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Westie Health Issues

Several health issues are seen with Westies. We've compiled a list here for your information.

Some Westie Health Issues

Atopic Dermatitis

The Canine Health Foundation has requested that the full research grant to isolate the DNA mutant gene that causes Atopy in the West Highland White Terrier be reviewed by their board of directors.

We believe that CHF will join with the Westie Foundation of America to fund this research by Dr. Thiery Olivery at North Carolina State University College of Veterinary Medicine.

Bob McCaskill, DVM—Westie Foundation of America



Chronic Hepatitis

Cirrhosis of the Liver

Cleft Palate

Copper-associated Hepatopathy

Coppertoxicosis (Copper-Associated Hepatitis)

Hepatitis related to high levels of copper occurs in the Doberman Pinscher, Bedlington Terrier, West Highland White Terrier and Skye Terrier. In Bedlingtons and Westies there is an inherited defect in copper metabolism that allows toxic concentrations of copper to accumulate in the liver. In Dobermans, copper concentrations are increased in most but not all affected dogs. It is unclear in the Doberman (and Skye Terrier) whether high copper levels are the cause of the hepatitis or the result. Copper can accumulate in the liver as a consequence of hepatitis alone.Ê As a rule, the higher the copper concentration, the more likely it is that copper is the cause. Genetic testing for Coppertoxicosis in Bedlington Terriers is available through the University of Pennsylvania.


Blood test, ultrasounds and CT scans provide useful information, but the only definitive test is biopsy of the liver. The prognosis for recovery depends on how long the dog has been ill, the extent of liver damage, and whether the disease can be surgically cured or controlled with medications.

Infectious diseases respond to treatment of the underlying condition. Drugs and poisons frequently exert temporary effects that reverse when the exposure is stopped. Bile duct obstructions and some primary tumors of the liver can be corrected by surgery.

The treatment of idiopathic chronic hepatitis involves the use of corticosteroids and immunosuppressants such as azathioprine (Imuran). The prognosis varies. Some dogs respond well and can be taken off medications, others require life-long treatment. Dogs that respond poorly generally have advanced liver disease with cirrhosis.

Cranial Cruciate Ligament Rupture

Your pet has tom the cranial cruciate ligament in its stifle (knee). As a result of this, the stifle is now unstable and "gives out" on your pet every time weight is placed on the leg. This instability results in lameness, a buildup of fluid in the stifle joint, inflammation (water on the knee), and oftentimes damages the medial meniscus (one of the cartilages of the stifle). Without surgery, there is a chance the knee will stabilize with scar tissue and your pet will once again start to use the leg. If the knee does spontaneously stabilize, it does so in an abnormal position, and arthritis rapidly builds up and becomes a significant problem. Good leg function rarely occurs if there is meniscal damage, as the damaged meniscus acts like a stone would in your shoe, causing significant discomfort and severe inflammation.

Surgery benefits your pet's stifle in many ways. It allows us to remove the fluid, remnants of the tom ligament, and any damaged portion of the medial meniscus. Following this, the stifle is stabilized by transposing other ligaments or creating a new ligament out of surrounding tissues. This results in a stable stifle and greatly slows down, but does not stop the progression of arthritis.

You may expect your pet to carry the leg for two to three weeks postoperatively, before starting to touch it down to the ground. It will then take at least four to six months following surgery for your animal to regain optimal function of this leg.

Following this type of surgery, the average dog can be expected to regain 80% normal use of the leg and only exhibit mild signs of arthritis (i.e. have a sore stifle after heavy exercise, be stiff when it first gets up in the morning, but then "warm out of it" and appear normal, etc.). This type of mild arthritis is readily treated by aspirin and other medications and is very minimal in relation to what would have developed without surgery. The percentage return to function you may expect in your pet may vary depending on its age, breed, weight, and the amount of arthritis already present in the affected stifle, whether both stifles are damaged, etc. A more accurate prognosis can be given at the time of preoperative evaluation.

The normal postoperative course of events includes two weeks with the lin1b in a bulky bandage, followed by leash walking only for a total of eight weeks postoperatively. Very strenuous activity should be avoided until after the third month following surgery. A strict rehabilitation program is not necessary but can be recommended should you desire.

If you have any questions regarding your pets condition, please do not hesitate to call our office. We are available to answer questions on evenings and weekends via our voice mail system. Please leave a message and a member of our staff will return your call as soon as possible.

5610 Kearny Mesa Road, Suite B, San Diego, California 92111. Phone: (858) 560-8006

Craniomandibular Osteopathy (CMO), Swollen Jaw

Description: Craniomandibular osteopathy or osteoarthropathy is a noncancerous growth of excess bone along the lower jaw (ramus of the mandible) or over the angle of the mandible and tympanic bulla. In most instances it is bilateral, but this is not always true. The disease can effect other parts of the jaw, skull and body. The dog's radius and ulna bones, located in the leg can be affected. The bone growth itself is dense, hard and has a rough surface that can usually be detected by external examination by an experienced Veterinarian. But the most common to positively identify and diagnosis is by taking an X-ray of the affected area.

