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General Information
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. Primary immunodeficiencies involving the cell-mediated, humeral, complement and phagocytic systems have all been described in veterinary literature. Defects involving the humeral immune response are associated with a high susceptibility to bacterial infection. Defects involving the cell-mediated immune response are associated with a high susceptibility to viral, fungal and protozoal infections. Defects in the phagocytic or complement system are associated with disseminated infection. 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 Ig A deficiency is the most common primary
immunodeficiency in man (approx. 1 in 600). Ig A Immunological
Disorders in the GSD 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. Primary immunodeficiencies involving the cell-mediated, humoral, complement and phagocytic systems have all been described in veterinary literature. Defects involving the humoral immune response are associated with a high susceptibility to bacterial infection. Defects involving the cell-mediated immune response are associated with a high susceptibility to viral, fungal and protozoal infections. Defects in the phagocytic or complement system are associated with disseminated infection. 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. Ig A dysfunction – a primary Ig A dysfunction has been described in the GSD and is probably at the root cause of many GSD specific immunological disorders. Aspergillosis in the GSD has been related directly to the Ig A dysfunction and has an almost 100% death rate. Other disorders seen in the GSD associated with a compromised immune system (usually involving Ig A) includes the following:-
Degenerative Myelitis – while not considered to be related to Ig A problems, was initially thought to have an immune-mediated basis. However, there have been few studies of the pathogenesis. The exact precipitating causes of the progressive demyelination and axonal degeneration is still poorly understood. There has been a DNA test developed to identify those that are “carrying” the problem, however, not all affected dogs develop the condition. Other triggering factors that are yet to be determined are postulated at this stage. Current Understanding of Ig A problems in the GSD. Ig A is primarily involved in mucous surfaces and skin/mucous surface junctions. This means the major areas involved are the skin, gut, eye and nose. Current understanding of the Ig A problem show this as a very complex problem with no simple answer at this stage:- 1. Measurements of Ig A levels show a wide variation of serum Ig A levels in normal GSD’S. 2. Reduced Ig A levels shown in tears and faeces of normal GSD but this can vary between studies. 3. Ig A serum levels do not appear to reflect mucosal Ig A secretion in the GSD, despite normal to increased Ig A plasma cell numbers in the lining of the gut. 4. It appears that GSD’s may have a “block” in the transportation of Ig A across the intestinal wall into the gut (and possibly other surfaces). Some of the current research involves 2 molecules that transport the Ig A from outside to inside the gut lumen. 5. It has recently been found that dogs can express at least 4 allotypes of Ig A. Interestingly, all GSD‘s examined so far express just one of these allotypes (type C). This occurs in the Ig A heavy chain hinge region. This could explain or potentially influence the ability of Ig A molecules to bind antigens. (K Allenspach 2009). It is clear that the GSD is predisposed to a whole slew of immunological or autoimmune diseases, primarily at this stage resulting from a dysfunctional Ig A transport system. In the case of bacterial and fungal infectious diseases, it has been proposed that weak immunological defenses at the mucosal or cutaneous surfaces permits the infection to gain foot hold in the body. The normal regulation of the immune system must be defective to allow an inappropriate attack on self tissues. Most autoimmunity is now considered to have an infectious trigger. Both types of disease may be related to an inability of dogs of this breed to deal effectively with infectious agents. There is no simple immunodeficiency in dogs of this breed, and the overall function of the humeral, cell mediated and phagocytic arms of the immune system are generally considered normal. There may however be a defect in the mucosal Ig A production. Serum, tear and salivary Ig A concentrations are usually normal in GSD’s, however there is a failure to adequately translocate Ig A across the intestinal epithelial barrier into the gut lumen. Current studies are continuing to address the molecular mechanism that underlies this selective defect in mucosal immunity. The laboratory tools are now available to permit further advances in the identification of the gene mutations that may be responsible for defective immunity in this breed. (Michael Day 2003.) References : Michael J Day
“Chronic German Shepherd Dog Illness.” 2003. Dr. Karen Hedberg
BVSc
Increasing weight & rapid growth
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).
