GSD CONDITIONS, DISORDERS AND DISEASES

The German Shepherd Dog Council of Australia has developed a number of schemes to combat conditions, disorders and diseases that adversely affect the German Shepherd Dog as a breed. Integral to that process, it has a Hereditary Diseases Subcommittee to monitor, investigate and recommend remedial action on emerging disorders that may affect breed development. Through these initiatives, the GSDCA and its affiliate members have built up much knowledge and resources on the veterinary aspects of many disorders/conditions. Also over the years, many articles have been published in the GSDCA National Review Magazine to inform GSD enthusiasts of topical veterinary and health matters.

If you wanted specific or general published veterinary articles, you may return to those streams of information by accessing the following links : 
 

This stream of information has items categorized under group headings to enable a systematic presentation of data.

GSD CONDITIONS, DISORDERS AND DISEASES

GSD Inherited and Acquired Disorders

By Dr Karen Hedberg, DVS. Consulting Veterinarian. Hereditary Diseases Registrar to the GSDCA.

User note :
The problems have been listed in a systematic approach, in order to group the various diseases or conditions affecting that system together. The section on immunological disorders has been grouped at the beginning, as this in turn can affect many other systems and the conditions seen.

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BREEDERS AIMS

When we are breeding dogs, in addition to producing better show animals, we should also be trying to breed as sound an animal as possible. This encompasses all of the following:- physical, mental and genetic soundness as well as breed type (ie. it must still resemble the breed!). All of these areas are of great importance, some are weighted more heavily than others in different breeds. Over time various areas come under heavier pressure, eg. With all the current adverse publicity from dog attacks, heavier emphasis is being placed on temperament issues (as it should). Compromises often have to be made when balancing out the relative importance of different problems both within that animal and the breed as a whole.

The bigger the number of issues we attack at any one time, the slower the relative rate of improvement of the breed as a whole. With breed improvement schemes, the larger the number of genes involved in any one condition, again the slower the rate of improvement as well as the larger the environmental effects.

Genetic problems that result in a high incidence of blindness, crippling arthritis or vastly shortened life span (eg. the storage diseases), where there is pain and suffering on behalf of both the dog and the owner (be it monetary or emotional stress), the greater the effort that should be made to decrease the incidence of these problems.

The most important point is to keep the problems a breed has within perspective. This means that if there is a minor problem that does not affect the animal's soundness either as a working animal or its quality and length of life, that it should be kept in proportion relative to other problems within the breed.

DEFINITIONS

Inherited Disorders - covers genetic disorders that have been inherited from one or both parents. Many of these disorders do not have a well documented means of the exact mode of inheritance. Hopefully over time this situation will improve. As a loose rule of thumb, the more genes involved in an inherited condition, the greater the effect of the environment (weight, diet), the greater the range of symptoms seen and the harder it is to control and/or reduce the incidence within the breed. Where there are exact tests that can positively identify affected and carrier animals for a condition (be it a blood test or DNA marker), then a condition can be readily removed from a breed within 2-3 generations if desired. In the polygenetic conditions, until reliable DNA tests are developed, the policy of removing the worst affected animal from breeding programs and promoting the soundest sires (with the best progeny results) is the only slow but sure long term policy.

Congenital Disorders - Means those present at birth. These conditions can be simple malfunctions during development (can be secondary to environmental insults, chemicals etc) while others can be inherited defects within that breed.

Acquired Disorders - Are those that develop over time and are listed here as conditions seen with some degree of frequency within the GSD breed.

Breed Predispositions - These are conditions where the breed in question, the GSD, shows a higher than average incidence of these diseases or conditions occurring than would be expected in the general population.

Immunological Disorders - Are defined by a diminished ability of the body to mount an effective immune response to a perceived threat.

Cutaneous - Of the skin.

IMMUNOLOGICAL.

General Information.

Immunodeficiency disorders are defined by a diminished ability by the body to mount an effective immune response to a perceived threat, eg. infection.

Primary immunodeficiency disease is caused by hereditable defects in the immune system.
Secondary immunodeficiency disease is a diminished immune response acquired as a consequence of some other primary disease.

Clinical Signs - Depend on the level at which the immune response is defective and range from chronic respiratory and gastro-intestinal signs and skin infections to life threatening conditions.

Gross and Histopathological Findings - Lesions vary, most are the result of recurrent or opportunistic infection involving the skin, ear canal, respiratory and gastro-intestinal infections. Refer to “The 5 Minute Veterinary Consult 1997”.

Ig A Dysfunction - A primary Ig A Deficiency has been described in the GSD and is probably at the root cause of several GSD specific immunological disorders. Aspergilosis in the GSD has been related directly to the Ig A deficiency and has an almost 100% death rate. Other disorders including Staph folliculitis and suppurative otits externa (ear infections) have also been directly linked to Ig A deficiencies.

Selective IgA deficiency is the most common primary immunodeficiency in man (approx. 1 in 600).

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BONE (and JOINT)

BONE DISEASES IN DOGS - The consequences of increasing weight and rapid growth.

Many of the joint diseases that occur in the dog arise often as the consequence of rapid growth in an increasingly heavy breed of dog (over time). Osteochondrosis (cartilage degeneration and damage) and joint dysplasias have been studied in many species, in particular in pigs.

In pigs, where the animals were selected for increasingly heavy end weight and rapidity of weight gain, the higher the incidence of symmetrical lesions in certain sites in joints and many growth plates. Experimentally the incidence and severity of osteochondrosis was directly related to rapid growth, ie. rate of weight gain. When the diet was restricted and the animals were grown at a low growth rate, the incidence of OCD was dramatically reduced (almost to zero).

All dog studies in this area have shown to support the concept that the high caloric intake rather than the specific intake of protein, minerals or vitamins influences the frequency and severity of osteochondrosis and HD. The causes of ED while not as thoroughly studied, show similarities and probably similar outcomes.

The common conclusion from studies in dog is that excessive calcium, phosphorus and vitamin D along with a high energy diet and rapid weight gain causing rapid growth, are almost a sure fire recipe for pushing the parameters for normal structural growth and joint soundness well beyond their normal limits, resulting in joint disorders. The higher incidence of osteochondrosis in males versus females is probably a direct reflection of this as males are often ¼ heavier than females at any one time, despite being born at a comparative weight.

Equally this is not to say that genetics does not pay an important part in the body’s structural soundness, however excessive rates of weight gain and thus rapid growth result in pushing the body’s parameters beyond which they can cope, particularly if they were not the most structurally stable to start with, ie. excessive rate of growth and weight will not create severe HD in itself; however, it can make an existing problem considerably worse.

Rate of Weight Gain - The causes of the development of hip dysplasia, as discussed below, are from a combination of genetic and environmental factors. Rapid weight gain and rate of growth through excessive nutritional intake can cause a disparity of development of supporting tissues. Factors affecting cartilage integrity (thickness and stability) and joint fluid composition, such as repeated trauma from excessive looseness of the joint and /or bacterial infections, can increase joint fluid production, thickening of the joint capsule, resulting in both joint pain and reduction in joint stability. These factors contribute to the development of joint looseness and subsequent subluxation, resulting in early clinical signs and joint changes. Control of the rate of weight gain, while it will not prevent hip dysplasia, it will allow a steady growth pattern allowing the hip structure to mature in concert with the strength of ligamentation in order to minimize excessive stress being placed on the hip joint.

Conversely to osteochondrosis, in breeds with a high incidence of HD, females generally have a higher average than males; due it is thought to the influence of female hormones. (a 4 point difference on average in the GSD).

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HIP DYSPLASIA

Hip Dysplasia (HD) - This is a disease that is very common throughout the dog breeds from Cocker Spaniels to Saint Bernards. It is most commonly seen in the heavier bone to muscle ratio breeds where the overall ligamentation is slightly loose.

Hip dysplasia is by definition an ill fitting hip. The hip is a ball and socket joint, and the deeper the socket (ideally sufficiently deep to hold 2/3rds of the head of the femur), the better fit of the femoral head and angle of the neck and the tighter the ligaments, the better the hip.

