FOXY DOXYS

Related terms: colour mutant alopecia, blue or fawn Doberman syndrome, fawn Irish setter syndrome, blue dog disease

What is colour dilution alopecia?

This condition develops in some, but not all dogs that have been bred for unusual coat colour, especially "fawn" (a dilution of a  normally red or brown coat) or "blue" ( a dilution of the normal black and tan coat colour). Alopecia means hairlessness - affected dogs have a poor, patchy haircoat progressing to widespread permanent hair loss. At the cellular level, there are abnormalities of the hair follicles and uneven clumping of pigment (melanin) granules in the hair shafts in affected areas

How is colour dilution alopecia inherited?

The inheritance is unclear. The condition is thought to be due to the interaction of different factors at the gene position for colour. It is not simply determined by the genes at that locus, because not all dogs with colour dilution develop coat problems.

What breeds are affected by colour dilution alopecia?

This condition is seen most commonly in Doberman pinschers with unusual coat colours (as many as 90% of blue Dobermans and 75% of fawns). The condition also occurs but is less common in other breeds bred for unusual coat colours: Bernese mountain dog, chihuahua (blue), chow chow (blue), dachshund (blue), Great Dane (blue), Irish setter (fawn), miniature pinscher (blue), saluki, schipperke (blue), Shetland sheepdog (blue), standard poodle (blue), whippet (blue), Yorkshire terrier (grey-blue).

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 colour dilution alopecia mean to your dog & you?

Dogs with this condition are born with a normal haircoat. Those with lighter blue or fawn hair coats usually start to show changes by 6 months while in dogs with darker steel blue coats, the changes may not be evident until 2 or 3 years of age. Your dog will experience hair loss and dry skin. Sometimes the earliest sign is a recurring bacterial infection (folliculitis), generally on the back, where you will see small bumps which are infected hair follicles. This clears up temporarily with antibiotics, but the affected area is very slow to regrow hair, or remains hairless.

Hair loss is usually first apparent on the back and by 2 or 3 years has spread over all the light coloured areas of the body. The exposed skin is often scaly and is susceptible to sunburn or extreme cold. Your dog's health is not otherwise affected by this condition.

How is colour dilution alopecia diagnosed?

Your veterinarian may suspect this disorder if your dog has typical haircoat changes and is an unusual colour for the breed. The diagnosis is confirmed through microscopic examination of plucked hairs or a skin biopsy. The latter is a simple procedure, done with local anesthetic, in which your veterinarian removes a small sample of your dog's skin for examination by a veterinary pathologist. The biopsy will show changes characteristic of this condition.

For the veterinarian: Careful microscopic examination of plucked hairs will show large clumps of melanin distributed unevenly along the hair shaft.

In young dogs, demodicosis or other inherited hair defects should be considered while in dogs with a later onset (2 to 3 years of age), endocrine disorders (particularly hypothyroidism) should be ruled out.

How is colour dilution alopecia treated?

Your dog can lead a normal healthy life with periodic symptomatic treatment as needed - moisturizing rinses for dry scaly skin or antibiotics for bacterial infections.

Since early hair loss occurs due to breakage, you may be able to slow the rate of loss by avoiding harsh shampoos and vigorous grooming.

For the veterinarian: There have been some early reports of hair regrowth using etretinate treatment . (See resource below.)

Breeding advice

Affected dogs, their parents and siblings should not be used for breeding. The condition can be entirely avoided by the use of non-colour-diluted dogs in breeding programmes.

FOR MORE INFORMATION ABOUT THIS DISORDER, PLEASE SEE YOUR VETERINARIAN.

Resources

Scott, D.W., Miller, W.H., Griffin, C.E. 1995. Muller and Kirk's Small Animal Dermatology. p. 777.  W.B. Saunders Co., Toronto.