What Price a Normal Hip Introduction The following article is an attempt to cover the many and varied aspects of hip dysplasia; its definition, the factors affecting the severity of the signs seen, the treatment of HD as well as the control of HD by (a) various schemes and (b) the genetic aspects. This somewhat rambling account is an attempt to show that the control of HD by concerned breeders is both difficult and complex. Additionally, the general public is being increasingly told that a “normal” hip is the only one acceptable, and anything above that may require surgical intervention. As both a breeder and a veterinarian, we need to look at this problem from all angles and present to the general public a more realistic view of the condition, not only for ourselves, but for all breeds where clubs are trying to lower the severity of the HD problem. As the general public is becoming far more litigious in these matters it behoves us to present a rational approach with realistic goals. 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. Bone Diseases in Dogs – the consequences of increasing weight and rapid growth. General Discussion 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).
Hip Dysplasia – its definition and structural components. 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), Where the socket is very shallow, the ligaments very loose and the femoral head either very steep in the neck or the head very small, these combination of factors lead to instability of the joint. Around the edges of the joint is attached the joint capsule, which in turn is attached to the periosteum. When the edges of the joint capsule are constantly being pulled, the periosteum is lifted and new bone is laid down in an attempt to stabilize the joint. Pain from hip dysplasia is largely from wearing of the cartilagenous surface within the joint, exposing pain fibres in subchondral bone. There are two groups of animals affected :-
Examination for HD 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 anaesthesia 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. # 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 1. 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. 2. The older patient – again weight should be considered as too heavy in condition will acerbate wear all the joints, not just the hips. Again 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*. 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. Costs - Generally
both hips are done at once, cost is around $6000.
3. Total Hip Replacement – 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 orthopaedic specialist. This is usually not done much on breeds or individuals that weight less than 20 kg (very hard to get small enough prosthetics at this time). Costs - Cost per hip is $3000 and up. 4. Femoral Head and Neck Excision – limits bony 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. Genetic and Breed Control Aspects of HD Genetic Aspects Definition - Inherited - this is the genetic material that is passed on to the next generation(s) unchanged by - although the "expression of" may be altered by - the environment. Inherited generally refers to trait(s) exhibited by the individual that breeders are interested in. Occasionally it may be a breed fault that they do not want exhibited eg. incorrect coat colour or texture; but mostly breeders are interested in maintaining particular virtues, and at the same time, removing the undesirable faults. Where a condition is affected by more than 3 genes, these are called polygenetic and are much harder to clear from the population as the effects are often a blend of the effects of the genes and the environment acting together. The more genes that are involved, the greater is the chance that the environmental factors will affect the end result. Environmental factors include diet, rate of weight gain, level of activity, stress factors etc. Breed Aspects in relation to Control Schemes Hip Dysplasia is a polygenetic condition, ie. many genes 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 condition 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. Population Means and Spread (of any measurable factor) Populations can be described by a bell curve which can apply to any feature you wish to look at, be it height through a breed, litter size, HD scores and so on. With this curve, the top of the curve is the mean of the population factor being assessed (eg. height) with the extremes at either end of the scale (eg. the shortest and tallest). Diagram of a Bell
(Normal) Curve
If in German Shepherds we apply this to height, and we have height limits on the breed; while we wish to breed strong, well boned dogs (who generally are on the large end of the scale), we have to fit (or attempt to fit) the vast majority of dogs under the limit, so the breeders will usually discard the tallest and the smallest, and generally work with the medium to large range of the population. This same principle can be applied to any genetic problem within a breed. If the incidence of a problem is small across the whole breed, eg. 5-10%, it can be fairly easy for breeders or clubs to say not to breed with affected animals. If, however, the problem has a variable expression and/or a complex means (polygenetic) of inheritance, this can affect virtually every member of a breed eg. Hip Dysplasia, to some degree. HD X-Ray Control Schemes 1. 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). 2. 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). 3. PENN Hip – dogs are anaesthetized and subjected to standard pressure, and 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 totalled 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, the 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. In other breeds the breed average may be much higher, the inheritance lower and the population spread much greater if one looks at the 75% of the population one wishes to keep, eg. the Golden Retriever, current breed average around 20, this mean has shifted very little despite hard work by breeders as well as breed improvement schemes LRL’s for hips, elbows and eyes. In this breed one would have to go to at least a score of 10 per hip if not slightly higher in order to retain sufficient breeding stock across the board. # If the breed average is above 20, efforts should be made to select and breed from stock under 20, as scores over 20 will generally result in significant arthritic changes over time (ie. as the dog ages). Where superior individuals have scores significantly higher, great care should be used if breeding from these animals, ideally using partners will very low scores and preferably where these partners have themselves already produced low scoring stock. 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. In the 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. Expectations of a Normal Hip What is Normal – Normal Grade or Normal/Average for that Breed.
