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Collie Eye Anomoly
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Hypothyroidism
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Dermatomyositis
Hip Dysplasia



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It is my belief that what we put into the bodies of our dogs directly affects their heath. Without proper nutrition, even the most genetically sound dogs will not reach their full potential and could also have health problems as a result. Though I always believed this and did much research into canine nutrition to determine what would be considered a suitable diet for my dogs, I found much conflicting information and many unsubstantiated claims. I changed foods as one food would cease to "work" and try another. I knew that the best diet for dogs would resemble their natural diet as closely as possible, but also be fully balanced. I believed (and still do) that a quality well balanced raw diet is the best we can do for our dogs as it mimics what they would eat in the wild. Having said that, I also understand that feeding a biologically appropriate raw food diet is more involved than feeding a high quality kibble, and can be cost/space prohibitive for a number of large dogs. Therefore, I wanted the components of a raw diet, but in an affordable kibble form. I also wanted ingredients that were healthy and identifiable (chicken meal instead of poultry by products, etc.), human grade meats, some fruit and veggies, so I did not have to add them every meal, though we still provide them as snacks.

There are many kibbles out there that tout themselves to be "natural" and "completely balanced" and/or "holistic". The ingredients vary though, so the next step was determining what ingredients were good for a dog and which ones were not. Around the time I was in the midst of trying to determine the good ones from the bad and why they were either, we had a guest speaker on the list I help moderate. Dogtor J's beliefs about certain foods, backed with research and experiences of himself (he is a celiac) and his clients, made me sit up and listen. He told of epileptic patients that previously were on heavy meds and still seized, that had not had a seizure in years without medication; diabetics that did not need insulin any longer; immune mediated conditions cleared and the list goes on. What was the big change? Eliminating foods that were not natural, which also happened to be high in glycoproteins- a complex of sugar and protein which has adhesive properties- read GLUE. This is found mostly in the gluten grains (wheat, barley, and rye), dairy (the casein), and soy protein AND to a lesser extent corn. Dr J surmises that "the glue from the wheat, barley, corn, soy, and dairy starts sticking to the duodenal villi from day one that they start eating it. Each meal puts some coating on it because each bite has some glue in it. The coating reduces the absorption of calcium, vitamins plus a whole lot more. The glue, at the same time, is invoking an immune response in the gut which creates the allergies." Eliminating these unnatural foods from the diet allows the body to absorb the nutrients it needs. "On the other hand, glutamate is a single amino acid that just so happens to be abundant in those same foods but also is present in high quantity in non-glue foods, like peanuts, almonds, and beans. Glutamate itself does not act like glue unless it is part of the glycoprotein complex (which it is in the gluten grains, dairy, and soy). " He also advises to avoid all but cold pressed natural oils. Read why here and here and here.

The point is that the foods that are bad for us and our dogs are bad in NUMEROUS ways. We have had PLENTY of warning that these foods are going to be our undoing....the allergies, heartburn, pain, etc.etc. It's just that the drug companies have covered all of those symptoms up. For a glimpse into this, look up the root of the word pharmacy, it is pharmakeia.

It was the missing information I had been searching for. I then put it into practice with my owns dogs, who I thought were in good condition and healthy. In just a few days time I saw the difference and over the next few months instead of gradually losing condition, they actually looked even better, had more energy, got lovelier coats and held them longer (the mom of my last litter held her coat until puppies were 4 months old), stools stayed good and no more upset tummies. For the first time in years, we did not have to change food after just a few months. We did make changes to adjust protein/fat and carb levels as needed, but the ingredients are always chosen with the low glutamate foods in mind and I found I could switch directly from one food to the next without fear of stomach upset. For more information on his theories please visit Dr. J's site at Http://www.dogtorJ.com .

To take this further, I needed to look into what my breed required for nutrient levels. Each breed has certain requirements. For instance, a toy breed would require more protein for lean muscle and less fat than a large breed who would need more fat for immediately available energy and to store for the rest of the days requirements. I was always told active dogs need more protein, and fell into the trap of giving higher protein food to more active dogs, and lower protein for less active. I could not understand it when my active dogs remained lean and the less active dogs gained, so I fed the more active dogs more food and the less active dogs less. Then one day I picked up a different bag of food- the same brand food I had been feeding with the same ingredients but much lower protein and fat. Since there was no time to bring it back and exchange it, I just fed it and added some stewed chicken to try to make up for some of the protein and fat that was missing, one week wouldn't hurt and they loved the chicken being added. At the end of the week I did weight checks and was amazed to find that everyone had put on at least 5 pounds and I was not feeding more than the "normal" amount. Over the following weeks I reduced the amount of food gradually until I was maintaining proper weight. In the end I was feeding all dogs at least 1/3 less food. It was not the amount of protein afterall- it was the quality of protein (ie the amount the body can assimilate) and fat. With the chicken added- it had enough natural protein and fat that they could use it.

Here are the dry foods that meet my expectations for kibble AND have the right amount of protein and fat for a collie, keep in mind if changing from a higher protein or lower quality food, you may need to lower the amount fed by 1/2 c each week until you find the right amount:

 

Orijen 42% protein/16% fat (I highly recommend this if you must feed kibble as it has no grains and is closest to a raw diet).

