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Here you can find information about Healthy issues
A healthy dog is the best thing you can have.

The Photo´s are from our dogs and dogs from our breed. They are all healthy dogs.


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More information about:

Dog’s canine epilepsy
Colour Dilution Alopecia
Hip dysplasia
Multidrug Sensitivity in Dogs
Cerebellar abiotrophy (CA)
Demodex Canex

Dog’s canine epilepsy

Dog’s canine epilepsy

NOTE: The photos of our kelpies all in good health. The photos are set to interrupt the text.

Canine epilepsy is a type of a neurological disorder which is of unprovoked, recurring seizures. It is caused due to any sort of disturbances in a part of the brain, mainly cerebrum. To be specific, canine epilepsy occurs due to an imbalance of the neurons and neurotransmitters in the brain. The neurons are the ones responsible for sending messages to the brain. It would enable the dog to move his body parts voluntarily. During the attack of epilepsy in the dogs, the nerves would not behave in normal coordinated style that would result in moderate to a serious seizure which is referred as epileptic fit. In case of a small attack, the dog will not have convulsions.
However, it will look as if collapsed.
Until and unless the dog is epilepsy results in a range of grand mal convulsions, the seizures will not be life intimidating.


You can seek help from a vet if you find your dog suffering from a series of epilepsy attacks. Recognizing epilepsy Epilepsy attacked dog would seem restless and would walk around restlessly. The dog might salivate and whine or maybe sit in a silent corner. This type of dog’s behavior might seem like this a couple of minutes prior to occurrence of a fit of canine epilepsy.


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Your dog might vomit or drool and would show certain unexpected and uncoordinated muscle activity. The epilepsy phase can last for about five minutes. After seizure, the dog might seem disoriented and he would move out a little oddly. Due to the epilepsy fit, the dog might go blind temporarily. Thus, you need to comfort your dog during this time. This phase could last for a couple of minutes to about several days. If you feel that your dog is not responding to you after epilepsy fit, then you need to consult a vet.

Sometimes, dogs suffering from epilepsy might get a little violent during the seizure. It is best not to come in contact with such dogs as they are not aware of what is actually happening. It is very much necessary to stroke the dog very gently soon after the attack. Treating epileptic dog If you think that your dog is suffering from dog epilepsy then you immediately need to take your dog to a vet. You should describe how the attacks occur, when they occur, and how much time they last for approximately to the vet. This would help the veterinarian to give appropriate diagnosis. Epilepsy cannot be removed completely easily.
However, under medication, epilepsy surely can be reduced. Phenobarbital is the most common drug used for curing epilepsy in dog. Primidone and Dilantin are some other drugs that are used as for treating dos with epilepsy. Do not let you dog go under any medication prior to consulting a vet. The medications would act by calming neurons in the dog’s brain and yet do not leave your dog in the sedated state. You would hardly notice that you dog is taking any epilepsy drugs.



Colour Dilution Alopecia

A "skin"(actually hair)  condition that you can find in kelpies, the dilution colour Fawn and Blue have sometimes Alopecia.
Fawn is a dilution from brown and Blue a dilution from black. These colours are possible in the breed but we think that it is not wise to want to breed these colors.
Read more about Colour Dilution Alopecia in this article.


A lot of people are dexing their dog but we think that you can better consider if you really want to do that. Often it is not in the interest of the dog. In our buyer contracts stood that it is not aloud to neutering your dog before 30 months except when there is a real medical problem.
Just read this article

Hip dysplasia

Hip dysplasia
by Professor John Innes RCVS Specialist in small animal surgery (orthopaedics)

What is hip dysplasia?
Hip dysplasia is a common developmental disease of the hip. As a puppy grows the soft tissue support for the hip may become loose (lax) and this can allow the head of the femur (the ball of the ball and socket joint) to slip in and out of the acetabulum (socket). This abnormal laxity of the hip can damage the tissues of the joint leading to osteoarthritis. Below - a radiograph showing severe hip dysplasia notice how the head of the femur is not fitting well in to the acetabulum Hip Dysplasia



What sort of dogs are affected?
Hip dysplasia occurs most commonly in medium-large breed dogs of any breed. Some breeds are commonly affected whereas others are rarely affected (e.g. Greyhound).
However, hip dysplasia can occur in smaller dogs and also sometimes in cats.