The various components that combine to give an unstable hip are combinations of the following:- 

shallow hip socket (the acetabulum),
an ill fitting head of the femur (head too small, neck too short and steep),
excessive looseness of ligamentation. 

Pain from hip dysplasia - Is largely from wearing of the cartilaginous surface within the joint, exposing pain fibers in subchondral bone. There are two groups of animals affected :-

1. Young group - 4.5 -10 months (rapid growth phase) and 
2. Older patients - with chronic degenerative disease.

Symptoms - Dogs with HD have a history of intermittent hindquarter lameness, pain on rising, poor hindquarter muscle development, narrow hindquarter action, reduced arc of movement, reduced exercise tolerance. Examination under anaesethic may show looseness while X rays will (if correctly positioned) give more definitive view of anatomical details as well as arthritic changes and the degree of joint looseness.

In should be remembered younger, overweight dogs will be looser in ligamentation than older, fitter individuals.

Different anaesethic agents and depths of anesthesia can vary slightly the looseness of ligamentation seen.

Positioning for X rays for HD assessment - It is most important that of the pelvis should be level, both from front to rear, and side to side. Too steep an angle of the pelvis front to rear will give the appearance of a shallower joint. Twisted, crooked pelvis side to side will have adverse effects on the hip tilted further away from the X ray plate.

Heavier, larger and looser ligamented breeds (and individuals) will exhibit the greatest arthritic changes. Some breeds tolerate looseness better than others.

# Clinical signs often do not correlate with radiographic changes. Some dogs with moderate or even severe HD are asymptomatic.

Differential Diagnosis - In both groups of affected dogs but particularly in the younger group, the back should be assessed, especially when accompanied by generalized soreness from excessively rapid growth. Soreness along the back, usually obvious by arching along the middle (lumbar section), will affect the dog in both rising and extension during movement and manipulation.

Rule outs - In the younger dog, lameness from other rapid growth associated conditions eg. Panosteitis, OCD, HOD or other injury to joints in the hindquarters. In the older dog, conditions such as cauda equina (neurological), acute or chronic knee injuries, bone neoplasia need to be taken into account.

# HD rarely if every presents as a sudden acute injury or onset. 

Methods of Treatment of HD

Treatment depends on the age of the patient and the severity of the symptoms, physical and radiographic findings and economics of the owner. Conservative and surgical options should both be looked at.

Many younger dogs (60%) spontaneously improve with increasing age after conservative management and return to acceptable clinical function (Barr, Denny, Gibbs 1987). The remainder requires further medical or surgical treatment at some time in their life.

Surgical intervention is indicated where conservative treatment is not effective, where athletic performance is desired, or in young patients where owners wish to slow the progression of degenerative joint disease and enhance the probability of good long term limb function.(Small Animal Surgery 1997).

Medical Management

The younger patient - Rest, correction of diet and weight if needed, use of drugs such as cartrophen to improve circulation to, and repair of cartilage, use of other anti-inflammatory drugs. Rest and recuperation for as short as 2-3 weeks can make remarkable improvements.

The older patient - Again weight should be considered as too heavy in condition will acerbate wear all the joints, not just the hips. Also use of the same drugs as above can give remarkable results. Rest with severe cases is always advised.

Non steroidal drugs include Aspirin, PBZ (phenylbutazone), Rimadyl*, Metacam*, Cu Algesic*. If dogs in either group fail to respond to appropriate treatment, dietary changes and rest, then surgical intervention may be necessary.

Surgical Intervention

1. Pectinomyotomy - This is the mildest (also cheapest and quickest) way to get some relief in the HD patient. This was used quite frequently in the past where there were fewer options available. This muscle cutting operation transects the pectinius muscle, a muscle that runs high on the inside of the thigh and pulls the leg medially. Cutting this muscle relieves tension on the joint capsule and eases movement by reducing medial pull of the limb. This can be very useful in the younger patient, particularly where funds do not permit the more radical operations. Can get good pain reduction, and does not interfere with any other surgical option at a later date.

2. Triple Pelvic Osteotomy - This is ideally done in dogs before they reach 9 months of age, where the pelvis has not yet finished growing. This is done to axially rotate and lateralize the acetabulum in order to increase the dorsal coverage to the femoral head. This operation is not suitable where there is insufficient depth of acetabulum to hold the femoral head. The results are best where there is minimal degenerative change. Generally both hips are done at once, cost is around $6000.

3. Total Hip Replacement - This is the replacement of a degenerative hip joint with a prosethetic acetabular cup and a femoral head/neck component. This is used on the older patient where conservative treatment is not effective. The success rate is good to excellent with an orthopedic specialist. This is usually not done much on breeds or individuals that weight less than 20kg (very hard to get small enough prosthetics at this time). Costs per hip is $3000 and up.

4. Femoral Head and Neck Excision - Limits boney contact between the acetabulum and the femur and a fibrous joint is formed. This is a type of operation routinely used with dislocations of the hip from trauma, in the case of HD dogs it is used where conservative treatment has failed and there are financial constraints against a total hip replacement. The results are no where near as good as with (3), as there are fibrous changes and restrictions of movement, but this is largely seen as a salvage procedure. However, many dogs do very well and have improved function. (# Once this operation has been done, other surgical options are virtually nil.)

Discussion

Given the very high percent of younger dogs that respond to rest, conservative treatment and weight/dietary management (60%), ideally the first route of treatment should be conservative, medical management. Many breeds are quite loose in their ligamentation when young and if weight factors are above breed norms for that age and sex, then conservative treatment with calorie limitation should be tried.

Unless there are substantial abnormalities present, ie. very shallow sockets, excessive luxation of the joint with arthritic changes developing and significant pain that is unresponsive, conservative treatment should be tried. If there are significant changes that are unresponsive to rest and treatment within the short term, then surgical options should be considered.

Older dogs should be tried on conservative management first, and again if not responsive, surgical options considered. The best responses are from total hip replacement, but the cost is high. If this cannot be afforded, the age of the dog should be considered, the older the dog, the more one leans to medical management, the younger the dog with severe symptoms, the more a surgical option should be considered.

Breed Aspects in relation to Control Schemes of HD

Hip Dysplasia is a polygenetic condition, that is many genes can affect the outcome. The more genes affecting a characteristic, the harder and slower it is to eradicate or affect the characteristic, and the more environmental effects come into play (diet, weight, rate of growth etc). Where there are ways to measure the condition, then progress can be made in controlling the effect of the polygenes in the overall population, eg. Hip Dysplasia - X raying of individuals and their progeny.

The schemes currently in use for control/reduction in severity of HD and ED aim to reduce the incidence and overall severity of these conditions across the breed (a) as a whole and (b) over time. Trying to shift the genetic structure of polygenetic conditions within a breed is a long term goal, and cannot be pushed rapidly without severe consequences in other areas (eg. type, temperament etc).

The overall picture must be considered. - Trying to eliminate all dogs with hip dysplasia did not work (attempted in both GSD's and Labradors), the end result was a greatly reduced genetic pool, cases of HD still occurring and breeds that did not resemble the standard. The main aim today of most hip schemes is a gradual reduction in the breed average while at the same time allowing breeders to preserve valuable bloodlines and decreasing the incidence of really severe HD. The hereditability of HD varies in different breeds, the higher the degree of inheritance, the more rapidly changes can occur within a breed when selecting for that characteristic. Also, a dog that has a good hip score, may not necessarily throw low scores in his progeny, a full litter brother with a similar score may have a far lower progeny average than his brother.

Until there are very reliable breed specific DNA markers or gene tests, rapid change within breeds, and therefore breed averages, will not be possible.

HD X-Ray Control Schemes

Grading - Where various aspects of hip construction, looseness of joints is looked at and assessed. The current international grading system has 0-6 grades, also called A-F (in some countries). The worst grade per hip gives the overall grade (ie. if grade 0 in 1 hip and 3 in the other, the overall grade is 3).

