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Veterinary Notes for Kuvasz Owners Canine Bloat Genetics of Deafness in Dogs
Patellar Luxation Registry: General Procedures Patellar Luxation Classification and Certification
What is Hypothyroidism Inherited Eye Disorders and Kuvasz

VETERINARY NOTES FOR KUVASZ OWNERS
By Dr.Carol Graham, B.Sc., D.V.M., DIP.Radiology

The Kuvasz is essentially a very healthy breed. A normal life expectancy would he more than 10 years with many reaching the age of 14 years. Because of the breed's rapid growth and large size, it is predisposed (prone) to developmental bone problems. Improper nutrition and trauma can contribute to the expression of clinical signs. Osteochondritis dissecans (OCD) is such a disease. OCD is seen most commonly in the shoulder but can also occur in the elbow, hock, or stifle joints. With OCD of the shoulder, lameness generally first occurs between 4 and 9 months and may be associated with a fall or accident playing with another dog. Lateral radiographs of the shoulder will reveal a flattening of the humeral head. Since many affected dogs (50%) have OCD in both shoulders, lameness is not always obvious. Bilaterally affected Kuvasz may only have a shortened anterior stride or " lack of reach". Treatment for OCD of the shoulder involves a surgical removal of the cartilage flap. Both shoulders can be operated on at the same time and recovery is rapid. The most common postoperative complication is the formation of a seroma (fluid buildup over the incision site). These are drained and are a short term problem and can be avoided or minimized by strict post-op cage rest. Mild cases of OCD may respond to conservative treatment if diagnosed early. A series of injections of a drug called Adequan may help in cases which are diagnosed early. However, severe arthritis of the shoulder can occur before the age of two with untreated OCD. The most common cause of hindleg lameness in the Kuvasz is anterior cruciate ligament injury of the stifle joint (knee). The lameness is usually of sudden onset with a characteristic holding up of the affected leg. The dog may marginally improve and toe touch the leg to the ground. The dog will sit with the affected leg off to the side. The damage to the ligament allows the femur and the tibia to slip when the dog puts his weight on the leg and this causes the characteristic gait. If the ligament is not replaced by surgery, arthritis will occur resulting in permanent lameness or pain. Cruciate ligament damage is diagnosed by palpation of laxity (looseness) in the stifle joint. However, in dogs with long standing lameness, the joint capsule will thicken and prevent the " drawer sign", thus frustrating diagnosis. Radiographs may help in the ruleout of other concurrent problems. A diagnosis of hip dysplasia does not rule out a stifle problem as many dogs with hip dysplasia are asymptomatic (not lame) until they injure their cruciates. Hip dysplasia is seen in the Kuvasz breed. The more generations of hip dysplasia certified-free dogs in the pedigree the less chance that the offspring will be dysplastic. Breadth of pedigree is as important as depth for selection of breeding stock. A dog from a dysplasia-free litter is a better breeding candidate than one who has dysplastic siblings. Most dysplastic dogs have a bilateral hip dysplasia. Less than one in five is dysplastic on one side. Dogs have variable clinical signs - some puppies may have severe gait problems between 4 and 6 months. They may have a very difficult time rising and may hop instead of gaiting smoothly. Other dysplastic dogs may have few, if any, clinical signs until they are geriatric and suffer from arthritis. Because of this, radiography of all breeding dogs is essential - a normal appearing gait does not rule out hip dysplasia. Occasionally, a young dog may have difficulty rising and start to shift weight onto the front legs causing straightening of the stifles and a characteristic "popping" of the hocks. These dogs may have a normal hip radiograph but have a bilateral cruciate ligament problem. This has been seen in large rapidly growing dogs. Again, if the injured cruciates are not diagnosed in the initial stages, thickening of the stifle joint capsule due to inflammation and arthrosis will prevent the palpation of joint laxity. An exploratory arthrotomy may be necessary for diagnosis in these cases. Hypertrophic osteodystrophy (H.O.D.) is a metabolic bone disease rarely seen in young Kuvasz. The typical age of onset would be 12-2O weeks. Puppies generally show swollen, painful ends of long bones and may have a fever as well as loss of appetite. If these puppies are not diagnosed early, permanent damage may necessitate euthanasia. Research with Great Danes (the breed showing a relatively high incidence of H. O.D.) shows that a high energy, high protein diet, or excess supplementation may predispose puppies to H.O.D. Treatment consists of putting the affected animal onto a high quality but more moderate diet as well as using analgesics to encourage the puppy to eat and stay mobile. Panosteitis (" pano" or growing pains) is rarely seen in the Kuvasz but can cause acute lameness in the immature animals. The affected leg is very sore, and the lameness occasionally shifts from leg to leg. The lame puppies generally show a severe pain response to palpation of the area around the blood vessel (nutrient foramen) in the affected long bone. The distal humerus and proximal radius are most commonly involved but panosteitis can affect any long bone in the body. Diagnosis is by palpation and radiography. Treatment is primarily rest and analgesics if necessary. In summary, it is important that the Kuvasz owner seek experienced veterinary attention when their dog is lame. Diagnosis is quicker in the early stage, and if surgical intervention is required, the prognosis is better. Surgery on an acute cruciate ligament injury will minimize future arthritis and return the dog more quickly to normal function than on a dog with long-standing arthritic changes and a grossly thickened joint capsule. Dr. Carol Graham studied at OVC with Dr. Paul Pennock, Canada's foremost authority on skeleton disorders. Dr. Graham and Dr. Pennock have spent many hours assisting breeders and owners of Kuvasz for which we thank them.
Copyright 12/15/94