Early in the disease there is an inflammatory component. The swollen jaw is extremely painful to the puppy. The hinge joints of the jaw may be involved, making it extremely difficult for the dog to open its mouth. Fever, drooling, and loss of appetite are characteristic. The eyes can appear 'cross-eyed' due to the severe pain. The disease is usually first recognizable when a puppy shows discomfort while chewing, when his mouth is being examined or has been bumped by a littermate or owner during play. Often the puppy will withdraw from the his littermates due to pain. The dog may cry out in pain when the jaw is forcefully opened. In the most sever of cases the dog can not open it's mouth to lap water. Dehydration can occur. Age of Onset: The disease is most often recognized between the ages of 4 and 10 months, but it can occur as early as 3 - 4 weeks and rarely as late as 10 months plus. Experienced breeders and veterinarians usually recognize it earlier than 4 months of age by clinical signs or by palpation.


The disease is most often diagnosed by clinical signs and palpation with definitive confirmation by lateral and/or ventral/dorsal radiographs of the skull, depending on the location of the specific lesion. All board-certified radiologists can diagnose the disease, as can many other experienced veterinarians. The Orthopedic Foundation for Animals maintain CMO registries for terriers in an attempt to diagnose and track the disease. The Westie Foundation of America has joined forces with the Cairn Terrier Foundation as well as the Scottish Terrier Foundation giving research grants to promote the scientific research of identification of a DNA marker for this disease. Mouth swabs from 'affected' dogs have been requested for on going research, as well as family pedigree history from known 'carriers'.


There is no effective treatment for the abnormal bone deposits. Tube feedings may be required during periods of appetite loss to support proper nutrition. The disease can be treated with most anti-inflam- matory drugs. But since long-term therapy may be required, consult your veterinarian about the drug of choice and the specific dosage. The disease usually stabilizes at one year of age. Partial or complete regression of the excess bone may then occur. The length of treatment may vary from 4 to 10 months. After therapy, some remodeling of the jaw occurs and by the time the dog is 2 - 3 years old, it may be impossible to visually detect the dog ever had the disease. However, there may also be a residual lump at the jaw line when palpated. Complete recovery is uncommon, most dogs are able to eat and maintain their weight however

Mode of Inheritance:

The disease is inherited as a simple autosomal recessive trait. This means that both parents must have at least one gene for CMO (i.e. they are defined 'carriers'). In this disease, the production of an affected puppy provides the only method of identifying 'carriers'. There are mathematical statistics regarding; affected, carrier and clear dogs from a litter. Test breeding to denote 'clear' breeding males or females can not be positively done unless that dog is test bred. This is when the dog to be test bred is bred with 'an affected' dog (either male or female). Statistics and several litters producing 9 or more puppies which are determined 'clear' currently is done by responsible breeders. Otherwise, the CMO gene is passed on undetected to future generations.

The disease is known to occur in West Highland White Terriers, Scottish Terriers, Cairn Terriers, Boston Terriers, Boxers, Doberman Pinschers, Great Danes, Labrador Retrievers and possibly Bulldogs. It is known to occur in the U. S., Canada and most European countries.

Common Treatment Regimen:

CMO is treatable in almost every case, except the MOST severe. The amount of medication and length of treatment varies depending on the severity of the disease. Early detection is essential in the treatment. Many puppies with CMO will need to be on a continuing dosage of Cortisone (steroid) until they are 10 months old or longer. The object being to medicate the puppy enough to keep him comfortable with the lowest possible dosage of a steroid. The symptoms from CMO usually run in 10 - 14 day pain/fever cycles. So even when on the steroid, the puppy may feel better for a while, regaining appetite and playing normally only to have another episode of fever, drooling, and pain. Prednisone is the current steroid which is administered. (Note: When giving this drug one must be careful to reduce the dosage in gradual steps. Stopping steroids abruptly will cause side effects).

Some cases are so mild they can be treated with baby aspirin or only an injection of Cortisone. Others, may require treatment until the dog reaches 14 months of age. It all depends on the severity of the case, the location of the inflammation, and the pain sensitivity of the dog. The object however is to keep the puppy comfortable and, if the disease is located near the hinge of the jaw, medicated enough to allow him to eat. Softened nutritious food or making a 'gruel' formula on painful days is suggested.

Cryptorchidism (Undescended Testicles)

Cryptorchidism is the failure of one or both of the testicles to descend into the scrotum. Normal descent is often complete by 6 to 8 weeks of age but may be delayed to as late as 6 months of age. The undescended testicle may be found within the abdominal cavity, in the inguinal canal or under the skin next to the penis. The condition is considered hereditary in most breeds. There is not complete agreement on the mode of inheritance. Because of the increased incidence of cancer in retained testicles, cryptorchid dogs should always be neutered. A neutered cryptorchid dog should have no other expected health risks due to this condition. Bilateral cryptorchid is sterile, unilateral fertile but barred from showing.

Inheritance: Threshold, possible recessive

What is hyperadrenocorticism?

Canine Hyperadrenocorticism (Cushing's Syndrome)

Hyperadrenocorticism or Cushing's syndrome occurs when a dog is chronically exposed to high levels of the hormone cortisol. Cortisol is produced by two small glands situated near the kidneys known as the adrenal glands. The production and release of cortisol from the adrenal glands is controlled by the hormone ACTH (adrenocorticotrophic releasing hormone). ACTH is produced by a pea-sized gland at the base of the brain called the pituitary gland. Cortisol is normally released into the bloodstream at times of stress to prepare the body for a "fight or flight" response. In dogs with Cushing's syndrome, cortisol is produced excessively all of the time and this eventually results in the development of the clinical signs of the syndrome.