What causes these diseases?
The cause of hip dysplasia is not fully understood. Certainly there is a complex genetic basis and it is likely that several different genes are involved. It is also likely that environmental factors (exercise, growth rate, nutrition) play a role and obesity will worsen the condition. At Liverpool we are investigating the genetic basis of the disease in collaboration with colleagues at CIGMA at the University of Manchester.



What are the signs of these diseases?
Hip dysplasia can cause pain and lameness although in some dogs the disease may remain clinically silent for many months or years. Often in puppies there is a swaying hindlimb gait and some dogs may sit down at exercise because of the discomfort. Usually the condition occurs in both hips and so signs may relate to joint stiffness in both hindlimbs. Later in life, the osteoarthritis initiated by hip dysplasia may progress to cause pain, stiffness and lameness.

How are these conditions diagnosed?
A clinical examination by a veterinary surgeon is the first step in diagnosis. Certain clinical tests can indicate if hip dysplasia is present but it may be necessary to perform these tests under heavy sedation or anaesthesia. If hip dysplasia is suspected, radiographs (x-rays) such as the one above are the most usual initial step in making a diagnosis.

What can be done to treat the condition?
The treatment of hip dysplasia in young dogs is controversial. Certainly only those dogs that have disability should be treated - many dogs with hip dysplasia never need treatment. Conservative treatment involves exercise restriction and possibly pain-relieving medication and can be very effective. As an affected dog matures the pain associated with hip dysplasia can subside although the hip will be prone to osteoarthritis which may cause stiffness and pain in later life. Some veterinary surgeons advocate surgical treatment in puppies. In older dogs where the osteoarthritis of the hip is causing intractable pain that does not respond to medical treatment and weight loss, one might consider a total hip replacement. This operation is similar to that performed in people and can relieve pain and provide excellent function. Careful specialist evaluation of the dog is required prior to such a surgery. At Liverpool we use the Biomedtrix canine hip system, which is probably the most widely used hip system for dogs in the world today.


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Multidrug Sensitivity in Dogs

Multidrug Sensitivity in Dogs

NOTE: The photos of our kelpies all in good health. The photos are set to interrupt the text.

In more and more articles they ment the Kelpie. We are really worried about this. At this time we haven't heard about a kelpie from our kennel who was affected with the MDR1 gen mutation. But because we want to keep this race healthy we plan to test our dogs on this mutation. Bron: Multidrug Sensitivity in Dogs
Some dog breeds are more sensitive to certain drugs than other breeds. Collies and related breeds, for instance, can have adverse reactions to drugs such as ivermectin and loperamide (Imodium). At Washington State University's College of Veterinary Medicine you can get your dog tested for drug sensitivity and keep up with the latest research.


tl_files/diversen/DSC_0276.jpgDrug sensitivities result from a mutation in the multi-drug resistance gene (MDR1). This gene encodes a protein, P-glycoprotein that is responsible for pumping many drugs and other toxins out of the brain. Dogs with the mutant gene cannot pump some drugs out of the brain as a normal dog would, which may result in abnormal neurologic signs. The result may be an illness requiring an extended hospital stay - or even death.
Affected Breeds Pictured from top: Collie, Australian Shepherd and Silken Windhound.Approximately three of every four Collies in the United States have the mutant MDR1 gene. The frequency is about the same in France and Australia, so it is likely that most Collies worldwide have the mutation.
The MDR1 mutation has also been found in Shetland Sheepdogs (Shelties). Australian Shepherds, Old English Sheepdogs, English Shepherds, German Shepherds, Long-haired Whippets, Silken Windhounds, and a variety of mixed breed dogs.
The only way to know if an individual dog has the mutant MDR1 gene is to have the dog tested. As more dogs are tested, more breeds will probably be added to the list of affected breeds. Breeds affected by the MDR1 mutation (frequency %) Breed Approximate Frequency Australian Shepherd 50% Australian Shepherd, Mini 50% Border Collie < 5% Collie 70 % English Shepherd 15 % German Shepherd 10 % Herding Breed Cross 10 % Long-haired Whippet 65 % McNab 30 % Mixed Breed 5 % Old English Sheepdog 5 % Shetland Sheepdog 15 % Silken Windhound 30 % Problem Drugs Many different drugs and drug classes have been reported to cause problems in Collies and other herding breed dogs that carry the MDR1 mutation.