Power, H.T., Ihrke, P.J. 1995. The use of synthetic retinoids in veterinary medicine. In S.J. Ettinger and E.C. Feldman (eds.) Textbook of Veterinary Internal Medicine. p 585-590. W.B. Saunders Co., Toronto.

Copyright © 1998 Canine Inherited Disorders Database. All rights reserved.
Revised: February 02, 2004.

This database is funded jointly by the Sir James Dunn Animal Welfare Centre at the Atlantic Veterinary College, University of Prince Edward Island, and the Canadian Veterinary Medical Association.

PLEASE SEE MY ARTICLE  "COAT CARE FOR DOGS WITH CDA - COLOR DILUTION ALOPECIA-AND FOR ROUTINE COAT CARE OF THE DILUTE COLORS".

The purpose of the cardiovascular system (heart and blood vessels) is to provide the cells of the body with oxygen, nutrition, and essential fluids. It also helps these same cells rid themselves of waste products, and distributes hormones and enzymes to allow for normal physiologic processes. It is even a big part of temperature regulation. all of this is no small feat when you consider the fact that the cardiovascular system must supply these needs to a body that contains billions of individual cells.

The whole point of the cardiovascular system is to provide the individual cells in each organ an adequate flow of blood (called perfusion) that gives them the nutrients and oxygen they need. When these cells have what they need they can perform their normal function. So for the kidneys, that means they can filter out waste products. For the muscles, that means they can initiate movement. For the liver, that means that liver cells can metabolize drugs we put into the body. This adequate perfusion equates back to how much fluid the heart can deliver to these cells. an adequate cardiac output is needed for this perfusion.

There is a difference between heart disease and heart failure. In heart disease the heart has some type of abnormality. If minor enough, the heart is able to deliver adequate perfusion to the cells, and there is no problem. In heart failure, the heart does not maintain an adequate perfusion for normal cell function. Pets that are relatively inactive may be able to stave off the effects of heart failure longer than active pets because they do not challenge the cardiovascular system. This has a bad side though, because by the time the symptoms of heart failure are finally apparent to an owner, the disease is well entrenched and more difficult to treat.

If the left heart becomes diseased it does not pump an adequate amount of blood (decreased cardiac output) through the aorta for distribution to the cells of the body. This inadequate flow of blood ((poor perfusion) prevents these cells from performing their normal functions The brain monitors this perfusion, and goes into action by regulating hormones and sodium in conjunction with the kidneys and the lungs. This increases the pressure in the arterial system as a whole, and satisfies the needs of the cells temporarily by supplying them with a greater flow of blood (better perfusion). This added blood pressure fills the diseased left ventricle with blood more than usual (increased preload), causing it to dilate and weaken further. It also increases the pressure the left ventricle has to pump against (increased afterload) to get the blood through the aorta and into the cells. These add further work to an already diseased heart, compounding the problem even further. Eventually, the blood presented to the left ventricle does not get pumped out effectively, which causes a back flow (added pressure) in the lungs. When the pressure reaches a certain point the fluid in the blood vessels in the lungs leaks out, causing pulmonary edema. This is congestive heart failure (CHF).

If the right heart becomes diseased, a similar set of physiologic sequences occurs. The higher blood pressure that results when the cells send their emergency signals to the brain results in a greater amount of blood being presented to the right heart (increased preload). Eventually, the weakened right heart cannot pump blood into the lungs faster than the venous system is presenting blood to it. This causes back pressure to build up in the venous system, especially the vena cava and other veins in the abdomen and even thorax. When the pressure gets high enough in these veins fluid leaks out, leading to ascites and pulmonary effusion. This problem can occur in both hearts at the same time, causing even more problems.

There are several factor, usually working in combination, that lead to cardiac disease:

They can buildup on the heart valves inhibiting their ability to flow blood in the proper direction through the heart.

They can directly affect the heart muscle (myocardium), causing cardiomyopathy. In the early years of parvo virus there was a form of the disease that attacked the myocardium and caused rapid death.