Scoring - Using the BVA System where 9 different areas of the hips are measured and scored (generally out of a 0-6 scale). Total score per hip given as well as overall total (maximum 106). Very useful in determining the breed average. If combined with a grading system, again the hip with the highest score will determine the overall grade (the ED scheme works on a similar score/overall grade basis).

The Australian ‘A’ Stamp is given by the GSDCA for hips that have a total score of 8 or less per hip, and are considered within normal limits of the breed and suitable for breeding purposes.

PENN Hip - Dogs are anaesthetized and subjected to standard pressure, then X rayed, to determine the degree of joint laxity. Many breeds exhibit varying degrees of joint laxity both across the breed and within the breed. The relevance of the joint laxity when done at an early age (4-6 months) needs to be seen relative to long term hip results (ie. against standardized HD X-rays at 12-18 months of age. Some breeds are more “laxity tolerant”, ie. the rate of change predicted is not as high in some breeds as others.

Breed Averages and Medians

Breed Average - Means all the scores from all the submitted animals being totaled and the divided to find the average for any member of a breed being checked for that characteristic (HD) will have a result (score or grade) close to that average score.

Breed Median - A breed median is the result for that breed where 50% of the breed will be better than that figure and 50% will be worse. In breeds where there are smaller populations being scored, the breed average may be considerably higher than the breed median. With increasing numbers (thousands) these figures are considerably closer.

With HD Schemes, we are working with empirical tests with large degrees of variability within them, it is therefore essential that every breed be looked at from as broad a spectrum as possible so that a relevant decisions can be made as to the breed worth of that individual. As we discussed above, when looking at a population, the spread of the population as well as the population mean is essential if making decisions as to what one can afford to discard from that population. Combined with this we need to estimate how many other individuals that are being culled for various other reasons so that in looking at a breed population as a whole, we need to retain at least 75% of the population for any one characteristic being selected for.

When breeding we obviously wish to breed from the best, soundest dogs, but as started before, this should be kept in perspective in relation to other genetic and breed soundness characteristics that are necessary. For that reason, we generally breed up to and often slightly past a breed average if we wish to retain sufficient breeding stock for the overall health and viability of the breed.

When discussing HD in the GSD, are breed average (BVA total score) is somewhere around 13 in Australia after some 20,000 dogs being scored/graded (the UK average is 18.73). When allowing for differences per hip as well, the average score per hip is around 7 to 8 (a maximum of Grade 3 if grading), a maximum of 8 per hip is allowed by our national governing body, the GSDCA if an A stamp is issued, indicating that the overall quality of the hips are suitable for breeding. As the total score per hip can go to a maximum of 53, a cut off of 8 per hip is quite low. 
 In the GSD as the heritability of HD is quite high, reasonably rapid improvements can be made, and generally 75% of the dogs submitted will pass these stringent requirements, indicating that the spread of the population is reasonably narrow.

Correct use of the Inherited Diseases Schemes by Breeders

The whole idea of these schemes is to give breeders information so as to give them knowledge prior to breeding an animal as to what one could afford to do.

BVA Scoring Scheme - Obviously an animal with a higher score should be used with more care and preferably to a sire or bitch of low score/grade and preferably where there are known family or sire averages. This type of system works where sire statistics are published, where the average score of the sire (where more than 20 progeny are scored) is of greater accuracy in predicting the average score of his progeny, than the score of the sire himself.

German Breed Value Scheme - Breed values are assigned along similar lines, where their data base encompasses litter mates, sire averages etc to give a more complete breed value per individual and outcomes for any expected mating. The breed values for an individual are out of 100, and the SV have gone 1 step further by saying that the combined breed value of the parent should be less than 200. This appears to be working quite well.

The conclusion one gets from these schemes, is that the more information one has both of the parents themselves and of the close relative, particularly offspring of the sire, the better one can plan and get successful results across a litter. In breeds where such information is limited and/or sire statistics are not available, breeders have much harder time selecting good sires and good breeding combinations.

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ELBOW DYSPLASIA

Elbow Dysplasia (ED) - There are 4 main subgroups of elbow dysplasia, which may occur alone or in combination. Generally they are considered inherited in most breeds and the incidence may be adversely affected by incorrect diets in some breeds. Excessive rate of weight gain can affect the incidence of many elbow conditions, often leading to joint incongruity (uneven rate of growth between the radius and ulna), and OCD seen particularly in males.

1. UAP - Ununited Anconeal Process - This process is a large triangular shaped piece of bone situated at the back of the elbow joint. This has a separate ossification center in a handful of breeds notably the GSD, Labrador, Great Dane, Irish Wolfhound, Newfoundlands, Bloodhound, Basset and Afghan hounds. This process normally is fully ossified (sealed) by 16-18 weeks of age. This condition is considered inherited with a possible 3 different genes being involved.

Symptoms - Clinically signs are seen from as young as 5-6 months with often an intermittent lameness, which is exaggerated by exercise. Full flexion and extension of the elbow will elicit pain. There is often an accompanying lateral bursitis (fluid swelling). X rays of the elbow in the flexed lateral position will readily show whether the process has unified or not. Long standing cases often have boney arthritic changes as well.

Treatment - Either (a) removal of the process, if done while young, reasonable prognosis with some arthritis later, or (b) fixation of the loose fragment by a lag screw, for reasonable prognosis in early cases. As the anconeal process is not a weight bearing surface, results following early surgery gives much better long term prospects than in the FCP cases (as loss of that process affects the weight bearing surfaces of the joint).

The majority of UAP cases in the GSD have good congruity of the head of the radius relative to the ulna. Where there is poor congruity, ie. the radius is too long for the ulna, osteotomy (cutting) of the ulna to allow it to lengthen naturally is another option.

Affected dogs should not be breed from. UAP is generally considered to be inherited as a separate condition from OCD and FCP in the GSD.

2. OCD - Osteochondrosis Dessicans - this occurs in many larger breeds, almost any breed greater than 18-20kg at adulthood. There is a higher incidence in males versus females. This can affect many joints, the commonest being the elbow. Breeds that see with a reasonably high incidence of elbow OCD would cover the following :- Rottweiler (high incidence), GSD, Golden Retriever, St Bernard, Great Dane, Border Collie, Rhodesian Ridgeback, Labrador.

Symptoms - Generally seen as a shifting lameness in the forequarter from around 5-8 months of age, some joint capsule swelling and usually a turning out of the front legs at stance as the inner edges of the elbow are most commonly affected. The cause of the problem is considered to be due to a faulty blood supply to the joint cartilage secondary to very rapid growth. On X ray the signs are often quite subtle in mild cases with minor “fluffiness” of the joint surfaces to the more distinct pot holes of larger lesions. Generally diagnoses of a straight extended and slightly medially rotated view of the elbow.

Treatment - If this condition is mild, treatment with drugs such as Cartrophen which increases the blood supply to cartilages, can be very effective along with complete rest, slowing down of the rate of weight gain, and low doses of anti-inflammatories. Repair and recovery can take up to 6-8 weeks of age depending on the severity of the condition, very heavy puppies may have to be kept reasonably restricted until 9 months of age by which stage all rapid growth has slowed dramatically. Severe cases of OCD are often found in conjunction with a FCP, and may require surgical intervention. Most cases >80% show good responses to medical, dietary and exercise management.

3. FCP - Fragmented Coronoid Process (of the Ulna) - this is generally referring to the medial coronoid process, a process that stabilizes the medial edge of the joint. Fragmentation of this process means that the inside edge of the elbow is not stable, hence the very typical lateral rotation of the leg away from the pain. Again, the same age group as above. On X ray the process can be seen as separated on a plate with the elbow extended straight out and a second view with slight medial rotation. If these are diagnosed when young, surgical intervention gives reasonable results, in the older dog where there are considerably secondary arthritic changes, medical management with tablets if probably preferred. Regardless of the treatment, the resulting joint incongruity (unevenness) will lead to ongoing osteoarthritis over time.