There are 2 forms of hyperadrencorticism

Pituitary-dependent hyperadrenocorticism (PDH) is the most common form (85% of cases) of the syndrome and occurs due to the development of a slow growing tumour in the pituitary gland. This tumour produces large amounts of the hormone ACTH.

Adrenal-dependent hyperadrenocorticism (ADH) occurs when a tumour producing large amounts of cortisol develops in one or possibly both of the adrenal glands. Both tumours result in excessive amounts of cortisol in the blood and over time the clinical signs of Cushing's syndrome will develop.

Clinical signs of hyperadrenocorticism

Hyperadrenocorticism (Cushing's syndrome) is usually seen in the older dog. Initially the signs may be attributed to normal aging.

A dog with hyperadrenocorticism will often:

  • Drink large amounts
  • Urinate frequently
  • Eat ravenously
  • Have a "pot belly"
  • Have thin skin and hair loss
  • Develop muscle wasting
  • Be lethargic

A dog may not necessarily have all of these symptoms.

The diagnosis of hyperadrenocorticism

Blood tests are performed to confirm a diagnosis. Cortisol levels in the blood of both normal dogs and dogs with hyperadrenocorticism fluctuate greatly throughout the day. As a result, a diagnosis cannot be confirmed by simply measuring the concentration of cortisol in a dog's blood. Instead, one of the most commonly used tests to aid in the diagnosis of hyperadrenocorticism, the "ACTH stimulation test" is routinely performed. This test assesses the capacity of a dog's adrenal glands to produce cortisol. This type of test requires the owner to leave the dog with the veterinary surgeon for a few hours or for a whole day.

Treating hyperadrenocorticism

Treatment requires reducing the level of cortisol in a dog's blood. A dog will need to take medication for life in order to halt and contain the debilitating effects of this syndrome. Given the complexity of the syndrome, it is important that a dog is carefully monitored at every stage. The veterinary surgeon will need to perform tests at regular intervals to assess progress and to make sure of the dog's well being. The owner is advised to keep checks on his/her dog and note any changes or new symptoms.

Vetoryl - the treatment for Cushing's Syndrome

Vetoryl is the only veterinary licensed treatment for canine hyperadrenocorticism in the UK.

Vetoryl contains the active ingredient trilostane that blocks the synthesis of cortisol by inhibiting an important enzyme which is key to that synthesis. Since Vetoryl is a short-acting drug, it needs to be taken every day.

Clinical trials have shown that Vetoryl is more effective if it is taken with food in the morning. The most common signs associated with Cushing's syndrome such as increased drinking, eating or urination tend to improve quickly ö often within two to three weeks after commencement of treatment. However skin changes including hair loss may take many months to improve.

Vetoryl therapy is only effective if a dog is carefully monitored. Regular revisits to a veterinary surgeon are necessary to assess progress. In the early stages after diagnosis, it is strongly recommended that a dog is tested and assessed at 10 days, 4 weeks and 12 weeks. Thereafter, a dog should be examined by a qualified veterinary surgeon every 3 months.

Idiopathic Pulmonary Fibrosis

A seminar presented by: Dr. Brendan Corcoran, Sponsored by: Westie Foundation of America, October 22, 2002

Summarized by: Donna Hegstrom

We were honored to have Dr. Brendan Corcoran from the Royal (Dick) School of Veterinary Studies at Edinburgh, Scotland as our speaker for the Montgomery County Educational Seminar. Dr. Brendan presented the history, current research and treatment of Idiopathic Pulmonary Fibrosis, known in Westie circles as "Westie Lung Disease", to an enthusiastic audience of breeders, pet owners, and veterinary staff. Information from his presentation is provided for the IMPRINT and for the Health Section of the W.H.W.T.C.A. web page.

Idiopathic Pulmonary Fibrosis is best described by analyzing the vocabulary utilized to describe the disease. Idiopathic, meaning from an unknown cause, Pulmonary, meaning the lung, and Fibrosis, meaning the formation of scar tissue makes up the analysis. Thus, in layman's terms: Lung scarring of an unknown cause. Clinicians often described the symptoms as "Cracklin Lungs."

Initial case histories, reported by Dr. Corcoran and his associates in 1999 in the United Kingdom, suggested that a "specific clinical entity consistent with chronic lung fibrosis occurs in specific breeds of terrier dogs." Since little data was available to confirm the radiographic and clinical findings in the canine, the study described a case of chronic pulmonary fibrosis in a terrier dog, where histopathological confirmation was possible and suggested that the condition might be analogous to idiopathic pulmonary fibrosis in humans. Utilizing this premise, Dr. Corcoran described the Interstitial Lung Disease Categories in dogs and cats based on the lung disease categories in humans. These categories were:

  • Primary Lung Disease including: neoplasia respiratory infection hypersensitivity disorders
  • Toxins
  • Idiopathic Pulmonary Fibrosis

Dr. Corcoran emphasized, "despite the major accomplishments in the understanding of the pathogenesis of lung fibrosis, the diagnosis and management of pulmonary fibrosis continues to pose significant challenges." He also stated the following: "The importance of Pulmonary Fibrosis in the West Highland White Terrier depends upon age." This suggests that younger dogs respond in a more positive manner to treatment, reflecting autoimmune conditions correlated with age.