Taurine, an essential amino acid in cats, can lead to dilated cardiomyopathy. Humans and dogs can produce taurine naturally (non-essential) and do not need it in their diet. A deficiency of taurine in the cat will also cause degeneration of the retina. Taurine was not included in adequate amounts in cat food many years ago. This problem has been corrected in almost all commercial cat foods, so we rarely see this problem anymore.

An inadequate amount of the thyroid hormone thyroxin can predispose a dog to heart disease. This problem is diagnosed with a blood sample and corrected with thyroxin hormone replacement. This problem is almost exclusively seen in dogs.

This cat problem occurs when the thyroid gland has a tumor and secretes excess thyroid hormone (thyroxin). You can learn about it in detail in our hyperthyroidism page. In this disease the heart is racing as it tries to keep up with the increased metabolic rate of the organs as they respond to the increased thyroid hormone.

Congenital abnormalities of the heart valves, usually a problem in young dogs, can lead to significant heart disease. These can include any of the valves. We get an indication of this early in a pets life by the presence of a heart murmur. Young animals can have what are called "innocent murmurs". These are heart murmurs that don't cause any problems and eventually resolve. If these murmurs persist, are of high intensity, or the pet is ill, they should be pursued further with diagnostic tests.

Older dogs get a problem with heart valves that also can be significant. We will go into this in more detail soon because it is the most common cause of heart disease in the dog.

Some drugs are toxic to the heart. It is ironic that one of the drugs used to treat heart disease, called digitalis, can be toxic to the heart also. This drug is commonly used to help slow down a racing heart. When used, we monitor digitalis levels with a blood sample at least every l6 months to make sure it does not go into the toxic range.

A heart that receives a severe blow can have problems with adequate pumping of blood or the normal electrical beating.

The heartworm parasite (dirofilaria immitis) can cause severe heart disease. This problem is not uncommon in dogs, and has been diagnosed with increasing frequency in cats lately.

Problems with hypertension in the lungs can cause the right heart to fail. These problems can include cancer, heartworms, infections, trauma, toxins, hypothyroidism, and Cushing's disease.

When vital internal organs like the kidney and liver are diseased there can be many changes that effect the heart. These include electrolyte abnormalities, calcium irregularities, and waste product buildup.

Some poisons selectively target the heart. Curare, the drug used in the tips of poison arrows and darts, is one of these drugs.

Typical symptoms of cardiac disease include:

These symptoms are found in many other diseases also, especially of the respiratory tract. To determine which disease is causing these symptoms we need to strictly adhere to the diagnostic process.

In some heart diseases, notably cardiomyopathy in cats, there might be no symptoms prior to a sudden death. These cats seem fine until a stress causes their diseased yet compensating heart to reach its limit.

Excerpts from: Long Beach Animal Hospital's web site

Luxating Patella
Race Foster, DVM
Marty Smith, DVM
Drs. Foster & Smith, Inc.

A dog from one of the smaller breeds runs across the yard chasing a tossed ball. In mid-stride, he yelps in pain and pulls his left hind leg off of the ground. After a second, he continues limping on in a three-legged fashion. After ten minutes, the rear leg drops back down to the ground and he uses it normally. This episode occurs maybe once a week. It never really seems to bother him that much – a yelp of pain, a short period of lameness, and in a few minutes he is back to his old self. Typically, he is a small or toy breed such as a Lhasa Apso, Pekingese, Pomeranian, Poodle, or Boston Bull.
A luxating patella may affect some animals much more severely. They may hold the leg up for several days and show considerable discomfort. Dogs who have a luxating patella on both hind legs may change their entire posture, by dropping their hindquarters and holding the rear legs farther out from the body as they walk. Those most severely affected may not even use their rear legs, walking by balancing themselves on their front legs like a circus act, or holding their hindquarters completely off the ground.

Normal knee anatomy

The patella is the bone we know as the knee cap. A groove in the end of the femur allows the patella to glide up and down when the knee joint is bent back and forth. In doing so, the patella guides the action of the quadriceps muscle in the lower leg. The patella also protects the knee joint.

