent to an owner is night blindness however a veterinary ophthalmologist may detect the disease at an earlier stage of disease during routine clinical examination. Over time, the disease progresses to advanced PRA in which vision loss is evident even at bright light levels.

CNGA1-PRA is inherited as an autosomal recessive disease in Shelties which means that dogs will only develop this form of PRA when they inherit two copies of mutant DNA, one from each parent.  Carriers of only one copy of the mutation will not develop the disease.

Degenerative Myelopathy (DM)

Degenerative Myelopathy in Shelties is an inheritable, recessive gene that can be passed on to future generations of puppies. What makes this a difficult disease to control is the fact that symptoms do not usually become evident until the dog is an older adult. This is long after a dog has been used for breeding multiple times.

The term Degenerative Myelopathy is descriptive of its effect on the dog. It wears away (degenerative) the myelin sheath (myelopathy) that surrounds the nerves of the spinal cord. As that protective covering around the nerves disintegrates, a variety of symptoms start showing.

The dog’s neurological function is slowly affected changing his ability to move normally, until he is unable to walk. He can also develop loss of control of bowel or bladder. Degenerative Myelopathy in Shelties is the dog’s version of Lou Gerig’s Disease.

There is no cure and there is no treatment other than palliative (keeping the dog comfortable). It is progressive and so the prognosis is poor. Many dogs with the disease may need to be euthanized.

Von Willebrand’s Disease Type III (VWD)

 Von Willebrand's disease, an inherited bleeding disorder, usually comes in two major types, type I and type III. (There is also a rarer Type II, not relevant to Shelties). Type III is a severe bleeding disorder with a high risk of spontaneous bleeding as well as a risk of serious bleeding from trauma and surgery. It is probably best known in Scottish Terriers, Shelties & Kooikerhondjies. Type I is milder, with most of the risk coming from trauma or surgery. It is probably best known in Doberman Pinschers. The Sheltie breed has type III vWD, the severe type. There may also be a second less prevalent defect, causing some Shelties to have the less severe Type I vWD, but this is uncertain at present.

Primary Ciliary Dyskinesia (PCD)

 Primary Ciliary Dyskinesia (PCD) is an inherited disorder of the cilia affecting some breeds. Cilia are microscopic, hair-like structures that line the nasal cavity, trachea, and bronchi of the respiratory system, the fluid filled cavities of the brain and portions of the reproductive tract. Normal cilia move in wave-like patterns to aid the movement of fluids in the brain and reproductive tracts and prevent large particles and pathogens from getting into the lungs. In PCD, affected dogs have cilia that are either malformed or do not move. Particles and pathogens cannot be removed from the upper respiratory tract and can lead to sinusitis, bronchitis and pneumonia. Affected dogs typically present a few days after birth with respiratory disease. Symptoms include coughing, sneezing, nasal discharge and frequent respiratory infections. This disorder also causes immobility of sperm, therefore affected male dogs are sterile. Dogs with PCD may also have a transposition of organs in the thoracic and/or abdominal cavities, resulting in a mirror image of the normal placement of the heart and lungs and sometimes other organs. This transposition is called situs inversus and does not usually cause clinical problems. Dogs with this disorder can live for years if their chronic respiratory infections are managed.

Hip Dysplasia

The cause…The first probable cause is genetics. It has been the thorn in the sides of breeders for decades now. Because there never seemed a simple inheritable pattern from parents to pups, it was felt to be polygenetic in nature. This means not one but several genes may play a role in whether a dog develops dysplasia. A specific gene has been found in the German Shepherd Dog, so finally there may be some objective means to determine which dogs to breed. It will take time to isolate the gene in other breeds but at least there is some progress. 

It is thought that genes cause the hip to develop in a less than functional manner.

A hip that has greater laxity (stretching ability) means that the ball and joint don’t sit snugly together. That would give the two pieces the chance to bounce around and wear away bone in the wrong places whenever the joint moved. Wearing down bone causes pain and bone spurs and eventually hip dysplasia in dogs.

 Depth of the socket is how deep does the ball of the femur sit in the socket. Even if it is a snug fit, a shallow socket can let the ball of the joint slosh around easier, and again wear away the socket in places it shouldn’t, like the edges.

This allows more and more movement in the wrong directions and again total wearing away of the joint.

A shallow hip joint can cause hip dysplasia in dogs as early as 4 to 6 months of age!

How a dog ages is another possibly hereditary factor. Osteoarthritis, usually develops as a dog ages. In the aging process, the cartilage loses protein and gains water making it softer and easier to wear away. Once the cartilage is gone, the bones rub against each other every time the joint is moved. This causes the bone to wear away, again causing pain and bone spurs.