The clinical features of the disease as experienced in the UK included:

Age of Onset

  • Middle to old age
  • Medium age of diagnosis 9 yrs. (range 4.5 - 13 years of age)

The Development and Prognosis

  • Gradual onset
  • Progressive deterioration
  • Medium survival from clinical signs first being noted: 15.5 months (range 3-41months)
  • Medium survival from diagnosis: 7 months (range 3-41 months)

The Clinical signs of Idiopathic Pulmonary Fibrosis include the following:

  • Dyspnea (labored breathing) tachyphoea
  • Crackles heard in lungs upon examination
  • Exercise intolerance
  • Cough
  • Otherwise presents as "normal"

Differential Diagnosis Considerations:

  • Pulmonary edema (an abnormal accumulation of fluid) associated with congestive heart failure.
  • Chronic bronchitis
  • Other extensive lung diseases

Diagnosis of Idiopathic Pulmonary Fibrosis should include the following:

  • The characteristic clinical presentation
  • The breed association
  • The presence of Pulmonary crackles
  • Use of Diagnostic Tests
    1. Imaging
    2. Bronchoscopy and airway cytology
    3. Pathology
    4. Blood gas analysis, haematology, biochemistry profile

Improvement is need in CT scanning technology. Tomography (HRCT) is beneficial in identifying the stage of the disease, but is very expensive. As with human diagnosis of IPF, canine diagnosis is difficult to identify. There are diffuse and patchy changes and variable findings, which may not improve diagnosis and may not affect therapy considerations. Disagreement about the classification of IPF in humans still abounds, but the degree of functional and structural changes caused by the disease correlates with the survival rate in humans and canines. Therefore the therapy prescribed for humans and canines is extremely variable and can be addressed in these general categories:

Idiopathic Pulmonary Fibrosis Therapies:

  • Anti-inflammatory therapy
  • Glucocorticosteriods
  • Azathioprine, Cyclophosphamide
  • Additional therapy
  • Bronchodilators
    Antibacterial therapy
  • Colchicines

Dr. Corcoran indicated that although treatments continue to improve, "The response is variable, but usually poor, with inevitable progressive deterioration."

At this time, the research into the causes of Idiopathic Pulmonary Fibrosis is SPECULATIVE. Again, turning to human research, some speculations are that the disease may be attributable to one or several of the following:

  • Inflammatory reaction in the lungs
  • Fibrotic reaction (We need to know WHY the lung scars so easily)
  • Immune mediated
  • Exposure to Toxins

Regardless of the cause, somehow the lungs get injured and disease begins. The question then becomes, "Is this disease inherited"? What is known is that it is a breed-associated disease, which suggests a genetic pool. In humans, there is a familial form, where family clusters have been affected. What is known on the human side is that both children and adults are affected. There is likely to be an autosomal dominant trait with penetrance. This means that the genes for the disease may be present, but do not necessarily manifest themselves. In order to determine the genetic basis of Idiopathic Pulmonary Fibrosis in canines and humans, there must be an accurate phenotype by which the affected individuals are identified. The use of molecular genetics and Microarray Technology to recognize the genes that are switched on in this disease is currently in the research stage and will affect drug protocols and gene therapy for both humans and canines.

According to Dr. Corcoran and his team of researchers, the future treatment of Idiopathic Pulmonary Fibrosis will be determined by the following:

  • Improved Diagnostics including:
    1. Earlier Diagnosis
    2. High resolution CT scanning
    3. Lung biopsy
  • Improved Therapy
    1. Controlled drug studies for the disease
    2. Adopt ideas from human medicine
  • Epidemiology
    1. Determine the exact incidence and prevalence of the disease
    2. Conduct pedigree analysis to identify patterns of inheritance
  • Molecular genetics


Demodectic Mange

Demodectic mange is caused by a tiny mite, Demodex Canis, too small to be seen with the naked eye. Nearly all dogs acquire mange mites from their mothers during the first few days of life. These mites are considered normal skin fauna when present in small numbers. They produce disease only when an abnormal immune system allows their numbers to get out of control. This occurs primarily in puppies and in adult dogs with lowered immunity. A high incidence of mange in certain bloodlines suggests that some purebred dogs are born with an inherited immune susceptibility.

Demodectic mange occurs in a localized and generalized form. The diagnosis is made by taking multiple skin scrapings and looking for the mites.

Localized Demodectic Mange

This disease occurs in dogs under one year of age. The appearance of the skin is similar to that of ringworm. The principal sign is thinning of hair around the eyelids, the lips and the corners of the mouth, and occasionally on the legs and feet. The thinning progresses to patches of moth-eaten hair loss about one inch in diameter. In some cases, the skin becomes red, scaly and infected.

Localized mange usually heals spontaneously in six to eight weeks, but may wax and wane for several months. If more than five patches are present, the disease could be progressing to the generalized form. This occurs in approximately 10 percent of cases.

Treatment: A topical ointment containing either benzoylperoxide gel (OxyDex or Pyoben), or a mild topical preparation used to treat ear mites can be massaged into affected areas once daily. This may shorten the course of the disease. The medication should be rubbed with the lay of the hair to minimize further hair loss. Treatment may cause the area to look worse for the first two to three weeks. There is no evidence that treating localized mange prevents the disease from becoming generalized. The puppy should be checked again in four weeks.

