Health, what you should Know

This page and information is here to give you the potential puppy buyer the information you may need in purchasing a puppy. in this page you will find information on MDR1 Gene ( canine multi drug Sensitivity test), Canine Cyclic Neutroenia ( Gray Collie Syndrome), HD (certification on hips ), CEA the new DNA test to prove you have a Non Carrier of CEA. We put this together for all so you can be better informed on collies and the latest studies please e-mail if you have any questions glasgow@hutontel.on.ca

We here at Glasgowhill Collies would like to address and dispel the rumors flying around about all the testing done at our kennel. Yes, we Show and win with our collies, but our foremost concern is breeding a healthy collie. And because of this the "collie world" is seeking to tear us down. The "collie world", for as long as I can remember, have professed that they have wanted to make the breed better. And as the years have progressed DNA markers have been found to help us eradicate some of these problems. But, if someone uses them to help eradicate these problems in their breeding program, they are talked about badly and rumors start flying about falsifying documents, buying off vets, etc. These rumors are killing our breed. I document every test I do, every problem I come up against and learn from them. Nowadays, it's not the dog itself that most people are buying, but the names in the pedigree. If you don't have top name kennels in the pedigree then your dogs are not worthy of breeding, according to some breeders. A Lot of breeders these days are playing the ostrich game. They will stick their heads in the sand and pretend these problems don't exist. People are saying that they want "honest" breeders to buy dogs from, but if you tell people about problems or test to eradicate them then you are ruining the "collie world". If you have problems and don't choose to let everyone know, then who is the "honest" breeder. I have never "knowingly" bred a dog with hip dysplasia, and those that have tested poorly have been eliminated from my breeding program and placed in pet homes. As we are finding out, hip dysplasia is poly genetic and even dogs with excellent hips can produce offspring with hip dysplasia. Breeding for normal eyes can be done in two generations, if carefully done. Those breeders who breed for just mild CEA are not "choosing" to eradicate this problem. But there are only a few kennels that are producing true normal eyed non carrier dogs and because of malicious rumors have been labeled "puppy mills" and people are afraid to buy or breed with these dogs. The consumer is getting smarter these days and are asking more informed questions. And if you aren't doing the testing that is available they move on until they find someone who does. If the "collie world" thinks that I am taking away their business then that's too bad. If they smartened up and did the testing available to them they would find their puppy buyers knocking their doors down. I WILL NOT apologize for trying to breed a healthier collie and doing the testing required for this. I WILL NOT apologize for taking informed puppy buyers away from other breeders who are not "interested" or won't do the testing puppy buyers are now requesting. I WILL NOT apologize for letting "the public" know when I come up against a problem. I WILL NOT apologize for trying to breed the healthiest collie I can. I WILL continue to do every test that is available to me and hope that other collie breeders will finally "get with the program" and turn this breed around. With regards to CEA...this is a disease not a condition. Several other breeds, such as Shetland Sheepdogs, Australian Shepherds to name a few, have eradicated this disease from their breed without adverse effects. And for the record, eye shape and size have nothing to do with the disease, so lets dispel the myth of "big eyed normal eyed collies". Most of this information is for those people who visit my site wishing to purchase a collie. We all have the freedom to "choose" what we want to do in our breeding program. There is no "collie police" telling you what you can and cannot do, but all the bad mouthing and misinformation about our breed has to stop. Let's touch on MDR1's. There are people out there that could care less about the MDR1 status of their dogs. Well, good for them, but as far as I'm concerned I DO care about that in my dogs. So, for all of you out there that are spreading rumors and badmouthing my breeding practices, KEEP IT UP! All you are doing is sending more puppy buyers my way because they are smart enough to want healthy dogs and because I do the testing and stand behind my contract they feel better about a dog purchased here.

