Health

 

No studies indicate that Norwich Terriers are predisposed to any particular health disorder.

 

The most common mode of of inheritance of genetic conditions in dogs is autosomal recessive. Because the recessive gene is carried in the population in outwardly normal animals, it is very difficult to eradicate these traits. However the incidence can be reduced by identification of carriers through genetic testing and the conscientious use of this information in breeding programmes. As long as the frequency of a gene for a recessive disorder remains low in the population, the particular gene may be passed along for many generations before by chance two carriers are mated and affected individuals are born. However, the gene frequency may become unusually high due to breeding of close family members (inbreeding), or because of the "popular sire" effect , where a sire with a harmful recessive gene is mated frequently because of desirable traits.  We strongly recommend that the Coefficient of Inbreeding (CoI) be less than 10.  The lower the better for healthy genetics.

 

The Norwich Terrier Club of America (NTCA) currently recommends that breeding animals be tested by a professional for:

 

• luxating patella,
• hip dysplasia, and
• eye exam (CERF).
   

Submitting results to the open registries of the Orthopaedic Foundation for Animals and Canine Eye Registry Foundation (CERF) permits breeders to make informed breeding decisions and is necessary for the health and longevity of any breed.
 

1. Luxating Patella

Luxating Patella, or trick knee, is a condition in which the patella, or kneecap, dislocates or moves out of its normal location. The luxation is usually medial, but can be lateral. It can be caused by some form of blunt trauma, or may be a congenital defect. In congenital cases, it is usually bilateral. Patellar luxation is a common condition in dogs, particularly small and miniature breeds. The condition usually becomes evident between the ages of 4 to 6 months.[1]

 

Diagnosis is made through palpation of the knee. X-rays are necessary in some cases. The luxating patella often causes no or very slight symptoms. There may be intermittent limping in the rear leg. Osteoarthritis can develop secondarily. There are several stages in patellar luxation, ranging from minor (the patella's position is normal most of the time) to very serious (the patella is permanently luxated). The more serious stages require surgery to correct, if the animal has difficulty walking. The surgery involves deepening the groove (trochlea) that the patella sits in.

 

Additional help can be given with the use of pet ramps, stairs, or steps. These can help the dog travel from one place to another, especially up and down, without adding any pain or damage to the patella.

 

References:

[1] Ettinger, Stephen J.;Feldman, Edward C. (1995). Textbook of Veterinary Internal Medicine, 4th ed., W.B. Saunders Company. ISBN 0-7216-6795-3.

 

 

2. Hip Dysplasia

Hip Dysplasia is a hereditary disease that, in its more severe form, can eventually cause crippling lameness and painful arthritis of the joints. It is caused by a combination of genetic and environmental factors. It can be found in many animals and occasionally in humans, but is most commonly associated with dogs, and is not uncommon in many dog breeds, particularly the larger breeds.

 

Hip dysplasia is one of the most studied veterinary conditions in dogs, and the most common single cause of arthritis of the hips.

 

Overview

Normal Hip Anatomy

In the normal anatomy of the hip joint, the femur (the thigh bone) is connected to the pelvis at the hip joint. The almost spherical end of the femur head (the caput, or caput ossis femoris) fits into the acetabulum (a concave socket located in the pelvis). The bony surface of the femur head and of the acetabulum are covered by cartilage. While bones provide the strength necessary to support body weight, cartilage ensures a smooth fit and a wide range of motion. Normal hip function can be affected by congenital conditions such a dysplasia, discussed in this article, trauma, and by acquired diseases such as osteoarthritis and rheumatoid arthritis.

 

Dysplastic Hip Anatomy

In a hip suffering from dysplasia, two things are commonly abnormal. First, the caput is not deeply and tightly held by the acetabulum. Instead of being a snug fit, it is a loose fit, or a partial fit. Secondly, the caput or acetabulum are not smooth and round, but are misshapen, causing abnormal wear and tear or friction within the joint as it moves. The body reacts to this in several ways. First, the joint itself is continually repairing itself and laying down new cartilage. However cartilage repair is a relatively slow process (the most rapid bodily repairs are often in systems with a blood flow, which cartilage lacks).

 

So the joint may suffer degradation due to the abnormal wear and tear, or may not support the body weight as intended. The joint becomes inflamed and a cycle of cartilage damage, inflammation and pain commences. This is a self-fueling process, in that the more the joint becomes damaged, the less able it is to resist further damage. The inflammation causes further damage. The bones of the joint may also develop osteoarthritis, visible on an x-ray as small outcrops of bone, which further degrade the joint.

 

The underlying deformity of the joint may get worse over time, or may remain static. A dog may have good x-rays and yet be in pain, or may have very poor x-rays and apparently almost no problems. The hip condition is only one factor to determine the extent to which dysplasia is causing pain or affecting the quality of life. In mild to moderate dysplasia it is often the secondary effects of abnormal wear and tear or arthritis, rather than dysplasia itself, which is the direct causes of visible problems.

 

Causes and Effects

In dogs, there is considerable evidence that genetics plays a large role in the development of this defect. There might be several contributing genetic factors, including a femur that does not fit correctly into the pelvic socket, or poorly developed muscles in the pelvic area. Large and giant breeds are susceptible to hip dysplasia, but smaller dog breeds may be affected as well.