 In addition to the genetics, there is a big nature vs nurture aspect to this illness of hip dysplasia in dogs. A gene may be present but the right circumstances allow it to be expressed in that individual dog:

Obesity - more pressure on a joint and it will fail faster and easier than if less stress is placed on it.

Onset of Sports / Pattern of Exercise –  Taking your puppy jogging long distances before they are mature and growth plates in the legs have closed (finished growing). Agility training the jumps. Repetitive jumping at a young age can cause damage to the joints.

Hip Dysplasia displays as lameness, or inability to bear weight on back legs, decreased range of motion in the back legs, loss of muscle tissue.

Elbow Dysplasia

 Elbow dysplasia in dogs is considered the leading cause of canine forelimb lameness. Elbow dysplasia is a general term meaning arthritis of the elbow, that encompasses several conditions of the elbow joint. All of these are causes of elbow dysplasia, but are different conditions with their own distinct pathophysiology:

Fragmented coronoid process – condition in which a small piece of bone on the inner side of the joint breaks off the ulna. The fragment irritates the joint and wears away the cartilage of the humerus.

Ununited anconeal process – condition in which a fragment of bone on the back side of the joint has failed to unite with the ulna during growth.

Osteochondritis dessicans – OCD is a condition in which a piece of cartilage becomes partially or fully detached from the surface of the elbow joint. This results in inflammation of the lining of the joint and causes pain.

Joint incongruity – a condition where the joint does not have the correct conformation and the cartilage of the joint wears out rapidly. This leads to progressive arthritis.

Corneal Dystrophy

Corneal dystrophy is characterized by white to grey opacities (lipid deposits) in the superficial layers of the cornea of one or both eyes. The deposits usually do not cause a problem, but some dogs may develop painful shallow erosions that require treatment. It is considered to be hereditary in some breeds. For Shelties, the American College of Veterinary Ophthalmologists classify this as “Breeder’s Option” since further studies are necessary to further define the disorder in Shelties.

Dermatomyositis (DMS)

Dermatomyositis (DMS)* is an autoimmune disease of the skin and muscle that occurs in both humans and dogs. In dogs, DMS is most often diagnosed in Shetland Sheepdogs and Collies and is caused by a combination of environmental and genetic factors. Skin lesions consist of hair loss and crusts on areas with minimal muscle overlying the bone such as the face, ear tips, legs and feet, and the tip of the tail. Muscle involvement is uncommon in Shelties. Onset of lesions may occur as early as 12 weeks of age or in mature dogs. In some affected puppies, lesions may diminish with age and may or may not return at an older age. Stress may induce worsening of lesions. Definitive diagnosis can only be made with a skin biopsy. Treatment with pentoxyphyline (Trental®), corticosteroids, and vitamin E has been helpful in some dogs

Epilepsy

Epilepsy (repeated seizure episodes) occurs in many animal species including dogs (purebred and crossbred). There are many causes, but when the cause is unknown, it is characterized as “idiopathic” epilepsy. Heredity likely plays a role in many dogs with idiopathic epilepsy. The typical age of onset of seizures in dogs with idiopathic epilepsy is 1 to 3 years.

The Canine Epilepsy Network, is an excellent website with understandable information about epilepsy, its causes, treatments, and living with epileptic dogs. After accessing the main page, click on “Canine Epilepsy Basics”. Another site with links to additional epilepsy resources (at bottom of page) is located at the AKC Canine Health Foundation Epilepsy Research Initiative.

Gallbladder Mucoceles

Bile is produced in the liver to aid in the digestion of food in the small intestine. Liver cells (hepatocytes) excrete bile into a tree-like system of branched ducts (bile ducts) within the liver. These ducts gradually coalesce into a large duct that extends between the liver and the small intestine. The gallbladder is an oval shaped sack-like structure that extends from the large bile duct via a short “cystic” duct. The gallbladder acts as a reservoir to store and concentrate bile between meals as some bile exiting the liver via the large bile duct enters the gallbladder. When food enters the intestine, the gallbladder is stimulated to contract, thus depositing bile into the intestine.

Gallbladder mucoceles (GBM) are characterized by distention of the gallbladder by a thick mass of sludge and mucus (rather than liquid bile) and may result in obstruction and rupture of the gallbladder. Clinical signs of affected dogs include vomiting, loss of appetite, and abdominal pain. Without surgical removal of the gallbladder, the dog may die if rupture occurs. Many other diseases cause similar clinical signs, and because gallbladder mucoceles are relatively uncommon, the diagnosis can be missed or delayed. The diagnosis is usually made via ultrasound examination, exploratory surgery, or at necropsy. In general, this appears to be a disease of older dogs.