Normal hips are technically a 0/0, going up to around a maximum of 2-3 per hips.
Discussion Technically by defining a normal hip score or grade, makes any higher score or grade dysplastic. However, an 8/8 hip for GSD is within the normal range of the Australian breed average, just as a 10/10 score can be “normal/average” for a Golden Retriever. We are often being penalized for breeding puppies that score or grade above the normal grade, rarely is the breed average for that breed considered. Legally we need to have a better definition of either what are normal hips, or better define what is considered as soundness for breeding purposes within that breed. Age factors - On looseness of ligamentation, just because a dog is loose at 6 months, but otherwise has good joint anatomy (deep sockets, good femoral heads and necks), it does not necessarily mean that the dog will be grossly dysplastic by either 12 months or even by middle age. If a dog hips are within a normal range or even slightly above average for that breed, and there are no signs of lameness, should one interfere just because we can? Because of that looseness, younger and younger dogs (puppies) are routinely being considered for surgery. Older dogs are similarly being targeted for hip operations even where changes are minimal. Often these dogs on further examination have either back (spondylitis) or other conditions present and have been often “diagnosed” by breed alone. Conclusion In conclusion, with increasing owner reliance on litigation, we as breeders (and the Kennel Controls) need to develop a broader definition of normal in regard to breeding stock. Is it within the normal breed average, that breeding stock should be selected at or preferably below the breed average. Ideally sire statistics should be looked at more carefully as well as sibling results. Broader expectations should be given to the public explaining while we as breeders can try as hard as possible to breed “normal” hips (and elbows), we can occasionally turn up bad results due to the polygenetic basis of the conditions we are looking at. Similarly it would be most prudent that breed clubs develop normal weight ranges for the differing sexes at various ages, that can be handed out, so that novices (owners, breeders and veterinarians alike) can be what is normal rate of weight gain for that breed, sex and age. Large variations in weight above normal are likely to exaggerate any inherited abnormalities of structure, particularly looseness of ligamentation. 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 - The part of the elbow involved 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. The 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. 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. There is no known hereditary component, and affected animal can be used for breeding. Hypertropic Osteodystrophy Hypertropic Osteodystrophy (HOD) - Inflammatory disease affecting the ends of the long bones in fast growing puppies of large, rapidly growing breeds. 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. 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. 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 Chondrodysplasia in GSD’s Dr Karen Hedberg BVSc, - 2003
Chondrodysplasia has appeared sporadically within the GSD population in the past and doubtless will do so again. It is not a new condition, nor specific to Australia - cases were seen and noted some 20 years ago and sporadically occur over the years. A quote from Willis in 1977 states :-
Chondrodysplasia can occur in many breeds, often on a sporadic nature. Some breeds have deliberately been selected for chondrodysplasia eg. the Dachshund, the Basset, etc. Chondrodysplasia can cause minor to severe shortening of the long bones. This again can vary between breeds. In the Alaskan Malamute, the chondrodysplastic “dwarfs” seen are as a result of a very breed specific anaemia with early death of red blood cells, creating a unique blood picture that can actually be tested. As far as we can find out, chondrodysplasia where it appears, is considered to be an autosomal recessive condition in most breeds - however, this too can vary - as stated in an article on the Havanese breed. Chondrodysplastic breeds eg. the Basset, the Dachshund or the Corgi breeds, which are chondrodysplasic by design, generally lead normal lives with minimal health problems. Current Situation in Australia : In the last 12-15 months there have been 7 confirmed cases of Chondrodysplasia in the GSD. What we are seeing is the 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 are very short in all 4 limbs with no intermediate cases, ie.varying lengths of foreleg. All but 1 of these cases have been sired by the same dog, but one should stress that there have been some 500 puppies born from this sire as of December 2003, and obviously the vast majority are normal, healthy puppies. The interesting case to note is the other puppy - the gene/condition is obviously floating around in the breed. Bitch lines of the affected litters vary considerably with numerous ¾ and sibling (to the dam) matings having normal litters. There is a reported unconfirmed case that has occurred in New Zealand – confirmation of this and pedigree information is currently being sought.
