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Professor Peter GC Bedford, BVetMed, PhD, FRCVS, DVOphthal, ILTM Primary glaucoma is an inherited disease of the eye in which the internal fluid pressure rises above normal. The high pressure destroys retinal and optic nerve tissues to render the eye blind. In acute onset disease there is considerable pain, but in the slower types of the disease the only signs are those of gradual loss of sight and globe enlargement In the Dandie Dinmont Terrier it is a slower type of disease that effects the late middle-aged and elderly dog. Sadly the cause is not known and our studies would suggest that it is the sum of several abnormalities that results in the disease. All are abnormalities associated with that part of the eye known as the drainage or iridocorneal angle (DA). Pectinate Ligament Dysplasia (PLD) is one of those abnormalities and it is this we look for when gonioscopy is completed. We also look for a narrowing of the DA, but the cause for the narrowing and the eventual closure of this structure is not known. That it happens is certain, but the changes at microscopic level that effect closure cannot be seen in a clinical examination of the eye It will take histological studies to provide the necessary detail, but, it must be remembered that the changes themselves may be destroyed by the glaucomatous process. Other changes may occur deep within the DA, but again these are not visible to the ophthalmoscope and not seen at gonioscopy. Here again histology will be necessary to describe these possible changes. Primary glaucoma in the Dandie Dinmont Terrier may be the sum of these three factors, but certainty at this time does not exist. At the moment, the gonioscopic work we are doing will give information on PLD and DA, but, as said earlier, histology will prove necessary to complete the jigsaw puzzle. We need to know about the disease in order to provide effective treatment and those same facts may eventually lead to a DNA based diagnostic test. Little fact at the moment and a lot of new hypothesis What can you do as a responsible owner or breeder ? - Really only one thing GONIOSCOPY I am suggesting currently that 3 gonioscopic examinations should be completed during the lifetime of the dog: In the young dog - 2 - 4 years of age In the middle aged dog - 6 - 7 years of age In the elderly dog - 9 - 10 years of age The early examination will pick up PLD and the later examinations will reveal subsequent possible narrowing and closure of the DA.   We have made a good start thanks to the tireless work of several committed breeders, but we need all the support possible if we are to get to the bottom of this particularly nasty disease © January 2004 by the Author. Reproduced with permission.
Tuesday, 01 January 2008 | 12004 hits
by C.A. Sharp Winner of 2002 AKC/CHF Golden Paw Award First published in the Aussie Times, May-June 2002 A complex and threatening storm is gathering on horizon. Reports of immune-mediated disease are on the rise in Australian Shepherds, as well as other purebred dogs. In magazines, on Internet discussion lists and at gatherings devoted to dogs autoimmune disease and allergies are regular topics. Immune-mediated disease results from excessive or inadequate action by the immune system. But what do we know about this rising storm of health problems, and is there anything breeder's can do about it? What is Happening Here? Mix-breed dogs and other species, including humans, have also experienced apparent increases in immune-mediated disease. Two factors are increased knowledge about the immune system by the scientific community and improved awareness on the part of the general public in the wake of the AIDS crisis. We know a lot more today about how the immune system works and how it fails than we did only a couple decades ago. Proper diagnosis of some of these diseases was once difficult. The presenting signs of diseases like thyroiditis are also seen in a variety of other conditions. Today improved knowledge and technology enable veterinarians to make more accurate diagnoses. Coupled with this, present day dog owners are more likely to take an ailing pet to the vet for conditions that do not present an obvious or immediate threat than was often the case in decades past. Both the increase in numbers of dogs being seen and improvements in veterinary medicine have without doubt contributed to the apparent increase in immune-mediated disease. However, not all the increase is an artifact of better reporting. Environmental factors also play a role. We and our dogs are exposed to potentially irritating substances' ranging from food preservatives to cleaning solvents to garden chemicals' which our grandparents, not to mention our dogs' great-great-grandparents, never encountered. Some of these substances have been shown to affect various bodily functions, including that of the immune system. Our technological culture has made changes in our environment that would never occur in nature and we are only beginning to understand what is going on. Vaccines are a part of this technological effect. Over-aggressive administration of vaccines can compromise immune function. However, the benefits of vaccination far outweigh the risks. The "core" diseases for which we commonly vaccinate our dogs, like distemper and parvo, can be fatal. Dog owners should not avoid vaccinating, but should work with their veterinarians to implement a vaccination protocol that gives the dog sufficient protection from infectious diseases without vaccine over-use. Vaccination should be administered only if a dog is at risk for that particular disease and adequate intervals should be left between vaccinations so that the dog's immune system is not overwhelmed. Over-vaccination has been implicated as a possible cause of autoimmune hemolytic anemia. Nutrition can also affect the efficiency of immune system function. Deficiencies in Vitamin E or selenium, a trace mineral, can result in a deficit of immune competent cells. These substances aid body mechanisms that counteract damaging free radicals that arise from normal metabolic functions such as breathing. As your dog ages, its immune system becomes less efficient in handling free radicals. Proper levels of Vitamin E and selenium in the diet can help the immune system function as well as possible for dogs that are sick or old. Most commercial dog feeds and the commonly used raw diets have sufficient selenium but may be lacking in Vitamin E, so supplementation may be advised. Some areas have selenium-deficient soils. (The Columbia River Gorge in Oregon and Washington is one example). If the products that form the basis of the diet you are feeding come from such an area, careful supplementing may be necessary. Excess selenium can be unhealthy, so follow professional advice and label directions carefully. But despite the improvements in diagnosis and the problems stemming from environmental conditions, a dog's genetic makeup has a significant part to play in how well its immune system works. Genetic Roots The immune system is governed by the Major Histocompatability Complex (MHC). This group of genes is referred to as a complex because they are all positioned close together on one chromosome. This positioning virtually guarantees that the genes will be inherited as a unit called a haplotype. The haplotype will be passed to offspring without the usual shuffling that occurs as genes are distributed into sperm or eggs. Every individual possesses two MHC haplotypes, one inherited from each parent. The MHC enables the immune system to respond appropriately to the intrusion of infectious agents, like viruses or bacteria. It is not unique to dogs, but exists in all species of mammals. Genes within the MHC are unusual in that they are highly polymorphic, each having many; sometimes as many as 100 different alleles, or forms. There are so many alleles it is probable that most individuals in a randomly breeding population, such as wild species, will have unique combinations of MHC genes. It is this very lack of similarity that leads to graft-vs.