I have become increasingly concerned about the rapid decline in the health of the 'Northern Inuit type dog' in recent years.   Recurring problems include hip dysplasia, elbow deformities, epilepsy, Addison's disease, von Willebrands disease, dwarfism, monorchidsm, sterile bitches, OCD, DM, overshot jaws, cataracts, organ failure (kidney, liver and heart) and various forms of cancer (lymphoma, bone cancer and brain tumours).   (Proof of these health problems occurring in Northern Inuit dogs is available to visitors on request)

Thankfully I have only experienced three of these problems in my lines during the time I have been breeding these dogs,  namely monorchid male puppies, epilepsy from one mating that I did over ten years ago and one pup with cataracts (possibly due to the mother having had a virus while pregnant and also the pup needing to be hand reared, which can lead to eye problems, however I am not taking any chances and will not be breeding from that bitch again).  

It is apparent to me, after discussing the genetic health problems with the top experts in the country, that these ailments are compounded by the chronic inbreeding within the breed causing gene mutations, also insufficient care being taken in the selection of the founder dogs.   The lack of genetic diversity means the future does not look promising and new blood is desperately needed. 

In this respect myself and a few responsible breeders have decided to bring in new blood and create our own unique, healthier lines of wolf-lookalike dogs, which will be registered as part of the Anglo Wulfdog breeding programme. Contrary to claims on some Northern Inuit dog websites we are not passing our dogs off as Northern Inuit dogs, but are in fact doing the opposite by making the point of distinguishing our dogs from Northern Inuit dogs by calling our dogs "Anglo Wulfdogs".  We do not wish to be associated with Northern Inuit or any other wolf lookalike dog in any way.

Monorchidism & Cryptorchidism

Monorchidism literally means one descended testis, and is very rare in most breeds but quite prolific in the Northern Inuit dog.

Cryptorchidism is the retention of one or both of the testes, usually in the abdomen. Cryptorchid testes can also be outside the body wall under the skin. The danger with cryptorchidism is that if the testis is in the abdomen, it is being exposed to a higher body temperature and is at great risk for Sertoli cell tumor (13 times more often than dogs with descended testes). Affected animals should be castrated (neutered). It is suspected to be a hereditary condition. Dogs which are unilateral cryptorchid (one testis is descended, one is not) can still be fertile and can pass the trait on to offspring. Cryptorchidism occurs most frequently in purebred dogs, in certain breeds, and within certain families of a breed. 

Sterile Bitches

There seems to be an increasing number of bitches who appear to be sterile and never have a season.

Addison's disease (Hypoadrenocorticism)

Addison's disease is also known as hypoadrenocorticism. It is an insufficient production of adrenal hormones by the adrenal gland. Since these hormones are essential for life, this is an extremely serious disease and it must be treated as such.

Most dogs with Addison's disease initially have gastrointestinal disturbances like vomiting. Lethargy it also a common early sign. Poor appetite can occur as well. These are pretty vague signs and it is extremely easy to miss this disease. More severe signs occur when a dog with hypoadrenocorticism is stressed or when potassium levels get high enough to interfere with heart function. Dogs with this problem will sometimes suffer severe shock symptoms when stressed, which can lead to a rapid death. When potassium levels get high heart arrythmias occur or even heart stoppage which also is fatal. In some cases, especially secondary Addison's disease, there are no detectable electrolyte changes.

You have to pay close attention to a dog with this problem. Don't ignore any changes in appetite, GI disturbances or anything else that makes you think your dog is ill. If you work with your vet and are careful about following his or her directions this disease has a good prognosis when it is discovered before a crisis occurs.

Clotting is a complex mechanism. In addition to platelets, clot formation is the result of a long chain of chemical reactions carried out by individual molecules called 'clotting factors.' Each factor is numbered such that factor I leads to a reaction with factor II forming a new substance. This then reacts with factor III and so on to factor XII.

In Von Willebrand's Disease, the dog is missing a substance, which helps the platelets form clots and stabilizes Factor VIII in the clotting process. This substance is called 'Von Willebrand's factor.' Because of the deficient clotting of blood, dogs with Von Willebrand's disease have excessive bleeding upon injury. This would be similar to hemophilia in humans.