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CANINE BLOAT
by Robert D. Hott, D.V.M.

Canine bloat is a serious medical condition of dogs. It is more properly termed " GASTRIC DILATATION-VOLVULUS COMPLEX" as this describes the course of events. Almost every breed of dog has been affected by GDV, but the condition is seen more commonly in large breeds. The Great Dane and German Shepherd dog seem to be especially susceptible.

The exact cause of GDV has never been determined with any certainty. Some doctors feel that these dogs are born with their stomachs slightly out of position allowing it to twist more easily. Dogs that eat rapidly and then exercise heavily may also be at increased risk. Apparently the heavy, food-filled stomach acts like a pendulum swinging back and forth until it twists on itself. Composition of the diet does NOT seem to be a cause nor does it seem to matter whether the dog eats canned or dry food. In older dogs, tumors of the spleen or stomach may cause twisting and subsequent blockage. Eating indigestible foreign material may also cause bloating. One dog in our clinic ate its dog blanket and bloated. We removed the blanket remnants at surgery and the dog survived. Whatever the inciting cause, affected dogs all show similar signs;

Initially they are anxious, restless, not interested in food or water, vomit once or twice, then follow this with retching and gagging motions which are usually unproductive. There are no abnormal bowel movements. After 30 to 60 minutes, the dog begins to appear SWOLLEN in its midsection due to accumulation of gas in the stomach. Dogs begin to pant heavily and breathing becomes rapid and shallow. In most cases of GDV, the stomach undergoes a " volvulus" or twist. This closes both the esophagus (inlet) and pylorus (outlet) preventing the dog from relieving the gas pressure. The condition is rapidly fatal in dogs causing shock, coma, and death within 6 to 12 hours.

Diagnosis is relatively easy based on breed, history, and clinical signs. Your veterinarian may take x-rays of the abdomen to confirm the diagnosis.

GDV is a true life-threatening emergency. If you suspect your dog may be showing signs, call your veterinarian or emergency clinic AT ONCE for instructions. Treatment is aimed at reducing the gas pressure and returning the stomach to its normal position. Your veterinarian will remove pressure via a stomach tube or trocar tube through the body wall then prepare the dog for exploratory surgery to find the exact problem and correct it. Usually, the surgeon will tack down the stomach (gastropexy) to help prevent recurrence, but these stitches may break down over time. Occasionally, bloat can be treated without surgery by washing out the stomach with a special stomach tube. Death loss due to GDV is very high for several reasons. Our clinic records over the last few years show that approximately half of the cases do not survive. Often, the owners delay in presenting the dog for emergency care because they are unaware of the seriousness of the condition. Also, once the stomach has undergone volvulus, many metabolic poisons build up resulting in damage to the stomach wall, liver, spleen, and heart muscle. Frequently, these poisons will cause the heart to stop during surgery or they may circulate for several days post-operatively and continue to pose a threat. Post-operative infection can also cause problems.

Newer, safer anesthesia methods have helped us treat this condition more successfully, but we are still unable to offer much in the way of preventive medicine. No medication or screen tests are available. The best advice at the present time is to feed these large breed dogs small amounts more frequently and avoid lots of twisting or rolling play. Affected dogs probably should not be used for breeding, but GDV may not show up until the dogs breeding career is almost over. The best plan is to a keep an eye out for GDV and call your veterinarian at the first sign of problems.