Looking at the lower front portion of the femur (the thigh bone) in a normal dog, you will notice two bony ridges that form a fairly deep groove in which the patella is supposed to slide up and down. These structures limit the patella’s movement to one restricted place, and in doing so, control the activity of the quadriceps muscle.

The entire system is constantly lubricated by joint fluid. It works so that there is total freedom of motion between the structures.

What occurs when the patella is luxated?

In some dogs, because of malformation or trauma, the ridges forming the patellar groove are not prominent, and a too-shallow groove is created. In a dog with shallow grooves, the patella will luxate (jump out of the groove) sideways, especially toward the inside. This causes the leg to 'lock up' with the foot held off the ground.

When the patella luxates from the groove of the femur, it usually cannot return to its normal position until the quadriceps muscle relaxes and increases in length. This explains why the affected dog may be forced to hold his leg up for a few minutes or so after the initial incident. While the muscles are contracted and the patella is luxated from its correct position, the joint is held in the flexed or bent position. The yelp is from the pain caused by the knee cap sliding across the bony ridges of the femur. Once out of position, the animal feels no discomfort and continues his activity.

Which dogs are at risk of having a luxated patella?

Smaller breeds of dogs, especially Miniature and Toy Poodles, have the highest incidence of patella luxation. Genetics can play a role.

In certain breeds that have extremely short legs such as the Basset Hound or Dachshund, patellar luxation is thought to be secondary to the abnormal shape of the femur and tibia. The curvatures of the bones in these breeds work in conjunction with the forces of the quadriceps muscles to displace the patella to the inside. Please do not misunderstand – not all members of these breeds are affected with patellar luxation, only a small portion.

What are the symptoms?

Most dogs are middle-aged, with a history of intermittent (on-again-off-again) lameness in the affected rear leg(s). An affected dog commonly stops and cries out in pain as he is running. The affected leg will be extended rearward, and for a while, the dog is unable to flex it back into the normal position.

What are the risks?

Uncorrected, the patellar ridges will wear, the groove will become even shallower and the dog will become progressively more lame. Arthritis will prematurely affect the joint, causing a permanently swollen knee with poor mobility. Therefore, a good evaluation needs to be done by your veterinarian early in the condition to prevent long-term arthritic crippling.

Treatment for luxating patellas

As would be expected, medical therapy has little corrective ability in this disorder and surgery is therefore required and is the treatment of choice. A surgical treatment is not necessary in every individual with this condition.

Surgery can alter both the affected structures and the movement of the patella. The groove at the base of the femur may be surgically deepened to better contain the knee cap. The knee cap itself may be 'tied down' laterally (on the outside) to prevent it from deviating medially (toward the inside). The bony protuberance at the site of the attachment of the quadriceps tendon on the tibia, may be cut off and then re-attached in a more lateral position. All of these procedures work well and the type performed depends on the individual case and the clinician. The animal should respond quickly after surgery and is usually completely recovered within thirty days, using his legs in normal fashion.

Breeding considerations

Because of the strong genetic relationships, we really feel that animals with this disorder should not be used for breeding. They can still be excellent pets - and those that do require surgery will usually lead perfectly normal lives without any restrictions on activity.



From: PetEducationcom

CATARACTS

What are 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 discoloration 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.

Breeding Advice

It is prudent to assume cataracts are inherited unless another specific cause can be identified. Since some cataracts cause no clinical signs, it is worthwhile to screen dogs of affected breeds annually that are used in breeding programmes. Where cataracts are identified, affected animals, their parents and littermates should not be used for breeding.

The fact that the age of onset is fairly specific for different breeds is helpful in making decisions about breeding programmes.

FOR MORE INFORMATION ABOUT THIS DISORDER, PLEASE SEE YOUR VETERINARIAN.

Where to find more information?