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We and other researchers have documented the toxicity that occurs with several of these drugs. Drugs that have been documented to cause problems in dogs with the MDR1 mutation include: ¡Acepromazine (tranquilizer and pre-anesthetic agent). In dogs with the MDR1 mutation, acepromazine tends to cause more profound and prolonged sedation. We recommend reducing the dose by 25% in dogs heterozygous for the MDR1 mutation (mutant/normal) and by 30-50% in dogs homozygous for the MDR1 mutation (mutant/mutant). ¡Butorphanol (analgesic and pre-anesthetic agent). Similar to acepromazine, butorphanol tends to cause more profound and prolonged sedation in dogs with the MDR1 mutation.We recommend reducing the dose by 25% in dogs heterozygous for the MDR1 mutation (mutant/normal) and by 30-50% in dogs homozygous for the MDR1 mutation (mutant/mutant). ¡Erythromycin. Erythromycin may cause neurological signs in dogs with the MDR1 mutation. A mutant/mutant collie exhibited signs of neurological toxicity after receiving erythromycin. After withdrawal of the drug, the dogs neurological signs resolved. There were no other potential causes of neurological toxicity identified in the dog. ¡Ivermectin (antiparasitic agent). While the dose of ivermectin used to prevent heartworm infection is SAFE in dogs with the mutation (6 micrograms per kilogram), higher doses, such as those used for treating mange (300-600 micrograms per kilogram) will cause neurological toxicity in dogs that are homozygous for the MDR1 mutation (mutant/mutant) and can cause toxicity in dogs that are heterozygous for the mutation (mutant/normal). ¡Loperamide (ImodiumTM; antidiarrheal agent). At doses used to treat diarrhea, this drug will cause neurological toxicity in dogs with the MDR1 mutation. This drug should be avoided in all dogs with the MDR1 mutation.

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¡Selamectin, milbemycin, and moxidectin (antaparasitic agents). Similar to ivermectin, these drugs are safe in dogs with the mutation if used for heartworm prevention at the manufacturer's recommended dose. Higher doses (generally 10-20 times higher than the heartworm prevention dose) have been documented to cause neurological toxicity in dogs with the MDR1 mutation. ¡Vincristine, Vinblastine, Doxorubicin (chemotherapy agents). Based on some published and ongoing research, it appears that dogs with the MDR1 mutation are more sensitive to these drugs with regard to their likelihood of having an adverse drug reaction. Bone marrow suppression (decreased blood cell counts, particulary neutrophils) and GI toxicity (anorexia, vomiting, diarrhea) are more likely to occur at normal doses in dogs with the MDR1 mutation. To reduce the likelihood of severe toxicity in these dogs (mutant/normal or mutant/mutant), we recommend reducing the dose by 25-30% and carefully monitoring these patients.