-host disease in transplant patients and why full siblings make the best transplant donors. MHC genes also have the highest mutation rate of genes for any germ-line cell. Germ line cells are those that ultimately produce sperm or eggs. In other genes, mutations usually confer little benefit to the individual and may cause considerable difficulty. MHC genes mutate readily because their diversity is important to species survival. Such extreme polymorphism is unusual. Biological systems tend to be conservative, keeping energy and resource needs to a minimum. The simpler a system, the less prone it is to breakdown. So why do we see all this complexity with the MHC? It is Nature's answer to the problem of infectious disease. The immune system must be prepared to tackle many different infectious agents. A mere handful of alleles would not allow the necessary flexibility to face down an ever-evolving array of pathogens. In most cases, each haplotype a dog has will differ from the other, thus increasing its odds of having something in its immune arsenal that will work against whatever nasty bug it may encounter. A plague may kill those individuals who don't have the correct combination of MHC alleles to fight the disease. It may even kill a major part of a population, as happened with bubonic plague among humans in centuries past. While each individual has only two haplotypes, the overall population of its species will have many. Therefore, when a new plague organism comes along, as they inevitably do, the species will survive even though some or even many individuals may be lost. As an example, HIV-positive individuals that have considerable MHC heterozygosity;meaning they have different, rather than similar (homozygous) pairs of MHC genes; are more likely to survive to 10 years without succumbing to AIDS. On the other hand, those who are homozygous for certain MHC genes are certain to die within the same period. Survivors of epidemics have the right? combination of MHC alleles to combat that particular infectious disease. The same plague may occur again and again, but as time goes by it becomes less virulent because those with inadequate MHCs will have died and been removed from the breeding population. The high MHC mutation rate guarantees that there will be plenty of ammunition for any new plagues that occur. MHC complexity is an excellent example of the importance of biological diversity; not only among species but also within them. All naturally reproducing species will avoid or significantly limit inbreeding. (For the purposes of this article, the term inbreeding includes what dog breeders refer to as linebreeding.) Studies in mice have shown that females, given a choice, show significant preference for mates with dissimilar MHCs, thereby conferring offspring sired by those males with more flexible immune systems. Even in humans a study has indicated females have some degree of preference for males with different MHCs, though no one argues that there are a plethora of other considerations that strongly influence a woman's mate choice. No studies have been done on dogs to date, but anecdotal reports of bitches that refuse to mate with closely related dogs are not unusual. In an inbred individual, the chance that both parents have passed on identical genes within the MHC increases. This situation diminishes the body's capability to mount an effective immune response. Such dogs are more prone to infections and are more likely to suffer autoimmune disease or allergies. Autoimmune Disease Every living thing, whether dog, human or microbe, will sooner or later experience ill health. The cause may be a virus or bacterium, an injury or even old age, But that your dog's own body might attack itself and cause serious illness seems bizarre. But this is the case with autoimmune disease. A bad combination of MHC genes can predispose an individual for this type of disease. Each of the more than three dozen recognized autoimmune diseases are influenced by certain MHC genes. In autoimmune disease, the immune system loses its ability to distinguish self from non-self and attacks the body's own tissues The immune system is designed to search out and destroy microscopic invaders. Its specialized cells circulate through the bloodstream, hunting down, disabling and consuming viruses and bacteria, which they recognize by their foreign proteins. Immune cells are genetically programmed to recognize the body's own proteins as well as those of the various organisms that lead their quiet and often beneficial lives on or within our dogs. But sometimes something goes terribly wrong, resulting in immune cells that target one or more of their own body's tissues, or attack the various benign residents. The author has personally experienced this; her eyes have suffered significant damage wrought by her own immune cells. Environmental conditions can induce autoimmune disease, but a dog's genetic make-up also plays a role. It is vital that breeders inform themselves about common canine autoimmune diseases, how they are diagnosed and whether they are inherited. Autoimmune disease does not just happen; it requires a trigger,? an event that starts the disease process. The cause will be some sort of stress factor; another disease, an injury, exhaustion, exposure, emotional distress, toxic exposures, or even something so subtle you may never know exactly what precipitated the illness. Sometimes the result will be temporary and the autoimmune reaction will cease as the body recovers, never to return. An example would be localized demodectic mange. The demodex mites live in the hair follicles of most if not all dogs. In normal circumstances, they are benign residents: they provide no apparent benefit but neither do they cause harm. Sometimes a puppy will have a reaction to the presence of these mites, resulting in localized demodectic mange. A small, coin-sized bald spot will develop, usually on the dog's face or forelegs. Most veterinarians will prescribe a miticide when they diagnose the disease, but treated or not it will eventually go away on its own. (There is another, more virulent, form of this disease that will be discussed below.) The disease is brought on by a temporary compromise of a young immune system still learning how to do its job. Once the crisis is past, the disease will go away. In most cases, there will be no sequel, but the author is aware of one dog that had localized demodex mange as a pup and went on to develop lupus in later life. Early autoimmune reactions may, in some dogs, indicate an inherently faulty immune system. If a dog with localized demodex has relatives who have also had it or relatives with chronic autoimmune disease, the mange could be a precursor of things to come. Of greater concern, especially to a dog breeder, are the chronic, genetically influenced forms of autoimmune disease the ones that, once started, will be a health concern for the balance of the dog's life. Chronic autoimmune disease is multi-factorial, meaning several things must happen for an individual to become ill. First, the dog must be genetically pre-disposed via the makeup of its MHC. The genetically predisposed dog must then experience a trigger. A dog which never experiences a trigger will never develop disease even though it has the necessary genes. While the affected dogs may be relatively free of symptoms when the disease is not active, there will be continuing flare-ups even with treatment. Some autoimmune diseases are readily identified, but others can be difficult to diagnose as they mimic other conditions. Diagnostic tests are available for some, but not all. These diseases cannot be cured and require life-long treatment for the affected dog. Sometimes they are fatal. Steroids are a common treatment for many autoimmune disorders. These are medications that can have serious side effects if taken in large enough doses or administered constantly over an extended period of time. Non-steroid medication may not be available for some diseases. There may come a point where the disease ceases to respond to one or all medications though most dogs can be maintained in reasonable comfort with proper treatment. These diseases usually do not appear until the dog is a young adult. Sometimes they will arise later in life. It is very possible affected dogs will have been bred prior to the disease becoming known. The Major Autoimmune Players Theoretically, any body system or tissue could fall prey to an autoimmune attack. In practice, however, there are some diseases that occur more frequently than others. The following are those most commonly encountered in Australian Shepherds: Thyroiditis is the most frequently reported autoimmune disease in dogs, both purebred and mongrel. The slow and eventually total destruction of the thyroid gland can cause a wide variety of signs in the affected dog, with the most common being hair loss with thickened oily skin, obesity and lethargy. Less frequently, affected dogs may develop other problems, including reproductive failure, seizures and corneal dystrophy. Sometimes these dogs will not display any of the more “classicâ€? signs of hypothyroid disease. All of these signs might also be the result of other conditions, so a thorough veterinary exam is indicated. Blood panels can be done to diagnose this