American College of Veterinary Ophthalmologists. 1996. Ocular Disorders Presumed to be Inherited in Purebred Dogs. Purdue University, W. Lafayette, Indiana.

Copyright © 1998 Canine Inherited Disorders Database. All rights reserved.

Revised: December 29, 2004.

 

GLAUCOMA

What is glaucoma?

Glaucoma is a leading cause of blindness in dogs. It is the result of increased fluid pressure within the eye (elevated intraocular pressure or IOP).  If the pressure can not be reduced, there will be permanent damage to the retina and optic nerve resulting in visual impairment. Complete blindness can occur within 24 hours if the IOP is extremely elevated or can occur slowly over weeks or months if the the elevation is mild. Glaucoma is usually very painful.

Glaucoma may be primary (inherited) or secondary to a number of eye disorders including luxation of the lens, tumours of the eye, and uveitis (inflammation of the eye).

Primary/inherited glaucoma causes an elevation of pressure within the eye because of abnormal drainage of fluid through the iridocorneal angle. When the angle at which the iris and cornea join is wide, the glaucoma is classified as open angle. If the base of the iris is pushed forward, the glaucoma is described as narrow angle. 

Goniodysgenesis is characterized by an abnormal sheet of tissue in the angle where drainage normally occurs. This may or may not cause an elevation in IOP and glaucoma.

In pigmentary glaucoma, the obstruction to fluid drainage is caused by an abundance of pigmented cells within the iridocorneal angle and sclera. The increase in IOP is progressive and often results in blindness.

How is glaucoma inherited?

Inherited open angle glaucoma is an autosomal recessive trait in beagles. Narrow angle glaucoma is inherited as an autosomal dominant trait in the Welsh springer spaniel. The mode of inheritance for glaucoma in other breeds has not been identified.

What breeds are affected by glaucoma?

Narrow angle glaucoma is much more common than open angle glaucoma. Both types occur in mixed breed dogs as well as purebreds.

open angle glaucoma: beagle, American cocker spaniel, basset hound, Boston terrier, miniature Schnauzer, Norwegian elkhound

narrow/closed angle glaucoma: Alaskan malamute, American and English cocker spaniel, basset hound, chow chow, dalmatian, Great Dane, wire and smooth fox terrier, toy, miniature, and standard poodle, samoyed, Siberian husky, Welsh springer spaniel

goniodysgenesis: basset hound, Bouvier des Flandres, American and English cocker spaniel, This is also seen in the chihuahua, Dandie Dinmont terrier, Norwegian elkhound, toy and miniature poodle, Siberian husky, wire hair fox terrier.

pigmentary glaucoma: Cairn 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 glaucoma mean to your dog & you?

Primary open angle glaucoma develops slowly over weeks to months. With closed angle glaucoma, which is much more common, there is usually a sudden, rapid elevation in the pressure within the eye. This affects all the structures in the eye. The effects on the optic nerve and retina cause loss of vision.

Glaucoma is moderately to extremely painful. The eye may be red and your dog may paw at it, or rub his or her head along the carpet. The eye may look cloudy due to swelling of the cornea and your dog will be very sensitive to light.  The affected eye may seem larger, or appear to bulge out, relative to the other eye. Other more general signs of pain include loss of appetite and depression.

Glaucoma is an emergency. Treatment must be started as soon as possible if your dog's sight is to be saved. Irreversible damage to the retina and optic nerve occur within a few hours of significant elevation of the intraocular pressure.

How is glaucoma diagnosed?

Glaucoma is one of the conditions your veterinarian will suspect if your dog has a painful eye. It is diagnosed by measuring the intraocular pressure with a tonometer. This can usually be done with  local anaesthetic drops placed in your dog's eye. To determine the type of glaucoma, gonioscopy is used to measure the iridocorneal angle.