4. Joint Incongruity - While most forms of elbow dysplasia can by their development result in joint incongruity, here we are looking at where there has been a possible early closure of a distal growth plate in the foreleg resulting in uneven growth of the radius (usually slightly shorter) in relation to the ulna. The resulting uneven ends of the bones within the joint can cause excessive wear on cartilages and in the worst cases, force the anconeal process distally (ie. create a UAP). Relatively uncommon in the GSD, however severe cases require surgery.

Other forms of elbow “dysplasia” exist, these forms generally involve the lateral displacement of the top of the radius in relation to the ulna (giving a cabriole effect) but these very rarely affect the GSD.

General Treatment of Elbow Dysplasia - As with any painful bone disorder, regardless of the age presented, common treatment is aimed at pain management, sensible diet and weight control and a restricted, suitable exercise regime. Where there are only minor changes in joint surfaces, medical management and conservative treatment with anti-inflammatory agents and rest is generally all that is needed. Those animals with UAP require surgical intervention to minimise future arthritis. Dogs with FCP or those with loose cartilaginous flaps, should in the younger dog be removed in order to minimise future damage to the joint. However due to the incongruity of the joint, there will be ongoing changes regardless. In the older dog with advanced arthritic changes, medical management and conservative exercise regimes is generally the preferred method of treatment.

Diet and Elbow Dysplasia - While diet may not of itself create elbow dysplasia, it can affect the severity OCD seen. Rapid weight gain will push factors such as joint congruity, as well as blood supply to the cartilages within the joints.

Rule outs (differential diagnosis) - Not all forelimb lameness is due to elbow dysplasia. Panosteitis and simple injuries should be checked for, particularly where there is a very sudden onset of lameness.

Controlling the incidence of Elbow Dysplasia - As elbow dysplasia is highly inherited, breeding from severely affected dogs should be heavily discouraged. Generally dogs with a UAP, FCP and arthritis of greater than 5mm are not used for breeding in the GSD in Australia. Breeding from dogs with mild changes should ideally be to normal partners and preferably to lines with low incidences of problems. As this is a group of highly inherited conditions, fairly rapid improvements can be made over reasonably short periods of time. 

Dogs with normal elbows and those with Grade I and Grade II changes are given the ‘Z’ Stamp by the GSDCA Council and are deemed to be within normal breeding limits for the breed. Care should be taken in breeding with Grade II elbows, preferably to normal status partners.

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PANOSTEITIS

Panosteitis - Affects any of the long bones with a shifting lameness pattern, one or more legs may be affected at any one time. Growth associated problem. Triggering factor(s) unknown, poorly understood inflammatory condition.

Breeds - Affected breeds :- most common in the Dobermann, relatively low incidence in the GSD.

Age - Dobermann s affected at about 4-8 months of age. GSD’s are affected at about 5-8 months of age.

Symptoms - Shifting lameness in young dogs, no swelling of growth plates. Affects long bones of any leg with a shifting lameness pattern, usually only one leg affected at any one time. Pain exhibited when firm pressure applied across the mid-shaft of the affected long bone. The pain can be quite acute. Most commonly affected bones are the humerus and femur. X-rays show increased intra-medullary density in the affected long bone.

Treatment - responds well to rest, the use of low grade anti-inflammatories and antibiotic therapy. May be required to treat for a minimum of 3-6 weeks. Diet should ideally ease off concentrated high protein foods in order to slow down the rate of weight gain. Recovery generally excellent.

There is no known hereditary component, and affected animal can be used for breeding.

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HYPERTROPIC OSTEODYSTROPHY

Hypertropic Osteodystrophy (HOD) - Inflammatory disease affecting the ends of the long bones in fast growing puppies of large, rapidly growing breeds.

Breeds - Great Danes, Mastiff most commonly affected breeds. Incidence in the GSD is very low. Age between 3-6 months. Males affected more than females.

Causes - Not fully known, it appears to be related to over nutrition, usually only affects one or two puppies in a litter; most likely infectious, may depend on timing of exposure to infective agent (bacterial or viral).

Symptoms - Often a sudden onset of acute lameness, rapidly progressing to a refusal to move, affected puppies spend most of their time lying down. All four legs are usually affected with painful swollen distal (lower) growth plates of the radius, ulna and tibia. These puppies present with high temperatures, depressed, reluctant to move. X rays show a very distinctive increased density around the growth plates to the lower limbs.

Treatment – Affected dogs respond well to rest, aspirin and antibiotic therapy. Restricted energy intake until recovering and then steady, not rapid weight gain. Recovery generally good – depending on the initial severity of symptoms. This condition is not considered to have hereditary components.

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CAUDA EQUINA

Cauda Equina (Acquired Lumbosacral Stenosis) - There can be three parts to this disease congenital stenosis (narrowing) of the spinal canal in the lumbar sacral area, sacral osteochondrosis (inflammation) and transitional lumbosacral vertebral segments. These three conditions may be congenital (few seen) or more commonly developmental, and can occur singularly or most often appear in concert with degenerative disc disease at the lumbo-sacral junction. The syndrome results in sensory and/or nerve disfunction due to compression, destruction or displacement of the nerve roots or their blood supply.

Breeds - GSD’s appear to be predisposed. Seen in many other medium to large breeds including the Labrador, St Bernard, cross breeds generally over 8 years of age.

Symptoms - The classic syndrome is seen in the older dog , usually over 5-6 years of age (over 8-9 years more frequently), with affected dogs showing difficulty in rising, pain and lameness in the hindquarters, often more severe in 1 leg than the other. The more advanced cases may have faecal incontinence (urinary incontinence less commonly), the tail may have limited movement or even a flaccid paralysis. On a lateral X-ray of the pelvis, the changes around the lumbo-sacral junction are very obvious. Stress radiographs can be taken (the hindquarters flexed up and/or down) showing instability or disc protrusion and calcification.

Differential Diagnosis - As these symptoms are very similar to HD in the older dog in particular, these different syndromes must be properly differentiated in order to treat them correctly. In the older GSD, the more severe cases showing nerve dysfunction also have to be differentiated from cases of degenerative myelitis. 

Treatment - Most dogs respond well to rest, use of strong anti-inflammatory agents for several weeks and will often stabilize on ongoing medication. In the younger animal and/or severely affected individual where there is considerable nerve pinching from disc protrusion, surgery to remove the disc may be warranted. Many of the older dears do appreciate long coats over their backs and pelvic areas during the colder months.

Prognosis - Depends on the severity of symptoms, however most respond well to rest, adequate medication and can survive for years on good management techniques. Those animals with feacal or urinary incontinence are obviously more severely affected and their long term prognosis can be poor unless there is very good (and rapid) response to medication; these dogs are candidates for disc removal surgery, but often their advanced age may preclude this being really feasible.

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SPONDYLITIS

Spondylitis - This condition results from inflammation around the base of the vertebral bodies, resulting in a lipping of new bone formation between many vertebrae along the back. It is not considered a genetic condition, however, GSD’s are considered to be over represented.

Breeds - Occurs in a many medium to large and giant breeds, especially GSD’s, Rottweilers and Great Danes. Spondylitis can also occur cross breeds, in reality can appear in any breed, the highest incidences in the heaviest, fast growing breeds and individuals.

Age - Seen from as young as 2-3 years of age, but generally from 5-6 years onwards, with the heaviest incidence above 8 years of age.

Cause - Specific causes yet to be defined, but as the incidence is highest in the heavier breeds, one has to consider whether rapid growth rates could in turn set of minor OCD lesions along the vertebral facets in the young rapidly growing dog. Many younger dogs can become quite sore over the back, arching is common and this generally settles with rest, and occasionally anti-inflammatories. This then may set the stage for future degenerative changes.

Symptoms - Arching over the back, pain on rising and on palpation along the back. On X-ray the characteristic lipping and new boney bridges linking between various thoracic and or lumbar vertebrae are clearly visible. Many dogs can have quite extensive changes that actually fuse the vertebrae together, these changes are stable over long periods of time, however they can flare up in colder weather and with excessive exercise. Slipping can fracture or crack the bridges, creating excruciating pain.

Treatment - Rest and use of anti-inflammatory drugs usually works very well. Acute cases may require 4-6 weeks rest. Weight should be reduced if well above normal. Care with adequate housing and coats in the colder weather will assist. 