disease, as well as identify probable carriers, but the tests do not always yield black and white results and may need to be repeated at intervals. Lupus comes in two forms. The less serious is discoid lupus, a skin disease resulting in hair loss and crusty, irritated areas of skin, usually on the face and head. Discoid lupus can advance to the more serious form, lupus erythematosus, a systemic disease. Dogs with systemic lupus can suffer a variety of problems. Other autoimmune diseases, including hemolytic anemia and thrombocytopenia can be secondary to systemic lupus. In serious cases the disease can prove fatal. Lupus can be diagnosed with a biopsy but there is no screening test that will reveal carriers or affected animals that have yet to become symptomatic. Generalized Demodectic Mange Sometimes a dog's immune system will be incapable of accepting the presence of demodex mites and will repeatedly react to them, with affected areas spreading across the body. Untreated, the entire skin surface can become involved and severe secondary bacterial infections may develop, a miserable and likely fatal state. Diagnosis is made on the appearance of the lesions and case history. There are no screening tests. Myasthenia Gravis In this disease the immune system targets the motor end plates—the connection between the nerves and the voluntary muscles. Affected dogs tire easily and may stumble for no apparent reason. They often also have megaesophagus. Vigorous exercise may bring on collapse and severe attacks can mimic toxic exposure. The disease can be acquired, but is more likely to be inherited. There is no screening test.   Other autoimmune diseases seen less frequently in Aussies include pemphigus, Vogt-Koyanagi-Harada (uveodermatologic) Sydrome, Addison's Disease, idiopathic thrombocytopenic purpura, inflammatory bowel disease, diabetes mellitus, and glomerulonephritis. The author's own family provides an example of the familial effect of autoimmune disease. As mentioned previously, the author suffers from an autoimmune eye disease, her sister has lupus erythematosus, her brother's daughter has rheumatoid arthritis, and her other sister's daughter has inflammatory bowel disease. All these diseases are different but all are autoimmune, indicating that the author's parents had an unfortunate combination of MHC haplotypes to pass on to their offspring. Based on her mother's extensive family genealogical studies, the author is confident that her family is not inbred. Unfortunately, Aussies and other purebred dogs generally are. The more inbred a population is, the more widespread the incidence of autoimmune disease can be. Allergies Dogs also get allergies, just as we do. Like us, dogs can have respiratory or digestive problems caused by allergies, but most likely they will itch. Allergic reactions are rarely fatal for dogs, though they are a persistent nuisance and, for some especially sensitive dogs, a source of ongoing misery. A severely allergic dog may itch constantly, damaging its skin and coat with continual scratching, biting and rubbing. The skin damage may result in secondary bacterial and yeast infections. An allergic dog may also have chronic and occasionally severe respiratory or digestive problems. Or, in the worst-case scenario, succumb to anaphylactic shock. However, with proper diagnosis and treatment, most dogs can live in relative comfort. Allergies are the physical expression of the immune system's over-reaction to substances, called “allergens.â€? Allergens are not normally irritants and will not bother a normal individual. Allergens can range from pollens and molds to common food items. Flea bite dermatitis is the most common canine allergy; the allergen involved is the saliva of fleas. Allergies are often discussed in the media, heightening our awareness and sometimes prompting us to call something an “allergyâ€? when it really is not. Diagnosis of canine allergies should be made by a veterinarian; not through the owner's assumptions. Even though allergies generally don't develop until a dog is at least six months old, allergen exposure usually takes place before four months of age. An allergy does not develop unless there has been prior exposure, which allowed the immune system to recognize the allergen and decide? that it needed to be attacked if encountered again. This attack upon subsequent exposure is what causes the allergic reaction. Exposure can occur through breathing or eating the allergen or getting it on the skin. Environmental factors that contribute to allergies include not only exposure to allergens, but parasite load and the administration of vaccines. If a dog has parasites, the immune system will react to their presence. The greater the parasitic load, the greater the stress on the dog’s immune system. This can lead to severe allergic reactions if the dog is also exposed to allergens. Fleas are the most problematic parasites where allergies are concerned, but heartworm and intestinal parasites can also set the dog up for allergy attacks. Both killed and modified live vaccines are potentially allergenic, though for very different reasons. Killed vaccines contain chemicals called adjuvants that enhance the efficacy of the vaccine without exposing the dog to the pathogen. The adjuvants can cause an allergic reaction. In the modified live vaccines, the toxins produced by the pathogen are what cause the reaction. One should keep in mind that in both cases, the vaccines are not the cause of the allergy, but the trigger. A dog must be genetically predisposed to allergies for the reaction to take place. Atopic dermatitis, a hypersensitivity reaction of the skin, is the second most common form of allergic reaction in dogs. When a dog is exposed to an allergen, usually by inhaling it, the immune system begins producing Immunoglobulin E (IgE), a special type of cell designed to target the allergen. The IgE activates mast cells that release several different substances including histamine, a chemical that causes itching, inflammation and swelling. Most mast cells are found around the feet, ears and anus so allergic reactions of the skin appear more commonly in these areas. If the skin within the ear is affected, the dog may also develop secondary ear infections. Dogs may also experience allergic respiratory problems, digestive problems and eye irritation, but these are much less frequent than the skin reactions. Respiratory reactions include an asthma-like chronic bronchitis. Affected dogs have a dry, hacking cough that can be brought on by exertion or by pressure on the trachea. Other dogs may have pulmonary infiltration with eosinophilia (PIE,) an allergic reaction in the lungs. Eosinophils are a type of white blood cell, the foot soldiers in the immune system's army. When faced with an infection or allergen, the body produces white cells to fight it. In PIE, the body produces too many of these cells in the lungs, causing respiratory distress. Food allergies can manifest as digestive problems or skin reactions. In humans, food allergy is over-diagnosed. This is probably also the case in dogs. A number of foods contain substances that can cause mast cells to release histamine, leading to an allergy-like reaction even in a normal individual. Any food can cause reactions in an allergy-prone dog, but some are more likely culprits than others. The portion of an allergen to which the immune system reacts is called an epitope. The proteins found in wheat have over 50 epitopes, so it is not surprising that allergic dogs often react to wheat-based feeds. Affected dogs tend to vomit within a couple hours of eating and may sometimes have loose stools. Skin reactions are not unusual. These dogs may have difficulty maintaining weight, despite a good appetite. Severely allergic individuals have chronic diarrhea, significant weight loss and poor coat quality. Food allergies often arise after a case of infectious enteritis. The most severe and potentially fatal form of allergic reaction is anaphylactic shock. It can occur after eating something containing an allergen, an injection of drugs or vaccine, or the bite of an insect. Affected dogs will have difficulty breathing. Their gums will be pale due to a drop in blood pressure. Immediate veterinary treatment is necessary. Some allergic females have fertility problems. It is uncertain whether these are secondary to the allergies or their level of inbreeding (i.e. inbreeding depression.) Allergies may commence as early as six months and have been reported to begin as late as seven years, though most affected dogs will have shown signs by the time they are two or three years old. Depending on the allergens that the dog reacts to, its problems may