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Success and mentoring
                                       When people seek the services of a doctor or a lawyer, they usually look for one with a good professional reputation and avoid  the “quacks” and “shysters.” When shopping for major purchases,  “brand names” and “quality” are sought in preference to the  unknown and untried.  Then why, oh why, does the novice breeder often select an unproved or less than adequate, breeder as their “mentor”? It is so often a case of the blind leading the blind!   This is not universal by any means. There are many novices who   have had the good fortune of enjoying the association of respected,  successful breeders. From them, the novice receives a valuable   education about many aspects of breeding and showing dogs, as well  as the basic rules of sportsmanship. Oftentimes, this association comes about purely by chance. Very seldom is it sought.    Most experienced and successful breeders neither need, nor want, the “coat-tail crowd”— those who look to them for every assurance, opinion, and then reflect his exact thoughts back  to him. Through experience, it is not difficult for this breeder to  discern fairly easily those worthy of his time and efforts. Novices  are NOT expected to know it all—those who act as though they do  are quickly given the cold shoulder. Novices ARE expected to ask  questions and shouldn’t feel their questions will be regarded as  silly and insignificant.  Perhaps it is the “fear” that the big-name breeder will not want to bother with him, that makes the novice seek out “second best.” Or, more than likely, an association with a lesser breeder is sought because in the eyes of the novice ANY accomplishment looms large beside his own insignificant or fumbling beginnings. To the novice, the word “champion” is truly the magic word—this before he develops the ability to discern that there are champions and THERE ARE CHAMPIONS! There are many breeders, both successful and near successful,  who are more than happy to lend a helping hand. They have usually  reached their own pinnacle of success due to another’s assistance   along the way. However, whereas successful breeders desire to help   those deemed worthy, many not-so-successful breeders encourage the association of one and all. In fact, the more the merrier! To gather a group of “disciples”around gives many less-than-successful breeders a prop for their sagging egos. It is not uncommon to find these breeders with their own personal retinue accompanying them everywhere, hanging onto their every word and taking all they have to say as the gospel truth. They are seen at dog shows clustered around the breeder’s  crates listening only to him. They pay little attention to the  other dogs, rarely watch the judging (where they may actually learn something!) and have eyes only for dogs belonging to their “friend.” The disciples end up with very little real knowledge of the breed   that they originally sought. Actually, they have been “used” rather  than helped. They are often kept within the fold by being made to  feel obligated as a result of a free stud service, gifts of dogs, and  deals. If they would only look around them and see the light, they would realize that “free” stud services are rarely offered on GOOD dogs; dogs that possess a monetary value and for which there is a demand are not “given away”, and “deals” rarely work out to everyone’s satisfaction.     Many of these people have long ago lost sight of their original goals and have become enmeshed in all sorts of dog activities that lead them nowhere. These are the ones who throw in  the towel and become another “five year statistic.” (Just look at the  magazine ads of five years ago and see how many are no longer  round.) Very few go on to become successful breeders on their  own, for that requires independent thought and they have not been conditioned to do this.   It should not be too difficult to establish criteria of some sort to distinguish between those breeders capable of assisting the novice and those who use the novice to further their own  interests. First off, what constitutes success? What assurance can the novice obtain that his would-be mentor has something to offer?  Is it because he has bred a champion? Realize, please, that many a  champion is the result of luck in breeding or persistence in showing.  Maybe he has bred several champions. Then ask, what kind of Champions? Did they finish quickly in good competition or were  they dragged through to their titles winning against even more   inferior competition? Also, ask how others regard these champions.  Do other well-known breeders desire their offspring or breed to them or does their “popularity” result from the novice and pet trade? Is this person known only Answers to these questions—honest answers, that is—should provide the beginning breeder with some insight as to where they should look for assistance. (Because of the need of the novice for “real” information was in their own locale or known throughout the state and country as well? started where factual information is available from some of the best and most EXPERIENCED people in dogdom). Then there is the matter of integrity. Does this breeder constantly knock other dogs belonging to others? Does he start, or perpetuate rumors, based on hearsay or inconclusive  evidence? Does he, when selling stock, “guarantee” that eight-  week-old puppies will finish their championships? Does he imply that his stud dogs will sire top quality—regardless of the bitches  bred to them? Does he profess expertise of bloodlines with which he has no experience? If the answer to most of these questions is yes, look elsewhere for your guidance. If you chose this kind of person as a role model, your chances for success are slim and none.     To become completely dependent on another person for your success in dogs will—in the long run—not serve you well. To be a good breeder you must be able to think independently and, when ready, begin to make your own decisions—to buy that puppy, to line breed correctly, to keep that ONE great puppy. Learn all you can from your competent mentor  and then go out and apply that knowledge on your own. Of course you will make mistakes, who doesn’t? Remember, you can learn as much from your failures as you can from success. Go over the dogs that are winning in good competition . Ask questions when you don’t understand something. Have  an inquiring mind, and by all means watch the judging and learn by  observing where the judge puts his hands, what he comes back  to when he goes over a dog a second time. Many judges “signal”   the ringside what they are looking for.  you will find some top breeders who are leery of helping a novice.  That is because they have no doubt had some bad experiences. They   have run into the know-it-alls, the stubborn ones who will only do it   their way and the troublemakers. Unfortunately, there are always novices out there who—in order to make a quantum leap to stardom—set out to accomplish something that have never been done before. Maybe an experienced breeder with a good knowledge of genetics may hazard such a venture, but the rank novice is headed for disaster, and when he crashes on the rocks he blames all but himself.     Let us say you have been fortunate enough to of  gotten yourself a good mentor. You set out on your own and Dame Fortune has smiled upon you. all is wonderful, you are a winner and you bask in the glory of your  winning dogs. Great, except that something is not quite right! You  have the uncomfortable feeling that all your winning is not going  over too well with your fellow exhibitors, where did you go wrong?  After all, isn’t the idea of this whole thing to be a winner? To be a good loser is not difficult; in fact, it happens frequently to most of us. But acting appropriately as a winner, is something else indeed.   At any show, whether it is a specialty or an all-breed show, there   can only be a few winners. Should one exhibitor’s entries account    for more than one win, the leftover pickings become even smaller.   This means that only a small number of people go home perfectly   happy from a dog show. The vast majority console themselves that there will be another day or, at least, the judge did a conscientious job and gave them a fair shake.    Let’s face it, we would rather win than lose on any given day. In the dog game we have learned that a top dog will probably win 3 out of 5 times and be close when he loses. The average competitor will probably finish in 15 shows, winning perhaps 6  times. So you see, losing is the norm. However, we go into each   show with the expectation of winning and, as a result, we get  disgruntled when we don’t. Turn to the person standing next to you  and remark about the poor job of judging that old Nicholas Applebeeis doing today and chances are you will get full agreement. What’s  so strange about that? However, point out that old Nicholas is really   on the ball today and is picking the top ones and you will most likely  get a baleful stare, unless you happen to be standing next to one of   the day’s few winners.     You learn that it’s hard to be a winner by any standard. Everyone’s goal is to be a winner and get to the top. But, for many, that winning spirit can get us into trouble with our peers and reaching the summit can become a hollow victory. Your dog has won, you are elated, thrilled, on   cloud 9 and you want to shout about it from the rooftops and let   the world know of your accomplishments. But you don’t, because—Lets face it—YOU are happy but most of the other exhibitors are  not. So you adopt the reserve of the English and smile inwardly. To have your dog’s wins greeted by indifference and often snide remarks takes the wind out of your sails and much that should be joyous becomes just the opposite. After coming up against the “wet dish rag” form of enthusiasm, you keep your enthusiasm to yourself to be taken out later and savored privately. While it will have to suffice, winning is not what it SHOULD be like. The losers of the day, on the other hand, are walking around muttering under their collective breaths that they “were robbed,” or “the judge was stupid,” or both. Perhaps some day there could be a cartoon that poses the question “Guess who the losers at the dog show are?” Not too many moons ago, a top-winning  special went up for Best of Breed and one of the losing handlers  came over to the handler of the winning dog and said “Nice win,  too bad he didn’t deserve it.” Comments like this cannot help to   make a winner’s day. As you can see being a winner is not easy, no matter how  desirable the position looks from afar. To come up with winning   dogs, year after year, places many breeders in the position of Being a prime target for the unsuccessful, jealous, and petty  Breeders still striving for success. Because of some quirk of  human nature, it seems that people feel the need to elevate their own  kennel’s status—not necessarily by breeding better dogs—but by downplaying those belonging to others. Everyone, at one time or  another has been guilty of this to some degree. However, the driven ones give little heed to the feelings of others and strive to demean other’s accomplishments at every turn. Perhaps this is their way of lessening the threat to their own aspirations.  This type of behavior is not solely confined to those engaged in dog activities. It is evidenced even more clearly in the business world by price cutting, false advertising, and disparaging your competition. It’s frowned upon by the Better Business Bureau. In dogdom, we have no BBB, only virtually “unenforceable” club codes of ethics.  By now, you must recognize that a healthy competitive spirit and a thick skin are prerequisites to success in the dog show game. Obviously when competitive spirit meets competitive spirit in the    ring, some sparks are going to fly. Think of it as two Terriers being  sparred against each other in the center of the ring. It’s a good show but when it’s over, it’s over! In order for any one breeder in an area to attain success, others must—by necessity—lose along the way. This cannot be helped, for it takes many losers to make a winner. Those on the threshold of success might do well to remember that the time will come when they must come face-to-face with those same losers—as they lose their grip on the top rung and slide downward. No matter how good we are as breeders, there can come a time when not every success is topped with yet another success and we lose our momentum and backslide a bit. Very few, if any, have the good fortune of having their cake  and eating it too. That is to say, that few breeders can continually   enjoy success without ruffling some feathers along the way. Some  people just cannot take the slings and arrows that come their way  as winners. They have thin skins and suffer grievously. What to do? Some just up and quit. To them, it’s just not worth it. Maybe they feel they have achieved what they set out to do and do not want to settle for second best. Many learn to compromise. That is, they can share the winner’s mantle with others without feeling they are a “failure.” These are the ones who survive. Their accomplishments and abilities are recognized but they no longer hold a monopoly on success. As a result they have a degree of popularity with their fellow breeders and have gotten out of the crossfire allowing them to enjoy their hobby. These people make excellent mentors. These “old timers” no longer have to prove themselves at every outing. The “comers,” on the other hand, strive and claw their way at every step. These are the ones who “work” the judge and demean the competition. This aggressiveness is what makes them tick and can lead to “success.” But at what cost? Many of you have run across such people in the dog show game. The desire for recognition is one thing, but you can carry the craving for success too far and alienate everyone around you. Once you have climbed that mountain and become “top dog,”   you may well find out that it’s very lonely at the top of that peak. There just isn’t much room at the top; the kind of personality  that’s driven you doesn’t allow for sharing the top perch. This fact is usually not recognized by those hell-bent on getting there. It can only be truly understood by those who have experienced this heady sort of success with all of its accompanying drawbacks.  It doesn’t have to be like this. In fact, in many instances it’s not. However, there are too many cases where this is the norm in a breed. They’ll love you while you are a “point maker.” In fact, your  dog may not be bad—and with a little help and some good luck—   might do some real winning. On the other hand, just as soon as you start to do real winning…well, after reading this it should be all too familiar.