 

To reduce pain, the animal will typically reduce their movement of that hip. In animals this may be visible as "bunny hopping", where both legs move together, or less dynamic movement (running, jumping), or stiffness. Since the hip cannot move fully, the body compensates by adapting its use of the spine, often causing spinal, stifle (a dog's knee joint), or soft tissue problems to arise.

 

In dogs, the problem almost always appears by the time the dog is 18 months old. The defect can be anywhere from mild to severely crippling. It can cause severe osteoarthritis eventually.

 

Clinical Detection and Testing

Symptoms

Dogs might exhibit signs of stiffness or soreness after rising from rest, reluctance to exercise, bunny-hopping or other abnormal gait (legs move more together when running rather than swinging alternately), lameness, pain, reluctance to stand on rear legs, jump up, or climb stairs, subluxation or dislocation of the hip joint, or wasting away of the muscle mass in the hip area. X-rays often confirm the presence of hip dysplasia, but radiographic features may not be present until two years of age in some dogs. Moreover, many affected dogs do not show clinical signs, but some dogs manifest the problem before seven months of age, while others do not show it until well into adulthood.

 

In part this is because the underlying hip problem may be mild or severe, may be worsening or stable, and the body may be more or less able to keep the joint in repair well enough to cope. Also, different animals have different pain tolerances and different weights, and use their bodies differently, so a light dog who only walks, will have a different joint use than a more heavy or very active dog. Some dogs will have a problem early on, others may never have a real problem at all.

 

Each case must be treated on its own merits, and a range of treatment options exist.

 

Diagnosis

The classic diagnostic technique is with appropriate x-rays and hip scoring tests. These should be done at an appropriate age, and perhaps repeated at adulthood - if done too young they will not show anything. Since the condition is to a large degree inherited, the hip scores of parents should be professionally checked before buying a pup, and the hip scores of dogs should be checked before relying upon them for breeding. Despite the fact that the condition is inherited, it can occasionally arise even to animals with impeccable hip scored parents.

 

In diagnosing suspected dysplasia, the x-ray to evaluate the internal state of the joints, is usually combined with a study of the animal and how it moves, to confirm whether its quality of life is being affected. Evidence of lameness or abnormal hip or spine use, difficulty or reduced movement when running or navigating steps, are all evidence of a problem. Both aspects have to be taken into account since there can be serious pain with little X-ray evidence.

 

It is also common to X-ray the spine and legs, as well as the hips, where dysplasia is suspected, since soft tissues can be affected by the extra strain of a dysplastic hip, or there may be other undetected factors such as neurological issues (eg nerve damage) involved.

 

There are several standardized systems for categorizing dysplasia, set out by respective reputable bodies (Orthopedic Foundation for Animals/OFA, PennHIP, British Veterinary Association/BVA). Some of these tests require manipulation of the hip joint into standard positions, in order to reveal their condition on an X-ray, and since this is very painful and must be held still for a clear image, often the animal will be anaesthetized or sedated to achieve clear diagnostic results.

 

Conditions which can Mimic or Replicate the Symptoms of Hip Dysplasia

According to www.petsurgery.com, a veterinary practice in California, the following conditions can give symptoms very similar to hip dysplasia, and should be ruled out during diagnosis:
 

• Cauda equina syndrome (i.e. lower back problems)
• Cranial (anterior) cruciate ligament tears
• Other rear limb arthritic conditions
   

They add that:

"Traditionally, the signs of hip dysplasia are rarely extreme. Usually, only mild to moderate lameness is noted which may suddenly worsen. Dogs with a cranial (anterior) cruciate ligament tear typically hold the affected leg up (which is unusual with hip dysplasia). Patients with back (spinal) problems often scuff their toenails when walking, have an uncoordinated gait, and are weak in the rear limbs. They may be very painful if they have a disc rupture (sciatica) or show no spinal pain in certain degenerative spinal cord conditions (German Shepherd myelopathy)."
 

It is also worth noting that a dog may misuse its rear legs, or adapt its gait, to compensate for pain in the forelegs, notably arthritis, osteochondritis (OCD) or shoulder dysplasia, as well as pain in the hocks and stifles or spinal issues. It is important to rule out other joint and bodily issues before concluding that only hip dysplasia is present. Even if some hip dysplasia is present, it is possible for a painful case of OCD or other diseases to be masked by mild dysplasia.
 

Long term pain It is important to note that a dysplastic animal has probably lived with the condition since it was only a few months old, and has therefore grown up taking the chronic pain for granted and have learned to live with it. Dogs suffering such pain do not usually cry out or show it. Sometimes, they will suddenly and abnormally sit down when walking, or suddenly refuse to walk or climb objects which they usually would, but this can equally be a symptom of many other things, including a thorn in the paw, or a temporary muscle pain. So pain recognition is less common a means of detection than the visible gait and other abnormalities described above.

 

Treatment

Overview

There is no complete cure, although there are many options to alleviate the clinical signs. The aim of treatment is to enhance quality of life. Crucially, this is a congenital condition and so will change during the life of an animal, so any treatment is subject to regular review or re-assessment if the symptoms appear to get worse or anything significantly changes.

 

If the problem is relatively mild, then sometimes all that is needed to bring the symptoms under control are suitable medications to help the body deal better with inflammation, pain and joint wear. In many cases this is all that is needed for a long time.

 

If the problem cannot be controlled with medications, then often surgery is considered. There are traditionally two types of surgery - those which reshape the joint to reduce pain or help movement, and hip replacement for animals which completely replaces the damaged hip with an artificial joint, similar to human hip replacements.