Possible Genetics : The hardest aspect about this condition is sorting out the probable genetics. What we need at the moment is input and information. The only thing in common with both the sires and the dams of affected litters is that they trace back in tail female line to various English lines on both sides. The odd case out, similarly traces to English lines via New Zealand lines. I would add however, the majority of these lines have been with us for many generations and often been linebred without producing any known problems in this area. At the moment, we have no definable pattern or pedigree information, sufficient to determine the exact nature of the genetic basis of this condition in the GSD. With regards to keeping puppies from a litter that has an affected puppy, a similar problem arose related to the pituitary dwarfs - people kept and bred from litter mates to pituitary dwarfs - yet we see/hear about remarkably few dwarfs, when by rights we should be overrun with them. Even if this is an autosomal recessive condition, as has been recorded in several breeds, technically one should see ¼ affected : ¼ carriers : ½ normals, yet we are seeing half of that in the affected litters. In each affected litter, only one puppy was affected. The Current Advice we would give is :
Current Areas Under Investigation :
Summary : Chondrodysplasia is readily diagnosed before 8-10 weeks of age. Affected animals can be removed from the breeding programs. The incidence should be noted, pedigree information forwarded to the GSDCA Hereditary Diseases Committee as soon as possible and we will continue to try to find a genetic pattern to these affected puppies, but it should at the same time be kept in perspective ! Had these puppies been pituitary dwarfs, from the number of affected cases to the total number of puppies, no one would have cared in the slightest, we may have noted the fact and kept going. However, because it appears as a "new" condition, great confusion and a degree of hysteria is being generated. GSDCA HDC Contact : Dr. Karen
Hedberg BVSc, GSDCA Hereditary Diseases Chairperson. References - additional information from :- 1. Genetics of the Dog - Hutt (1979) :- Extract, quote :-
2. Hereditary Bone and Joint Diseases in the Dog - JP Morgan et al (2000) :- Discusses many of the sub groups of elbow dysplasia - including the one discussed below listed as ‘elbow sub-luxation associated with chondrodysplasia occurring occasionally as a unique trait in a non-chondrodysplastic breed (discussing the radiographic findings on a chondrodysplastic Dobermann puppy 15 weeks old), quote :-
Article above issued by the GSDCA Hereditary Diseases Committee (HDC) - 18 December 2003. ----------------------------------------- Update Chondrodysplasia Update – the possible Genetics - 12.2.04 Dr Karen Hedberg BVSc, - 2004 The genetics of the cluster of chondrodysplasia cases that GSDCA has recorded in Australia are such that in the 6 cases from the one sire, Aimsway Abacus; there have been no consistent bloodline connections to support a standard simple recessive pattern of inheritance. Analysis of all the cases concerned and of the pedigrees of all the bitches that have gone to the dog, show that there is enough doubling up of all our major bloodlines, as well as close siblings being put to the dog, such that had this been a case of a simple recessive gene pattern, the number of cases seen would be far higher ie. approaching 25% in litters from "carrier" bitches. There have been a number of full litter sisters (3), and a mother to the 3 bitches all used to this dog, with only one bitch throwing one affected puppy. There are several cases of ¾ litter sisters being used, again one affected puppy in one litter. The bloodlines of the dams of the litters are those predominantly the major lines that have been heavily used and doubled up on across Australia, with no previous history of cases of chondrodysplasia occurring with any such line breedings. This again supports the theory that it is not a simple recessive pattern of inheritance. When the genetics do not match up within the number of cases seen on a per litter basis nor with any consistent pedigree data, then one then must look at the picture from the total progeny produced ie. 6 cases from 500 odd puppies, around 1.25% affected progeny to 98.75% normal progeny. With input from Danielle La Grave a highly respected genetic counsellor and German Shepherd enthusiast in the USA, she comments :-
In Ms LaGrave’s opinion :
The input from Ms LaGrave is invaluable and fits the population genetics seen. What this translates to in real terms is that if this theory is correct, then :-
In order to test this pattern of inheritance, to prove this conclusively, we propose that 2 test breedings be undertaken. The first litter would be from an affected dog to a normal unrelated bitch – where 50% of the progeny should be affected and 50% normal even one affected puppy from this mating would give strong evidence that this disorder is not a recessive; the second litter would be an affected dog to an affected bitch (if possible) – if this is a recessive condition then 100% of the progeny should be affected. Even one unaffected puppy would prove that this is not a recessive. The GSDCA is continuing to investigate the problem and have been fortunate in getting the interest of Dr. Mark Neff, a researcher at UC Davis School of Veterinary Medicine, who is an expert on dwarfism in the dog. Dr Neff’s reply as of 12.2.04 is :