The Rising Storm: What Breeders & Pet Owners Need to Know about the Immune System

A complex and threatening storm is gathering on horizon. Reports of immune-mediated disease are on the rise in 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 ?classic? 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.? 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 ?allergy? 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 ?fix? 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 ?cured? 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.

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Bloat in Dogs

The probitoic/digestive enzyme is called FCN Breeder Pack Probiotics/Digestive Enzymes and it comes in a 4 lb tub for breeders. It only takes a little per animal - and double it for the males when girls are in season.
you can order that here 1-765-287-8288

An Excellent read from My friend the Great Dane lady
Excellent information regarding Bloat

 

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Collie Nose (Nasal Solar Dermatitis)

 

MDR1

Testing for CEA and PRA
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Canine Cyclic Neutroenia ( Gray Collie Syndrome)

DESCRIPTION Canine Cyclic Neutropenia is a stem cell disorder that occurs in collies. Puppies are usually smaller and weaker than their litter mates and by 8 to 12 weeks of age they develop clinical signs such as fever, diarrhea, joint pain, or other signs associated with eye, respiratory, or skin infections. The disorder is caused by an abnormality of the stem cells in the bone marrow, from which all blood cells are developed. The result is a cyclic fluctuation in blood cell numbers. Every 10 to 12 days the number of neutrophils drops dramatically, and then rebounds.

There is an increased susceptibility to infection corresponding to the dip in neutrophil numbers. Affected dogs are subject to severe recurring bacterial infections, primarily of the respiratory or gastrointestinal tract. These dogs are also prone to bleeding episodes due to the drop in blood cells numbers. This is a serious genetic disorder. Even with the best of care, affected dogs rarely live beyond 2 or 3 years of age. Most die within the first few weeks.

The disease occurs in all gray (not merle) collies. Affected puppies have a silver gray hair coat that ranges in color from very light, to darkish pewter gray, sometimes with a slight yellowing due to a mixture of light beige and light gray hair. No matter what color variation or type, all Collies have black noses EXCEPT those with gray collie syndrome. If the nose continues to come in gray, then that is pathognomonic (absolutely diagnostic) for "gray collie syndrome". Sable "gray collie syndrome" dogs have brown or pale sable noses, but never black noses as they should have.

DNA TEST
HealthGene Laboratory is the first DNA diagnostic laboratory that has developed and offered a DNA-based test for Canine Cyclic Neutropenia. HealthGene's test provides a reliable identification of dogs that carry mutant gene(s). This test allows a breeder to control the mutant gene frequency in the Collie breed thus preventing the production of puppies affected with Canine Cyclic Neutropenia. This DNA test accurately and specifically identifies normal, carriers (heterozygous) and affected dogs. this test has been developed for the breeder so we can avoid this disorder

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HD (certification on hips ) Hip dysplasia

Hip dysplasia literally means an abnormality in the development of the hip joint. It is characterized by a shallow acetabulum (the "cup" of the hip joint) and changes in the shape of the femoral head (the "ball" of the hip joint). These changes may occur due to excessive laxity in the hip joint. Hip dysplasia can exist with or without clinical signs. When dogs exhibit clinical signs of this problem they usually are lame on one or both rear limbs. Severe arthritis can develop as a result of the malformation of the hip joint and this results in pain as the disease progresses. Many young dogs exhibit pain during or shortly after the growth period, often before arthritic changes appear to be present. It is not unusual for this pain to appear to disappear for several years and then to return when arthritic changes become obvious.

Dogs with hip dysplasia appear to be born with normal hips and then to develop the disease later. This has led to a lot of speculation as to the contributing factors which may be involved with this disease. This is an inherited condition, but not all dogs with the genetic tendency will develop clinical signs and the degree of hip dysplasia which develops does not always seem to correlate well with expectations based on the parent's condition. Multiple genetic factors are involved and environmental factors also play a role in determining the degree of hip dysplasia. Dogs with no genetic predisposition do not develop hip dysplasia.

At present, the strongest link to contributing factors other than genetic predisposition appears to be to rapid growth and weight gain. In a recent study done in Labrador retrievers a significant reduction in the development of clinical hip dysplasia occurred in a group of puppies fed 25% less than a control group which was allowed to eat free choice. It is likely that the laxity in the hip joints is aggravated by the rapid weight gain.

If feeding practices are altered to reduce hip dysplasia in a litter of puppies, it is probably best to use a puppy food and feed smaller quantities than to switch to an adult dog food. The calcium/phosphorous to calorie ratios in adult dog food are such that the puppy will usually end up with higher than desired total calcium or phosphorous intake by eating an adult food. This occurs because more of these foods are necessary to meet the caloric needs of puppies, even when feeding to keep the puppy thin.

If clinical signs of hip dysplasia occur in young dogs, such as lameness, difficulty standing or walking after getting up, decreased activity or a bunny-hop gait, it is often possible to help them medically or surgically. X-ray confirmation of the presence of hip dysplasia prior to treatment is necessary. There are two techniques currently used to detect hip dysplasia, the standard view used in Orthopedic Foundation for Animals (OFA) testing and X-rays (radiographs) utilizing a device to exaggerate joint laxity developed by the University of Pennsylvania Hip Improvement Program (PennHIP). The Penn Hip radiographs appear to be a better method for judging hip dysplasia early in puppies, with one study showing good predictability for hip dysplasia in puppies exhibiting joint laxity at 4 months of age, based on PennHIP radiographs.