EVO 42% protein/22% fat (I highly recommend this if you must feed kibble as it has no grains and is closest to a raw diet).

If impossible to find either of the above- the following will do with the addition of raw or cooked meat or poultry to add quality protein and fat:

Canidae maintenance 24% protein/14.5 fat

Innova Dog Dry 24% protein/14.5 fat

Eagle Natural 23% protein/12% fat

Nutro Natural Choice Chicken,Rice and Oatmeal 21% protein/12% fat

California Natural Chicken meal and rice 21.5% protein/11% fat

Burns food for Dogs 18.5% protein/7.5% fat

California Natural Chicken meal and rice 21.5% protein/11% fat

Solid Gold MMILLENNIA Beef and barley DOG FOOD 22% protein/12% fat

Nature's Variety Prairie Brand Canine Chicken & Rice Medley 24% protein/14 fat

Artemis Holistic Dog Food 23% protein/14% fat

Breeder's Choice Active Care Healthy Joint Formula Lamb Meal & Brown Rice 22% protein/12% fat

Breeder's Choice AvoDerm Adult Chicken Meal & Rice Formula 23% protein/13% fat

 

If the food you choose does not have probiotics in it, I recommend feeding some daily. Not only does it keep the digestive tract bacteria balanced, it also aids in utilizing the food to its full extent so you need to feed less. These occur naturally in raw foods, but is not present in processed diets (unless added back in) as cooking destroys them. Also it would be adviseable to keep some on hand for dogs which become ill or go off of thier normal diet (therefore not getting little if any probiotics). The best product line I have found is Fastrack®. Fastrack® Canine Gel is great for dogs who are suffering from digestive ailments due to illness or stress and has specialized proteins which act against Parvo Virus, E. Coli strains 0101K99 and 08 K88, coronavirus and rotavirus as well as newborn puppies. You may contact Kit for more information.

I also believe that large breed puppies do not need a diet higher in protein. Collie puppies should not be fat. Fat puppies are puppies that are getting too much protein and fat and are growing faster than is healthy for their joints. Rapid growth can produce heavy muscle mass which puts undue strain on immature bones. It is well established that high intake of protein and fat during puppyhood leads to health problems in the adult; for example obesity and skeletal disorders, especially hip dysplasia.
I recommend feeding a high quality adult diet of no more than 25% protein with one spoonful of scraped meat or chicken added or 21%-23% protein with a 2 spoonfuls of scraped meat or chicken added until 6 months old. If the food does not contain Vit C, I add 500 mg.

For puppies if a bit higher protein/fat food is desired:

Royal Canin Sensible Choice chicken and rice adult maintence 25% protein/15% fat

Breeder's Choice Pinnacle Canine Chicken & Oats Formula 25% protein/15% fat

Breeder's Choice Active Care Healthy Joint Formula Chicken Meal & Brown Rice 25% protein/15% fat

Life's Abundance 25% protein/15% fat

Precise Chicken and rice adult 25% protein/15% fat

As I said before, I do believe that a biologically correct diet is the best we can do for our dogs. I was determined to find a way to feed a raw diet that was completely balanced but also economical. Thanks to David Mroz founder of St. Francis Animal Sanctuary & Retreat , and a couple of Raw feeding groups, I was able to get my dogs started on a diet that would be the best for them. The diet we feed now includes a variety of meats, fish, organ meats and some veggies and potatoes. Variety is the key in a raw diet.

We feed mainly chicken quarters, as they are readily available and inexpensive at Walmart. I feel that feeding chicken backs and necks to a large breed dog is not enough meat, though it is fine for puppies and smaller dogs. We also get organ meats for free or inexpensively from the butcher.

Here is a sample menu of what we feed:

Sunday: Chicken quarters and ground raw veggies, sprinkled with kelp and garlic with a cheap multivitamin for pets.

Monday: Chicken quarters and ground raw veggies, sprinkled with kelp and garlic with a cheap multivitamin for pets.

Tuesday: Beef liver, kidney, beef lung and baked potatoes sprinkled with kelp and garlic with a cheap multivitamin for pets. (every other tues, alternating the fish meal)

Wednesday: Chicken quarters and ground raw veggies, sprinkled with apple cider vinegar,brewers yeast and garlic.

Thursday: Chicken quarters and ground raw veggies, sprinkled with kelp and garlic with a cheap multivitamin for pets.

Friday: Beef liver, kidney, beef lung and baked potatoes with kelp and garlic with a cheap multivitamin for pets.

Saturday: Canned mackerel and salmon, eggs and baked potatoes sprinkled with kelp and garlic with a cheap multivitamin for pets.

When we can get other meat or (RMB's) raw meaty bones inexpensively we feed that also or if in a rush, I will pick up some fresh ground or pork (not sausage) and serve with some potatoes and garlic. I also get venison scraps from the hunters when available. I plan on eventually raising rabbits to both cut costs and to give the dogs more variety.

We occassionally give recreational bones for chewing but avoid weight bearing bones of large animals.

Some benefits to feeding raw:

Convenience- I don't have to travel to the closest large town to get kibble- most everything I need is 20 mins away. I don't have to worry about what time the pet food store closes anymore, holidays or if they have my brand in stock. No more wasting time checking the labels to see if they changed the formula.

Easy clean up- Stools are such that they disinegrate to a powder in a few days or less. When fed a raw diet the dog is able to use all of the nutrients, thereby much less is passed.