 

Non Surgical Interventions

Non-surgical interventions include three elements: weight control, exercise control, and medication. Weight control is often "The single most important thing that we can do to help a dog with arthritis", and consequentially "reducing the dog's weight is enough to control all of the symptoms of arthritis in many dogs". Reasonable exercise stimulates cartilage growth and reduces degeneration (though excessive exercise can do harm too),[2] and also regular long walks in early or mild dysplasia can help prevent loss of muscle mass to the hips. Medication can reduce pain and discomfort, and also reduce damaging inflammation.[2]

 

Non surgical intervention is usually via a suitable non-steroidal anti-inflammatory drug ("NSAID") which doubles as anti-inflammatory and painkiller. Typical NSAID's used for hip dysplasia include carprofen and meloxicam (often sold as Rimadyl and Metacam respectively), both used to treat arthritis resulting from dysplasia, although other NSAIDs such as tepoxalin (Zubrin) and prednoleucotropin ("PLT", a combination of cinchophen and prednisolone) are also sometimes tried. NSAIDs vary dramatically between species as to effect - a safe NSAID in one species may be unsafe in another.[2] It is important to follow veterinary advice.

 

A glucosamine based nutritional supplement may possibly be suggested to give the body additional raw materials used in joint repair. Glucosamine can take 3-4 weeks to start showing its effects, since it can take up to 6 weeks to reach full therapeutic effect in the body, so the trial period for medication is usually around 3-5 weeks minimum before assuming it isn't working. It's important to remember that glucosamine is not a medication, it's a raw material, so the body still takes considerable time to build more cartilage once it has access to this raw material. Note that the efficacy of glucosamine for such conditions is uncertain; it is supported by some veterinary sources, and considered unsupported by others.

 

It is also common, if necessary, to try multiple anti-inflammatories over a further 4-6 week period. This is since an animal will often respond to one type, but will fail to respond to another. If one anti-inflammatory does not work, a vet will often try one or two other brands for 2-3 weeks each, also in conjunction with ongoing glucosamine, before necessarily concluding that the condition does not seem responsive to medication.

 

Carprofen, and other anti-inflammatories in general, whilst very safe for most animals, can sometimes cause problems for some animals, and (in a few rare cases) sudden death through liver toxicity. This is most commonly discussed with carprofen but may be equally relevant with other anti-inflammatories too. As a result it is often recommended to have monthly (or at least, twice-annually) blood tests performed, to confirm that the animal is not reacting badly to the medications, if these are being used. Such side effects are rare but worth being aware of, especially if long term use is anticipated.

 

This regime can usually be maintained long term, for as long as it is effective in keeping the symptoms of dysplasia at bay.

 

Surgical Interventions

If medications fail to maintain an adequate quality of life, surgical options may need to be considered. These may attempt to modify or repair the hip joint, in order to allow pain free usage, or may in some cases completely replace it.

 

Hip modification surgeries include excision arthroplasty, in which the head of the femur is removed and reshaped or replaced, and pelvic rotation (also known as triple pelvic osteotomy, or pubic symphodesis) in which the hip socket is realigned, may be appropriate if done early enough. These treatments can be very effective, but as a rule tend to become less effective for heavier animals - their ability to treat the problem becomes reduced if the joint has to handle more pressure in daily life. Pelvic rotation is also not as effective if arthritis has developed to the point of being visible on x-rays.

 

Femoral head ostectomy (FHO), sometimes appropriate for smaller dogs and cats, is when the head of the femur is removed but not replaced. Instead, the resulting scar tissue from the operation takes the place of the hip joint. In such surgeries, the weight of the animal must be kept down throughout its life in order to maintain mobility. FHO surgery is sometimes done when other methods have failed, but is also done initially when the joint connection is particularly troublesome or when arthritis is severe.

 

Hip modification surgeries such as these usually result in reduction of hip function in return for improved quality of life, pain control, and a reduction in future risk.

 

Hip replacement is expensive but (since it completely replaces the faulty joint) has the highest percentage of success especially in severe cases, usually restores complete mobility if no other joint is affected, and also completely prevents recurrence.

 

Hip replacement for dogs, can sometimes also be a preferred clinical option for serious dysplasia in animals over about 40 - 60 lbs (20-30 kg), a weight that excludes certain other surgical treatments. For additional information and considerations for canine hip replacement and other surgeries, see main article: Hip replacement (animal).

 

Other options under exploration include:

 

• DARthroplasty (Dorsal Acetabular Rim arthroplasty) is a technique developed by Dr. Barclay Slocum and Theresa Devine Slocum whereby cortico-cancellous bone strips, taken from the iliac crest, are contoured over the femoral head and sutured to the dorsal hip joint capsule and packed with additional cancellous bone graft dorsally to eventually anchor to drill holes in the original dorsal acetabulum. The new "shelf" eventually becomes an extension of the original acetabulum, thereby providing support and eliminating subluxation of the hip joint. The joint capsule becomes the new joint surface.
   
• Pubic symphysiodesis (also known as juvenile pubic symphysiodesis, or JPS), is a procedure for very young dogs that manipulates the way the pelvis grows to create a tighter hip. It involves cauterizing the growth plates of the pelvis, in other words, the part of the pelvis which would usually grow and spread in puppyhood, no longer does so. To compensate, the rest of the pelvis grows outward, in a manner which enhances the "socket" of the hip and provides better support than that dog would have had naturally. Since it relies on growth in puppyhood, it has a very tight window for surgery -- currently no sooner than about 4 months and no later than about 5 months. This is compatible with hip scoring of puppies at 4 months.
   