Once a determination is made that hip dysplasia is present, a treatment plan is necessary. For dogs that exhibit clinical signs at less than a year of age, aggressive treatment may help alleviate later suffering. In the past a surgery known as a pectineal myotomy was advocated but more recent evidence suggests that it is an ineffective surgical procedure. However, administration of glycosaminoglycans (Adequan Rx) may help to decrease the severity of arthritis that develops later in life. Surgical reconstruction of the hip joint (triple pelvic osteotomy) is helpful if done during the growth stages. For puppies with clinical signs at a young age, this surgery should be strongly considered. It has a high success rate when done at the proper time.

Dogs that exhibit clinical signs after the growth phase require a different approach to treatment. It is necessary to determine if the disorder can be managed by medical treatment enough to keep the dog comfortable. If so, aspirin is probably the best choice for initial medical treatment. Aspirin/codeine combinations, phenylbutazone, glycosaminoglycosans and corticosteroids may be more beneficial or necessary for some dogs. It is important to use appropriate dosages and to monitor the progress of any dog on non-steroidal or steroidal anti-inflammatory medications due to the increased risk of side effects to these medications in dogs. If medical treatment is insufficient then surgical repair is possible.

The best surgical treatment for hip dypslasia is total hip replacement. By removing the damaged acetabulum and femoral head and replacing them with artificial joint components, pain is nearly eliminated. This procedure is expensive but it is very effective and should be the first choice for treatment of severe hip dyplasia whenever possible. In some cases, this surgery may be beyond a pet owner's financial resources. An alternative surgery is femoral head ostectomy. In this procedure, the femoral head (ball part of the hip joint) is simply removed. This eliminates most of the bone to bone contact and can reduce the pain substantially. Not all dogs do well following FHO surgery and it should be considered a clear "second choice".

Hip dysplasia may not ever be eliminated by programs designed to detect it early unless some effort is made to publish the results of diagnostic tests such as the OFA evaluation or PennHIP evaluations and in canada OVC Guelph university , openly. This is the only way that breeders will be able to tell for certain what the problems have been with hip dysplasia in a dog's ancestry.

When an older dog is exhibiting signs of pain associated with this condition it is often possible to help them dramatically through medication and simple steps like providing a warm bed or warm spot to rest during the day. There is no advantage to pain and steps should be taken to ensure that the older dog is not in pain. Regular exercise can be very helpful and weight loss can have dramatic effects on the amount of discomfort a dog experiences.

Working with your vet to come to the best solution for your dog and your situation will enable you and your dog to enjoy life to its fullest, despite the presence of hip dysplasia.

OFA Web Site

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What is dermatomyositis?

This condition is one of inflammation (itis) of the skin (dermato) and muscle (myo) that is seen in young collies and Shetland sheepdogs. There appears to be a defect in the immune system that predisposes dogs to this disorder. The skin lesions typically develop first with variable muscle problems occurring later. There are many similarities to dermatomyositis in people.Ulcerative dermatosis may be a variant of this condition. It is a rare disorder that occurs in middle-aged to older dogs of the same breeds, and is manifest by skin lesions (blisters, crusting) that are seen primarily in the groin and underarm regions. Occasionally there are muscle abnormalities.

How is dermatomyositis inherited?

The trait is believed to be autosomal dominant with variable expressivity. This means that if either parent is affected, all puppies have a susceptibility to the disorder, but not all will be affected equally. The variability suggests there is more involved than simple inheritance, including internal factors such as the individual's immune system (also affected by heredity) and external factors (including possibly viral infection). The most severely affected dogs may be homozygous for the trait.

What breeds are affected by dermatomyositis?

This disorder is seen primarily in the collie, Shetland sheepdog, and their crosses. It has been diagnosed in other breeds, including the Australian cattle dog, German shepherd, chow chow, Pembroke Welsh corgi, and Kuvasz. Ulcerative dermatosis is seen in Shetland sheepdogs and collies.

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 listed breeds for which there is a consensus among those investigating in this field and among veterinary practitioners, that the condition is significant in this breed.

What does dermatomyositis mean to your dog & you?

With this condition, the skin is almost always affected before, and worse than, muscle. Typically, skin lesions occur by 6 months of age. There is reddening, hair loss, blisters or small bumps, crusting and where severe, ulceration of the skin. Most often affected are the face (especially the muzzle and ear tips, and around the eyes), the tip of the tail, bony prominences (over the elbows for instance) and the toes. Over time, the affected skin becomes scarred.The muscles are not always affected in dermatomyositis, or the abnormalities may be so slight as to go unnoticed. When there is muscle involvement, the puppies may be weak and lethargic and have a slow rate of growth. Muscles (especially of the face and head) may appear smaller due to muscle atrophy (shrinkage and loss of use). The most severely affected dogs may have difficulty in chewing or swallowing. The leg muscles may also atrophy.The degree to which pups are affected varies considerably. Muscle inflammation is generally less severe in Shelties.Generally the clinical signs fluctuate over time for no apparent reason, and many mildly affected dogs will outgrow the condition before a year of age, although some may have permanent scars on their face or legs. In severely affected dogs, the condition is progressive and these dogs may have to be euthanized due to severe muscle atrophy and associated problems such as an inability to eat and drink properly, which may be complicated by pneumonia.

How is dermatomyositis diagnosed?

This disorder is usually suspected in a young collie or Sheltie with crusting facial skin lesions, with or without muscle weakness. There are other conditions which can cause these types of lesions and your veterinarian will do tests such as a skin biopsy to pinpoint the diagnosis. This is a simple procedure done with local anesthetic, in which your veterinarian removes a small sample of your dog's skin for examination by a veterinary pathologist. The biopsy will show changes in the skin consistent with this condition.For the veterinarian: CBC, biochemical profile and urinalysis are usually normal, and the results of standard tests for autoimmunity are usually negative. In addition to history and physical exam findings, diagnosis is made by biopsy (affected skin and muscle), electromyography (EMG), and ruling out other conditions. The main differential diagnosis, especially where the muscle component is mild, is epidermolysis bullosa. The skin lesions have a similar age of onset and clinical progression, but with dermatomyositis, erythematous plaques or vesicles can not be induced in normal skin by applying mild friction.Dermatomyositis may be complicated by localized or generalized demodicosis. Megaesophagus (+/- aspiration pneumonia) may occur in dogs with severe muscle involvement.

How is dermatomyositis treated?

Skin lesions are exacerbated by trauma and by exposure to ultraviolet light, so these should be avoided (by the use of sunscreens for example). This may be all that is required in mildly affected dogs, who are likely to outgrow the condition with time.Dermatomyositis can usually be managed fairly well in moderately affected dogs, with the above precautions and the use of Vitamin E and occasional use of corticosteroids for flare-ups. Your veterinarian will work with you to determine how best to manage the condition in your dog. Unfortunately, it is very difficult to maintain the health and comfort of severely affected dogs, and euthanasia is sometimes the best option..For the veterinarian: Pentoxifylline may help by improving microvascular blood flow. A response may take 2 or 3 months. Short term use of glucocorticoids may be necessary for acute flare-ups of skin or muscle inflammation, but long term use should be avoided as it will exacerbate skin and muscle atrophy.