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Drugs that are known to be pumped out of the brain by the protein that the MDR1 gene is responsible for producing but appear to be safely tolerated by dogs with the MDR1 mutation:¡Cyclosporin (immunosuppressive agent). While we know that cyclosporin is pumped by P-glycoprotein (the protein encoded by the MDR1 gene), we have not documented any increased sensitivity to this drug in dogs with the MDR1 mutation compared to "normal" dogs. Therefore, we do not recommend altering the dose of cyclosporin for dogs with the MDR1 mutation, but we do recommend therapeutic drug monitoring. ¡Digoxin (cardiac drug). While we know that digoxin is pumped by P-glycoprotein (the protein encoded by the MDR1 gene), we have not documented any increased sensitivity to this drug in dogs with the MDR1 mutation compared to "normal" dogs. Therefore, we do not recommend altering the dose of digoxin for dogs with the MDR1 mutation, but do recommend therapeutic drug monitoring. ¡Doxycycline (antibacterial drug). While we know that doxycycline is pumped by P-glycoprotein (the protein encoded by the MDR1 gene), we have not documented any increased sensitivity to this drug in dogs with the MDR1 mutation compared to "normal" dogs. Therefore, we do not recommend altering the dose of doxycycline for dogs with the MDR1 mutation. Drugs that may be pumped out by the protein that the MDR1 is responsible for producing, but appear to be safely tolerated by dogs with the MDR1 mutation:¡Morphine, buprenorphine, fentanyl (opioid analgesics or pain medications). We suspect that these drugs are pumped by P-glycoprotein (the protein encoded by the MDR1 gene) in dogs because they have been reported to be pumped by P-glycoprotein in people, but we are not aware of any reports of toxicity caused by these drugs in dogs with the MDR1 mutation. We do not have specific dose recommendations for these drugs for dogs with the MDR1 mutation.


The following drugs have been reported to be pumped by P-glycoprotein (the protein encoded by the MDR1) in humans, but there is currently no data stating whether they are or are not pumped by canine P-glycoprotein. Therefore we suggest using caution when administering these drugs to dogs with the MDR1 mutation. ¡Domperidone ¡Etoposide ¡Mitoxantrone ¡Ondansetron ¡Paclitaxel ¡Rifampicin There are many other drugs that have been shown to be pumped by human P-glycoprotein (the protein encoded by the MDR1 gene), but data is not yet available with regard to their effect in dogs with the MDR1 mutation. MDR1 Breeding Guidelines This chart provides guidelines for consideration when owners are contemplating breeding dogs that may be affected by the MDR1 mutation. While it is ideal to use only "Normal/Normal" breeding pairs, one must always consider other genetic factors in addition to the MDR1 gene. Because the MDR1 gene is present in such a large percentage of Collies and Australian Shepherds, it may be necessary to breed "Normal/Mutant" dogs in order to maintain a large enough pool of good breeding stock. By using thoughtful breeding strategies including these guidelines, future generations of dogs will have a substantial decrease in the frequency of the mutant MDR1 gene. MDR1 Breeding Pair Combinations and Outcomes Normal/Normal Male Normal/Mutant* Male Mutant/Mutant Male Normal/Normal Female 100% Normal/Normal puppies Normal/Normal and/or Normal/Mutant puppies 100% Normal/Mutant puppies Normal/Mutant* Female Normal/Normal and/or Normal/Mutant puppies Any combination of puppies Normal/Mutant and/or Mutant/Mutant puppies Mutant/Mutant Female 100% Normal/Mutant puppies Normal/Mutant and/or Mutant/Mutant puppies 100% Mutant/Mutant puppies *Normal/mutant is the same as mutant/normal and "heterozygote"


Cerebellar abiotrophy (CA)

Cerebellar Abiotrophy (CA)

NOTE: The photos of our kelpies all in good health. The photos are set to interrupt the text.

What is cerebellar abiotrophy?

The cerebellum is the part of the brain that regulates the control and coordination of movement. With this condition, cells in the cerebellum mature normally before birth, but then deteriorate prematurely causing clinical signs associated with poor co-ordination and lack of balance.
The Purkinje cells in the cerebellum are primarily involved; cells in other areas of the brain may also be affected.