Less $$$ spent at vets- No more dental cleanings (or bad breath), teeth and gums are kept healthy by RMB's. Dogs are healthier eating what nature intended and it shows in thier skin and coats.

Less $$$ spent on food- Hunters and butchers are happy to give you thier cast offs of offal and scraps. Veggies and fruits grown in the garden or extras from neighbors cost nothing extra. Chicken is pretty inexpensive as well. Expensive supplements are a thing of the past- the dogs get most all of what they need from thier food and it is in proper balance.

Better muscle development- when eating RMB's the dog must use jaw and neck muscles to tear the meat and chew.

More energy- I had old dogs that acted like a puppy once again.

Reproduction- Before starting raw, my girls whelped 4-8 pups each time. After switching, I have noticed that all litters are 8 or more- usually 10 or 11. Personally, I believe it is because of the nutrients that are readily available in raw form increase the amount available to the developing fetuses, resulting in more puppies that are able to be supported to term instead of being resorbed early on.

 

Concerns-

Won't dogs choke on bones?

They can. We are sure to supervise during meal times, but we always have anyways. Dogs have died choking on kibble as much as they have eating raw bones. It is much easier to dislodge a chicken leg than to extract kibble from the throat, so in my opinion, less of a risk. Feed large meaty bones that they must chew into pieces. Feeding a large dog small meaty bones is asking for trouble. Dogs who like to gobble up thier meals instead of chew should be given larger bones until they learn to eat properly. Never give large marrow bones, these can break teeth. NEVER FEED COOKED BONES

Won't my dog get salmonella, bacterial infection, etc.from raw meat?

Dogs digestive systems are much shorter than ours hence digestion takes place at a faster rate than our does, not allowing bacteria to have a chance to colonize in the gut. In a healthy dog, this is not a problem. In a dog who is ill, and digestion is slowed, it may be adviseable to avoid poultry until it is healthy.

But my vet says that a well balanced kibble is the best for my dog.

Vets have the knowledge they were taught in college, unfortunately nutrition is a very small part of what they learn and is sponsored by major dog food companies. Some vets also reccommend (and even sell) kibble that contains known allergens because they don't know any better. Many vets and even pet food companies recognize that a natural diet is the best for dogs and will usually provide support for you. Burn's Pet foods supports a cooked diet and will even give you recipes, but raw is better as the natural enzymes are not destroyed in cooking and also provides needed calcium through bones, which a cooked diet lacks. It is also easier and less time consuming.

Won't it make my dog blood thirsty or aggressive?

No, either a dog is aggressive or it isn't. Feeding raw will not make a dog what it isn't. I feed chicken often, but the dogs do not attack my chickens. They will instead herd them and protect them. Some will even let the birds take bites of thier food. Yes, some dogs will eat mice and birds- but that is what they would do if they were fed kibble too.

As far as aggression- no, it will not make them more aggressive. They may however love thier food so much they will fight with another dog that tries to come near it or attempt to steal someone elses food. This is normal no matter the diet. That is why I advise feeding dogs separate- no matter what is fed. I also would not recommend letting a child put thier hands or faces in a dogs bowl or near its food, no matter the diet nor how wonderful you think the dog is with allowing it. No matter how sweet and well trained- your wonderful family member is still a dog and as such has natural instincts that they may not be able to control and a child is usually the lowest ranking member of the human pack- and as such may be seen by the dog as even lower than its ranking from time to time.

In this section of the page we will discuss some of the hereditary defects that can occur in the Collie. Please don't get the impression that the Collie is a breed plagued by more defects than other breeds, as this is not the case. ALL breeds are predisposed to certain defects. The purpose of this page is to inform you so that you are aware of the possibilities, and can insist upon proof and /or guarantee, from the breeder you are buying from, that the puppy/dog is free from these defects. On some of these issues you will find information, on others, there will be links to sites which I believe have factual information on the subject. If you have any questions regarding a specific defect, please consult a veterinarian that specializes in that field.

Collie Eye Anomaly

Collie eye anomaly, known as CEA is prevalent in Collies. Collie Eye Anomaly or CEA affects approximately 2/3 of all Collies. It is believed that 85% of Collies are either affected or carry the gene. There is no doubt that CEA has existed for a great many years before the discovery of it's existence, making it extremely difficult to breed out of Collies.


CEA is the most common form of eye problem found in the Collie, both rough and smooth variety. It is also found in the Border Collie, and the Shetland Sheepdog. CEA is a simple recessive, as shown by research at Ohio State; however a cluster of genes controls the severity of CEA in an affected dog and that can complicate diagnosis.


There is no correlation between CEA and sex, coat color, type of coat (rough or smooth), or presence of the merling gene. Although, in blue merles it is especially important to have an ophthalmologist who is experienced examine the eyes, as the merle gene can cause some lack of pigment that can be mistaken for CEA. Usually both eyes are affected, but not necessarily to the same degree. Those dogs with minor anomaly make fine pets and do not lose their eyesight.