Breeding advice

Affected dogs should not be bred. Also, because it is difficult to identify dogs that have only a mild form of this condition, close relatives of affected dogs (siblings and parents) should not be used for breeding. It is important to remember that because of the variation in expressivity, offspring of only mildly affected dogs may have much more serious clinical signs

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Demodectic Mange

Demodectic mange is the result of Demodex canis, a microscopic mite multiplying out of control. Most dogs have demodex mites on their skin in small numbers. These mites are acquired by puppies shortly after birth, from their mother.
The causative factors as to why some dogs develope demodectic mange while other dogs do not is not fully understood. The tendancy to be suseptible to demodectic mange appears to be hereditary. It is known that dogs with demodectic mange have an immune system defect. It is this defect that appears to be inherited, making the pup unable to keep the demodex mites under control.
Demodectic mange occurs in one of two forms. The first form is the localized form. This form most often appears in dogs under 1 year of age. The first sign is a thinning of hair around the eyelids, the lips, the corners of the mouth and the front legs. The dog has a moth-eaten appearance. The patches of hair loss can progress into circles of approximately one inch in diameter (occasionally confused with ringworm). Mite removal/reduction normally consists of cleansing shampoos, antibiotic therapy, and immune stimulants. Not all young animals that experience demodicosis are immunologically impaired for life. A significant percentage will "self cure" as their immune system matures. This maturity normally takes place between the ages of 8 months and 3 years, depending on the breed of dog.
During treatment it is critical that the dog is making continuous improvement. If the animal has 5 or more patches, or is not showing a marked improvement; the demodex could be progressing into the generalized form.
The generalized form is the second presentation type of this condition. Generalized demodex can begin as a localized case or can present itself as a sudden onset. Numerous patches appear on the head, legs, and trunk. These patches continuously spread developing into large areas of hair loss. The hair follicles become congested with debris and mites. The breakdown of the skin leads to the formation of sores, with crusting and draining sinus tracts.
Treatment of dogs experiencing generalized demodex can be very prolonged. The reponse to treatment is slow and often requires frequent changes in the medication. In spite of the number of mite removal dips, topical ointments and antibiotics availale a cure is not always possible. Generalized demodectic mange must be treated under veterinary supervision.
Older dogs that develop demodectic mange (in either form) should be screened for underlying causative factors in immune system dysfunction. Diseases such as diabetes, cancer or Cushing's disease can all impact therapy.
Dogs treated for generalized demodectic mange should be neutered

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Patent Ductus Arteriosis (PDa)

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 patency, 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 Collie 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, 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. Their parents should not be bred either, and siblings should only be used after careful screening. If any affected offspring are born, breeding of the parents should be discontinued.

On a Personal Note I had a problem with PDA about 15 years ago I suspected A dog so I contacted Dr. Michael O'Grady Dip-ACVIM Cardiology and along with my vet embarked on some research I breed the male to his Daughter and the results was very obvious this line had PDA in it four of the eight pups had PDA none of them survived long enough to have the surgery to fix the PDA . when the pups were born one could feel a thrill or vibration in there hand . PDA is graded from 1 to 4 four being the worse we had a 2, and three grade fours . the sire the daughter and all related to them in my breeding program were neutered and places in homes . I learned that this was a very serious problem in collies and have taken precautions to prevent this in my breeding program all pups are screened at birth for PDA

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Seizures

Seizures occur for many reasons. There are a number of classification schemes for seizures based on why they occur or what they look like when they do occur. A short explanation of one of those schemes might help to understand what the possibilities are.

Seizures can occur for no apparent reason --- and no reason can be found despite careful examination. This type of seizure activity is referred to by some vets as primary epilepsy, or idiopathic epilepsy. Most of the time the onset of seizures in dogs with primary epilepsy is between one and five years of age and there usually is a fairly long interval between the first seizure and subsequent seizures when they occur. While primary epilepsy is common it is not the most likely problem in Eddie's case because he was older when the seizures started and because the interval between seizures was short.

Seizures can occur as a reaction to medication, allergies, toxins, other diseases, fevers and anything else that disturbs brain function. These seizures are sometimes referred to as reactive seizures or secondary seizures. It is often possible to figure out the cause of this type of seizure based on the history of another illness known to lead to seizure activity, the clinical signs at the time of seizuring or a known history of using a medication that may lead to seizure activity. Allergies are a lot harder to rule out as a cause of seizures, especially food allergies. It may be worth following an limited antigen diet. This is a diet with one meat source, preferably a meat source that the dog hasn't eaten before, and limited carbohydrate sources, such as just rice or just potatoes. I think that seizures due to allergies probably occur, based on several clinical case reports in the literature, but I think that they are pretty rare. Still, when seizures won't respond to medication it seems reasonable to rule out this possibility. Reactive seizures can occur at any age. A careful review of Eddie's prior medical history to try to rule out exposure to distemper, toxins such as lead, chronically administered medications and other illnesses can be helpful, sometimes, in discerning the cause of
seizures.

Another cause of seizures is anatomical or structural disease in the brain. This can be from a brain tumor, hydrocephalus (inadequate drainage of fluid in the skull), bleeding in the brain, circulatory problems in the brain and other structural or anatomical problems. Unfortunately, in older dogs (over five years of age) with seizures that occur without a prior history of seizure activity and that recur quickly, the most likely diagnosis is a brain tumor. This means that this possibility is high in Eddie's case. Magnetic resonance imaging (MRI) and computed tomagraphy (CT) scans are very helpful in diagnosing brain tumors. Due to the cost of these procedures it may be a good idea to think about the next step for a brain tumor, which would be radiation therapy or surgery, before spending the money for the scans. If you know that these options are not available or not suitable in Eddie's case, then it may not be worth making a definite diagnosis. A really careful neurologic exam might reveal clues about the possibility of a seizure but most of the time there aren't discernible neurologic signs in dogs with brain tumors, at least early on.

The last cause of "seizures" are things that look a lot like seizures, but aren't. The most common problems that are sometimes mistaken for seizures are fainting due to heart disease and low blood sugar (hypoglycemia), which is most commonly associated with overproduction of insulin due to insulinomas (a tumor of the pancreas). I don't think these problems are very likely as it seems like your vet is being cautious about testing for them.

Potassium bromide does make a good addition to phenobarbital for seizures that are hard to control. In addition it does seem like some dogs need to be at the high end of the serum levels ( 30 to 40 ug/dl at trough times ) in order to have seizure control

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If you like nothing better than coming home from a hard day's work and finding that your dog decided to "go" on the couch or use your favorite slippers as a new chew toy, then crate training isn't for you. But, if you're like most people, then using a crate to properly train your dog will be time well spent. Crate training takes some time and effort, but it is a proven way to help train dogs who act inappropriately without knowing any better. If you have a new dog or puppy, you can use the crate to limit his access to the house until he learns all the house rules—like what he can and can't chew on and where he can and can't eliminate. A crate is also a safe way of transporting your dog in the car or taking him places where he may not be welcome to run freely. If you properly train your dog to use the crate, he'll think of it as his safe place and will be happy to spend time there when needed.