• Capsular Neurectomy, is a procedure in which the hip joint capsule is de-nerved to reduce pain in the hip. This allows the dog to exercise moderately with less pain, thus preventing the leg muscles from weakening from disuse and providing less support to the bad joint. Both hips can be done at one surgery. This surgery should not prevent a future hip replacement, if a more complete fix is desired.

 

Prevention

Overfeeding puppies and young dogs, might aggravate the problem or bring it on earlier, because pups tend to be more active, less aware of their physical limitations, and have immature bones and supporting structures carrying their weight. Dogs from breeds which are known to be prone to dysplasia, can be kept slightly leaner than normal until around 2 years old, by which time the bones are full strength and the animal can be easily brought up to its normal adult weight. Over exercising young dogs whose bones and muscles have not yet fully developed might also be a contributing factor.

 

Responsible breeders who track the incidence of hip dysplasia have been able to reduce the incidence in some breeds but not to eliminate it altogether.

 

Additional Help

There are many products on the market now to help dogs suffering from hip dysplasia to get around. These consist of pressure-reducing pet beds, ramps, stairs, and steps built with wood, plastic, metal, or foam that help the dog get from one place to another without causing pain or hurting themselves further.

 

References:

[1] Ettinger, Stephen J.;Feldman, Edward C. (1995). Textbook of Veterinary Internal Medicine, 4th ed., W. B. Saunders Company. ISBN 0-7216-6795-3.

[2] ^ a b c d vetrica.com: http://www.vetrica.com/care/dog/arthritis.shtml

[3] Siegal, Mordecai (editor); UC Davis School of Veterinary Medicine Book of Dogs, 1995. Harper Collins. ISBN 0-06-270136-3.

[4] Slocum, B. & Slocum, T. D. DARthroplasty. In: Bojrab, M. J., ed. Current Techniques in Small Animal Surgery, 4th Ed. Baltimore: Williams & Wilkins 1998: 1168 - 1170

 

3. Cataracts

A cataract is any opacity or loss of transparency of the lens of the eye. The opacity may be confined to a small area of the lens or capsule, or it may affect the whole structure. A complete cataract affecting both eyes will result in blindness, whereas small non-progressive cataracts will not interfere with vision. Primary cataracts occur in some breeds; in other breeds the cataract may develop secondarily to another inherited disorder such as progressive retinal atrophy or glaucoma.

 

Most cataracts are inherited. Non-hereditary cataracts also occur, as a result of other diseases, trauma, toxicity, or metabolic disturbances.

 

How are cataracts inherited?

The genetics have not yet been defined for most affected breeds. In others, the mode of inheritance is autosomal recessive, autosomal dominant, or with incomplete dominance.

 

What breeds are affected by cataracts?

 

As you can see from the following list, inherited cataracts have been identified in many breeds. In general, the age of onset, the ophthalmoscopic abnormalities seen, the rate of progression, and the degree of symmetry are specific to each breed. Congenital cataracts are those that are present when the eyes open or before 8 weeks of age; juvenile or developmental cataracts occur in young animals up to about 4 years of age; and later onset cataracts develop in mature animals. Afghan hound (early developing cataracts progressing to visual impairment by 2 - 3 years of age), akita (cataracts associated with microphthalmia), Alaskan malamute (juvenile), American cocker spaniel (juvenile), Australian cattle dog (blue heeler), Australian shepherd (congenital, juvenile, adult), Basenji (congenital), beagle (congenital), bearded collie (juvenile, adult), Bedlington terrier (juvenile), Belgian sheepdog (cataracts non-progressive, do not cause visual impairment), Belgian tervuren (non-progressive, do not cause visual impairment), Bichon frise (juvenile), border collie (adult), Boston terrier (early onset cataracts, bilateral, progress to complete cataract and blindness by 2 - 3 years of age, and later onset cataracts, only occasionally interfere with vision, seen before 8 years of age), Bouvier des Flandres (congenital, juvenile, adult), Brussels griffon (adult), Cavalier King Charles spaniel (early onset cataracts appear by 6 months, progress to complete cataract and blindness by 2 years), Chesapeake Bay retriever (cataracts seen as young adult, may progress to impair vision), chow chow (congenital cataracts), Clumber spaniel, collie (rough and smooth - congenital), curly-coated retriever (cataracts develop as adults and progress slowly), dachshund , dalmatian , Doberman pinscher (cataracts develop before 2 years of age and may cause significant vision loss), English cocker spaniel (juvenile), English springer spaniel (congenital, juvenile, adult), German shepherd (congenital or early developing cataracts that are non-progressive after 1 or 2 years of age), German short-haired pointer (juvenile), Golden retriever (cataracts develop at varying ages, and at different lens locations, usually without visual impairment), Gordon setter (juvenile or adult), Great Dane (juvenile), Havanese, Irish setter (juvenile), Irish wolfhound (juvenile, adult), Italian greyhound (juvenile), Jack Russell terrier, Japanese chin, Labrador retriever (mostly see stationary or very slowly progressive cataracts by 1 to 3 years of age, that do not interfere with vision), Lhasa apso (adult), Lowchen, Mastiff, miniature schnauzer (congenital, juvenile, adult, also cataracts in association with microphthalmos), Newfoundland, Norbottenspets, Norwegian elkhound (juvenile), Nova Scotia duck tolling retriever, Old English sheepdog (congenital, juvenile, adult), Papillon (juvenile, adult), Pekingese, Pembroke Welsh corgi (congenital, juvenile), Portuguese water dog, rottweiler (juvenile, adult), Saint Bernard (juvenile), samoyed (congenital, juvenile, adult), Scottish terrier (adult), Shar Pei, Shetland sheepdog, Shih tzu, Siberian husky (juvenile), smooth fox terrier, soft-coated Wheaten terrier, Staffordshire bull terrier (early onset cataracts are seen by 12 months and progress to blindness by 3 years of age), standard poodle (cataracts are bilateral, symmetrical, and progressive to blindness by about 2 years of age), standard schnauzer (juvenile), Tibetan spaniel, Tibetan terrier (juvenile), Welsh springer spaniel (cataracts develop as early as 8 to 12 weeks of age and progress rapidly, impairing vision), West Highland White terrier (congenital, juvenile), whippet (adult), wire-haired fox terrier (juvenile), Yorkshire terrier (juvenile)