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GENETICS OF DEAFNESS IN DOGS
by Dr. George M. Strain, Louisiana State University School of Veterinary Medicine Baton Rouge, Louisiana 70803

Congenital deafness in dogs (or other animals) can be acquired [caused by intrauterine infections, ototoxic drugs like gentamicin, liver disorders, or other toxic exposures before or soon after birth] or inherited. Inherited deafness can be caused by a gene defect that is autosomal dominant recessive, sex-linked, or may involve multiple genes (more on this later). It is usually impossible to determine the cause of congenital deafness unless a clear problem has been observed in the breed or carefully planned breedings are performed. In this article, I will discuss what is currently known about the genetics of deafness in dogs so that breeders can make the best informed decisions possible when attempting to reduce or eliminate deafness.

Congenital deafness has been reported for approximately 40 breeds with the list growing at a regular rate; (Table 1)

Table 1 - Dog Breeds with Reported Congenital Deafness

Akita American, Staffordshire Terrier, Australian Cattle Dog, Australian Heeler, Australian Shepherd, Beagle, Border Collie, Boston Terrier, Bulldog, Bull Terrier, Catahoula Leopard Dog, Cocker Spaniel, Collie Dalmation, Dappled Dachshund, Doberman Pinscher, Dogo Argentino, English Bulldog, English Setter, Foxhound, Fox Terrier, Great Dane, Great Pyrenees, Ibizan Hound, Kuvasz, Maltese, Miniature Poodle, Mixed Breed, Norwegian Dunkerhound, Old English Sheepdog, Papillon Pointer, Rhodesian Ridgeback, Rottweiler, Scottish Terrier, Sealyham Terrier, Shetland Sheepdog, Shropshire Terrier, Walker American Foxhound, West Highland White Terrier

It can potentially appear in any breed. The deafness has often been long established in a breed, but kept hidden from outsiders to protect reputations. The disorder is usually associated with pigmentation patterns where increasing amounts of white in the hair coat increase the likelihood of deafness. Two pigmentation genes, in particular, are often associated with deafness in dogs: the merle gene (seen in the Collie, Shetland Sheepdog, Dappled Dachshund, Harlequin Great Dane, American Foxhound, Old English Sheepdog, Norwegian Dunkerhound, among others) and the piebald gene (Bullterrier, Samoyed, Greyhound, Great Pyrenees, Sealyham Terrier, Beagle, Bulldog, Dalmation, English Setter). Not all breeds with these genes have been reported to be affected. The deafness, which usually develops in the first few weeks after birth while the ear canal is still closed, normally results from the degeneration of part of the blood supply to the cochlea (the stria vascularis). The nerve cells of the cochlea subsequently die and permanent deafness results. The cause of the vascular degeneration is not known, but appears to be associated with the absence of pigment producing cells (melanocytes) in the blood vessels. The function of these cells is not known but appears to be critical for survival of the stria. Deafness may also occur later in life from causes such as toxicities, infections, or injuries, or due to aging presbycusis. These forms of deafness almost never have a genetic cause in animals, and thus do not present a concern in breeding decisions.

The incidence of congenital deafness in different breeds is seldom known because of the limited number of studies. In the Dalmation, where the incidence is highest, 8% of all dogs are bilaterally deaf and 22% are unilaterally deaf. In the English Setter, where fewer numbers of dogs have been hearing tested, the incidence appears to be about 1/3 of that of Dals. Unilateral or bilateral deafness is found in 75% of all white Norwegian Dunkerhounds, but the incidence in normal color dogs is unknown. Other breeds with a high incidence are the Australian Heeler and Australian Shepherd. The incidence of all types of deafness in the general dog population is low, reported to be 2.56 to 6.5 cases per 10,000 dogs seen at veterinary school teaching hospitals. Recognition of affected cases is often difficult because unilaterally deaf dogs appear to hear normally unless a special test (the brainstem auditory evoked response, BAER) is performed; facilities to perform the BAER are usually only available at veterinary schools. It should be noted that a unilaterally deaf dog can be as great a genetic risk for transmission of deafness to its offspring as is a bilaterally deaf dog.

The method of genetic transmission of deafness in dogs is usually not known. There are no recognized forms of sex-linked deafness in dogs, although this does occur in humans. The disorder has been reported to have an autosomal recessive mechanism in the Rottweiler, Bull Terrier, and Pointer. References usually state that deafness transmission in most other breeds is autosomal dominant, but there is reason to believe that this is not always true as will be discussed below. Pigment associated inherited deafness is not restricted to dogs. Similar defects have been reported for mice, mink, pigs, horses, cattle, cats, and humans.