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CA has been seen in the Australian Kelpie, Gordon Setter, Border Collie, Labrador Retriever, Airedale, English Pointer, Scottish Terrier, Kerry Blue Terrier, Miniature Schnauzer, and other dog breeds. Time of onset varies. In a few breeds, such as the Beagle, Rough Collie, and Miniature Poodle, Purkinje cells begin to die off at or shortly before birth, and pups are born with symptoms or develop symptoms by three to four weeks of age.
Most breeds prone to the condition, such as the Kerry Blue Terrier, Border Collie, Australian Kelpie, and Labrador Retriever, begin showing symptoms between six and sixteen weeks of age. In a very few breeds, such as the American Staffordshire Terrier, Old English Sheepdog, Brittany Spaniel, and Gordon Setter, symptoms do not appear until adulthood or even middle age. In dogs, CA is also usually an autosomal recessive gene, but in a few breeds, such as the English Pointer, the gene is sex-linked. New information about the progress of the research (February 2010): Update on CA research in Kelpies at University of New South Wales. (Feb 2010) Previously we have reported that we have identified the region of DNA containing the Cerebellar Abiotrophy gene that results in ataxia in affected kelpies.


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This was made possible partly through funding from Terry Snow and from Working Kelpie Council to use newly available technology. We have localised the ataxia mutation to a region of 5 million bases (0.2% of the dog genome) which still makes the search for the mutation like looking for a needle in a haystack. There are 44 genes in this region, and at first glance, none stand out as likely to be involved in ataxia. Recent work has been to pull this haystack apart and examine the contents closely in search of differences between ataxia affected dogs and unaffected dogs. Utilising recent technological advances this entire region has been isolated from two affected dogs and one unaffected control dog. Using next generation sequencing technology at the Ramaciotti Centre at UNSW we have obtained the genetic sequence for almost the entire 5 million base region for each of the two ataxia affected dogs and the unaffected control dog. Comparing the affected dogs to the control dog identifies 2107 differences, any of which could be the actual cause of Ataxia. By employing a process of elimination, 691 of these differences are within gene regions, 27 are within regions that code for protein (cellular machinery) production and 9 of these change the protein. Six other differences have also been identified which may be the cause of ataxia. Each of these 15 differences are currently being investigated by checking all our 200 other kelpie DNA samples to see if the difference is inherited exclusively with the disease. While we have chosen to focus our attention on these 15 differences it is possible that the real cause is not one of these 15 and we may have to check all of the differences to find the cause. The genetic cause of the disease looks to be very difficult to identify but we will persevere until a DNA test is developed. Jeremy Shearman Alan Wilton

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Demodex Canex

Demodex Mites

Demodex Mites
Advocate®: Effective Against Demodicosis
Demodex is part of the physiological fauna of the skin in many, if not all, mammalian species, including the dog and man. Demodex canis is responsible for one of the most important skin diseases of dogs: canine demodicosis.

The Parasite
Life Cycle
Pathogenesis and Clinical Appearance
Zoonotic significance
Efficacy of Advocate®
The Parasite
Demodex canis (Leydig, 1858), the hair-follicle mite, is a white, oblong mite. Adult female mites measure 300 µm and the males about 250 µm (Fig.1).

It normally lives as a commensal in the skin of most animals, spending its entire life cycle in the hair follicles and sebaceous glands. Mites can be found in healthy dogs, albeit in small numbers. For Demodex canis, so-called ‘short-bodied’ and ‘long-bodied’ mites have been described, although whether these are individual species, subspecies or races currently remains undetermined.

The capitulum is horseshoe-like with clearly visible mandibles. The cuticula of the body resembles transverse wrinkles. Four pairs of stump-like legs end with 2 claw-like structures. The mites feed on cells, sebum and epidermal debris.

Fig. 1: Adult Demodex canis

Life Cycle
Demodex mites are transmitted from the bitch to the nursing puppies within the first days after birth. Mites spend their entire life on the skin of dogs, where they reside in the hair follicles and, rarely, the sebaceous glands.

Four stages have been described for Demodex canis (Fig.2).