Prognosis - Severe cases may have a poor prognosis if there is nerve dysfunction and pinching secondary to the arthritic changes. However most cases can be reasonably well managed for years.

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DISKOSPONDYLITIS

Diskospondylitis- Inflammation and infection of the ends of vertebral bodies, usually only in 2-3 sites along the back. It is not considered a genetic condition

Breeds - Occurs in medium to large and giant breeds, GSD’s, Rottweilers and Great Danes, and also crossbreds, males outnumber females 2:1.

Age - Average age 4-6 years.

Symptoms - Can vary from mild to acute onset. Signs of pain include difficulty in rising, arching over the back, reluctance to jump, stilted gait, occasionally ataxia or paresis of the hindquarters. Any disk space can be affected, most commonly the lumbar vertebrae and the lumbar sacral junction.

Causes - Bacterial, generally staph infections.

Treatment - For minimum 6 weeks on strong antibiotics and anti-inflammatories. Ongoing treatment with anti-inflammatories is often required, occasional bouts of severe inflammation may require repeat long courses of antibiotics.

Prognosis - Long term outcome depends on the infection and degree of spinal cord damage. Generally good long term with variable degrees of nerve damage - usually stable after treatment.

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CHONDRODYSPLASIA

Chondrodysplasia - Shortened long bones, normal to slightly shorter depth of body, normal head. From the term achondrodysplastic - meaning a lack of development of the long bones of the legs, with well developed head, chest and trunk. Chondrodysplastic “dwarf” and/or achondrodysplastic “dwarf” refers to the “dwarfed” nature of the shortened limbs, and is a condition that is unrelated to the true pituitary dwarf.

Breeds - Occurs in many breeds, including reports of GSD's, Dobermanns and Alaskan Malamutes, etc, most often on a sporadic nature. Some breeds have deliberately been selected for chondrodysplasia eg. the Corgi, the Vallhund, the Dachshund, and the Basset, etc.

Age - Can be readily diagnosed before 8-10 weeks of age.

Symptoms - Shortening of the long bones with full development of the normal width of bone ie. body size is relatively normal - similar to the Basset in leg length, heavy bone, big body, short legs (all 4). All the cases seen in the GSD, those dogs are very short in all 4 limbs with no intermediate cases, ie.varying lengths of foreleg.

Causes - As far as known, chondrodysplasia where it appears, is considered to be an autosomal recessive condition in most affected breeds.

Treatment - Not applicable, as process cannot be stopped or reversed and there are usually minimal health problems.

Prognosis - Generally good long term, as affected dogs lead relatively normal lives with normally only further aquired health problems.

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BLOOD

HAEMOPHILIA

Haemophilia A - X chromosome sex linked recessive bleeding disorder, primarily affecting males. This condition has been seen in several breeds, most notably in the GSD. Haemophilia A is now nearly cleared from the GSD breed, with many countries regularly testing of males of suspect bloodlines. Within Australia, no cases have been reported within the registered population of GSD’s in the last 5 years.

VON WILLEBRANDS

Von Willebrands - This is another clotting disorder, equally affecting both sexes, rarely causes major haemorrhage, seldom seen or reported within the GSD within Australia.

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NEUROLOGICAL

EPILEPSY

Epilepsy - Exact mode of inheritance not fully understood. Age first seen - 5-6 months to 5 years; average 6 months to 3 years.

Breeds - Affects many breeds, GSD included.

Signs - Most seizures occur at night or early morning, animal stiffens up, falls to the ground on its side, and various combinations of the following are seen - jaw champing, salivation, urinating, defecating, paddling of all 4 limbs; this lasts 2-3 minutes and is followed by a short period of disorientation that usually lasts 5-10 minutes. Seizure frequency tends to increase over time if the animal is left untreated.

Treatment - Can be treated quite successfully for many years. Drug of choice generally the phenobarbitone family of drugs.

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TAIL CHASING

Tail Chasing - This has been linked with both behavioral abnormalities and with epilepsy. ? if an inherited condition.

Breeds - Affects several breeds, most commonly the Australian Cattle Dog and the GSD. The tail chasing starts at around the same age as epilepsy (5-6 months), but has been linked with boredom syndromes.

Treatment - Some dogs can with good activity programs grow out of the problems, others are unresponsive, will continue to tail chase, often heavily chewing the tail and these dogs may require an ongoing treatment regime with similar drugs as the epileptic dogs.

*As a general comment, both epileptics and tail chasers are found to be very “hyper” (or over the top) dogs.

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GUN/NOISE SENSITIVITY

Gun/Noise Sensitivity - This is considered an inherited trait in many breeds, and the dogs that are affected often get worse with age with increasingly severe reactions to thunder storms, fireworks etc.

Breeds - Most commonly affected (within my experience) are the Golden Retriever and the GSD.

Treatment - Severely affected dogs need to be either tranquilized or placed on anti-epileptic drugs ahead of anticipated storms or fireworks, if not, these dogs will either take off over fences or rip their way through doors to get either into houses or out as the case maybe.

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DEGENERATIVE MYELOPATHY

Degenerative Myelopathy - This is a slowly progressing degeneration of the myelin around the nerves of the middle of the back, slowing down the transmission of messages which results in increasingly severe effects on the mobility and manoeuvrability of the hindquarters.

Breeds - This disease is almost exclusive to the German Shepherd Dog and is generally seen from 7-8 years onwards, the most common age is around 10-11 years, the earliest age I have seen this is in a 6 year old.

Symptoms - There is a characteristic scraping of the hind feet, knuckling of the hind feet, wearing of the tops on the nails, a tangling of the hocks if they turn fast, troubling negotiating stairs especially descending, a very characteristic swaying pacing gait (almost an inability to trot correctly).  There are proprioreceptive deficits in both hindlegs, one leg can be more affected than another. To test this, turn the toes of the hind foot underneath and see if they remain in that position for any length of time. In a normal dog, the return to the normal position is instantaneous (“righting reflex”), in affected dogs this is significantly slower and may take up to 10-15 seconds or longer.

There are several characteristics in this disease that are similar to multiple sclerosis (MS) in that similar abnormalities of the immune system and the type of nerve degeneration. The degeneration in these dogs always only affects the hindquarters.

The dogs follow a course of always step wise degeneration, plateauing out for a while before gradually getting worse again. The course of the disease generally takes 12-18 months, from the time symptoms are recognised, some dogs may last up to 2 years before the hindquarters no longer support them in any significant degree.

Treatment - The only good point in this disease is that it is not painful. Cortisones and other anti-inflammatory drugs have no effect on the progression of the disease but can help to cover any other degenerative joint disease present (HD, spondylitis etc). Some dogs benefit from additional Vitamin E (300-500 iu daily) and I find, some Selenium (Selim E tabs, 1 tab 2 x weekly). Some therapeutic benefit has been reported with the use of aminocaproic acid (Amicar, Lederle), 500mg given every 8 hours - progression of the degenerative process was slower in about 50% of treated dogs, and improvement occurred in some, benefits usually occurred within 8 weeks. [Neurology Textbook - reference - ]

This condition is an immune system failure. As it occurs almost exclusively in the GSD, there are obviously genetic factors involved. In my experience I have not been able to directly link and family groups/lines etc, and I feel, reflects more a failing in the immune system in general across the breed. This condition would affect around 5-8% of older German Shepherd Dogs.

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HEART

Heart Defects - As a rule of thumb, cardiac defects that are severe, will usually affect the rate of growth early, ie. by 6-8 weeks of age. These individuals usually have to be put down. Cardiac defects that are detected at 6-12 weeks where the growth and weight of the affected puppy is the same as its litter mates, these puppies often will grow with few problems. Generally, where a defect is detected and the puppy is of good size etc; the puppy is checked every 3-4 weeks, preferably until 16 weeks of age. Some defects will correct, others may become more severe (not that commonly). Overall the incidence of heart defects in the GSD is relatively low. Affected animals should not be bred with.