FOR THE VETERINARIAN: Because of the potential for elevated IOP to quickly cause irreversible damage to the visual structures of the eye, the timely diagnosis of glaucoma is very important. IOP should be measured in all red eyes for which the cause is not immediately obvious, and in eyes with unexplained pupillary abnormalities, corneal edema, or visual impairment, particularly if these signs occur in a dog that is of a breed with a predisposition to glaucoma.  (See references below for a good discussion of accurate IOP measurement, as well as therapy).

Although the normal range of  IOP varies (based on tonometer and other factors), generally a measurement of >25 mm Hg indicates glaucoma. An IOP of 50 mm Hg or more can lead to permanent optic nerve and retinal damage within hours if not relieved.

How is glaucoma treated?

Preserving vision in an eye with glaucoma is difficult and requires aggressive medical and surgical therapy. Your veterinarian may choose to provide initial emergency medical therapy and refer you immediately to a larger veterinary centre.

Treatment depends on several factors - the type of glaucoma present, the degree of elevation of IOP, and the extent of visual impairment. Primary open angle glaucoma tends to be slower in onset and may, at least initially, be controlled by medical therapy (drugs) alone. With closed angle glaucoma, which is much more common, there is usually a sudden, rapid elevation in IOP. Ultimately, most forms of glaucoma require surgery.

If vision is present or has just recently been lost, a combination of medical and surgical therapy will be used to try and maintain your dog's sight . Aggressive medical therapy (meaning a combination of anti-glaucoma drugs administered frequently and monitored closely) is used to reduce IOP prior to surgery to prevent further damage to the eye. Some of these drugs will be used as well for additional minor IOP reductions following surgery. The aim of surgery in an eye that is still visual (or potentially visual) is to decrease the production of fluid within the eye, and to improve the drainage from the eye. There are a few different methods that a veterinary ophthalmologist can use to achieve this.

If the eye is irretrievably blind, glaucoma can be treated by removing the globe of the eye (enucleation). This will eliminate the pain for your dog. There are also procedures that can be done that preserve the globe such as placing a prosthesis.

Inherited glaucoma usually occurs in both eyes eventually. Your veterinarian will monitor the pressure in the other eye regularly, and discuss with you recognition of early signs of glaucoma. He or she  may also recommend preventive medication for the unaffected eye.

Breeding Advice

Animals of predisposed breeds should be screened for glaucoma before being used for breeding. Affected dogs and their close relatives should not be bred. Unfortunately, glaucoma does not generally become apparent until after breeding age has been reached, usually 3 years of age or greater.

FOR MORE INFORMATION ABOUT THIS DISORDER, PLEASE SEE YOUR VETERINARIAN.

Where to find more information?

Both have good information on diagnosis and therapy, including prophylactic therapy for high risk eyes.

Miller, P.E. 1995. Glaucoma. In J.D. Bonagura and R.W. Kirk (eds.). Kirk's  Current Veterinary Therapy XII Small Animal Practice, p. 1265-1272.  W.B. Saunders Co., Philadelphia

Slatter, D. 1990. Fundamentals of Veterinary Ophthalmology. W. B. Saunders Co., Philadelphia

Copyright © 1998 Canine Inherited Disorders Database. All rights reserved.
Revised: March 28, 2002.

 

PRA (PROGRESSIVE RETINAL ATROPHY)

What is progressive retinal atrophy?

The cells of the retina receive light stimuli from the external environment and transmit the information to the brain where it is interpreted to become vision. In progressive retinal atrophy (PRA), deterioration of the retinal cells causes blindness.

The retina lines the back of the eye. The inner layer is the neural retina (called simply the retina) which has 9 layers, the outermost of which consists of the photoreceptor cells - the rods and cones. The outer layer of the retina is the retinal pigmented epithelium (RPE). In dogs the retina is not mature until 6 or 7 weeks of age.

The term progressive retinal atrophy covers several types of inherited degeneration (deterioration) of the retina. Sub-classifications of PRA are based on the age at which dogs show signs of the disease and the type of retinal cell which is affected.