With Dr Neff’s input, this problem maybe completely resolved in the fairly short term. The HDC will be sending material out to various vets once we sort out which dogs are required. This would be of great help to us in understanding all aspects of the genetics involved. Aimsway Abacus is producing above average progeny in type and quality, with excellent hip and elbow results to date. In light of the above information, the dog can be used at stud in relation to this condition, taking into account the 1% risk of an affected puppy. Until such time as the genetic pattern of inheritance can be confirmed, it is suggested that there be no close linebreeding to the dog or his close relatives. The dog’s name was withheld until such time as the genetics of the situation could be looked into, as if it had been a recessive condition, then the dams of the affected litters would automatically have to have been carriers and equally should have been named. I would sincerely like to thank both the breeders of Aimsway Abacus , John and Lee Marten, and his co-owners Kay and Alan Doyle for their unfailing support and assistance with the many pedigrees in researching this problem. Summary It is most important to keep this issue in perspective – the problem of Pituitary Dwarfism which first arose in the late 70’s created equal furore at the time with letters backwards and forwards. This condition is supposed to be a simple recessive disorder, yet the numbers seen are far lower than expected and would possibly indicate a slightly different pattern from that which is commonly accepted. Such notable dogs as Uran Wildsteiger Land, Ingo Hafenlorhtal, Prima Zorba and Masuta Piaute all threw dwarfs. No one removed their breed survey status, nor was there any suggestion that these dogs be forcibly removed from public stud. Chondrodysplasia is readily diagnosed before 8 weeks of age. Affected animals can be removed from the breeding programs. The incidence should be noted, diagnostic X rays and/or photos, pedigree and complete litter information forwarded to the GSDCA Hereditary Diseases Committee as soon as possible. It is most important that the data is correctly reported and recorded, such that the correct diagnosis is made in each case. Dr. Karen Hedberg BVSc
Fibromyositis of the Gracillus Muscle
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. 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!).
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.
Epilepsy
Epilepsy Epilepsy - Exact mode of inheritance not fully understood. Age first seen - 5-6 months to 5 years; average 6 months to 3 years. Tail Chasing Tail Chasing - This has been linked with both behavioral abnormalities and with epilepsy. ? if an inherited condition. *As a general comment, I have found both epileptics and tail chasers to be very “hyper” (or over the top) dogs. 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. Gun Test James Rodger (Victoria), GSDCA Breed Surveyor and Specialist Judge. Introduction Due to the many misconceptions and misunderstandings of a large number of German Shepherd Dog enthusiasts, (both old and new), as to the actual purpose and requirements of the guntest, it was thought that a short article would be helpful to address this situation. It is my view that due to the demanding requirements of a working dog, the gun test is a critical part of the evaluation of a dog’s temperament and therefore a firm reaction to the gun is required, rather than the current requirement survey rule of being only “sufficiently firm” for the Class I classification. (Note: This matter was discussed at the NBC meeting in July 2001, where it was decided to put the above on the agenda for the forthcoming AGM in February 2002.) Whilst I do not believe that a major problem exists in this country with regard to gunshy dogs, however we must never allow a problem to arise. The gun test is a vital test for working dogs, as illustrated by the following example. A number of years ago whilst talking to Herr Erich Orschler about the gun test and interpreting a dog’s reaction, he told the following true story as to the importance of working dogs being gun sure. The West German Police Training School, as part of their introduction tests for new dogs, was to walk them through various parts of the city to observe and assess their reactions to various situations, noises, people, other dogs and animals, etc before their actual training commenced. On this occasion a handler was walking with a “new dog” along a busy canal when suddenly they were confronted by armed assailants and a revolver was discharged several times. The dog took fright and reacted by running round and round the handler thus entangling his legs with the lead, which in turn resulted in the handler overbalancing and falling to the ground, whereupon his head struck a rock and he was killed instantly. Thus, my earlier view was confirmed, that all working dogs should have a firm reaction to the gun test. Background Current ANKC Standard Quotes: (1)
Old WUSV Standard Quotes: (2)
The Biology of the Ear Hearing is accomplished by pressures. Everyone knows what a dog’s ear looks like and the hole, which it surrounds, which leads into the head. All the delicate mechanism of hearing is embedded in the heavy bone at the base of the skull. Technically the outer ear, which we see, is the auricle. In natural dogs with erect ears, these cone-shaped organs can be moved to better collect the sound waves and conduct them down into the cavity where these vibrate against the eardrum. This is a membrane (the tympanic) which lies across the end of the auditory opening and is very thin and delicate. It has no vibrations of its own and is able to pick up vibrations of a variety of lengths and intensities. Behind the ear drum, there is a small cave (tympanic cavity), a tube (the Eustachian) drains it from its lowest part down to the throat of the dog and allows air to enter to insure equal pressure on both sides of the ear drum. Within the tiny cave, there is a most ingenious