Generalized Demodectic Mange

Dogs with the generalized disease develop patches of hair loss on the head, legs and trunk. These patches coalesce to form large areas of hair loss. The hair follicles become plugged with mites and skin scales. The skin breaks down to form sores, crusts and draining tracts, presenting a most disabling problem. Some cases are a continuation of localized mange; others develop spontaneously in older dogs.

When generalized DEMODECTIC mange develops in dogs under one year of age, there is a 30 to 50 percent change that the puppy will recover spontaneously. It is uncertain whether medical treatment accelerates this recovery.

In dogs older than a year of age, a spontaneous cure is unlikely but the outlook for improvement with medical treatment has improved dramatically over the past decade. Most dogs can be cured with intense therapy. Most of the remaining cases can be controlled if the owner is willing to commit the necessary time and expense.

Treatment: Generalized DEMODECTIC mange must be treated under close veterinary supervision. Therapy involves the use of medicated shampoos and dips to remove surface scales and kill mites. Shave or clip hair from all affected areas to facilitate access to the skin.

The FDA protocol involves first bathing the dog with a medicated benzoyl peroxide shampoo (OxyDex or Pyoben) to remove skin scales. Allow the shampoo to remain on the dog for 10 minutes before rinsing it off. Completely dry the dog.

Amitraz (Mitaban) currently is the only miticide approved by the FDA for use on dogs. Make up an Amitraz dip by adding Mitaban to two gallons of water, according to the directions. Be sure to treat in a well-ventilated area and wear rubber or plastic gloves to keep the chemical off your skin. Sponge on the dip over a 10-minute period, allowing the dog's feet to soak in the rinse. Allow the dip to dry on the dog. Repeat every two weeks, or as directed by your veterinarian. Try to keep the dog from getting his coat and feet wet between dips.

Continue this protocol for 60 days beyond the day when skin scrapings first became negative. Side effects of Mitaban include drowsiness, lethargy, vomiting, diarrhea, dizziness and a staggering gait. Puppies are more susceptible than adults are to these effects. Should such a reaction occur, immediately remove the miticide by thoroughly rinsing the coat and skin.

If the FDA protocol is not completely effective, your veterinarian may suggest an alternative treatment.

Secondary skin infections should be treated with antibiotics, based on culture and sensitivity tests. Corticosteroids, often used to control sever itching, lower the dog's immunity to the mites and should NOT be used to treat this disease.

Because of an inherited immune susceptibility, dogs that recover from DEMODECTIC mange should not be bred.

Ectopic Ureter

Epidermal Dysphasia

Enlarged Orbit

Fatty Liver Syndrome

Globoid Cell Leukodystrophy (Krabbe's Disease)



Inguinal Hernia

Keratoconjuncitivitis Sicca

Legg-Perthes Disease—Avascular aseptic necrosis of femoral head

Luxating Patella

malassezia dermatitis
malassezia dermatitis

Malassezia Dermatitis

Over the last several years, an alarming number of Westie owners have been seeking assistance for their Westies that are suffering from the troublesome condition of Malassezia dermatitis.

Despite countless visits to their veterinarian and an assortment of medications, their Westie's condition just gets worse and worse. As a result, the owner becomes more and more frustrated and, all too often, the Westie ends up being abandoned at the vet's office, relinquished to a shelter or rescue group, or euthanized.

Most often, the inquiry is a desperate plea similar to the following: "I own a Westie with severe skin allergies. We have been to the vet on numerous occasions and tried all sorts of medications, but nothing is working. My Westie is constantly itching and losing its hair. I feel so bad for him/her. Do you have any suggestions for what I can do to help him/her?"

Does this sound familiar? Is your Westie suffering from itching, hair loss, black oily skin and/or crusty skin, a musty/yeasty odor, and usually accompanied by an ear infection?

If your response is "yes," than it is quite possible that your Westie has Malassezia.

Yeast infections are especially itchy, crusty, and smelly. Often the Westie starts with a rash or a simple itching, and the skin may begin to thicken to an "elephant-like" skin appearance. The itch gets extreme, and the odor can become especially troublesome.

What is Malassezia?

Malassezia is the name of a type of yeast (fungus) that is found on both normal and abnormal canine skin and ears. On normal healthy skin, it causes no problems. To get a yeast infection, conditions on the skin surface have to change to favor the proliferation of the yeasts. Some conditions which could lead to a yeast proliferation include: high environmental humidy, an increase in skin oils (from an allergic flare up), an immune deficiency, flea and/or food allergies, or seborrhea (excessive oil production of the skin). Some Westies are actually allergic to the yeasts themselves.

There are a number of breeds predisposed genetically to yeast infections; unfortunately, the West Highland White Terrier is one of them.

How is a Malassezia infection diagnosed?

The most common way to diagnose Malassezia is with a positive identification of the organism under the microscope. Your veterinarian can take a microscope slide and press it onto the affected area, then the sticky, oily stuff that clings to the slide can be stained and examined for the organism. Other methods your vet may use include collecting the material with a cotton swab or scraping the skin and applying it to the slide. However, because Malassezia is a common resident of normal skin of dogs and cats, there may always be some doubt as to if it is the causative agent of the symptoms. Therefore, diagnosis is usually confirmed by response to treatment. (Please note: A Staph infection can have very similar symptoms as Malassezia...loss of hair, bad odor, etc. When your veterinarian takes the slide, if the yeast organism is found, it could be Malassezia; if a bacteria organism is found, it could be Staph. Treatment of Staph is very similar. Always consult with your veterinarian.)