Generalized PRA:These diseases affect primarily the photoreceptor cells. Both eyes are similarly affected and dogs eventually become totally blind.

i) Early onset photoreceptor dysplasia:  In these conditions, the photoreceptor cells develop abnormally in the first few weeks after birth, and then degenerate along with the inner layers of the retina.

ii) Later onset photoreceptor degeneration (progressive rod-cone degeneration): Here the retina matures  and functions apparently normally for varying periods of time before degenerating. Dogs are not usually clinically affected until 1 year of age or more, although abnormalities can be seen in the eye and on the electroretinogram (ERG) long before owners notice signs of visually impairment.

Progressive rod-cone degeneration has similarities to retinitis pigmentosa in people.

Central PRA:(also called RPE dystrophy) The abnormality is in the retinal pigmented epithelium (RPE). The photoreceptor cells will also degenerate eventually. The rate of vision loss is much slower than with generalized PRA, and not all dogs become totally blind.

How is progressive retinal atrophy inherited?

In the Siberian husky, PRA is an X-linked trait. In most breeds studied to date, PRA is inherited as an autosomal recessive trait.

What breeds are affected by progressive retinal atrophy?

Many breeds are affected by one or sometimes more than one form of PRA.

Generalized PRA - early onset: Cardigan Welsh corgi, collie (rod-cone dysplasia type II), Cairn terrier, Gordon setter, Great Dane, Irish setter (rod-cone dysplasia type I), miniature schnauzer (photoreceptor dysplasia), Norwegian elkhound (rod dysplasia, also early retinal degeneration), Tibetan terrier (progressive rod degeneration causing night blindness only)

Alaskan malamute - progressive cone degeneration causing hemeralopia (day blindness) - this condition occurs rarely.

Generalized PRA (progressive rod-cone degeneration) - later onset (usually older than 1 year): Akita, Australian cattle dog, Australian shepherd, American and English cocker spaniel, Basenji, beagle, Belgian sheepdog, Briard, Brittany spaniel, Chesapeake Bay retriever, collie (rough and smooth), dachshund, English springer spaniel, German shepherd, German short-haired pointer, golden retriever, greyhound (without typical initial night blindness), Irish setter, Labrador retriever, mastiff, Nova Scotia duck tolling retriever, old English sheepdog, papillon, pekingese, poodle (miniature and toy), Portuguese water dog, Rottweiler, samoyed, Shetland sheepdog, Shih tzu, Siberian husky, Tibetan spaniel, Tibetan terrier, Welsh springer spaniel, Yorkshire terrier

Central PRA - retinal pigment epithelial dystrophy (RPED): This disease occurs mostly in dogs in the United Kingdom, of the following breeds: border collie, Cardigan Welsh corgi, English cocker spaniel, English springer spaniel, golden retriever, Labrador retriever, rough and smooth collie, Shetland sheepdog 

Retinal degeneration in the Borzoi: Unlike other forms of PRA, the eyes are affected asymmetrically and the retinal lesions appear inflammatory. Males are affected more often than females. Ultimately, the ophthalmoscopic lesions are similar to those of PRA.

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 progressive retinal atrophy mean to your dog & you?

Generalized PRA - early onset:  The first sign is generally failing night vision, as early as 6 weeks of age, and this progresses to complete loss of vision by about 1 - 2 years of age. Collies may retain some vision until the age of 2 - 3 years.  In miniature schnauzers, poor night vision usually develops later (6 months to a year) and there is advanced loss of vision by 3 to 4 years. Affected Alaskan malamutes are day-blind (hemeralopia) at 8 to 10 weeks of age; night vision is never affected.

Generalized PRA (progressive rod-cone degeneration) - late onset:   Generally night blindness is noticed between 2 and 5 years of age (depending on the breed) progressing to total blindness within a year or so. Peripheral vision is lost first.