initially be seasonal, but most cases will advance into a year-round condition. The Genetic Problem The over-all canine gene pool probably contains as much MHC diversity as it ever did. However, the division of that gene pool into mutually exclusive sub-sets, or breeds, has guaranteed that any one breed cannot have the full range of MHC alleles present in the species. This limiting factor is further exacerbated by standard breeding practices such as inbreeding and the use of popular sires. Without diversity within the MHC, the dog will catch a disease. If the disease is bad enough, the dog may die. If there were only a few possible MHC haplotypes in a breed or species, the risk of an entire population being wiped out by a virulent plague would be very high. The cheetah provides an example from nature. This wild cat species went through an extreme genetic bottleneck sometime in the last ice age. All modern cheetahs are descended from a very few individuals, possibly from a single pregnant female. Thanks to Nature’s harsh culling practices' far more stringent than those applied by any dog breeder - the cheetah has survived, but even so it is extremely susceptible to some kinds of disease. But purebred dog breeds have been artificially selected to meet human needs. In recent decades that selection, especially in show breeds or lines, has included significant inbreeding. The regular use of popular sires over several generations can play havoc with MHC diversity. Since any individual can only have two MHC haplotypes, if a significant portion of a breed descends from a relative few individual dogs the population may not be able to respond effectively to the next canine plague that comes along. Nor may they be able to effectively utilize vaccines. Rottweilers, for example, responded poorly to early parvo vaccines. This often left them vulnerable to the disease if they encountered it. Before the immune system can mount a response to an antigen, the antigen must be first broken into pieces inside the cell and transported to special cell surface receptors. These antigen-binding molecules are called histocompatibility molecules. In Rotts, the parvo vaccines did not work because the body couldn't react to it and thereby protect itself from the disease. Fortunately, the newest generation of vaccines seems to be much more effective in this breed. For more than a century, inbreeding has been the norm in domestic dogs. The technique is used quite effectively to “fixâ€? traits deemed desirable. This works very well with traits that can readily be observed and measured, such as shape, size and color. It also works, though less well, with complex traits which do not lend themselves to quantification (behavior, temperament, performance drives, etc.) The practice of inbreeding to improve breed traits has inadvertently led to a reduction of MHC diversity within the various breeds. When added to genetic bottlenecks due to wars, loss of popularity and other drastic population-reducing events, combined with the extensive use of popular sires, MHC diversity may be lowered to critical levels. Popular sire use is especially pernicious because each such sire can have only two MHC haplotypes--nowhere near the hundreds that exist in the canine genome. Therefore, when a significant portion of a breed descends from one individual, those dogs' resistance to infectious disease or susceptibility to autoimmune disease can be seriously affected. A correlation has been drawn between the coefficient of inbreeding (COI) and MHC heterozygosity. The COI is a measure of how inbred an individual is. Individuals with low COIs (less inbred) are more likely to have two different MHC haplotypes. Indications of MHC homozygosity are not always as obvious as an Aussie's susceptibility to autoimmune diseases like thyroiditis or a Rott's inability to react to parvo vaccine. Sometimes the effects are quite subtle. The dog may be a "poor keeper"? Or it may be sickly, catching one minor infection after another, but never coming down with anything really serious. Or it may be unable to shake an infection in spite of diligent treatment. What to do? While homozygosity of some genes is desirable, particularly those for breed traits like physical type or character, it clearly is not where the MHC is concerned. Most important breed traits are already fixed one doesn't see a purebred Aussie that looks like a Chinese Crested or trails with the obsession of a Bloodhound. Aussies look and act like Aussies, however much we quibble over the fine points. Given that, breeders must give the prevention of immune-mediated disease a much higher priority, maintaining MHC heterozygosity through reduced inbreeding and not using individuals with chronically impaired immune systems Unfortunately, there is no way for a dog breeder to determine what MHC haplotypes his breeding stock have. However, there are several steps he can take to limit the risk of producing dogs with immune-mediated disease. First, no dog affected with chronic autoimmune disease or serious allergies should be bred. If an animal is being maintained successfully on medication, the breeder should not delude himself that it is “curedâ€? and the disease is not a problem. The sickly and poor keepers should also be removed from breeding programs. At all costs, avoid the over-use of any individual dog, no matter how fine a specimen it might be. When making breeding decisions, the breeder should avoid crosses that increase the COI above that of the parents and, wherever possible, seek to reduce it. Breeders should be aware of their dogs' COIs. To detect inbreeding that is not apparent in the common three- to five- generation written pedigrees, the COI should be calculated over several more generations. How many generations depends on the genetic history of the breed, but for most, including Aussies, ten will be adequate. If the COI is high (12.5% or more), mates should be selected which will give a COI in the puppies that is lower than that of the parent with the family history of immune-mediated disease. No matter what the COI, any dog from a family with these diseases should be bred to mates whose families do not. Neither parents, siblings nor offspring of affected individuals should be bred back on the affected pedigree. Members of affected families used for breeding should be paired with mates from families free of disease. Breeding pairs should be selected that produce puppies with a lower COI than that of the parent from the autoimmune affected family. This will increase the probability of diversity in the MHC. The closer the relationship between an individual and its affected family member, the more care should be taken in mate selection as regards this kind of disease. If an individual dog has produced multiple cases of autoimmune disease or allergies, especially in different and relatively unrelated mates, serious consideration should be given to withholding it from further breeding. Crosses that produce autoimmune disease or allergies should never be repeated. If there is significant risk that a particular dog may develop autoimmune disease or allergy, as is the case with the siblings or offspring of one already affected, it would be wise to hold off breeding that dog until it is 3 or 4 years old to be reasonably assured it will not develop disease. As with any inherited problem, breeders would do well to record as much information as possible on the allergy and autoimmune disease status of numerous relatives of the dogs they intend to use for breeding. This includes his sisters and his cousins and his aunts - those dogs not directly on the pedigree. The more affected family members a dog has, the more likely it is to develop allergies or produce young who will. If screening tests are available for a disease that is frequently encountered, such as thyroiditis they should be used, as should screening tests for diseases that have occurred in a dog's family. It is up to us The storm is upon us and will not soon dissipate. Due to the complex nature of immune-mediated disease, its total eradication is unlikely in the foreseeable future. Potential impact on breed health is great. Even though we lack the ability to eliminate this kind of disease, damage control must be instituted. We can shelter our dogs from this rising storm if we commit to working within our own breeding programs and in cooperation with fellow breeders to make that reduction a priority. While no breeder can guarantee he will not produce a dog affected with immune-mediated disease, with good record keeping, diligence and foresight the risk of producing these costly, potentially devastating, and sometimes-fatal diseases can be significantly reduced.