It is important to note that before a primary diagnosis of Malassezia is rendered, other conditions should be ruled out. Allergies to contacted surfaces, reactions to medications, skin infections (like mange), and atopy (food allergy) may cause similar symptoms. The goal is to determine if Malassezia is the primary problem or is occurring secondary to another condition. In either case, the yeast infection must be cleared up.

It is also important to note that yeast infections are not contagious; however, they can recur if the underlying allergy, seborrhea, etc., is not controlled.

How are Malassezia infections treated?

Treatment can be oral, topical, or both. Topical treatment alone is not usually adequate, but since oral medications are expensive, often topical management alone is attempted first, especially if only a small body area is involved. (For localized treatment of very small areas, miconazole cream can be applied twice daily for several weeks.)

To provide an inhospitable environment for Malassezia, lipids on the skin need to be removed. There are specifically anti-yeast shampoos that we prefer, such as Malaseb (available from your vet or via mail order - the least expensive we've found is Valley Vet Supply at www.valleyvet.com), Nizoral (easily obtainable over-the-counter at any drug store and works well), and Micro-Tek Medicated Shampoo (a combination anti-bacterial, anti-fungal, and anti-microbial product also available through www.valleyvet.com).

The Westie must be bathed twice a week to start for several weeks. The shampoo should remain lathered on the skin for 10-15 minutes before rinsing. Occasionally, the Westie may become pruritic after topical treatment. This is not a reaction to the shampoo, but more likely it reflects the release of the toxin zymogen from the yeast cell wall as the organisms die. This reaction will resolve as the infection is eliminated. As the condition improves, the Westie should be bathed once a week for several more weeks or until the skin is clear. Leave on conditioners such as ResiCort and ResiChlor (available from your vet or via mail order - the least expensive we've found is at www.upco.com) have also proven to be of some benefit in some cases.

For dogs with more severe cases, or those cases which are resistant to topical treatment, oral ketoconazole (brand name: Nizoral) can be administered for several weeks (in addition to the baths). A response is generally seen within 1-2 weeks, but therapy needs to continue for an additional 3-6 weeks. Ketoconozale is very effective, but because of its potentially toxic side effects and expense, it should only be used under direct veterinary supervision.

Please note: Malassazia responds poorly to prednisone, and it should not be used as the main treatment. However, depending on the severity of any internal swelling the Westie may be experiencing, a cortisone shot and/or a short course of prednisone may be helpful in getting the Westie on the right road to recovery.

How Ketoconazole works

Ketoconazole works by interfering with the structure of the fungal cell wall. Depending on the fungus and depending on the dose used, ketoconazole may kill the fungus or just inhibit its ability to reproduce.

The most common side effects are nausea, vomiting, and diarrhea. These may be reduced by giving ketoconazole with food or by dividing the dose into several smaller doses (we normally use ½ or ¼ tablet twice a day - depending on the severity of the condition). If nausea is severe, it should resolve with discontinuation of the medication.

It is best to avoid using ketoconazole in patients with pre-existing liver disease or with decreased platelet (blood clotting cell) levels. When ketoconozale therapy will continue for months at a time, many veterinarians will monitor liver enzymes and complete blood counts. (Contraindications: Imadazole antifungal drugs have been associated with life-threatening cardiac arrhythmias in man when administered concomitantly with certain antihistamines. Accordingly, we prefer to avoid using any antihistimines while the ketoconozale is being given.)

Note: Ketoconozale is an expensive "human" medication and, while some vets stock it, sometimes it must be obtained from your neighborhood or online mail order pharmacy. The least expensive place we have found it to date is via mail order from Costco (www.costco.com) or Mexico.


Veterinarian Information Network, Inc. (www.vin.com)
Drs. Foster & Smith, Inc. (www.peteducation.com)
VetCentric (www.vetcentric.com)
Animal Dermatology Specialty Clinic (www.skinvet.com)
University of Prince Edward, Canine Inherited Disorders Database (www.upei.ca~cidd)
Singapore Veterinary Association (www.sva.org.sg)
The Westie Foundation of America, Inc. Newsletter


Pulmonary Fibrosis

Contributed By: Dorinda Dew

What is Pulmonary Fibrosis?

Very little is known at this time about Pulmonary Fibrosis. It is mostly seen in Westies, although Scotties and Cairns do develop it. Idiopathic Pulmonary Fibrosis, also known as Westie Lung Disease, is a scarring and fibrosing of the alveoli and interstitium (air sacs and connective tissue) of the lungs. The scarring may be the result of chronic inflammation of the alveoli, and can replace much of the normal structure of the lungs. It is suspected that this disease is similar to the same disease in people.

What causes it?

At this writing, we do not know, because research has yet to be done. Some veterinary researchers feel that there may be a link between Pulmonary Fibrosis, the immune systems and allergies. Most researchers agree that Westies are predisposed to Pulmonary Fibrosis, relative to other dog breeds.

What are the symptoms?

Symptoms may be caused by other factors or diseases, so caution should be exercised when diagnosing Pulmonary Fibrosis in the Westie. In a recent talk, Dr. Elizabeth Rozanski DVM from Tufts Veterinary School reported a number of signs to look for in diagnosing Pulmonary Fibrosis. They included the following, although not all symptoms need be present:

  • Rapid Shallow Breathing Pattern or Labored Breathing
  • Loss of Exercise Tolerance
  • Build up of Scar Tissue in the Lungs
  • Crackles in the Lungs
  • Dry Cough

These dogs can also develop pulmonary hypertension or can have an enlargement of the heart, due to breathing patterns.