Central PRA (CPRA)  - retinal pigment epithelial dystrophy (RPED):  Loss of vision occurs much more slowly than in generalized PRA, without initial night blindness.  Affected dogs may not lose vision completely. Because the changes are in the centre of the retina, affected dogs initially have trouble locating still objects in bright light.

How is progressive retinal atrophy diagnosed?

There are no obvious external changes to the eyes. You may notice that your dog has difficulty getting around when the lights are turned off, or when outside at night. If you suspect that your dog has impaired vision, your veterinarian will look for abnormalities with an ophthalmoscope. PRA may also be detected by electroretinogram (ERG) before your dog has any apparent visual difficulties. Electroretinography, which measures electrical patterns in the retina, is usually only available in specialty veterinary centres. (See CERF website listed in references below.)

Genetic testing is quickly becoming available for different forms of PRA in different breeds. The advantage of such testing is that it can identify dogs whose sight is unaffected, but who are carriers of the disorder (heterozygotes).

FOR THE VETERINARIAN:

Generalized PRA

1. Ophthalmoscopic exam: retinal thinning is seen as hyper-reflectivity of the tapetal fundus, attenuation of the retinal vessels, and shrinking and pallor of the optical disc; cataracts and/or retinal detachment may occur late in the disease.

2. Electroretinogram: Generalized PRA can be detected by ERG long before it is apparent clinically.

3. DNA testing: Rod-cone dysplasia or rcd1 can be detected in Irish Setters by polymerase chain reaction. DNA testing for PRA is also available for Chesapeake Bay retrievers, Labrador retrievers and Portuguese water dogs. For more information, see resources below.

CPRA

1. Ophthalmoscopic exam: initially central multiple light to dark brown spots within tapetal fundus, varying in size, shape and density, due to accumulation of lipopigment within the photoreceptor layer. You will also see hyper-reflectivity and retinal vessel attenuation as the disease progresses.

2. Electroretinogram: The ERG has not been found useful in the early diagnosis of CPRA because the photoreceptor cells are only affected later in the course of the disease.

How is progressive retinal atrophy treated?

There is no treatment for PRA. The degree of visual impairment varies with the breed and specific type of retinal degeneration as described above, but most affected dogs will ultimately be completely blind. With their acute senses of smell and hearing, dogs can compensate very well, particularly in familiar surroundings, to the point where owners may be unaware of the extent of vision loss.

You can help your dog by developing regular routes for exercise, maintaining consistent surroundings, introducing any necessary changes gradually, and being patient.

Breeding Advice

Breeding is not advised for any dog with PRA, or for the parents (assumed to be carriers). Siblings should be carefully screened by electroretinogram if they are considered for breeding.  Generalized PRA can often be detected by electroretinography at least a year before clinical signs are apparent.

For some disorders (eg. rod-cone dysplasia type I in Irish setters), blood-based DNA tests are available which can distinguish normal animals from those who are clinically normal but are carriers, and from those that are affected but are not yet showing any signs. Test results are registered through the Canine DNA Registry administered by the Canine Eye Registration Foundation (CERF). DNA testing for PRA is also available for Chesapeake Bay retrievers, Labrador retrievers and Portuguese water dogs. For more information see the resources below.

FOR MORE INFORMATION ABOUT THIS DISORDER, PLEASE SEE YOUR VETERINARIAN.

Where to find more information?

American College of Veterinary Ophthalmologists. 1995. Ocular Disorders Presumed to be Inherited in Purebred Dogs. This reference is helpful in differentiating disorders specific to different breeds.

Ackerman, L. 1999. The Genetic Connection. p. 162-167. AAHA Press. Lakewood, Colorado. This reference contains good information on inheritance, age of onset and form of PRA in different breeds.

This database is funded jointly by the Animal Welfare Unit at the Atlantic Veterinary College, University of Prince Edward Island, and the Canadian Veterinary Medical Association.

 

Copyright © 1998 Canine Inherited Disorders Database. All rights reserved.
Revised: September 15, 2003

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