PATENT DUCTUS ARTERIOSIS

Patent Ductus Arteriosis (PDA) - Most common canine congenital heart defect. This condition is as a result of the persistence of the connection between the aorta and pulmonary artery. This normally closes off after birth once the lungs start being used.

Breeds - Predilections are Miniature Poodle, GSD, Collie, Pomeranian, Toy Breeds.

Symptoms - Signs are usually picked up by 6-8 weeks of age, often at the initial veterinary check. Severely affected puppies may be picked up earlier. The degree of severity depends on the relative size of the defect. Most are euthanased. For those that are not picked up early, with continued growth, the stress across the duct increases and most will come down with signs of cardiac failure by 5-6 months of age. Few GSD’s ever reach this stage. Symptoms consistent with cardiac failure; puppies usually small, pot bellied, easily stressed, cyanotic (blue in the gums).

Treatment - For those that are diagnosed later, surgery can rectify the problem , however there are considerable risks as these dogs already have considerable cardiac stress. Surgery should only be attempted where no other existing heart defects are present, ie. all cases should be Doppler Ultrasounded before considering surgery.

Affected dogs should not be used for breeding. Incidence in the GSD is low. 

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SUBVALVULAR AORTIC STENOSI

Subvalvular Aortic Stenosi (SAS) - Second most common canine congenital heart defect. This is considered inherited with a polygenetic mode of inheritance. Studies show that this develops post natally and can progress with maturity (ie. get worse with age). The stenosis or narrowing can be mild to severe. Mildly affected dogs may have no symptoms, moderately to severely affected dogs may have exercise intolerance or congestive heart failure, severely affected dogs present with either congestive heart failure, sudden collapse or sudden death.

Symptoms - Mildly affected dogs may remain undetected under 16 weeks of age. More severely affected dogs are usually picked up at vaccination time (6-8 weeks of age). Affected dogs, even if only mildly affected should not be bred from.

Breeds - Affected breeds include Newfoundlands, Golden Retrievers, Rottweilers, Boxers and GSD’s. Incidence in the GSD low, but not uncommon.

Treatment - If the condition is suspected, the best diagnostic tool is a Doppler Ultrasound, usually only available at a specialist centre or university clinic.

Prognosis - For mildly affected dogs is usually good. Severely affected dogs may have a limited life span.

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ATRIO-VENTRICULAR VALVE DYSPLASIA

Atrio-ventricular Valve Dysplasia (AVD) - Mitral valve defect. Not as common as the other defects seen.

Breeds - Seen in the Great Dane, GSD, Afghan Hound.

Symptoms - Most commonly seen in males. Usually picked up at 6-8 weeks of age. The severity of the condition can vary greatly. Severely affected individuals may show symptoms of cardiac failure at an early age.

Treatment - Suggested that a Doppler Ultrasound is done to determine the severity of the defect. If mild, these dogs may be reasonable normal for long periods of time, as they age, they may require cardiac drugs to assist the blood circulation.

Affected dogs should not be bred with.

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PERSISTENT RIGHT AORTIC ARCH

Persistent Right Aortic Arch (PRAA) - Discussed under mega-oesophagus (INTESTINAL GROUP) below.

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CARDIOMYOPATHY

Cardiomyopathy - Affects older dogs, any age, most commonly seen over 5-6 years of age.

Breeds - Seen primarily in Dobermanns, Newfoundlands, Great Danes, St Bernards ie. mostly the larger or giant breeds. Incidence is relatively low in the GSD. 

Symptoms - Usually very sudden onset of cardiac failure signs, tiredness, enlarged abdomen, occasional sudden death.

Treatment - Most respond very well to therapy within several days, drugs to stabilize the heart include Enafor, Fortecor; additional Vitamin E and low doses of Selenium for muscle strength can assist. Others with severe changes may respond very poorly.

Long Term Prognosis - For those that respond well, these dogs can have quite good quality of life for several years or longer, depending on other existing conditions. Some dogs (20-30%) do not respond to therapy and require almost immediate euthanasia.

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INTESTINAL

MEGA-OESOPHAGUS

Congenital Mega-oesophagus - Inherited, seen in various breeds including the GSD (possibly an autosomal dominant with incomplete penetration.). These present at around 4-5 weeks of age when solid feeds are started. The typical picture is one of vomiting within 5-10 minutes of eating, puppies affected are often small and weedy due to lack of adequate food getting through to the stomach. Many have a dilation of the throat after eating and a persistent gurgle.

There are two basic types of congenital mega-oesophagus, Persistent Right Aortic Arch and Mega-oesophagus :

1. PERSISTENT RIGHT AORTIC ARCH

Persistent Right Aortic Arch (PRAA) - This is actually a vascular abnormality that results in constriction of the oesophagus over the base of the heart, causing a build up of food forward of the obstruction.

Symptoms - Signs are regurgitation of solid foods almost immediately after eating (seen from 3-4 weeks of age). These are diagnosed by their very characteristic appearance on barium X ray. In this type of abnormality, the actual musculature of the oesophagus is normal.

Treatment - These can be corrected surgically (usually not before 12-14 weeks of age), however as the operation is intra-thoracic, the puppy usually has to be of a reasonable size and weight before operation. The prognosis can be guarded as the puppies are often thin, undersized and there can be secondary pneumonia.

Prognosis - Most improve dramatically after the operation, however some can persist in having some dilatation in the 1st 1/3 of the oesophagus. Feeding of these puppies is by giving them a more liquid diet and feeding them with the food in an elevated position so as to provide a straighter passage through the chest to the stomach.

2. MEGA-OESOPHAGUS

Mega-oesophagus - These puppies have a grossly dilated oesophagus affecting the entire length of the oesophagus. These cases often have secondary chest infections due to vomiting and regurgitation.

Symptoms - Regurgitation of solid foods almost immediately after eating. Again these are diagnosed by barium X ray.

Prognosis - This is extremely poor as the major defect in the muscles affects the passage of food to the stomach and the condition is not readily correctable. 

Mega-oesophagus - (Acquired) - This condition can develop in the older animal from a variety of reasons. 

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BLOAT

Bloat or Gastric Dilation and Volvulus (GDV) - This is common in large deep chested breeds of dogs, often those with a rather narrow spring of rib being at higher risk.

Breeds - Affected breeds include the Borzoi, Bloodhound, Great Dane, St Bernard, Irish Setter, Basset, GSD and the list goes on.

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LIVER

PORTASYSTEMIC SHUNTS

Portasystemic Shunts - Congenital, vascular anomaly, it is usually a multiple shunt and can be acquired secondary to pre-existing liver disease. Dogs with multiple shunts are recognised at later age than dogs with single major shunts, most not being recognised before 1-2 years of age.

Breeds - Found in the Doberman, GSD and Cocker Spaniel.

Symptoms - Depression, vomiting, weight loss, blood chemistry changes suggestive of liver function abnormality.

Treatment - Restricted protein, low residue, balanced diet, small feeds regularly. Some abnormalities are surgically correctable.

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IDIOPATHIC HEPATIC FIBROSIS

Idiopathic Hepatic Fibrosis - Young dog predisposition, suggests a congenital or genetic basis. Various types of idiopathic hepatic fibrosis exist; these are non-inflammatory fibrosing diseases whose cause is generally unknown. Idiopathic hepatic fibrosis is not common, but is probably under diagnosed because of unfamiliarity with the symptoms. It is most common in young dogs, most less than 2 years of age, however some as young as 4 months and as old as 6-7 years may have the disease diagnosed.

The type of fibrosis that shows a marked breed predisposition in the GSD is Central Perivenous Fibrosis. The GSD is also over represented in cases of Pericellular Fibrosis. There is no sex predisposition. The cause of either of these types of fibrosis is as yet unknown. The young age of affected animals and the marked breed predisposition in the GSD suggests an inherited pattern.

Symptoms - Both types of fibrosis present the same. Most dogs are presented with abdominal distension due to fluid build up (ascites), vague gastro-intestinal signs such as vomiting, diarrhoea, anorexia (not eating) and weight loss. Duration of signs is variable, some as short as 1-2 weeks, others several months. Some dogs present with neurological signs secondary to liver toxin build up. Jaundice is uncommon.