A recessive trait means there are three types of dogs: unaffected dogs that do not display the trait NOR have genes for the trait; carriers that do not display the trait, but DO have one of the genes for the trait; and affected dogs that have the trait and can only pass along genes for the trait. If a dog is "mildly affected", it is an affected dog and will always pass along CEA to it's puppies. So breeding two "mildly affected" dogs will never result in unaffected, or even carrier puppies. Breeding two apparently normal dogs may result in puppies with CEA if both dogs turn out to be carriers. If a dog ever produces a puppy with CEA, then that dog must be either a carrier or an affected dog itself. Each variation is carried independently (If a dog is affected with a coloboma it is possible that it does not carry Choroidal Hypoplasia) therefore it is possible to get all normal eyed pups if you were to breed a carrier of one variation to a carrier or affected of another variation and get all normal eyed pups. Although you would not know which pups carried which variation until they were bred.


There are five grades of CEA.


GRADE 1 Choroidal Hypoplasia is the mildest and most common form, distinguished by an area, or areas, lacking in pigment on the Choroid layer at the back of the eye. It does not affect vision and it isn't progressive. The sight of the Collie will not deteriorate as it gets older. Pin point Colobomas are also graded as a 1.


GRADE 2- Coloboma or Staphyloma. Colobomas can be pinpoint which grades at a 1 to large which would be a 3. This manifests itself as a hole or very thin area adjacent to the optic nerve. As long as it is not so large that it affects attachment of the retina, this is also a non-progressive state and will only slightly affect the Collies field of vision. The grade 3 colobomas can cause slight blurring of vision.


GRADE 3- Partial or complete detachment of the retina. This results in partial or complete blindness, depending on the severity of the condition.


GRADE 4- Intra Ocular Hemorrhage or bleeding in the eye. This sometimes follows the detached retina stage and can be due to a blow on the head or from bumping into an object. It causes severe pain that can only be relieved by removing the eye.


GO NORMALS- There is one other grade known as Go Normal Syndrome. This happens when a certain lack of pigment in the back of the eye, detectable in a six- week-old puppy, colors in at a later stage becoming indistinguishable from a CEA clear eye. A dog tested at a later age will often be given a clear eye grading. This dog is not a true clear and for breeding purposes is an affected animal.


Persistent Papillary Membranes- This happens when the tiny veins which feeds the eye are larger than normal. This is not CEA and so the dog can have this and be given a normal eye check (if all else is normal). It does not affect vision.


Microphthalmos- This simply means that the globe (eyeball) is smaller than usual. This is not a desirable trait. Please keep in mind that this refers to the size of the globe and not the size of the skin surrounding the eye. The eye can look small to an observer and the dog can still have a normal sized globe, and vice versa.


The best age at which CEA can be accurately and permanently diagnosed is at 5 7 weeks of age. A puppy that is clear then, is known to be clear for life.


Puppy buyers should ask to see the eye papers of their puppy, and if they want to breed from their puppy, should insist it has a clear or mild grade 1 eye check between 5-7 weeks of age. If the puppy is to be a pet, then a Grade 1 to Grade 3 coloboma would be acceptable. It will mean the puppy's eyes will not deteriorate and he will never have problems with his vision. CEA is virtually impossible to detect without the aid of sophisticated ophthalmic instruments. Even severely affected animals, due to their heightened sense of smell and hearing, can show very little evidence of their defective sight.

Another thing I will mention here is the affect of the merle gene on eyes and ears. The merle gene in one dose has no serious effects on either, though may cause blue or partially blue iris's- it is purely asthetics. In a double dose (from a merle to merle breeding- which includes sable merles) it results in double merle or white merle puppies (also known incorrectly as double dilutes) which will appear to be mostly white usually with a mostly white head as well. Not to be confused with a merle headed white who only has one copy of the merle gene,(though a double merle may look like a merle headed white) the merle headed white is colored as such because of the white gene- not the merle gene. The merle gene in duplicate MAY cause vision problems as listed above from slight to blindness due to lack of pigmentation in the retina and/or micropthalmia, but can also cause a puppy to be born lacking an eye or both eyes. It MAY also cause loss of hearing due once again to lack of pigmentation in the ear canal. It is most common (though not always the case) that the areas that are covered by white on the head will be affected to at least some degree. The defects may be unnoticable if only one ear or eye is affected. Most breeders who breed merle to merle (either on purpose or accidentally) will euthanize any puppies with white over ears and/or eyes at birth because of this. Others have raised these puppies along side thier full colored littermates and found almost none to have defects (most common if one or both parents are free of CEA and/or a non-carrier of CEA). Others have raised them and tested them only to find that they have defects. Other than eyes and ears- these puppies are just as strong and healthy as thier normal colored litter mates and if not severely defective, can make a wonderful companion. Double merles will not pass on any defects (that are due to doubling up on the merle gene) to any puppies they produce IF bred to a full colored non merle partner. They will only produce puppies with one copy of the merle gene when bred to a full colored dog (when bred to tri- all blue merles, when bred to a pure for sable- all sable merles, when bred to a tri factored sable- merles and sable merles).


Puppy buyers should never buy a puppy whose eyes have not been tested by an ophthalmologist. The result could be heartbreaking.


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Progressive Retinal Atrophy and Central Progressive Retinal Atrophy

 

Progressive Retinal Atrophy (PRA) is a condition in which the retina slowly deteriorates over years. The deterioration will result in blindness. A well known and widely used stud dog in the '70s was found to be a carrier and did produce blind puppies, because of that, PRA is present in a number of lines. Most reputable breeders who know or suspect that PRA is in their lines do test-breed. Since PRA in Collies is a simple recessive gene, and is not as wide spread as CEA, it has been easier to control than CEA.