Deafness in blue-eyed white cats is common and is known to be passed on as an autosomal dominant defect. Blue eyes, resulting from an absence of pigment in the iris, is common with pigment associated deafness, but is not in and of itself an indication of deafness or the presence of a deafness gene. Waardenburg's syndrome in humans presents with deafness a stripe of white in the hair and beard, blue eyes (even in blacks and Asians), no pigment behind the retina, and structural deformities around the nose and eyes. This is an autosomal dominant disorder with incomplete penetrance which means that individuals that inherit the disorder may not show all components of the syndrome, i.e. they may not be deaf. Incomplete penetrance of a defect greatly complicates the determination of mode of inheritance. At present, there is no documentation that incomplete penetrance is a factor in any canine deafness.

In simple Mendelian genetics, each dog carries two copies of each gene, one from each parent. The possible outcomes of breedings can be demonstrated with tables showing the genotype of both parents and the possible combinations of their offspring. If deafness is carried as a simple autosomal recessive gene (d), the breeding of two carriers (Dd), and 25% free of the defect (DD). The breeding of a carrier to a dog free of the defect (Table 3) will result in no affected dog to a carrier (Table 4) will result in 50% affected, 50% carriers, and no free. Finally, the breeding of an affected dog to a dog free of the defect (Table 5) will result in 100% carriers and no affected or free.

If, instead deafness, is carried as a simple autosomal dominant gene (D), the breeding of an affected dog (Dd) to a free dog (dd) (Table 4) would result on average in 50% affected and 50% free. Dogs with the genotype DD would be unlikely to occur unless two deaf dogs had been bred. All of the above assumes that incomplete penetrance is not acting. If more than one gene (recessive and/or dominant) is involved in producing deafness, the possible combinations become much more complicated. It is estimated for humans that there are 10-15 different autosomal recessive deafness genes, so that children of two deaf parents can be unaffected but carry both genes. If deafness in dogs results from more than one recessive gene, the possible outcomes of breedings are more numerous and determination of the mechanisms of transmission will be difficult.

As stated above, deafness is often associated with the merle (dapple) gene, which produces a mingled or patchwork combination of dark and light areas. This gene (M) is dominant so that affected dogs (Mm) show the pattern which is desirable in many breeds. However, when two dogs with merle are bred, 25% will end up with (MM) genotype (i.e., Table 2). These dogs have a solid white coat and blue irises, are often deaf and/or blind and are sterile. Breeders of these dogs know not to breed merle to merle. In this case, the deafness is neither dominant nor recessive, but is linked to a dominant gene that disrupts pigmentation and secondarily produces deaf dogs.

Genetic transmission of deafness in dogs with the piebald (Sp) and extreme piebald (Sw) pigment genes, such as the Dal, is less clear. These genes affect the amount and distribution of white areas on the body. Deafness in Dals does not appear to be a simple recessive disorder: we have twice bred pairs of deaf Dals and obtained mostly hearing puppies when all should have been deaf if it was recessive. These findings might be explained by a multi-gene cause, the presence of two different autosomal recessive genes or a syndrome of incomplete penetrance. Further studies will be required to determine the mechanisms.

So what should breeders do when deafness crops up? The most conservative approach would be not to breed the affected animal and not repeat the breeding that produced deafness. As a general rule, bilaterally deaf puppies should be euthanized since they make poor pets, are prone to biting, frequently die from misadventure (cars), and require excessive care. Unilaterally deaf dogs can make good pets but usually should not be bred. When deafness is uncommon in a breed, affected dogs should not be bred, but this does not mean that all related dogs are a risk and must be retired from breeding. An understanding of simple autosomal recessive and dominant patterns, as explained above, can allow the breeder to make informed decisions and likely avoid future deaf animals without sacrificing a breeding line that has been shaped over many years. However, extreme caution must be used when line breeding of dogs related to deaf dogs, whether the deafness is unilateral or bilateral. To make these decisions in an informed manner for breeds with known deafness, it is important that advantage be taken of hearing testing facilities at veterinary schools. Unilaterally deaf dogs cannot be detected by other means, and these dogs will pass on their deafness genes.

Orthopedic Foundation for Animals (OFA) 2300 E. Nifong Blvd. Columbia, MO. 65201-3856
Phone 1 314 442 0418 Fax 1 314 875 5073

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PATELLAR LUXATION REGISTRY: GENERAL PROCEDURES
Picture Of Knee

1. Purposes - To identify those dogs that are phenotypically normal prior to use in a breeding program and to gather data on the genetic disease - patellar luxation.
2. Examination and Classification - Each dog is to be examined and classified by an attending veterinarian according to the enclosed application and general information instructions.
3. Certification - A certificate and breed registry number will be issued to all dogs found to be normal at 12 months of age or older. The OFA fee is $15.00 and no charge will be made for recertification at a later age. The breed registry number will contain the age at evaluation and it is recommended that dogs be periodically re-examined as some luxations will not be evident until later in life.
4. Preliminary Evaluation - Evaluation of dogs under 12 months of age is encouraged if the owner desires to breed at this age. OFA will enter the information in a data bank at a fee of $10.00 for those found to be normal.
5. Dogs with Patellar Luxation - The attending veterinarian and owner is encouraged to submit all evaluations, whether normal or abnormal, for the purpose of completeness of data. There is no OFA fee for entering an abnormal evaluation of the patellar in the data bank.