Tuesday, 01 January 2008 | 12861 hits
by C.A. Sharp   "Inbreeding was once a valuable tool in shaping today's breeds. As these have now reached a high degree of homogeneity, it has lost its importance and turned into a fatal and disastrous habit." -Hellmuth Wachtel, PhD Inbreeding (which, for the purposes of this article, includes "linebreeding" ) has been the rule in dog breeding for the better part of two centuries. Before that, breeders bred "like-to-like." Records may or may not have been kept, depending on the literacy, social status or interest of the breeder. Pedigrees were of marginal interest, if they were considered at all. Registries, as we know them now, did not exist. New individuals might be introduced to the breeding pool at any time, so long as they displayed characteristics that the breeder wanted to perpetuate. Even an unplanned mating with a dog that would never have been deliberately selected might be shrugged off so long as some of the offspring proved useful. In the nineteenth century, prominent European breeders of various domestic species, including dogs, became interested in maintaining the "purity" of their bloodlines. They had no knowledge of genetics, indeed the science had yet to be born. Their breeding theories were a reflection of social attitudes of the times. It should also be kept in mind that these individuals were mostly wealthy men whose human pedigrees were considered better than those of "common" people. As pedigrees became more important, so did the regular appearance of significant names in those pedigrees. Eventually registries were established to keep official records. At some point, virtually all dog registries became closed. Most of this occurred before breeders had even a rudimentary knowledge of genetic science. At first, inbreeding proved beneficial. Breeders learned that by mating related individuals of the desired type, the resulting quality and uniformity of the offspring improved As people began to learn basic genetics in the early part of this century, they deliberately sought to fix desired traits, particularly in production livestock, by breeding near relatives. This practice continues to the present day. A sire will be "progeny-tested" by being bred to a group of his daughters. If the offspring measure up, he will be kept for stud. If they don't, everybody goes to market. This drastic culling serves its purpose in livestock, but it is impractical and unacceptable in companion animals such as dogs. Nature goes to great lengths to discourage inbreeding. Related animals rarely mate, which prevents genes for diseases and defects from coming together with any great frequency. Wild animals have a variety of behaviors which will eliminate or severely restrict inbreeding. In wolves, the species most closely related to dogs, only the alpha pair will breed. Pups stay with the pack for their first year. After that time they must find a place, often low-ranking, within the adult hierarchy. If a yearling cannot accept this or it becomes the brunt of too much negative social interaction, it will disperse. Dispersers may have to travel many miles before they can find an available territory and a mate, if they can find them at all. Those individuals which do not disperse will not be breeders unless they should someday attain alpha status, so the breeding of relatives is unlikely. Sometimes circumstances give animals no choice but to mate with relatives. If those conditions persist for any length of time they create a "genetic bottleneck." The wolves of Isle Royale in Lake Michigan descend from a very small number of animals which crossed from the mainland decades ago during a hard winter when the lake froze over. Their present-day descendants have proved more than usually vulnerable to an assortment of diseases and parasites. When canine parvovirus reached Isle Royale, the wolf population plummeted so badly that some observers at the time feared the wolves would die out entirely. In recent years, purebred dogs have experienced increasing problems with hereditary diseases and defects. The causes are complex, including genetic load, the presence of lethal equivalents in all individuals, genetic bottlenecks, closed gene pools, gene pool fragmentation, and genetic drift, but all are attributable to inbreeding. Thanks to closed registries, breeds form exclusive gene pools. All gene pools, no matter how large or diverse, will have a genetic load - the difference between the fittest possible genotype and the average fitness of the population. "Fitness" is the individual's over-all health, vigor and ability. It may or may not directly relate to traits breeders select for. (The English Bulldog, for instance, has an "ideal" physical form which virtually precludes females from being able to naturally whelp their young.) The greater the genetic load, the more genetic difficulties members of a breed are likely to suffer. In a closed gene pool, the situation may remain stable or deteriorate. It cannot get better. Each individual within a breed also carries it's own kind of load - four or five genes for potentially fatal diseases or defects. These are called "lethal equivalents." In most cases they will not affect the individual carrying them because a single allele, or form of the gene, will be insufficient to cause the problem. But when relatives are mated, the odds of matching up those alleles increases and as does the frequency the disease. Every population must deal with genetic load and lethal equivalents, but when the population is prevented having genetic exchange with other similar populations, genetic diversity within the population begins to diminish. Some of this may be beyond anyone's control. A breed's function may have become obsolete, resulting in only a few surviving members. This was the case with the Portuguese Water Dog. All present-day PWDs descend from a handful of dogs. Social, political or environmental difficulties may also preclude breeding, causing populations to crash. Many breeds experienced a genetic bottleneck at the time of World War II. With much of the world at war, dog breeding was not a high priority and populations in areas of military action were often wiped out or severely depleted. In such a situation, breeders can only make do with what remains. It's a tough row to hoe for the truly rare breeds, especially since the prevailing attitude that breeds must be kept "pure" prevents supplementing with fresh genetic material from similar, less impacted, populations. Breed gene pools can fragmented into so many gene puddles when they are arbitrarily split along size, color or coat-type lines, with dogs of one color or variety prohibited from mating with those of another. No matter how diverse a breed may have been before such distinctions were made, afterwards breeders have fewer options when choosing mates and the eventual result will be increased inbreeding because there isn't anywhere else to go. One striking example of this is the Belgian Sheepdog in the United States. Outside the US this breed contains four varieties, all of which might occur in a single litter. The American Kennel Club lists three of varieties as entirely separate breeds. The fourth isn't even recognized. In the US they cannot be interbred though throughout the rest of the world, they can. Changes in social conditions may also fragment breed gene pools. The Australian Shepherd was originally a working ranch and farm dog. Today there are far more Aussies than there are "jobs" on farms and ranches; so most are companion animals. Over the past three decades, the breed has clearly split between working and conformation strains with a third, smaller, category of "versatility" animals whose breeders work toward a multi-purpose animal .There is also a population of "mini" Aussies dogs whose size is below the breed norm. They are often registered as Australian Shepherds along with listing in a registry for minis. There is very little breeding between these various sub-groups though all trace back to more-or-less overlapping sets of founder animals. One of the results of gene pool fragmentation is loss of alleles that may exist in the breed but didn't happen to occur in the founders for that variety. Genetic drift can cause further loss. Genes not being specifically selected for tend to "drift" out of the gene pool. Many of these will be for things so subtle they might never come to a breeder's direct attention. A dog has some 100,000 genes, only a relative few of which are for things we can readily observe or measure. Many of these genes cause minor variations in form or bodily function. Cumulative losses of such genes through genetic drift can reduce overall health and fitness without presenting consistent or identifiable signs; a dog may seem to be a poor keeper, unusually subject to minor ailments, or lacking in endurance. Even "typical" breed behaviors, such as herding ability, can be diminished in this manner, if breeders are not using the behavior as part of their selection criteria. The use of popular sires, particularly multiple generations of them, can accelerate loss of alleles. A dog can only have a maximum of two alleles for any given gene. Excessive use of a single individual will skew the gene pool toward the alleles that dog happened to carry. Obviously, such a dog gets heavy use because he has desirable traits. Genes for those traits will become more common, but so will those for his lethal equivalents and more subtle ills. And if a deleterious gene is "linked" (sits close on the chromosome) to a desired gene the sire carries, the breed may suddenly find itself riddled with the problem that bad gene causes. It won't be easy to eliminate unless breeders are also willing to give up the linked desired trait. Proponents of inbreeding often point out that mongrels have more genetic problems than purebreds. While it is true that mongrels, as a group, have more individual kinds of diseases and defects than any single pure breed, it must be remembered that each breed represents only a portion of the canine gene pool, whereas mongrels encompass all of it. If mongrels' defects are compared to those found among all pure breeds, the discrepancy disappears. Since mongrels usually are the result of random, unplanned breeding, the incidence of defects is low in the overall population. In pure breeds many of those same defects are common. For instance, progressive retinal atrophy and collie eye anomaly are rare in mongrels. Incidence of both is high in Collies. It is becoming more and more apparent that the short-term gains of inbreeding are outweighed by its long-term costs. Present-day breeders need to re-think their strategy. Assortative mating - the mating of phenotypically similar but unrelated or less-related individuals - will allow breeders to reach their breeding goals while reducing the loss of alleles in the over-all population. To accomplish this it is vital that each breeder has a thorough knowledge of breed pedigrees. The typical three to five generation pedigree may