A latent form of PRA known as central progressive retinal atrophy has now been diagnosed. As it's name would suggest, it starts in the center of the eye and spreads outwards. Appearance can be delayed for up to eight or nine years. It is thought to be inherited from close ancestors. It is impossible to delay breeding from a collie until such an advanced age, which adds to the difficulties of eradicating PRA from the breed.
It is vital that collies used for breeding should have their eyes checked annually for CPRA. Ophthalmoscopic signs may be detected on occasion in dogs of just over 12 months of age, but it is more usual to make the diagnosis from about 18 months of age onwards.
The disease is caused by the inability of the retinal pigment epithelial cells to degrade spent photoreceptor metabolites, with the resultant accumulation of lipopigment within the retinal pigment epithelium. There are focal concentrations of lipopigment-laden cells which migrate into the true retinal layers. Degeneration of the photoreceptors (rods and cones) is secondary to the lipopigment epithelial cell malfunction.
Unlike generalized progressive retinal atrophy, central progressive retinal atrophy rarely causes blindness and secondary cataract formation is also unusual. The inheritance of the disease appears complex and environmental factors (for example, poor quality diet) may influence the phenotypic expression. Until more information is available, it is prudent to advise against breeding from affected dogs and their relatives.

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Hip Dysplasia

According to current OFA statistics out of 1,840 collies tested, 24.3 percent were graded excellent and 3.2 percent were dysplasic. The remaining 72.5 percent tested within normal limits. Although the incidence of HD in the collie is lower than most breeds (it ranks 115 out of 126 breeds-1 being the worst rank),it is still a concern. Without continued efforts by breeders, HD could easily become a major concern in the collie once again. Please click on the collie to access the link which describes this hereditary condition in detail.





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Canine Hypothyroidism

What is it? Canine hypothyroidism is the absence of sufficient thyroid hormone to maintain healthy body functions. 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.

What are the Symptoms? 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. 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.
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.


The diagnosis can be complex; the treatment as simple as supplementing a basic essential hormone.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.

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.

Who is at risk? 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. Even though the Collie is not one of the most commonly affected breeds, I have included it here because it can affect them.

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 had symptoms of thyroid disease or are taking thyroid medication and if there have been any thyroid disease in their background. Pre-breeding

 




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Patent Ductus Arteriosis

What is patent ductus arteriosus (PDA)?
At birth, mammals must adapt from living in a fluid environment (the amniotic fluid) and acquiring oxygen through the mother's blood, to breathing air and acquiring oxygen through their own lungs. The ductus arteriosus is very important in the adaptation process. This is a small communicating blood vessel between the pulmonary artery (which carries blood to the lungs), and the aorta (which carries blood to the rest of the body). Before birth, most of the blood from the fetal heart bypasses the fetal lungs via the ductus arteriosus. The lungs gradually become functional fairly late in fetal development. At birth, the blood supply from the mother is of course cut off, the dog (or other mammal) begins breathing on its own, and blood flow through the ductus arteriosus decreases dramatically. Within a few days, the ductus closes off completely.
Where the ductus does not close, the dog is left with a patent ductus arteriosus (PDA). The extent to which this affects the dog depends on the degree of latency, or opening, of the ductus.
How is patent ductus arteriosus inherited?
Inheritance is complex.
What breeds are affected by patent ductus arteriosus?
PDA is the most commonly diagnosed congenital heart defect in dogs. It occurs in many breeds and is seen more often in females.
The breeds at most risk for this disorder are the Maltese, Pomeranian, Shetland sheepdog, and Kerry blue terrier.
Other breeds with an increased risk are the Keeshond, miniature and toy poodle, Bichon frise, Yorkshire terrier, English springer spaniel, collie, cocker spaniel, German shepherd, Irish setter and Chihuahua.
For many breeds and many disorders, the studies to determine the mode of inheritance or the frequency in the breed have not been carried out, or are inconclusive. We have only listed breeds for which there is a strong consensus among practitioners that the condition is significant in this breed.
What does patent ductus arteriosus mean to your dog & you?
The degree to which your dog is affected depends on the magnitude of the defect. This can range anywhere from a small blind pocket off the aorta which doesn't cause any problems, to varying degrees of abnormal blood flow through the ductus between the aorta and the pulmonary artery. Most commonly there is a shunt from the left to the right side of the heart , with blood from the higher pressure aorta continuously shunted to the main pulmonary artery. This means an increased volume of blood to the lungs which results in fluid build-up (pulmonary edema) and volume overload to the left heart. You may see coughing, reduced tolerance of exercise, loss of weight, and eventually, congestive heart failure. Without surgery, premature death is likely.
Less commonly, there is a right-to-left shunt. This may be the case from birth or, it may develop because the PDA is so large that the pressure in the lungs, and resultant resistance to this pressure, markedly increase. In effect, the circulation is the same as when the dog was a fetus - that is, some of the blood leaving the right side of the heart bypasses the lungs entirely. This results in circulation of poorly oxygenated blood. Your dog may have shortness of breath and weakness or collapse in the hind limbs.
How is patent ductus arteriosus diagnosed?
Usually a PDA is first suspected when the veterinarian hears the characteristic continuous "machinery" heart murmur when your dog is examined at the time of vaccination. There are radiographic and electrocardiographic signs to confirm the diagnosis. At this point your puppy will not likely show any clinical signs relating to the PDA.
FOR THE VETERINARIAN:

MURMUR: continuous "machinery" murmur - (disappears with right-to-left shunt).
ELECTROGARDIOGRAM: left atrial enlargement, left ventricular dilation and hypertrophy, (right ventricular hypertrophy with right-to-left shunt).
RADIOGRAPHS: pulmonary over-circulation, left atrial and ventricular enlargement, possibly dilation of the descending aorta and main pulmonary artery (right ventricular hypertrophy with right-to-left shunt).
ECHOCARDIOGRAPHY: left sided cardiac enlargement and dilation of aorta and pulmonary artery (right ventricular hypertrophy with right-to-left shunt).
OTHER: signs of pulmonary edema and left-sided heart failure. In a right-to-left shunt, unoxygenated blood directly from the pulmonary artery mixes with blood from the lungs in the descending aorta causing differential weakness and cyanosis in the hind end. Desaturated arterial blood also goes to the kidneys, causing hypoxemia, polycythemia, and hyperviscosity. The PCV often exceeds 65 per cent.
How is patent ductus arteriosus treated?
Surgery is recommended in all dogs less than 2 years of age in which a left-to-right shunting PDA has been diagnosed. Surgical treatment consists of tying off the patent ductus and is quite successful. Surgery should be performed as soon as possible - as early as 8 to 16 weeks of age - before changes have occurred as the heart tries to compensate for the defect. The prognosis for a normal life with early surgery is usually very good. Where there are signs of heart disease, there are increased risks associated with surgery and your veterinarian will recommend medical stabilization before surgery.
The problems associated with the less common right-to-left shunt are managed medically rather than surgically. Treatment includes rest, exercise restriction, and avoidance of stress. Your veterinarian will monitor and work with you to manage the changes which occur due to the circulation of poorly oxygenated blood.
Breeding advice
Dogs in whom PDA has been diagnosed, with or without surgical correction, should not be used for breeding.


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Gastric dilatation-volvulus

Please be aware of the symptoms and emergency treatment of bloat BEFORE you need it.

What is meant by the term " Bloat" in dogs?

This is a term that is synonymous with the more scientific term "Gastric Dilatation/Volvulus." It is often called GDV. That means that a dog's stomach distends with air to the point that it goes into shock and may die.

Dilatation means that the stomach is distended with air, but it is located in the abdomen in its correct place. Volvulus means that the distention is associated with a twisting of the stomach on its longitudinal axis.

How or why does this occur?

We really do not know the answer to either of those questions. Original theories suggested that it occurred when a dog ate a large meal of dry food and then drank a lot of water. The water caused the dry food to swell. At the same time, the dog was supposed to be engaged in strenuous exercise that included running and jumping. That resulted in the dog's stomach twisting on itself as the heavy organ was jostled about in the abdomen.

Although that is the most common explanation given, there is no scientific evidence to support this theory. In most dogs experiencing GDV, the stomach is not excessively full of dry food and the dog has not recently engaged in strenuous exercise. The most current theory is that the stomach's contractions lose their regular rhythm and trap air in the stomach; this can cause the twisting event. However, the sequence of events for most cases defies a good explanation.

While the genetics of GDV are not completely worked out, most breeders and veterinarians feel there is some degree of heritability. Therefore, while prophylactic gastroplexy will probably help an individual dog, it makes sense not to breed dogs who are affected or who are close relatives of those suffering from GDV.

How is it diagnosed?

The first step in diagnosis is to determine if the correct breed is involved. This condition almost always occurs in deep-chested dogs of large breeds. Some of the more commonly affected breeds include Great Danes, Irish Setters, German Shepherds, and Afghan Hounds. Collies are also a deep chested breed and are susceptable.

The next step is to establish that the stomach is distended with air. An enlarged stomach will cause the body wall to protrude prominently, especially on the dog's left side. The swelling will be very firm and obvious enough to see across the room. Occasionally, this distention is not very apparent. This occurs in dogs which have a large portion of the stomach up under the rib cage. In most cases, however, the owner is able to detect the distention. A dog which experiences significant pain will be very depressed. It may lie in what is commonly called a "praying position" with the front legs drawn fully forward. This should occur quickly, within two to three hours at the most.

The presence of a rapidly developing distended abdomen in a large breed dog is enough evidence to make a tentative diagnosis of GDV. A radiograph (x-ray) is used to confirm the diagnosis of dilatation. It can also identify the presence of volvulus, in most cases.

What happens when the stomach is distended with air?

The first major life-threatening event that occurs is shock. This occurs because the distended stomach puts pressure on the large veins in the abdomen that carry blood back to the heart. Without proper return of blood, the output of blood from the heart is diminished, and the tissues are deprived of blood and oxygen.

The reduced blood output from the heart and the high pressure within the cavity of the stomach cause the stomach wall to be deprived of adequate circulation. If the blood supply is not restored quickly, the wall of the stomach begins to die; the wall may rupture. If volvulus occurs, the spleen's blood supply will also be impaired. This organ is attached to the stomach wall and shares some large blood vessels. When the stomach twists, the spleen is also rotated to an abnormal position and its vessels are compressed.