arrangement of delicate bones – the mallet (malleus), the anvil (incus) and the stirrup (stapes). The mallet is attached to the ear drum while its body attaches to the body of the anvil. This bone in turn attaches by its other end to the stirrup, the flattened area of which fills the end of a crooked tube called the cochlea. While these three small bones undoubtedly make hearing more acute, a dog can hear fairly well without them, as was shown by a student who surgically removed them from a dog who was still able to hear after the operation. Intense sound can destroy the end organ of hearing, the sensory part of the cochlear duct, called the Organ of Corti. Changes which are permanent can be produced by certain sound frequencies of considerable duration. This is nowhere nearly as severe as a loud blast, which may deafen by rupturing the ear drum and is of an entirely different nature. In the matter of hearing, dogs and human beings live in the same world, but a times quite different tones. By that, I mean that the dog can hear everything we can hear, but a lot more too. He can hear fainter sounds coming from a somewhat greater distance. But he really puts us to shame when it comes to hearing notes of a higher pitch – higher on the musical scale, for example, the stereo system. In the same way, dogs can hear cycles far up the scale. A man’s hearing capacity begins at about twenty and stops at about 20,000 cycles per second. Dog’s start at about twenty but go up above 30,000 and some experimenters claim as high as from to 35,000 to 70,000. (Cats hear up to 50,000.) Besides the cycles, we must consider pitch. This is the quality of sound that depends on the rapidity of the vibrations. We hear best at about 2,000 vibrations per second, a dog hears best at about 4,000. Dogs respond to sounds to which we are deaf, because of the higher pitch. (3) Current Requirements of the GSDCA Breed Survey Manual Para 7.6 Gun Test
Para 11.4.4 Gun Test
Appendices & Forms Working Dog Requirements :
Scale of Reaction to the
Gun Test :
A gun sure dog normally reacts to the gun shot by standing in one spot and either, being alerted, or showing lack of interest. A gun shy dog adversely reacts to the gun shot by not standing in one spot and either, moves around, jumps up on the handler, walks around the handler, hyperventilates, moves closer to the ground, looks fearful and anxious, sits or cringes. If the dog moves, retest. The major assessment is stability to the discharge sound. The Assessment A careful observation of the dog’s immediate reaction to the rapid firing of two shots, will in the vast majority of cases, determine whether the dog’s reaction is “gunshot indifference”, being the desired reaction or not. Matters to be observed and subject to assessment by the surveyor are as follows, which is not as simple as it first seems (Note: Remember that the dog is standing away from its handler on a loose lead.) :
As the surveyor is approximately twelve paces away from the dogs being gun tested, he or she is in the best position to judge these matters, as opposed to someone being thirty or forty metres away. Yes, sometimes the assessment can be a little subjective, but that is where a surveyor’s experience, knowledge and powers of observation come into play. Remember that whilst a surveyor’s accountability and credibility are at stake, surveyors have absolutely no joy in failing a dog. Rather, it is a sick, empty and hollow feeling. Please remember that a surveyor has a serious job to do and is not there to be “popular”. Sometimes the reaction to the gun test is one of lack of conditioning and/or socialisation, which should not be confused with actual gun shyness. These dogs should be represented after suitable and careful conditioning to the gun. There are numerous scientific experiments, as well as practical experiences with the gun dog breeds, which support this statement. In reality, the major problem with gun shyness is a physiological one. That is, physically the eardrum cannot take the “pitch” of the sound and causes the dog great stress and discomfort and hence the dog wants to run away. The higher the pitch, the greater the problems. By way of interest, Germany uses 6mm gun whereas in some other countries they use 9mm which is not as severe. Remember that this dog may well have otherwise a generally sound temperament. Alternatively, the above dog may still be of a generally nervous disposition, as evidenced by its behaviour generally, as well as to the gun. Of course, gun shyness is highly inheritable. Therefore, we have to be very firm in assessing dogs on the gun test for suitability for breeding in our survey scheme. Obviously it is very upsetting to all to see a dog obviously in distress because of the gun test. Consequently it is a serious fault, similar to incorrect dentition, monorchidism, cryptorchidsm, coat, size, etc and therefore should be always kept in the forefront of breeders mind when selecting or keeping dogs for breeding. Finally, I trust that this article has assists in your understanding of the requirements of the gun test, as well as the actual physical assessment by the surveyor. Always remember that the purpose of the gun test for working dogs is “gunshot indifference”, "that is alert, but not skittish" – a quote obtained from the Walt Disney program on Guide Dogs in New Jersey. A nervous or aggressive reaction to the gun not only detracts, but also in many cases, destroys a dog’s ability to concentrate and work. References # : 1. Current GSD Breed
Standard (ANKC - FCI - WUSV). Degenerative Myelitis Degenerative Myelitis - 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. 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. 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.