Selecting a Crate

Crates may be plastic (often called "flight kennels") or collapsible, metal pens. They come in different sizes and can be purchased at most pet supply stores. Your dog's crate should be just large enough for him to stand up and turn around in. If your dog is still growing, choose a crate size that will accommodate his adult size. Block off the excess crate space so your dog can't eliminate at one end and retreat to the other.

The Crate Training Process

Crate training can take days or weeks, depending on your dog's age, temperament, and past experiences. It's important to keep two things in mind while crate training: The crate should always be associated with something pleasant, and training should take place in a series of small steps. Don't go too fast.

Step 1: Introducing Your Dog to the Crate

Place the crate in an area of your house where the family spends a lot of time, such as the family room. Put a soft blanket or towel in the crate. Bring your dog over to the crate and talk to him in a happy tone of voice. Make sure the crate door is open and secured so that it won't hit your dog and frighten him.
To encourage your dog to enter the crate, drop some small food treats nearby, then just inside the door, and finally, all the way inside the crate. If he refuses to go all the way in at first, that's okay; don't force him to enter. Continue tossing treats into the crate until your dog will walk calmly all the way into the crate to get the food. If he isn't interested in treats, try tossing a favorite toy in the crate. This step may take a few minutes or as long as several days.
Step 2: Feeding Your Dog His Meals in the Crate
After introducing your dog to the crate, begin feeding him his regular meals near the crate. This will create a pleasant association with the crate. If your dog is readily entering the crate when you begin Step 2, place the food dish all the way at the back of the crate. If instead your dog remains reluctant to enter the crate, put the dish only as far inside as he will readily go without becoming fearful or anxious. Each time you feed him, place the dish a little further back in the crate.
Once your dog is standing comfortably in the crate to eat his meal, you can close the door while he's eating. The first time you do this, open the door as soon as he finishes his meal. With each successive feeding, leave the door closed a few minutes longer, until he's staying in the crate for ten minutes or so after eating. If he begins to whine to be let out, you may have increased the length of time too quickly. Next time, try leaving him in the crate for a shorter time period. If he does whine or cry in the crate, it's imperative that you not let him out until he stops. Otherwise, he'll learn that the way to get out of the crate is to whine, so he'll keep doing it.
Step 3: Conditioning Your Dog to the Crate for Longer Time Periods

After your dog is eating his regular meals in the crate with no sign of fear or anxiety, you can confine him there for short time periods while you're home. Call him over to the crate and give him a treat. Give him a command to enter, such as "kennel." Encourage him by pointing to the inside of the crate with a treat in your hand. After your dog enters the crate, praise him, give him the treat, and close the door. Sit quietly near the crate for five to ten minutes and then go into another room for a few minutes. Return, sit quietly again for a short time, then let him out of the crate.
Repeat this process several times a day. With each repetition, gradually increase the length of time you leave him in the crate and the length of time you're out of his sight. Once your dog will stay quietly in the crate for about 30 minutes with you out of sight the majority of the time, you can begin leaving him crated when you're gone for short time periods and/or letting him sleep there at night. This may take several days or several weeks.
Step 4, Part A: Crating Your Dog When Left Alone
After your dog can spend about 30 minutes in the crate without becoming anxious or afraid, you can begin leaving him crated for short periods when you leave the house. Put him in the crate using your regular command and a treat. You might also want to leave him with a few safe toys in the crate. You'll want to vary at what point in your "getting ready to leave" routine you put your dog in the crate. Although he shouldn't be crated for a long time before you leave, you can crate him anywhere from five to 20 minutes prior to leaving.
Don't make your departures emotional and prolonged, but matter-of-fact. Praise your dog briefly, give him a treat for entering the crate, and then leave quietly. When you return home, don't reward your dog for excited behavior by responding to him in an excited, enthusiastic way. Keep arrivals low key to avoid increasing his anxiety over when you will return. Continue to crate your dog for short periods from time to time when you're home so he doesn't associate crating with being left alone.
Step 4, Part B: Crating Your Dog at Night

Put your dog in the crate using your regular command and a treat. Initially, it may be a good idea to put the crate in your bedroom or nearby in a hallway, especially if you have a puppy. Puppies often need to go outside to eliminate during the night, and you'll want to be able to hear your puppy when he whines to be let outside.
Older dogs, too, should initially be kept nearby so that they don't associate the crate with social isolation. Once your dog is sleeping comfortably through the night with his crate near you, you can begin to gradually move it to the location you prefer, although time spent with your dog—even sleep time—is a chance to strengthen the bond between you and your pet.
Potential Problems

Too Much Time In The Crate. A crate isn't a magical solution. If not used correctly, a dog can feel trapped and frustrated. For example, if your dog is crated all day while you're at work and then crated again all night, he's spending too much time in too small a space. Other arrangements should be made to meet his physical and emotional needs. Also remember that puppies under six months of age shouldn't stay in a crate for more than three or four hours at a time. They can't control their bladders and bowels for longer periods.
Whining. If your dog whines or cries while in the crate at night, it may be difficult to decide whether he's whining to be let out of the crate, or whether he needs to be let outside to eliminate. If you've followed the training procedures outlined above, then your dog hasn't been rewarded for whining in the past by being released from his crate. If that is the case, try to ignore the whining. If your dog is just testing you, he'll probably stop whining soon. Yelling at him or pounding on the crate will only make things worse.
If the whining continues after you've ignored him for several minutes, use the phrase he associates with going outside to eliminate. If he responds and becomes excited, take him outside. This should be a trip with a purpose, not play time. If you're convinced that your dog doesn't need to eliminate, the best response is to ignore him until he stops whining. Don't give in; if you do, you'll teach your dog to whine loud and long to get what he wants. If you've progressed gradually through the training steps and haven't done too much too fast, you'll be less likely to encounter this problem. If the problem becomes unmanageable, you may need to start the crate training process over again.

Separation Anxiety. Attempting to use the crate as a remedy for separation anxiety won't solve the problem. A crate may prevent your dog from being destructive, but he may injure himself in an attempt to escape from the crate. Separation anxiety problems can only be resolved with counter-conditioning and desensitization procedures. You may want to consult a professional animal-behavior specialist for help

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Vaccinations for the new puppy........

Susan Thorpe Vargas Ph.D.

Thank you Susan for this Info

One of the most controversial issues in veterinary science today concerns vaccinations. What people are questioning is the frequency of vaccination, some safety vs. efficacy concerns and even whether to vaccinate at all. So when you ask your vet when to bring your new puppy back for its next shot, be aware there is no one correct answer, how often to vaccinate will depend upon quite a few different factors. Some of these considerations include your puppy's environment, its breed, the age at which the first shot was given and the interval between shots. Also important are the kinds of vaccines necessary for the area you live in and what type, e.g., whether a killed, recombinant or a modified live-type vaccine is being used.