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PATELLAR LUXATION CLASSIFICATION AND CERTIFICATION
by Donald L. Pierrnattei, D.V.M., Ph.D. and Steven P. Arnoczky, D.V.M.

Patellar luxations fall into several categories:

1. Medial luxation; toy, miniature, and large breeds.
2. Lateral luxation; toy and miniature breeds.
3. Lateral luxation; large and giant breeds.
4. Luxation resulting from trauma; various breeds, and is of no importance to the certification process.

Numbers 1, 2 and 3 are either known to be heritable or strongly suspected.

Classification

A method of classifying the degree of luxation and bony deformity is useful for diagnosis and can be applied to either medial or lateral luxations by reversing the medial-lateral directional references. The position of the patella can most easily be palpated by starting at the tibial tubercle and working proximally along the patellar ligament to the patella.

Grade 1

Intermittent patellar luxation causing the limb to be carried occasionally. The patella easily luxates manually at full extension of the stifle joint, but returns to the trochlea when released. No crepitation is apparent. The medial, or very occasionally, lateral deviation of the tibial crest (with lateral luxation of the patella) is only minimal, and there is very slight rotation of the tibia. Flexion and extension of the stifle is in a straight line with no abduction of the hock.

Grade 2

There is frequent patellar luxation which, in some cases, becomes more or less permanent. The limb is sometimes carried, although weight bearing routinely occurs with the stifle remaining slightly flexed.

Especially under anesthesia, it is often possible to reduce the luxation by manually turning the tibia laterally, but the patella reluxates with ease when manual tension of the joint is released.

As much as 30 degrees of medial tibial torsion and a slight medial deviation of the tibial crest may exist. When the patella is resting medially, the hock is slightly abducted. If the condition is bilateral, more weight is thrown onto the forelimbs.

Many cases in this grade live with the condition reasonably well for many years, but the constant luxation of the patella over the medial lip of the trochlea causes erosion of the articulating surface of the patella and also the proximal area of the medial lip. This results in crepitation becoming apparent when the patella is luxated manually.

Grade 3

The patella is permanently luxated with torsion of the tibia and deviation of the tibial crest of between 30 degrees and 50 degrees from the cranial/caudal plane. Although the luxation is not intermittent, many animals use the limb with the stifle held in a semi-flexed position. Flexion and extension of the joint causes abduction and adduction of the hock. The trochlea is very shallow or even flattened.

Grade 4

The tibia is medially twisted and the tibial crest may show further deviation medially with the result that it lies 50 degrees to 90 degrees from the cranial/caudal plane.

The patella is permanently luxated. The patella lies just above the medial condyle and a space can be palpated between the patellar ligament and the distal end of the femur. The trochlea is absent or even convex.

The limb is carried or the animal moves in a crouched position with the limb partly flexed.

1. Medial Luxation in Toy, Miniature, and Large Breeds

These luxations are often termed congenital because they occur early in life and are not associated with trauma. Although the luxation may not be present at birth, the anatomical deformities that cause these luxations are present at that time and are responsible for subsequent recurrent patellar luxation. Patellar luxation in these breeds should be considered an inherited disease.

Medial luxation is far more common than lateral luxation in all breeds representing 75 to 80 percent of cases with bilateral involvement seen 20 to 25 percent of the time.

Clinical Signs

Three classes of patients are identifiable:

1. Neonates and older puppies often show clinical signs of abnormal hind-leg carriage and function from the time they start walking; these present grades 3 and 4 generally.
2. Young to mature animals with grade 2 to 3 luxations usually have exhibited abnormal or intermittently abnormal gaits all their lives but are presented when the problem symptomatically worsens.
3. Older animals with grade 1 and 2 luxations may exhibit sudden signs of lameness because of further breakdown of soft tissues as result of minor trauma or because of worsening of degenerative joint disease pain.

Signs vary dramatically with the degree of luxation. In grades 1 and 2, lameness is evident only when the patella is in the luxated position. The leg is carried with the stifle joint flexed but may be touched to the ground every third or fourth step at fast gaits. Grade 3 and 4 animals exhibit a crouching, bowlegged stance (genu varum) with the feet turned inward and with most of the weight transferred to the front legs. Permanent luxation renders the quadriceps ineffective in extending the stifle. Extension of the stifle will allow reduction of the luxation in grades 1 and 2. Pain is present in some cases, especially when chondromalacia of the patella and femoral condyle is present. Most animals however, seem to show little irritation upon palpation.