When the stomach is distended, digestion stops. This results in the accumulation of toxins that are normally removed from the intestinal tract. These toxins activate several chemicals which cause inflammation, and the toxins are absorbed into circulation. This causes problems with the blood clotting factors so that inappropriate clotting occurs within blood vessels. This is called disseminated intravascular coagulation (DIC) and is usually fatal.

What is done to save the dog's life?

There are several important steps that must be taken quickly.

1)Shock must be treated with administration of large quantities of intravenous fluids. They must be given quickly; some dogs require more than one intravenous line.

2)Pressure must be removed from within the stomach. This may be done with a tube that is passed from the mouth to the stomach. Another method is to insert a large bore needle through the skin into the stomach. A third method is to make an incision through the skin into the stomach and to temporarily suture the opened stomach to the skin. The last method is usually done when the dog's condition is so grave that anesthesia and abdominal surgery is not possible.

3)The stomach must be returned to its proper position. This requires abdominal surgery which can be risky because of the dog's condition.

4)The stomach wall must be inspected for areas that may have lost its blood supply. Although this is a very bad prognostic sign, the devitalized area(s) of the stomach should be surgically removed.

5)The stomach must be attached to the abdominal wall (gastropexy) to prevent recurrence of GDV. Although this is not always successful, this procedure greatly reduces the likelihood of recurrence.

6)Abnormalities in the rhythm of the heart (arrhythmias) must be diagnosed and treated. Severe arrhythmias can become life-threatening at the time of surgery and for several days after surgery. An electrocardiogram (ECG) is the best method for monitoring the heart's rhythm.

What is the survival rate?

This will largely be determined by the severity of the distention, the degree of shock, how quickly treatment is begun, and the presence of other diseases, especially those involving the heart. Approximately 60 % of the dogs will survive if treatment is started reasonably soon after onset of signs. Some dogs may survive the initial treatment and surgery only to have areas of the stomach wall die and slough 2 to 4 days after surgery. These areas may have looked fine during surgery but were deprived of blood long enough to permanently affect the tissue.

What can be done to prevent it from occurring again?

The most effective means of prevention is gastropexy, the surgical attachment of the stomach to the body wall. This will not prevent dilatation (bloat), but it will prevent volvulus in most cases. Various dietary and exercise restrictions have been used, but none of these have proven value.

Fortunately, this is not something that is a routine occurrence but it does happen often enough that owners of "deep chested" large breeds should be aware of the potential.

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Demodectic Mange

 

Demodectic mange is a common skin disease in dogs. It is known by a variety of names such as red mange, and is caused by a mite known as Demodex canis. The mite is cigar shaped when viewed under a microscope, but is not visible to the naked eye.

It is generally believed that all dogs have a small number of these mites living in their hair follicles at all times. The mite is not contagious from dog to dog in the usual sense, nor is it transmissible to humans. Dogs acquire the mites during the first two to three days of life while nursing their dams. In a large number of dogs, the mites cause no problem, but in some individuals, skin disease does result.

Two theories exist about why certain dogs develop demodectic mange, both of which deal with suppression of the immune system. While not proven to be inherited, most researchers believe the tendency to develop demodectic mange is hereditary, and most breeders seem to find evidence of certain families that are more prone to the problem. One theory regards the cause to be a defect in t- lymphocytes (a type of white blood cell) which respond to an immunosuppressive substance produced by the mites, resulting in a dog whose immune system cannot get rid of the mites. The second theory holds that it is not the mites, but a tendency to develop a bacterial infection along with the mange, which results in the bacteria suppressing the immune system. Either way, the result is the same, the mites and bacteria proliferate on the skin, causing hair loss, redness, etc.

Demodectic mange is seen primarily in two forms, juvenile and adult. Juvenile mange is further subdivided into localized and generalized mange. The age at the onset of symptoms determines the diagnosis, with mange beginning before about 15 months of age considered juvenile.

Localized juvenile mange is a common problem resulting in patches of hair loss, primarily involving the face and front legs, but which may be found anywhere on the body. The symptoms begin between three months and a year of age, and 90% of the dogs cure themselves within 4-8 weeks. The remaining dogs progress on to have generalized mange, which is characterized by more than 10 areas of hair loss, itching, bacterial infection and redness.

Adult onset mange is that which begins in dogs more than about two years of age, and is not considered hereditary. Many dogs with adult onset of mange have an underlying health problem that is suppressing the immune system and leads to the development of the mange. A dog with adult onset of mange should be carefully examined and have lab work performed to rule out any underlying cause.

Diagnosis of demodectic mange involves finding a large number of mites in affected areas. The skin is scraped with a scalpel blade and the resulting material is examined under the microscope. A skin scraping is a simple, inexpensive test and should be performed on every dog with hair loss of any description in order to rule out mange as a cause.

Treatment varies with the severity of the symptoms. As localized mange will resolve even without treatment, most veterinarians regard treatment for localized mange as a case of treating the owner, rather than the patient. Treatment may involve regular bathing to clear the hair follicles, application of insecticidal ointments to the affected areas, or antibiotics. There is no evidence that spot treatment of localized lesions will prevent generalized mange. It is not considered advisable to treat localized mange with amitraz (Mitoban ) dips. In many cases, no treatment at all is the best treatment, with periodic visits to the veterinarian for scrapings to determine if the numbers of mites are increasing.