The developmental cycle starts with the larvae hatching from the fusiform eggs. The six-legged larvae moult to become the eight-legged first nymphal stage. This is followed by a second nymphal stage, which in turn moults to give rise to the final adult stage. The whole life cycle is completed in about 3 weeks. All stages of the mite can be found in the hair follicles, as well as the lymphatic system, bloodstream, and other bodily organs. Mites in these „extra-cutaneous“ locations are dead and have relocated to these areas by means of lymph or blood drainage.

Fig.2: Life Cycle of Demodex canis

To watch or download the animation of this life cycle please visit our download area.

Pathogenesis and Clinical Appearance
While Demodex canis may be present in the normal canine dermis, transmission occurs from the nursing bitch to the puppies within the first 3 days of life. Mites have been demonstrated in pups as young as 16 hours old. In contrast, puppies born by caesarean section and kept apart from an infected bitch do not harbor mites – a clear sign that no intrauterine transmission occurs.

Two forms of the condition are recognized: a localized and a generalized form. The generalized type may be further subdivided into juvenile-onset and adult-onset demodicosis.

Factors that adversely affect the immune system are important in determining the occurrence and severity of demodicosis.

Generalized demodicosis involves several areas of the body and these may be quite large in size. A dog with five or more localized lesions, involvement of an entire body region, or involvement of two or more feet is considered as having generalized demodicosis.

Generalized demodicosis may occur at a young age and if it does not resolve spontaneously with the maturation of the immune system, it will require treatment.

The pathological mechanisms involved in juvenile-onset demodicosis remain unclear.

Adult onset demodicosis could affect any age and is most likely to be triggered by factors such as an underlying deficiency of the immune system, diseases such as infection or neoplasia, and certain therapies, especially immunosuppressive agents.

In addition to the demodicosis, secondary pyoderma is common and can result in a pustular form of the condition, which is severely pruritic.

Zoonotic significance
Human infection is rare, thus the mite has a low zoonotic potential.

The standard method for diagnosis of infection with Demodex mites is microscopic examination of deep skin scrapings and detection of mites.

To perform a skin scraping, the skin should be squeezed, thus expelling the mites from the depths of the hair follicles to the surface. Demodex mites are present in the skin of healthy dogs and a single mite found in a scraping may be consistent with a diagnosis of healthy skin. However, while it is not common to detect mites in healthy dogs, such a finding should not be ignored. Skin scrapings from several areas are necessary to confirm infestation.

Special care should be taken when the face and paws are affected to avoid causing excessive bleeding. Another option is to examine plucked hair for the presence of mites.

Efficacy of Advocate®
Eighteen dogs with severe generalized demodicosis were treated with Advocate to assess its efficacy against Demodex canis.1 Prior to inclusion, infection was determined by mite counts from deep scrapings. A minimum of two and a maximum of four treatments were applied; treatment days were 0, +28, +56 and +84.

On day 0 all dogs were treated. The number of subsequent treatments per dog depended on the presence or absence of Demodex spp. mites as determined during assessments one day prior to the second, third and fourth treatments.

If mites were found the animal was given another treatment; if mites were absent the animal was also given another treatment, unless it had been negative at the previous assessment.

In this study, two to four treatments with Advocate, applied at four-week intervals, were effective against Demodex spp. infestations in dogs. The reduction in the geometric mean numbers of mites at the end of the study compared to the pre-treatment numbers was 97.84% (Table 1).

Clinical symptoms of demodicosis, namely the occurrence of erythema, casts, scales, crusts and alopecia, improved accordingly, body weight increased and the overall condition of the animals improved markedly.

As indicated above, demodicosis is a multifactorial disease, and wherever possible, one should also identify and treat any underlying disease appropriately.



NOTE: The photos of our kelpies all in good health. The photos are set to interrupt the text.