indicate few, if any, common ancestors. But what happens if the pedigree is extended a few more generations? If two dogs share no ancestors for four generations, but share many in the 5th, 6th and so on, breeding them would be inbreeding. All members of a single breed are, of course, related to some degree, though how much varies from breed to breed. Somewhere back in each breed's history there is a group of founders from whom all present-day dogs descend. Portuguese Water Dogs have very few, Australian Shepherds have quite a number, though not every Aussie goes back to all of them. It is important to know who the founder individuals were, particularly if the breed is rare, split into varieties or experienced a significant bottleneck at some point in its history. A large number of founders allows for greater diversity (assuming those founders were, themselves, unrelated), but if some are heavily represented in comparison to others due to inbreeding on their descendents, diversity is at risk. Breeders should strive to increase the representation of the neglected founders whenever possible. Calculation of inbreeding coefficients will give an indication of how inbred a dog or a prospective cross is. Knowing these numbers enables the breeder to make choices that will reduce inbreeding. Good books on animal breeding will have a section explaining how this is done, but calculating them by hand becomes cumbersome when working with a full pedigree. There are pedigree programs on the market which will perform these calculations. Perhaps the most important issue is making health a top priority. It is obvious even to those who promote inbreeding that screening for genetic diseases and not breeding affected individuals is important. As tests become available which will detect carriers of genetic problems, they should be put to use. However, carrier status should not automatically preclude breeding of otherwise good individuals. Care should be taken that they aren't bred to other carriers and those who buy puppies from a carrier parent should be advised to screen the pup if they want to breed it. But eliminating proven carriers as breeding stock is throwing our their many good genes while avoiding one bad one. Australian Shepherd breeders are doing this with Pelger-Huet Anomaly. PHA is lethal to offspring that inherit two copies of the gene, resulting in reduced litter size and neonatal deaths. Carriers rarely suffer any effects. Knowledgeable breeders use a blood test to screen and carriers are bred to non-carriers. Less specific aspects of health must also be considered. A dog that is a "hard keeper, or repeatedly comes down with one minor ill or another should not be a breeding prospect. These individuals likely carry a surplus of genes which individually have only a small negative effect on health but cumulatively have produced an unthrifty individual. A common result of inbreeding is "inbreeding depression," typified by small litter size or difficulty producing or rearing young. Bitches from families that consistently produce small litters may be suffering inbreeding depression. Animals which can only be bred or raise their puppies if they receive extraordinary human assistance are poor breeding candidates. This is not to say that people shouldn't properly house and care for their animals, but if a dog is indifferent to bitches in standing heat or a bitch needs to be physically restrained to keep her from resorting to fight or flight in an attempt to prevent mating, or won't settle without veterinary intervention, or is apt to kill or damage her puppies through intent or neglect, these are signs of inbreeding depression and that animal shouldn't be bred. Breeders should not go to excessive, near surgical, lengths to control the environment for newborns, nor should they use heroic measures to keep failing whelps alive. (For those who find this too callous: Save them if you will, but don't breed them.) Inbreeding gave us the many breeds of dog we enjoy today, but its time is past. If purebred dogs are to remain viable into the next century breeders need to rethink their strategy and work toward their goals with more emphasis on over-all health and concerted efforts to reduce the level of inbreeding in their dogs.   C.A. Sharp is editor of the "Double Helix Network News". This article appeared in Vol. VII, No. 1 (Winter 1999). It may be reprinted providing it is not altered and appropriate credit is given.  
Tuesday, 01 January 2008 | 11971 hits
By Norma Bennett Woolf   Introduction | Thyroid Gland | Diagnosis | Treatment | Inherited Disease Introduction Canine thyroid disease can be tough to diagnose.The symptoms can be legion and sometimes contradictory: lethargy, mental lassitude, weight gain, dull coat, skin infections, constipation, diarrhea, cold intolerance, skin odor, hair loss, greasy skin, dry skin, reproductive problems, aggression, and more. The associated diseases or conditions can be serious: megaesophagus, ruptured knee ligaments, testicular atrophy, cardiomyopathy, excessive bleeding, and corneal ulcers. The disease can be inherited or of unknown or uncertain origin. The diagnosis can be complex; the treatment as simple as supplementing a basic essential hormone. This is the description of canine hypothyroidism, the absence of sufficient thyroid hormone to maintain healthy body functions. Thyroid Gland  The mammalian body has 10 systems - skeletal, muscle, digestive, circulatory, excretory, integumentary (skin), respiratory, nervous, endocrine (ductless glands), and reproductive - that must be working properly for the animal to stay in good health. Endocrine glands secrete hormones that help manage the body's processes. The thyroid gland lies on the dog's trachea, just below the larynx; triiodothyronine and levothyroxine, the hormones produced by the thyroid, govern the body's basic metabolism - including control of growth and development and maintenance of protein, carbohydrate, and lipid metabolism - throughout life. Failure of the thyroid gland means trouble of one sort or another for the body. The clinical signs can mimic other diseases. Weight gain, lethargy, mental dullness, skin abnormalities, weakness, and a decrease in tolerance for exercise are most often seen, along with behavioral changes that owners may not attribute to physical causes often occur: the sweet dog can become aggressive and the steady dog may become flighty or fearful. Diagnosis Thyroid disease is considered the most common endocrine disease of dogs. Because susceptibility to one form of the disease may be inherited, it is of great concern to breeders. However, in spite of the attention the disease has received from researchers and the development of more precise diagnostic tests, hypothyroidism is not easy to identify. Part of the problem is that chronic or temporary illness, reproductive hormones, drugs, obesity, and exposure of the dog to temperature extremes can affect the test. Sometimes the only sure test is to supplement with thyroid hormone; if symptoms subside, the diagnosis was accurate. Veterinarians may suggest a thyroid test if a pet has gained weight or is having chronic skin infections or if a breeding dog is experiencing reproductive difficulties, especially if the animal lacks energy and has a scruffy or dull coat. The veterinarian draws the blood and sends it to one of several laboratories with the equipment for conducting the test. The blood sample should be taken when the dog is otherwise healthy, is not approaching or in a heat cycle, and is not taking pharmaceuticals such as steroids, non-steroidal anti-inflammatories, or anti-seizure drugs. The latest tests include measurement of two forms of the thyroid hormones T3 (triiodothyronine) and T4 (levothyroxine) and a search for antibodies that could indicate autoimmune thyroiditis, the genetic form of the disease. Interpretation of the numbers recorded is as important as the numbers themselves, for the relationship between the hormones is complex. In addition, normal ranges of hormone vary somewhat with the breed or mix. Treatment Treatment consists of two daily doses of levothyroxine, the hormone identified in the test as T4. Levothyroxine is converted to triiodothyronine by the body; dogs that cannot make this conversion will need both levothyroxine and triiodothyronine. The dosage is based on body weight; thyroid hormones are quickly metabolized and excreted from the body, so splitting the dose is most effective. One to two months after starting the dog on thyroid therapy, the veterinarian will probably want to redo the tests to make sure the levels are within the normal range. Blood should be drawn four-to-six hours after the morning dose. Dogs on long-term thyroid therapy should have a complete panel of tests every six to 12 months. Inherited Disease Some dogs have a genetic susceptibility to diseases that attack their own immune system. Researchers suspect that these immune-mediated diseases may be triggered by environmental chemicals, viruses, repeated inoculation with multi-valent modified live vaccines, and other immune system challengers. The presence of autoantibodies in the thyroid test is considered by some researchers and breeders to be a forecaster of autoimmune lymphocytic thyroiditis - the inherited form of the disease - but other researchers consider the data base of information to be too small to make that call. However, breeders should test their dogs and bitches, keep good records, and be wary of using animals with the potential to further spread the disease. Studies indicate that the breeds most commonly affected by autoimmune lymphocytic thyroiditis include Golden Retriever, Great Dane, Beagle, Borzoi, Shetland Sheepdog, American Cocker Spaniel, Labrador Retriever, Rottweiler, Boxer, Doberman Pinscher, German Shepherd, Akita, Old English Sheepdog, and Irish Setter. Symptoms usually appear between one and five years of age, but blood tests can indicate the potential for disease before clinical signs appear. Unfortunately, a clean thyroid test at one year of age does not mean the dog will remain free of disease throughout its life. In August 1996, the American Kennel Club Canine Health Foundation hosted an international symposium on canine hypothy-roidism at the University of California at Davis. Here the world's experts on the disease shared findings, asked and answered questions, and suggested avenues for further study to increase understanding of the disease, improve diagnostic tests, and identify a genetic marker for the inherited form of the disease. Until more is known, however, dog owners can watch their pets for the classic signs of thyroid disease manifestation as outlined above and potential dog owners can ask breeders if the sire and dam of that wonderful litter have been screened for thyroid disease or are taking thyroid medication. Even though the tests are not perfect, the answer will indicate a breeder's commitment to ridding his dogs of thyroid disorder.   © 2002 by Canis Major Publications. Reproduced with permission.    