Certain breeds have a higher incidence of vWD than others. German Shepherds, Doberman Pinschers, Shetland Sheepdogs, Chesapeake Bay Retrievers, German Shorthaired Pointers, Golden Retrievers, Standard Poodles, and Scottish Terriers all have a higher than normal incidence, showing that it can be inherited.

What are the symptoms?

Excessive bleeding is the main symptom. Bleeding generally occurs after a wound or surgery. In these cases, the blood simply does not clot in the normal time, and bleeding is extensive. Dog's with Von Willebrand's disease may also develop nosebleeds, or bleeding from the gums. Bleeding may also occur in the stomach or intestine in which case the stool may either have blood in it, or be black and tarry. Some dogs will have blood in their urine. Bleeding into the joints also occurs, which can cause symptoms similar to those of arthritis.

The diagnosis of Von Willebrand's is made through a test, which checks for the level of Von Willebrand's factor in the blood.

What are the risks?

These dogs, without treatment, can bleed to death following surgery, or what might be normally considered less than life threatening injuries.

What is the management?

Transfusions with blood collected from normal dogs is the only proven way to treat Von Willebrand's disease. Some dogs with Von Willebrand's disease also are hypothyroid - meaning they have lower than normal levels of thyroid hormone. These dogs will benefit from thyroid hormone replacement therapy.

Some studies have been done which suggest a drug called desmopressin acetate (DDAVP) may help dogs with a bleeding episode. The drug can be administered intranasally (into the nose) to increase clotting. There is still some controversy over whether this treatment is effective.

There is no cure for Von Willebrand's disease. Prevention through eliminating affected individuals from any breeding program is the goal of veterinary medicine today. Tests are available to determine which dogs may have this trait. All individuals with a history of this disorder in their backgrounds should be tested.

Congenital defects are those that have been present since birth. Thankfully, they are comparatively rare, accounting for only 5% of the cases seen by vets.   These will usually cause the blood flow through the heart to become turbulent; making a distinctive whooshing noise that vets can hear using a stethoscope. That's what is meant by a 'heart murmur'. However, if your vet tells you they've detected a heart murmur in your dog, it's not necessarily cause for concern.   Many puppies are born with a slight heart murmur (or puppy murmur) that clears up by itself after 4-6 months. In many cases, vets will simply recommend a later checkup, just to be sure that the condition has resolved itself.
 

To understand what hip dysplasia really is we must have a basic understanding of the joint that is being affected. The hip joint forms the attachment of the hind leg to the body and is a ball and socket joint. The ball portion is the head of the femur while the socket (acetabulum) is located on the pelvis. In a normal joint the ball rotates freely within the socket. To facilitate movement the bones are shaped to perfectly match each other, with the socket surrounding the ball. To strengthen the joint, the two bones are held together by a ligament. The ligament attaches the femoral head directly to the acetabulum. Also, the joint capsule, which is a very strong band of connective tissue, encircles the two bones adding further stability. The area where the bones actually touch each other is called the articular surface. It is perfectly smooth and cushioned with a layer of spongy cartilage. In the normal dog, all of these factors work together to cause the joint to function smoothly and with stability.

Hip dysplasia results from the abnormal development of the hip joint in the young dog. It may or may not be bilateral, affecting both right and left sides. It is brought about by the laxity of the muscles, connective tissue, and ligaments that should support the joint. Most dysplastic dogs are born with normal hips but due to genetic and possibly other factors, the soft tissues that surround the joint start to develop abnormally as the puppy grows. The most important part of these changes is that the bones are not held in place but actually move apart. The joint capsule and the ligament between the two bones stretch, adding further instability to the joint. As this happens, the articular surfaces of the two bones lose contact with each other. This separation of the two bones within a joint is called subluxation, and this causes the resulting problems we associate with the disease.