2. Lateral Luxation in Toy and Miniature Breeds

Lateral luxation in small breeds is most often seen late in the animal's life from 5 to 8 years of age. The heritability is unknown. Skeletal abnormalities are relatively minor in this syndrome, which seems to represent a breakdown in soft tissue in response to, as yet, obscure skeletal derangement. Thus, most lateral luxations are grades 1 and 2, and the bony changes are similar but opposite to those described for medial luxation. The dog has more functional disability with lateral luxation than with medial luxation.

Clinical Signs

In mature animals, signs may develop rapidly and may be associated with minor trauma or strenuous activity. A knock-knee or genu valgum stance, sometimes described as seal like, is characteristic. Sudden bilateral luxation may render the animal unable to stand and so simulate neurological disease. Physical examination is as described for medial luxation.

3. Lateral Luxation in Large and Giant Breeds

Also called genu valgum, this condition is usually seen in the large and giant breeds. Rudy postulated a genetic pattern of occurrence and noted Great Danes, St. Bernards, and Irish Wolfhounds as being the most commonly affected. Components of hip dysplasia, such as coxa valga (increased angle of inclination of the femoral neck) and increased anteversion of the femoral neck, are related to lateral patellar luxation. These deformities cause internal rotation of the femur with lateral torsion and valgus deformity of the distal femur which displaces the quadriceps mechanism and patella laterally.

Clinical Signs

Bilateral involvement is most common. Animals appear to be affected by the time they are 5 to 6 months of age. The most notable finding is a knock-knee (genu valgum) stance. The patella is usually reducible, and laxity of the medial collateral ligament may be evident. The medial retinacula tissues of the stiffly joint are often thickened, and the foot can often be seen to twist laterally as weight is placed on the limb.

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WHAT IS HYPOTHYROIDISM

Thyroid Deficiency is a condition due to inadequate output of thyroid hormones from the thyroid gland in the neck. Since the rate of metabolism is under the influence of the thyroid, a deficiency of thyroid hormone in the system slows down energy production. The signs of thyroid deficiency are lethargy, obesity, drooping of the eyelids, mental dullness, skin and ear problems, irregular heat cycles, and infertility problems. Hypothyroidism is easy to treat with thyroid hormone given daily. Usually it is permanent and requires lifetime treatment.

Note: Dogs that have been sick or recovered from Parvovirus should be tested for acquired thyroid deficiency that may be related to disease. Titer testing for diseases including Parvo and Distemper is now available.

The following is an interesting article regarding show dogs and Hypothyroidism.

A few years ago two independent polls of purebred dog breeders, handlers, and owners listed hypothyroidism as the most common inherited disease in dogs. These surveys accurately reported their perceptions, but how accurate are those perceptions? Some breeders and handlers estimate that up to 80 percent of dogs shown in some breeds are being treated for hypothyroidism. Unfortunately, the great majority have never been tested to confirm hypothyroidism, making the treatment purely arbitrary.

These dogs are routinely treated due to the ease of obtaining thyroid drugs and their relative low costs. Breeders and handlers have also heard that thyroid drug treatment results in a beautiful full coat, makes a bitch extra-fertile, or helps a dog show better.

This treatment is usually not harmful and is the treatment of choice if the dog is truly hypothyroid. But there is no scientific data to suggest there may be any value in using thyroid substitutes in dogs with a normal (euthyroid) thyroid gland. Thyroid treatment is unnecessary in this situation and could even be potentially harmful.

Arbitrary treatment makes it impossible to ascertain the true incidence of hypothyroidism. It is entirely possible the disease is not nearly as common as believed. But it would be useless or misleading to test treated animals because significant information cannot be derived if a dog has received thyroid medication in the last three months.

Presently, the OFA will accept thyroid results from five labs, the Endocrinology Laboratory at Michigan State University, Cornell Veterinary Laboratory, the Laboratory at Guelph in Canada, and the veterinary laboratories at the University of Minnesota, and the University of California at Davis. These laboratories can be contacted for information on fees and instructions for sample preparation and shipping. For information on inherited and acquired Hypothyroidism contact the above.

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INHERITED EYE DISORDERS & KUVASZ
by Susan Secor

It has been six years since the Kuvasz literature had something to say about heritable eye disorders. An article written by Mayling Koval (Koval, 1988) informed Kuvasz owners and breeders about the CERF eye registry. It was reported there that only 6 Kuvasz had been registered with the CERF by August 1988.