Generalized mange, either juvenile or adult onset, is a serious and potentially life threatening disease, as unresponsive cases sometimes require euthanasia. Treatment of generalized mange should only be undertaken with the knowledge that it will probably take a long time, be expensive, and may not work. Adult onset is particularly difficult to treat, due the common presence of another underlying condition.

Treatment of generalized mange usually involves clipping the hair to better reach the skin, bathing with antibacterial shampoos, regular dipping with amitraz (Mitoban ) and appropriate antibiotics. Many individuals will relapse if not treated every eight weeks or so, even after an apparent cure. Many animals treated with amitraz develop side effects, most notably sleepiness and depression. While frightening to owners, these are rarely serious. Due to the presumed hereditary nature of the disease, the American Academy of Veterinary Dermatologists recommends the surgical neutering of any animal affected with, or recovered from, generalized demodectic mange.

In cases which do not respond to amitraz, some success is being obtained with milbemycin (Interceptor ), an oral heartworm preventive, but this requires daily treatment, is very expensive and is not approved for this use. Some researchers feel higher concentrations of amitraz, used more frequently, may also help, although these doses are not approved in this country.

Other suggested treatments such as ivermectin (Heartgard ) have been demonstrated to have no beneficial effect. Thyroid hormone is not indicated unless the animal is hypothyroid, as well as having mange. Corticosteroids (cortisone) should not be given even if the animal is experiencing itchiness, due to the immunosuppressive effects of these drugs.

Juvenile demodectic mange is a common problem in Italian Greyhounds. Data from the IGCA health survey indicates some 10% of IG's have had localized mange. Only about 5% of the affected individuals went on to develop generalized mange, a somewhat lower figure than might be expected. What conclusions can we draw from this information?
Probably that while localized mange is a common problem in IG puppies, most dogs do not develop generalized mange. This would seem to indicate that removing these animals from a breeding program would serve no purpose, but conversely, due to the relative infrequency of generalized mange, any affected individual should be surgically neutered

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Dermatomyositis

 

Dermatomyositis (DM), AKA sheltie skin syndrome, is a skin-and-muscle disorder that is known to affect collies (both varieties) and shelties, but is not generally seen in any other breed. Most of the research on canine DM (several varieties also occur in humans) has been done on collies.
The mode of inheritance appears to be autosomal dominant with variable expression.
"Autosomal" means it is non-sex-linked, and occurs with equal frequency in males and females. "Dominant" means that one parent must HAVE IT to pass it on to offspring (or, possibly, it can occur as a new mutation; however, while possible, I believe this is highly unlikely, because if new mutations occured in canines, DM would be a problem in almost every breed). "Variable expression" means that disease severity can vary from very mild--too mild to be diagnosed--to very severe.

Because the gene is dominant, there is no such thing as a "carrier." A dog either HAS it, or he doesn't--whether or not he gets diagnosed is the sticky part of the equation (see next paragraph). Affected dogs may have one gene for the disorder (D) and one normal gene (d). Such a dog would be referred to as heterozygous, and his genetic make-up would be Dd. Or, an affected dog may have two genes for the disorder (having inherited one from each parent). That dog would be referred to as homozygous, and his genetic make-up would be DD. It is probable that the more severely affected dogs are homozygous (DD), but nobody knows for sure.

The "variable expression" component is the scary part; it means that a dog who is heterozygous for the gene may be so mildly affected as to never be diagnosed. For example, as a young puppy, an affected dog may have show no signs other than a VERY small area of hair loss around the eyes or muzzle (or somewhere else, like the inside of a leg near the foot). That spot may clear up and the dog may show NO OTHER SIGNS EVER. Another dog, who also is heterozygous for the gene, may have more extensive hair loss and muscle atrophy, and probably will be diagnosed. The second dog will probably never be bred; but the first dog may be. The important point is that BOTH dogs have the same genetic make-up when it comes to DM and if bred, both are EQUALLY LIKELY to produce affected puppies.

Because of the way DM is transmitted, one affected dog can contaminate a pedigree for years to come. Breeders should be suspicious about ANY skin problem OR muscle-wasting condition that shows up at ANY age. Sure, it might just be demodectic mange, or an allergy.. but you won't know for sure without a biopsy for DM (for accuracy, the biopsy must be done on an affected area of the body during a "flare-up"). Also, research with collies showed that some affected puppies had BOTH demodectic mange AND DM. So a positive diagnosis of demodectic mange DOES NOT rule out dermatomyositis. Breeders cannot affort to be complacent about this condition. Taking a wait-and-see attitude about even small amounts of hair loss, small scabs or small crusty areas--which may well clear up on their own--can result in a mildly affected dog entering (and contaminating) your breeding program.

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Preceeding thyroid excerpts taken from the Dog Owner's Guide: Canine thyroid disease Copyright © 2001 Canis Major Publications.
Preceeding bloat excerpts taken from Dr Ken Diestler.
Article on Demodectic Mange written by Teri Dickinson, DVM
Article on DM written by Kim Schive.

Copyright © 2001-2003 Willowynd Collies, all rights reserved. Other existing copyrights of material on this page also reserved.