 

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 do cataracts mean to your dog & you?

This depends on whether the cataracts are localized to a small area or are more general, and whether they affect one or both eyes. A small cataract in one eye will not affect your dog's vision at all. At the other end of the spectrum, cataracts may progress rapidly or slowly to cause complete blindness.

 

Congenital cataracts or those that develop at a young age may mature and be reabsorbed, resulting in improved vision. This is unpredictable. In the process of resorption, liquefied lens material may leak into the eye causing inflammation and possibly glaucoma.

 

With their acute senses of smell and hearing, dogs can compensate very well for visual difficulties, particularly in familiar surroundings. In fact owners may be unaware of the extent of vision loss. You can help your visually impaired dog by developing regular routes for exercise, maintaining your dog's surroundings as constant as possible, introducing any necessary changes gradually, and being patient with your dog.

 

How are cataracts diagnosed?

You may suspect your dog is having visual difficulties and/or you may notice discolouration of your dog's pupil(s). Your veterinarian will be able to see the cataract with an ophthalmoscope. Even when not causing visual problems, cataracts may be discovered on a routine ophthalmoscopic exam.

 

How are cataracts treated?

Cataracts can be removed surgically. The decision whether to do so is based on several factors, such as whether the cataracts are progressive, the degree of visual impairment, and the dog's temperament. To prevent postoperative problems, the dog must be cooperative and quiet, especially in the first week following surgery.

 

 

4. Mitral Valve Disease

 

Anterior (frontal) view of the opened heart. White arrows indicate normal blood flow. (Mitral valve labeled at centre right.) 

 

Base of ventricles exposed by removal of the atria. (Bicuspid valve visible at bottom left.) The mitral valve (also known as the bicuspid valve or left atrioventricular valve), is a dual flap (bi = 2) valve in the heart that lies between the left atrium (LA) and the left ventricle (LV). The mitral valve and the tricuspid valve are known collectively as the atrioventricular valves because they lie between the atria and the ventricles of the heart and control flow.

 

Overview

A normally functioning mitral valve opens to pressure from the superior surface of the valve, allowing blood to flow into the left ventricle during left atria systole (contraction), and closes at the end of atrial contraction to prevent blood from back flowing into the atria during left ventricle systole. In a normal cardiac cycle, the atria contracts first, filling the ventricle. At the end of systole, the bicuspid valve shuts, and prevents back flow as the ventricle begins its systole phase. Back flow may occur if the patient suffers from mitral valve prolapse, causing an audible "murmur" during auscultation.

 

Anatomy

The mitral valve has two cusps/leaflets (the anteromedial leaflet and the posterolateral leaflet) which guards the opening. The opening is surrounded by a fibrous ring known as the mitral valve annulus. (The orientation of the two leaflets were once thought to resemble a bishop's miter, which is where the valve receives its name.[1]) The anterior cusp protects approximately two-thirds of the valve (imagine a crescent moon within the circle, where the crescent represents the posterior cusp). These valve leaflets are prevented from prolapsing into the left atrium by the action of tendons attached to the posterior surface of the valve, chordae tendinae.

 

The inelastic chordae tendineae are attached at one end to the papillary muscles and the other to the valve cusps. Papillary muscles are finger like projections from the wall of the left ventricle. Chordae tendinae from each muscle are attached to both leaflets of the mitral valve. Thus when the ventricle contracts, the intraventricular pressure forces the valve to close, while the tendons prevent the valve from opening in the wrong direction.

 

Normal Physiology

During left ventricular diastole, after the pressure drops in the left ventricle due to relaxation of the ventricular myocardium, the mitral valve opens, and blood travels from the left atrium to the left ventricle. About 70-80% of the blood that travels across the mitral valve occurs during the early filling phase of the left ventricle. This early filling phase is due to active relaxation of the ventricular myocardium, causing a pressure gradient that allows a rapid flow of blood from the left atrium, across the mitral valve. This early filling across the mitral valve is seen on doppler echocardiography of the mitral valve as the E wave.

 

After the E wave, there is a period of slow filling of the ventricle.

 

Left atrial contraction (left atrial systole) (during left ventricular diastole) causes added blood to flow across the mitral valve immediately before left ventricular systole. This late flow across the open mitral valve is seen on doppler echocardiography of the mitral valve as the A wave. The late filling of the LV contributes about 20% to the volume in the left ventricle prior to ventricular systole, and is known as the atrial kick.