How is it diagnosed?

Diseases of the interstitium of the lungs are difficult to identify because they usually require a lung biopsy for correct diagnosis. Lung biopsy is not simple in normal patients, and may be quite risky in affected dogs. Furthermore, many different lung diseases exist, and differentiation is difficult. Not enough samples have been taken, and pathologists vary in expertise in reading these samples. Radiographic changes in the lungs can be seen in X-rays, and the blood gases are abnormal, showing hypoxia, or lack of oxygen to the tissues. Tests that will easily diagnose Pulmonary Fibrosis and indicate the prognosis are needed. A specialized machine exists that can effectively screen people for the similar disease, and it is presently being tested on a control group of Westies.

What is the treatment?

Very few treatment options exist at this time. Once scarring occurs, there is little that can be done. Preventing respiratory tract infections, limiting exercise, and planned weight loss for overweight patients are all important. Drugs such as bronchial dilators (theophylline and terbutaline) may strengthen the respiratory muscles, but tend to lose effectiveness with time. Some dogs may benefit from controlled use of steroids, such as Prednisone and Interferon. Experimental usage of inhaled steroids has been tried in some cases. Cough suppressants can be helpful.

What is the prognosis?

The prognosis for affected dogs is very poor. Lung disease appears to affect older Westies, with the average age of onset being about nine years of age. Patients live 17-24 months after diagnosis, although some live less and some live longer. Our very limited data shows the average survival time after diagnosis to be about eighteen months, although some dogs have survived for more than three years. Very recently an international study group has been formed among veterinary respiratory specialists, which should help to speed research.

Is the Westie prone to Lung Disease?

We honestly do not know. It appears to be breed-specific, which could indicate a genetic basis. Pedigree studies have shown that some affected individuals have been related, but so little data has been collected for the general population that these observations should not be taken as proof that Pulmonary Fibrosis is inherited.

What can Westie owners do?

Owners of affected dogs can contribute significantly to the data collection and research programs. Make your veterinarian aware of the research being done. Monitor your own dogs for signs of respiratory disease. The earlier a diagnosis is made, the more likely treatment may be beneficial.

The Westie Foundation of America has funded research and is working with several institutions to develop future research. Information and tissue samples cannot be handled at this time but we hope to be able to at a later date. (6/02)

Pyruvate Kinase (PK) Deficiency


Pyruvate Kinase deficiency (synonym: erythrocyte pyruvate kinase deficiency) in red blood cells (erythrocytes) causes a severe hemolytic (red cell rupture) anemia as a result of the premature destruction of PK deficient red blood cells. PK is a key regulatory enzyme in a metabolic pathway that generates almost all energy from glucose (sugar) in red blood cells. The clinical signs of anemia are very pale mucous membranes (gums), increased heart rate and pounding pulses, weakness and exercise intolerance. The liver and spleen may be enlarged, and after one year of age, the density of all bones, particularly long bones and skull, appear radiographically increased. Affected dogs that are well confined may not show any obvious signs, but may acutely decompensate and die when severely exercised or stressed.

Age of Onset:

The disease is most often recognized between 4 months and 1 year of age, but may not be detected until later in life, if a dog is not very active. Affected dogs develop relatively mild clinical signs during the first year of life, despite severe anemia.


After excluding the more common causes of hemolytic anemia (autoimmune, toxic and infectious hemolytic anemia), PK deficiency should be considered. A chronic, severe, highly regenerative hemolytic anemia (PCV 15 - 27%) associated with increased radiographic bone density in older animals is highly suggestive of PK deficiency. PK deficiency is diagnosed through DNA analysis. A simple determination of PK activity does not provide a diagnosis of an affected dog, but does allow the detection of carriers. Blood samples must be specially handled and arrangements must be made prior to submitting the sample to a specialized laboratory.


There is no simple treatment. Splenectomy and glucorticosteroid therapy are not helpful. Iron chelation may be considered when large iron deposition occurs in tissues. Experimentally, bone marrow transplantation has been shown to cure the disease. Affected dogs usually die at a young age (1 - 4 years) because of progressive anemia or hepatic (liver) failure.

Mode of Inheritance:

The disease is inherited as an autosomal recessive trait. Carriers can be detected by measuring PK activity in erythrocytes. Carriers have half-normal PK activity in erythrocytes and are asymptomatic.

The disease occurs in West Highland White and Cairn Terriers, Basenjis, and Beagles.

Seborrhea, primary


Tapeworms can conjure up many images and thoughts of a ghastly infestation. However, in comparison to other intestinal worms it is probably the parasite with the least direct health problems. Although they compete with the infected pet for the nutrients of ingested food, they do not generally harm the host. Tapeworms, which include several types, reside in the intestines of dogs, cats, horses and others animals. They consist of a head and a long flat body made up of segments. This body can be several feet, if not more, long. Segments, each having the ability to reproduce, are passed in the animal's feces, leaving the head still attached to the animal's intestinal lining, where it produces new segments. One of the worst case scenarios is that if left untreated it may become so long that it obstructs the intestines.