Dogs of all ages are subject to the symptoms of hip dysplasia and the resultant osteoarthritis. In severe cases, puppies as young as five months will begin to show pain and discomfort during and after vigorous exercise. The condition will worsen until even normal daily activities are painful. Without intervention, these dogs may be unable to walk at all by several years of age. In most cases, however, the symptoms do not begin to show until the middle or later years in the dog's life.

Genetics: Almost all researchers agree that there is a genetic link involved. If a parent has hip dysplasia, then the offspring are at greater risk for developing hip dysplasia. Some researchers feel that genetics are the only factor involved, where others feel that genetics contribute less than 25% to the development of the disease. The truth probably lies in the middle. If there are no carriers of hip dysplasia in a dog's lineage, then he will not contract the disease. If there are genetic carriers, then he may contract the disease. We can greatly reduce the incidence of hip dysplasia through selective breeding. We can also increase the incidence through selectively breeding. We cannot, however, completely reproduce the disease through selective breeding. In other words, if you breed two dysplastic dogs, the offspring are much more likely to develop the disease but will not all have the same level of symptoms or even necessarily show any symptoms. The offspring from these dogs will, however, be carriers and the disease may show up in their offspring in later generations. This is why it can be difficult to eradicate the disease from a breed or specific line.

Nutrition: Experimentally, we can increase the severity of the disease in genetically susceptible animals in a number of ways. One of them is through obesity. It stands to reason that carrying around extra weight will exacerbate degeneration of the joint in a dog with a loose hip. Overweight dogs are therefore at a much higher risk. Another factor that may increase the incidence is rapid growth in a puppy during the ages from three to ten months. Experimentally, the incidence has been increased in genetically susceptible dogs when they are given free choice food. In a study, Labrador Retriever puppies fed free choice for three years had a much higher incidence of hip dysplasia than their littermates who were fed the same diet but in an amount that was 25% less than that fed to the dysplastic group.

There have also been studies looking into protein and calcium levels and their relationship to hip dysplasia. Both of these studies were able to increase the level of hip dysplasia by feeding increased amounts of calcium and protein. In the studies, though, puppies were fed greatly increased amounts over normal recommended values and compared to animals fed decreased amounts. They failed to compare puppies fed a normal amount of food that had the recommended amount of protein, fat, and calcium to those fed a diet with slightly less protein, fat, and calcium (similar to a 'large breed puppy food').

Exercise: Exercise may be another risk factor. It appears that dogs that are genetically susceptible to the disease may have an increased incidence of disease if they over-exercised at a young age. But at the same time, we know that dogs with large and prominent leg muscle mass are less likely to contract the disease than dogs with small muscle mass. So exercising and maintaining good muscle mass may actually decrease the incidence of the disease. Moderate exercise that strengthens the gluteal muscles, such as running and swimming, is probably a good idea. Whereas, activities that apply a lot of force to the joint are contraindicated. An example would be jumping activities such as playing Frisbee.

In most cases this condition happens because of another problem causing diarrhoea or vomiting, which can often cause very violent diarrhoea or vomiting which is what causes the violent contractions of the muscles in the intestines when the dog strains. From this the sections overlap each other and more and more waste will get stuck in the pocket produced, making it grow and stretch longer and become painful.

Lymphoma

The “typical” canine lymphoma patient is a middle aged dog presented to the veterinarian because one or more lumps have been found.  The veterinarian rapidly determines that all of the peripheral lymph nodes (those near the skin surface) are enlarged and firm. Usually the dog has not been showing any signs of illness.  The next step is a blood panel and urinalysis to more completely assess the patient’s health and one or more lymph nodes are aspirated or biopsied to confirm the diagnosis of lymphoma.

Thee average life expectancy for a patient with untreated lymphoma is about 2 months from the time of diagnosis.

There are many types of cancer and many possible causes of cancer (chemicals in our environment – especially cigarette smoke, sun exposure, assorted viruses and infections). There are important genetic factors as well. Cancer starts with one or a small group of cells that have “gone wrong.” It appears that such cells arise in our bodies all the time and we have an assortment of natural mechanisms to destroy these cells before they get out of hand. Sometimes these cancer cells escape our natural mechanisms and cancer develops.  At this time, there is no way to know what caused lymphoma development in a given patient.