Patent Ductus Arteriosis (PDA)
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. Affected dogs should not be used for breeding. Incidence in the GSD is low.
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.
Atrio-Ventricular Valve Dysplasia Atrio-ventricular Valve Dysplasia (AVD) - Mitral valve defect. Not as common as the other defects seen. Affected dogs should not be bred with.
Persistent Right Aortic Arch Persistent Right Aortic Arch - Discussed under mega-oesophagus (INTESTINAL GROUP) below.
Cardiomyopathy Cardiomyopathy - Affects older dogs, any age, most commonly seen over 5-6 years of age. For those that respond well to treatment, 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.
Congenital Mega-oesophagus
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 :
Mega-Oesophagus (Acquired) Mega-oesophagus - (Acquired) - This condition can develop in the older animal from a variety of reasons.
Canine Bloat Definition : Bloat or Gastric Dilation of the stomach is a condition of quite sudden onset and threat to life of an afflicted dog. Technically, this condition is known as Gastric Dilation - Volvulus (GDV). Causes : Relatively little information appears to be available on this subject. Until significant research is undertaken, it cannot be proven as to which factors determine bloat. Some non-scientific observations are :
Risk Factors : Any breed of dog may well be susceptible to bloat. Most cases have been reported in the larger breeds, including the German Shepherd Dog. There seems to be a very strong correlation between bloat and dogs with deep and narrow chests. Older or mature dogs, say over two years of age, have the greatest incidence of the condition, whereas in young dogs it rarely happens. Risk Reduction : In light of the lack of knowledge on bloat, the following points should be taken as the best suggestions to place your dog in the lowest risk category:
External Signs : Any of the following may be signs of bloat :
Internal Effects : The dog's stomach fills with gas, which may result in any one or more of the following :
Treatment : This must be administered immediately. To delay is critical. The longer there is delay, the chances for recovery or survival are diminished. Confirmation of bloat by veterinary diagnosis is needed. Bloat can be so quick, ruthless and complicated that emergency treatment by a veterinarian is essential. Contact your veterinarian to organise appropriate and instant attention at an adequately equipped surgery. Endeavour to keep your dog as calm and warm until treatment can be undertaken. Normally, the following emergency procedures are taken by the veterinary surgeon : 1. Decompression and
stabilisation: 2. Corrective and
preventative surgery: 3. Recovery treatment:
Rehabilitation : It is estimated that approximately half of the dogs that suffer bloat are able to make a relatively complete recovery from this severe condition. Given that the intensive post operative period of treatment has elapsed, a best suggestion for recuperation to normality is as follows :
Summary : Practise the outlined methods of risk reduction as prevention is better than the cure. Monitor for external signs of bloat in your dog on a regular basis. Seek veterinary assistance immediately if you suspect your dog may have bloat. Reference to future scientific studies is needed. References : Compiled from various sources by John Fenner - January 1997.
Portasystemic Shunts
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.
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.
Wheat (Gluten) Allergies
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 - 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. 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. 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).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. 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. Eosinophilic Enteritis Eosinophilic Enteritis - Inflammatory disease of the small intestine characterised by the infiltration of eosinophils. 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.
Pituitary Dwarfism Pituitary Dwarfism - Thought to be inherited as a simple autosomal recessive. 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.
Collagen Disorders of the Footpads
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]. 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. Severely affected dogs, if not treated adequately, should be euthanased.
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). 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.