 

Surface Anatomy

The opening and closing of the mitral valve is difficult to hear directly, but the flow of blood to the left ventricle is most audible at the apex of the heart, and so auscultation is usually performed at the intersection of the fifth intercostal space and the midclavicular line.

 

 

5. Elongated Soft Palate

This is breathing disorder found in some breed lines. The soft palate is the flap of skin at the back of the throat. If the palate is too long, it blocks the airway making it difficult for the dog to breathe. Signs are excessive panting, unable to calm down quickly when excited, and possibly vomiting. Loud, raspy breathing when overheated is another symptom.

 

A vet can check the palate by looking down the dog’s throat, while the dog is awake if he/she is calm and will allow it. Otherwise, a mild sedative can be given so the vet can do a thorough check.

 

Surgery can be done to shorten the palate but is not suggested until the dog is about a year old as the palate may still grow when they are pups, and another procedure may be required at a later date. Sometimes the dog may need to have laryngeal saccules or tonsils removed also, and the vet will do this during the palate clip if required.

 

Laser surgery is now the most common way to shorten the palate. It cauterizes as it cuts, which cuts down the bleeding and swelling, and lessens recovery time. During post-op recovery, only soft food should be given to allow the throat time to heal. Hard kibble can be irritating. Rice/ground beef or chicken, soft dog food, eggs, oatmeal and even baby food are some of the meals that can be fed. Kibble can also be softened with hot water or a gravy.

 

Healing time varies by dog but normal time is between 2-3 weeks.

 

 

 

6. Ischemic Dermatopathy / Cutaneous Vasculitis

A little known and often misdiagnosed reaction to the rabies vaccine in dogs, this problem may develop near or over the vaccine administration site and around the vaccine material that was injected, or as a more widespread reaction. Symptoms include ulcers, scabs, darkening of the skin, lumps at the vaccine site, and scarring with loss of hair. In addition to the vaccination site, lesions most often develop on the ear flaps (pinnae), on the elbows and hocks, in the center of the footpads and on the face. Scarring may be permanent.

 

Dogs do not usually seem ill, but may develop fever. Symptoms may show up within weeks of vaccination, or may take months to develop noticeably. Dogs with active lesion development and / or widespread disease may be treated with pentoxyfylline, a drug that is useful in small vessel vasculitis, or tacrolimus, an ointment that will help suppress the inflammation in the affected areas.

 

Owners and veterinarians of dogs who have developed this type of reaction should review the vaccination protocol critically and try to reduce future vaccinations to the extent medically and legally possible. At the very least, vaccines from the same manufacturer should be avoided. It is also recommended that the location in which future vaccinations are administered should be changed to the rear leg, as far down on the leg as possible and should be given in the muscle rather than under the skin.

 

 

 

7. Canine Epilepsy

Epilepsy is characterized by recurrent unprovoked seizures. In dogs, epilepsy is often an inherited condition. It is more common in certain breeds than others. There is no genetic test that currently exist to screen breeding dogs. Thankfully it is not very common in Norwich Terriers. Affected dogs should not be part of a breeding program.

 

Treatment

Treatments can include the drugs phenobarbital, phenytoin, potassium bromide and diazepam. Potassium bromide and phenobarbital are often paired for the treatment of animals with epilepsy (other drugs such as gabapentin are only recently being introduced into the treatment of animals). A veterinarian will often prescribe Zentinol in an effort to minimize the damaging effects of bromides on the liver enzymes.

 

References:

Canine Epilepsy Resources

Seizure Disorders In Dogs And Cats

Seizure Disorders (in pets)

 

8.  Atypical Seizure Disorder / Paroxysmal Dyskinesia (PD)

While Norwich Terrier Breeders have long been aware of siezure disorders in the breed, the Norwich Terrier genome has not yet mapped epilepsy.  Norwich Terrier DNA analysis has not yet identified a gene or complex of genes associated with seizures.  In fact when breeders refer to Norwich siezure disorder as either “epilepsy” an inherited genetic disorder, or “Norwich Cramp”, an environmentally trigered disease, not necessarily inherited, they are expressing their opinion, not scientific fact.

 

“Norwich Cramp” is not a version of “Scotty Cramp”, a condition suffered by Scottish Terriers, a hereditary neurotransmitter defect.  A problem in seratonin metabolism causing its deficiency.  The Scotty disorder, can be verified with a diagnostic test.  Both Scotties and Norwich remain conscious during the episode.  To be clear, Norwich seizures are completely distinct from Scotty Cramp.  

 

A diagnosis of idiopathic epilepsey means there is no underlying cause and does not address its cause or pathology. Epilepsy is a general term used for neurological disorders that are characterized by recurrent seizures.

 

Paroxysmal dyskinesias (PDs) are episodic movement disorders in which abnormal movements are present only during attacks. Although increasingly being recognised they are often poorly characterised in veterinary literature and are commonly mistaken for an epileptic seizure, both by owners and by vets.

 

The term ‘paroxysmal’ indicates that the signs occur suddenly against a background of normality. The term ‘dyskinesia’ broadly refers to a movement of the body that is involuntary, which means that your dog has no control over the movement and remains fully aware of its surroundings. Between attacks, dogs are neurologically normal and there is no loss of consciousness during the attacks, though some dogs find the episodes disconcerting and do not respond normally. The attacks can last anything from a few minutes to a couple of hours and can sometime occur in clusters.