Osteochondritis Dissecans (OCD)

This disorder of immature long bones is seen primarily in the human, horse and dog.  Due to a various set of circumstances which include diet, trauma, genetics and body size and weight, growing long bones may develop cracks in the cartilage of the weight bearing surface.  These cracks may extend deep to the soft (cancellous) bone beneath the cartilage and eventually a section of the joint cartilage will separate from the underlying structure.  This cartilage flap, varying in size from less than a quarter of an inch to over and inch in diameter, acts as an irritant in the joint.  Subsequent inflammation and attempts at healing can lead to scar tissue and calcium deposits in the affected joint.  Not a happy situation for a creature who is growing and active!

Pituitary Dwarfism  or Hyposomatotrophism

In Pituitary dwarfism / hyposomatotrophism a deficiency in pituitary stimulation of growth hormone production leads to dwarfism. This occurs most commonly in German shepherds but has been reported in several other breeds. It is an inherited disease in German shepherds (autosomal recessive trait). This disorder must be distinguished from other conditions leading to stunted growth, including malnutrition, congenital hypothyroidism and other congenital defects leading to poor growth. Dogs with this condition do not grow like their litter mates. Their hair retains its "puppy" appearance, feeling soft to the touch. Hairloss along the sides that is symmetrical often occurs. Abnormalities in bone growth lead to a deformed appearance to the legs. As other puppies in the litter appear to mature, affected dogs continue to have a puppy-like appearance and bark. Dogs with this condition may be deficient in other hormones in which the pituitary gland controls part of the process of stimulating the hormone's production. It is a good idea to check for hypothyroidism and hypoadrenocorticism in dogs with hyposomatotrophism. Human growth hormone will work to treat affected dogs but it is expensive and may be hard for the average veterinary practitioner to obtain.

The age at onset is 5 to 14 years, which corresponds to the third to sixth decades of human life. Although a few cases have been reported in other large breeds of dogs, the disease appears with relative frequency only in the German Shepherd breed, suggesting that there is a genetic predisposition for German Shepherd dogs (GSD) in developing DM. The work presented here and by others on the nature of DM has been performed in the German Shepherd breed. Care must be taken in extrapolating this information to other breeds of dogs. It is currently not known whether the exact condition exists in other breeds of dogs. Many dogs may experience a spinal cord disease (myelopathy) which is chronic and progressive (degenerative); but, unless they are caused by the same immune-related disease which characterizes DM of GSD, the treatments described herein may be ineffectual. The breeds for which there is data to suggest that they also suffer from DM of GSD are the Belgium Shepherd, Old English Sheep Dog, Rhodesian Ridgeback, Weimaraner and, probably, Great Pyrenees. Confirmation of the diagnosis is important in other breeds before assuming that they have DM of GSD.

Diagnosis of DM is made by a history of progressive spinal ataxia and weakness that may have a waxing and waning course or be steadily progressive. This is supported by the neurologic findings of a diffuse thoracolumbar spinal cord dysfunction. Clinical pathologic examinations are generally normal except for an elevated cerebral spinal fluid (CSF) protein in the lumbar cistern. Electromyographic (EMG) examination reveals no lower motor unit disease, supporting the localization of the disease process in the white matter pathways of the spinal cord. Spinal cord evoked potentials recorded during the EMG do show changes which help determine the presence of spinal cord disease. Radiographs of the spinal column including myelography are normal (other than old age changes) in uncomplicated DM. Unfortunately, myelography can be associated with worsening of clinical signs and carries some degree of risk for certain patients.