The Vaccine Controversy

The first point to consider is the safety issue. Vaccines can be harmful. We vaccinate because the advantages outweigh the risks. Just ask anyone who has seen a beloved pet die of parvo or distemper. But one should question the sense of vaccinating against Lyme disease or Leptospirosis in an area where these diseases are not a problem. This is why the dog's environment is so important. High-risk dogs are those that live in close proximity with each other, as in a shelter or kennel situation, or show dogs constantly exposed to dogs from all over the country. However, there are risks associated with vaccinations and when such risks weighed against the benefits usually are considered acceptable, except when it is your dog that suffers the untoward reaction. For instance some dogs, after being vaccinated with modified live canine distemper vaccine (see types of vaccines) can develop aggression, seizures, a lack of coordination and other neurological dysfunctions caused from a rare condition called postvaccinal canine distemper virus encephalitis. Another problem noted with genetically susceptible animals is that it is possible for vaccinations to trigger various autoimmune diseases, including several blood disorders and rabies vaccine-induced encephalitis.

Another source of controversy is the recommended frequency of vaccinations. Although yearly boosters are recommended by most vets, for many diseases the yearly booster really is not obligatory and may be counter productive and increase the risk for adverse reactions. However, a yearly checkup is necessary for the same reasons you would have one yourself. For the low-risk pet, once the initial puppy series is completed, a booster at one year and another at three years should suffice until your dog's senior years. With the new licensing requirements duration of efficacy studies are now available. These data were only recently required. However, animal vaccines should compare favorably with the duration of human vaccines, and the results certainly reflect that. On the other hand, no data supports yearly vaccinations either.
Below is a table from an article by Dr. Robert D. Schultz, Duration of Immunity to Canine Vaccines:
What We Know and Don't Know. Ronald D. Schultz is Professor and Chair of the Department of Patho-biological Sciences, School of Veterinary Medicine, University of Wisconsin-Madison.

http://critterfixer.com/pages/petcare_duration_immunity.asp

"Duration of protective immunity was assessed primarily by two procedures; the first is held to be the "gold standard and that is to challenge the vaccinated animal with the virulent organism, the second method is to measure antibody and compare the antibody titer to that which is known to prevent infection (e.g. provide sterile immunity). The studies we report here include challenge studies as well as studies that determine antibody titers. A summary of our results show the following (Table 1). "

Table 1: Minimum Duration of Immunity for Canine Vaccines
Vaccine Minimum Duration of Immunity Methods Used to Determine Immunity
CORE VACCINES
Canine Distemper Virus (CDV
Rockbom Strain 7 yrs / 15 yrs challenge / serology
Onderstepoort Strain 5 yrs / 9 yrs challenge / serology
Canine Adenovirus-2 (CAV-2) 7 yrs / 9 yrs challenge-CAV-1 / serology
Canine Parvovirus-2 (CAV-2) 7 yrs challenge / serology
Canine Rabies 3 yrs / 7yrs challenge / serology
NON-CORE VACCINES
Canine parainfluenza 3 yrs. serology
Bordetella bronchiseptica 9 months challenge
Leptospira interrogans ser. canicola ?
Leptospira icterohaemorrhagiac ?
Borrelia burgdorferi 1 yr. challenge
Giardia ?
Canine Coronavirus Lifetime (whethervaccinated or notvaccinated) Challenge / serology

Why Is Breed Important?

If your puppy is a Rottweiler, Greyhound or Doberman, or even a mix of one of these breeds, you should be aware that the normal series of shots for parvovirus may not be enough to produce noticeable antibody titer. It may take multiple shots given over a year's time before your dog is protected adequately. Why is that, you ask? At this point no one is quite sure. The basis most likely is genetic because it seems more prevalent in certain lines, but some data indicate that upward of 5 percent of Rottweilers are going to be poor responders. On the other hand, the immune system is very complex, and just because the antibody titer is low does not mean the dog will not survive exposure to the disease.

A Short Course in Immunology

So what is antibody titer? Antibody titer is going to be the new veterinary buzzword. Simply put, when your body is exposed to a foreign protein such as the outer coat of a virus or bacteria, your immune system is able to recognize that this is a foreign body. Why? Because everyone carries on most cells a glycoprotein (a sugar-protein molecule) that identifies his or her cells as unique to himself or herself. These molecules are called the Major Histocompatibility Complex I and II proteins, and why they are important will become clear later in this article. Once an invasive agent is recognized as "non-self" your body is able to mount a specific immune response that targets that precise foreign protein. This is called the humoral response and involves the making of antibodies. An antibody is another protein whose job is to attach itself to the target molecule so another type of cell, called a macrophage, can eliminate it. However, the body takes quite a while to mount this specific immune response on the first exposure to an antigen, or more correctly an epitope. Epitope is "science speak" for a fragment of a foreign protein. This immune system learning process is the reason why both you and your puppy get multiple vaccinations during the first initial series. After being exposed once to a particular antigen (which is antibody-generating), some of these cells turn into memory cells with the ability to manufacture antibodies against that specific antigen with a much shorter response time. Once firmly established, immunity against the particular antigen can last a very long time, sometimes for the entire lifetime of the animal.

The humoral response is just one way the immune system defends the body against pathogens. There are the native defense mechanisms such as the complement system, enzymes in the saliva and tears, acids in the stomach and even beneficial bacteria in the gastrointestinal tract that can be considered the first line of defense. For our purpose here, with respect to vaccinations, the other most important immune response is known as cell-mediated immunity. This type of immunity is the result of the interaction of several different types of white blood cells and is controlled by a class of cells called T- cells. Some pathogens, such as viruses, have learned to hide from the immune system by inserting themselves into different types of body cells. Once established within the cell the virus can either go dormant or proceed to take over the genetic replication machinery of the host cell. It is possible for the body to recognize those host cells infected by virus because certain changes occur on the affected cell surface that alert the T-cells to the presence of virus. Once aware of the threat, the cytotoxic T-cells either destroy the infected host cell or secrete an array of protein molecules that can eliminate targeted host cells. However, cytotoxic T-cells only will attack virus-infected host cells if they are expressing MHC class I molecules on their surface. A virus-infected cell also will release a glycoprotein called interferon. Not only does interferon have antiviral activity, but its presence induces the production of two other proteins that inhibit viral reproduction.

Current thinking suggests that when vaccination is known to prevent reinfection, it is the humoral system that is regulating protection. However, it appears cell-mediated immunity is the primary regulator of vaccines that prevent clinical expression of disease but do not always prevent reinfection. Hence, the ideal vaccine should elicit both types of immune response.