Diagnosis - Elevated liver enzymes, radiographs show a small liver, ultrasound may show up abnormal blood vessel flow, complete diagnosis may require a reasonable sized biopsy of the liver.

Treatment - Antibiotics and anti-fibrotic agents (often includes prednisolone). Diet – moderately to severely protein restricted disease, supplements with lactulose and antibiotics as needed. Fluid build up is a less consistent problem and can usually be managed with dietary sodium restriction and diuretics.

Prognosis - Guarded, but some may survive for long periods on symptomatic management.

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GASTRO-INTESTINAL - DIGESTIVE

There are a group of conditions/disorders that affect the digestion and/or intestinal stability of the GSD. Many of these probably have an allergy or immunological basis. On an overview of these type of problems, as they affect our breed, the GSD is certainly overrepresented.

WHEAT (GLUTEN) ALLERGIES

Wheat (Gluten) Allergies - Tests run have suggested that over 30% of dogs suspected of having food allergies are sensitive to gluten. Many of the features seen in gluten allergies are also seen in other types of inflammatory bowel diseases eg. lympocytic-plasmacytic enteritis, and it highlights the need with this group of diseases to try elimination diets to ensure that what appears as a chronic disease is not a simple allergy driven condition. Many dogs that exhibit this condition often show few signs prior to 8-9 months of age (the earliest I have seen this is around 5 months), as it takes time to sensitise an individual by continual low grade insult.

Breeds - These are very common in many breeds.

Symptoms - Usually present as failure to maintain body weight, often despite increasing the food intake; chronically loose to sloppy motions.

Treatment - As this is around a similar age to the diagnosis of pancreatic insufficiency in GSD’s, my first step is to try these dogs on a wheat or gluten free diets for a minimum of 6 weeks and limit the type of meat proteins fed (usually I limit the meat to either chicken or mutton, cut out beef entirely). If using a dry food, the safest cereal base to use is rice. The other grains that contain some gluten include barley, rye, buckwheat and oats. I would estimate around 10-15% of GSD’s have a definite wheat/gluten sensitivity and this figure can be higher within certain bloodlines.

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EXOCRINE PANCREATIC INSUFFICIENCY

Exocrine Pancreatic Insufficiency - Assumed to be inherited in the GSD and postulated to be inherited as an autosomal recessive trait. Age from 8 months onwards, usually in the younger dog.

Diagnosis - Tests TLI - fasted TLI <2.5mg/L is diagnostic - Low serum cobalamin is associated with EPI and distal bowel malabsorption. Low serum folate is associated with proximal small bowel malabsorption, small bowel intestinal bacterial overgrowth may raise serum folate and lower serum cobalamin

Symptoms - Chronic diahorrea, often pasty coloured motions, weight loss/failure to hold weight.

Treatment - Low fat diets, supplementation with panreatic enzymes. Place these dogs on low allergy diets in addition to pancreatic supplementation. If the dog picks up really well over 4-6 weeks (good weight and firm motions), try gradually removing the pancreatic enzyme supplement, if the weight stays good and the motions stay firm, the majority of the problem could have been a chronic allergic response.

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PANCREATIC ATROPHY

Pancreatic Atrophy - The causes for this are considered possible abnormal immune mediated responses. GSD’s represent over ½ the cases seen. In the older dog, these cases are often as the result of chronic bouts of pancreatitis (inflammation of the pancreas which results in loss of enzyme producing cells).

Diagnosis - In the GSD however, these dogs are seen at a young age. Even so, signs do not appear prior to 6-12 months of age, so presumably sufficient enzymes are produced prior to this time. # Ensure that the diagnosis of the chronic bowel condition your GSD is diagnosed as having, is correct, as chronic wheat (gluten) allergy can present a similar picture of poor absorption of food and/or irritable bowel symptoms.

Treatment - Remove wheat/gluten sources from the diet and see if symptoms abate, try a rice based diet, remove beef proteins as well as this is the most common meat based protein that dogs can be allergic to. If symptoms still exist, these dogs require ongoing pancreatic enzyme supplementation.

The number of GSD’s affected by pancreatic insufficiency or atrophy, once the chronic allergy cases are eliminated would be quite small, certainly less than a tenth of the number with gluten allergies.

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INFLAMMATORY BOWEL DISEASE

Inflammatory Bowel Disease - This is a name covering several different types of diseases, usually classified according to the type of inflammation present and the area of the intestine where the majority of the inflammation occurs. These diseases have an immune mediated component.

Symptoms - As the Ig A system is intricately involved in dampening the body’s reaction to gut antigens, a defect in the system will have an immune response reacting to various gut antigens, be it a bacterial product, a food antigen, or a self antigen (autoimmune). The resulting response induces gastrointestinal irritation and inflammation.

Breeds - Some breeds are more predisposed to more than one type of inflammatory bowel disease such as the Boxer and the GSD, reflective of these diseases having an immune mediated component.

Treatment - For these dogs, aims at stabilizing the gut sufficiently that food can be absorbed. The food given should ideally be concentrated, of easily assimilated form so as to be highly digestable with low residue. Despite these diets, some dogs have to remain on a combination of drugs including metronidazole, motility modifiers, pancreatic enzyme replacers and/or low doses of cortisone.

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EOSINOPHILIC ENTERITIS

Eosinophilic Enteritis - Inflammatory disease of the small intestine characterised by the infiltration of eosinophils. 

Breeds - GSD, Rottweiler and Sharpei may be predisposed.

Age - Younger animals usually less than 5 years of age, but any age can be affected.

Symptoms - Intermittent vomiting, diahorea, anorexia, weight loss, thickened bowel loops.

Causes - Immune related, food allergies, parasites.

Treatment - Feed with low allergy diets, limited food sources, high digestibility. Long term dietary control may be required.

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CHRONIC COLITIS (LYMPHOCYTIC-PLASMACYTIC)

Chronic Colitis (Lymphocytic-Plasmacytic) - Inflammatory bowel disease characterised by infiltration of lymphocytesand/or plasma cells into the walls of the intestines.

Breeds - GSD’s and Sharpeis may be predisposed.

Age - Most present before 6 years of age.

Symptoms - Signs vary considerably between individuals in type severity and frequency, increasing over time. Symptoms chronic diarrhoea, vomiting common, anorexia followed by bouts of ravenous appetite, chronic weight loss, blood in faeces occasionally seen. Thickened loops of gut, enlarged mysenteric lymph nodes.

Causes - Infections (bacterial guardia, salmonella, campylobacter); dietary (food additives, meat or milk proteins, wheat glutens); genetic factors (breed predilections).

Treatment - Low allergy diets. Cortisone and long term antibiotics may be needed.

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OTHER GASTRO-INTESTINAL - DIGESTIVE

Bacterial Overgrowth

Malabsorption Syndrome

Stress Induced Diarrhea

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HORMONAL

PITUITARY DWARFISM

Pituitary Dwarfism- Thought to be inherited as a simple autosomal recessive.

Symptoms - Affected puppies fairly obvious by 8-10 weeks of age. Puppies affected fail to develop beyond ¼- 1/3rd normal size, bilateral symmetrical alopecia (hair loss, abnormal coat, hyperpigmentation), most are also hypothyroid as well. Adrenal and gonadal abnormalities also occur.

Treatment - Some supplementation with thyroid hormones can assist hair growth, some increase in final size (marginal at best). Growth hormone would obviously be of more use, however its use is severely restricted and is not available for use in animals in Australia.

Number of puppies affected per year is hard to determine but would have to be around 20-50 per year Australia wide, these are very obvious usually by 8-10 weeks of age, are usually euthanased and thus removed as an immediate problem. They are also, due to the nature of the problem, sterile. Carrier status animals (ie. parents) would have to involve a reasonable percentage of the population, possibly as high as 20%. Whether these animals, who should, by all terms, be producing slightly lower than normal pituitary hormones, are therefore more prone to developing other conditions, is at this time, yet to be determined.