Tuesday, 01 January 2008 | 13561 hits
Policy & Procedure for compiling Judges Lists 1) The Club will use the A1, A2 & A3 lists as recommended by the Kennel Club 2) The Club will formulate B & C lists and anyone wishing to be considered for these lists should complete the DDTC Judges Questionaire. 3) Applicants will be informed of the Committee's decision in writing. 4) The list will be available to Secretaries of Show Societies to help promote judges of the Breed who are supported by the Club
Tuesday, 01 January 2008 | 6255 hits
5th July 2003.  Judge: Mrs P Stallard (Huntershill)   Main Results Dog CC & B.O.B Buist & Chapman-King's CH INZIEVAR WILLIAM WALLACE Reserve Dog CC Sample's DENTGATE WATERMARK Bitch CC Tinsley's CLOVERWOOD MINNOW Reserve Bitch CC Cameron & Chapman-King's INZIEVAR SILVER JUBILEE Best Puppy Bromley's MISHAHDA CINNAMON CRUMBLE     Class Results - Dogs Junior 1st: Gilluley & Haron's PENACTIV BLUE MOON 2nd: Fisher's DENGOLD CAPTAIN ARCHER OF GYPSYWISH Post Graduate 1st: Hamilton's MARGHAM LORD OF THE DANCE 2nd: Hughes' MAGANBAR BLACK MULBERRY 3rd: Lowton's MAGANBAR SUNDANCER Limit 1st: Sample's DENTGATE WATERMARK 2nd: Burnett's OAKSLEIGH BIGGLES FLYS EAST 3rd: James' ZANNEUS ZIMBA Open 1st: Buist & Chapman-King's CH INZIEVAR WILLIAM WALLACE 2nd: Wheble's CH FERNROYAL MISTER CHUCKLES AT PENACTIV 3rd: Wither's SWANWILLOW STONECHAT WITH PAJANTICKS Res: James' ZANNEUS ZIMBA Class Results - Bitches Puppy 1st: Bromley's MISHAHDA CINNAMON CRUMBLE 2nd: Justice's DANDALEITH ADVENT SPICE 3rd: Burnett's OAKSLEIGH CHRISTMAS CAROL Junior 1st: Wheble's PENTACTIV LUST FOR LIFE 2nd: James' ZANNEUS ZANDIE 3rd: Bailey's STINCHCOMBE PENNY CRESS Res: Wheble's PENTACTIV EVERGREEN Post Graduate 1st: Dennis & Green's PENTACTIV MADE IN HEAVEN OF ABBEYWATER 2nd: Tinsley's CLOVERWOOD BORDER GOLD 3rd: Fisher's OAKSLEIGH MAGGIE MAY OF GYPSYWISH Res: Hows' KUDDLEMEE ON A MOONBEAM VHC: Hamilton's MARGHAM RUBY TUESDAY Limit 1st: Tinsley's CLOVERWOOD MINNOW 2nd: Hamilton's PENACTIV MONDAY MONDAY AT MARGHAM 3rd: Bailey's STINCHCOMBE LOVE IN A MIST Res: James' ZANNEUS ZARA VHC: Sample's BENCHARRA STARE IF YOU DARE Open 1st: Cameron & Chapman-King's INZIEVAR SILVER JUBILEE 2nd: Deacon's CASSENCARRIE CALVADOS 3rd: Bailey's STINCHCOMBE MEADOW SAFFRON Res: James' ZANNEUS ZARA VHC: Bromley's FINLOREN FANTASIA AT MISHADA
Saturday, 05 July 2003 | 3777 hits
9th May 2003.  Judge: Mr P Chappell (Mariquita)       Main Results Dog CC & B.O.B Buist & Chapman-King's CH INZIEVAR WILLIAM WALLACE Reserve Dog CC Derry's VISTCA VAN DER VALK Bitch CC Shore's SWANWILLOW FORGET-ME-NOT Reserve Bitch CC Bromley's FINLOREN FANTASIA AT MISHAHDA Best Puppy Derry's VISTCA VAN DER VALK     Class Results - Dogs Puppy 1st: Derry's VISTCA VAN DER VALK 2nd: Fisher's DENGOLD CAPTAIN ARCHER OF GYPSYWISH 3rd: Harpwood's FINLOREN NICHOLAS NICKELBY Junior 1st: McLeod's HEALAVAL USQUEBAE Post Graduate 1st: Sample's DENTGATE WATERMARK Limit 1st: Coleman's FOLLYCOTT FRANK LEE 2nd: Gibson's SOMERCLOUD HANDYMAN Open 1st: Buist & Chapman-King's CH INZIEVAR WILLIAM WALLACE 2nd: Shore's CH FINLOREN THE LAIRD OF SWANWILLOW Class Results - Bitches Puppy 1st: Gibson & Halliwell's DENGOLD NERYS Junior 1st: Shore's SWANWILLOW FORGET ME NOT 2nd: Heywood's SCHALULLEKE LIZZYWEAVER 3rd: Camm's SWANWILLOW PRIMULA AT SOMERCLOUD Post Graduate 1st: Tinsley's CLOVERWOOD MINNOW 2nd: Fisher's OAKSLEIGH MAGGIE MAY OF GYPSYWISH Limit 1st: Russell's HENDELL GOLDEN DAWN WITH HAWKESMILL 2nd: Cameron & Chapman-King's INZIEVAR SILVER JUBILEE Open 1st: Bromley's FINLOREN FANTASIA AT MISHAHDA 2nd: Harpwood's FINLOREN LADY JANE GREY 3rd: Tinsley's CH HENDELL DAMASK ROSE AT CLOVERWOOD
Friday, 09 May 2003 | 3824 hits