Types of Vaccines

Killed vs. Modified Live

When designing a vaccine, efficacy and safety are the primary considerations. These two principles appear to be mutually incompatible. In order to offer immunity against disease the vaccine model should mimic the native antigen and yet should not cause pathology, i.e., clinical signs of disease. Killed vaccines, also known as fully attenuated vaccines, until recently have been the safest vaccine option available. They are safer because unlike the modified live vaccines they do not shed virus into the environment nor can they ever revert to virulence. However, in order to maximize their effectiveness, killed vaccines are normally used with adjuvants that can cause their own problems. The immune system is antigen-driven. This means that in order to mount an effective immune response, the body must "see" the antigen for as long as possible. Once the antigen is eliminated the response is terminated. Many different compounds have been used to enhance the efficacy of killed vaccines, but the rational behind their use is to prolong the antigenic stimulus of the primary immune response.

In comparison, the modified live vaccines are more like the original pathogen in the way they elicit a immune reaction. In general, vaccines that contain the living organisms will produce a stronger and a longer-lasting immunity, but their virulence must be reduced to a safe level. This process is called attenuation. Reducing the virulence of bacteria is accomplished by culturing them under unusual conditions. For example, one can make them dependent on a growth medium that is not available in the living animal so they cannot reproduce. Once introduced into the body these bacteria can elicit the expected immune response, but die off so rapidly they do not cause the disease. When the pathogen is a virus a different strategy is used-cell culture in cells or in a species for which the organism is not normally adapted. After many passages through these foreign cell lines the virus is unable to produce disease when reintroduced into its original host. Another issue associated with the use of MLV is possible contamination with other pathogens. One also should be aware this not just one organism, but a population. Therefore it is conceivable that deleterious mutations might occur. So you can see there are problems associated with both types of vaccines and some choices between safety and efficacy that need to be made.

Recombinant

Great strides have been made in recombinant technology and the future will bring even more advances leading to vaccines that may offer better protection and greater safety. A recombinant is defined as a virus, a bacterium or other microorganism in which the genetic material has been artificially modified. This alteration usually involves deletion of all or part of a gene or the insertion of one or more genes from another organism. So far the United States Department of Agriculture has classified three different types of recombinant vaccines.

The first class is called Subunit Vaccines. It really is not necessary for an animal's immune system to "see" the entire infectious organism in order to mount an immune response. Often all that is required is for only a small portion or protein fragment to act as the antigen. An example of a subunit vaccine is one developed by Rhone Meriux scientists (now known as Merial) against Lyme disease. This vaccine is made of purified Outer surface protein A. After mapping the genome of the bacteria Borrelia burgdorferi, it was determined that this protein evoked the greatest antigenic response. Recombinant techniques allow for the isolation of this DNA fragment and its amplified expression. It then is purified and used to manufacture the vaccine. Besides safety, one of the greatest advantages of this type of vaccine is that a simple blood test can distinguish between animals that have been vaccinated and those that are infected naturally.

The second category is recombinant: Gene-Deleted vaccines. These can be considered a type of genetically attenuated modified live vaccine. Those parts of the pathogen that can cause disease are either removed or rendered nonfunctional.

The third type is called Recombinant: Vectored Vaccines. Recombinant techniques are used to isolate and remove the immune-inducing genes from a pathogenic virus. These genes then are inserted into a nonvirulent vector virus. Once innoculated into the host the vector virus produces both its genes and those of the 'crippled' pathogenic virus. This has the potential to be a very effective type of vaccine because both a humoral and a cell-mediated immune response are elicited. Class III vaccines may also allow for alternative methods of vaccination, for instance, an oral mode of administration. They also have the potential for immunization against more than one type of infection. The advances in safety and efficacy made possible by this new technology bode well for the future health of our pets.

Vaccine Failure

It may require one to two weeks or more to develop an effective immune response after a course of vaccination. If the animal is exposed to an infectious agent prior to vaccination or shortly after, the vaccine will not have had time to induce immunity and the puppy will develop clinical signs of the disease. This also will occur if the puppy was incubating the disease at the time it was vaccinated. In fact, the modified live vaccines can cause something called immunosuppression, so vaccinating a puppy that already is sick only will make matters worse. Canine parvovirus, canine distemper and the use of polyvalent vaccines that contain these attenuated viruses have been implicated in inducing immune dysfunction. Other factors that can cause immunosuppression are stresses including pregnancy, malnutrition, concurrent infections, not allowing enough time between scheduled vaccinations and the use of drugs such as prednisone. Another cause of vaccine failure is incorrect administration, including splitting a vial between puppies.

However, the most common reason for vaccine failure is thought to be the presence of maternal antibodies. This is a passive immunity gained from the dam's colostrum during the first 72 hours of nursing. Maternal antibody interferes more with viral vaccines than bacterial vaccines and with the parvovirus vaccines more than any other type of viral vaccine. Unfortunately, the amount of antigen that causes disease is less than that needed to overcome maternal antibodies, so there is a period of vulnerability when the protection afforded by maternal antibodies is not sufficient to prevent disease and the puppy's immune system is not yet fully functioning. It is very important not only to isolate the puppy from contact with other dogs, but to maintain a strict hygienic regime. A bleach solution diluted 1:10 with water will kill even the parvo virus, but remember to thoroughly rinse with clean water before allowing the puppy to contact a bleached surface.

A Possible Vaccination Schedule for the Low-Risk Puppy

With the stipulation previously mentioned that there is no one correct vaccination protocol and that each individual animal's needs should be assessed by its veterinarian, what follows is an example of an optimal vaccination schedule.

Ideally the initial vaccination should begin no earlier than 6 weeks of age. Older technology suggested that the first shot would contain a modified live measles/distemper vaccine. Measles? Yes, measles. This is an example of a process called heterotypic immunity. It is possible to induce an immune response to one microorganism by immunizing with another microorganism. Since the measles virus is antigenically related to (the body sees it the same way as) the distemper virus, it was possible to confer temporary protection against distemper while avoiding interference from distemper maternal antibodies. We now have available a recombinant distemper vaccine that is able to overcome maternal antibodies and is considerably safer.

If giving the core vaccines in a polyvalent form the second shot should given approximately 3 to 4 weeks after the first injection. Most practitioners also will recommend the puppy be inoculated against canine adenovirus type 2 (CAV-2), which causes a respiratory tract disease. This vaccine will cross-protect against infectious canine hepatitis as well. In some rare cases, if given jointly with the distemper MLV, it can cause temporary immunosuppression. The use of low passage/high titer vaccines now have made it possible to overcome maternal antibody vaccine inactivation at an earlier age and thus shorten the window of vulnerability to canine parvovirus, but remember greater efficacy means you lose some safety factors.

Many veterinarians will vaccinate every two weeks, although a three- or four- week interval is considered optimal. So the third shot should be given in that time frame. At six months a rabies vaccination is required by law. A killed rabies vaccine in the most commonly given and the preferred route is intramuscular.

There is no question that one should vaccinate. Vaccinations protect both the individual dog and the canine population as a whole. What you as a pet health consumer should be aware of is that there are some very real concerns within the veterinary community on the vaccination issues. It is difficult to obtain agreement among academics as to the necessity of certain vaccines, much less the question of yearly vaccinations. You will find just as little consensus among practitioners, but it is you, the puppy owner, who needs to make the final decision.