Dogs afflicted with DM have depressed lymphocyte blastogenesis to plant mitogens. The depression of their cell mediated immune responses correlates with the clinical stage and severity of the disease. Furthermore, this suppression has been shown to be due to the genesis of a circulating suppressor cell. Some dogs with DM exhibit antigen-binding cells specific to canine myelin basic protein. Immunoglobulins have been shown to be bound within lesions within the spinal cords of dogs with DM. These patients also show increased circulating immune-complexes in their sera. The antigens in these immune-complexes have been examined and appear to be markers of inflammation as they have been found to exist in patients who have other inflammatory diseases of the central nervous system. 2-Dimensional electrophoresis of CSF proteins indicates that the elevated proteins in the CSF of DM patients represent changes which are related to inflammation. While these changes are not specific for DM, the other conditions in which the inflammatory proteins have been found in CSF can be differentiated by clinical signs. The 2-dimensional electrophoresis of CSF proteins appears to be one of the most specific change seen in DM. Recently, we have found that CSF levels of the enzyme, acetylcholinesterase, are elevated in patients with DM. Again, this occurs in other forms of central nervous system inflammation in dogs. However, when combined with the history, neurologic signs, CSF protein concentration and EMG, the elevated CSF acetylcholinesterase level helps confirm the diagnosis. This allows the inclusion of DM in the diagnosis, even if other problems are uncovered during the examination.

The gross pathologic examination of dogs with DM generally is not contributory toward the diagnosis. The striking features being the reduction of rear limb and caudal axial musculature. The microscopic neural tissue lesions consist of widespread demyelination of the spinal cord, with the greatest concentration of lesions in the thoracolumbar spinal cord region. In severely involved areas, there is also a reduced number of axons, an increased number of astroglial cells and an increased density of small vascular elements. In the thoracic spinal cord, nearly all funiculi are vacuolated. Similar lesions are occasionally seen scattered throughout the white matter of the brains from some dogs, as well. Many patients have evidence of plasma cell infiltrates in the kidneys on throughout the gastrointestinal tract, providing a hint to the underlying immune disorder causing DM.

During the past two decades, we, at the University of Florida, have provided important new insights into the pathoetiology of DM. The release of antigens during the disease process could explain the immune deficits seen in DM and suggests that processing these immune-complexes by circulating macrophages leads to the development of the circulating suppressor cells that were previously noted. This provides a logical explanation for the presence of immune abnormalities in GSD with DM. Electrophoresis of immune-complexes demonstrates that the proteins present are inflammatory proteins which increase in inflammatory diseases of the dog nervous system. It is hoped that working with the antigens present in the immune-complexes will lead to a major breakthrough in our understanding of DM and that this also could lead to an early serodiagnostic test for the condition. However, the development of a serodiagnostic test will await the availability of antibodies specific to unique markers within the inflammatory proteins of DM dog immune-complexes.

While the cause of the altered immune system is not known, what is increasingly clear is that DM is caused by an autoimmune disease attacking the nervous systems of patients, leading to progressive neural tissue damage. In many respects, DM is similar to what has been discovered about the pathogenesis of Multiple Sclerosis in human beings. In fact, based upon new data concerning the pathology of MS, we can now say with some degree of certainty that DM is MS in dogs. We believe that, due to some triggering factor, immune-complexes circulate. These immune-complexes lead to endothelial cell damage in the vessels of the CNS. Subsequently, fibrin is deposited in the perivascular spaces. When this degrades (point of action of aminocaproic acid), inflammatory cells are stimulated to migrate into the lesions. The inflammatory cells release prostaglandins and cytokines (point of action of vitamin E and C) which leads to the activation of tissue enzymes and the formation of oxygen free-radicals (point of action of acetylcysteine) which, in turn, leads to tissue damage. Treatment of DM of GSD, which we recommend, is directed at these pathologic processes.

This disease is rife throughout the Northern Inuit breed - there is a very simple DNA test that will show whether a dog is clear (n/n), a carrier (n/DM) or affected (DM/DM).   Sansorrella and all Anglo Wulfdog breeders are testing for this and if a breeding bitch is shown to be a 'carrier' then she will only be mated to a 'clear' dog - all 'outside' dogs included in the Anglo Wulfdog breeding programme are only used if tests show they are 'clear'.   This disease can be bred out if breeders test and take care with their breeding, but sadly not many breeders are testing for this horrific disease and are unwittingly mating 'carrier' to 'carrier' and 'carrier' to 'affected'.