 

Most neurologists consider that PD results from dysfunction an area of the brain called the basal nuclei (often call the basal ganglia). Nerve cells in this area play an important role in initiating and controlling movement and any abnormal activity here can result in spontaneous and uncontrolled muscle activity. The underlying cause of many PDs is unknown, with the majority being described as idiopathic (meaning of unknown cause).

 

In veterinary medicine, PD have been described in a number of breeds (Cavalier King Charles spaniel, Border terrier, Cairn terrier, Scottish terrier, Dalmatian and Norwich terrier, Boxer, Bichon Frise, Pugs, Chinook, in which they have been ‘labelled’ as breed-specific entities (see below). Although not reported in the literature, similar paroxysmal movement disorders are increasingly seen in other breeds, particularly Jack Russell terriers (JRT) or Labrador retrievers in the UK. The most common appearance of affected dogs is ‘cramping’/’spasm’ involving the hind limbs, which is seen as an increase in the muscle tone of the limbs. While all four limbs may be affected, the hind limbs are often affected to a greater degree than the fore limbs. During an attack, animals can be severely incapacitated, since the spasm overcomes any attempts at voluntary movement; however, many dogs will still attempt to walk. In some cases, episodes can be triggered by excitement or exercise.

 

It has long been a subject of controversy among Norwich breeders as to whether certain episodes of some of their dogs represented a form of epilepsy ... or something else - called "cramp" or "epileptoid cramping syndrome" and now called "paroxysmal dyskinesia". Even veterinary neurologists disagree.

 

The 2016 scientific paper Paroxysmal Dyskinesia in Norwich Terrier Dogs Movement Disorders Clinical Practice, 2016 Luisa De Risio, DVM, MRCVS, PhD, Dipl ECVN, Oliver P. Forman, PhD, Cathryn S. Mellersh, PhD, Julia Freeman, BSc

 

From the paper:

Paroxysmal dyskinesias (PxDs) are a heterogeneous group of disorders in humans and animals characterized by recurrent episodes of sudden, abnormal, involuntary movements of variable duration.

 

The episodes [of the dogs in the study] were characterized by sustained muscular hypertonicity in the pelvic limbs, lumbar region, and thoracic limbs, impairing posture and locomotion without loss of consciousness. ... Episode duration generally was from 2 to 5 minutes ... The majority of affected dogs were related.

 

It is unlikely that the paroxysmal disorder described in the [Norwich Terrier] dogs in this study represents a form of epilepsy, considering the episode phenomenology (e.g., normal level of consciousness and awareness, lack of autonomic signs, the tendency to continue performing certain activities during the episode, and the absence of postictal signs), the similarities with PxDs in other canine breeds, the lack of response to antiepileptic drugs commonly used in canine epilepsy, and the absence of electroencephalogram (EEG) abnormalities in the 2 tested dogs.

 

However, differentiation between PxD and epilepsy can be very challenging,...The stereotyped licking movements movements (observed in 38% of [the Norwich Terrier] dogs in this study) can occur in epileptic patients.

 

A British study on Paroxysmal Dyskinesia identified that, “all dogs were neurologically normal between episodes. No significant abnormalities were detected on diagnostic investigations.  Mean age at the first episode was three years.  The episodes were characterized by sustained muscular hypertonicity in the pelvic limbs, lumber region, and thoracic limbs, imparing posture and locomotion without loss of conciousness.  Episode frequency varied both between and within individuals. Stress, anxiety, excitement and variation in daily routine were recognized as episode triggers in 6.5% of the sample population.  Episode duration generally was from 2-5 minutes.  The majority of affected dogs were related.”

 

De Risio L., Forman O.P., Mellersh C.S., and Freeman J. (2016) Paroxysmal Dyskinesia in Norwich Terrier Dogs, Movment Disorders Clinicla Practise, 3:573-579. Doi: 10.1002/mdc3.12334

 

Treatment  

Following any one or all three of the following presecriptions did see a significant redution in the frequency and duration of siezures.  Treatment varies from diet change, to anticonvulsants, to supplemets of Vitamin E and Selenium.

 

• Diet change included refraining from eating certain types of protien or protien rotation between single protiens.

• Anticonvulsants included Phenobarbital, Bromide, Levetiracetam, Valporoic acid and Zonisamide.
• Vitamin E (50 units) and Selenium (12.5 mcg) every for days to a protocal of Vitamin E (400 units twice a day) and Selenium (50 mcg twice a day). 

 

Clearly more research needs to be done and better diagnostic tests developed. Currently all we have are the opinion of canine neurologists based upon videos of episodes provided by owners. While not trying to minimize this health problem, in terms of the dog's quality of life, these episodes seem to be more distressing to the owners than to the dog (although the dog clearly knows that something is wrong). The episodes are over in a few moments, and no surgical intervention is necessary

 

 

 

9. Atopy

Atopy can be considered the canine equivalent of hay fever. It is quite common, affecting around 10 per cent of dogs. Animals with this condition become sensitized to substances (allergens) in the environment, that are inhaled or absorbed through the skin (and which cause no problems for non-atopic animals). The resultant allergic reaction is primarily seen as extreme itchiness (pruritis).

 

The main allergens involved are house dust mites, house dust, human dander, feathers, molds, and pollens from trees, weeds, and grasses. Atopic dogs are also prone to seborrhea, secondary bacterial skin infections (pyoderma) and probably yeast (Malassezia) infections as well

 

How is atopy inherited?