Since then, more Kuvasz have had their eyes examined and some breeders have started to pay attention to this aspect of their breeding programs. The most recent AKC Awards publication (AKC, 1994) reported eleven CERF registrations during the first quarter 1994 alone. This is encouraging, but there is much more to be done. To avoid the heartbreak experienced in other breeds where little was known about eyes, more of our dogs must be examined and examined repeatedly over their entire life spans. In the past three years (1991-1993), only 50 dogs were examined; since some breeders are already examining their dogs multiple times, the actual number of individual dogs may be even less than that. Yet, in that same three year period, there were 304 AKC Kuvasz litters produced. An educated guess is that very few of those litters had parents with recent eye exams. The present state of knowledge and awareness suggests a widespread belief that ignorance is bliss. The purpose of this article is to change that.

People who care about genetic eye health include not only conscientious breeders, but also owners who hope their dogs will lead high quality lives that include good eye sight and the absence of pain. This article presents recent Kuvasz eye research data from CERF, discusses implications of these data, and provides specific recommendations about breeding and about learning more about the status of genetic eye disorders in our breed. It is written with detail that breeders need to have, yet provides information for the educated buyer who cares about the background of the dog being acquired.

Tell Me Again, What's CERF?

The Canine Eye Registration Foundation (CERF), founded in 1974 by concerned owner/breeders, has the goal to eliminate heritable eye disease in purebred dogs through research, education, and maintenance of a centralized national registry. The CERF registry and research databases have been maintained at Purdue University's School of Veterinary Medicine since 1988 as a subsidiary of the massive Veterinary Medical Data Base there. To be eligible for a CERF number, a dog must have an ophthalmologic examination and be certified free of major heritable eye disease by an American College of Veterinary Ophthalmologists (ACVO) Board-certified veterinary ophthalmologist. A major disease is one that can cause pain or blindness. A number of other less severe eye conditions can exist in a dog which is CERF-cleared of major eye disease. The CERF registration is valid for twelve months; a dog must be re-examined and certified annually to maintain its registration number.

CERF, a group of non-veterinarians who maintain the registry, relies on the ACVO Genetics Committee for the technical guidelines as to what constitute genetic disorders. There are four disorders for which recommendations exist against breeding and for which CERF will not issue a number (this applies to all breeds): progressive retinal atrophy (PRA), certain cataract conditions, congenital retinal dysplasia (geographic or detached), and retinal detachment. In addition, there may be breed specific disorders that make an affected member of that breed ineligible for CERF registration. There are no such disorders for Kuvasz at this time due to insufficient information.

The Kuvasz Data

It is through CERF and the process described above that data about eye problems in the Kuvasz are available. Tables 1 and 2 present information about Kuvasz whose eyes were examined during 1991 (the year in which computerized forms were instituted) through 1993. They are reported from the CERF research database which consists of data generated by all exams performed by veterinary ophthalmologists. The database does not include identifying information about the dogs, hence the data are strictly anonymous.

Table 1 contains annual summaries of total Kuvasz examined including number that were evaluated normal (not showing any problems); number that had one or more problems; and number of different problems that were observed.

Table 2 lists the disorders seen in the Kuvasz examined in order of appearance on the CERF examination form. In reviewing this table, recall from Table 1 that the number of dogs examined is extremely small. It would be unwarranted to draw conclusions about such things as the presence of distichiasis or the relative absence of retinal atrophy.

Table 3 contains the definitions and breeding recommendations for the problems seen among Kuvasz. They are based on information provided by the ACVO Genetics Committee and augmented by personal conversations with veterinary opthalmologists, Dr. Todd Hammond and Dr. Denise Lindley, who is also a member of the Genetics Committee and the CERF liaison. There are two categories of breeding advice (ACVO, 1992):
1. NO, for where substantial evidence exists that supports heritability of the disorder and/or the disorder represents a potential compromise of vision or other ocular function, and
2. BREEDER'S OPTION, where disorder is known or suspected to be inherited but does not necessarily represent potential compromise.

What Do These Numbers Really Mean?

It is an unavoidable statistical reality that the sensitivity of detecting genetic disorders in a breed is greater when large numbers of dogs are examined. Furthermore, the relative lack of disorders is often only a reflection of the paucity of examinations reported (ACVO, 1992). Because so few Kuvasz have been examined and because no more than five of them are seven years or older, virtually nothing is known about eyes in the mature Kuvasz.