Tapeworms can be detected by the human eye in your dog's stool. The segments appear as white 'grains of rice' like objects. If unseen or if a heavy flea infestation has occurred on the animal, a stool check is recommended. Once a year stool sample checks are a good health routine preventative.

Vet treatment is to administer either a one time shot or medication (pills) if the sample is positive for tapeworms. Re-infestation can occur when infected fleas are ingested by the animal.

White Shakers Syndrome

Contributed by: Christine Swingle, Bonniebriar Westies, CT


This syndrome is a unique generalized tremor that occurs in young, predominately small dogs. Because this syndrome was initially seen in larger numbers of dogs with white coats, the name White Shaker Dog Syndrome has also been used to describe it.

Dogs with WSS have a fine tremor of the entire body. Young dogs (9 months to 3 years old) of either sex are most frequently affected. The tremor is usually persistent throughout the day and will worsen with handling, excitement or stress. The magnitude of the tremor may increase or remain persistent without therapy. Other clinical signs associated with a neurological system abnormality, such as head tilts, limb weakness and seizures are occasionally seen.

The disease is most often associated with a mild central nervous system inflammation (nonsuppurative encephalomyelitis). This inflammation commonly affects the cerebellum, and dysfunction of this part of the brain may be one of the initiators of the tremor. Some veterinarians hypothesize that the cause might be from an underlying virus, but there has been no research to support that theory and no definitive infectious cause has been found for this inflammation. Also, it is not known if the inflammation is the true cause of the tremor or if there is some other associated neurotransmitter abnormality that results in abnormal firing of nerves.


Generally made with clinical descriptions and symptoms. Blood cytology, chemistry and x-rays, as well as a physical exam, are usually normal and have not proven valuable to aid in a diagnosis. The disease is rarely fatal.


WSS is characterized by a sudden onset of constant tremors all over the body, including the head and eyeballs. Chaotic random eye movement is called opsoclonus. Rapid, involuntary, rhythmic eye movements, often indicative of central nervous system dysfunction is called nystagmus. The tremors are exaggerated by handling, forced locomotion, excitement and high levels of stress. It decreases but may not completely disappear with total relaxation. Putting the dog in a crate in a minimally darkened room, where there is quiet, has helped reduce the tremors during times of stress. The dogs are alert and responsive and have no deficiency in cranial nerve function. The tremors may be severe enough to cause an ataxic gait, but strength remains normal. On occasion, one of these dogs convulses. At the onset of the syndrome, and usually for a short period of time, the animal may refuse to eat. Therefore, great care and TLC must be given to encourage eating and drinking, or, this must be done by hand. Eventually, they return to eating and drinking on their own. Some dogs benefit by elevating their food and water bowls off the ground, so the dog does not have to lower its head as much.


No specific therapy exists but supportive therapy includes reducing the tremors with diazepam (Valium) and anti-inflammatory drugs (corticosteroids). It has been suggested that neither alone is rapidly and consistently effective. The use of both types of drug simultaneously has been more effective and reliable, according to Dr. Alan Parker's experience. Early diagnosis is beneficial when beginning treatment, as many dogs will respond in a few days to immunosuppressive levels of corticosteroids. Some dogs may have to be maintained on low levels of these drugs for a number of months, but there are some dogs that never require them. When giving steroids, it is very important not to decrease the corticosteroid dose too quickly.

According to Dr. Parker, if treated, the duration of therapy is critical; premature cessation of therapy usually leads to a relapse. Simultaneous use of oral prednisolone (1-2[rarely 4] mg./kg, Q24h for four weeks, then ½-1 mg/kg, Q24h for two weeks, then ½-1 mg/kg Q48h for two weeks, and then ½-1 mg/kg Q72h for four weeks) with oral diazepam (1/2-1 mg/kg, Q8h for four weeks, then ½-1 mg/kg, Q12h for four weeks and then ½-1 mg/kg, Q24h for four weeks) is preferable. Clinical signs usually decrease during the second day and the dogs are usually 80 percent normal by the fifth day. Vaccinations are not recommended for WSS dogs as relapses could occur within a month of vaccination.

Personal Experience:

I had a WSS Westie (diagnosed at age 3) that got worse when given the drugs. I felt as if I was going to have to put Cody down but I persisted. He did not eat or drink unless I put it directly into his mouth. It was approximately two and a half weeks from the start of the symptoms, through diagnosis, when Cody began to eat and drink on his own. Today, when things get stressed, Cody is isolated in a quiet and peaceful room for about 15 minutes to one half-hour. I have also found that a homeopathic remedy called Calming Essence or Rescue Remedy (Back Flower Remedies Ltd., and available in health food stores) helps him greatly during times of excitement and stress. There might come that moment when you think the only answer is euthanasia. DON'T GIVE UP. If I had, my Cody would not be here today, and at age 10 he is going strong.


Dr. Alan J. Parker, MRCVS, PhD, Diplomat ACVIM (Neurology)
Chief of Staff, Small Animal Hospital
Dept. of Veterinary Clinical Medicine
College of Veterinary Medicine
University of Illinois
1008 West Hazelwood Drive
Urbana, IL 61801
Phone: 217-333-5311

Alexander deLahunta, DVM, PhD
College of Veterinary Medicine
Cornell University
Ithaca, New York 14853-6401
Phone: 607-253-3547

Rodney S. Bagley, DVM

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