20th June 2003.  Judge: Mrs Jane Withers (Pajanticks)       Main Results Dog CC & B.O.B Gilbert's CASSENCARRIE KEYMASTER Reserve Dog CC Harpwood's FINLOREN NICHOLAS NICKELBY Bitch CC Jarvis' CH MOSTERLADA FOXY LADY Reserve Bitch CC Deacon's CASSENCARRIE KALVADOS Best Puppy Harpwood's FINLOREN NICHOLAS NICKELBY     Class Results - Dogs Puppy 1st: Harpwood's FINLOREN NICHOLAS NICKELBY 2nd: William's WESTWELL SKYLARK 3rd: Harper & Barbour's OAKSEAL ZORIL OF KIRKBRAE Junior 1st: McLeod's HEALAVAL USQUEBAE 2nd: Peacock & Styler's FERNROYAL MAGICAL 3rd: Fisher's DENGOLD CAPTAIN ARCHER OF GYPSYWISH Novice 1st: McLeod's HEALAVAL USQUEBAE 2nd: Heaton's MOORBARROW DUNCAN Limit 1st: Mannia's FINLOREN THE LION IN WINTER AT KIRSKILL 2nd: Sample's DENTGATE WATERMARK Open 1st:Gilbert's CASSENCARRIE KEYMASTER 2nd: Shore's CH FINLOREN THE LAIRD OF SWANWILLOW 3rd: Harpwood's CH FINLOREN FRIAR TUCK Veteran 1st: Halliwell's DENGOLD MULBERRY Class Results - Bitches Puppy 1st: Bromley's MISHAHDA CINNAMON CRUMBLE Junior 1st: Heywood's SCHALULLEKE LIZZY WEAVER 2nd: Camm's SWANWILLOW PRIMULA AT SOMERCLOUD 3rd: Shore's SWANWILLOW FORGET-ME-NOT Post Graduate 1st: Robinson's POYNTON PUSHMATAHA 2nd: Fisher's OAKSLEIGH MAGGIE MAY OF GYPSYWISH 3rd: Oakes & Searle's OAKSEAL ZEPHYR Limit 1st: Motler's FINLOREN LADY ELOISE AT WAZZLY 2nd: Oakes & Searle's BRACKENFORD CAMEO 3rd: Sample's BENCHARRA STARE IF YOU DARE Open 1st: Jarvis' CH MOSTERLADA FOXY LADY 2nd: Deacon's CASSENCARRIE KALVADOS 3rd: Bromley's FINLOREN FANTASIA AT MISHADA
Friday, 20 June 2003 | 4302 hits
14th June 2003.  Judge: Mr John Burrows       Main Results Dog CC & B.O.B Buist & Chapman-King's CH INZIEVAR WILLIAM WALLACE Reserve Dog CC Derry's VISTCA VAN DER VALK Bitch CC France's TORBRAE DANCE ON DREAMS Reserve Bitch CC Chapman-King & Hislop's MOSTERLADA WILD HEATHER OF INZIEVAR Best Puppy Bromley's MISHADA CINNAMON CRUMBLE     Class Results - Dogs Puppy 1st: Harper & Barbour's OAKSEAL ZORIL OF KIRKBRAE Junior 1st: Derry's VISTCA VAN DER VALK 2nd: McLeod's HEALAVAL USQUEBAE 3rd: Peacock & Styler's FERNROYAL MAGICAL Novice 1st: McLeod's HEALAVAL USQUEBAE 2nd: Heaton's MOORBARROW DUNCAN Post Graduate 1st: Heaton's MICKLAM MOSS TROOPER Limit 1st: Walkley's BENCHARRA BACK IN THE FRAME FOR FOLLYCOTT 2nd: Chapman-King's INZIEVAR TINKERS GOLD 3rd: Mannia's FINLOREN THE LION IN WINTER AT KIRSKILL Open 1st: Buist & Chapman-King's CH INZIEVAR WILLIAM WALLACE 2nd: Shore's CH FINLOREN THE LAIRD OF SWANWILLOW 3rd: Halliwell's DENGOLD MULBERRY Class Results - Bitches Puppy 1st: Bromley's MISHAHDA CINNAMON CRUMBLE 2nd: Morrice's SHONILLIAN DANDILLY MILLY Junior 1st: Shore's SWANWILLOW FORGET-ME-NOT 2nd: Gibson & Halliwell's DENGOLD NERYS 3rd: McKenzie's VISTCA VANITA Novice 1st: McKenzie's VISTCA VANITA Post Graduate 1st: Chapman-King's & Hislop's MOSTERLADA WILD HEATHER OF INZIEVAR 2nd: Bedborough's PITFIRRANE LADY JANE 3rd: Lind's STRATHMONT OCEAN SPIRIT Res: Heaton's MOORBARROW TANZINE VHC: Heaton's MOORBARROW BLUEBELL Limit 1st: Kerrush's MICKLAM STEEL BONNET 2nd: Cameron & Chapman-King's INZIEVAR SILVER JUBILEE 3rd: Motler's FINLOREN LADY ELOISE AT WAZZLY Open 1st: France's TORBRAE DANCE ON DREAMS 2nd: Jarvis' CH MOSTERLADA FOXY LADY 3rd: Bromley's FINLOREN FANTASIA AT MISHADA Res: Morrice's CASSENCARRIE DIANTHUS OF SHONILLIAN
Saturday, 14 June 2003 | 4312 hits
11th August 2003.  Judge: Mrs S Linter       Main Results Dog CC & B.O.B Derry's VISTCA VAN DER VALK Reserve Dog CC Deacon's CASSENCARRIE BLITHE SPIRIT Bitch CC France's TORBRAE DANCE ON DREAMS Reserve Bitch CC Tinsley's CLOVERWOOD MINNOW Best Puppy Tinsley's CLOVERWOOD DANDIE DAZZLE     Class Results - Dogs Puppy 1st: Tinsley's CLOVERWOOD DANDIE DAZZLE Junior 1st: Williams' WESTWALL SKYLARK Post Graduate 1st: Hamilton's MARGHAM LORD OF THE DANCE 2nd: Lowton's MAGANBAR SUNDANCER Limit 1st: Derry's VISTCA VAN DER VALK 2nd: Sample's DENTGATE WATERMARK Open 1st:Deacon's CASSENCARRIE BLITHE SPIRIT 2nd: Wheble's CH FERNROYAL MISTER CHUCKLES AT PENACTIV Class Results - Bitches Puppy 1st: Bromley's MISHAHDA CINNAMON CRUMBLE 2nd: Tinsley's CLOVERWOOD ENGLISH ROSE Junior 1st: Wheble's PENACTIV EVERGREEN Post Graduate 1st: Hamilton's MARGHAM RUBY TUESDAY Limit 1st: Tinsley's CLOVERWOOD MINNOW 2nd: Sample's BENCHARRA STARE IF YOU DARE 3rd: Hughes' LACANMOR LEADING LIGHT Open 1st: France's TORBRAE DANCE ON DREAMS 2nd: Bromley's FINLOREN FANTASIA AT MISHADA 3rd: Hamilton's PENACTIV MONDAY MONDAY AT MARGHAM
Monday, 11 August 2003 | 4609 hits

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