Here is a very simple explanation of the process by which a dog "sees": Light passes through the lens and is directed onto the retina, which contains specialised photoreceptor (light-sensitive) cells called rods and cones. These cells convert the light into electrical nerve signals, which pass along the optic nerve to the brain, where they are "translated" into images. ~ rods are responsible for vision in dim light i.e. night vision ~ cones are responsible for vision in bright light i.e. daytime and colour vision


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~ Progressive a slowly developing disease process ~ the affected dog will gradually lose its sight and will usually adjust to its handicap ~ Retinal of the retina ~ the light-sensitive area at the back of the eye ~ Atrophy degeneration or deterioration ~ of the specialised light-sensitive cells in the retina


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Initially, a dog with PRA will develop "night-blindness" i.e. it will eventually be unable to see in dim light conditions or in the dark. This is due to atrophy, or degeneration, of the rods. The owner may notice that the dog is reluctant to go out in the dark and hesitant to do down stairs in poor light. The dog may also appear to be a little "clumsy" i.e. bumping into things. In the later stages of the disease, the cones are affected, and the dog's daytime vision will gradually deteriorate. PRA in Glens is thought to be "late onset" i.e. it is very unlikely that a Glen would show any degenerative changes (at eye examination) as a puppy. The range of ages, at which PRA has been first diagnosed in Glens, covers more than five years i.e. the youngest age, at confirmation of diagnosis,is 2 years and 2 months, and the oldest age, following previous "clear" eye examinations, is 7 years and 10 months.


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The "genetic marker" for PRA has been identifed in a number of breeds of dog. A blood sample is sent to a specialist laboratory for testing and the dog can then be classified as normal, a carrier, or affected. Please see LINKS for a list of the breeds for which blood testing is currently available. Unfortunately, for the Glen of Imaal Terrier, and many other breeds, there is currently no test to determine genetic status for PRA i.e. we cannot do a simple blood test to identify whether a Glen is normal, a carrier or affected. For the time being, we have to rely on eye testing by a veterinary ophthalmologist. Eye testing can identify affected Glens.


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However, a "clear" test result cannot differentiate the normal Glen from the carrier Glen or even the Glen who goes on to test affected at a later date. A "clear" test result simply means that the dog does not have any clinical signs of PRA on the day of the eye examination. Eye examination should be carried out by a certified veterinary ophthalmologist. Your dog will be given some eye drops, to dilate the pupils. After about 20 minutes, your dog can be examined. The examination takes place in a darkened room; the vet will look into your dog's eyes using an instrument called an indirect ophthalmoscope. This examination takes just a few minutes, and is a non-invasive and painless procedure for your dog! You need to bring your dog's registration documents with you when you have your dog's eyes tested. The veterinary ophthalmologist will provide you with a certificate, valid for one year, detailing his/her findings. Please see LINKS for a list of (UK) certified ophthalmologists.
Professor Peter Bedford is a certified ophthalmolgist in the UK. He is patron of the Glen of Imaal Terrier Association and attends one of their breed shows each year to conduct a subsidised eye testing session. Professor Bedford recommends that breeders have their litters routinely screened for congenital and hereditary eye anomalies. He suggests annual screening thereafeter.


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Inheritance of PRA in a couple of breeds of dog is known to be sex-linked, and it has a dominant form of inheritance in another couple of breeds. However, in the majority of breeds affected by PRA, the mode of inheritance is known or thought to be autosomal recessive. The mode of inheritance of PRA in Glens is believed to be autosomal recessive, which means that the PRA gene has to be inherited from both parents for the dog to be affected. A dog with the PRA gene from only one parent will be a carrier; and a dog with no PRA genes will be normal. ~ Affected (pp) PRA gene from both parents ~ dog will eventually go blind ~ may test "clear" before being tested affected ~ if tested regularly, all affected dogs will eventually be identified ~ Carrier (Pp) PRA gene from only one parent ~ dog will have normal vision and will test "clear" ~ Normal (PP) No PRA genes ~ dog will have normal vision and will test "clear" The dominant gene is denoted with a capital letter, in this case P. The recessive gene is then denoted with the same letter, but in lower case. The "dominant" letter goes before the "recessive" letter e.g. Pp represents a carrier i.e. the (dominant) normal gene (P) from one parent and the (recessive) affected gene (p) from the other parent.


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