We can use retinal atrophy for an example of this absence of knowledge. CERF data in the late 1980s recorded incidence of progressive retinal atrophy in 79 breeds (Freer, 1988); it has also been seen in mixed breeds. We do not have data to know with certainty whether this is a problem in Kuvasz, but it is generally believed that progressive retinal atrophy is common to nearly all breeds.

In the single Kuvasz occurrence of the disorder in 1991-1993, a seven year old dog had generalized retinal atrophy. We know nothing else about this particular dog, but that disorder typically leads to blindness. Since there is presently little evidence to suggest that Kuvasz are going blind at an early age, we might suspect that if retinal atrophy exists in the Kuvasz, it occurs later in life. In other breeds with late onset (e.g. Tervurens), it is often not identified by routine ophthalmoscopic examination until as late as eight or nine years of age. Earlier diagnosis is possible through electroretinography which records the electrical response that follows stimulation of the retina by light. Another diagnostic tool has just recently been announced that is revolutionary because it deals directly with genotype. This blood-based DNA test to identify a certain form of PRA (rod-cone dysplasia 1) in Irish Setters unequivocally identifies genetically normal, affected, and carrier dogs. The test holds promise for all purebred dogs as research in this area continues.

In the meanwhile, for other breeds and other forms of PRA, retinal atrophy that is late in clinical onset and not diagnosed is particularly bad news where it involves breeding stock. By the time a routine exam would detect the disorder, a dog may have been bred several times. In that case, damage control is often limited; about all that can be done is to identify the original carriers and avoid breeding to their descendants.

So, again, what do the Kuvasz numbers mean? They really mean that we don't know very much about anything, and that could mean serious trouble for our beloved breed.

Then What Should We Do?

First, be aware that having a CERF number means only that no major inherited disorder is clinically present at the time of exam; it does not rule out the possibility that the dog has a disorder that is not detectable by the routine opthalmologic exam. Also, a CERF number does not preclude the existence of other disorders of concern. Some of the information needed to make breeding decisions is contained on the owner's copy of the exam form. The other information that you'd want to have, such as, is the dog going to be affected in the future or is it a carrier of undesirable traits, might not be available.

The ACVO Genetics Committee strongly recommends annual evaluations of dogs of all breeds as the first step in control of hereditary eye disorders. This is necessary not just for popular stud dogs, but for any dog that has been bred or that is being otherwise watched closely by its owner. It is the frequency needed to detect a problem in a timely fashion, and to identify trends in eye disease and breed incidence.

There is help available to accomplish screening on a continuous basis. ACVO board certified veterinary ophthalmologists are highly trained and dedicated specialists who have entered a demanding profession because they care about keeping our best friends free of eye problems. Their advice is given to that end. We are fortunate that such resources are there for us, however, those ophthalmologists who do breeding exams are in the unenviable position of sometimes having to deliver bad news. To wit, animals affected with major problems should be removed from breeding programs so genes responsible for these diseases are not spread throughout the gene pool before it becomes almost impossible to find animals that are free of the traits.

These doctors are available at eye clinics sometimes held at dog shows or sponsored elsewhere by local breed clubs. While these clinics provide a welcome service, many ophthalmologists prefer examinations in their own offices where they have their support staff and other diagnostic tools available. Time is scheduled there for a thorough exam and for counseling.

There are approximately 150 veterinary ophthalmologists in the US. If you are not aware of one in your area, Susan Secor (Telephone 719-495-3783) has a current ACVO list and can put you in touch with one closest to you.

Not having our dogs checked doesn't mean they don't have a problem. It must be kept in mind that no news is not necessarily better than bad news. It is only with this information -- good and bad -- that we can make intelligent, informed decisions. If widespread and frequent examination reveals that our breed is relatively free of eye disease, so much the better. If not, then we have the responsibility to save our breed from irreparable harm. The more forthcoming Kuvasz enthusiasts are about examining their dogs and exchanging information, the better off our breed will be in the future.

References

• American College of Veterinary Ophthalmologists, 1992, Ocular Disorders Proven or Suspected to Be Hereditary in Dogs, ACVO.
• American Kennel Club, 1994, AKC Awards, May:CRF11.
• Freer, Hilary, 1988, CERF: Better Eyes, Better Dogs, AKC Gazette, July:48-50.
• Canine Eye Registration Foundation, Eliminating Heritable Eye Disease in Purebred Dogs pamphlet, undated.
• Koval, Mayling, 1988, What Kuvasz Owners and Breeders Should Know about C.E.R.F., Kuvasz Club of America Newsletter, October 3.
• Hammond, Todd B., DVM, DACV0, 1994, personal conversations, May.
• Lindley, Denise, DVM, MS, DACVO, 1994, personal conversation, May.

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