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. Can be associated with Acanthosis Nigricans. Hypothyroidism - Thyroid Insufficiency Dr Don Barrett, BVSc. Consulting Veterinarian – February 1998. Background : Iodine is an absolute requirement for the production of two active hormones T3 and T4. The thyroid hormones have a marked general effect on most tissues. They stimulate metabolic rate, in the young and have a marked effect on growth and development. This applies particularly to the epiphysical growth plates of the skeleton. * How T3 and T4 work is still somewhat of a mystery. Hypothyroidism : In dogs hypothyroidism is mostly a disease of middle to old age and follows inflammatory destruction or idiopathic atrophy of the thyroid gland. Congenital and acquired disorders of the adenohypophysis occasionally produce secondary hypothyroidism in the dog through a total or partial deficiency of TSH. May lead to early death in puppies. Primary hypothyroidism - Usually adult dogs with 2 major pathological patterns: Progressive immunological destruction of follicles. The gland is atropied and contains many lymphocytes. Almost as common – atrophy of the gland with no evidence of inflammation, this is a so-called ideopathic thyroid atrophy and may be the result of end stage lymphocytic thyroiditic (a rare form of congenital hypothyroidism seen in Scottish Deerhounds) Secondary hypothyroidism - 5% only – follows congenital or acquired abnormalities in the pituitary gland (basically similar to primary hypothyroidism). The animal may exhibit abnormalities referable to deficiencies of other pituitary hormones such as ACTH, growth and gonadal hormones. Congenital secondary
hypothyroidism is seen in German Shepherd Dog dwarfs. Acquired secondary
hypothyroidism is almost always due to pituitary neoplasms.
Symptoms : Thyroid hormones maintain the basal metabolic rate within a very narrow range. Dogs with hypothyroidism are :
All of the above are due to change in the metabolic rate. Abnormalities of the skin and hair coat are more difficult to explain:
Clinical signs :
Treatment : a. L-thyroxine 20mg/kg
orally SID Response : Usually mental attitude improvement and activity after 10 days. D x T3,T4 assay Cholestoral 400/500mg/100ml References : Compiled from Lecture Notes by Dr Don Barrett, BVSc. Consulting Veterinarian – February 1998. 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. 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. Nasal Keratitis Nasal Keratitis - Refer to Dyscoid Lupus Erythematosis above. Pemphigus Pemphigus - Again an immune system problem of the skin.
Aspergilosis
Perianal Fistula (Anal Furunculosis) - Anal skin condition probably of an auto-immune basis.
Pannus (Chronic Superficial Keratitis)
Pannus (Chronic Superficial Keratitis) Pannus (Chronic Superficial Keratitis) - Affects the cornea of the eye resulting in the increasing deposition of black pigment across the cornea. This is considered to be an auto-immune disorder due to the type and chronic nature of the inflammatory response Plasmoma Plasmoma - Similar condition to pannus, affecting the conjunctiva and 3rd eyelids. Not seen very often, affecting GSD’s primarily. Incidence within the breed is less than 1%. Not necessarily seen in conjunction with pannus. The cornea in these cases is unaffected. This is considered to be an auto-immune disorder due to the type and chronic nature of the inflammatory response.
Otitis Externa Otitis Externa - Certain breeds have a higher incidence of external ear disease. The GSD has an adequate lumen size proportional to their ear canals, but it is offset by unusually heavy wax production that begins early in life. Unless ear infections are cleared up fairly quickly, they can rapidly become chronic. Humid conditions acerbate the condition, so if your dog is prone to these problems, increased care and attention is needed. *Where there is just inflammation of the inside edge of the outer ear (the Pinna) and the outer third of the ear canal with reddening, thickening, waxiness combining to result in increasing pigmentation (black) can be seen in association with hypothyroidism and acantosis nigricans. These dogs have associated skin conditions.
Haemangiosarcoma
Haemangiosarcoma Haemangiosarcoma - These are predominantly tumours of the spleen and/or of the liver, the majority of cases involve primarily the spleen in the earlier stages of the disease. Skin Haemangiosarcoma. Skin Haemangiosarcoma - Also called Malignant Haemangio-Endothelioma. Thought to have a genetic predisposition. May require aggressive surgical intervention and or chemotherapy. Very low incidence in the GSD.
Lymphosarcoma Lymphosarcoma - Affects all the lymph nodes of the body, most commonly first seen in the lymph nodes under the chin, at the corner of the jaw. Length of life expectance with conservative treatment can be as short as 6-12 weeks. The average is about 5-6 months. Decisions to euthanase are generally based on quality of life, mobility, etc. Definitions of Conditions, Disorders and Genetic Conditions 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.
Text References : Veterinary Paediatrics
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