The exact mode of inheritance is unknown. There is a strong breed predilection for this condition, and marked familial involvement (ie. if both parents are allergic, there is a very strong likelihood the offspring will be as well).

 

What breeds are affected by atopy?

This condition occurs in many breeds. It is most common in the following: Boston terrier, boxer, Cairn terrier, Chinese shar-pei, dalmatian, English setter, golden retriever, Irish setter, Labrador retriever, Lhasa apso, miniature poodle, miniature schnauzer, pug, Scottish terrier, West Highland White terrier, and wire-haired fox terrier. 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 atopy mean to your dog & you?

The condition is usually first seen between 1 and 3 years of age, although it may develop as late as 6 or 7. Initially atopy may be seasonal (eg. from spring to fall) but most affected dogs eventually have signs all year round.

 

Dogs with atopy are very itchy. The areas most affected are the face, paws, lower legs, groin, and, less often, the ears and eyes. In addition to scratching themselves with their hind feet, they often lick or chew the affected areas, or rub along the carpet to scratch the face or ears. The intense itching can make them irritable and less tolerant of being handled.

 

Initially, there are no apparent skin abnormalities, except possibly slight reddening, even though the dog is clearly itchy. (This is important because in other conditions there is often a rash or some visible lesion.) Over time, lesions develop as a result of the scratching and self-trauma, bacterial or yeast infections, and seborrhea, all of which can contribute to the objectionable odor of these dogs. The skin becomes reddened and eventually darkened (hyperpigmentation), abraded, thickened, and wrinkled, with loss of hair and bronze staining from saliva.

 

The concept of "allergen load" is important in understanding and treating this disorder. Atopic dogs are generally allergic to more than 1 agent. A small amount of allergens may be tolerated without developing a reaction, but an increase in any one of those (ie. an increase in allergen load such as occurs during pollen season) may push your dog over the edge to an allergic reaction of extreme discomfort.

 

How is atopy diagnosed?

There are many skin diseases that cause itching, and they can all look rather similar on physical examination. Your veterinarian will ask you questions about your dog's diet, environment, any kind of skin care you are already providing, whether any other pets or people in the house are itchy, where and how quickly did the skin lesions start, and is there any seasonal pattern to the itching. The answers, as well as the age and breed of your dog, will provide diagnostic clues. For example, itching that begins suddenly and rapidly gets worse, is more typical of a flea allergy, scabies, or a drug hypersensitivity. Itching that begins insidiously and gradually worsens, is seen more often with atopy, food allergy, bacterial or yeast skin infection, and seborrhea. Skin infections and seborrhea commonly develop secondary to atopy and may have to be cleared up before your veterinarian can diagnose atopy.

 

Diagnostic tests may include multiple skin scrapings and smears (for mites or yeast infection), fecal examination (for parasites), skin biopsy, skin testing (for allergies to different substances), elimination diets or change in environment (if food or contact allergy is suspected).

 

For the veterinarian: A tentative diagnosis can be made based on history, physical exam, and laboratory tests to rule out other possibilities. Intradermal testing (and to a lesser extent, serologic allergy testing) is necessary for definitive diagnosis and identification of allergens involved. Diagnosis should not be made based solely on intradermal (because of low specificity) or serologic testing (very common false-positive reactions).

 

Intradermal testing is the preferred method of diagnosing canine atopy and determining appropriate immunotherapy. However to get good results requires experience, practice, and close attention to detail. Many factors can lead to false-positive and false-negative reactions. Where possible, it is desirable to refer cases to specialists in this area.

 

How is atopy treated?

Atopy can be satisfactorily controlled in at least 90 percent of affected dogs. There are three components to successful treatment, which will be life-long and will likely require modification from time to time. A combination approach is generally most effective.

 

Reduction in exposure to allergens. This requires identification of the substances to which your dog is sensitive (ie. allergy testing). You may be able to avoid some allergens altogether (if your dog is allergic to feathers or tobacco smoke for example), and reduce exposure to others (by keeping your pet out of carpeted areas to reduce house dust mite exposure for example). Your veterinarian will discuss this with you, in conjunction with the results of your dog's allergy testing.

 

Hyposensitization (immunotherapy or "allergy shots"). This is recommended when the allergens involved can't be avoided, and your dog has clinical signs more than 4 to 6 months of the year which can not be kept under control with medical therapy. Immunotherapy is carried out after your dog's allergens have been identified by allergy testing. Injections of low doses of the appropriate allergens are given at short intervals at first, and then boosters given as needed when clinical signs begin to reappear.

 

Medical treatment. Long term management may include gentle moisturizing anti-pruritic (control itching) shampoos, fatty acids, antihistamines (more likely effective when given as preventative), and short-acting corticosteroids on alternate days (given for short periods at times when there are flare-ups, to minimize the potentially serious side-effects).

 

Resources

[1] Scott, D.W., Miller, W.H., Griffin, C.E. 1995. Immunologic Skin Diseases. In Muller and Kirk's Small Animal Dermatology. p. 500-518. W.B. Saunders Co., Toronto. This reference contains detailed information on allergy testing and on hyposensitization. Page 515 has practical suggestions for environmental management in atopic dogs.

[2] Ihrke, P.J. 1995. Pruritis. In E.J. Ettinger and E.C. Feldman (eds.). Textbook of Veterinary Internal Medicine, pp. 214-219. W.B. Saunders Co., Toronto.