Welcome To: Glasgowhill Collies

Award Winning Glasgowhill Collies® Rough & Smooth

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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 these pages you 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

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Crate training

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.

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(MDR1)

DESCRIPTION
Some dog breeds are more sensitive to certain drugs compared to other breeds. For example, Australian Shepherds, Collies, Longhaired Whippets and other breeds are more sensitive to antiparasitic and anticancer drugs. The problem is due to a mutation in the multidrug resistance gene (MDR1). The product of MDR1 gene, P-glycoprotein, is an important component of the blood-brain barrier that is responsible for pumping many drugs out of the brain. Dogs with mutant MDR1 gene cannot remove some drugs out of the brain as normal dogs would, which may result in abnormal neurological signs. The result may be an illness requiring an extended hospital stay or even death of the dog.

In addition to its expression in the blood-brain barrier, P-glycoprotein expression occurs also in the intestinal tract, liver, and kidney. In these organs, the absence of P-glycoprotein will alter the pharmacokinetic properties of drugs identified as P-glycoprotein substrates, resulting in enhance oral bioavailability and/or reducing drug elimination through the liver, kidney, and gut. In consequence, plasma concentrations will increase and adverse drug reactivity may occur.

Drugs that have been documented, or are strongly suspected to cause problems in dogs with MDR1 mutation:
- Acepromazine (tranquilizer):
- Butorphanol (pain control);
- Cyclosporin (immunosuppression drug);
- Digoxin (heart drug);
- Doxorubicin (anticancer drug);
- Ivermectin (antiparasitic drug);
- Loperamide (Imodium®, antidiarrheal drug);
- Moxidectin;
- Vinblastine (anticancer drug);
- Vincristine (anticancer drug).

Biochemical studies have shown that mutant MDR1 gene has the potential to act on over 50 different drugs. The following drugs may potentially cause problems when given to dogs that have the mutation:
- Domperidone;
- Etoposide;
- Mitoxantrone;
- Morphine;
- Ondansetron;
- Paclitaxel;
- Quinidine;
- Rifampicin.

INHERITANCE
Multidrug sensitivity in dogs shows an autosomal recessive mode of inheritance.

DNA TEST
Dogs affected with multidrug sensitivity typically display neurological symptoms after drug admission such as hypersalivation, ataxia, blindness, tremor, depression, coma, respiratory compromose, and death. Carriers of the mutant gene may display mild neurological manifestations. Recently, a DNA-based test for the detection of the gene responsible for multidrug sensitivity became available. Since this test directly targets the mutant gene, it is 100% accurate and provides breeders with definitive information on the genetic status of their animals. Instead of avoiding drugs as ivermectin in known susceptible breeds, veterinarians can now determine if a dog is normal, in which case the drug can be administered, or dog is affected, in which case an alternative treatment can be given. Breeders can use this information to detect carriers and eliminate this disease from their breeding lines.

BREEDS:
Australian Shepherd
Collie (rough)
Collie (smooth)
English Shepherd
Longhaired Whippet
McNab
Old English Sheepdog
Shetland Sheepdog
Silken Windhound

Note: As more dogs are tested, more breeds will probably be added to the list of affected breeds.

TEST RESULTS:

Result Interpretation
Normal/Normal These dogs do not carry the mutation, and will not pass on the mutation to their offspring. These dogs would not be experiencing unexpected adverse reaction to normal doses of drugs.
Normal/Mutant These dogs carry both mutant and normal genes, and may pass on the mutant gene to their offspring. These dogs may experience some toxicity after normal doses of drugs.
Mutant/Mutant These dogs carry two mutations, and will not pass on the normal gene to their offspring. These dogs would be expected to experience toxicity after normal doses of drugs.

SAMPLES:
Two types of samples can be submitted for this DNA test:
- A blood sample in a lavender (EDTA) tube;
- Cheek swabs - Order a FREE Sample Collection Kit!

PRICE:
-$75.00 CDN*
Special contract prices are available for Breeder Clubs. Please contact us for more information.

* - subject to the applicable taxes (7% GST)

CERTIFICATION OF RESULTS:
HealthGene will provide a certificate for each test result.
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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.

http://www.offa.org/hipinfo.html

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CEA Collie Eye Anomaly .

there is a test know to prove that you have a Non Carrier of CEA please visit this site www.opigen.com/pot9_test_cea_ch.html for more info .there is more info on CEA please see the page on this site

October 24th 2008

News Release:

Ithaca, NY --- October 24, 2008. It has been a long time coming but rough and smooth collie breeders can now celebrate the news that a definitive DNA test for PRA is available for their breeds. Thanks to years of dedicated work by researchers in the laboratories of Dr. Greg Acland and Dr. Gus Aguirre, and aided by early support from Morris Animal Foundation and the Collie Health Foundation, the mutation responsible for the collie PRA called rod cone dysplasia type 2 (rcd2) has been identified. OptiGen has been granted exclusive rights worldwide to offer this test by Cornell University and the test is now available at OptiGen.

For more information, please visit our website at www.optigen.com

Sincerely,
Becky Iddings
Administrative Support Associate

**********************************************
OptiGen, LLC
Cornell Business & Technology Park
767 Warren Road, Suite 300
Ithaca, NY 14850

phone: 607-257-0301
fax: 607-257-0353
email: genetest@optigen.com
web: www.optigen.com

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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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This is sally's Story

I bought Sally on July 15th 2007 she had demodetic Mange so did her three litter mates it was generalized mange . All her litter mates cleared up and were well on there way to recovery . But sally was not she was left untreated by Her owner and she did not want her anymore so I bought her ( Through Lawyers ). she was shipped to me in this condition

Day she arrived Open soars on her back and covered in Mange from head to toe

Third day in my home and the same day she came home from the VET's she had to be shaved . and treatment was started

This picture was taken today of Sally August 30th she had two treatments of Taktic and every other day bathing and she was free of Mange within two weeks of arriving . her owner wanted to have her put down . Her mother and all her litter mates have been Spayed or neutered Including sally .

Sally has made a full recovery . Please if your dog breaks in mange DO YOUR HOMEWORK there was no need to put poor sally down Nor should she have suffered for such a long time. sally is a year old she is a wonderful loving happy dog considering the condition of her skin and all she went through I will never regret buying sally .

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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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Hypothyroidism Article
http://www.mirage-samoyeds.com/thyroid3.htm

The most resent study's and other info will be posted as time goes on