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MUSCULAR

FIBROMYOSITIS OF THE GRACILLUS MUSCLE

Fibromyositis of the Gracillus Muscle - This is an uncommon condition seen almost exclusively in GSD and less commonly in the Belgian Shepherd and the Dobermann. This is a progressing disorder affecting the gracillus muscle (and secondarily the semi-tendenosis muscle) on the inside of the hindquarter. The condition results in the progressive replacement of normal muscle tissue with fibrous tissue, resulting in severe contraction of the affected muscle.

Symptoms - As the gracillus muscle runs from the inside of the pelvic floor to just below the knee (stifle), these dogs have a very characteristic double swing to the hindquarter gait, as though the leg cannot straighten fully (which it can’t!). Most cases seen are bilaterally affected. The age seen is anywhere from 2-3 years onwards, more commonly around 4-6 years, uncommon in older dogs.

Cause - Several causes have been postulated, the most likely being initial micro-insults to the muscles concerned followed by an inappropriate response from the immune system, resulting in a fibrous reaction that once started, continues to affect the entire muscle, and often affects the neighbouring muscles as well.

Treatment - Generally unresponsive with anti-inflammatories. Surgical removal of the affected muscle will give some instant relief, however the fibromyositis then starts to affect the neighbouring muscles and the dogs generally are back to square 1 within 3-4 months.

Prognosis - This does not appear to be a painful condition in of itself, however movement of the hindquarter becomes progressively more restricted and the hindquarters pulled downwards, creating more wear and tear along the back and a shifting of the weight forwards in order to balance better when walking. Rate of degeneration is variable, some dogs progress very rapidly within a 6 month period, others (less commonly) may slowly progress over several years. Average length of time with reasonable movement 12-18 months.

This condition is not considered genetic in origin, but again, some abnormality of the immune system creating the abnormal change within this affected muscle group. The numbers seen with this condition are very small, usually only a handful of affected GSD’s every year in Australia (when they are picked up!).

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SKIN

The GSD has a very impressive list of skin conditions that can affect it as a breed.

COLLAGEN DISORDERS OF THE FOOTPADS

Collagen Disorders of the Footpads - Thought to be inherited, it is an ulcerative disorder of the pads, which generally regresses spontaneously by 12 months of age. However, affected animals usually die of renal amyloidosis later in life. [This condition has to my knowledge never been reported in Australia].

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DEEP STAPH PYODERMA

Deep Staph Pyoderma (Furunculosis/Folliculitis/Cellulitis) - Seen almost exclusively in middle aged GSD’s, usually over 5-6 years of age, with probably a slightly higher incidence being seen in females. Most cases have a pattern of frequent relapses and the condition is thought to have an immunological basis.

Symptoms - Often with a history pattern of intense puritis prior to condition breaking out. Areas affected rump, back, flanks and thighs in a bilaterally symmetrical pattern. Some individuals have more extensive lesions affecting the chest and neck. The head, ears and front legs are rarely involved.

Causes - The condition is thought to have an immunological basis. Bacterial hypersensitivity, genetic predisposing factors, immune deficiencies and hypothyroidism have all been considered as precipitating or complicating factors.

Treatment - Consists of periodic courses of antibiotics, and ongoing use of low doses of cortisone 2-3 times weekly. Numbers of these cases are low, but due to the severity of the infections that occasionally build up, these dogs require constant care and ongoing medication. Treated carefully, these dogs can be kept comfortable over 4-6 years, but will not cure, and gradually over time may get more severely affected. Severely affected dogs, if not treated adequately, should be euthanased.

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ACANTHOSIS NIGRICANS

Acanthosis Nigricans - Often this condition is associated with a hypothyroidism. It is considered to be secondary to endocrinopathies (including hypothyroidism, sex hormone “imbalances” etc) and hypersensitivities (chronic reactions, atrophies, etc; ie. arising from auto-immune deficiencies or hyper-sensitivities).

Age - Can start as early as 12-18 months of age, average age of onset around 3-4 years of age, gradually getting worse with age and in the hotter humid months.

Symptoms - Characterised by auxiliary hyperpigmentation, thickening of the skin, sebhorrea of the auxiliary skin areas and of the ears, and hair loss in a bilateral symmetrical pattern. Earliest signs are hyper-pigmentation of the auxiliary areas followed by thickening of the skin and increasing sebhorrea (greasy, rancid skin).

These dogs again would have to be considered as having an immune system problem. These dogs are not that uncommon and most surgeries that seen reasonable numbers of GSD’s would have around 10 cases ongoing at any one time.

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HYPOTHYROID

Hypothyroid - Not a high incidence within the GSD breed, but as with all chronic conditions affecting large areas of the body or involving several body systems, eg. acanthosis, then it should be considered as a possible underlying factor. Equally true (chicken and the egg problem), is that the thyroid levels can be lower in any chronic debilitating condition. Rarely seen under 2-3 years in the GSD.

Symptoms - Include thinning of the coat, poor top coat, excess weight and sluggish disposition with no change in diet/amounts fed, poor reproductive history (often where initial history was very good).

Diagnosis - Test T4 levels, dogs showing symptoms and below or on the lower end of the normal range should be supplemented to see the affect, if needs be, re test levels 6 weeks later.

Treatment - Usually use drugs such as Oroxine, dosages in dogs is generally much higher than in humans due to lower absorption of the drug from the intestine. Can be associated with Acanthosis Nigricans.

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DYSCOID LUPUS ERYTHEMATOSIS

Dyscoid Lupus Erythematosis - Cutaneous (of the skin), this is an immune system problem, where the exposed skin is over sensitive, particularly to the summer sun.

Breeds - Predisposed breeds include the GSD, Collie, Sheltie, Siberian Husky and Malamute.

Age - Onset varies, but usually the cases seen are over 3-4 years of age.

Symptoms - Signs initially are depigmentation of nose and lips, this progresses to ulceration, tissue loss and scaring. Ears, eye rims, feet and genitalia may also be affected. Exposure to ultraviolet radiation will acerbate the condition. In the GSD it is primarily to nasal area that is affected.

Treatment - With suitable creams (zinc, sun block) and cortisone orally. This condition is largely controllable. Excessive exposure to summer sun should be avoided. This is an immune system problem. Numbers seen are very small proportionally.

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NASAL KERATITIS

Nasal Keratitis - Refer to Dyscoid Lupus Erythematosis above.

PEMPHIGUS

Pemphigus - Again an immune system problem of the skin.

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SYSTEMIC

Aspergilosis - Nasal, bone condition.

Systemic Lupus Erythematosus

Sebhorrea

Deep Staph Dermatitis - cellulitis (folliculitis, furunculosis).

Calcinosis Circumscripta

PERIANAL FISTULA (ANAL FURUNCULOSIS)

Perianal Fistula (Anal Furunculosis) - Anal skin condition probably of an auto-immune basis.

Breeds - Seen in the predominantly in the GSD and less commonly, the Irish Setter. Generally seen in the older dog (over 5-6 years) but can be as young as 2 years of age. Intact dogs have a higher prevalence. GSD’s have a high density of sweat glands around the edge of the rectum.

Causes - Many have been proposed. Thought to have an auto-immune basis - there is a high incidence of ongoing diarrhea in affected dogs, such cases have been identified as having chronic colitis. Combined with the broad based and low set tail, there is a reduced aeration of the anal area. Chronic diarrhea may contribute by increasing soiling of the anal area. Additionally, infections of the anal glands are thought to be a contributing factor.

Symptoms - Often detected when the dog show pain on defecation, excessive licking in the anal area, painful tail movements etc. Symptoms can vary with the severity of the condition. Small ulcerations appear which when examined penetrate quite deeply into the tissue behind. Over time these sinuses become deeper and more extensive.

Treatment - Can be either extensive antibiotic therapy, more recently with cyclosporins and/or surgery. Re-occurrence is very common. Good local hygiene with trimming of the hair at the base of the tail and on either side of the rectum (creating a ‘breezeway effect’), can be very beneficial in long term controlling the condition. Removal of the anal glands where the sinuses are